\r\n\tFrederick Law Olmsted, who is considered the father of American landscape architecture, often commented that landscape architecture is a profession that creates natural design approaches in human interaction with the environment.
\r\n\tLandscape design answers the people's need for parks and gardens in urban areas.
\r\n\tIt is a necessary design tool to understand to make more livable places in our living environment. Landscape Planning gives an option to protect our natural resources and natural environment. It draws a balance between the use and protection of natural areas. Urban Design is one of the important issues for landscape architecture. It is a common point of architecture, planning, and the landscape architecture profession. It helps to create sustainable, healthy spaces in urban development. Rural planning and development is the core issue of landscape architecture that makes a balance between natural and human interactions.
\r\n\r\n\tThis book project welcomes research papers related to all Landscape Architecture topics. We hope to provide an opportunity for Landscape Architecture researchers to distribute information to the academic community.
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Askeland, Mark R. Newton, Jonathan R. Henning and\nMichael A. O’Donnell",authors:[{id:"46467",title:"Prof.",name:"Yi",middleName:null,surname:"Luo",fullName:"Yi Luo",slug:"yi-luo"},{id:"95257",title:"Dr.",name:"Jonathan",middleName:null,surname:"Henning",fullName:"Jonathan Henning",slug:"jonathan-henning"},{id:"95258",title:"Prof.",name:"Michael",middleName:null,surname:"O'Donnell",fullName:"Michael O'Donnell",slug:"michael-o'donnell"},{id:"155748",title:"Dr.",name:"Eric",middleName:null,surname:"Askeland",fullName:"Eric Askeland",slug:"eric-askeland"},{id:"155749",title:"Dr.",name:"Mark",middleName:null,surname:"Newton",fullName:"Mark Newton",slug:"mark-newton"}]},{id:"44479",title:"Anti-Angiogenic Active Immunotherapy for Cancers: Dawn of a New Era?",slug:"anti-angiogenic-active-immunotherapy-for-cancers-dawn-of-a-new-era-",signatures:"Jianping Pan and Lihuang Zhang",authors:[{id:"157217",title:"Dr",name:null,middleName:null,surname:"Pan",fullName:"Pan",slug:"pan"}]},{id:"44354",title:"Nutrigenomics and Cancer Prevention",slug:"nutrigenomics-and-cancer-prevention",signatures:"Júlio César Nepomuceno",authors:[{id:"50743",title:"Ph.D.",name:"Júlio César",middleName:null,surname:"Nepomuceno",fullName:"Júlio César Nepomuceno",slug:"julio-cesar-nepomuceno"}]},{id:"44607",title:"The Impact of Vitamin D in Cancer",slug:"the-impact-of-vitamin-d-in-cancer",signatures:"Khanh vinh quoc Luong and Lan Thi Hoang Nguyen",authors:[{id:"48032",title:"Dr.",name:"Khanh",middleName:null,surname:"Luong",fullName:"Khanh Luong",slug:"khanh-luong"}]},{id:"44299",title:"The Treatment of Cancer: A Comprehensive Therapeutic Model Entailing a Complex of Interaction Modalities",slug:"the-treatment-of-cancer-a-comprehensive-therapeutic-model-entailing-a-complex-of-interaction-modalit",signatures:"R. Saggini and M. Calvani",authors:[{id:"60231",title:"Prof.",name:"Raoul",middleName:null,surname:"Saggini",fullName:"Raoul Saggini",slug:"raoul-saggini"}]},{id:"44356",title:"Supportive and Palliative Care in Solid Cancer Patients",slug:"supportive-and-palliative-care-in-solid-cancer-patients",signatures:"Bassam Abdul Rasool Hassan, Zuraidah Binti Mohd Yusoff,\nMohamed Azmi Hassali and Saad Bin Othman",authors:[{id:"155124",title:"Dr.",name:"Bassam",middleName:"Abdul Rasool",surname:"Hassan",fullName:"Bassam Hassan",slug:"bassam-hassan"}]},{id:"44609",title:"Impact of Cancer Treatment on Reproductive Health and Options for Fertility Preservation",slug:"impact-of-cancer-treatment-on-reproductive-health-and-options-for-fertility-preservation",signatures:"Kenny A. Rodriguez-Wallberg",authors:[{id:"157692",title:"Dr",name:"Kenny",middleName:null,surname:"Rodriguez-Macias Wallberg",fullName:"Kenny Rodriguez-Macias Wallberg",slug:"kenny-rodriguez-macias-wallberg"}]},{id:"43661",title:"Sialyl Salivary–Type Amylase Associated with Ovarian Cancer",slug:"sialyl-salivary-type-amylase-associated-with-ovarian-cancer",signatures:"Takanori Moriyama",authors:[{id:"162211",title:"Prof.",name:"Takanori",middleName:null,surname:"Moriyama",fullName:"Takanori Moriyama",slug:"takanori-moriyama"}]},{id:"44421",title:"Role of CREB Protein Family Members in Human Haematological Malignancies",slug:"role-of-creb-protein-family-members-in-human-haematological-malignancies",signatures:"Francesca D’Auria and Roberta Di Pietro",authors:[{id:"60267",title:"Prof.",name:"Roberta",middleName:null,surname:"Di Pietro",fullName:"Roberta Di Pietro",slug:"roberta-di-pietro"},{id:"167139",title:"Dr.",name:"Francesca",middleName:null,surname:"D'Auria",fullName:"Francesca D'Auria",slug:"francesca-d'auria"}]},{id:"44358",title:"Life-Cycling of Cancer: New Concept",slug:"life-cycling-of-cancer-new-concept",signatures:"Marina Shaduri and Marc Bouchoucha",authors:[{id:"16822",title:"Dr.",name:"Marina",middleName:null,surname:"Shaduri",fullName:"Marina Shaduri",slug:"marina-shaduri"}]}]}]},onlineFirst:{chapter:{type:"chapter",id:"74100",title:"Approach to the Newborn with Disorders of Sex Development",doi:"10.5772/intechopen.94570",slug:"approach-to-the-newborn-with-disorders-of-sex-development",body:'\nSex development involves many autosomal and X-linked genes acting and interacting along a short duration in a precise synergy. The process of sex determination includes 4 layers:
Determination of the chromosome sex
Determination of the gonadal sex
Development of the internal genitalia
Determination of the external genitalia
DSD is a heterogeneous group of congenital abnormalities associated with atypical development of the external and internal genitalia with an estimated incidence of 1:200–1:4500 [1]. Some of the abnormalities seem to have increased in incidence along the years with hypospadias reported to reach an incidence of 1:125 newborn males and cryptorchidism reaching an incidence as high as 3% of full-term male newborns.
