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Barely three months into the new year and we are happy to announce a monumental milestone reached - 150 million downloads.
\n\nThis achievement solidifies IntechOpen’s place as a pioneer in Open Access publishing and the home to some of the most relevant scientific research available through Open Access.
\n\nWe are so proud to have worked with so many bright minds throughout the years who have helped us spread knowledge through the power of Open Access and we look forward to continuing to support some of the greatest thinkers of our day.
\n\nThank you for making IntechOpen your place of learning, sharing, and discovery, and here’s to 150 million more!
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However, this book on Hydraulic Conductivity presents comprehensive reviews of new measurements and numerical techniques for estimating hydraulic conductivity. This is achieved by the chapters written by various experts in this field of research into a number of clustered themes covering different aspects of hydraulic conductivity. The sections in the book are: Hydraulic conductivity and its importance, Hydraulic conductivity and plant systems, Determination by mathematical and laboratory methods, Determination by field techniques and Modelling and hydraulic conductivity. Each of these sections of the book includes chapters highlighting the salient aspects and most of these chapters explain the facts with the help of some case studies. Thus this book has a good mix of chapters dealing with various and vital aspects of hydraulic conductivity from various authors of different countries.",isbn:null,printIsbn:"978-953-307-288-3",pdfIsbn:"978-953-51-4396-3",doi:"10.5772/744",price:139,priceEur:155,priceUsd:179,slug:"hydraulic-conductivity-issues-determination-and-applications",numberOfPages:448,isOpenForSubmission:!1,isInWos:1,isInBkci:!0,hash:"77f359622d92baeaf977c1632585e1b4",bookSignature:"Lakshmanan Elango",publishedDate:"November 23rd 2011",coverURL:"https://cdn.intechopen.com/books/images_new/220.jpg",numberOfDownloads:80982,numberOfWosCitations:81,numberOfCrossrefCitations:26,numberOfCrossrefCitationsByBook:2,numberOfDimensionsCitations:79,numberOfDimensionsCitationsByBook:2,hasAltmetrics:0,numberOfTotalCitations:186,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"October 20th 2010",dateEndSecondStepPublish:"November 17th 2010",dateEndThirdStepPublish:"March 24th 2011",dateEndFourthStepPublish:"April 23rd 2011",dateEndFifthStepPublish:"June 22nd 2011",currentStepOfPublishingProcess:5,indexedIn:"1,2,3,4,5,6,7,8",editedByType:"Edited by",kuFlag:!1,featuredMarkup:null,editors:[{id:"47726",title:"Prof.",name:"Lakshmanan",middleName:null,surname:"Elango",slug:"lakshmanan-elango",fullName:"Lakshmanan Elango",profilePictureURL:"https://mts.intechopen.com/storage/users/47726/images/1851_n.jpg",biography:"Professor L. Elango is a specialist in the field of hydrogeological characterisation, hydrochemical studies, hydrogeophysics and groundwater modelling. He had professional training in Danish Hydraulic Institute, Swiss Federal Institute of Technology, University of Newcastle, University of Bath, University of Birmingham and Ruhr University. He has carried out sponsored research projects on various aspects of hydrogeology, including the ones funded by the British Geological Survey, Australian Research Council, Russian Academy of Sciences and the European Commission. He has published about 50 research papers in various journals and four books. He is a Vice President of International Commission on Water Quality of IAHS. He has organised many training programmes, workshops and conferences in the field of hydrogeology, including capacity building programmes under The World Bank funded Hydrology Project and UNESCO’s International Hydrology Programme. He is in the editorial board of a few international journals. 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\r\n\tNatural products of spiroketals have shown a wide range of significant biological activities. The purpose of this book is to discuss the isolation, structure elucidation, biological activities of various spiroketals of monoterpenoids, sesquiterpenoids, diterpenoids, sesterpenoids, and triterpenoids. In addition, spirostanol saponins are one kind of important class compounds in medicinal plants. Spiroketals also contain specific chromophores. Thus, this book also provides a powerful approach to the determination of their absolute configuration using electronic circular dichroism (ECD) in combination with ECD calculations by time-dependent density functional theory (TDDFT). This book aims to cover topics such as introduction to spiro compounds, spiroketals of monoterpenoids and sesquiterpenoids: isolation, structure elucidation, biological activity, spiroketal of diterpenoids and sesterpenoids: Isolation, structure elucidation, and biological activity, spirostanol saponin and Pharmacological aspects, absolute configuration determination of spiroketals using NMR and CD methods, total synthesis of spiroketals from natural products.
",isbn:null,printIsbn:"979-953-307-X-X",pdfIsbn:null,doi:null,price:0,priceEur:0,priceUsd:0,slug:null,numberOfPages:0,isOpenForSubmission:!1,isSalesforceBook:!1,hash:"fa002b6b35caf5b7eca35ab6e1387909",bookSignature:"Associate Prof. Nguyen Xuan Nhiem",publishedDate:null,coverURL:"https://cdn.intechopen.com/books/images_new/9187.jpg",keywords:"Spiro Compounds, Carbocyclic Spiro, Heterocyclic Spiro, Spiroketal, Monoterpenoids and Sesquiterpenoids, Structure Elucidation, Biological Activity, Spirostanol Saponin, Pharmacological Aspects, Cytotoxicity, NMR and CD, Total Synthesis, Chaetoquadrin",numberOfDownloads:null,numberOfWosCitations:0,numberOfCrossrefCitations:null,numberOfDimensionsCitations:null,numberOfTotalCitations:null,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"November 7th 2019",dateEndSecondStepPublish:"November 28th 2019",dateEndThirdStepPublish:"January 27th 2020",dateEndFourthStepPublish:"April 16th 2020",dateEndFifthStepPublish:"June 15th 2020",remainingDaysToSecondStep:"2 years",secondStepPassed:!0,currentStepOfPublishingProcess:5,editedByType:null,kuFlag:!1,biosketch:null,coeditorOneBiosketch:null,coeditorTwoBiosketch:null,coeditorThreeBiosketch:null,coeditorFourBiosketch:null,coeditorFiveBiosketch:null,editors:[{id:"66831",title:"Associate Prof.",name:"Nguyen Xuan",middleName:null,surname:"Nhiem",slug:"nguyen-xuan-nhiem",fullName:"Nguyen Xuan Nhiem",profilePictureURL:"https://mts.intechopen.com/storage/users/66831/images/system/66831.jpg",biography:"Nguyen Xuan Nhiem got his Ph.D. in 2011 from Chungnam National University, Korea with the topic of curcubitanes from Momordica charantia and their anti-diabetic activity. Dr. Nhiem received his postdoc in the College of Pharmacy, Yonsei University, Korea (2011-2013). He is currently working at the Institute of Marine Biochemistry, Vietnam Academy of Science and Technology (VAST) as well as a lecture at the Graduate University of Science and Technology, VAST. He is author/co-author of over 140 SCI/SCIE papers. His current research interests are isolation and structure elucidation of medicinal plants and marine sponges and evaluation of inflammatory, anticancer, and anti-diabetic effects.",institutionString:"Vietnam Academy of Science and Technology",position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"2",totalChapterViews:"0",totalEditedBooks:"0",institution:{name:"Vietnam Academy of Science and Technology",institutionURL:null,country:{name:"Vietnam"}}}],coeditorOne:null,coeditorTwo:null,coeditorThree:null,coeditorFour:null,coeditorFive:null,topics:[{id:"8",title:"Chemistry",slug:"chemistry"}],chapters:null,productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"},personalPublishingAssistant:{id:"270935",firstName:"Rozmari",lastName:"Marijan",middleName:null,title:"Ms.",imageUrl:"https://mts.intechopen.com/storage/users/270935/images/7974_n.png",email:"rozmari@intechopen.com",biography:"As an Author Service Manager my responsibilities include monitoring and facilitating all publishing activities for authors and editors. From chapter submission and review, to approval and revision, copyediting and design, until final publication, I work closely with authors and editors to ensure a simple and easy publishing process. I maintain constant and effective communication with authors, editors and reviewers, which allows for a level of personal support that enables contributors to fully commit and concentrate on the chapters they are writing, editing, or reviewing. I assist authors in the preparation of their full chapter submissions and track important deadlines and ensure they are met. I help to coordinate internal processes such as linguistic review, and monitor the technical aspects of the process. As an ASM I am also involved in the acquisition of editors. 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It was estimated more than 1.8 million new cases in 2018 according to American Institute for Cancer Research and Continuous Update project panel. It is linked to the transition nutrition to the western lifestyle, consuming processed meat, red meat and alcoholic drinks, greater body fatness and adult height increase the risk of the disease. The incidence of the disease continues to rise especially in low and middle income countries and it is considered one of the clearest markers for rapid societal and economic changes that are associated with cancer development [1].
Genetic knowledge is essential for understanding of carcinogenic colorectal cancer, and can develop strategies for prevention, diagnosis and treatment. A list of genes in which mutations are capable of interfering with both cancer creation and treatment, has grown a lot in recent years, helping to understand risks for cancer formation and identifying several promising therapeutic targets. Today focused on a best treatment, but research on colorectal cancer genetics began with a focus on diagnosis, much of our understanding of pathogenesis came from study of hereditary syndromes of colorectal diseases that advanced into cancer, showing a huge diversity in types of colorectal cancer and genetic involvement.
In 1882 W. Harrison Cripps associated in his work that multiple intestinal polyposis had hereditary nature and also potentially malignant nature. Subsequently in 1913 Aldred S. Warthin reported on 1600 cases of carcinoma treated at University of Michigan for 19 years, collecting detailed family histories of approximately 500 patients and mapping a predisposition to gastrointestinal and endometrial carcinogenesis of three generations. In 1950, Eldon J. Gardner at University of Utah conducted a long genetic study in patient families with multiple polyps and established a link between this event and a predisposition to carcinomatosis only in 1986 Herrera et al. described a case of a patient with polyposis and multiple carcinomatosis, with an amputation in a long arm of chromosome 5, suggesting a location of tumor suppressor gene. Subsequent studies in families with polyps have identified the 5q21 region as adenomatous polyposis coli or APC gene. Since then, we have identified numerous genetic defects and genetic expressions showing a diversity of mutations with distinct pathways of progression [2].
There have been significant advances in the last years and more than understanding the risk factors for CCR, recent progress in the field of molecular biology, has allowed us to identify the oncogenesis basis to the development of the disease. Then apply these knowledge in the research of new drugs that lead to better outcomes even in the advanced disease.
In medical practice, patients with cancer present with great frequency, clinical evolution in a differentiated way in response to the treatment performed. As a result, there is a high margin of uncertainty as to the effectuation of the treatment performed, not infrequently counting initially favorable prognostic evaluations [3].
