Differentiation of ICUS, IDUS, CCUS and CHIP [8].
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These books synthesize perspectives of renowned scientists from the world’s most prestigious institutions - from Fukushima Renewable Energy Institute in Japan to Stanford University in the United States, including Columbia University (US), University of Sidney (AU), University of Miami (USA), Cardiff University (UK), and many others.
\\n\\nThis collaboration embodied the true essence of Open Access by simplifying the approach to OA publishing for Academic editors and authors who contributed their research and allowed the new research to be made available free and open to anyone anywhere in the world.
\\n\\nTo celebrate the 50 books published, we have gathered them at one location - just one click away, so that you can easily browse the subjects of your interest, download the content directly, share it or read online.
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IntechOpen and Knowledge Unlatched formed a partnership to support researchers working in engineering sciences by enabling an easier approach to publishing Open Access content. Using the Knowledge Unlatched crowdfunding model to raise the publishing costs through libraries around the world, Open Access Publishing Fee (OAPF) was not required from the authors.
\n\nInitially, the partnership supported engineering research, but it soon grew to include physical and life sciences, attracting more researchers to the advantages of Open Access publishing.
\n\n\n\nThese books synthesize perspectives of renowned scientists from the world’s most prestigious institutions - from Fukushima Renewable Energy Institute in Japan to Stanford University in the United States, including Columbia University (US), University of Sidney (AU), University of Miami (USA), Cardiff University (UK), and many others.
\n\nThis collaboration embodied the true essence of Open Access by simplifying the approach to OA publishing for Academic editors and authors who contributed their research and allowed the new research to be made available free and open to anyone anywhere in the world.
\n\nTo celebrate the 50 books published, we have gathered them at one location - just one click away, so that you can easily browse the subjects of your interest, download the content directly, share it or read online.
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This natural phenomenon is known as a tsunami event. By December 26, 2004, an event in the Indian Ocean, this word suddenly became known to the public. The effects were indeed disastrous and 227,898 people were killed. Tsunami events are a natural part of the Earth's geophysical system. There have been numerous events in the past and they will continue to be a threat to humanity; even more so today, when the coastal zone is occupied by so much more human activity and many more people. Therefore, tsunamis pose a very serious threat to humanity. The only way for us to face this threat is by increased knowledge so that we can meet future events by efficient warning systems and aid organizations. This book offers extensive and new information on tsunamis; their origin, history, effects, monitoring, hazards assessment and proposed handling with respect to precaution. Only through knowledge do we know how to behave in a wise manner. This book should be a well of tsunami knowledge for a long time, we hope.",isbn:null,printIsbn:"978-953-307-552-5",pdfIsbn:"978-953-51-4521-9",doi:"10.5772/573",price:159,priceEur:175,priceUsd:205,slug:"the-tsunami-threat-research-and-technology",numberOfPages:730,isOpenForSubmission:!1,isInWos:1,isInBkci:!0,hash:null,bookSignature:"Nils-Axel M?rner",publishedDate:"January 29th 2011",coverURL:"https://cdn.intechopen.com/books/images_new/41.jpg",numberOfDownloads:102594,numberOfWosCitations:36,numberOfCrossrefCitations:61,numberOfCrossrefCitationsByBook:2,numberOfDimensionsCitations:145,numberOfDimensionsCitationsByBook:3,hasAltmetrics:0,numberOfTotalCitations:242,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"April 28th 2010",dateEndSecondStepPublish:"May 26th 2010",dateEndThirdStepPublish:"September 30th 2010",dateEndFourthStepPublish:"October 30th 2010",dateEndFifthStepPublish:"December 29th 2010",currentStepOfPublishingProcess:5,indexedIn:"1,2,3,4,5,6,8",editedByType:"Edited by",kuFlag:!1,featuredMarkup:null,editors:[{id:"15619",title:"Dr.",name:"Nils-Axel",middleName:null,surname:"Morner",slug:"nils-axel-morner",fullName:"Nils-Axel Morner",profilePictureURL:"https://mts.intechopen.com/storage/users/15619/images/1648_n.jpg",biography:"Nils-Axel Mörner took his PhD in Quaternary Geology at Stockholm University in 1969. He was head of a personal institute at Stockholm University and the Swedish National Council on Paleogeophysics & Geodynamics (P&G) from 1991 up to his retirement in 2005. He has written hundreds of research papers and a number of books. He is a global traveller and has undertaken field studies in all continents. Several students have taken their doctoral degree at the P&G institute, which became an international centre for paleoseismics, neotectonics, paleomagnetism and global sea level changes. He was president of the INQUA Neotectonics Commission (1981-1989) and president of the INQUA Commission on Sea Level Changes and Coastal Dynamics (1999-2003). From 1996 he has been deeply engaged in paleotsunami research in Sweden and the Maldives. 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\r\n\tWith this rapid transformation of the computing and communication world, information-system security has moved from a largely self-contained bounded environment interacting with a generally known and disciplined user community to a worldwide scope with a body of users that may not be known and are not necessarily trusted. Importantly, security control now must deal with circumstances over which there is largely no control or expectation of avoiding their impact. Computer security, as it has evolved, shares a similarity with liability assurance: they each face a threat environment that is known in a very general way and can face attacks over a broad spectrum of sources. However, the exact details or even time or certainty of an attack are unknown until an incident occurs.
\r\n\tThe purpose of this book is to discuss some of the critical security challenges in today’s computing world and to discuss mechanisms for defending against those attacks by using classical and modern approaches to cryptography and other security solutions. With this objective, the book invites contributions from researchers in the field of cryptography and its applications in network security. Some illustrative topics of interest (but not limited to) are cryptography algorithms, authentication, authorization, integrity, confidentiality, privacy, security in wireless networks, security in wireless local area networks, wireless sensor networks, wireless ad hoc networks, vehicular ad hoc networks, security and privacy in the Internet of Things. Privacy of information, Blockchains, and Machine Learning in Security are three additional topics that the book will also deal with.
Myelodysplastic syndromes (MDS) are clonal stem cell disorders with a relatively heterogeneous spectrum, characterized by morphological dysplasia in hematopoietic cells and by bone marrow failure and varying degrees of peripheral blood cytopenias. MDS have been recognized for more than 70 years and named refractory anemia, oligoblastic leukemia and smoldering acute leukemia.
\nThe risks of MDS include infection, anemia, bleeding and transformation to acute myeloblastic leukemia (AML) in approximately 30% of cases. MDS incidence increased from less than 5/100,000 for patients less than 60 years to 36.2 per 100,000 in patients more than 80 year old and more common among men.
\nIn the last 20 years, different MDS classification and prognostic scoring systems have been proposed [1]. French-American-British (FAB) classification was recommended in early and as modified by the World Health Organization (WHO). The WHO classification system uses percentages of blasts in bone marrow, ring sideroblasts and dysplastic changes to differentiate MDS subtypes. The International Prognostic Scoring System (IPSS) is based on a multivariate to evaluate the prognosis. The updated and recent scoring system combine with WHO classification for identification transfusion need was modified by Malcovati and co-workers, the so-called WPSS (World Prognostic Scoring System). This score suggests that patients with unilineage erythroid dysplasia do not need transfusion [2].
\nThe risk of MDS increased with advancing age; approximately 86% of patients with newly diagnosed MDS predominate in the elderly, with a median age at diagnosis 65 years [3]. The age of MDS patients at diagnosis was different according to residency; the results of some studies on patients show that the median age of diagnosis in German, Japan, and Korea were 74, 60, and 57 years, respectively [4].
\nThe chosen diagnostic criterion of MDS is the dysplasia in ≥10% of total count, this morphology features can point to underlying pathological cytogenetic changes which suggestive MDS diagnosis according to the World Health Organization (WHO) 2016 revision [5].
\nThe minimal prerequisites diagnostic guidelines for MDS according to an International Working Group (IWG) are: (1) stable cytopenia for >6 months unless accompanied a specific chromosomal analysis (Karyotype) or bilineage dysplasia [6]; (2) the exclusion of other potential disorders as a primary reason for dysplasia or cytopenia or both.
\nMDS diagnosis based on morphological characteristics of bone marrow dysplasia in patients with clinical manifestations evidence of hematopoiesis impairments by different combinations of anemia, leukopenia, neutropenia and thrombocytopenia. The National Comprehensive Cancer Network (NCCN) recommend specific guidelines for evaluation of MDS include physical examination; peripheral blood examination, bone marrow examination with iron stain and cytogenetic, RBC folate and vitamin B12 and serum ferritin [7]. The combination peripheral cytopenias despite of bone marrow hypercellularity is the hallmark of MDS, and is a consequence of bone marrow dysfunction with an increase apoptosis rate of bone marrow cells.
\nAccording to NCCN the diagnosis of MDS requires ≥1 of MDS-related criteria: (1) dysplasia (≥10% in ≥1 of bone marrow cell line); (2) presence of 5–19% blast cells; and (3) presence of a specific MDS-linked chromosomal abnormalities like del(5q), del(20q), +8, or −7/del(7q) [8].
\nBefore treatment, the major role is to distinguish MDS from other causes of cytopenia and dysplastic changes and from other clonal stem cell disorders [9]. The investigations work-up is important to rule the possible differential diagnosis and pre-MDS conditions (Table 1).
\n\n | Characteristics | \n
---|---|
IDUS | \nMild cytopenias for >6 months (Hb ≥ 11/dl, neutrophils ≥ 1500/μl, platelets ≥ 100,000/μl, all below lower limit of normal) or no cytopenias but marked dysplasia in >10% of cell lineages and no clonal cytogenetic/molecular markers | \n
ICUS | \nMild cytopenias (hemoglobin <11.0 g/dl, neutropenia <1500/μl and/or thrombocytopenia <100,000/μl and lack of significant dysplasia in the bone marrow but exclusion of other diseases and/or no clonal cytogenetic/molecular markers | \n
CCUS | \nHemoglobin, <11 g/dl, ANC <1500/μl, platelet count <100,000/μl, ≥10% dysplasia in the granulocytic, erythroid, or megakaryocytic lineage, myeloblasts comprise ≥5% of total cellularity. Common mutations; TET2, DNMT3A, ASXL1, SRSF2, TP53 | \n
CHIP | \nThe presence of clonal hematopoiesis in the absence of cytopenias and dysplastic changes. The incidence of CHIP increases with age. Common mutations; TET2, DNMT3A, ASXL1, PPM1D, JAK2, TP53, | \n
Differentiation of ICUS, IDUS, CCUS and CHIP [8].
ICUS, idiopathic cytopenia of uncertain significance; ICUS, idiopathic dysplasia of unknown significance; CCUS, clonal cytopenia of undetermined significance; CHIP, clonal hematopoiesis of indeterminate potential.
An absence of mutation and unexplained cytopenias are criteria do not meet World Health Organization (WHO)-defined requirements for myelodysplastic syndrome.
Chronic liver diseases
Drug induced cytopenia
Excessive alcohol intake
Cytotoxic therapy
B12/folate deficiency
Autoimmune cytopenia
Anemia of chronic disorders
Parasitic manifestation (hypersplenism in malaria and leishmaniasis)
Human immunodeficiency virus infection (HIV)
Other stem cell disorder
Clinical presentation of MDS is nonspecific and varies considerably depending on subtypes and severity of cytopenias. This should include family history, tobacco, alcohol intake, pesticides, heavy metals, prior chemotherapy, irradiation, radioiodine, radioimmunotherapy, concomitant medication including “alternative medication”, infection, tendency for bleeding/bruising, and a complete physical examination including spleen size. Symptoms can include general weakness, pallor, shortness of breathing, bleeding manifestations; gum bleeding and petechiae.
\nComplete blood count (CBC) includes white blood cell count (WBC) with differential blood count including erythrocyte morphology, hemoglobin, platelet count, red blood cell indices, mean corpuscular volume (MCV), and reticulocyte count.
\nSerum tests of erythropoietin, protein electrophoresis, folic acid, cobalamin, iron, total iron binding capacity (TIBC), ferritin, lactate dehydrogenase (LDH), bilirubin, Coombs test, alanine aminotransferase (ALT) test, aspartate aminotransferase (AST), alkaline phosphatase, albumin, uric acid, creatinine (S-immunoglobulins), B2 microglobulin and thyroid function tests.
\nAlso some investigations are mandatory to exclude viral infection especially; anti-HIV, anti-Parvovirus B19 (hypoplastic MDS), hepatitis C antibody, hepatitis B surface antigen (HBsAg) and cytomegalovirus test (CMV) in transfusion dependent patients.
\nCytogenetic study for BCR-ABL and JAK2 (Janus kinase 2) are important for differential diagnosis of myeloproliferative disorders.
\nThe WHO recommendations for the definition of cytopenia are the same reported in the International Prognostic Scoring System (IPSS), when the hemoglobin less than 10 g/dl, the leukocyte count 3000/mm3, an absolute neutrophil less than 1800/mm3 and platelets less than 100,000/mm3. These thresholds have been a matter of debate, and as a result, any cytopenia should be differentiated from MDS in case of clear morphologic or the result of genetic features consistent with MDS [5, 6]. Anemia is represent in most patients, the mean corpuscular volume (MCV) is often increased and an increased erythrocyte distribution width (RDW) which the erythropoiesis disturbances. A dimorphic red blood cell (RBC) population (macrocytes and microcytes), anisocytosis, poikilocytosis, nucleated red blood cells, basophilic stippling and Howell-Jolly bodies are also indications that the erythrocyte has undergone abnormal development [10]. Peripheral blood may reveal very abnormal nuclei such as Pelger-Huet anomalies and hypo-or hypersegmentation and ring forms nuclei also occur in neutrophils are important morphological features in MDS/MPN peripheral blood when diagnosing and distinguishing MDS/MPN is important to understand the similarities and differences in pathologic mechanism from similar diseases (AML, infectious diseases and other causes of cytopenia). The platelet morphological changes include giant platelets and platelets hypogranulation or agranulation. Some platelets may possess large fused granules. Circulating micromegakaryocytes (dwarf cells), multiple small nuclei separated by strands of nuclear material, and large mononuclear cells with dysmorphic nuclear features have been described in peripheral blood from patients with MDS [11].
\nThe diagnosis of MDS requires a careful light microscopic examination of optimally stained peripheral blood and bone marrow smear and trephine biopsy sections with presence of 1% blast in peripheral blood, with <5% BM blasts and uni- or multilineage dysplasia is defined as unclassifiable MDS. Monocytic hyperplasia accounting for >10% of the white blood cells is a common finding in chronic myelomonocytic leukemia (CMML) and is a common finding in dysplastic marrows and can be dominant manifestation of the hematopoietic abnormality in CMML for months and years.
\nA diagnosis of MDS often requires repeated bone marrow aspiration/biopsy examinations a few weeks or months, or even years apart in order to firmly establish the diagnosis and to identify cases with rapid disease progression. Bone marrow morphology evaluation and dysplasia in blood and bone marrow follow guidelines in the WHO 2016 classification. A good quality diagnostic bone marrow analysis includes marrow aspirate May-Grunewald Giemsa (MGG)/equivalent and bone marrow iron stain and a bone marrow biopsy either decalcified/paraffin embedded or plastic embedded. Degree of fibrosis should be estimated. The cytochemistry staining should include iron staining, Peroxidase-Staining, in addition to hematoxylin-eosin/equivalent [12].
\nThe cell counting of bone marrow and blood smear should include at least 200 cells in blood smear, 500 cells in bone marrow and 25 megakaryocytes and at least 100 erythroblasts should be evaluated. An optimal staining of blood and marrow slides prepared from freshly drawn aspirates is important for evaluation of dysplasia (Table 2) [12, 13, 14, 15].