\nThe nomenclature used to describe the genital abnormalities was initially descriptive, and on many occasions offensive. The advances in genetics and genomics knowledge substantially improved our understanding of the etiology of these conditions and resulted in a need to change the nomenclature. Thus, a new concept was introduced at the Chicago Consensus Conference 2005 [2] which defined the DSD as a congenital condition in which the development of chromosomal, gonadal or anatomical sex is atypical (instead of abnormal or ambiguous).
\nDSD can be divided into isolated or non-isolated/associated with other major abnormalities (Figure 1). When non-isolated they are usually associated with a variety of chromosome abnormalities, single gene or developmental field disorders which involve different body organ and systems (Figure 2). This review will mainly highlight the isolated/non-syndromic group of disorders of sex development.
\nDisorders of sex development—initial assessment.
Differential diagnosis in isolated disorders of sex development.
In humans, the gonads are populated by primordial germ cells, deriving from the yolk sac wall early in week five post conception. Normally, it is the presence or absence of the of the SRY gene in the Y chromosome in the germ cells that starts the chain of events which cause the gonadal determination as testis in males. The secretion of testicular hormones in males and their attachment to their action through receptors results in normal development of the male internal and external genitalia (Figures 3 and 4). The absence of the SRY gene or function and the expression of genes induced by them will result in the development of ovaries. The lack of hormones produced by the testis will determine the normal formation of female internal and external genitalia (Figures 3 and 4).
\nGonadal differentiation and function.
Diagram of the known major genes involved in testicular and ovarian differentiation and function (adapted from [
It was previously thought that the absence of SRY gene in the gonadal ridge will result in ovarian differentiation while the existence of the SRY gene will result in testicular development. However it is currently clear that gonadal sex is determined by antagonistic actions of ovarian and testicular cascades [5, 6] around week six post conception. In the female embryo, high levels of retinoic acid around the germ cells induces the STRA8 gene expression, resulting in germ cell meiosis and formation of oocytes. The absence of retinoic acid in the developing testis, results in formation of gonocytes which differentiate into spermatogonia and proliferate through mitosis with the meiosis happening after puberty [7].
\nThere are three main differences between ovarian and testicular activities (Figure 3):
The testes produce testosterone early in embryogenesis which induce the formation of the male external genital while the ovaries produce hormones only from puberty
Oogenesis starts and ends prior to 20 weeks gestation while spermatogenesis starts only at puberty
The ovarian hormonal production/function is linked to the process of follicle development and/or maintenance. The testes on the other hand can continue producing testosterone even in the lack of spermatogenesis.
The management of a newborn with abnormal genitalia has to be individualized taking into account the specific genital abnormalities as well as the parental and family as a whole. The decision regarding the sex of rearing should take into account the, surgical and non-surgical treatment, future pubertal development and fertility. This should be considered an urgent clinical situation and requires immediate assessment and counselling, and if possible, involvement of the DSD multidisciplinary core team including endocrinology, clinical genetics, genetic counselling, urology, obstetrics and gynecology, social work and psychology/psychiatry among others.
\nAlthough the majority of sex chromosome abnormalities do not have genital differences as a clinical finding, some do. At conception 2% of all pregnancies are Turner syndrome and is one of the most common chromosome abnormality associated with first trimester miscarriages. The condition is highly lethal in-utero and thus the incidence at birth is 1:2500 female newborn. In almost 2/3 of cases, i.e. 60%, the karyotype is 45,X while in 15%, the condition is associated with mosaicism, i.e. 45, X/47,XXX, 45,X/46, XX/47,XXX, 45,X/46, XY, and 45,X/46, XX. Other chromosome abnormalities associated with Turner syndrome include structural abnormalities involving the X chromosome, e.g., 46,X,r(X), 46,X,Xp-, and 46,X,i(Xq) in 10% of cases, structural abnormality of the X chromosome in mosaic state in 10% of cases, with 5% in the other [8]. The condition can be detected prenatally, due to abnormalities in the lymphatic system, with the fetus presenting with heart lesions, specifically left-sided, hydrops fetalis, increased nuchal translucency or cystic hygroma. Postnatally, female babies can present with typical facial features, including epicanthic folds, droopy eyelids, down slanting palpebral fissures, micrognathia, and low set and prominent ears. The neck is often webbed and short with a nuchal hairline that is low, as well as swelling (lymphedema) of the feet and hands, and deep set nails. Left-sided cardiac anomalies are seen in 50% of the cases (hypoplastic left heart, coarctation of the aorta, bicuspid aortic valve, and aortic stenosis) with an increased risk for aortic dissection during pregnancy and the puerperal period if they decide to conceive using a donor egg. It is also associated with horseshoe kidneys as well as short stature, streak gonads and thus lack of spontaneous puberty. However, they can conceive using a donor egg.
\nGenetic analysis for Y chromosome material, including in a mosaic state can be picked up by chromosome microarray analysis and is important since girls with mosaicism for 46, XY [45,X/46,XY] have an increased risk for gonadoblastoma and dysgerminoma and may have absent uterus. A large British series in the literature, looking at women with Turner syndrome, showed an increased incidence not only of gonadoblastoma, but also uterine cancer, as well as possibly pediatric brain cancers. This study also demonstrated a lower incidence of breast cancer [9, 10, 11].