Cancer results from a long process of at least three phases: initiation, promotion and progression, which reflect accumulated genetic alterations, responsible for the transformation of normal cells into neoplastic cells. The mechanisms of transformation of a normal cell into neoplastic involve a number of genetic and molecular events that affect proliferation and differentiation. In the pathogenesis of neoplastic processes, two groups of genes are involved: proto-oncogenes, which stimulate cell growth and impede differentiation, and tumor suppressor genes, which promote differentiation and limit cell proliferation. The imbalance in the regulation of this system, through the activation of proto-oncogenes or loss of the function of tumor suppressor genes, can lead to the uncontrolled proliferation of cells and to the accumulation of successive genetic abnormalities characteristic of neoplastic cells [4, 5, 6, 7].
The development of cancer (oncogenesis) results from mutations in one or more genes, responsible for the regulation of cell growth and programmed cell death called apoptosis (Figure 1) [8]. When cancer occurs as part of a hereditary cancer syndrome, the initial mutation causing the cancer is inherited through germ lineage. However, most cancers are sporadic because mutations occur in a single somatic cell, which then divides and proceeds to develop cancer [9].
Mechanism of oncogenesis. General scheme for mechanism of oncogenesis by proto-oncogene activation, loss of tumor suppressor gene expression, activation of anti-apoptotic genes or loss of pro-apoptotic gene expression. The effect of the genes that induce a process is shown as +, while the effect of the genes that suppress a process is shown as −. Modified from Thompson and Thompson [
Considering a frequency of 10-10 replication errors per DNA basis, cell division, and about 1015 cell divisions over the life span of an adult, only replication errors would result in thousands of mutations in the DNA of the genome [8].
Once initiated, a cancer progresses through additional accumulation of genetic damage through mutations in maintenance genes, which encode the DNA repairing cellular machinery. Changes in these genes produce mutations in increasing numbers, leading to failures in controlling cell proliferation and repairing DNA damage. In this way, the original clone of neoplastic cells functions as a reservoir of genetically unstable cells, known as cancer stem cells. These give rise to multiple underlining of varying degrees of malignancy, each carrying a set of mutations. In this context, cancer is a multifactorial disease with an important genetic component, and mutations are central to its etiology and progression [8] (Figure 2).
Stages in the evolution of cancer. Increasing degrees of abnormalities are associated with sequential loss of tumor suppressor genes from various chromosomes and activation of proto-oncogenes, with or without a defect, concomitant in DNA repair. Modified from Thompson and Thompson [
The classical CCR carcinogenesis model is based on the adenoma-carcinoma sequence in which tumor onset occurs from a sequential and progressive process. This involves the activation of oncogenesis (K-ras) and the inactivation of tumor suppressor genes (APC, DCC, p53) [10, 11]. This model of carcinogenesis, where there is chromosomal instability, is usually found in the distal segments of the colon and rectum [11]. The adenoma-carcinoma sequence was described for the first time by Hill et al. (Figure 3) [12].
The adenoma-carcinoma sequence. Postulated mechanism for progression from normal tissue to adenoma to carcinoma. n: normal gene; p: adenoma gene (recessive), so that cell pp: is adenoma-prone. A: environmental agent causing adenomas only in adenoma-prone cell. B: environmental agent causing adenomas to grow. C: agent causing adenomas to develop into carcinomas. Modified from Hill et al. [
In the colorectal carcinogenesis, there are a complex interaction between environmental and lifestyle factors and multiple molecular pathways contributes to its occurrence. Three different molecular mechanisms are implicated in colorectal carcinogenesis: chromosomal instability (CIN), genetic instability (GIN) and the serrated pathway. However, although they differ at the beginning of the chain of events, their signaling pathway, implicated in the transformation of the normal epithelial colorectal cell to the neoplastic one, appear to be similar and converge to the clinical and pathological manifestation of the disease. These genetic mechanisms can be acquired after birth and the occurrence of cancer is called sporadic or they can be inherited from the genitors and in this case is called hereditary. In the recent past, only clinical and pathological manifestations were considered when proposing the optimal treatment. However, after the understanding of the patterns implicated in the carcinogenesis, the tumors could be classificated according to molecular standards and individual treatment schemes were developed [13].
The most frequent model of phenotype group in colorectal cancer are allelic losses in the short arm of chromosome 17 and 8 and in the long arm of chromosomes 5, 18 and 22, being approximately 80% of the sporadic form and are related to mutations in tumor suppressor genes of TP53 genes, APC, SMAD2, and SMAD4.
The first major accepted model for cancer development in colon was described by Fearon and Vogelstein in 1990. The majority of the sporadic CCR tumors originates from premalignant precursor lesions known as polyps, which over time progress to clinically relevant tumors. In this model, the sequence of events leading from the adenoma (polyps) to carcinoma was based on mutation on APC and TP53 genes [13, 14].
The proto-oncogene K-ras (Kirsten-ras) tumor suppressor genes, APC protein (adenomatous polyposis coli), DCC protein (deleted in colorectal cancer) and TP53; and DNA repair or mismatch repair genes (MSH2, MLH1, PMS1, PMS2 and MSH6) are fundamental in development of CCR. Repetitive nucleotide sequences form approximately 25–40% of the DNA molecule being observed several times across the genome as dispersed replicates and tandem or satellite replicates [15]. These replicates can be classified according to the extension of the repetitive sequence in: satellite, minisatellite and microsatellite, depending on the number of nucleotides [16].
Most of the cases of CCR originate from polyps, but it was evidenced that about 45% of the tumors located in the proximal colon originated from epithelium without preexisting polyps, being considered new cancer [17]. In this model of carcinogenesis, which affects 10–15% of cases of sporadic CCR, instead of chromosomal instability there would be genomic instability due to mutations of DNA repair proteins, a phenomenon known as microsatellite instability (IMS) [18]. This pathway of colorectal carcinogenesis due to chromosomal instability is more frequently observed in tumors in the proximal colon, presenting characteristic histological features, being diploid, exophytic growth, worse histological grade, greater tendency to mucus production and lower mutation index in the TP53 gene, and paradoxically, they are associated with a better prognosis [18, 19].
DNA is a molecule that often undergoes changes through loss of segments, mutations that occur during the process of cell division. To correct these changes, it has proteins with the function of performing the repairs necessary to maintain its integrity. These proteins are produced from some genes known as repair (mismatch repair genes—MMR) and this function is carried out continuously, preserving the cellular tissues [20, 21, 22]. The hMLH1 gene is located on chromosome 3p21-23 [23, 24], hMSH2 on chromosome 2p21 [25, 26, 27] and hMSH6 is on 2p16 [28].
In hereditary CCR there are two genetic pathways of carcinogenesis: a chromosomal instability pathway, which occurs in PAF (familial adenomatous polyposis), where the patient inherits a mutation of the APC (adenomatous colonic polyposis) tumor suppressor gene, and DNA hypermutability pathway, which occurs in HNPCC (inherited non-polyposis colorectal cancer) in which the inherited genetic change is the inactivation of one of the alleles of genes involved in DNA repair (hMSH2 and hMLH1 genes). However, other genes are involved in colorectal carcinogenesis, such as K-ras gene, DCC gene, Tp53 gene, etc. [29].
DNA is a molecule that often undergoes changes through loss of segments, mutations that occur during the process of cell division. To correct these changes, it has proteins with the function of performing the repairs necessary to maintain its integrity. These proteins are produced from some genes known as repair (mismatch repair genes—MMR) and this function is carried out continuously, preserving the cellular tissues [20, 21, 22]. The hMLH1 gene is located on chromosome 3p21-23 [23, 24], hMSH2 on chromosome 2p21 [25, 26, 27] and hMSH6 is on 2p16 [28].
MMRs have the function of recognizing the occurrence of the mutation and blocking cell division in order to prevent the emergence of a defective cell line, which is done by inducing cell death (apoptosis) or performing DNA repair. For the latter, these proteins remove a segment of DNA containing the change and insert a new segment containing the right sequence, based on the “template” of the complementary DNA [30].
The failure of these proteins to function will cause a great instability in the genome, that is, defects in the sequence of base pairs occurring at random in DNA replication cannot be adequately repaired, generating an accumulation of genetic abnormalities that favor the emergence of cancer [30].
A genetic instability that appears in 12–15% of CCR cases, named MSI (microsatellite instability) as a result of a mismatch repair (MMR), what leading to the accumulation of mutations in genes controlling cell cycle and apoptosis (TGFBRII, BAX or CASPASE5) [31].
Cells with changes in MMRs are not able to correctly repair errors during DNA replication. Because of their repetitive structure, microsatellite regions in DNA are particularly prone to these repair errors [32, 33]. The DNA of cells of certain tumors presents differences in the number of repetitive units in one or more microsatellites, when compared to the same microsatellites in the DNA of normal cells, a fact called microsatellite instability (MSI). as positive for replication errors, that is, RER (+) [34].
More than 90% of HNPCC patients present RER (+), while about 15% of sporadic CCRs present this genetic trait [30].
Repair proteins in their normal state form heterodimers [35, 36, 37, 38]. MSH2 dimerizes with MSH6 forming the MutSα [38] functional complex, and MLH1 dimerizes with PMS2 to form MutLα [37, 39]. It has been shown that MSH2 and MLH1 proteins are obligatory parts of their respective heterodimers [40, 41, 42]. Their abnormalities may result in a proteolytic degradation of their dimers and consequently loss of both mandatory and secondarily associated proteins, the exception includes only MLH1 mutations, when the mutations result in the antigenically activation of the mutated MLH1 protein, which may be the loss of PMS2 only. The reverse, however, is not true, when mutation occurs in the genes of secondary proteins, for example, in MSH6 and PMS2, loss of MSH2 and MLH1 proteins that may not occur, inasmuch as other proteins compensate the function of the secondary proteins, such as MSH3, MLH3 and PMS1. In effect, mutations of MLH1 or MSH2 routinely cause loss of MLH1/PMS2 or MSH2/MHS6, respectively, while mutations of PMS2 or MSH6 cause isolated loss of PMS2 or MSH2 only [43].
Figure 4 shows the model of DNA repair proteins in patients with colorectal cancer [44].
Model of DNA repair proteins and molecular pathways for CCR with microsatellite instability. Modified from Kohzoh and Yamamoto [
Studies performed in CCR demonstrated a positivity index for greater microsatellite instability in young patients or located in proximal segments of the colon. A study restricted to rectum tumors, the incidence of repair errors was only in 2% of cases, confirming the relationship between microsatellite instability and tumors located in the right or transverse colon [45]. The CCR associated with repair errors tend to present the same location and biological behavior independent of their sporadic or hereditary nature (HNPCC) [45].
The serrated pathway was first described by Longacre and Fenoglio-Preiser in 1990 and differs from the classical adenoma-carcinoma sequence one because in this way there is the participation of other genetic alterations other than chromosomal instability and KRAS mutations like BRAF mutations and gene promoter hypermethylation. But in the serrated pathway, microsatellite instability can also be detected.
The serrated polyps are characterized by glandular serration in which the colonic epithelial crypts show luminal “saw-toothed” pattern. The nomenclature is not well established but the World Health Organization in 2010 classified them into three main groups: hyperplastic polyps, sessile serrated adenomas/polyps and traditional serrated adenomas [46].