\nCell line | \nPeripheral blood | \nBone marrow | \n
---|---|---|
Erythroid | \nDimorphic; macrocytic; anisocytosis; polychromatic; hypochromasia, tear drop cells Pappenheimer bodies; basophilic stippling | \nErythroid hyperplasia; megaloblastic changes; dyserythropoiesis; multinuclearity, nuclear bridges, nuclear budding, atypical mitosis, ring sideroblasts | \n
Granulocytes | \nHypersegmented neutrophils; hypogranular or agranular neutrophils; pseudo-Pelger cells | \nShift to left, promyelocytes with absent or spares azurophilic granules; hypogranular myelocytes, metamyelocytes and neutrophils, Auer rods, pseudo-Pelger cells, nuclear anomalies | \n
Monocytes | \nMature monocytes | \nIncrease and morphological abnormalities of monocytes | \n
Megakaryocytes | \nThrombocytosis; giant platelets | \nIncrease or decrease; mononuclear megakaryocytes, micromegakaryocytes, hypersegmented megakaryocytes | \n
Blasts | \nFigure 2 | \n
The highly specific dysplastic changes in granulocytes of patients with MDS are hypoagranularity and nuclear abnormality of neutrophils in peripheral blood smear and positive on peroxidase reaction or Sudan black. The highly specific dysplastic changes in erythropoiesis are sideroblastic rings and megaloblastoid changes. The highly specific for dysmegakaryopoiesis are micromegakaryocytes.
Dysplastic changes are the most important diagnostic features of myelodysplastic syndrome. A marrow cell lineage is considered picture of MDS if >10% of cells are affected.
\nDyserythropoiesis is the presence of oval macrocytes and erythroblast may resemble megaloblasts that have nuclear-cytoplasmic maturation asynchrony, nuclear fragmentation, or cytoplasmic nuclear remnants. This pattern is referred to as megaloblastoid erythropoiesis [14, 15, 16]. A dimorphic red blood cell population, anisocytosis, poikilocytosis, nucleated red blood cells, Howell-Jolly bodies and basophilic stippling are indications that the erythrocyte has undergone abnormal development. The RBC with abnormally round nucleus may have lobes or buds, internuclear bridging, nuclear fragments and abnormal mitosis are occasionally present. Pathologic sideroblast may be identified when the marrow treated with Prussian blue stain (Figure 1) [14, 15].
\nMorphological abnormalities of myelodysplastic syndrome: Leishman stain. (I) Erythroid dysplastic changes; (A) megaloblastic changes, (B) cytoplasmic fraying, (C) internuclear bridging, (D) nuclear lobulation, (E) nuclear lobulation (F) karyorrhexis (II) granulocytic dysplastic changes; (G) hypogranulation band neutrophil, (H) pseudo-Pelger anomaly, (I) nucleus ring or doughnut shaped (III) megakaryocytic dysplastic changes; (J) hypersegmented, (k) micromegakaryocyte, (L) giant abnormal platelet.
The most striking abnormalities are hypogranulated neutrophils. The defect in granulation may be seen in myelocytes early in the course of disease. Very abnormal nuclei, such as Pelger-Huet anomalies and hypo- or hypergranulation, and ring shaped nuclei in neutrophils. Monocytic hyperplasia is a common finding in dysplastic marrows and can be the dominant manifestation of the hematopoietic abnormalities of CMML for months or years (Figure 1) [11]. Cytoplasmic changes may include uneven staining such as a dense ring of basophilia around the periphery with a clear unstained area around the nucleus [14, 15]. Occasionally there are Auer rods, either in circulating or BM blast cells, entails an unfavorable prognosis and this could lead to misclassification the disease in the AML. Myeloperoxidase and the study of specific immunophenotypic markers are helpful to differentiate between MDS and other types of AML [17].
\nThe common changes include giant platelets and abnormal platelet granulation, either hypogranulation or agranulation. Some platelets may possess large fused granules. Circulating micromegakaryocytes, multiple small nuclei separated by stands of nuclear material and large mononuclear cell with dysmorphic nuclear features have been described in peripheral blood of patients with MDS (Figure 1) [13, 14, 15].
\nFor significant dysplasia, dysplastic features should be present in at least 10% of the nucleated cells in the lineage in consideration.
\nMyeloblast cell should be differentiated from promyelocyte. The promyelocyte is larger than myeloblast and characterized by clear Golgi zone and azurophilic granulations. Myeloblast was defined in terms of several nuclear characteristics, including a high nuclear/cytoplasmic ratio, easily visible nucleoli and usually contain fine nuclear chromatin and viable nuclear shape. The International Working Group (IWGM) recommended that myeloblast in MDS should be classified as agranular or granular [12]. The agranular blast corresponds to the type I blast of the FAB classification. Type II have scanty granules [18] and type III blast with more than 20 fine azurophilic granules as defined by Goasguen et al. [13]. The nuclear characteristic of promyelocytes included an eccentric or central nucleus and intermediate or fine chromatin and azurophilic granulation (Figure 2) [12].
\nBlasts, promyelocytes, abnormal promyelocytes, modified of Mufti et al. [
The cytogenetic study of bone marrow aspirate has a major role in determining clonality in patients with MDS. Karyotyping should be done in all patients, at least 25 metaphases, whenever possible, and described according to International System recommendations. Chromosomal abnormalities are reported in more than 50% of patients with MDS by counting 25 metaphase cytogenetic analysis, but not by fluorescence in situ hybridization (FISH) or sequencing technologies. The technique by using FISH method may be helpful to detect monosomy 7 and to clarify complex aberrations. Screening FISH (5q−, −7, +8) from peripheral blood may be performed in patients of dry tap bone marrow and this may influence management of the patient [19]. Different cytogenetic abnormalities are considered MDS-defining [20]. The presence monosomy 5, 7, or 13; 5q, 7q and 13q deletions; i(17p) and t(17p); 11q deletion; 9q or 12p deletion or t(12p), idic (X)(q13) allows for the diagnosis of MDS even in the absence of dysplastic changes. Cytogenetic is strongly correlated with not only the calculation prognosis but also selection of the most effective therapy; thus, a complete BM karyotype remains the standard work up evaluation procedure of the patient with MDS according to IPSS-R (Table 3) [21, 22].
\nPrognostic category | \nChromosomal categories | \nMedian survival (months) | \n
---|---|---|
Very good | \nDel(11q), −Y | \n60 | \n
Good | \nNormal, del(5q), double aberrations including del(5q), del(12p), del (20q) | \n40.5 | \n
Intermediate | \nDel(7q), +8.i(17q), +19, any other | \n25.0 | \n
Poor | \nInv(3)/t(3q), −7, −7/7q, double aberrations including −7/7q−, complex karyotypes with 3 abnormalities | \n15.0 | \n
Very poor | \nComplex karyotypes with >3 abnormalities | \n5.7 | \n
IPSS-R, Revised International Prognostic Scoring System.
MDS prognosis is calculated by utilizing the International Prognostic Scoring System (IPSS) score, which includes cytogenetics analyzed categories, in addition to number of cytopenias and counting of blast percentage. The present of >3 chromosomal abnormalities indicate very poor prognosis.
The most important mutated genes for MDS prognostication involved in epigenetic regulation are acquired mutation have been detected in several genes: (
By flow cytometry and immunohistochemistry, immunophenotyping of the blast population can be useful for emerging pathological CD34 and or CD117 and myeloperoxidase (MPO) positive populations are suggestive of transformation.
\nAccording to WHO classification 2016, the best method for diagnosis of MDS is the percentages of blast cells in bone marrow. The immunophenotyping can be useful to study the expression of maturation and anomalies as marker of dysplasia of a particular lineage [26].
\nMultiple aberrant features (>3) in maturation patterns of erythroid and myeloid lineage are highly specific for MDS, but single aberrancies are not diagnostic [27]. The role of flow cytometry can be useful in the diagnostic work-up of MDS, and to detect minimal residual disease after treatment according to the European Leukemia Net (ELN) work package for flow cytometry [28]. For prognostic follow up, the increase expression of CD33, CD34, CD13, HLA-DR/human leukocyte antigen-DR and decreased reactivity for CD11b in the bone marrow have been associated with shorter survival and high risk of transformation to acute leukemia.
\nSeveral classifications have been developed to predict the transformation of MDS to acute myeloid leukemia (AML). In 1982, the FAB system, was introduced based on percentage of blasts and morphological features in blood and bone marrow, namely medullary and peripheral blast cell count, ringed sideroblasts, number of monocytes in peripheral blood, and Auer rods. According to this classification, patients are diagnosed with MDS when dysplastic changes in bone marrow are present and/or myeloblast cells are between 5 and 30% of all bone marrow cells. Five subgroups with significantly different prognoses were established: refractory anemia (RA) with blasts <5% in BM, refractory anemia with ringed sideroblasts (RARS) with blasts <5% and ring sideroblasts >15%, refractory anemia with excess of blasts between 5 and 20% (RAEB), RAEB in transformation to acute leukemia and blast cells ranged between 20 and 30% (RAEB-T) and chronic myelomonocytic leukemia characterized by increase of peripheral blood monocytes (CMML) (Table 4) [20, 29]. For more than 20 years this classification served as the standard for the evaluation of MDS [30]. Hypercellular MDS, and MDS with bone marrow fibrosis were not recognized by the FAB classification [31].
\nType | \nBlasts in blood | \nBlasts in bone marrow | \n
---|---|---|
1. Refractory anemia (RA) | \n<1% | \nBlasts <5%, ring sideroblastic <15% | \n
2. Refractory anemia with ring sideroblastic (RARS) | \n<1% | \nBlasts <5%, ring sideroblasts >15% | \n
3. Refractory anemia with excess of blast (RAEB) | \n<5% | \nBlasts 5–20% | \n
4. Refractory anemia with excess blast in transformation (RAEB-t) | \n<30% | \nBlasts 20–30% | \n
5. Chronic myelomonocytic leukemia (CMMoL) | \n<5% with increase monocytes | \nBlasts 0–20% | \n
AML | \n>30% | \n>30% | \n
Myelodysplastic syndrome (MDS) according to FAB classification [20].
Modified of Ref. [20].
CMML, chronic myelomonocytic leukemia blast cells <20% and monocytes ≥1000/μl); RA, refractory anemia <1% in PB and <5% blasts in BM; RAEB, RA with excess blasts in PB <5% and 5–20% blasts in BM; RAEB-t, RAEB with excess blasts in transformation between 20 and 30%; RARS, RA with ringed sideroblasts >15%.
The World Health Organization (WHO) classification of MDS revised in 1999 and redefine subtypes of MDS [32]. The definitions of refractory anemia (RA) and refractory anemia with ring sideroblastic (RARS) unchanged became more consistent and characterized by the presence of dysplastic morphology in the erythroid cell line. Refractory anemia with ring sideroblastic (RARS) is morphologically similar to
Refractory anemia with excess of blasts (RAEB) recognized by the World Health Organization (WHO) classification in all versions and remains unchanged but distinguishes between two categories of RAEB: RAEB-1 with 5–10% blast cells and RAEB-2 with 11–20% blasts in the bone marrow.
\nThe other new subgroups of MDS were incorporated: (1) refractory cytopenia with multilineage dysplasia (RC1Dys), is a frequent subtype of MDS, which is equivalent to RA or RARS in the FAB classification with the presence of dysplasia but lacking an increase in blast cells with no Auer rods or increase of monocytes;(2) del (5q) syndrome is a myelodysplastic disorder characterized by macrocytic anemia, dysplastic changes in the erythroid cell line only, thrombocytosis and increase of hypolobulated micromegakaryocyte; (3) MDS unclassifiable; myelodysplastic syndromes that do not meet criteria of a specific WHO entity.
\nRAEB-T and CMML subgroups were removed from the new MDS classification: RAEB-T, because of distinctive biologic features and similarities in treatment strategies with acute myeloid leukemia (AML), and CMML, because of having overlapping dysplastic and proliferative features and its close relation to myeloproliferative diseases [33].
\nIn 2001, the WHO proposed an alternative classification for MDS that was modified from the original French-American-British (FAB) definitions [18]. Since then, the WHO classification has been updated twice (2008 and 2016) (Table 5) [22, 33].
\n2008 WHO classification | \n2016 WHO classification | \n
---|---|
Refractory cytopenia with unilineage dysplasia (RCUD) encompassing refractory anemia (RA), refractory neutropenia (RN), and refractory thrombocytopenia (RT) | \nMDS with single lineage dysplasia (MDS-SLD) | \n
Refractory cytopenia with multilineage dysplasia (RCMD) | \nMDS with multilineage dysplasia (MDS-MLD) | \n
Refractory anemia with ringed sideroblasts (RARS) | \n|
\n | MDS-RS with single lineage dysplasia (MDS-RS-SLD) | \n
\n | MDS-RS with multilineage dysplasia (MDS-RS-MLD) | \n
Myelodysplastic syndrome associated with isolated del(5q) | \nMDS with isolated del(5q) | \n
\n | |
Refractory anemia with excess blasts-1 (RAEB-1) | \nMDS-EB-1 | \n
Refractory anemia with excess blasts-2 (RAEB-2) | \nMDS-EB-2 | \n
Myelodysplastic syndrome, unclassified (MDS-U) | \n|
\n | With 1% blood blasts | \n
\n | With single lineage dysplasia and pancytopenia | \n
\n | Based on defining cytogenetic abnormality | \n
Refractory cytopenia of childhood | \nRefractory cytopenia of childhood | \n
WHO, World Health Organization; MDS, myelodysplastic syndromes; RS, ring sideroblasts; RCUD, refractory cytopenia with unilineage dysplasia; RCMD, refractory cytopenia with multilineage dysplasia; MDS-MLD, MDS with multilineage dysplasia; MDS-SLD, MDS with single lineage dysplasia; MDS-EB, MDS with excess blasts; MDS-U, MSD, unclassifiable; RCC, refractory cytopenia of childhood.
The last edition of WHO classification guidelines identify 6 types of MDS: MDS with single lineage dysplasia (MDS-SLD); MDS with ring sideroblasts (MDS-RS); MDS with multilineage dysplasia; MDS with excess blasts (MDS-EB); MDS with isolated del(5q); and MDS unclassifiable (MDS-U). There is an additional provisional entity termed “refractory cytopenia of childhood.” MDS-SLD includes refractory anemia (unilineage erythroid dysplasia), refractory neutropenia (unilineage dysgranulopoiesis), and refractory thrombocytopenia (unilineage dysmegakaryocytopoiesis). The latter 2 were previously classified as MDS-U in 2001 but were reclassified in the 2008 update [34].
\nAccording to 2016 WHO classification guidelines identify MDS subtypes based on the results of blood and bone marrow test. The classification of 2016 WHO of MDS was according to factors that differ from those of the FAB system and defined by precise criteria including: (1) dysplastic changes (2) number of cytopenia in peripheral blood (3) percentage of sideroblastic rings (Table 6) [5].
\nSubtype | \nBlood | \nBone marrow | \n
---|---|---|
(1) MDS with single lineage dysplasia (MDS-SLD) | \nSingle of bicytopenia | \nDysplasia in ≥10 of one cell line, <5% blasts | \n
(2) MDS with ring sideroblasts (MDS-RS) | \nAnemia, no blasts | \n≥15% of erythroid precursors w/ring sideroblasts, or ≥5% of ring sideroblasts, <5% blasts | \n
(3) MDS with multilineage dysplasia (MDS-MLD) | \nCytopenia(s*), <1 or 109/l monocytes | \nDysplasia in ≥10 of cells in ≥2 hematopoietic lineages, ±15% ring sideroblasts, <5% blasts | \n
(4.1) MDS with excess blasts-1 (MDS-EB-1) | \nCytopenia(s), ≤2–4% blasts#, <1 × 109/l monocytes | \nUnilineage or multilineage dysplasia, 5–9% blasts, no Auer rods | \n
(4.2) MDS with excess blasts-2 (MDS-EB-2) | \nCytopenia(s), 5–19% blasts#, <1 × 109/l monocytes | \nUnilineage or multilineage dysplasia, 10–19% blasts, ±Auer rods | \n
(5) MDS with isolated del(5q) | \nAnemia, platelets normal or increased | \nUnilineage erythroid dysplasia, isolated del(5q), <5% blasts | \n
(6) MDS, unclassifiable (MDS-U) | \nCytopenia(s), +1% blasts on at least 2 occasions | \nUnilineage dysplasia or no dysplasia but characteristic MDS cytogenetics, <5% blasts | \n
(7) Refractory cytopenia of childhood | \nCytopenias, <2% blasts | \nDysplasia in 1–3 lineages, <5% blasts | \n
Cytopenias defined as: hemoglobin, 10 g/dl; absolute neutrophil count, 1800/mm3 and platelet count less than 100,000/mm3; S; bicytopenia may be observed in most cases of MDS.