\nThe incidence of Klinefelter syndrome, i.e. 47, XXY is approximately 1 in 500 males. Clinically, they can present with testes on the smaller end of the spectrum, which can impact production of testosterone and normal sperm. Otherwise, they do not have genital differences. They have normal appearing facies but can be taller in height than average and about 50% develop gynecomastia at puberty. Boys with Klinefelter syndrome can present with neurodevelopmental/neurobehavioral issues; however encouraging results, for behavioral as well as for the physical features described above, have been seen with early administration of testosterone. The optimal timing and dosage of hormonal therapy has not been established and further studies and long term follow-up are needed prior to this becoming standard treatment [12].
\nMosaicism for 45,X/46, XY, also previously called mixed gonadal dysgenesis, is a rare condition with an approximate incidence reported in Denmark of less than 1/15,000 live births [8]. It has been suggested that transformation of the indifferent gonad to testes [13, 14, 15] is due to the existence of Y chromosome in the gonadal ridge. The spectrum of genital differences with this karyotype is varied, ranging from females presenting with Turner syndrome, to males with ambiguous genitalia, to phenotypically normal males. Gonadal function in most 45,X/46, XY males, even those with genital ambiguity, seems sufficient for spontaneous puberty and patients appear to benefit from GH treatment when needed [16].
\n46, XY DSD can be divided into categories;
Disorders of testicular (gonadal) development
Disorders of androgen synthesis
Both categories lead to feminization or abnormal genitalia.
\nDisorders of testicular (gonadal) development are characterized by absent or small testes on palpation and/or ultrasound. Müllerian structures (uterus and fallopian tubes) can be present with the external genitalia feminized to varying degrees along with decreased levels of testosterone, dehydroepiandrosterone and androstenedione [17].
\nAt approximately 6 weeks, the gonads can form ovaries or testis [3]. The process of testicular differentiation involves multiple genes (Figure 4). Mutations causing haploinsufficiency with a loss of function and duplication with gain of function are known to be associated with 46, XY gonadal DSD. The
The
The ligand
The Wilms tumor factor 1 (
Disorders of androgen synthesis are characterized by a lack of Müllerian structures. The testes in 46, XY individuals produce Anti-Müllerian hormone and have genital abnormalities including normal female external genitalia.
\nTwo categories can be used to describe Disorders of Androgen Synthesis:
Congenital adrenal hyperplasia (CAH) in patients with female chromosome sex
Associated with normal adrenal function.
Seven enzymes involved in the production of testosterone and dihydrotestosterone, responsible for 46, XY disorders of sex differentiation have been identified (Figure 5).
\nSteroid hormone synthesis pathway and associated biochemical abnormalities in 46, XY DSD. POR: P450 oxidoreductase; StAR: steroid acute regulatory protein; 17α-OH: 17α-hydroxylase; 3β-HSD: 3β-hydroxysteroid dehydrogenase; 21-OH: 21-hydroxylase; 18-OH: 18-hydroxylase; 11β-OH: 11β-hydroxylase; 17β-HSD: 17β-hydroxysteroid dehydrogenase; 5α-R: 5α-reductase; CAH: congenital adrenal hyperplasia (adapted from [
Defects early in the pathway result in congenital adrenal hyperplasia and adrenal insufficiency. These enzymes are present in both the adrenal cortex and the gonads.
\nThe first enzymatic step involves the steroidogenic acute regulatory (
3β-hydroxysteroid dehydrogenase (3β-HSD) is the next major enzyme involved in multiple steps including converting pregnelone to progesterone, 17α-OH pregenelone to 17α-OH progesterone and DHEA to androstenedione. Defects in 3β-HSD enzyme activity result in salt wasting and decreased testosterone production resulting in genital abnormalities in males. The findings include hypospadias, micropenis and bifid scrotum (OMIM 201810).
\n17α-hydroxylase is involved in the conversion pregnelone and progesterone to their 17α hydroxylated forms. Defects to this enzyme pathway also present with increased risk for adrenal insufficiency and ambiguous genitalia. Patients presenting with a combined deficiency in 17α-hydroxylase and 17,20-lyase present similarly to isolated 17α-hydroxylase deficiency. Patients with isolated 17,20-lyase deficiency have normal adrenal function and variable abnormalities of male phenotype. This is because 17,20-lyase is present in the gonads only.
\n17β-hydroxysteroid dehydrogenase type III (Figure 5) leads to the conversion of androstenedione into testosterone, this occurs within the gonads. Pathogenic variants cause an autosomal recessive disorder (OMIM 264300) with female external genitalia in 46, XY individuals, male gonadal derivatives, absent Müllerian structures, infertility and decreased testosterone [33]. These patients are sometimes difficult to distinguish from 5α-reductase deficiency and partial androgen insensitivity syndrome [34]. Further biochemical testing with ACTH stimulation or hCG stimulation may be needed [17] although DNA analysis is probably the easiest to perform.
\nTestosterone and dihydrotestosterone (DHT) are the end products for testis steroid hormone synthesis. Pathogenic variants occurring in the 5α-reductase gene (
The most common cause of 46, XY DSD are the androgen insensitivity syndromes (AIS) [OMIM # 300068]. The androgen receptor (AR) is unable to activate due to the inability of testosterone or DHT to bind to the receptor [35] (Figure 5). Androgens have a lack of effect on genital development. These conditions are X-linked inherited and present with a wide range in phenotypes. Complete Androgen Insensitivity Syndrome (CAIS) has an estimated prevalence of at least 1:99,000 [36] presenting with normal female genitalia and blind ending vaginal pouch. Partial Androgen Insensitivity Syndrome (PAIS) has an estimated prevalence of 1:8000. This conditions occurs when there is residual AR receptor function and hypospadias are the common finding. Mild Androgen Insensitivity Syndrome (MAIS) is the least severe. MAIS usually presents with no genital abnormalities. This condition can be suspected in the context of pubertal gynecomastia or unexplained infertility [33]. Pathogenic variants in AR have been associated with AIS. These pathogenic variants can be located outside of the coding region [37, 38]. There have been some cases where no pathogenic variants in AR have been detected. This suggests other proteins located beyond AR that influence testosterone signaling [39].
\n46, XX DSD can occur due to:
\nAbnormal ovarian development.
Excess androgen levels due to abnormal synthesis or androgen exposure.