Genetically, carcinoma arising from serrated polyps are MSI-H and shows epithelial serrations, clear, eosinophilic and abundant cytoplasm, vesicular nuclei, absence of necrosis, mucin production and presence of cell balls and rods. The finding of serrated lesion in the peripheral of an invasive carcinoma also leads to the diagnostic of this pathway.
Serrated adenocarcinoma is found in about 10% of sporadic colorectal cancers and is originated in the serrated polyp-carcinoma pathway. In this way, hyperplastic polyps now are recognized as neoplastic lesions because they may predispose to cancer in a sequence in which they progress to serrated adenomas and then to colorectal cancer in at about 7 years. It is not clear why only a few groups of hyperplastic polyps, mainly the ones located in the right colon, will progress to carcinoma and the answer is probably dependent on the genetic findings not elucidated until now. A great number of studies have shown that the right colon is not the same organ as the left colon and the right-sided cancer tends to be more aggressive and this difference is caused by the difference of genetic standard between the sides.
The clinical management of hyperplastic polyps and serrated polyps is essential for avoiding the carcinoma transformation. The most important procedure for prophylaxis is the complete removal of these polyps in colonoscopy and the subsequent surveillance but it is not well established how to follow up. Just for comparison, in the classical adenomatous polyps, the size, number and histological variants (if tubular, villous or tubulovillous) are taken in account to determine the interval of surveillance and this knowledge is more than a decade old. For serrated polyps, as the understanding of this pattern of via is recent, the follow up is not clear hence studies have not shown yet which features are important to determine the risk of progression of these lesions. Moreover, the majority of serrated polyps will not progress to carcinoma and studies answering why are not yet available. A few studies have demonstrated that sessile serrated lesions larger than 10 mm are at high risk for carcinoma progress. But despite the lack of information and in order to prevent cancer arising via serrated pathway, the complete removal of serrated polyps is the goal in these cases.
If there are significant differences regarding the genetic markers and pathological findings in serrated pathway, it is expected to have differences in the presentation of the disease and response to therapy. And some evidences have showed these: carcinomas arising from serrated pathway tends to have lesser 5-year survival but again the causes of this comportment are not available, and the answer may be found as the genetic alterations becomes evident [47].
For now, it is clear that serrated pathway is a well-established pattern that explains the behavior of some hyperplastic and serrated polyps that could not have been explained in the classical adenoma-carcinoma sequence using CIN and MSI models. Even with lacks in knowledge for profound understanding, the pathological and molecular characterization of these polyps are constantly progressing and studies in the next few years will probably show the best way to manage these cases in clinical practice [47].
There have been significant advances about tumor molecular biology, will allow us to apply this knowledge in more specific diagnostic techniques, a proper diagnosis, with the possibility of detecting earlier pre-malignant lesions and diagnoses. This applied research knowledge would allow the development of more efficient therapies for cancer, moreover, it can act in prevention.
The application of molecular biology knowledge in the diagnosis and treatment of colorectal cancer generates a great impact on the accuracy of diagnosis and optimization of cancer therapy in order to individualize the treatment, thereby trying to reduce the uncertainty about the effectiveness of the treatment that will be accomplished.
Adenomyosis consists of a term that describes the presence of endometrial glands in a layer deep in the myometrium, in a random arrangement and similar histological lesions can be also appeared outside of the uterus, such as the area of the rectal septum [1, 2, 3]. Pathogenesis and etiology of adenomyosis development have not been elucidated thoroughly.
Studies in humans and experiments in animals support the hypothesis of endometrial insertion from the myometrium, although the development of adenomyosis from Müller’s duct debris at locations outside the uterus is possible from the outset.
The conditions for the development of adenomyosis can be either some “weakness” of the smooth muscle fibers of the myometrium or the increased pressure in the uterine cavity or both. To maintain adenomyosis, relatively high concentrations of estrogen and impaired control of the development of the ectopic endometrium, which is associated with the immune system, may be necessary. Hyperplasia and hypertrophy of smooth muscle fibers are a reflection of the reactive changes in the proliferation of ectopic endometrium. The definitive diagnosis is made after hysterectomy, although efforts have been made to confirm the diagnosis preoperatively with magnetic resonance imaging and endometrial biopsies [4, 5, 6].
Adenomyosis, one of the most common diseases in gynecology with a frequency ranging between 5% and 70%, can significantly affect the quality of life of women with clinical symptoms such as menorrhagia, dysmenorrhea and infertility [7, 8, 9]. There are two prevailing theories concerning the origin of adenomyosis. One supports “migration”, which concerns the penetration of the endometrium into the myometrium, while the other is based on the metaplastic differentiation of the remaining endometrial stem cells in the myometrium. Mutations that have been observed, almost exclusively, in the KRAS genes, in the presence of adenomyosis, underscore the importance of these genes in the pathogenesis of the disease at the genetic level. This discovery of the cause-effect relationship between the presence of mutations in the aforementioned [7, 8, 9] KRAS genes and adenomyosis refuted the recent theory that the reported molecular abnormalities in adenomyosis are mainly epigenetic or associated with abnormal expression in different genes [7, 8, 9]. Most recognized abnormalities regarding gene expression, were associated with excess estrogen formation, progesterone resistance and were related to steroid hormone receptors and other transcription factors. More specifically, mutations have been found, such as the following two P129R, M427I/L429M, which are the most predominant ones, in the ESR1 gene of the estrogen receptor α (ERa) located on chromosome 6q25.1 and appear to be involved in the etiology of adenomyosis [7, 8, 9]. It has also been described an association between adenomyosis and deregulation of mechanisms involved in the transition process of epithelial to mesenchymal cells, as occurs in cases of decreased expression of Cadherin-1 (CDH1) protein, as well as in cases of increased Notch I and TGF-β levels [7, 8, 9]. Regarding epigenetic factors, it has been suggested that Class I histone deacetylases (HDACs) are involved in promoting gene transcription, as well as DNA methyltransferase (DNMT) proteins involved in DNA methylation are associated with adenomyosis. High levels of HDAC1 and HDAC3 as well as DNMT1 and DNMT3B were found in cases of adenomyosis at the ectopic endometrium. Consequently, epigenetic alterations seem to play an important role in the pathogenesis of adenomyosis, which along with the other aforementioned genetic factors provides knowledge that could potentially lead to advances in the diagnosis and treatment of the disease [7, 8, 9].
In the mid-nineteenth century, Rokitansky described a condition in which elongated endometrial glands were embedded in the hyperplastic endometrial layer. The author mentioned two variants of this condition: the first, in which the glands developed in the muscular wall of the uterus and the second, in which the glands extended to the intrauterine cavity, forming polyps [10]. Several researchers in the 1880s and 1890s considered adenomyosis to be either an embryonic error in the distribution of Müller’s ducts or the penetration of the hyperplastic basal endometrium into the myometrium [10, 11, 12, 13, 14]. Von Recklinghausen, then argued that adenomyosis is the result of displacement of the mesonephric elements. The researcher reported that these ectopic glands are more commonly found in the posterior wall of the uterus and the area of the cornea, and that these areas consist of remnants of Wolff’s pores rather than Müller’s ducts [10, 11, 12, 13, 14]. Marcus, later described the lymphatic transmission of endometrial elements [14]. Although, this theory has been used to interpret pelvic endometriosis, it also provides a possible explanation for adenomyosis. Marcus, then suggested that there are some miller pluripotent cells in the myometrium, which can differentiate into endometrial cells, offering another possible interpretation for the development of adenomyosis [14]. The cycle is now complete, and most researchers believe that adenomyosis is caused by the penetration of the basic endometrium into the hyperplastic layer of the myometrium. It should be noted that all the organs of the human body, which show cavities, present a sub-orogenic area, except for the uterus. It is believed that the main function of the sub-orogenic region is to inhibit the growth of the glands that line these cavities. The term “uterine adenomyosis” was first used by Frankl in 1925. In 1972 Bird and his colleagues defined adenomyosis as “benign, penetration of the endometrium into the myometrium, which causes diffuse enlargement of the uterus and microscopically presents ectopic, non-neoplastic, endometrial glands and layer, surrounded by hypertrophic and hyperplastic endometrium” [15]. This definition still applies today.
However, it has been described by some researchers as “the presence of endometrial glands and a layer, which are diffuse and deep inside the myometrium”. The issue of depth is important as the normal endometrial contribution is usually irregular. Thus, adenomyosis must be distinguished from cases in which there is minimal adhesion of the basal layer of the endometrium surrounded by myometrium and there are two ways to treat it. The first case is the detection of myometrial hypertrophy (“collar around the foci of adenomyosis”), because this type of change is not observed in the intramuscular junction. The second way is to measure the distance between the endomyometrial junction and the nearest adenomyotic site, the size of which must correspond to at least 25% of the total thickness of the myometrium. The second approach is particularly useful in the postmenopausal and pregnant uterus, as in these cases there is generally no muscle hypertrophy around the foci of adenomyosis. Although, many researchers consider adenomyosis as a variety of endometriosis and call it internal endometriosis, adenomyosis should be defined as the presence of endometrial glands and mattresses, located outside the myometrium [10, 11, 12, 13, 14, 15, 16, 17, 18].
The incidence of adenomyosis varies widely, with rates ranging from 5.7% to 69.6% [19, 20]. Although, some of this discrepancy can be explained by the different histological definitions of adenomyosis, the difference is mainly due to the interest of pathological volumes in making the diagnosis. As a result of the local entity of the condition, the diagnosis of adenomyosis is particularly difficult. In the excellent prospective study by Bird et al. [15], 200 consecutive hysterectomy specimens were examined histologically. When three sections of the myometrium were examined, adenomyosis was found in 62 women (31%). When six more incisions were made, three from the anterior and three from the posterior wall of the uterus, another 61 cases of adenomyosis were diagnosed, increasing the rate from 31 to 61.5% [21, 22, 23, 24, 25].
The main reason for the difficulty in determining the true incidence of adenomyosis is mainly due to the fact that published studies report the number of adenomyosis cases, but without mentioning the total number of hysterectomies per age group, so the relative impact of adenomyosis with age has not been defined. Another problem is determining the true frequency is also the fact that in the various studies, only women who undergo a hysterectomy are evaluated, and a selection of cases is applied. Ιn two necropsy studies, the incidence of adenomyosis was reported between 50 and 53.7% [21, 22, 23, 24, 25]. Although, these studies had a different choice of cases (excluding women who underwent hysterectomy), they show that the true incidence of adenomyosis is at the highest end of the published frequency range. The woman’s interest appears to be related to adenomyosis, as 93% of the women treated had children [21, 22, 23, 24, 25]. Although, the numbers tend to mimic the general population, their importance is questionable. If these numbers are real, the observation will confirm an interesting paradox, that is, the number of pregnancies protects against endometriosis, but it is a risk factor for the development of adenomyosis. There does not appear to be a significant association between adenomyosis and another gynecological entity. In a retrospective study of 134 women who underwent a hysterectomy, Vercillini and colleagues found a similar coexistence of adenomyosis with fibroids (23%), with uterine prolapse (19%), with endometrial cancer (28%), with ovarian cancer (28%) and with ovarian cysts (21%) [26].