Present of 5–9% myeloblast in BM and 2–4% myeloblasts in the blood, the diagnostic is MDS-EB-1 and 10–19% myeloblast in BM and 5–19% myeloblasts in the blood, the diagnostic is MDS-EB-2. Cases with pancytopenia with unilineage or absent dysplasia with 1% myeloblasts in the blood should be classified as MDS-U.
One dysplastic lineage with dysplasia in at least 10% of the early cells of 2 or 3 cell types (red blood cells, white blood cells, and/or megakaryocytes in the bone marrow. No Auer rodes blast cells less than 5% in BM and <1% in PB. Sideroblastic ring less than 15% in BM and <5% in PB.
\nMDS-RS previously named as refractory anemia with ring sideroblasts (RARS). In this type of MDS, there is increased sideroblastic rings of nucleated red blood and for diagnosis, ring sideroblasts seen in nucleated red blood cells or at least 5% if the cells also have high of
MDS-RS include 2 subtypes based on dysplastic bone marrow:
MDS-RS with single lineage dysplasia (MDS-RS-SLD): one dysplastic lineage, one or two PB cytopenia, sideroblastic rings >15% in BM or 5% in cases with SF3B1 mutation, blast cells <5% in BM and <1% in PB and no Auer rods.
MDS-RS with multilineage dysplasia (MDS-RS-MLD): dysplasia in more than one lineage, one to three PB cytopenias, sideroblastic ring in BM 15 and 5% if SF3B1 mutation is present. Blast cells in BM <5% and in PB <1% without Auer rods.
This type of MDS is not common. It rarely turns into AML, and the outcome for people with this type is generally better than for some other types of MDS.
\nDysplastic changes in two or three lineages and PB cytopenia in one to three lineages, sideroblastic ring in 15% in BM or 5% in cases with SF3B1 mutation, blast cell without Auer rods <5% in BM and <1% in PB.
\nIn this type of MDS, the blasts are present in the bone marrow and/or peripheral blood. Dysplastic changes present in one to three lineage and cytopenia in one to three lines. Sideroblastic ring not present.
\nThere are 2 types, based on how many of the cells in the bone marrow or blood are blasts:
“5q− syndrome” is a specific type of myelodysplastic syndrome (MDS). Is not common and it occurs most often in older women. It is characterized by missing part of chromosome number 5. The patient also has cytopenia in one or two blood cell lines with common manifestations including severe anemia, typical dysmegakaryopoiesis, frequent thrombocytosis and favorable outcome [5]. The median survival of patients with isolated 5q– syndrome of 9 years and they have good prognosis and rarely transform to develop AML [35].
\nThis type of MDS is uncommon. For MDS-U, the pathological findings in bone marrow more than in peripheral blood. We observe that, one or more cytopenias are a standard feature of MDS-U but other clinical features are variable. Dysplastic changes in bone marrow in less than 10% but typical cytogenetic abnormality was reported [5].
\nUsually hypocellular with similar picture of aplastic anemia. The mutations are less common than in adult MDS (24% of patients) and have a different profile NRAS/KRAS, SETBP1, ASXL1, RUNX1, BCOR/BCORL, PTPN.
\nChronic myelomonocytic leukemia (CMML) is a clonal hematopoietic stem cell disorder classified by the WHO as an overlapping feature of myelodysplastic syndromes and myeloproliferative neoplasms (MPN). It is characterized by peripheral blood monocytosis, dysplastic features in at least 1 hematopoietic cell line and increased risk of progression to AML [36].
\nThe disease annual incidence became stable at around 0.4 per 100,000 population in Western countries [37]. CMML is occurring in elderly patients whose median age at diagnosis is 71–75 years. The incidence of CMML was higher in men than in women whose origin remains unclear [37].
\nDiagnosis is based on the presence of sustained (>3 months) peripheral blood monocytosis (≥1 × 109/l; monocytes ≥10%), along with bone marrow dysplastic changes. Bone marrow and BCR-ABL are recommended to exclude acute leukemia and a classic myeloproliferative neoplasms. Atypical monocytes differ from promonocytes and monoblasts. They contain no nucleolus, exhibit swelling, abnormally folded nuclei, aggregated chromatin, nucleus-cytoplasm asynchrony. Their presence is usually associated with increase of neutrophils and shift to left picture with increase of platelet count but the association of macrocytic anemia and thrombocytopenia are the most common [38]. The CMML classified into three groups/categories for precise prognostication include: CMML0; a group with <2% blasts in PB and <5% blast in BM, the second group CMML1 include patients with 2–5% blasts in PB and 5–9% blasts in BM and third group include patients with 5–9% blasts in PB and 10–19% blasts in BM (Table 7) [5, 39].
\nPersistent monocytosis ≥1 × 109/l and monocytes ≥10% of WBC in peripheral blood | \n
<20% blasts in peripheral blood and bone marrow aspiration* | \n
No criteria and no previous history of CML, ET**, PV, and PMF | \n
If eosinophilia, no | \n
≥1 following criteria: \n
| \n
Diagnostic criteria of CMML modified according to Daniel Arber of 2016 WHO classification Blood 2016 [5].
Total blast cells include monoblast, promonoblasts and myeloblasts.
Exclude of myeloproliferative neoplasms (MPN) associated with monocytosis by bone marrow cytology and/or of MPN-associated mutations (JAK2, calreticulin gene “CALR”, or myeloproliferative leukemia mutation “MPL”) tend to confirm the diagnosis of MPN with monocytosis rather than chronic myelomonocytic leukemia (CMML).
The mutations associated with CMML which may support confirmation of diagnosis like ASXL1, SRSF2, SETBP1, TET2.
CML, chronic myeloid leukemia; ET, essential thrombocythemia; PV, polycythemia vera; PMF, primary myelofibrosis; WBC, white blood cell.
An international nomenclature has been used to help diagnose CMML [40]. Human monocytes can be divided into three subsets; MO1, CD14+/CD16− (classical), MO2, CD14+/CD16+ (intermediate) and MO3, CD14−/CD16+ (nonclassical). CMML is characterized by the accumulation of classical monocytes with an MO1 threshold to 94% of total circulating monocytes and with different gene expression profiles, chemokine receptor expressions and phagocytic activities [41].
\nClonal cytogenetic abnormalities identify non-specific chromosomal abnormalities in 30–40% of CMML patients. Peripheral blood/bone marrow for BCR-ABL rearrangement for all patients should be done to exclude any pathological disorder related to myeloproliferative disorders and PDGFRA, PDGFRB, FGFR1 rearrangements or PCM1-JAK2 (Table 7) [5, 42]. The most common alterations include; trisomy 8 (4–11%),—Y (5–20%), abnormalities of chromosome 7 (monosomy 7 and del7q) in 2–14%, trisomy 21, and complex karyotypes [43].
\nMyelodysplastic syndrome diagnosis based on data accumulated since the 2008 WHO classification of MDS, much of which relates to adequate medical information, cytomorphology and dysplastic assessment and new molecular genetic information about these neoplasms. The revised WHO classification is the more accurate classification introduces refinements in morphologic interpretation and cytopenia assessment and addresses the influence of genetic information in MDS diagnosis and classification of patients and will allow for better guidance of treatment.
\nThe evaluation of cytogenetic results is important for the classification and determination of the prognosis according to the revised International Prognostic Scoring System (IPSS-R). Immunophenotyping and molecular analysis will provide valuable information on diagnosis and prognosis.
\nThe field of learning disabilities has a long history, stemming back diagnostically over the past century to the work of Hinshelwood [1] and Morgan [2] in the 1890’s, and the work of Orton in the 1920’s and 1930’s with children characterised as “word blind” [3, 4]. Methodologically, it can be traced to the techniques for treating reading, writing and spelling difficulties pioneered by Dearborn [5, 6], Monroe [7], Gates [8], Durrell [9], and Fernald [10], to the application of Orton’s theories by Gillingham and Stillman [11] and to the differing conceptualisations of treatment developed by Strauss and Lehtinen in the 1940’s [12] and by clinicians such as Cruickshank [13], Ayres [14], Dubnoff [15], Frostig [16], Kephart [17], Getman [18], Kirk [19], Spalding and Spalding [20], Freidus [21], and Johnson and Myklebust [22] in the 1950’s and 1960’s.
In teaching children to read there has also been intense debate between proponents of phonically based techniques and visually-based methods as summarised in Chall [23], as well as between those who have advocated or rejected the practice of classifying and labelling different types of reading disabilities, as outlined by Elliott and Grigorenko [24]. These debates are ongoing [25].
At this point in time, based on over a hundred years of clinical and academic work in the field, the value of teaching reading using phonologically and phonically based methods at entry point to school and also at foundation level in school has become widely accepted [26, 27, 28]. In addition, a number of different types of learning disabilities have been identified [29, 30].
Despite these advances, there is still lack of agreement as to typologies of learning disabilities, as well as to how these apply to children and adults. There is also a lack of consensus as to whether it is better to base diagnosis of learning disabilities on purely functional descriptions of the behaviours associated with how learning disabilities manifest in particular children (using terms such as “backward reading”, “specific learning disorder, with impairment in reading”, or “specific reading retardation”), or whether it is helpful to also apply a label such as “dyslexia”, “developmental dyslexia”, “dysgraphia”, or “dyscalculia” to children for diagnostic purposes.
This chapter describes a programme which uses a response to intervention model of classification [31, 32, 33], working from the standpoint that classifications of learning difficulties are provisional and emergent, with the potential of changing from hypotheses to firm and persistent categories as treatment progresses. The model is based on a process of incremental and treatment validity, in which evidence concerning a child’s response to particular procedures or techniques can add to an existing combination of assessment methods [34, 35, 36].
The model is then discussed in relation to the methods for assessment and treatment of functional difficulties with reading, writing, spelling and arithmetical concepts applied in the programme. As the difficulties of children are specific and manifest in the context of particular households and school environments, initial functional descriptions of behaviour are used in the programme as the basis for treating learning difficulties associated with difficulties with reading, writing, spelling and numeracy.
The approach to diagnosis and treatment is evidence-based, and described in Potter [37, 38]. Initial assessment provides descriptive information concerning a child’s functioning, which is then linked to specific treatment programmes. Firm classification of dyslexia, dysgraphia and dysgraphia is then linked to both ongoing assessment and to progress evaluation linked to indicators of progress to establish effects of treatment, and through this to firm classification as learning disabled [39].
Lyon et al. [40] suggest that classification research involves forming groups or categories, which can then be evaluated for reliability, validity, and coverage. This implies that all classifications are essentially hypotheses about variables, and the relationships between variables. Classifications applying in the area of learning disabilities thus relate to both variables indicating difficulties as well as variables relating to the treatment of difficulties. Classification researchers then evaluate the reliability, validity, and coverage of hypothetical groupings of both independent and dependent variables relating to both difficulties and treatment of difficulties. This is done by conducting and analysing research on the relationships between these variables, as well as the relationships between variables conceptualised as either dependent or independent [41].
Following this logic, classifications applying in the area of learning disabilities are based on the interrelationships between a wide range of variables based on indicators associated with the learning difficulties experienced by particular children at school. As many types of behaviour are associated with both successful and unsuccessful performance in particular school environments, it would also imply that it would be unlikely that learning difficulties can be conceptualised as related to a single disability. Instead learning disability would need to be represented as a general category, which is composed of disabilities in any one or a combination of several areas or domains as these apply to the development of particular children [42].
This is the standpoint adopted in the programme described in this chapter, based on the position previously taken by others. In the 1968 federal definition of learning disabilities adopted in the United States, for example, seven domains are identified: (1) listening; (2) speaking; (3) basic reading (decoding and word recognition); (4) reading comprehension; (5) arithmetic calculation; (6) mathematics reasoning; and (7) written expression [30, 43], while Fletcher et al. [44] have suggested that the evidence supports six subgroups of learning disability involving reading (word recognition, fluency, and comprehension), math (calculations and problem solving), and probably written expression. The latter could involve either the generation of text (handwriting, spelling) or composition. Further research would be needed on these written expression components to establish whether these are distinct categories or categories which overlap other forms of learning disability.
Within these domains, the programme described in this chapter focuses on three main subgroups of learning disability:
Reading disabilities (often referred to as dyslexia)
Written language disabilities (often referred to as dysgraphia)
Math disabilities (often called dyscalculia)
Other related categories treated in the programme include disabilities that affect focus and attention, working memory, social skills, and executive functions such as personal organisation and deciding how to approach or begin a task. These difficulties are initially described functionally [37]. This is followed by a process of firmer classification based on analysis of response to intervention to programmes focused on improving functioning and performance in these areas, based on a process of evaluation which is empirical, multimethod and evidence-based [45, 46, 47].
A response to intervention instructional model uses intervention as a treatment variable and response to intervention as an indicator of underlying learning disabilities. Firm classification is then based on evidence of learning difficulties which are persistent or resistant to treatment. This is the approach adopted in Dr. Charles Potter’s Reading Fluency Programme [48], which is described in this chapter. Given the difficulties inherent in measurement particularly where anxiety and emotion are involved, the programme uses a response to intervention approach in which diagnosis can be emergent, based on evidence from both response-to-intervention (RTI) and norm-referenced ability testing collected over time [49].
Since difficulties with reading, writing and/or math are recognisable problems during the school years, the signs and symptoms of learning difficulties in a particular school programme form the point of departure for treatment. Functional description of different types of learning difficulties forms the basis for establishing treatment programmes. Response to intervention then provides the basis for classification as learning disabled.
Learning disabilities are thus initially defined as functional difficulties, based on evidence of unexpected underachievement in a child relative to the achievement which would be typical of other children in a particular school or learning environment. Indicators of unexpected underachievement are used at the outset to describe the difficulty, based on inability to respond to the instruction which is benefitting other children. The definition would also include other functional indicators of learning difficulties, such as ratings or test scores indicating reading, writing and spelling difficulties or difficulties with number concept and mathematical problem-solving, and would also include ratings or test scores indicating neurological markers and signs, as well as unevenness in cognitive functions.
A firm classification as learning disabled would then be based on evidence of difficulties persisting both during as well as after treatment based on longitudinal, incremental assessment and evaluation [50, 51] as outlined in Table 1.
Classification of learning disabilities based on response to intervention.
The model in Table 1 is a generic one which can be applied by others. How this has been applied in practice is described in the rest of this chapter with reference to a particular programme applying specific methods of assessment and treatment in a particular country context. As there are a number of different variables which can affect the development of reading, writing and spelling, the methods and materials used with each child vary, based on initial assessment to identify areas of strength and difficulty, as well as specific areas requiring intervention.
Intervention then takes place to address the variables related to the areas of difficulty. As this takes place, firm diagnosis and classification of learning disability then becomes possible, based on assessment linked to ongoing assessment and progress evaluation of the effects of multivariate treatment, based on use of particular types of methods and materials. Classification as learning disabled can then be linked to concessions to compensate for the areas of difficulty which have been demonstrated to be resistant to particular forms of treatment, as well as to ongoing treatment and learning support.
The assessment process used in Dr. Charles Potter’s Reading Programme1 is based on the child’s family and scholastic history in either the private or government schooling system in South Africa, which is a country classified as both first and third world [52]. The assessment procedures conform to similar procedures used by other educational psychologists in South Africa to provide evidence which can be used for diagnostic purposes against what are termed the ICD DSM IV and ICD DSM V criteria by South African medical aid societies.2
The ICD DSM IV and ICD DSM V criteria are designed to enable initial diagnosis to be made against functional descriptions of the learning difficulties experienced by children. These can then be used as the basis for both functional classification as well as for the development of treatment programmes.