There are two types of abnormal development that can cause XX sex reversal:
Patients who have the presence of the
Patients who are XX males and
Loss of function mutations in genes coding for ovarian formation and function are associated with ovarian dysgenesis and/or accelerated loss of primordial follicles. This can cause premature ovarian failure (POF) and/or premature menopause.
\nThe gene responsible for the differentiation of the bipotential gonad into ovaries is the
In humans, duplication of chromosome 1p31-p35 causes a duplication of the
Another important gene is the
In mice models the continued expression of
\n
Other genes associated with ovarian dysgenesis and premature ovarian failure include:
In 46,XX female, increased fetal androgen synthesis or prenatal exposure to androgen leads to musculinization of the female external genitalia (Figure 6) [26].
\nSteroid hormone synthesis pathway in 46, XX DSD. 3β-HSD: 3β-hydroxysteroid dehydrogenase; 21-OH: 21-hydroxylase; 11β-OH: 11β-hydroxylase (adapted from [
Maternal androgen producing tumors can cause virilization of a female infant. These include adrenal tumors and ovarian tumors. There have been reports including a maternal luteoma of pregnancy which caused virilization of both mother and child [53]. There are also various drugs with androgenic activity. These include androgens, danazol, progestins and potassium sparing diuretics that are known to cause virilization [17, 53].
\nPlacental Aromatase Deficiency is another cause of virilization in a female. This is a rare autosomal recessive condition caused by mutations in
Steroid synthesis defects leading to congenital adrenal hyperplasia with androgen excess cause clitoral enlargement, partial or complete fusion of the labia majora and a short vagina [26] with virilization Prader stage above III [55].
\nThe most common cause of 46, XX disorders of sexual differentiation (Figure 6) is 21-hydroxylase (21-OH) deficiency. This occurs in 90% of cases [55] and has a prevalence of 1:14,000–1:15,000 worldwide [54, 55]. This autosomal recessive condition is caused by mutations in the 21-OH gene (
Patients with classic 21(OH) deficiency are at high risk (approximately 70%) for neonatal salt wasting [17]. These patients present with high 17α-hydroxyprogesterone, androstenedione and testosterone levels (Figure 6) and decreased sodium, elevated potassium and elevated renin at the end of the first week of life [17]. The high androgens levels result in virilization of the female external genitalia in female fetuses. This can be seen as early as 12 weeks gestation [54] and varies from mild clitoromegaly to complete male external genitalia with rugated and pigmented labioscrotal folds and a phallic structure [17].
\nNon-classic 21(OH) deficiency is more common than the classic form. The world wide incidence is 1:300, the Ashkenazi Jewish population has a higher incidence described as 1:27 [54]. They generally present in adolescence with a presentation is similar to Polycystic Ovarian Syndrome, namely premature pubarche, acne, hirsutism and irregular menses.
\n11β-OH is present in the adrenals and coded by the CYP11B1 gene. Defects lead to congenital adrenal hyperplasia which present with a similar picture to classical CAH. This is the second most common cause of congenital adrenal hyperplasia with an incidence of less than 1:100,000 births. The condition is inherited in an autosomal recessive manner and homozygote or compound heterozygote mutations in the
There are rare forms of defects in steroid synthesis causing CAH. These include 3β-hydroxysteroid dehydrogenase (3β-HSD) deficiency and 11β-hydroxylase (11β-OH) deficiency. There are two enzymes that mediate 3β-HSD. The type 1 enzyme (
Type 2 (
The initial investigation should include a careful physical examination to determine if the presentation is isolated or non-isolated (Figure 1). In view of the association between IUGR and undervirilization in chromosomal male fetuses, results of maternal serum screening, placental growth factor and detailed fetal ultrasound findings and biophysical profile as well as the birth weight should be obtained.
\nExamination of the external genitalia should include:
Assessment of the labioscrotal folds—the labioscrotal folds should be assessed for pigmentation, rugation, asymmetry and fusion. High insertion of the labioscrotal folds (above the penis) as well as “buried penis” should be differentiated from micropenis.
Assessment of the phallic structure, the length, breadth, urogenital openings—the phallic structure should be assessed for length, breadth, chordee and relationship with the labioscrotal folds looking for complete or incomplete penoscrotal transposition. The normal penile length at term is 3.5 cm with 2.5 cm being at −2SD. The normal clitoral length at term is 2–8.5 mm and breadth 2–6 mm [56].
Location, structure and volume of the gonads—gonads located in the inguinal canal and labioscrotal folds are always testes although ovotestes is also a possibility.
The perineum should also be examined for the number and position of the openings and then compared to the Prader scale [57].
\nInvestigations should be targeted to identify:
The chromosome sex
The gonadal sex
The internal genitalia [using ultrasound and/or MRI to find if], is there is a uterus, is the uterus normal and are there intrabdominal gonads
The external genitalia
Since gonads in the inguinal canal and labioscrotal folds are almost always testis finding them on palpation usually indicates the existence of the SRY gene. However, the chromosome sex should be determined using quantitative fluorescent PCR (QF-PCR) or fluorescent in-situ hybridization (FISH) analysis. Microarray analysis should be completed, looking for submicroscopic deletion or duplication involving the
Unique situations to be aware of include the most severe cases (46,XY with complete feminization and 46,XX with complete masculinization) it is difficult to diagnose an abnormal phenotype. Other scenarios include isolated grade 1 (glandular) and 2 (penile shaft) hypospadias, especially when associated with intrauterine growth restriction (IUGR) the investigative yield is low. Most cases are the result of the IUGR – Placental dysfunction – abnormal genitalia syndrome [59]; however, since this is a diagnosis by exclusion and there is no objective way of differentiating the condition from PAIS and mild 5α reductase deficiency, DNA analysis using 46,XY panel or for these conditions is recommended. Further investigations are also indicated with hypospadias associated with bilateral or unilateral undescended testes, micropenis, clitoromegaly, posterior fusion of the labia majora.
\nThe most common cause of abnormal genitalia in female is CAH. When initial investigations show XX karyotype, 17-hydroxyprogesterone (17-OH) and renin at 48 hours of age (after the surge of adrenal hormones at birth) should be done. The abnormal sodium and potassium blood levels will present only in the second week of life.