Although, the exact etiological factors of endometriosis have not been clarified yet, there are many theories on this subject, such as the ones proposed by Ridley [27]. According to the most popular view, adenomyosis is the result of the attachment of the basal layer of the endometrium to the myometrium. In non-uterine areas, the predominant theory concerning the pathogenesis of adenomyosis is the de novo development of ectopic fetal residues of Müller’s ducts, since an invasive mechanism of the endometrium into the myometrium has not been established. There are significant differences in the cellular level between the basal layer of the endometrium and the functional layer, such as increased DNA synthesis in the nucleus, and margin formation in the functional layer. In general, the functional layer is considered to be the site of blastocyst implantation while the basal layer provides the possibility of intrauterine regeneration after menstruation. During the period of regeneration of the endometrium, cells from the basal layer glands are in close contact with the endothelial cells having intracellular microfiber/tubular and squamous cell systems [28, 29, 30].
These findings support the location of possible migration through amoebic contraction-extension. Such morphological changes have not yet been described in the intrauterine epithelium of adenomyosis. However, in vitro studies have shown that endometrial cells have the penetrating capacity and that their penetration rate is similar to that of cell lines from metastatic bladder carcinoma. This penetrating ability can facilitate the expansion of the basal layer of the endometrium to the myometrium. In MCF-7 cells from breast cancer, tenascin production is stimulated by epidermal growth factors (EGF), which are regulated by hormones. The fact that fibroblasts of the endometrial layer produce tenascine, a fibronectin inhibitor that in turn facilitates the migration of epithelial cells, suggests that there is a complex physicochemical relationship during the growth process of the endometrium in the production phase. Tenascin has been immunohistochemically located around the endometrial glands during the productive phase of the cycle, but not in this position after ovulation [28, 29, 30]. Tenascin may mediate the interactions between epithelial and mesenchymal cells, where it inhibits cell adhesion to fibronectin in the endometrial adenomyotic type in the same way as in the normal endometrium.
In a study within situ hybridization and immunohistochemistry, it was found that the endometrial glands in adenomyosis selectively express more human chorionic gonadotropin (hCG) receptor mRNA and immunoreactive receptor protein, compared to the present [31, 32, 33, 34]. It seems that ΗCG/LH receptor expression levels do not differ at different sites of the normal endometrium, but increased expression of this receptor may give epithelial cells the ability to invade the myometrium and form adenomyotic islets. Furthermore, quite interesting is the fact that there is an increased expression of hCG/LH receptors in endometrial carcinomas as well as in non-invasive choriocarcinoma trophoblast cells [31, 32, 33, 34]. Studies on steroid hormone receptors in adenomyosis foci have shown dubious results. Thus, some studies reported the absence of progesterone receptors in 40% of adenomyosis cases, while others showed higher concentrations of progesterone receptors than estrogens. Relatively high concentrations of estrogen and progesterone receptors were found in both the basal and adenomyotic endometrium using immunohistochemical detection techniques. Estrogen receptors are a prerequisite for the development of the uterus, which is caused by estrogen [35, 36, 37, 38]. Although, there is no clear evidence of a disturbed hormonal environment in most women with adenomyosis, hyperestrogenemia may play a role in the process of endometrial infiltration, as women with adenomyosis have a high rate of endometrial hyperplasia. According to some researchers, a relatively high concentration of estrogen is necessary for the development of both endometriosis and adenomyosis [31, 32, 33, 34, 35, 36, 37, 38]. The clinical observation that the destruction of the estrogenic environment with danatrol causes regression of the ectopic endometrium and remission of the associated symptoms of menorrhagia and dysmenorrhea reinforces this hypothesis [31, 32, 33, 34, 35, 36, 37, 38]. As in uterine fibroids, estrogen is synthesized and secreted in adenomyotic tissues [31, 32, 33, 34, 35, 36, 37, 38]. It was found, therefore, that there is aromatase activity of estrogen sulfatase in the upper part of the myometrium, which contained foci of adenomyosis, by the method of steroid biochemical analysis. The activity of estrogen sulfatase and, in particular, aromatase was higher than that observed in normal adjacent endometrium, leiomyomas and suprauterine endometrium. In addition, endometrial aromatase enzyme activity was inhibited in vitro by up to 50% with the addition of 106 M of danatrol [31, 32, 33, 34, 35, 36, 37, 38]. Finally, the presence of aromatase was confirmed in foci of adenomyosis from human matrices by immunohistochemical method and, in particular, in the cytoplasm of glandular epithelial cells, but not in the cytoplasm of stratum cells. The production of estrogen by adenomyotic tissue is further enhanced by the finding of a large number of women with adenomyosis and a high concentration of estradiol (30 pg/ml) in menstrual material compared to those without adenomyosis and normal menstrual cycles [31, 32, 33, 34, 35, 36, 37, 38].
Adenomyotic tissue appears to respond well to progesterone with secretory differentiation. Progestogens also enhance aromatase activity in both eutopic endometrium and adenomyotic tissues, thus contributing to the biosynthesis of estrogen in adenomyotic foci.
It is possible, however, that the bioavailability of race steroids alone is not sufficient to develop adenomyosis. It is possible that the myometrium, in cases of adenomyosis, is either predisposed to penetrate the main endometrium, so that benign “penetration” of the endometrium occurs secondarily due to “weak” myometrium, or the morbidity of the uterine scraping, fibromyectomy and cesarean section. Thus, adenomyosis was induced in pregnant rabbits, after scraping one horn of the uterus and fallopian tube, while maintaining the pregnancy in the opposite horn [31, 32, 33, 34, 35, 36, 37, 38]. Penetration into the myometrium of the basal layer of the endometrium is enhanced, possibly, by increased intrauterine pressure, which, according to Cullen, can be caused by high circulating progesterone concentrations. The immunohistochemical method has been observed, increased expression of class II antigens of the major histocompatibility complex (HLA-DR) in the glandular cells of the idiopathic endometrium, endometriosis and adenomyosis [31, 32, 33, 34, 35, 36, 37, 38]. In addition, the number of macrophages in the myometrium of women with adenomyosis appears to be increased. These macrophages can activate helper T- and B-cells to produce antibodies [31, 32, 33, 34, 35, 36, 37, 38]. Phospholipid autoantibodies and significant deposition of immunoglobulins (lgs) or complement factors have been found in women with endometriosis or adenomyosis [31, 32, 33, 34, 35, 36, 37, 38]. The exact importance of these immune aberrations in adenomyosis or endometriosis is not currently understood. In vitro experiments have shown that activated CD3+ T cells in the uterus and their secretory product, interferon γ, promote the expression of HLA-DR immunoreactivity in endometrial glandular cells and inhibit their proliferation [31, 32, 33, 34, 35, 36, 37, 38]. The closer the endometrial cells are to the activated T cells, the greater the inhibition of their growth. It appears that lymphocyte-like formations, located mainly at the endomyometrial junction, are rich in activated T cells. Their appearance coincides with the maximum suppression of endometrial growth, which is observed both morphologically and with proliferation indices [31, 32, 33, 34, 35, 36, 37, 38]. On the contrary, the proliferation of the endometrium is observed, to the greatest extent, near the surface of the endometrium, that is, far enough away from the basal layer, in which these lymphoid formations are found [31, 32, 33, 34, 35, 36, 37, 38].
During a hysterectomy, the adenomyotic uterus is usually spherical or soft. It is swollen in 60% of cases, but rarely exceeds the size of a 12-week pregnant uterus [39]. The uterus weighs from 80 to 200 g. In his classic study, in which a woman’s interest determined the weight of the uterus, Langlois reported the upper limit of the normal uterus weight at 130 g for the unmarried woman, at 210 g for the firstborn to the third child, and at 250 g for women with four or more children [40]. With these criteria, excluding cases of fibroids, the weight of the uterus does not increase significantly with adenomyosis. Uterines with adenomyosis are usually hyperemic with thick walls. Although, many researchers have reported that adenomyosis is more common in the posterior wall of the uterus than in the anterior. Bird and colleagues found that the foci of adenomyosis were evenly distributed when receiving six additional incisions for histopathology [15]. These foci may be diffusely dispersed in the myometrium, and may sometimes be large and localized, forming structures called adenomas. The characteristic macroscopic appearance of adenomyosis is due to hypertrophy of the myometrium, which surrounds the endometrium [40, 41, 42, 43, 44]. When the entire myometrium, or one of the layers of the uterine wall, is diffusely affected, the uterus increases in size and takes on a spherical shape. During the cross-section of the uterus, the hypertrophic muscular beams are visible, which develop in all directions and surround the foci of adenomyosis. The latter, in some cases, may contain “old” blood with a brown appearance, corresponding to hemolyzed blood and hemosiderin deposits [40, 41, 42, 43, 44].
Local infection of the uterus by adenomyosis resembles fibroid. The term adenomyoma is used for the frequent occurrence of adenomyosis. Because the treatment is not neoplastic, the term focal adenomyosis is preferred by Hendrickson and Kempson [40, 41, 42, 43, 44]. As adenomyoma is often confused clinically with leiomyoma, which is a benign but neoplastic condition, the term adenoma is accepted. Typically the adenoma does not have clearly defined boundaries because they merge with the normal myometrial environment. In contrast, leiomyomas compress the myometrial environment and have well-defined boundaries [45, 46, 47, 48, 49, 50].
Leiomyoma can be nucleated, while adenomyoma can not. Histologically, by the immunohistochemical method, the endometrial glands and the layer in foci of adenomyosis resemble the basal layer of the endometrium. Rarely do they respond to hormonal stimuli, a phenomenon that explains, at least in part, that only in certain cases are hemorrhagic or regenerative morphological findings observed in foci of adenomyosis. The reason for the increased tendency of focal bleeding in deep-seated adenomyotic foci is not understood [45, 46, 47, 48, 49, 50]. In contrast, the ectopic endometrium at foci of endometriosis often undergoes circular changes, including degeneration, bleeding, and regeneration, which are similar to those seen in the functional layer of the endometrium. The different frequency of menstrual-type changes may be due to the relatively poor vascularity of the ectopic endometrium, which is a type of primary endometrium, compared to the endometriosis of the endometrium, which is rich in perspiration and is a type of functional layer of the endometrium. However, it appears to retain the ability to proliferate as a result it can develop and be responsible for the failure of amenorrhea or submenorrhea after endometrial destruction operations [45, 46, 47, 48, 49, 50]. The secretory changes, which include the degradation of the layer in foci of adenomyosis, are observed mainly during pregnancy and treatment with exogenous progestogens and these changes are made through estrogen and progesterone receptors.