As has been described in a previous publication on the work of the programme [37], four screening tests are used at the outset of the assessment process. These are designed to yield information about reading single words and reading words in sequence, and writing and spelling single words and words in sequence. Results on these tests are then reported using reading, spelling and dictation ages, for the reason that the South African ICD DSM IV and DSM V are based on age-related expectancies which are then used by the medical aid societies for the management of claims and benefits.3
Besides following the medical aid society guidelines in focusing on basic skills in reading and written expression, the assessment procedures are also based on the procedures suggested by Luria [58] for clinical assessment of reading and writing. Qualitative analysis of an initial parent interview is combined with analysis of drawings, pragmatic writing-based tasks and observation in an initial ice-breaking session with the child. This is then followed by a second session with the child during which four screening tests are used to establish levels of basic skills in reading, writing and spelling. This information is also combined with additional evidence from a biographical inventory, parental interview, analysis of school reports and more formal psychometric testing. This includes assessment of arithmetical and mathematical problem-solving skills if these are highlighted as areas of difficulty by the child’s school and the child’s parents.
Overall, the procedures used in the assessment process thus follow Luria’s suggestion [58] that assessment should start with a preliminary conversation, and then include a careful history, detailed observation of behaviour, analysis of neurological symptoms and a series of additional objective tests. Luria suggests that the examination needs to be relatively short, and involve methods of experimental psychological investigation applied to clinical practice.
The methods of examination used in the initial sessions spent working with the child also include pragmatic assessment of repetitive and spontaneous speech, writing, reading, comprehension of texts and the solution of problems, in order to establish how reading, writing and spelling are used by the child as a functional system. This informal evidence is then combined with more formal testing of reading, writing and spelling skills, and interpreted, as Luria suggests, against a framework of knowledge of the types of difficulties normally associated with the functional system under investigation, based on current literature [59].
Assessment leads to a functional description of deficits sufficient for diagnosis of learning disability to meet medical aid requirements,4 as opposed to an attempt to link this to possible labelling of the child as dyslexic, or labelling in terms of the other types of learning disability commonly described in the literature [37]. This is consistent with the standpoint adopted by Elliott and Grigorenko [24] and Elliott [61], namely, that adding a label adds little of clarity to a functional description of deficits for purposes of intervention. Similarly, the pattern of scores on subtests of an IQ test would best be used functionally, to indicate areas of cognitive and language strength and weakness, as well as areas in sequencing and working memory which may need to be worked with in therapy.
Following Luria [62], the aim is to move from assessment to statement of areas of deficit, and from this to specific programmatic intervention. The statement of areas of deficit can then be used as the basis for diagnosis for medical aid purposes, recommendations concerning the need for additional more in-depth testing (e.g. cognitive testing, speech and language and/or visual assessment, more in-depth analysis of phonological and phonic skills) or for more in-depth neurological or paediatric investigation,5 as well as to recommend specific types of programmatic activities which can be used to address the areas of deficit.
Being based on the DSM IV criteria,6 the diagnosis is related to the ICD10 classifications of possible types of developmental disorders affecting the development of scholastic skills, which are as follows:
F81 Specific developmental disorders of scholastic skills
F81.0 Specific reading disorder
F81.2 Mathematics disorder
F81.8 Other developmental disorders of scholastic skills
F81.81 Disorder of written expression
F81.89 Other developmental disorders of scholastic skills
This classification then enables parents to be able to claim benefits from their medical aid societies. At the same time, the statement of areas of deficit then enables recommendations to be made for more in-depth testing, as well as for commencing treatment. This is done matching the behaviours tapped by the tests used in the assessment process with the functional descriptions associated with the following literature-based based categorisation of types of learning disability associated with the ICD 10 developmental disorders of scholastic skills [42, 64, 65]:
Dyslexia: learning difficulties affecting reading and related language-based processing skills.
Auditory processing problems: difficulties with the sound system of the language, with phonological awareness, with listening in the classroom, and with processing and remembering the sounds associated with the letters in reading, writing and spelling.
Language processing problems: difficulties in processing spoken language, affecting both receptive and expressive language.
Reading Comprehension Deficits: learning difficulties affecting an individual’s understanding of what they read.
Dysgraphia: learning difficulties affecting a person’s handwriting ability and fine motor skills.
Visual, Visual perceptual or visual motor deficits: poor eye-hand coordination, difficulties in navigating surroundings, difficulties in visual tracking of print or losing one’s place when reading.
Non-Verbal Learning Deficits: learning difficulties affecting the child’s social interactions, manifesting in difficulties interpreting nonverbal cues such as facial expressions or body language, or difficulties relating to poor coordination.
Dyscalculia: learning difficulties affecting a person’s ability to understand numbers and learn arithmetic or mathematical facts.
As the work done in my practice is related to the ICD 10 classification and medical aid codes, the functional difficulties associated with the ICD 10 codes related to the above categories (dyslexia, reading comprehension deficits, dysgraphia and dyscalculia) form the basis for the types of treatment initially developed for working with the child. Functional difficulties in the other four areas are referred to other therapists (e.g. occupational therapists, physiotherapists, visual therapists and speech and language specialists) working in the field.
This enables the work done in the practice to meet medical aid requirements, while at the same time focusing on use of particular methods and materials in working with reading, writing and spelling difficulties, difficulties with numeracy and mathematical problem-solving, as well as the attentional, emotional and social aspects which accompany difficulties at school (Table 2) [37, 38, 66].
Diagnosis of learning disability based on response to intervention prior to, during and subsequent to treatment.
The model for evidence-based classification can be represented as follows:
The model thus involves evidence-based multivariate treatment as the basis for firm classification of particular types of learning disability based on response to intervention over time. At each stage in the application of the model, classification of learning disability is based on incremental validity based on specific evidence relating to particular types of treatment. It is also related to the emotional, social, family and classroom issues involved in treating learning difficulties at school.
How the model has been applied in practice is outlined in the following sections. While this is done with reference to the multivariate programmes developed in the practice for treating learning disabilities, the model could also be applied in other programmes working in a similar evidence-based way.
Dr. Charles Potter’s Reading Programme is a fluency-based programme for treating learning difficulties [67]. The methods used for treating reading difficulties in the programme are based on the theories of the Russian neuropsychologist A.R. Luria [58, 68, 69] and have been described in a number of previous publications [37, 38, 66, 70, 71]. The materials used in the programme are electronic, and can either be downloaded or sent out by email.
At pre-reading level, the material is activity-based and focuses on developing phonological and phonemic awareness. The methods used in working with the material are described in accompanying manuals [72, 73, 74, 75, 76, 77, 78, 79, 80, 81, 82, 83, 84, 85, 86] which can be used by parents, teachers and therapists, and form the basis for the training of programme implementers.
The programme works with children from pre-reading and school readiness level. The transition to foundation level is made once the child has developed alphabetic awareness and the associations between the letters of the alphabet and the sounds used to represent the letters in English. The child is then introduced to reading through a series of fifteen foundation level reading books, using a structured language experience approach which integrates reading, writing, phonics and spelling with drawing and illustration. This is done through six activity books based on families of rhyming words, which accompany the first six of the foundation level reading books, with the methods used described in accompanying manuals [75, 82, 86].
Once the child has developed the ability to read three letter words and words based on short vowel sounds and beginning and ending consonant blends and clusters, repetitive paired reading is introduced, focusing initially on reading of sentences. Comprehension is developed through drawing and illustration of reading content.
Once the child can read and write phonically based words as well as sentences using three letter words in context, reading fluency work is commenced using large print phonically based reading books, based on the model for treatment of reading acquisition, reading fluency and reading comprehension development represented in Table 3.
Model for Reading fluency development.
The procedures used are documented in a user’s manual which includes both theory and the methods used in programme implementation [72]. In addition, there is a parent implementer’s manual which presents a step by step approach to implementation [78].
The development of the large-print, phonically based material used for developing reading fluency in the programme has been described in a separate publication [66]. The methods used for developing reading fluency involve use of a paired reading method called the 3 x 3 Oral Impress Method. This is designed to be used with a series of electronic reading fluency books which are graded, and written in a way which builds repetition into the words used, as well as phrases used in sentences.
The material presents letters and letter strings associated with particular sounds repetitively in an uncluttered format. Repetitive oral reading is then used together with visual tracking of the printed words to develop and then automatise the associations between the configuration of the letters within phonically regular words and their sounds as used in the written language the child sees, the spoken language the child hears, and the words read by both adult and child [87].
This is done by working with the reading material three paragraphs at a time in the following way (Table 4).
Child reads | Parent and Child read together | Parent reads | |
Parent reads | Child reads | Parent and Child read together | |
Parent and Child read together | Parent reads | Child reads |
The 3 x 3 Oral impress method.
The aim, as Luria suggests [58, 68], is to enhance cerebral organisation based on a repetitive process. This was also Heckelman’s view when he pioneered the use of paired reading as a procedure [88, 89, 90], suggesting that paired reading is “one of the most direct and fundamental systems of reading” involving a “combination of reflexive neurological systems.” We have reported similar positive results [38, 66], supporting Heckelman’s position that gains made are based on increasing neurological integrity.
The model for developing using the phonically-based, large print reading materials to develop reading fluency would be conceptualised as based on the coding and recoding of phonic associations [91, 92, 93]. Following Dehaene [94, 95], what the 3 x 3 Oral Impress Method does when used with our phonically based large-print reading fluency books is to present the visual word form area in the brain with strings of letters representing sounds repeatedly. This would have the effect of strengthening the connections between the visual areas in the brain and the areas of the brain involved in processing sounds and oral language, thus enabling the child first to read, and then to read fluently.
The relationship between rapid naming and reading difficulties has been established by a number of researchers [96, 97, 98, 99, 100, 101, 102]. What has not been clearly established is whether rapid naming is a separate factor influencing reading performance, and whether it is responsive to training [103, 104]. Recent research indicates that training interventions in this area are possible [105, 106], but that more controlled studies are still necessary on whether rapid naming can be trained, and how it can be trained. The descriptions provided in this section should be viewed in this context.
Our methods focus on teaching rapid naming of letters, words and numbers, as well as teaching rapid reading. At initial stages in the programme, rapid naming of letters is conducted using phonogram cards. Rapid naming of words is conducted using key words drawn from our phonically-based large print reading material. Rapid naming of numbers is trained through rapid marking of arithmetic worksheets. Rapid reading is also taught developmentally using the 3 x 3 Oral Impress Method [72], which focuses on accurate naming of phonically regular words and sentences, and then on rapid and accurate reading of a wider range of reading material.
The material used is phonically graded as well as repetitive, and the aim in the initial stages is to work with words which become increasingly familiar to the child, to develop accurate and rapid naming ability for individual words and words in sequence. This is done through the repetitive methods used to develop automaticity in reading [74], as well as through activities in which the child is asked to name letters and numbers in worksheets based on both familiar and unfamiliar content. Tachistoscopic work is then introduced at later stages in the programme [107], working repetitively with words of increasing length drawn from an electronic dictionary, as well as with words drawn from graded revisualisation materials and the child’s school books.
Using computer-based presentation, length of words presented, time exposure of the presentation of each word and time between the exposure of each word can be treated as variables. Other variables involve the ways in which words can be presented, read, revisualised and written down, following the procedures outlined in Table 5.
Methods for treating rapid naming difficulties.
The methods used for developing rapid naming in the child’s programme thus link with the methods used for training fluency in reading, and include activities methods designed to develop rapid naming of words as well as activities aimed at developing increasing familiarity with words. Based on Luria’s theories of automaticity [58], repetition would be intrinsic to the development of fluency in reading. As Dehaene [95] has noted, familiarity with material influences fluency. The aim of our methods is to use repetitive paired reading to develop the coding, recoding, working memory and rapid naming abilities necessary for fluent and accurate reading, and for self-teaching [108].
Fluency in writing and spelling is addressed in our programme through a variety of methods involving linking the teaching of phonic associations with training in basic skills in writing and copying. This is done by teaching the child how to work from print to sound, how to analyse words based on phonic analysis of how words work, and how to use the letters and letter combinations used to represent the vowels in words as the basis for remembering how words are spelled both individually and in sequence. This is done through a process we call “phonological referencing” which focuses on the coding and recoding of phonic associations [80].
This is done using word families of between five and six words, supported by sentences in which the words are analysed in sequence, revisualised and then tested. The aim is to use revisualisation of words and sequences of words as an integral part of the process of learning to write and spell, with the aim of developing the phonological, phonic and sequential working memory processes involved in writing rapidly and accurately in sequence [84, 85].
The model for using our phonically-based, large print materials for developing writing and spelling fluency, is represented in Table 6.
Model for developing writing and spelling fluency based on activities involving development of reading, writing, spelling, phonic analysis and revisualisation.
Following Luria’s theories [58], our methods use repetition as intrinsic to the development of automaticity in writing and spelling fluency. As with reading fluency, the aim is to develop the coding, recoding and working memory abilities necessary for fluent and accurate writing and spelling [91, 92, 93, 108, 109].
At initial stages in the programme, the aim is to build phonological, orthographic and morphological awareness through phonological referencing [86]. This involves developing the child’s phonic analysis, visual memory and sequential working memory skills by methods which combine phonic analysis and revisualisation [74].
The phonic abilities of the child are established from analysis of the child’s errors on spelling tests, in the child’s descriptive writing, creative writing and school work, as well as through a series of phonic inventories [79]. Based on the pattern of errors, we initially involve the child in work with word families and phonogram cards targeting specific phonic errors in the profile. In the process, the child is introduced to working with the Seven Vowel Phonic Analysis System, which is a procedure for teaching children through activities involving mapping the combinations of letters used in writing words to the sounds made when those words are spoken orally [73, 74].
The aim is to combine phonic analysis and revisualisation in developing skills in word attack, spelling and sequential working memory. This is done through activities focusing on analysis of the letters and letter combinations used to represent the vowel sounds in words, combined with revisualisation activities focused on remembering sequences of words [84]. The sequence of instruction followed, and the links between phonological referencing, the introduction and application of the Seven Vowel Phonic Analysis System, and the combination of phonic analysis and revisualisation in the Targeted Revisualisation Programme [83], are represented in Table 7 below.
Introducing phonological referencing and the seven vowel phonic analysis system.
The sequence of instruction followed in implementing the programme thus integrates reading, writing and spelling through activities which are phonically-based, linking phonological, phonemic, visual memory and sequential working memory development. The methods used are outlined in a series of manuals which can be used by therapists, teachers, schools and parents [81, 82, 83, 84, 85].
Both phonological referencing and the Seven Vowel Phonic Analysis System are used for point to point analysis of the links between the sequences of letters used in written words and the sequence of sounds made which the words are spoken orally. This is done through activities in which the child is taught to map the associations between the sequences of letters used in written words and the sequences of sounds used when the words are spoken orally [80].
The sequence of instruction followed in teaching the child is as follows:
After the child has learned the associations between sounds and letters, the child works with word families as well as with phonogram and rime cards, which are used side by side with the process of phonological referencing. The basis for mapping is to link the individual letters and sequences of letters with the sequences of sounds made when the words are spoken out loud, based on the principle that “what we say is what we write.”
This stage involves activities in which the hand is placed under the chin to increase the ease by which the vowel sounds in words can be identified as part of the process of mapping letters to sounds and sounds to letters.
Particular focus is placed on identifying the vowel sounds in words (which are spoken when the mouth opens) and the consonant sounds (which are spoken when the mouth closes). The letters the child has written or typed form the departure point for linking what is written on paper with both sounds and mouth movements.
The aim is to enable the child to identify the vowel letters and the consonant letters used in written words, and then to link these back to the sounds made when the word is spoken orally.
Reverse mapping between the sequence of sounds in the word and the letters used in writing the word then takes place. Once the vowel sound in the word has been identified, the letters used to represent the vowel sound are then colour coded. In the process, short vowel sounds are identified as normally being made by one letter working by itself, while long vowel sounds are identified as normally being made by two letters working together.
As the focus lies on mapping the consistency between the sequences of letters used in written words with the sequences of sounds used when the words are spoken orally, the aim is to enable the child to build the variety of phonic associations necessary to read, write and spell in sequence. Visual memory, revisualisation and dictation activities are also used to develop the metacognitive and working memory processes necessary to remember and write sounds and letters in sequence, and words in sequence [110, 111, 112, 113, 114, 115, 116].