\nIn cases with XY karyotype, the testosterone, LH and FSH levels should be measured looking for low testosterone and dihydrotestosterone (DHT) levels. Answering the above four questions will guide further investigations which include assessment of adrenal function, testicular function and internal genitalia using ultrasound, MRI and/or genitogram or laparoscopy [17].
\nGenetic testing plays an important role in finding the etiology and thus providing genetic counselling regarding the recurrence risks and the prenatal/preimplantation options in future pregnancies. The use of DSD genetic panels can investigate multiple genes simultaneously and accelerate the diagnostic process. Using massive parallel sequencing looking at a variety of genes causing DSD in a cohort of 278 patients with 46, XY DSD and 48 with 46, XX DSD of an unknown etiology, Eggers et al., found a likely genetic diagnosis in 43% of patients with 46, XY DSD and 17% of patients with 46, XX DSD [60]. If no gene mutation is identified, whole exome/genome sequencing is recommended.
\nWhen a newborn presents with ambiguous genitalia, a thorough physical examination, as well as various genetic (e.g. karyotype, microarray) and non-genetic investigations are ordered. From this, the health care team is able to have discussions with parents regarding the gender for sex of rearing. With regards to genital surgery, the current suggestion is that if genital surgery is not medically indicated, then to wait until the patient him/herself is able to make this decision. In cases with substantial ambiguity such as in PAIS, mixed gonadal dysgenesis, ovotesticular DSD and females with CAH and severe masculinization, a multidisciplinary DSD team including pediatric endocrinologists, geneticists, genetic counsellors, urologists, gynecologists, social workers and psychologists/psychiatrists with expertise in this field should be part of the care team. The findings, plan for investigations, gender assignment and treatment should be discussed among the group members prior to meeting the parents. Factors which have to be taken into consideration include type of gonads and potential function of these, present or future treatment with hormones, including for inducing puberty or for fertility if this can be predicted, as well as any medically necessary surgical treatment. When meeting with the parents, the team should present this information at a level that the parents can understand, using visual aids to facilitate the discussion. At the same time, if information is known from the literature about certain conditions that parents should be aware of, e.g. female babies with CAH and exposure to high and early levels of androgen levels prenatally can show more behaviors attributable to the male personality and sexual orientation [61, 62, 63, 64], and the challenges in repairing severe hypospadias in patients diagnosed with PAIS [65], then this should be shared with them. In this way, the parents, together with the healthcare team’s input can come to an informed decision about sex of rearing.
\nDysgenetic gonads with a Y chromosome material are associated with an increased risk for malignancy, mainly gonadoblastoma, dysgerminoma and germ cell tumors, including seminoma, non-seminoma, juvenile granulosa cell and germ cell neoplasia in situ [66, 67]. Gonadoblastoma (GB) presents with a mixture of germ cells and stromal elements as well as immature Sertoli cells and may contain calcifications with pure gonadoblastomas being not metastatic. About 80% of patients with GB are phenotypic females and 20% are phenotypic males, many of them with hypospadias and bilateral or unilateral cryptorchidism. The incidence of GB in dysgenetic gonads varies from 4.7% to as high as 25%. Germ cell neoplasia in-situ cells are found lining the seminiferous tubules in dysgenetic testes and resemble immature germ cells. Thus, they cannot be diagnosed before puberty when they are normally present. However, when found in the testes in late childhood or post puberty they are pathological and are capable of transforming into seminomas in males and dysgerminoma in females and this tumor can metastasize. Removal of the gonad prior to puberty in patients with complete androgen insensitivity is controversial in view of the data indicating low risk for malignancy until early adult years [68, 69]. In these patients, if the testes are located in the labia majora, they are amenable to ultrasound surveillance and biopsies, if needed which makes post-pubertal monitoring simpler. When the testes are undescended, laparoscopic gonadopexy to bring them near the anterior abdominal wall to allow surveillance may be an option for patients who decide to avoid gonadectomy [68, 69]. Delayed surgery can help in involving the patient in the decision making [67, 70, 71]. Persistent Mullerian Duct Syndrome is associated with the usual cancer risk associated with cryptorchidism as well as an unknown incidence of a possible tumor risk of the Mullerian duct structures.
\nIn 2006, a new definition of genetic counseling was published in the Journal of Genetic Counseling, by a task force that was convened by the National Society of Genetic Counselors (NSGC). The definition is as follows: “Genetic counseling is the process of helping people understand and adapt to the medical, psychological and familial implications of genetic contributions to disease. This process integrates the following:
Interpretation of family and medical histories to assess the chance of disease occurrence or recurrence.
Education about inheritance, testing, management, prevention, resources and research.
Counselling to promote informed choices and adaptation to the risk or condition” [72].
Genetic counselling has an important role in the management of DSD patients and their families. In most cases, counselling involves the woman/couple, following the birth of a child with DSD and/or in discussing the implications of their future reproductive plans. Genetic counselling can also be extended to other family members and the implications to themselves and their future pregnancies. Discussions with other family members require consent from the parents of the index patient or the index patient himself/herself if of age of maturity. Other indications for genetic counselling include an adolescent or young adult with DSD who wishes to learn more about their own diagnosis and the implications for her/his reproductive plans as well a woman/couple during their pregnancy when discordance between the genotypic and phenotypic sex is identified.
\nFollowing the birth of a child with DSD, parents are often overwhelmed and confused by their child’s condition. Although gender assignment and naming of the child are pressing issues for the parents, these actions should not be unduly rushed. Parents should be provided with information so as to help them in making informed decisions, together with their healthcare team. Adequate counseling and support for parents includes education regarding sexual development in utero (including brain imprinting of gender identity), genetic counseling, ethical considerations of the child’s rights to make decisions regarding gender, and information regarding current guidelines and recommendations.