Progesterone effect in the non-pregnant uterus is observed in approximately 30–50% of foci of adenomyosis. During intrauterine pregnancy, 57% of the studies evaluated by Azziz found degeneration [39]. Other authors observed degeneration during pregnancy, only in deep foci, at a depth of at least two low-magnification optical fields, while degeneration was absent or insignificant in foci less than two low-magnification optical fields, the boundary of the basal layer of the endometrium-myometrium [45, 46, 47, 48, 49, 50, 51, 52]. It is worth to be mentioned that adenomyosis can often be complicated by hyperplastic disorders up to atypia, while squamous cell carcinoma, mucosal metaplasia, and adenocarcinoma can occur in parallel with adenomyosis.
When the carcinoma is confined to an adenomyotic lesion, it should be considered “intravenous” as the prognosis is no worse than the carcinoma for which the patient underwent surgery. It is not possible to determine histologically whether the adenocarcinomas found in the supracervical uterus in foci of adenomyosis are the primary foci or the expansion of the endometrium into the foci of adenomyotic foci [45, 46, 47, 48, 49, 50, 51, 52].
Approximately 35% of adenomyosis cases are symptomatic [53, 54, 55, 56]. In other cases, the most common symptoms are menorrhagia (50%), dysmenorrhea (30%) and uterine bleeding (20%). In some cases, discomfort may be an additional symptom. The frequency and severity of symptoms depend on the extent and depth of adenomyosis [53, 54, 55, 56].
The exact cause of menorrhagia in patients with adenomyosis is not known. Menorrhagia may be due to poor contractility of the adenomyotic myometrium and compression of the endometrium by submucosal adenomas or leiomyomas. Mefenamic acid may reduce blood loss, suggesting that prostaglandin F2a (PGF2a) may play a role in the greater blood loss in women with adenomyosis [53, 54, 55, 56, 57]. Other factors may include anovulation, hyperplasia and, rarely, endometrial adenocarcinoma. Dysmenorrhea, finally, is due to the irritability of the uterus, which in turn is secondary to the increased amount of blood loss [58, 59, 60]. The symptoms associated with adenomyosis have not been analyzed by all researchers. For example, in a study of 136 patients with histologically confirmed adenomyosis, the symptoms were varied, non-specific and, according to the researchers, associated with co-existing pathological conditions such as leiomyomas, endometriosis and polyps, rather than with adenomyosis [58, 59, 60]. In another prospective study, there were no differences in the incidence or severity of dysmenorrhea and pelvic pain between 28 women with adenomyosis and 157 controls [58, 59, 60, 61, 62]. A study of 23 women with myometrial adenomyosis reported no qualitative differences in spontaneous motility of isolated myometrial tissue during the menstrual cycle, compared with normal uterine fibroids [58, 59, 60, 61, 62]. The type of mobility was low-intensity and high-frequency automatic contractions during the reproductive phase, both of which increased during the secretory phase. Histamine-induced contractions of the myometrium were similar to all myometrial tissues tested [58, 59, 60, 61, 62].
Because the symptoms of adenomyosis are not specific, it is natural for the disease to be rarely diagnosed preoperatively. Most researchers report a correct preoperative diagnosis in less than 10% of cases [58, 59, 60, 61, 62]. However, due to the way the cases are selected, the incomplete pathological examination of the surgical specimens, and the limited number of well-designed studies, the true ability to diagnose adenomyosis is difficult to assess.
The clinical diagnosis of adenomyosis is, at best, hypothetical (50%) and more often, it either does not occur (75%) [63, 64, 65, 66] or the disease is overdiagnosed (35%) [63, 64, 65, 66]. Menorrhagia and dysmenorrhea in a large woman, aged 40–50 years, raise the suspicion, but not the diagnosis, of adenomyosis. The uterus may be diffusely swollen, about the size of a 12-week pregnant uterus, and soft and tender to the touch. In addition, the presence of endometrial hyperplasia at the time of hysterectomy is the only variable directly related to adenomyosis [63, 64, 65, 66].
Several researchers have used radiological methods to diagnose adenomyosis. In the largest hysterosalpingography study, Marshak and Eliasoph diagnosed adenomyosis in only 38 of 150 patients with proven adenomyosis [67]. However, they did not report either the total number of patients examined or the frequency of a false-positive diagnosis. The most common findings in hysterosalpingography are endometrial diversions and cellular invasions within the myometrium [67].
This test was considered inaccurate because myometrial adhesions attributed to adenomyosis resemble lymphatic or vascular infiltrations of the pigment. Intra-abdominal ultrasound is not useful in diagnosing adenomyosis. In the late 1970s, a group suggested that abnormal ultrasound areas of the myometrium, 5–7 mm in size, were an ultrasound finding characteristic of generalized adenomyosis [63, 64, 65, 66].
This view was subsequently challenged by Siedler et al., who reported generalized uterine enlargement, normal uterine echogenicity, and retention of uterine shape in the majority of women with established adenomyosis. Subsequent studies have failed to clarify this issue [68].
Vaginal ultrasound has been used to diagnose adenomyosis since the early 1990s. Fedele estimated 43 women who would undergo hysterectomy for menorrhagia with preoperative transvaginal ultrasound. He described numerous small subsonic areas of the myometrium, with an abnormal ultrasound outline in 22 women [69].
The sensitivity of the method was estimated at 80% and specialization at 74%. Other researchers reported lower sensitivity, at 48 and 53% [70, 71, 72, 73, 74, 75, 76, 77, 78, 79, 80]. Other studies, with a larger number of women, are needed to address this issue [81, 82, 83, 84, 85].
Magnetic resonance imaging (MRI) has been applied to pelvic pathology and the initial results in women with adenomyosis are encouraging [75, 76, 77, 78, 79, 80, 81, 82, 83, 84]. Mark and his colleagues predicted adenomyosis in eight of 20 women studied with T2 images. Ten of the remaining 12 women were correctly diagnosed with adenomyosis free, while in two the diagnosis was uncertain [70].
The researchers described a typical, wide, low-density area surrounding the normal, high-density, endometrium in women with diffuse adenomyosis. Tiny foci of adenomyosis could not be diagnosed. T2 imaging has a significant advantage over shadowless imaging and that with T1 amplification. MRI has been used to differentially diagnose adenomyosis from leiomyomas [75, 76, 77, 78, 79, 80, 81, 82, 83, 84, 85].
Ninety-three patients were evaluated preoperatively and the results were related to surgical pathology. The 16 cases of adenomyosis were diagnosed preoperatively. The wider application of new technology needs, however, further evaluation. In addition, the cost can prevent MRI from becoming a widely used diagnostic test [75, 76, 77, 78, 79, 80, 81, 82, 83, 84, 85].
CA-125 is an antigen produced by the ovarian epithelial cells. It is secreted from these cells into the blood and is determined in a variety of gynecological diseases. Some researchers have used the determination of CA-125 levels to predict recurrences of non-mucosal ovarian cancers, while others have used it to diagnose recurrences of endometriosis. In the second case, successive determinations of CA-125 levels [75, 76, 77, 78, 79, 80, 81, 82, 83, 84, 85].
was required. In 1985, Takahashi and colleagues reported high preoperative CA-125 levels in six out of seven women with adenomyosis [70]. Although, CA-125 levels were elevated in these women, they were significantly lower than in patients with ovarian cancer. One month after hysterectomy, all women showed normal CA-125 levels. The same researchers, by immunohistochemical method, observed CA-125 production in the glandular epithelium of adenomyosis foci in eight hysterectomy specimens [75, 76, 77, 78, 79, 80, 81, 82, 83, 84, 85, 86, 87, 88]. In another study, it was not possible to reproduce these results. In the report of 22 women, 11 of whom had adenomyosis, Halila and colleagues found normal preoperative CA-125 levels in all women with adenomyosis [71, 72]. These levels did not change significantly at one and five weeks after surgery. The cause of the different results in these studies was not clear, but it is hoped that future research will lead to some conclusions [71, 72].
Cysteine and leucine aminopeptidase levels have been used as possible markers of adenomyosis. Levels of these enzymes are elevated in various benign and malignant conditions of the uterus and ovaries [75, 76, 77, 78, 79, 80, 81, 82, 83, 84, 85, 86, 87, 88].
However, no control studies have been performed to evaluate the clinical utility of these measurements. Although, adenomyosis can be diagnosed after a needle biopsy of the uterus, the sensitivity of this method is low and depends on the number of biopsies and the depth of penetration of the adenomyosis. This technique is of little or no importance in the diagnosis of minimal or moderate disease, but can provide histological confirmation in cases with extensive myometrial infiltration. If the biopsy confirms the diagnosis, women should be identified based on their history and tested for transvaginal ultrasound and MRI. These diagnostic methods can also help determine the location of the biopsy. However, myometrial biopsy, as a routine method, in women with pelvic pain should not be performed [75, 76, 77, 78, 79, 80, 81, 82, 83, 84, 85, 86, 87, 88].
Hysterectomy surgery remains the key approach in both the diagnosis and treatment of adenomyosis until a safer and more effective method of immediate biopsy is found. The only way to accurately diagnose adenomyosis is to remove the uterus, which also provides treatment for this condition, whereas prolactin, progesterone and growth hormone appear to accelerate the development of the disease [89, 90, 91, 92, 93, 94].
RU 486, an anti-progesterone agent that inhibits the action of progesterone on its receptors in the uterus, suppresses the development of adenomyosis if administered for 30 days. Of course, they also require studies in humans [89, 90, 91, 92, 93, 94]. There is evidence that progesterone promotes the development of adenomyosis in humans as well as in muscles [89, 90, 91, 92, 93, 94]. Danazol, an antigonadotropic derivative of testosterone 17α-ethinyl, has not been widely used in the treatment of adenomyosis [88].
From June 1993 to August 2000, Tamaoaka et al. treated adenomyosis women with endometrial glomeruli containing danatrol, and observed a marked reduction in dysmenorrhea and levels of CA-125 in women with endometrial hyperplasia. The histopathological findings of hyperplasia disappeared during the use of these endometrial glomeruli. The mechanism of the direct action of danatrol in endometrial hyperplasia has not been fully elucidated [89, 90, 91, 92, 93, 94].
Hormone therapy with progestogens or gonadotropin-releasing hypothalamic hormone analogs (GnRH-α) could be as effective as in endometriosis [94, 95, 96]. However, an increase in uterine size and a recurrence of symptoms occur within six months of stopping treatment. Conservative surgical treatment may be helpful in some patients, although follow-up of women after such surgery is limited to three years [96, 97, 98].
The activity of one orally administered metalloproteinase inhibitor (ONO-4817) in the development of adenomyosis was recently tested experimentally by anterior pituitary gland transplantation into muscle. The results indicate that this drug could be activated the development of adenomyosis [96, 97, 98].