Much has been written about the transparency of the English language compared to other languages [117, 118, 119, 120, 121, 122], for the reason that the phonic associations underpinning English orthography are varied, with similar sounds being represented by different letter combinations. This means that both reading and spelling in English are not as easy for children to learn as in many other languages such as Italian, Afrikaans, Welsh, German, or French [123, 124, 125, 126, 127, 128, 129, 130]. This has potentially negative effects on the progress of children with learning disabilities [118, 119, 131, 132, 133].
Our materials attempt to overcome this problem at initial stages in the programme through the use of carefully chosen vocabulary. Phonic associations are initially taught through graded rhyming word activities, and then developed through activities involving reading, writing and use of working memory in spelling. Once the child has been introduced to the phonological referencing and colour coding process with individual words and families of rhyming words, he or she is also introduced to activities involving use of visual memory and revisualisation of words in sequence.
Word families of written words are used as the basis for analysing individual words, while written sentences are used as the basis for analysing words in sequence. This is done through activities based on sentences and paragraphs which include words in which the y and w combine with other letters to form long vowel sounds. These letter-sound associations are identified and then mapped using the Seven Vowel Phonic Analysis System [73, 74, 83].
In the process, the child is taught that a, e, i, o and u are the letters normally used to represent the vowel sounds in words, but that y and w can also be used to represent the represent the vowel sounds in positions at or near the end of written words in English. The Seven Vowel Phonic Analysis System is then worked with and applied through activities in which the child speaks the word out loud and then identifies the letters used as vowels in the word. Through activity-based learning, the child is introduced to the principle that there needs to be a vowel in every word, that the letters a, e, i, o and u are used to represent the vowels in all positions in words, and that the use of y and w as vowels at the end of words is both logical and consistent, applying to nearly all words in English.
The use of the Seven Vowel Phonic Analysis System thus enables the letters used to represent the sounds in both simple and complex written words to be identified through phonological referencing, and to be analysed following the principle that “what we say we write.” The aim is make written English as transparent as written Welsh, in which the use of the seven vowels a, e, i, o, and u, as well as y and w, also applies [122, 123, 133], making it logical and easier for children to learn.
The methods for teaching spelling in our programme have been described in Potter [38, 70] and follow the phonologically and phonically-based stages in spelling described by Moats [134, 135], as well as the stages in a set of three phonic inventories based on the foundation level curriculum taught in primary schools in South Africa [79]. Phonic associations are initially introduced through graded rhyming word activities involving reading, writing and use of working memory in spelling. Focus is placed on teaching through synthetic phonic approaches incorporating teaching children to isolate sounds and blend sounds into words, as well as how to create families of rhyming words based on similar phonological and phonemic elements [75].
These are introduced side by side with reading fluency activities using our foundation level and then our basic level readers, through methods which use activity-based learning to build the variety of phonic associations necessary to read, write and spell. Phonic analysis is then introduced using phonological referencing [80], which is applied working with families of between five and seven words, each of which are based on a similar consonant blend of cluster. These are then contextualised in short sentences in which the words are then phonically analysed and revisualised in sequence. The aim is to develop the working memory integrities necessary to write accurately in sequence.
In the ck word family, for example, the following words would be written in the child’s writing book.
shock
brick
check
stack
cluck
trick
The vowel in each word would then be underlined in colour and matched with the way the mouth opens in making each vowel sound and the way the mouth closes in making each consonant sound. After this, the child would work with his or her reading partner and phonologically reference each word in the ck word family, by linking the sounds in each word when the word is spoken out loud with the letters used when the word is written down.
This would be done through an activity-based process, in which the child is asked to:
Point to the written word on the page and say it.
Look at the two letters at the beginning of the written word. Say the sound of these letters out loud.
Look at the vowel in the middle of the written word. Say the sound of this letter out loud.
Look at the two letters at the end of the written word. Say the the sound of these letters out loud.
The phonic rule applied in each of the words would then be focused on working with the reading partner. This would be done by focusing on how the beginning sound, the middle sound and the ending sound work together to make each word, and how the ck ending applies in each word.
Each of the words in the family would then be contextualised in sequence in a short sentence. The sentence would be written down by the child, and the vowel or vowels in each word in the sentence underlined in colour. After this, each word in the sentence would then be revisualised in sequence working memory tested by asking the child to rewrite the sentence from memory. These sequential revisualisation techniques would then be used further at higher levels in the programme [84].
The sequence of instruction followed with each child varies based on evidence of how the child learns, but is conducted with the aim of linking the development of phonic analysis, visual memory and working memory skills as represented in Table 8.
Methods linking phonic analysis, visual memory for strings of letters and words and sequential working memory for written words, phrases, sentences and paragraphs.
It will be apparent from Table 8 that the aim at each level of the programme is to work to combine phonological and phonic skills development with the development of visual memory and sequential working memory. This is done through methods which to combine the process of phonic analysis with the process of revisualisation in developing sequential working memory for words [83, 84], through a longitudinal process in which:
The child is taught to map the associations between the sequences of letters used in words and the sequences of sounds used when words are spoken orally through phonological referencing, as well as through use of phonogram and rime cards.
The child is taught that each written word is logical and can be analysed on the principle that “what we say is what we write.”
The child is shown how to use revisualisation to remember the sequences of letters used in individual words and the sequences of words in used in sentences.
Both phonic analysis and revisualisation are thus used to develop the child’s ability to store each word in working memory in sequence. This is initially done working with words in the context of sentences, and then with sequences of sentences. The child’s sequential working memory is tested through dictation.
At each level in the programme, the methods used are repetitive and follow the procedures for developing automaticity outlined by Luria [58, 68, 69], and are summarised in illustrated implementer manuals for users [74, 81, 83, 84, 85]. Once the child is able to recall sentences of between five and seven words accurately, span of sequential working memory is increased by phonic analysis and revisualisation of sentences of increasing length, as well as by phonic analysis and revisualisation of increasing numbers of sentences in sequence.
As our reading fluency materials are graded and phonically based, sentences and paragraphs from these can be used as the basis for activities which link reading, writing, spelling and sequential working memory work. More complex graded paragraphs and sequences of paragraphs are then introduced once the Targeted Analysis, Revisualisation and Sequential Spelling Programme is commenced, as described in the section following.
Once the child is able to recall the words used in individual sentences and sequences of sentences accurately, the materials used in the Targeted Analysis, Revisualisation and Sequential Spelling Programme are introduced. The methods target words with more than one vowel, which are first written, then typed, then colour coded and then syllabified. The target words are then revisualised and tested [136].
After analysing and recalling the target words, the text of the graded materials is then worked with, focusing on each word in each sentence in sequence. Sequential revisualisation techniques are used. We call this process “targeted revisualisation” as each word is targeted in sequence, using techniques which combine the procedures used for phonic analysis of the target words with the types of mental imagery the child uses in recalling words. These build on the activities linking phonic analysis and revisualisation, and the methods used for developing sequential working memory used at previous levels in the programme.
The aim is to use accuracy in use of sequential working memory for words as the basis for developing fluency and automaticity in writing and spelling [38]. This is done in four stages, as outlined in Table 9.
Level of mediation | Focuses of phonic analysis | Focuses of revisualisation | Focuses of use of sequential working memory |
---|---|---|---|
Stage One: Focus on Words based on Short Vowel Sounds | Introduce concept that vowels are used in all spoken and written words. Identify and mediate short vowel sounds a, e, i, o, and u. | Construct, deconstruct, mentally image and revisualise words and rhyming word families containing short vowel sounds. | Use working memory in writing rhyming words based on short vowel sounds in sequence. |
Stage Two: Focus on Words based on Long Vowel Sounds | Identify and mediate long vowel sounds involving use of digraphs involving a, e, i, o, and u. Introduce the letters y and w as vowels in positions at or near the end of words. | Construct, deconstruct, mentally image and revisualise words and rhyming word families containing long vowel sounds, including use of the letters y and w as vowels in positions at or near the end of words. | Use working memory in writing sequences of words containing both long and short vowel sounds, including use of the letters y and w as vowels in positions at or near the end of words. |
Stage Three: Focus on Sequentialisation of Words in Sentences | Identify letters used as vowels in words used in sequence in sentences. | Identify, phonically analyse, mentally image and revisualise single syllable and polysyllabic words in sequence in sentences. | Use working memory in writing single syllable and polysyllabic words in sequence in sentences and sequences of sentences. |
Stage Four: Focus on Sequentialisation of Words and Sentences in Paragraphs | Identify letters used as vowels in words used in sequence in sentences, and in sentences used in sequence in paragraphs. | Identify, phonically analyse, mentally image and revisualise single syllable and polysyllabic words in sequence in paragraphs. | Use working memory in writing sentences in sequence in paragraphs of increasing length and phonic complexity. |
Stages and focuses of mediation in the targeted analysis, revisualisation and sequential spelling programme.
The Targeted Analysis, Revisualisation and Sequential Spelling Programme is applied using graded paragraphs, which increase in complexity as well as length. As these are worked with, the process of combining phonic analysis and revisualisation in using the Seven Vowel Phonic Analysis System is applied repetitively. This is done by working from printed word to sound, and from sound back to print. These phonological recoding skills provide the building blocks on which writing and spelling fluency is developed [71].
On a phonological and phonic level, the methods used are based on the coding and recoding of phonic associations through activities in which the child writes, types and colour codes the vowels in words by underlining the letters used to represent the vowel sounds in colour as well as using the colour coding feature in a word processing programme. This adds a visual dimension to the targeted revisualisation process, as the methods used are designed to make the letters used to represent the vowel sounds in words stand out in colour [83].
Both phonic associations and visual contrasts are then used to identify the letters representing the vowel sounds in words, with the aim of enabling the child to develop working memory for individual words as well as sequential working memory for words in sequence. Fluency in writing and spelling is then based on increasing span of sequential working memory as well as automaticity in recalling the sequences of letters used in individual words, the sequences of words used in sentences, and the sequences of sentences used in paragraphs.
At higher levels in the programme, rapid reading of words and working memory for words are also developed through use of tachistoscopic methods conducted side by side with targeted revisualisation [107]. Children who have worked in this way report effects in improving word attack in reading, as well as improvements in rate of processing words, rate of reading, spelling accuracy and rate of work.
In addition to the strands in the child’s programme focused on treating difficulties with reading, writing and spelling, numerical and problem-solving activities are also included in the programme, using electronic materials which can be worked with online, as well as sent to parents and children by email [71]. The aim of using this format-based multivariate treatment system is to enable treatment of the functional difficulties identified in assessment, while at the same time addressing needs indicated by the errors made by the child in his or her school work.
The format system is flexible and comprehensive enough to be able to focus on areas of strength as well as needs, while also enabling email delivery of the activities included in each child’s individual programme. Number concept development can also be linked to language and problem-solving activities, with support programmes linked to the developmental model outlined in Table 10. These activities are then implemented side by side with the mathematical curriculum taught at school.
Model for development of number concept, numerical fluency, numerical reasoning and numerical problem solving.
It will be apparent from Table 10 that at the same time as treating numerical and mathematical difficulties identified in the initial assessment, the learning support provided is both diagnostic and based on clinical teaching, as well as linked to numerical and mathematical concepts covered in the child’s work at school. As with other areas of our programme, the aim is to treat functional difficulties as well as to evaluate the child’s response to specific types of interventions, as outlined in the section following.
Work with each child is conducted longitudinally, and is based on a cycle in which evaluation forms an integral part of both planning and implementation. Feedback on specific activities in the format is also provided by photographs sent by email or WhatsApp, enabling the planning of the next format in the child’s programme to be evidence-based, linked to ongoing evaluation of learning needs. Assessment is then built into programme implementation at regular intervals.
The model used for implementation is action research based [137, 138, 139], and can be summarised as follows (Table 11).
Action research cycle for planning and implementation of activity-based online programmes.
As the programme’s data base is extensive, the planning and implementation model implies that each child’s programme is evidence-based and multivariate, addressing a number of different learning needs through use of a variety of graded activities. The programme is then implemented using online sessions supported by learning materials provided by email [71].
The aim is that programme implementation can take place with support from parents, teachers, tutors or au paires as reading partners, working with a variety of electronic materials delivered by email or made accessible online via links to websites. Methods used in the programme are documented in illustrated implementer manuals, and are demonstrated working online, supported by cell phone and email contact.
Both evaluation programme activities and evaluation of progress are linked to evidence from the child’s school work and school reports at regular points in primary, with full re-assessment and summative evaluation being conducted at point of transition to high school. The aim at this point is to make a firm diagnosis of learning disability which can be linked to concessions.
The aim is to ensure that firm classification and labelling of a child as learning disabled is valid [36], based both on longitudinal analysis of test results as well as response to specific interventions [140, 141], on the model described in the section following.
In implementing the different types of interventions which have been described in this chapter, the programme focuses on a number of different variables related to the areas of difficulty. Interventions are normally longitudinal and conducted side by side with the curriculum taught in the child’s school.
The programme works with the aim of providing fluency-based interventions which can develop basic skills and competences in reading, writing, spelling as well as numeracy. At the same time, evidence-based learning support is provided focused on areas of the school curriculum with which the child is experiencing difficulties. This type of multivariate intervention is implemented using formats based on an online session providing counselling followed by an intervention, supported by electronic materials which can then be used by parents and children working in conjunction with a teacher or therapist, or independently [71].
At the outset the child’s difficulties are described functionally. This enables labelling to be avoided, until such time as the child has had benefit of focused multivariate treatment, and is also likely to be more developmentally and neurologically mature [142, 143, 144, 145]. As maturation takes place, firm diagnosis and classification of learning disability then becomes to the child’s benefit, as it can be linked to concessions related to areas of ongoing difficulty. This can be linked both to cross-sectional assessment as well as evaluation of response to interventions which have been based on multivariate treatment using particular types of methods and materials.
In our programme, firm classification as learning disabled is thus normally undertaken at the end of a child’s primary school years, based on evidence collected by use of different methods over time [146, 147], within a model of inference based on a process of incremental validity [34, 35, 148]. Diagnosis can then be linked to concessions to compensate for those areas of difficulty which have been demonstrated to be resistant to particular forms of treatment, as well as to ongoing treatment and learning support in particular areas of the high school curriculum.
The model for classification of learning disabilities is reflected in Table 12 on the previous page. It will be noted that the model is multimethod, based on summative assessment linked to progress evaluation of longitudinal interventions conducted across a number of areas of functional difficulty, enabling triangulation across different data points over time [131].
Classification of learning disabilities based on response to multivariate fluency-based interventions.
This enables firmer conclusions as to the type of learning disability involved, as well as classification of learning disability based on specific evidence relating to response to particular types of treatment [141].
This chapter has focused on treatment of the functional learning difficulties associated with dyslexia, dysgraphia and dyscalculia, as three dimensions of learning disability. As each of these dimensions can be associated with a range of reading, writing, spelling and working memory difficulties, the model of classification described in this chapter has been described with reference to a particular programme which uses a large data base to implement a variety of different activities with children diagnosed as having learning problems.
Owing to the measurement error implicit in testing young children who may have attention and focus difficulties in addition to functional difficulties with reading, writing, spelling and maths, the model of classification assumes that initial diagnosis of learning disabilities is at best provisional. For this reason, labelling of children is avoided at the outset. Functional indicators based on actual versus expected performance are used in preference, using ICD10 codes and descriptors as opposed to labelling using terms such as Dyslexia, Auditory Processing Problems, Language Processing Problems, Reading Comprehension Deficits, Dysgraphia, Visual Perceptual or Visual Motor Deficits, Non-Verbal Learning Deficits or Dyscalculia.
Detailed description of the initial assessment process has been provided in order to show that functional ICD 10 descriptors can be used instead of labels as the basis for establishing needs and areas of treatment. Treatments can then be targeted at these descriptors, being related to focus on specific problems with reading, writing and spelling, as well as numerical concepts and mathematical problem-solving. Difficulties outside these areas are then referred to other specialists.
Detailed description of particular methods, materials and programmes has also been provided in this chapter to indicate that once initial functional classification has taken place linked to specific areas of difficulty, multivariate interventions can then be developed and implemented. Firm classification then becomes possible based on the child’s progress over time.