\nA three generation family history should be obtained with careful inquiry. Information about family history of infertility, women with no menstrual periods, stillbirth, recurrent miscarriages, neonatal death, congenital abnormalities, intellectual disabilities and consanguinity should be obtained. When drawing the family history, it should be kept in mind that chromosome sex and phenotypic sex may be interpreted differently by the family; for the family, it is the phenotypic sex that identifies the family members as male or female (versus chromosome sex). Furthermore, in X-linked conditions the phenotypic infertile female may be chromosomally male (such as in androgen insensitivity or ATRX).
\nWhen a diagnosis is established from genetic investigations, then the family can be provided with information regarding the clinical manifestations and natural history, mode of inheritance, medical management recommendations, if any, recurrence risk for future pregnancies, implications to their other children/other family members, as well as information regarding appropriate patient support groups. Cultural differences need to be respected and taken into consideration during the counselling process [73].
\nIn some cases, a DSD is diagnosed incidentally during pregnancy, with no previous family history. This could be following the finding of fetal abnormal external genitalia or finding of discrepancy between the phenotypic sex as determined by fetal ultrasound and the genotypic sex as determined by chorionic villus sampling, amniocentesis or non-invasive prenatal testing (NIPT) done for other reasons. The differential diagnosis for the cases detected incidentally is broad but it should be kept in mind that in a 46,XX fetus, the most likely diagnosis is congenital adrenal hyperplasia. In a 46,XY fetus, the differential diagnosis includes a variety of conditions including androgen insensitivity syndrome, 46,XY gonadal dysgenesis and testosterone biosynthesis defects, when no other abnormalities are identified. When other abnormalities are detected, such as on ultrasound, more rare conditions such as campomelic dysplasia and Smith-Lemli-Opitz syndrome should be considered [74]. Following prenatal diagnosis of a DSD the family may choose to continue with the pregnancy with no further investigations, they may decide to terminate the pregnancy based on the information provided or they may decide to further investigate the etiology of the abnormalities identified. Prior to this however, the genetics health care team should facilitates a discussion with the family outlining each option with the pros/cons of each, including what to expect from a procedure, if applicable, as well as the impact on puberty and fertility and the potential psychosocial perspective. This information is important to allow an informed decision to be made in keeping with their value and belief system. The family should be made aware that the genetics health care team will support whatever decision they make. In situations where the family decides to terminate the pregnancy and the etiology of the condition is not known, the benefits of a fetal autopsy and molecular analysis should be reviewed with the family.
\nGenetic counselling should be made available to couples who are planning to have more children, following the birth of a child with DSD. The provision of genetic counselling in these cases, in addition to providing psychosocial support, includes information regarding their recurrence risk and their available reproductive options:
Accepting the risk of having another affected child and have no prenatal/preimplantation genetic diagnosis.
Deciding not to have any more biological children and choosing instead to use donor gametes, donor embryos or adoption.
Conceive naturally and have pre-natal diagnosis with the option of either continuing or terminating an affected pregnancy.
Pre-implantation genetic diagnosis (PGD).
Patients with DSD may be infertile. For these patients, conception using donor gametes and/or surrogate mother may be possible and should be discussed. However, to lower the recurrence risk, when applicable, the donor should not be a genetic relative/carrier of the condition.
\nNormal sex development includes determination of chromosome sex, gonadal sex, development of internal and external genitalia as well as the psychosocial sex. This is a complex process involving genetic and non-genetics components, many of them are yet unknown. Disorder of sex development is an etiologically a heterogenous group of disorders with a major lifelong impact on the patients and their families.
\nIn view of the complexity of these group of patients they should be seen by a DSD team including but not limited to pediatric endocrinologist, pediatric urologist, medical geneticist, genetic counsellor, psychologist/psychiatrist and social worker and the findings and current knowledge should be presented to the parents so that they can make an informed decision regarding the gender, when appropriate. The child with DSD should continue be followed into puberty and adulthood to achieve optimal treatment, psychosocial well-being, sexual satisfaction, and fertility in view of the patients gender role and identity [75].
\nWeb-based educational resources for families include:
\n\nwww.aboutkidshealth.ca/En/HowTheBodyWorks/SexDevelopmentAnOverview\n
\nThis website provides detailed graphically illustrated explanations of sex development and DSDs that health professionals can use when working with families.
\nAndrogen Insensitivity Syndrome: Differences of Sex Development Support Group.
\n\nCARES foundation: Congenital Adrenal Hyperplasia Research, Education and Support.
\n\nhttp://www.caresfoundation.org\n
\nHypospadias and Epispadias Association.
\n\n"Open access contributes to scientific excellence and integrity. It opens up research results to wider analysis. It allows research results to be reused for new discoveries. And it enables the multi-disciplinary research that is needed to solve global 21st century problems. Open access connects science with society. It allows the public to engage with research. To go behind the headlines. And look at the scientific evidence. And it enables policy makers to draw on innovative solutions to societal challenges".
\n\nCarlos Moedas, the European Commissioner for Research Science and Innovation at the STM Annual Frankfurt Conference, October 2016.
",metaTitle:"About Open Access",metaDescription:"Open access contributes to scientific excellence and integrity. It opens up research results to wider analysis. It allows research results to be reused for new discoveries. And it enables the multi-disciplinary research that is needed to solve global 21st century problems. Open access connects science with society. It allows the public to engage with research. To go behind the headlines. And look at the scientific evidence. And it enables policy makers to draw on innovative solutions to societal challenges.\n\nCarlos Moedas, the European Commissioner for Research Science and Innovation at the STM Annual Frankfurt Conference, October 2016.",metaKeywords:null,canonicalURL:"about-open-access",contentRaw:'[{"type":"htmlEditorComponent","content":"The Open Access publishing movement started in the early 2000s when academic leaders from around the world participated in the formation of the Budapest Initiative. They developed recommendations for an Open Access publishing process, “which has worked for the past decade to provide the public with unrestricted, free access to scholarly research—much of which is publicly funded. Making the research publicly available to everyone—free of charge and without most copyright and licensing restrictions—will accelerate scientific research efforts and allow authors to reach a larger number of readers” (reference: http://www.budapestopenaccessinitiative.org)
\\n\\nIntechOpen’s co-founders, both scientists themselves, created the company while undertaking research in robotics at Vienna University. Their goal was to spread research freely “for scientists, by scientists’ to the rest of the world via the Open Access publishing model. The company soon became a signatory of the Budapest Initiative, which currently has more than 1000 supporting organizations worldwide, ranging from universities to funders.