The uterine artery embolization (UAE) has been used successfully for refractory gynecologic problems in premenopausal women like: hemorrhage, pain, bulk symptoms, or a combination of them despite previously performed surgical procedures (myomectomy, adenomectomy) or medical treatment. The desire for minimally invasive alternatives for the management of symptomatic adenomyosis premenopausal women prompts interventional radiologists to propose UAE as an alternative treatment to surgical treatment of adenomyosis. According to various reports, the ability to improve menstrual disorders and symptoms of premenopausal women through UAE without the need for surgical procedures led to this method becoming famous. However, despite the positive comments of several reports exist no prospective randomized trials to determine the relative safety effectiveness of UAE compared either to surgical or medical options [78, 79, 80, 81, 82, 83, 84]. The cooperation between a gynecologist and interventional radiologist is obligatory to establish optimal clinical guidelines for premenopausal women care due to preinterventional consultation, procedural course and postprocedural follow up require gynecological and also radiological services.
The target of the UAE is to administrate material polyvinyl alcohol (PVA). Microspheres or gelatin-coated tris-acryl polymer microspheres bilateral in uterine arteries to interrupt or reduce the blood supply at the level of the arterioles and to produce irretrievable ischemic damage, degeneration and shrinkage of adenomyosis focus without causing permanent damage to uterus. The target of UAE is an interruption or reduction of the blood supply of fibroids at the level of the arterioles after bilateral (from left and right) super-selective catheterization with microcatheters of the arteries that supply the fibroids and injection of acryl polymer embolospheres with a diameter of 500–900 μm for provocation of irretrievable ischemic damage to the fibroids. The aspects of the technical approach of UAE are summarized and described as follows: A single right femoral artery is typically catheterized after intravenous local analgesia and after that is performed pelvic arteriography to define the vascular tree and identifiy both uterine arteries. All UAE procedures were carried out in the angio suite with a digital subtraction angiography (DSA) system. Except this is of great importance to exclude present vascular abnormalities. The goal of UAE is partial or complete occlusion of both uterine arteries branches which led to adenomyosis focus with polyvinyl alcohol (PVA). Microspheres or gelatin-coated tris-acryl polymer microspheres and after the embolization of the above-mentioned vessels may produce effective infraction of adenomyosis focus associated due to moderate or severe pain. It is very important to sparing of cervical and vaginal branches, vasoconstriction avoidance, catheter 4-F retraction in the internal iliac artery, after the microcatheter placement.
Caution for anatomic variances:
atypical origin of uterine arteries, ovarian/uterine tube arteries deriving from uterine arteries, multiple arteries branching instead of one artery, absence of uterine arteries, origin from ovarian arteries or round ligament arteries, avoidance of embolization of the ascending branches to the ovary and descending branches to the cervix and the vagina.
After the selective catheterization of the uterine artery visualization with contras, if major ovary branch is visualized micro catheter is moved superelectively inside the ovary branch and the embolization of the supply to the ovary is done first with microspheres or big embolospheres with a diameter 900 μm. Technical difficulties include severe cannulating of arteries due to anatomic variations, arterial spasm, recently use of gonadotropin releasing hormone agonist, uterine perfusion from collateral ovarian vasculature. During the procedure, analgesic treatment (paracetamol and morphine) is administered wherever it is necessary.
Between April 2008 and 2021 sixty-four premenopausal women from our department Obstetrics and Gynecology, with symptomatic adenomyosis (diffuse adenomyosis), focal (adenomyoma) or coexisting with uterine myomas in fourty cases, ten cases and fourteen cases respectively underwent uterine artery embolization (UAE) in cooperation with Interventional Radiology department of Democritus University of Thrace, Greece. All procedures were performed by the institutional ethical standards and with the 1964 Helsinki Declaration.
Informed consent was obtained from all individual participants included in the study. All study participants with adenomyosis with or without concomitant fibroids were assessed for treatment by an experienced gynecologist.
With a medical history, the main symptoms were divided into the following categories: menstrual bleeding, pelvic pain (rated on a VAS score from 0 to 10, with 0 representing no pain and 10 unbearable pain), urinary discomfort, bleeding pain, massive symptoms, combination despite previous treatment, and health-related quality of life effects (restrictions on daily activities, energy/mood, self-awareness, and sexual function). Each participant then underwent a gynecological clinical examination, also transvaginal ultrasound followed by an MRI study. All imaging findings [US/MRI transvaginal ultrasound in either a Tesla 1 scanner (GE Healthcare) or a 1.5 Tesla magnet (Philips Multiva)] were then evaluated by an experienced gynecologist and invasive radiologist for possible treatment in the UAE. We present from our study participants Figures from a case with mixed adenomyosis and myoma uteri (Figures 1
Uterus myoma straight vessels.
Adenomyosis uteri spiral vessels.
Mixed type adenomyosis, myomas predominate, pressing and repelling the endometrium. MRI section, T2-WI, Sagital. Notice the increase in the width of the myometrial transition zone and hemosiderin granule (arrow) in the enlarged transition zone.
MRI section, T2-WI, Sagital of the patient, six months after bilateral embolization. The myomas have completely degenerated and shrunk, however they continue to repel the endometrium to a lesser degree. The myometrial band anatomy has been restored to normal. The examination was performed with sections T2-WI, D-WI and T1-WI, simple and with spectral suppression of the magnetic fat signal, before and after intravenous administration of paramagnetic substance—situation after UAE 6 months ago. Degeneration, complete elimination of vasculitis and very significant further shrinkage of the two submucosal myomas, degeneration, ischemia and mild further shrinkage of the subarachnoid myoma of the anterior myometrium are observed, while the muscles of the fibroids are completely indistinguishable. The (normal) endometrium is slightly repelled by the two submucosal myomas. In the present examination, the uterus, which has been reduced in size, is presented with normal belt anatomy. Normal imaging of the cervix—a little free peritoneal liquid is shown in the Douglas pouch—the ovaries are normal—no pathological lymph nodes are not detected.
Hyperelective catheterization and imaging before embolization of the left uterine artery, using a microcatheter. Observe the spiral vessels of adenomyosis and the straight lines of the myomas.
Hyperelective catheterization and imaging before embolization of the right uterine artery, using a micro-catheter.
The clinical results of the study were based on evaluations concerning the overall satisfaction of the patients, the relief of clinical symptoms, the need for reoperation and hysterectomy and the amenorrhea rates during the follow-up period, which varied from 1 to 12 months.
Included were postmenopausal women, patients with severe co-morbidities, patients who wished to maintain their fertility, patients with a known allergy to the contrast agent used during the procedure, and patients with suspected malignancy. There was no planned pregnancy or pelvic inflammation in the participants, while patients with only symptoms of back pain, asymptomatic, fibroid pendulum and rapidly improved size were excluded from the present study.
A total of 64 patients met the inclusion criteria, with a mean admission age of 51 years (36–53). 40 patients (62.5%) were diagnosed with pure adenomyosis, 10 patients (15.62%) with focal adenomyosis (adenomyoma) and 14 patients (21.87%) with adenomyosis and fibroids. 50 participants (78%) had a history of pregnancy and childbirth in the past.
Reported symptoms included: dysmenorrhea (98%) with a mean VAS score of 8.8 (range 6–10), menorrhagia with menstrual clots (88%), menorrhagia without menstrual clots (53%) and urinary problems (12%). In terms of quality of life data, 76.5% of women complained of limited daily activities and low energy due to heavy menstrual bleeding, while 73.5% had problems with their sex life.
According to our results, we confirm the following data:
Successful embolization (100%) was observed in all participants. On average, patients spent two days in the hospital, one day before the procedure and one on the day of the intervention. Elimination of clinical symptoms and reduction in pelvic pain intensity, assessed using VAS, was observed in 62 participants (96.87%). Pain in these cases decreased by an average of 7.5 points (from 8.2 to 1.0 points) during the follow-up period (from 1 to 12 months, average 3 months). Severe pain immediately after embolization and for approximately 24 h was observed in 8 cases with diffuse adenomyosis, 4 cases with adenomyoma and 2 cases with coexisting adenomyosis, in which analgesics and non-steroidal anti-inflammatory drugs were administered. In the majority of participants in our study, there were no significant complications associated with the procedure. However, in 4 participants (6.2%) recurrence of pain was observed within one to 2 months after embolism. In these cases, fractional dissolution is required, because submucosal fibroids coexist and adenomyosis diffuses. A postpartum neonatal ward of focal adenomyosis, sepsis, and surgical resection of necrotic sections was established, subject to the uterus. In no case was either reoperation or hysterectomy required. Restoration of normal menstruation was immediately observed in the subgroup of participants under 45 years of age. The other subgroup, which included participants over the age of 45, had normal menstruation. Only in 93% of cases immediately and only in 4 participants reported experience of the absence of menstruation for at least 3 months after embolization, resulting in the appearance of the period later after three months than in the other participants. In participants of the older participants over 45 years with a delayed onset of menstruation, low levels of AMH were established depending on biological age. Based on the findings of the MRI, partial or complete restoration of the normal zone anatomy in the uterus was confirmed after 6 months. All participants reported a decrease in menstrual bleeding and consequently improvement of everyday life quality. In one woman aged 49 years old, the decrease was not satisfactory and she underwent two months of analgesics therapy and after that the clinical symptoms were successfully improved. In our participants, the avoidance of hysterectomy was achieved in 100% of the women. All participants reported to be very or fairly satisfied with the results and would recommend this treatment to colleagues and friends.
Adenomyosis is reasonable, although it has not been proven, that matrices with adenomyosis are deficient in activated T-cells, with the result that the basal endometrium in adenomyosis has an advantage in terms of growth potential over non-adenomyotic and lymphoid-rich basal formations. The adenomyosis led to reducing the junctional zone thickness whereas the latter results in the reduction of uterine volume. It remains a major problem that the diagnosis is based on its variable presentation and common coexistence of other gynecologic disorders like fibroids or endometriosis. Growth of adenomyosis focus proved due to contrast-enhanced MRI and TVUS are recommended currently as the most accurate imaging techniques for the diagnosis of the disease. The classical surgical procedure, hysterectomy, is recommended as the only definite treatment modus, while the other treatment alternatives medical and UAE are widely implemented and exist controversially reports [94, 95, 96, 97, 98].
Both treatments are reported to be successful, especially in the short term, but there are some long-term reports of UAE adenomyosis treatment being poor in success rate and reaching almost 50% of patients receiving treatment without reporting clinical improvement. Regarding the previously published reports, a recurrence rate of 38% was reported, satisfactory life results were observed in 76% of the participants. However, the question remains unanswered whether such an abnormality is necessarily associated with acquired “morbidity” of the myometrium or whether it is an independent condition for the development of adenomyosis. The exact cause of hyperplasia-hypertrophy of the myometrium, located around the deep foci of the endometrium, is not known [94, 95, 96, 97, 98].
Myometrial hyperplasia-hypertrophy may indicate either an attempt to control endometrial penetration or simply represent bundles of smooth muscle fibers displaced by the expanding endometrium. After examination, by immunohistochemical technique, it was found that the myometrium, which surrounds the ectopic endometrium either diffuse (adenomyosis) or focal (adenomyoma), does not show abnormalities. Smooth muscle cells in adenomyotic foci, normal myometrium and leiomyomas, whether or not coexisting with adenomyosis, are rich in actin and desmin [94, 95, 96, 97, 98]. Several experimental “models” have been reported to study the pathogenesis of adenomyosis. In one of them, endometrial grafts of the anterior pituitary gland in mice led to the development of adenomyosis [98, 99, 100]. Prolactin may amplify this, as the uterine horn that did not contain isografts showed relatively less development of adenomyosis. In this experimental model ovarian resection was prevented, while benzoic estradiol favored the development of adenomyosis.