One implication is that initial diagnosis of learning difficulties can be rigorous despite being provisional, providing detailed descriptions of specific areas of difficulty which are made with a view to undertaking multivariate treatment. Firm classification can then be made based on response to intervention at a time in the child is likely to be more developmentally and neurologically mature, and prior making a transition to new forms of teaching and new areas of learning at high school level.
Another implication is that the process of establishing firm diagnosis and classification would best be conducted at the end of a child’s primary school years, with a view to establishing concessions as well as the possibility of further treatment at higher levels in the curriculum. At this point firm diagnosis as having dyslexia, dysgraphia or dyscalculia can act to the child’s maximal benefit, in maximising the chances of obtaining the concessions and further treatments necessary to making the grade.
As the response to intervention classification model described in this chapter has been successfully applied in practice,7 a third implication is that the model is feasible and may have wider relevance. It offers the possibility that firm classification as learning disabled can be based on the child’s response to treatment which has been focused, multivariate and multimethod. In terms of the model, firm diagnosis of children as dyslexic, dysgraphic or dyscalculaic becomes an outcome taking place after treatment, linked to the possibility of concessions as well as additional interventions.
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All published Book Chapters are licensed under a Creative Commons Attribution 3.0 Unported License. Monographs are licensed under the Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0) license granted to all others. Our Copyright Policy aims to guarantee that original material is published while at the same time giving significant freedom to our Authors. IntechOpen upholds a flexible Copyright Policy meaning that there is no copyright transfer to the publisher and Authors hold exclusive copyright to their work.
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On September, 29th 2006 he has won a post PhD fellowship from the university of Bologna (from October 2006 to October 2008), at the competitive examination he was ranked first in the industrial engineering area. He extensively served as referee for several international journals. He is author/coauthor of more than 100 research papers. He has been involved in some projects supported by MURST and European Community. 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Delac received his B.Sc.E.E. degree in 2003 and is currentlypursuing a Ph.D. degree at the University of Zagreb, Faculty of Electrical Engineering andComputing. His current research interests are digital image analysis, pattern recognition andbiometrics.",institutionString:null,institution:{name:"University of Zagreb",country:{name:"Croatia"}}},{id:"557",title:"Dr.",name:"Andon",middleName:"Venelinov",surname:"Topalov",slug:"andon-topalov",fullName:"Andon Topalov",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/557/images/1927_n.jpg",biography:"Dr. Andon V. Topalov received the MSc degree in Control Engineering from the Faculty of Information Systems, Technologies, and Automation at Moscow State University of Civil Engineering (MGGU) in 1979. He then received his PhD degree in Control Engineering from the Department of Automation and Remote Control at Moscow State Mining University (MGSU), Moscow, in 1984. From 1985 to 1986, he was a Research Fellow in the Research Institute for Electronic Equipment, ZZU AD, Plovdiv, Bulgaria. In 1986, he joined the Department of Control Systems, Technical University of Sofia at the Plovdiv campus, where he is presently a Full Professor. He has held long-term visiting Professor/Scholar positions at various institutions in South Korea, Turkey, Mexico, Greece, Belgium, UK, and Germany. And he has coauthored one book and authored or coauthored more than 80 research papers in conference proceedings and journals. 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Whizar-Lugo"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"9829",title:"Biosimilars",subtitle:null,isOpenForSubmission:!1,hash:"c72171c1d1cf6df5aad989cb07cc8e4e",slug:"biosimilars",bookSignature:"Valderilio Feijó Azevedo and Robert Moots",coverURL:"https://cdn.intechopen.com/books/images_new/9829.jpg",editedByType:"Edited by",editors:[{id:"69875",title:"Dr.",name:"Valderilio",middleName:"Feijó",surname:"Feijó Azevedo",slug:"valderilio-feijo-azevedo",fullName:"Valderilio Feijó Azevedo"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}}],booksByTopicTotal:1834,seriesByTopicCollection:[{id:"3",title:"Dentistry",numberOfPublishedBooks:8,numberOfPublishedChapters:129,numberOfOpenTopics:2,numberOfUpcomingTopics:0,issn:"2631-6218",doi:"10.5772/intechopen.71199",isOpenForSubmission:!0},{id:"6",title:"Infectious Diseases",numberOfPublishedBooks:13,numberOfPublishedChapters:113,numberOfOpenTopics:3,numberOfUpcomingTopics:1,issn:"2631-6188",doi:"10.5772/intechopen.71852",isOpenForSubmission:!0},{id:"13",title:"Veterinary Medicine and Science",numberOfPublishedBooks:11,numberOfPublishedChapters:106,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2632-0517",doi:"10.5772/intechopen.73681",isOpenForSubmission:!0}],seriesByTopicTotal:3,mostCitedChapters:[{id:"19013",doi:"10.5772/21983",title:"Cell Responses to Surface and Architecture of Tissue Engineering Scaffolds",slug:"cell-responses-to-surface-and-architecture-of-tissue-engineering-scaffolds",totalDownloads:10483,totalCrossrefCites:132,totalDimensionsCites:303,abstract:null,book:{id:"314",slug:"regenerative-medicine-and-tissue-engineering-cells-and-biomaterials",title:"Regenerative Medicine and Tissue Engineering",fullTitle:"Regenerative Medicine and Tissue Engineering - Cells and Biomaterials"},signatures:"Hsin-I Chang and Yiwei Wang",authors:[{id:"45747",title:"Dr.",name:"Hsin-I",middleName:null,surname:"Chang",slug:"hsin-i-chang",fullName:"Hsin-I Chang"},{id:"53659",title:"Ms.",name:"Yiwei",middleName:null,surname:"Wang",slug:"yiwei-wang",fullName:"Yiwei Wang"}]},{id:"46479",doi:"10.5772/57353",title:"Floating Drug Delivery Systems for Eradication of Helicobacter pylori in Treatment of Peptic Ulcer Disease",slug:"floating-drug-delivery-systems-for-eradication-of-helicobacter-pylori-in-treatment-of-peptic-ulcer-d",totalDownloads:2838,totalCrossrefCites:136,totalDimensionsCites:293,abstract:null,book:{id:"3839",slug:"trends-in-helicobacter-pylori-infection",title:"Trends in Helicobacter pylori Infection",fullTitle:"Trends in Helicobacter pylori Infection"},signatures:"Yousef Javadzadeh and Sanaz Hamedeyazdan",authors:[{id:"94276",title:"Prof.",name:"Yousef",middleName:null,surname:"Javadzadeh",slug:"yousef-javadzadeh",fullName:"Yousef Javadzadeh"},{id:"98229",title:"Dr.",name:"Sanaz",middleName:null,surname:"Hamedeyazdan",slug:"sanaz-hamedeyazdan",fullName:"Sanaz Hamedeyazdan"}]},{id:"25512",doi:"10.5772/30872",title:"Epidemiology of Psychological Distress",slug:"epidemiology-of-psychological-distress",totalDownloads:8790,totalCrossrefCites:90,totalDimensionsCites:243,abstract:null,book:{id:"727",slug:"mental-illnesses-understanding-prediction-and-control",title:"Mental Illnesses",fullTitle:"Mental Illnesses - Understanding, Prediction and Control"},signatures:"Aline Drapeau, Alain Marchand and Dominic Beaulieu-Prévost",authors:[{id:"84582",title:"Dr.",name:"Aline",middleName:null,surname:"Drapeau",slug:"aline-drapeau",fullName:"Aline Drapeau"},{id:"84605",title:"Dr.",name:"Alain",middleName:null,surname:"Marchand",slug:"alain-marchand",fullName:"Alain Marchand"},{id:"84606",title:"Dr.",name:"Dominic",middleName:null,surname:"Beaulieu-Prévost",slug:"dominic-beaulieu-prevost",fullName:"Dominic Beaulieu-Prévost"}]},{id:"64762",doi:"10.5772/intechopen.82511",title:"Mechanism and Health Effects of Heavy Metal Toxicity in Humans",slug:"mechanism-and-health-effects-of-heavy-metal-toxicity-in-humans",totalDownloads:10236,totalCrossrefCites:100,totalDimensionsCites:229,abstract:"Several heavy metals are found naturally in the earth crust and are exploited for various industrial and economic purposes. Among these heavy metals, a few have direct or indirect impact on the human body. Some of these heavy metals such as copper, cobalt, iron, nickel, magnesium, molybdenum, chromium, selenium, manganese and zinc have functional roles which are essential for various diverse physiological and biochemical activities in the body. However, some of these heavy metals in high doses can be harmful to the body while others such as cadmium, mercury, lead, chromium, silver, and arsenic in minute quantities have delirious effects in the body causing acute and chronic toxicities in humans. The focus of this chapter is to describe the various mechanism of intoxication of some selected heavy metals in humans along with their health effects. Therefore it aims to highlight on biochemical mechanisms of heavy metal intoxication which involves binding to proteins and enzymes, altering their activity and causing damage. More so, the mechanism by which heavy metals cause neurotoxicity, generate free radical which promotes oxidative stress damaging lipids, proteins and DNA molecules and how these free radicals propagate carcinogenesis are discussed. Alongside these mechanisms, the noxious health effects of these heavy metals are discussed.",book:{id:"7111",slug:"poisoning-in-the-modern-world-new-tricks-for-an-old-dog-",title:"Poisoning in the Modern World",fullTitle:"Poisoning in the Modern World - New Tricks for an Old Dog?"},signatures:"Godwill Azeh Engwa, Paschaline Udoka Ferdinand, Friday Nweke Nwalo and Marian N. Unachukwu",authors:[{id:"241837",title:"Mr.",name:"Godwill Azeh",middleName:null,surname:"Engwa",slug:"godwill-azeh-engwa",fullName:"Godwill Azeh Engwa"},{id:"274194",title:"BSc.",name:"Paschaline Ferdinand",middleName:null,surname:"Okeke",slug:"paschaline-ferdinand-okeke",fullName:"Paschaline Ferdinand Okeke"},{id:"286975",title:"Dr.",name:"Friday",middleName:null,surname:"Nweke Nwalo",slug:"friday-nweke-nwalo",fullName:"Friday Nweke Nwalo"},{id:"286976",title:"Dr.",name:"Marian",middleName:null,surname:"Unachukwu",slug:"marian-unachukwu",fullName:"Marian Unachukwu"}]},{id:"27687",doi:"10.5772/29869",title:"Heavy Metals and Human Health",slug:"heavy-metals-and-human-health",totalDownloads:18954,totalCrossrefCites:83,totalDimensionsCites:191,abstract:null,book:{id:"1012",slug:"environmental-health-emerging-issues-and-practice",title:"Environmental Health",fullTitle:"Environmental Health - Emerging Issues and Practice"},signatures:"Simone Morais, Fernando Garcia e Costa and Maria de Lourdes Pereira",authors:[{id:"13875",title:"Prof.",name:"Simone",middleName:null,surname:"Morais",slug:"simone-morais",fullName:"Simone Morais"},{id:"79715",title:"Prof.",name:"Maria De Lourdes",middleName:null,surname:"Pereira",slug:"maria-de-lourdes-pereira",fullName:"Maria De Lourdes Pereira"},{id:"87294",title:"Prof.",name:"Fernando",middleName:null,surname:"Garcia E Costa",slug:"fernando-garcia-e-costa",fullName:"Fernando Garcia E Costa"}]}],mostDownloadedChaptersLast30Days:[{id:"64851",title:"Herbal Medicines in African Traditional Medicine",slug:"herbal-medicines-in-african-traditional-medicine",totalDownloads:14207,totalCrossrefCites:30,totalDimensionsCites:52,abstract:"African traditional medicine is a form of holistic health care system organized into three levels of specialty, namely divination, spiritualism, and herbalism. The traditional healer provides health care services based on culture, religious background, knowledge, attitudes, and beliefs that are prevalent in his community. Illness is regarded as having both natural and supernatural causes and thus must be treated by both physical and spiritual means, using divination, incantations, animal sacrifice, exorcism, and herbs. Herbal medicine is the cornerstone of traditional medicine but may include minerals and animal parts. The adjustment is ok, but may be replaced with –‘ Herbal medicine was once termed primitive by western medicine but through scientific investigations there is a better understanding of its therapeutic activities such that many pharmaceuticals have been modeled on phytochemicals derived from it. Major obstacles to the use of African medicinal plants are their poor quality control and safety. Traditional medical practices are still shrouded with much secrecy, with few reports or documentations of adverse reactions. However, the future of African traditional medicine is bright if viewed in the context of service provision, increase of health care coverage, economic potential, and poverty reduction. Formal recognition and integration of traditional medicine into conventional medicine will hold much promise for the future.",book:{id:"6302",slug:"herbal-medicine",title:"Herbal Medicine",fullTitle:"Herbal Medicine"},signatures:"Ezekwesili-Ofili Josephine Ozioma and Okaka Antoinette Nwamaka\nChinwe",authors:[{id:"191264",title:"Prof.",name:"Josephine",middleName:"Ozioma",surname:"Ezekwesili-Ofili",slug:"josephine-ezekwesili-ofili",fullName:"Josephine Ezekwesili-Ofili"},{id:"211585",title:"Prof.",name:"Antoinette",middleName:null,surname:"Okaka",slug:"antoinette-okaka",fullName:"Antoinette Okaka"}]},{id:"76640",title:"Control of Clinical Laboratory Errors by FMEA Model",slug:"control-of-clinical-laboratory-errors-by-fmea-model",totalDownloads:1131,totalCrossrefCites:0,totalDimensionsCites:0,abstract:"Patient safety is an aim for clinical applications and is a fundamental principle of healthcare and quality management. The main global health organizations have incorporated patient safety in their review of work practices. The data provided by the medical laboratories have a direct impact on patient safety and a fault in any of processes such as strategic, operational and support, could affect it. To provide appreciate and reliable data to the physicians, it is important to emphasize the need to design risk management plan in the laboratory. Failure Mode and Effect Analysis (FMEA) is an efficient technique for error detection and reduction. Technical Committee of the International Organization for Standardization (ISO) licensed a technical specification for medical laboratories suggesting FMEA as a method for prospective risk analysis of high-risk processes. FMEA model helps to identify quality failures, their effects and risks with their reduction/elimination, which depends on severity, probability and detection. Applying FMEA in clinical approaches can lead to a significant reduction of the risk priority number (RPN).",book:{id:"9808",slug:"contemporary-topics-in-patient-safety-volume-1",title:"Contemporary Topics in Patient Safety",fullTitle:"Contemporary Topics in Patient Safety - Volume 1"},signatures:"Hoda Sabati, Amin Mohsenzadeh and Nooshin Khelghati",authors:[{id:"340486",title:"M.Sc.",name:"Hoda",middleName:null,surname:"Sabati",slug:"hoda-sabati",fullName:"Hoda Sabati"},{id:"348872",title:"M.Sc.",name:"Amin",middleName:null,surname:"Mohsenzadeh",slug:"amin-mohsenzadeh",fullName:"Amin Mohsenzadeh"},{id:"348874",title:"MSc.",name:"Nooshin",middleName:null,surname:"Khelghati",slug:"nooshin-khelghati",fullName:"Nooshin Khelghati"}]},{id:"64762",title:"Mechanism and Health Effects of Heavy Metal Toxicity in Humans",slug:"mechanism-and-health-effects-of-heavy-metal-toxicity-in-humans",totalDownloads:10236,totalCrossrefCites:100,totalDimensionsCites:229,abstract:"Several heavy metals are found naturally in the earth crust and are exploited for various industrial and economic purposes. Among these heavy metals, a few have direct or indirect impact on the human body. Some of these heavy metals such as copper, cobalt, iron, nickel, magnesium, molybdenum, chromium, selenium, manganese and zinc have functional roles which are essential for various diverse physiological and biochemical activities in the body. However, some of these heavy metals in high doses can be harmful to the body while others such as cadmium, mercury, lead, chromium, silver, and arsenic in minute quantities have delirious effects in the body causing acute and chronic toxicities in humans. The focus of this chapter is to describe the various mechanism of intoxication of some selected heavy metals in humans along with their health effects. Therefore it aims to highlight on biochemical mechanisms of heavy metal intoxication which involves binding to proteins and enzymes, altering their activity and causing damage. More so, the mechanism by which heavy metals cause neurotoxicity, generate free radical which promotes oxidative stress damaging lipids, proteins and DNA molecules and how these free radicals propagate carcinogenesis are discussed. Alongside these mechanisms, the noxious health effects of these heavy metals are discussed.",book:{id:"7111",slug:"poisoning-in-the-modern-world-new-tricks-for-an-old-dog-",title:"Poisoning in the Modern World",fullTitle:"Poisoning in the Modern World - New Tricks for an Old Dog?"