\\n\\nAt IntechOpen today, we are still as committed to working with organizations and people who care about scientific discovery, to putting the academic needs of the scientific community first, and to providing an Open Access environment where scientists can maximize their contribution to scientific advancement. By opening up access to the world’s scientific research articles and book chapters, we aim to facilitate greater opportunity for collaboration, scientific discovery and progress. We subscribe wholeheartedly to the Open Access definition:
\\n\\n“By “open access” to [peer-reviewed research literature], we mean its free availability on the public internet, permitting any users to read, download, copy, distribute, print, search, or link to the full texts of these articles, crawl them for indexing, pass them as data to software, or use them for any other lawful purpose, without financial, legal, or technical barriers other than those inseparable from gaining access to the internet itself. The only constraint on reproduction and distribution, and the only role for copyright in this domain, should be to give authors control over the integrity of their work and the right to be properly acknowledged and cited” (reference: http://www.budapestopenaccessinitiative.org)
\\n\\nOAI-PMH
\\n\\nAs a firm believer in the wider dissemination of knowledge, IntechOpen supports the Open Access Initiative Protocol for Metadata Harvesting (OAI-PMH Version 2.0). Read more
\\n\\nLicense
\\n\\nBook chapters published in edited volumes are distributed under the Creative Commons Attribution 3.0 Unported License (CC BY 3.0). IntechOpen upholds a very flexible Copyright Policy. There is no copyright transfer to the publisher and Authors retain exclusive copyright to their work. All Monographs/Compacts are distributed under the Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0). Read more
\\n\\nPeer Review Policies
\\n\\nAll scientific works are Peer Reviewed prior to publishing. Read more
\\n\\nOA Publishing Fees
\\n\\nThe Open Access publishing model employed by IntechOpen eliminates subscription charges and pay-per-view fees, enabling readers to access research at no cost. In order to sustain operations and keep our publications freely accessible we levy an Open Access Publishing Fee for manuscripts, which helps us cover the costs of editorial work and the production of books. Read more
\\n\\nDigital Archiving Policy
\\n\\nIntechOpen is committed to ensuring the long-term preservation and the availability of all scholarly research we publish. We employ a variety of means to enable us to deliver on our commitments to the scientific community. Apart from preservation by the Croatian National Library (for publications prior to April 18, 2018) and the British Library (for publications after April 18, 2018), our entire catalogue is preserved in the CLOCKSS archive.
\\n"}]'},components:[{type:"htmlEditorComponent",content:'The Open Access publishing movement started in the early 2000s when academic leaders from around the world participated in the formation of the Budapest Initiative. They developed recommendations for an Open Access publishing process, “which has worked for the past decade to provide the public with unrestricted, free access to scholarly research—much of which is publicly funded. Making the research publicly available to everyone—free of charge and without most copyright and licensing restrictions—will accelerate scientific research efforts and allow authors to reach a larger number of readers” (reference: http://www.budapestopenaccessinitiative.org)
\n\nIntechOpen’s co-founders, both scientists themselves, created the company while undertaking research in robotics at Vienna University. Their goal was to spread research freely “for scientists, by scientists’ to the rest of the world via the Open Access publishing model. The company soon became a signatory of the Budapest Initiative, which currently has more than 1000 supporting organizations worldwide, ranging from universities to funders.
\n\nAt IntechOpen today, we are still as committed to working with organizations and people who care about scientific discovery, to putting the academic needs of the scientific community first, and to providing an Open Access environment where scientists can maximize their contribution to scientific advancement. By opening up access to the world’s scientific research articles and book chapters, we aim to facilitate greater opportunity for collaboration, scientific discovery and progress. We subscribe wholeheartedly to the Open Access definition:
\n\n“By “open access” to [peer-reviewed research literature], we mean its free availability on the public internet, permitting any users to read, download, copy, distribute, print, search, or link to the full texts of these articles, crawl them for indexing, pass them as data to software, or use them for any other lawful purpose, without financial, legal, or technical barriers other than those inseparable from gaining access to the internet itself. The only constraint on reproduction and distribution, and the only role for copyright in this domain, should be to give authors control over the integrity of their work and the right to be properly acknowledged and cited” (reference: http://www.budapestopenaccessinitiative.org)
\n\nOAI-PMH
\n\nAs a firm believer in the wider dissemination of knowledge, IntechOpen supports the Open Access Initiative Protocol for Metadata Harvesting (OAI-PMH Version 2.0). Read more
\n\nLicense
\n\nBook chapters published in edited volumes are distributed under the Creative Commons Attribution 3.0 Unported License (CC BY 3.0). IntechOpen upholds a very flexible Copyright Policy. There is no copyright transfer to the publisher and Authors retain exclusive copyright to their work. All Monographs/Compacts are distributed under the Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0). Read more
\n\nPeer Review Policies
\n\nAll scientific works are Peer Reviewed prior to publishing. Read more
\n\nOA Publishing Fees
\n\nThe Open Access publishing model employed by IntechOpen eliminates subscription charges and pay-per-view fees, enabling readers to access research at no cost. In order to sustain operations and keep our publications freely accessible we levy an Open Access Publishing Fee for manuscripts, which helps us cover the costs of editorial work and the production of books. Read more
\n\nDigital Archiving Policy
\n\nIntechOpen is committed to ensuring the long-term preservation and the availability of all scholarly research we publish. We employ a variety of means to enable us to deliver on our commitments to the scientific community. Apart from preservation by the Croatian National Library (for publications prior to April 18, 2018) and the British Library (for publications after April 18, 2018), our entire catalogue is preserved in the CLOCKSS archive.