In another mouse model, which received high doses of diethylstilbestrol (DES) during fetal life, adenomyosis developed. These genera of mice appear to be prone to developing adenomyosis when there are high concentrations of prolactin, estrogen and progestogens. More recently, other researchers have induced adenomyosis in uncastrated rats with hyperprolactinaemia [98, 99, 100, 101, 102, 103, 104].
The researchers argued that high concentrations of prolactin cause degeneration of the myometrium, with the concomitant presence of ovarian steroids, which leads to its weakening, resulting in the invasion of the basal layer of the endometrium. Also of great interest were the observations of Mori and Nagasawa in mice, in which the penetration of stromal fibroblasts along the branches of the myometrial blood vessels preceded the invasion of the endometrial glands [105].
In another study, Sakamoto et al., caused severe adenomyosis of the uterus in mice by placing ectopic anterior pituitary lobe isografts [106]. DNA synthesis-related activities and related enzymes, such as thymidyl synthetase and thymidine kinase, were significantly increased in adenomyosis matrices, compared with controls in the control group. In the same experimental model, it was found that finding low molecular weight metalloproteinases plays a role in the development of adenomyosis, at the level of gene transcription, activation and repression [99, 100, 101, 102, 103, 104, 105, 106, 107, 108]. Specific experimental observations suggest that hereditary factors may be involved in the pathogenesis of adenomyosis. For example, the matrices of recombinant SMXA mice automatically develop adenomyosis-like histological changes and contain tenascin around the adenomyotic glands [100, 101, 102, 103, 104, 105, 106, 107, 108]. These observations, together with the biological properties of tenascin, reinforce the view of the endometrial origin of adenomyosis and the idea of endometrial penetration into the myometrium, which is genetically predisposed.
Also, compared to SMXA mice, the matrices of F1 mice, a genus found between SMXA and NJL, contain even more obvious spontaneous changes, resembling human adenomyosis. It should be noted, however, that it has not yet been determined whether heredity is an important factor in the development of adenomyosis in humans [100, 101, 102, 103, 104, 105, 106, 107, 108]. The early development of adenomyosis from remnants of Müller’s ducts, in positions outside the uterus, is enhanced by the finding of adenomyosis in the rectal septum [100, 101, 102, 103, 104, 105, 106, 107, 108]. In this anatomical position can be found endometrial glands and layers, which are associated with hypertrophy of the adjacent smooth muscle fibers and form adenomyotic nodules [100, 101, 102, 103, 104, 105, 106, 107, 108]. Although, these nodules can develop as a result of penetration of the peritoneal endometriosis of their origin from remnants of Müller’s resources. Thus, according to Nisolle and Donnez, in most cases, adenomyotic nodules are located deep in the septum and in some cases in the muscular layer of the rectum, away from the pelvic peritoneum [106, 107, 108]. The co-expression of vimentin and cytokeratin in the endometrium, when it is located in the endometrial cavity and when it is located in adenomyotic foci, is a typical feature of tissue, derived from Müller’s ducts. Morphologically and in terms of receptor content, adenomyosis of the atrial septum is similar to that of the myometrium, including poor or no response to the post-ovulatory effect of progesterone. Despite the high doses of progestogens in women with rectal adenomyosis to induce secretory differentiation, hormone therapy has poor results. The definitive treatment of the rectal lesions with surgery also suggests the existence of a metaplastic process from the beginning, from remnants of Müller’s ducts in this position, despite the implantation and penetration by peritoneal endometriosis [109, 110, 111, 112, 113, 114, 115, 116, 117, 118, 119].
Therefore, as the pathogenetic mechanisms of adenomyosis remain unclear, more studies are needed to reveal the pathophysiology of the disease. In the present study, all patients presented improvement in menorrhagia and had less blood loss during menstruation, while the effectiveness of the method appeared to be higher than that of other conservative surgeries such as intra-myometrial resection/excision and adenoectomy and laparoscopic myometrial electrocoagulation [119, 120, 121, 122, 123, 124, 125]. Radical surgery such as hysterectomy was eventually avoided in all participants, in 100% of the 64 patients. We did not observe the occurrence of permanent menopause, except in 0.6% of the participants, while transient amenorrhea within the first 3 months, occurred in the subgroup over the age of 45 years [119, 120, 121, 122, 123, 124, 125]. Premature menopause induction and subclinical reduction of ovarian functional reserve after the UAE is a known complication of this procedure, however, we have not observed any cases [119, 120, 121, 122, 123, 124, 125]. We know that our study has limitations and that the small sample size precludes a more detailed statistical analysis. Also, when adenomyosis coexists with uterine fibroids, it is very difficult to determine if the symptoms are caused by adenomyosis or the other. The incidence of pure adenomyosis is relatively low and due to a rare condition, individuals with co-existing fibroids were included [119, 120, 121, 122, 123, 124, 125].
In conclusion, despite the small number of participants, our preliminary study showed promising results with a very high rate of satisfied patients confirming that UAE might be a safe and effective method of treatment for premenopausal women with symptomatic adenomyosis in different if occurs with or without fibroids. It is a non-amputating treatment, alternative to hysterectomy UAE, for the treatment of symptomatic adenomyosis, when conservative treatment fails associated with few complications and allowed an option for the new session for recurrent disease.
None.
I would like to many thanks to Emeritus Professor George Iatrakis for his scientific helpful contribution.
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A number of options are suggested for development of global water resource and food production.",book:{id:"7645",slug:"desalination-challenges-and-opportunities",title:"Desalination",fullTitle:"Desalination - Challenges and Opportunities"},signatures:"Sheikh Mohammad Fakhrul Islam and Zahurul Karim",authors:[{id:"288119",title:"Prof.",name:"S.M. Fakhrul",middleName:null,surname:"Islam",slug:"s.m.-fakhrul-islam",fullName:"S.M. Fakhrul Islam"},{id:"288121",title:"Prof.",name:"Zahurul",middleName:null,surname:"Karim",slug:"zahurul-karim",fullName:"Zahurul Karim"}]},{id:"60850",doi:"10.5772/intechopen.76624",title:"Wastewater Treatment Using Membrane Technology",slug:"wastewater-treatment-using-membrane-technology",totalDownloads:2971,totalCrossrefCites:14,totalDimensionsCites:29,abstract:"Water contamination by heavy metals, cyanides and dyes is increasing globally and needs to be addressed as this will lead to water scarcity as well as water quality. Different techniques have been used to clean and renew water for human consumption and agricultural purposes but they each have limitations. Among those techniques, membrane technology is promising to solve the issues. Nanotechnology present a great potential in wastewater treatment to improve treatment efficiency of wastewater treatment plants. In addition, nanotechnology supplement water supply through safe use of modern water sources. This chapter reviews recent development in membrane technology for wastewater treatment. Different types of membrane technologies, their properties, mechanisms advantages, limitations and promising solutions have been discussed.",book:{id:"6539",slug:"wastewater-and-water-quality",title:"Wastewater and Water Quality",fullTitle:"Wastewater and Water Quality"},signatures:"Azile Nqombolo, Anele Mpupa, Richard M. Moutloali and Philiswa\nN. 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This chapter presents a review on fundamentals and applications of conventional Fenton, leading advanced technologies in the Fenton process, and reuse methods of iron containing sludge to synthetic and real wastewaters are discussed. Finally, future trends and some guidelines for Fenton processes are given.",book:{id:"9415",slug:"advanced-oxidation-processes-applications-trends-and-prospects",title:"Advanced Oxidation Processes",fullTitle:"Advanced Oxidation Processes - Applications, Trends, and Prospects"},signatures:"Min Xu, Changyong Wu and Yuexi Zhou",authors:[{id:"307479",title:"Dr.",name:"Changyong",middleName:null,surname:"Wu",slug:"changyong-wu",fullName:"Changyong Wu"},{id:"307546",title:"Prof.",name:"Yuexi",middleName:null,surname:"Zhou",slug:"yuexi-zhou",fullName:"Yuexi Zhou"},{id:"311139",title:"Dr.",name:"Min",middleName:null,surname:"Xu",slug:"min-xu",fullName:"Min Xu"}]},{id:"67689",doi:"10.5772/intechopen.86952",title:"Membrane Distillation: Basics, Advances, and Applications",slug:"membrane-distillation-basics-advances-and-applications",totalDownloads:1450,totalCrossrefCites:9,totalDimensionsCites:20,abstract:"Membrane technology as an emerging separation process has become competitive with other separation techniques in recent decades. Among pressure-driven and isothermal membrane processes, membrane distillation (MD) as a thermally driven process has come out to put an end to hardships of such processes like distillation. MD process can be used in a wide variety of applications such as desalination and wastewater treatment. Generally, MD is a process which water is a main component of the feed solution and only water vapor can pass through a hydrophobic membrane pores. With four main configurations different from each other by their condensation procedure, the performance of MD process is limited due to the lack of appropriate module, membrane, and energy consumption rate. In recent years, many experiments have been carried out to find well-suited membrane type and module. Also, applying solar or waste heat as heat source and the capability of coupling with other processes like forward osmosis and osmotic distillation distinguish MD process from other membrane processes. This chapter addresses membrane characteristics, MD applications, transport mechanisms, and process challenges.",book:{id:"8915",slug:"advances-in-membrane-technologies",title:"Advances in Membrane Technologies",fullTitle:"Advances in Membrane Technologies"},signatures:"Mohammad Reza Shirzad Kebria and Ahmad Rahimpour",authors:[{id:"289042",title:"Associate Prof.",name:"Ahmad",middleName:null,surname:"Rahimpour",slug:"ahmad-rahimpour",fullName:"Ahmad Rahimpour"},{id:"289043",title:"Mr.",name:"Mohammad Reza",middleName:null,surname:"Shirzad Kebria",slug:"mohammad-reza-shirzad-kebria",fullName:"Mohammad Reza Shirzad Kebria"}]}],mostDownloadedChaptersLast30Days:[{id:"70242",title:"Advancements in the Fenton Process for Wastewater Treatment",slug:"advancements-in-the-fenton-process-for-wastewater-treatment",totalDownloads:1873,totalCrossrefCites:9,totalDimensionsCites:21,abstract:"Fenton