},signatures:"Godwill Azeh Engwa, Paschaline Udoka Ferdinand, Friday Nweke Nwalo and Marian N. Unachukwu",authors:[{id:"241837",title:"Mr.",name:"Godwill Azeh",middleName:null,surname:"Engwa",slug:"godwill-azeh-engwa",fullName:"Godwill Azeh Engwa"},{id:"274194",title:"BSc.",name:"Paschaline Ferdinand",middleName:null,surname:"Okeke",slug:"paschaline-ferdinand-okeke",fullName:"Paschaline Ferdinand Okeke"},{id:"286975",title:"Dr.",name:"Friday",middleName:null,surname:"Nweke Nwalo",slug:"friday-nweke-nwalo",fullName:"Friday Nweke Nwalo"},{id:"286976",title:"Dr.",name:"Marian",middleName:null,surname:"Unachukwu",slug:"marian-unachukwu",fullName:"Marian Unachukwu"}]},{id:"65467",title:"Anesthesia Management for Large-Volume Liposuction",slug:"anesthesia-management-for-large-volume-liposuction",totalDownloads:5965,totalCrossrefCites:0,totalDimensionsCites:0,abstract:"The apparent easiness with which liposuction is performed favors that patients, young surgeons, and anesthesiologists without experience in this field ignore the many events that occur during this procedure. Liposuction is a procedure to improve the body contour and not a surgery to reduce weight, although recently people who have failed in their plans to lose weight look at liposuction as a means to contour their body figure. Tumescent liposuction of large volumes requires a meticulous selection of each patient; their preoperative evaluation and perioperative management are essential to obtain the expected results. The various techniques of general anesthesia are the most recommended and should be monitored in the usual way, as well as monitoring the total doses of infiltrated local anesthetics to avoid systemic toxicity. The management of intravenous fluids is controversial, but the current trend is the restricted use of hydrosaline solutions. The most feared complications are deep vein thrombosis, pulmonary thromboembolism, fat embolism, lung edema, hypothermia, infections and even death. The adherence to the management guidelines and prophylaxis of venous thrombosis/thromboembolism is mandatory.",book:{id:"6221",slug:"anesthesia-topics-for-plastic-and-reconstructive-surgery",title:"Anesthesia Topics for Plastic and Reconstructive Surgery",fullTitle:"Anesthesia Topics for Plastic and Reconstructive Surgery"},signatures:"Sergio Granados-Tinajero, Carlos Buenrostro-Vásquez, Cecilia\nCárdenas-Maytorena and Marcela Contreras-López",authors:[{id:"273532",title:"Dr.",name:"Sergio Octavio",middleName:null,surname:"Granados Tinajero",slug:"sergio-octavio-granados-tinajero",fullName:"Sergio Octavio Granados Tinajero"}]},{id:"30178",title:"Chest Mobilization Techniques for Improving Ventilation and Gas Exchange in Chronic Lung Disease",slug:"chest-mobilization-techniques-for-improving-ventilation-and-gas-exchange-in-chronic-lung-disease",totalDownloads:31193,totalCrossrefCites:0,totalDimensionsCites:5,abstract:null,book:{id:"648",slug:"chronic-obstructive-pulmonary-disease-current-concepts-and-practice",title:"Chronic Obstructive Pulmonary Disease",fullTitle:"Chronic Obstructive Pulmonary Disease - Current Concepts and Practice"},signatures:"Donrawee Leelarungrayub",authors:[{id:"73709",title:"Associate Prof.",name:"Jirakrit",middleName:null,surname:"Leelarungrayub",slug:"jirakrit-leelarungrayub",fullName:"Jirakrit Leelarungrayub"}]}],onlineFirstChaptersFilter:{topicId:"3",limit:6,offset:0},onlineFirstChaptersCollection:[{id:"82321",title:"Noncanonical (Non-R132H) IDH-Mutated Gliomas",slug:"noncanonical-non-r132h-idh-mutated-gliomas",totalDownloads:3,totalDimensionsCites:0,doi:"10.5772/intechopen.105469",abstract:"Mutations in IDH1 or IDH2 confer a significant survival advantage compared to their isocitrate dehydrogenase (IDH) wild-type counterparts and, as such, are the most significant prognostic factors in this group. The mutations in the IDH1 gene are heterozygous and almost always involve only a single residue (arginine 132), which is replaced by histidine in roughly 90% of tumors. Regardless, the non-p.R132H (noncanonical) mutations in the IDH1 gene were also documented in around 20% of mutated glioma. The noncanonical IDH mutations have distinguishing radiological and histological features. The existence of such tumors seems to be associated with a genetic predisposition to cancer development.",book:{id:"11597",title:"Glioblastoma - Current Evidences",coverURL:"https://cdn.intechopen.com/books/images_new/11597.jpg"},signatures:"Tariq D. Al-Saadi and Roberto J. Diaz"},{id:"82492",title:"Treatment of Patients with Newly-Diagnosed Multiple Myeloma",slug:"treatment-of-patients-with-newly-diagnosed-multiple-myeloma",totalDownloads:2,totalDimensionsCites:0,doi:"10.5772/intechopen.105774",abstract:"Multiple Myeloma is an incurable disease. It is responsible for 1.8% of all cancers. The median age is 69–71 years. The treatment of MM is challenging and is affected by several factors such as the patient’s age, comorbidity index, and fitness. The main combination regimen consists of the addition of proteasome inhibitors and IMIDs to steroids. In all studies conducted to date, the results obtained in transplanted patients are better than in patients who did not proceed into transplantation. Before starting treatment, risk stratification should be performed for all patients, and they should be treated accordingly. Recently, there have been advances in the treatment with the introduction of new agents, particularly monoclonal antibodies.",book:{id:"11600",title:"Recent Update on Multiple Myeloma\ufeff",coverURL:"https://cdn.intechopen.com/books/images_new/11600.jpg"},signatures:"Ali Zahit Bolaman and Atakan Turgutkaya"},{id:"82458",title:"Perspective Chapter about Surgical Management of Symptomatic Rectocele",slug:"perspective-chapter-about-surgical-management-of-symptomatic-rectocele",totalDownloads:0,totalDimensionsCites:0,doi:"10.5772/intechopen.105505",abstract:"Rectocele is defined as a herniation of the anterior rectal wall through the posterior vaginal wall into the vaginal lumen caused by rectovaginal septum weakness. This entity is more common in postmenopausal female patients. Approximately one-third of adult women affected with pelvic organ prolapse have a significant impact on their quality of life and emotional well-being. Up to more than 90% of woman can be asymptomatic. In symptomatic cases, constipation, defecatory disorders such as obstructed syndrome (ODS) or incontinence, vaginal mass, and pelvic discomfort are the main complaints. Surgical treatment is indicated after failure of conservative management. Talking about ODS, nearly 20% of the patients need surgery. Surgical options can be classified as abdominal (being laparoscopic colposacropexy the technique of choice) or perineal approach. In the latter group, the alternatives are transanal (TA), transperineal (TP), and transvaginal (TV) approaches with or without prosthetic material or grafts. Native-tissue transvaginal approach should be preferentially performed as it has shown better results. Nowadays, there is no consensus on what the gold-standard technique is given the lack of strong evidence.",book:{id:"11272",title:"Benign Anorectal Disorders - An Update",coverURL:"https://cdn.intechopen.com/books/images_new/11272.jpg"},signatures:"Esther María Cano Pecharromán, A. Teresa Calderón Duque, Juan Carlos Santiago Peña and Tomás Balsa Marín"},{id:"82480",title:"The Role of Microglia in Neuroinflammation",slug:"the-role-of-microglia-in-neuroinflammation",totalDownloads:2,totalDimensionsCites:0,doi:"10.5772/intechopen.105865",abstract:"Microglia typically exist in a resting state of a mature brain and monitors the brain environment. In response to brain injuries or immunological stimuli, however, microglia are readily activated. In their activated state, they can serve diverse beneficial functions essential for enhancing neuron survival through the release of trophic and anti-inflammatory factors. Under certain circumstances, such as sustained epilepsy, however, microglia become overactivated and can induce significant and highly detrimental neurotoxic effects by the excessive production of a large array of cytotoxic factors, such as nitric oxide and proinflammatory cytokines. Neuroinflammation has been identified in epileptogenic tissue and is suspected of participating in epileptogenesis. Recent evidence has shown the effects of anti-inflammation and protection against ischemic brain injury by inhibiting soluble epoxide hydrolase (sEH) pharmacologically and genetically. We assume that sEH inhibition might be also beneficial to prevent inflammatory processes caused by seizures and subsequent chronic epilepsy. In the present study, we investigated whether sEH is involved in overactivated microglia-induced neuroinflammation and subsequent epileptogenesis in a mouse model of temporal lobe epilepsy. Overactivated microglia will be detected by using imaging techniques. It is hoped that the results of the present study would provide a better understanding of the roles of sEH and microglia in epileptogenesis.",book:{id:"11585",title:"Epilepsy - Seizures Without Triggers",coverURL:"https://cdn.intechopen.com/books/images_new/11585.jpg"},signatures:"Shao-Wen Hung, Chia-Chi Chen, Hsiao-Yun Chen, Ying-Ching Hung, Ping-Min Huang and Chia-Yu Lin"},{id:"82489",title:"Changes in Brain Metabolism Induced by Metabolic Challenges and Their Beneficial Roles for Brain Aging",slug:"changes-in-brain-metabolism-induced-by-metabolic-challenges-and-their-beneficial-roles-for-brain-agi",totalDownloads:1,totalDimensionsCites:0,doi:"10.5772/intechopen.105778",abstract:"Life expectancy has been increasing globally along with the risk of developing Alzheimer’s or other dementias. Diets high in saturated fats, refined sugars and a sedentary lifestyle are determining factors in the development of a metabolic syndrome. These factors induce energy imbalance and dysfunctional brain metabolism, hence increasing the risk of cognitive impairment and/or dementia. A cohort study with mild cognitive impairment found that it was found that the presence of three or more components of a metabolic syndrome increased the risk of Alzheimer’s. On the other hand, hyperglycemia induces glutamate excitotoxicity in neurons, β-amyloid accumulation, tau phosphorylation and oxidative stress. The present chapter will cover the dysregulation of brain metabolism during physiological and pathological aging, and how metabolic challenges such fasting, caloric restriction and ketogenic diet reverts many of the deleterious effects of brain aging, favoring energy balance and cognitive function.",book:{id:"11710",title:"Lifestyle-Related Diseases and Metabolic Syndrome",coverURL:"https://cdn.intechopen.com/books/images_new/11710.jpg"},signatures:"Claudia Carvallo"},{id:"81607",title:"Does Physical Activity Mediate the Effect of Loneliness on Inflammatory and Metabolic Processes?",slug:"does-physical-activity-mediate-the-effect-of-loneliness-on-inflammatory-and-metabolic-processes",totalDownloads:4,totalDimensionsCites:0,doi:"10.5772/intechopen.104915",abstract:"The study to be presented in the chapter explores one potential behavioral mechanism by which loneliness affects inflammatory and metabolic processes in old age. Specifically, it addresses whether physical activity mediates the loneliness—inflammatory/metabolic dysregulation association. Multivariate linear regressions were applied to data derived from the Health and Retirement Study (HRS). The findings revealed that loneliness was prospectively associated with elevated values of log C-reactive protein (log-CRP) and with amplified levels of Glycated hemoglobin (HbA1c), Cystatin C (CysC), and Body Mass Index (BMI), after controlling for socio-demographics. Second, physical activity mediated the association between loneliness with prospective values of log-CRP and also mediated associations between loneliness and prospective levels of metabolic biomarkers. 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He worked as a post-doctoral fellow at the Public Health Research Institute (PHRI), Newark, NJ for four years before accepting a three-year faculty position at Brigham Young University-Hawaii. Dr. Engohang-Ndong is a tenured faculty member with the academic rank of Full Professor at Kent State University, Ohio, where he teaches a wide range of biological science courses and pursues his research in medical and environmental microbiology. 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He has an excellent track record in the herpesvirus field, and his group is engaged in clinical research in the field of Epstein-Barr virus diseases. He is the editor of the online Encyclopedia of Environment and he coordinates the Universal Health Coverage education program for the BioHealth Computing Schools of the European Institute of Science.",institutionString:null,institution:{name:"Grenoble Alpes University",country:{name:"France"}}},{id:"131400",title:"Prof.",name:"Alfonso J.",middleName:null,surname:"Rodriguez-Morales",slug:"alfonso-j.-rodriguez-morales",fullName:"Alfonso J. Rodriguez-Morales",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/131400/images/system/131400.png",biography:"Dr. Rodriguez-Morales is an expert in tropical and emerging diseases, particularly zoonotic and vector-borne diseases (especially arboviral diseases). He is the president of the Travel Medicine Committee of the Pan-American Infectious Diseases Association (API), as well as the president of the Colombian Association of Infectious Diseases (ACIN). He is a member of the Committee on Tropical Medicine, Zoonoses, and Travel Medicine of ACIN. He is a vice-president of the Latin American Society for Travel Medicine (SLAMVI) and a Member of the Council of the International Society for Infectious Diseases (ISID). Since 2014, he has been recognized as a Senior Researcher, at the Ministry of Science of Colombia. He is a professor at the Faculty of Medicine of the Fundacion Universitaria Autonoma de las Americas, in Pereira, Risaralda, Colombia. He is an External Professor, Master in Research on Tropical Medicine and International Health, Universitat de Barcelona, Spain. He is also a professor at the Master in Clinical Epidemiology and Biostatistics, Universidad Científica del Sur, Lima, Peru. In 2021 he has been awarded the “Raul Isturiz Award” Medal of the API. Also, in 2021, he was awarded with the “Jose Felix Patiño” Asclepius Staff Medal of the Colombian Medical College, due to his scientific contributions to COVID-19 during the pandemic. He is currently the Editor in Chief of the journal Travel Medicine and Infectious Diseases. His Scopus H index is 47 (Google Scholar H index, 68).",institutionString:"Institución Universitaria Visión de las Américas, Colombia",institution:null},{id:"332819",title:"Dr.",name:"Chukwudi Michael",middleName:"Michael",surname:"Egbuche",slug:"chukwudi-michael-egbuche",fullName:"Chukwudi Michael Egbuche",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/332819/images/14624_n.jpg",biography:"I an Dr. Chukwudi Michael Egbuche. I am a Senior Lecturer in the Department of Parasitology and Entomology, Nnamdi Azikiwe University, Awka.",institutionString:null,institution:{name:"Nnamdi Azikiwe University",country:{name:"Nigeria"}}},{id:"284232",title:"Mr.",name:"Nikunj",middleName:"U",surname:"Tandel",slug:"nikunj-tandel",fullName:"Nikunj Tandel",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/284232/images/8275_n.jpg",biography:'Mr. Nikunj Tandel has completed his Master\'s degree in Biotechnology from VIT University, India in the year of 2012. He is having 8 years of research experience especially in the field of malaria epidemiology, immunology, and nanoparticle-based drug delivery system against the infectious diseases, autoimmune disorders and cancer. He has worked for the NIH funded-International Center of Excellence in Malaria Research project "Center for the study of complex malaria in India (CSCMi)" in collaboration with New York University. The preliminary objectives of the study are to understand and develop the evidence-based tools and interventions for the control and prevention of malaria in different sites of the INDIA. Alongside, with the help of next-generation genomics study, the team has studied the antimalarial drug resistance in India. Further, he has extended his research in the development of Humanized mice for the study of liver-stage malaria and identification of molecular marker(s) for the Artemisinin resistance. At present, his research focuses on understanding the role of B cells in the activation of CD8+ T cells in malaria. 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She is currently an Adjunct Professor at Feevale University in Medicine and Biomedicine courses and a permanent professor of the Academic Master\\'s Degree in Virology. She has experience in the field of Microbiology, with an emphasis on Bacteriology, working mainly on the following topics: bacteriophages, bacterial resistance, clinical microbiology and food microbiology.",institutionString:null,institution:{name:"Universidade Feevale",country:{name:"Brazil"}}},{id:"229220",title:"Dr.",name:"Amjad",middleName:"Islam",surname:"Aqib",slug:"amjad-aqib",fullName:"Amjad Aqib",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/229220/images/system/229220.png",biography:"Dr. Amjad Islam Aqib obtained a DVM and MSc (Hons) from University of Agriculture Faisalabad (UAF), Pakistan, and a PhD from the University of Veterinary and Animal Sciences Lahore, Pakistan. 