is considered to be one of the most effective advanced treatment processes in the removal of many hazardous organic pollutants from refractory/toxic wastewater. It has many advantages, but drawbacks are significant such as a strong acid environment, the cost of reagents consumption, and the large production of ferric sludge, which limits Fenton’s further application. The development of Fenton applications is mainly achieved by improving oxidation efficiency and reducing sludge production. This chapter presents a review on fundamentals and applications of conventional Fenton, leading advanced technologies in the Fenton process, and reuse methods of iron containing sludge to synthetic and real wastewaters are discussed. Finally, future trends and some guidelines for Fenton processes are given.",book:{id:"9415",slug:"advanced-oxidation-processes-applications-trends-and-prospects",title:"Advanced Oxidation Processes",fullTitle:"Advanced Oxidation Processes - Applications, Trends, and Prospects"},signatures:"Min Xu, Changyong Wu and Yuexi Zhou",authors:[{id:"307479",title:"Dr.",name:"Changyong",middleName:null,surname:"Wu",slug:"changyong-wu",fullName:"Changyong Wu"},{id:"307546",title:"Prof.",name:"Yuexi",middleName:null,surname:"Zhou",slug:"yuexi-zhou",fullName:"Yuexi Zhou"},{id:"311139",title:"Dr.",name:"Min",middleName:null,surname:"Xu",slug:"min-xu",fullName:"Min Xu"}]},{id:"71660",title:"Applications of Chemical Kinetics in Heterogeneous Catalysis",slug:"applications-of-chemical-kinetics-in-heterogeneous-catalysis",totalDownloads:1104,totalCrossrefCites:3,totalDimensionsCites:3,abstract:"Chemical kinetics is a key subdiscipline of physical chemistry that studies the reaction rate in every elemental step and corresponding catalytic mechanism. It mainly concludes molecular reaction dynamics, catalytic dynamics, elemental reaction dynamics, macrodynamics, and microdynamics. Such a research field has wide applications in heterogeneous catalysis. Based on the Arrhenius plot fitted by the catalytic conversions below 15% without the mass transfer effect and heat transfer effect, the apparent activation energy echoing with the intrinsically catalytic sites and the pre-exponential factor echoing with the relative number of active sites can be, respectively, derived from the slope and intercept of the Arrhenius plots, which can be used to compare the intrinsically catalytic activity of different catalysts and the relative amount of active sites. Reaction orders of both reactants and products are derived from the reaction rate equation and also fitted by the catalytic conversions below 15% without the mass transfer effect and heat transfer effect. According to the acquired reaction orders, the reaction mechanism can be proposed and even defined in some simple reactions. Therefore, investigations of chemical kinetics are of extreme importance and meaning in heterogeneous catalysis.",book:{id:"9415",slug:"advanced-oxidation-processes-applications-trends-and-prospects",title:"Advanced Oxidation Processes",fullTitle:"Advanced Oxidation Processes - Applications, Trends, and Prospects"},signatures:"Zhenhua Zhang, Li-Ping Fan and Yue-Juan Wang",authors:[{id:"312555",title:"Prof.",name:"Zhenhua",middleName:null,surname:"Zhang",slug:"zhenhua-zhang",fullName:"Zhenhua Zhang"},{id:"316868",title:"Ms.",name:"Li-Ping",middleName:null,surname:"Fan",slug:"li-ping-fan",fullName:"Li-Ping Fan"},{id:"316869",title:"Prof.",name:"Yue-Juan",middleName:null,surname:"Wang",slug:"yue-juan-wang",fullName:"Yue-Juan Wang"}]},{id:"77416",title:"Application of Water Quality Index for the Assessment of Water from Different Sources in Nigeria",slug:"application-of-water-quality-index-for-the-assessment-of-water-from-different-sources-in-nigeria",totalDownloads:516,totalCrossrefCites:0,totalDimensionsCites:1,abstract:"Water quality index (WQI) provides a single number that expresses the overall water quality, at a certain location and time, based on several water quality parameters. The objective of WQI is to turn complex water quality data into information that is understandable and usable by the public. A number of indices have been developed to summarize water quality data in an easily expressible and easily understood format. The WQI is basically a mathematical means of calculating a single value from multiple test results. This chapter discusses, in detail, the application of a water quality index for the assessment of water quality to different several water sources in Nigeria.",book:{id:"9921",slug:"promising-techniques-for-wastewater-treatment-and-water-quality-assessment",title:"Promising Techniques for Wastewater Treatment and Water Quality Assessment",fullTitle:"Promising Techniques for Wastewater Treatment and Water Quality Assessment"},signatures:"Ruth Olubukola Ajoke Adelagun, Emmanuel Edet Etim and Oko Emmanuel Godwin",authors:[{id:"256167",title:"Dr.",name:"Emmanuel",middleName:null,surname:"Edet Etim",slug:"emmanuel-edet-etim",fullName:"Emmanuel Edet Etim"},{id:"345734",title:"Mr.",name:"Oko",middleName:null,surname:"Emmanuel Godwin",slug:"oko-emmanuel-godwin",fullName:"Oko Emmanuel Godwin"},{id:"345735",title:"Dr.",name:"Ruth",middleName:null,surname:"Olubukola Ajoke Adelagun",slug:"ruth-olubukola-ajoke-adelagun",fullName:"Ruth Olubukola Ajoke Adelagun"}]},{id:"71348",title:"Water Treatment and Desalination",slug:"water-treatment-and-desalination",totalDownloads:1049,totalCrossrefCites:2,totalDimensionsCites:3,abstract:"Water covers a large area of the earth that reaches about three quarters of the surface of this planet, but we cannot say that all of this water is fresh or drinkable; according to many statistics, the percentage of fresh water reaches about 1% of the total water on earth. But with the great need for fresh water, whether for drinking or other purposes such as agriculture, the search for water treatment methods has become much larger. One of the most important of these methods that have been developed is desalination of seawater using desalination plants; therefore, we will address here the most important methods used in desalination and water treatment.",book:{id:"7645",slug:"desalination-challenges-and-opportunities",title:"Desalination",fullTitle:"Desalination - Challenges and Opportunities"},signatures:"Mona M. Amin Abdel-Fatah and Ghada Ahmed Al Bazedi",authors:[{id:"286268",title:"Associate Prof.",name:"Mona",middleName:null,surname:"Abdel-Fatah",slug:"mona-abdel-fatah",fullName:"Mona Abdel-Fatah"},{id:"295973",title:"Dr.",name:"Ghada",middleName:null,surname:"Al-Basedi",slug:"ghada-al-basedi",fullName:"Ghada Al-Basedi"}]},{id:"69228",title:"Advances in Passive Cooling Design: An Integrated Design Approach",slug:"advances-in-passive-cooling-design-an-integrated-design-approach",totalDownloads:2073,totalCrossrefCites:1,totalDimensionsCites:4,abstract:"Incorporating passive cooling devices within building design requires analysis of device variables and actions to improve cooling performance, maximize efficiency, and integrate with building elements. Improving devices performance requires understanding the relation of devices to design stages, building elements, and working mechanism, and actions performed by devices to enhance cooling process and effectiveness. Therefore, designers could integrate passive devices as intrinsic design elements. The current research introduces SARS as an innovative classification of passive devices based on cooling actions that are performed by a device like storing, avoidance, removal or slowing (SARS). All actions, devices, and variables were discussed and analyzed to help integrate them within design stages: analysis, designing, and performance. Understanding actions will help maximize the performance of the devices, combine two or more devices together, and integrate the devices’ deign in design process. Combining more devices together to perform more than one function will move passive design to a new level to become as whole building design approach and to be a core design element.",book:{id:"8496",slug:"zero-and-net-zero-energy",title:"Zero and Net Zero Energy",fullTitle:"Zero and Net Zero Energy"},signatures:"Ahmed A.Y. Freewan",authors:[{id:"284866",title:"Dr.",name:"Ahmed A.Y.",middleName:null,surname:"Freewan",slug:"ahmed-a.y.-freewan",fullName:"Ahmed A.Y. Freewan"}]}],onlineFirstChaptersFilter:{topicId:"287",limit:6,offset:0},onlineFirstChaptersCollection:[],onlineFirstChaptersTotal:0},preDownload:{success:null,errors:{}},subscriptionForm:{success:null,errors:{}},aboutIntechopen:{},privacyPolicy:{},peerReviewing:{},howOpenAccessPublishingWithIntechopenWorks:{},sponsorshipBooks:{sponsorshipBooks:[],offset:8,limit:8,total:0},allSeries:{pteSeriesList:[{id:"14",title:"Artificial Intelligence",numberOfPublishedBooks:9,numberOfPublishedChapters:87,numberOfOpenTopics:6,numberOfUpcomingTopics:0,issn:"2633-1403",doi:"10.5772/intechopen.79920",isOpenForSubmission:!0},{id:"7",title:"Biomedical Engineering",numberOfPublishedBooks:12,numberOfPublishedChapters:98,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2631-5343",doi:"10.5772/intechopen.71985",isOpenForSubmission:!0}],lsSeriesList:[{id:"11",title:"Biochemistry",numberOfPublishedBooks:27,numberOfPublishedChapters:287,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2632-0983",doi:"10.5772/intechopen.72877",isOpenForSubmission:!0},{id:"25",title:"Environmental Sciences",numberOfPublishedBooks:1,numberOfPublishedChapters:9,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2754-6713",doi:"10.5772/intechopen.100362",isOpenForSubmission:!0},{id:"10",title:"Physiology",numberOfPublishedBooks:11,numberOfPublishedChapters:139,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2631-8261",doi:"10.5772/intechopen.72796",isOpenForSubmission:!0}],hsSeriesList:[{id:"3",title:"Dentistry",numberOfPublishedBooks:8,numberOfPublishedChapters:129,numberOfOpenTopics:0,numberOfUpcomingTopics:2,issn:"2631-6218",doi:"10.5772/intechopen.71199",isOpenForSubmission:!1},{id:"6",title:"Infectious Diseases",numberOfPublishedBooks:13,numberOfPublishedChapters:107,numberOfOpenTopics:3,numberOfUpcomingTopics:1,issn:"2631-6188",doi:"10.5772/intechopen.71852",isOpenForSubmission:!0},{id:"13",title:"Veterinary Medicine and Science",numberOfPublishedBooks:10,numberOfPublishedChapters:103,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2632-0517",doi:"10.5772/intechopen.73681",isOpenForSubmission:!0}],sshSeriesList:[{id:"22",title:"Business, Management and Economics",numberOfPublishedBooks:1,numberOfPublishedChapters:12,numberOfOpenTopics:2,numberOfUpcomingTopics:1,issn:null,doi:"10.5772/intechopen.100359",isOpenForSubmission:!0},{id:"23",title:"Education and Human Development",numberOfPublishedBooks:0,numberOfPublishedChapters:0,numberOfOpenTopics:2,numberOfUpcomingTopics:0,issn:null,doi:"10.5772/intechopen.100360",isOpenForSubmission:!1},{id:"24",title:"Sustainable Development",numberOfPublishedBooks:0,numberOfPublishedChapters:10,numberOfOpenTopics:4,numberOfUpcomingTopics:1,issn:null,doi:"10.5772/intechopen.100361",isOpenForSubmission:!0}],testimonialsList:[{id:"13",text:"The collaboration with and support of the technical staff of IntechOpen is fantastic. 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