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Professor Derbel is presently working at the Clinique les Oliviers, Sousse, Tunisia. His hospital activities are mostly concerned with laparoscopic, colorectal, pancreatic, hepatobiliary, and gastric surgery. He is also very interested in hernia surgery and performs ventral hernia repairs and inguinal hernia repairs. He has been a member of the GREPA and Tunisian Hernia Society (THS). During his residency, he managed patients suffering from diabetic foot, and he was very interested in this pathology. For this reason, he decided to coordinate a book project dealing with the diabetic foot. 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She has published several articles in diffrent journals.",institutionString:"Sidi Bouzid Regional Hospital",institution:null},{id:"229481",title:"Dr.",name:"Erika M.",middleName:"Martins",surname:"de Carvalho",slug:"erika-m.-de-carvalho",fullName:"Erika M. de Carvalho",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/229481/images/6397_n.jpg",biography:null,institutionString:null,institution:{name:"Oswaldo Cruz Foundation",country:{name:"Brazil"}}},{id:"186537",title:"Prof.",name:"Tonay",middleName:null,surname:"Inceboz",slug:"tonay-inceboz",fullName:"Tonay Inceboz",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/186537/images/system/186537.jfif",biography:"I was graduated from Ege University of Medical Faculty (Turkey) in 1988 and completed his Med. PhD degree in Medical Parasitology at the same university. I became an Associate Professor in 2008 and Professor in 2014. I am currently working as a Professor at the Department of Medical Parasitology at Dokuz Eylul University, Izmir, Turkey.\n\nI have given many lectures, presentations in different academic meetings. I have more than 60 articles in peer-reviewed journals, 18 book chapters, 1 book editorship.\n\nMy research interests are Echinococcus granulosus, Echinococcus multilocularis (diagnosis, life cycle, in vitro and in vivo cultivation), and Trichomonas vaginalis (diagnosis, PCR, and in vitro cultivation).",institutionString:"Dokuz Eylül University",institution:{name:"Dokuz Eylül University",country:{name:"Turkey"}}},{id:"71812",title:"Prof.",name:"Hanem Fathy",middleName:"Fathy",surname:"Khater",slug:"hanem-fathy-khater",fullName:"Hanem Fathy Khater",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/71812/images/1167_n.jpg",biography:"Prof. Khater is a Professor of Parasitology at Benha University, Egypt. She studied for her doctoral degree, at the Department of Entomology, College of Agriculture, Food and Natural Resources, University of Missouri, Columbia, USA. She has completed her Ph.D. degrees in Parasitology in Egypt, from where she got the award for “the best scientific Ph.D. dissertation”. She worked at the School of Biological Sciences, Bristol, England, the UK in controlling insects of medical and veterinary importance as a grant from Newton Mosharafa, the British Council. Her research is focused on searching of pesticides against mosquitoes, house flies, lice, green bottle fly, camel nasal botfly, soft and hard ticks, mites, and the diamondback moth as well as control of several parasites using safe and natural materials to avoid drug resistances and environmental contamination.",institutionString:null,institution:{name:"Banha University",country:{name:"Egypt"}}},{id:"99780",title:"Prof.",name:"Omolade",middleName:"Olayinka",surname:"Okwa",slug:"omolade-okwa",fullName:"Omolade Okwa",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/99780/images/system/99780.jpg",biography:"Omolade Olayinka Okwa is presently a Professor of Parasitology at Lagos State University, Nigeria. She has a PhD in Parasitology (1997), an MSc in Cellular Parasitology (1992), and a BSc (Hons) Zoology (1990) all from the University of Ibadan, Nigeria. She teaches parasitology at the undergraduate and postgraduate levels. She was a recipient of a Commonwealth fellowship supported by British Council tenable at the Centre for Entomology and Parasitology (CAEP), Keele University, United Kingdom between 2004 and 2005. She was awarded an Honorary Visiting Research Fellow at the same university from 2005 to 2007. \nShe has been an external examiner to the Department of Veterinary Microbiology and Parasitology, University of Ibadan, MSc programme between 2010 and 2012. She is a member of the Nigerian Society of Experimental Biology (NISEB), Parasitology and Public Health Society of Nigeria (PPSN), Science Association of Nigeria (SAN), Zoological Society of Nigeria (ZSN), and is Vice Chairperson of the Organisation of Women in Science (OWSG), LASU chapter. She served as Head of Department of Zoology and Environmental Biology, Lagos State University from 2007 to 2010 and 2014 to 2016. She is a reviewer for several local and international journals such as Unilag Journal of Science, Libyan Journal of Medicine, Journal of Medicine and Medical Sciences, and Annual Research and Review in Science. \nShe has authored 45 scientific research publications in local and international journals, 8 scientific reviews, 4 books, and 3 book chapters, which includes the books “Malaria Parasites” and “Malaria” which are IntechOpen access publications.",institutionString:"Lagos State University",institution:{name:"Lagos State University",country:{name:"Nigeria"}}},{id:"273100",title:"Dr.",name:"Vijay",middleName:null,surname:"Gayam",slug:"vijay-gayam",fullName:"Vijay Gayam",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/273100/images/system/273100.jpeg",biography:"Dr. Vijay Bhaskar Reddy Gayam is currently practicing as an internist at Interfaith Medical Center in Brooklyn, New York, USA. He is also a Clinical Assistant Professor at the SUNY Downstate University Hospital and Adjunct Professor of Medicine at the American University of Antigua. He is a holder of an M.B.B.S. degree bestowed to him by Osmania Medical College and received his M.D. at Interfaith Medical Center. His career goals thus far have heavily focused on direct patient care, medical education, and clinical research. He currently serves in two leadership capacities; Assistant Program Director of Medicine at Interfaith Medical Center and as a Councilor for the American\r\nFederation for Medical Research. As a true academician and researcher, he has more than 50 papers indexed in international peer-reviewed journals. He has also presented numerous papers in multiple national and international scientific conferences. His areas of research interest include general internal medicine, gastroenterology and hepatology. He serves as an editor, editorial board member and reviewer for multiple international journals. His research on Hepatitis C has been very successful and has led to multiple research awards, including the 'Equity in Prevention and Treatment Award” from the New York Department of Health Viral Hepatitis Symposium (2018) and the 'Presidential Poster Award” awarded to him by the American College of Gastroenterology (2018). He was also awarded 'Outstanding Clinician in General Medicine” by Venus International Foundation for his extensive research expertise and services, perform over and above the standard expected in the advancement of healthcare, patient safety and quality of care.",institutionString:"Interfaith Medical Center",institution:{name:"Interfaith Medical Center",country:{name:"United States of America"}}},{id:"93517",title:"Dr.",name:"Clement",middleName:"Adebajo",surname:"Meseko",slug:"clement-meseko",fullName:"Clement Meseko",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/93517/images/system/93517.jpg",biography:"Dr. Clement Meseko obtained DVM and PhD degree in Veterinary Medicine and Virology respectively. He has worked for over 20 years in both private and public sectors including the academia, contributing to knowledge and control of infectious disease. Through the application of epidemiological skill, classical and molecular virological skills, he investigates viruses of economic and public health importance for the mitigation of the negative impact on people, animal and the environment in the context of Onehealth. \r\nDr. Meseko’s field experience on animal and zoonotic diseases and pathogen dynamics at the human-animal interface over the years shaped his carrier in research and scientific inquiries. He has been part of the investigation of Highly Pathogenic Avian Influenza incursions in sub Saharan Africa and monitors swine Influenza (Pandemic influenza Virus) agro-ecology and potential for interspecies transmission. 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His research work has been published in various high-impact factor journals (Science, PNAS, Nature Medicine) with a high number of citations. He has received many awards and honors in India and abroad including various Young Scientist Awards, BBSRC India Partnering Award, and Dr. JC Bose National Award of Department of Biotechnology, Min. of Science and Technology, Govt. of India. Dr. Saxena is a fellow of various international societies/academies including the Royal College of Pathologists, United Kingdom; Royal Society of Medicine, London; Royal Society of Biology, United Kingdom; Royal Society of Chemistry, London; and Academy of Translational Medicine Professionals, Austria. He was named a Global Leader in Science by The Scientist. He is also an international opinion leader/expert in vaccination for Japanese encephalitis by IPIC (UK).",institutionString:"King George's Medical University",institution:{name:"King George's Medical University",country:{name:"India"}}},{id:"94928",title:"Dr.",name:"Takuo",middleName:null,surname:"Mizukami",slug:"takuo-mizukami",fullName:"Takuo Mizukami",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/94928/images/6402_n.jpg",biography:null,institutionString:null,institution:{name:"National Institute of Infectious Diseases",country:{name:"Japan"}}},{id:"233433",title:"Dr.",name:"Yulia",middleName:null,surname:"Desheva",slug:"yulia-desheva",fullName:"Yulia Desheva",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/233433/images/system/233433.png",biography:"Dr. Yulia Desheva is a leading researcher at the Institute of Experimental Medicine, St. Petersburg, Russia. She is a professor in the Stomatology Faculty, St. Petersburg State University. She has expertise in the development and evaluation of a wide range of live mucosal vaccines against influenza and bacterial complications. Her research interests include immunity against influenza and COVID-19 and the development of immunization schemes for high-risk individuals.",institutionString:'Federal State Budgetary Scientific Institution "Institute of Experimental Medicine"',institution:null},{id:"238958",title:"Mr.",name:"Atamjit",middleName:null,surname:"Singh",slug:"atamjit-singh",fullName:"Atamjit Singh",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/238958/images/6575_n.jpg",biography:null,institutionString:null,institution:null},{id:"333753",title:"Dr.",name:"Rais",middleName:null,surname:"Ahmed",slug:"rais-ahmed",fullName:"Rais Ahmed",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/333753/images/20168_n.jpg",biography:null,institutionString:null,institution:null},{id:"252058",title:"M.Sc.",name:"Juan",middleName:null,surname:"Sulca",slug:"juan-sulca",fullName:"Juan Sulca",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/252058/images/12834_n.jpg",biography:null,institutionString:null,institution:null},{id:"191392",title:"Dr.",name:"Marimuthu",middleName:null,surname:"Govindarajan",slug:"marimuthu-govindarajan",fullName:"Marimuthu Govindarajan",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/191392/images/5828_n.jpg",biography:"Dr. M. Govindarajan completed his BSc degree in Zoology at Government Arts College (Autonomous), Kumbakonam, and MSc, MPhil, and PhD degrees at Annamalai University, Annamalai Nagar, Tamil Nadu, India. He is serving as an assistant professor at the Department of Zoology, Annamalai University. His research interests include isolation, identification, and characterization of biologically active molecules from plants and microbes. He has identified more than 20 pure compounds with high mosquitocidal activity and also conducted high-quality research on photochemistry and nanosynthesis. He has published more than 150 studies in journals with impact factor and 2 books in Lambert Academic Publishing, Germany. He serves as an editorial board member in various national and international scientific journals.",institutionString:null,institution:null},{id:"274660",title:"Dr.",name:"Damodar",middleName:null,surname:"Paudel",slug:"damodar-paudel",fullName:"Damodar Paudel",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/274660/images/8176_n.jpg",biography:"I am DrDamodar Paudel,currently working as consultant Physician in Nepal police Hospital.",institutionString:null,institution:null},{id:"241562",title:"Dr.",name:"Melvin",middleName:null,surname:"Sanicas",slug:"melvin-sanicas",fullName:"Melvin Sanicas",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/241562/images/6699_n.jpg",biography:null,institutionString:null,institution:null},{id:"337446",title:"Dr.",name:"Maria",middleName:null,surname:"Zavala-Colon",slug:"maria-zavala-colon",fullName:"Maria Zavala-Colon",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"University of Puerto Rico, Medical Sciences Campus",country:{name:"United States of America"}}},{id:"338856",title:"Mrs.",name:"Nur Alvira",middleName:null,surname:"Pascawati",slug:"nur-alvira-pascawati",fullName:"Nur Alvira Pascawati",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Universitas Respati Yogyakarta",country:{name:"Indonesia"}}},{id:"441116",title:"Dr.",name:"Jovanka M.",middleName:null,surname:"Voyich",slug:"jovanka-m.-voyich",fullName:"Jovanka M. 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\r\n\tPollution is caused by a wide variety of human activities and occurs in diverse forms, for example biological, chemical, et cetera. In recent years, significant efforts have been made to ensure that the environment is clean, that rigorous rules are implemented, and old laws are updated to reduce the risks towards humans and ecosystems. However, rapid industrialization and the need for more cultivable sources or habitable lands, for an increasing population, as well as fewer alternatives for waste disposal, make the pollution control tasks more challenging. Therefore, this topic will focus on assessing and managing environmental pollution. It will cover various subjects, including risk assessment due to the pollution of ecosystems, transport and fate of pollutants, restoration or remediation of polluted matrices, and efforts towards sustainable solutions to minimize environmental pollution.
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Dr. Rahman was also adjunctly attached with Kanazawa University, Japan (Visiting Research Professor, Dec 2014 to Mar 2015; JSPS Postdoctoral Research Fellow, Apr 2012 to Mar 2014), and Tokyo Institute of Technology, Japan (TokyoTech-UNESCO Research Fellow, Oct 2004–Sep 2005). \nHe received his Ph.D. degree in Environmental Analytical Chemistry from Kanazawa University, Japan (2011). He also achieved a Diploma in Environment from the Tokyo Institute of Technology, Japan (2005). Besides, he has an M.Sc. degree in Applied Chemistry and a B.Sc. degree in Chemistry, all from the University of Chittagong, Bangladesh. \nDr. Rahman’s research interest includes the study of the fate and behavior of environmental pollutants in the biosphere; design of low energy and low burden environmental improvement (remediation) technology; implementation of sustainable waste management practices for treatment, handling, reuse, and ultimate residual disposition of solid wastes; nature and type of interactions in organic liquid mixtures for process engineering design applications.",institutionString:null,institution:{name:"Fukushima University",institutionURL:null,country:{name:"Japan"}}},editorTwo:{id:"201020",title:"Dr.",name:"Zinnat Ara",middleName:null,surname:"Begum",slug:"zinnat-ara-begum",fullName:"Zinnat Ara Begum",profilePictureURL:"https://mts.intechopen.com/storage/users/201020/images/system/201020.jpeg",biography:"Zinnat A. Begum received her Ph.D. in Environmental Analytical Chemistry from Kanazawa University in 2012. She achieved her Master of Science (M.Sc.) degree with a major in Applied Chemistry and a Bachelor of Science (B.Sc.) in Chemistry, all from the University of Chittagong, Bangladesh. Her work affiliations include Fukushima University, Japan (Visiting Research Fellow, Institute of Environmental Radioactivity: Mar 2016 to present), Southern University Bangladesh (Assistant Professor, Department of Civil Engineering: Jan 2015 to present), and Kanazawa University, Japan (Postdoctoral Fellow, Institute of Science and Engineering: Oct 2012 to Mar 2014; Research fellow, Venture Business Laboratory, Advanced Science and Social Co-Creation Promotion Organization: Apr 2018 to Mar 2021). 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