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I am also a member of the team in charge for the supervision of Ph.D. students in the fields of development of silicon based planar waveguide sensor devices, study of inelastic electron tunnelling in planar tunnelling nanostructures for sensing applications and development of organotellurium(IV) compounds for semiconductor applications. I am a specialist in data analysis techniques and nanosurface structure. I have served as the editor for many books, been a member of the editorial board in science journals, have published many papers and hold many patents.",institutionString:null,institution:{name:"Sheffield Hallam University",country:{name:"United Kingdom"}}},{id:"54525",title:"Prof.",name:"Abdul Latif",middleName:null,surname:"Ahmad",slug:"abdul-latif-ahmad",fullName:"Abdul Latif Ahmad",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"20567",title:"Prof.",name:"Ado",middleName:null,surname:"Jorio",slug:"ado-jorio",fullName:"Ado Jorio",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Universidade Federal de Minas Gerais",country:{name:"Brazil"}}},{id:"47940",title:"Dr.",name:"Alberto",middleName:null,surname:"Mantovani",slug:"alberto-mantovani",fullName:"Alberto Mantovani",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"12392",title:"Mr.",name:"Alex",middleName:null,surname:"Lazinica",slug:"alex-lazinica",fullName:"Alex Lazinica",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/12392/images/7282_n.png",biography:"Alex Lazinica is the founder and CEO of IntechOpen. After obtaining a Master's degree in Mechanical Engineering, he continued his PhD studies in Robotics at the Vienna University of Technology. Here he worked as a robotic researcher with the university's Intelligent Manufacturing Systems Group as well as a guest researcher at various European universities, including the Swiss Federal Institute of Technology Lausanne (EPFL). During this time he published more than 20 scientific papers, gave presentations, served as a reviewer for major robotic journals and conferences and most importantly he co-founded and built the International Journal of Advanced Robotic Systems- world's first Open Access journal in the field of robotics. Starting this journal was a pivotal point in his career, since it was a pathway to founding IntechOpen - Open Access publisher focused on addressing academic researchers needs. Alex is a personification of IntechOpen key values being trusted, open and entrepreneurial. Today his focus is on defining the growth and development strategy for the company.",institutionString:null,institution:{name:"TU Wien",country:{name:"Austria"}}},{id:"19816",title:"Prof.",name:"Alexander",middleName:null,surname:"Kokorin",slug:"alexander-kokorin",fullName:"Alexander Kokorin",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/19816/images/1607_n.jpg",biography:"Alexander I. Kokorin: born: 1947, Moscow; DSc., PhD; Principal Research Fellow (Research Professor) of Department of Kinetics and Catalysis, N. Semenov Institute of Chemical Physics, Russian Academy of Sciences, Moscow.\r\nArea of research interests: physical chemistry of complex-organized molecular and nanosized systems, including polymer-metal complexes; the surface of doped oxide semiconductors. He is an expert in structural, absorptive, catalytic and photocatalytic properties, in structural organization and dynamic features of ionic liquids, in magnetic interactions between paramagnetic centers. The author or co-author of 3 books, over 200 articles and reviews in scientific journals and books. He is an actual member of the International EPR/ESR Society, European Society on Quantum Solar Energy Conversion, Moscow House of Scientists, of the Board of Moscow Physical Society.",institutionString:null,institution:{name:"Semenov Institute of Chemical Physics",country:{name:"Russia"}}},{id:"62389",title:"PhD.",name:"Ali Demir",middleName:null,surname:"Sezer",slug:"ali-demir-sezer",fullName:"Ali Demir Sezer",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/62389/images/3413_n.jpg",biography:"Dr. Ali Demir Sezer has a Ph.D. from Pharmaceutical Biotechnology at the Faculty of Pharmacy, University of Marmara (Turkey). He is the member of many Pharmaceutical Associations and acts as a reviewer of scientific journals and European projects under different research areas such as: drug delivery systems, nanotechnology and pharmaceutical biotechnology. Dr. Sezer is the author of many scientific publications in peer-reviewed journals and poster communications. Focus of his research activity is drug delivery, physico-chemical characterization and biological evaluation of biopolymers micro and nanoparticles as modified drug delivery system, and colloidal drug carriers (liposomes, nanoparticles etc.).",institutionString:null,institution:{name:"Marmara University",country:{name:"Turkey"}}},{id:"61051",title:"Prof.",name:"Andrea",middleName:null,surname:"Natale",slug:"andrea-natale",fullName:"Andrea Natale",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"100762",title:"Prof.",name:"Andrea",middleName:null,surname:"Natale",slug:"andrea-natale",fullName:"Andrea Natale",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"St David's Medical Center",country:{name:"United States of America"}}},{id:"107416",title:"Dr.",name:"Andrea",middleName:null,surname:"Natale",slug:"andrea-natale",fullName:"Andrea Natale",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Texas Cardiac Arrhythmia",country:{name:"United States of America"}}},{id:"64434",title:"Dr.",name:"Angkoon",middleName:null,surname:"Phinyomark",slug:"angkoon-phinyomark",fullName:"Angkoon Phinyomark",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/64434/images/2619_n.jpg",biography:"My name is Angkoon Phinyomark. I received a B.Eng. degree in Computer Engineering with First Class Honors in 2008 from Prince of Songkla University, Songkhla, Thailand, where I received a Ph.D. degree in Electrical Engineering. My research interests are primarily in the area of biomedical signal processing and classification notably EMG (electromyography signal), EOG (electrooculography signal), and EEG (electroencephalography signal), image analysis notably breast cancer analysis and optical coherence tomography, and rehabilitation engineering. I became a student member of IEEE in 2008. During October 2011-March 2012, I had worked at School of Computer Science and Electronic Engineering, University of Essex, Colchester, Essex, United Kingdom. In addition, during a B.Eng. I had been a visiting research student at Faculty of Computer Science, University of Murcia, Murcia, Spain for three months.\n\nI have published over 40 papers during 5 years in refereed journals, books, and conference proceedings in the areas of electro-physiological signals processing and classification, notably EMG and EOG signals, fractal analysis, wavelet analysis, texture analysis, feature extraction and machine learning algorithms, and assistive and rehabilitative devices. I have several computer programming language certificates, i.e. Sun Certified Programmer for the Java 2 Platform 1.4 (SCJP), Microsoft Certified Professional Developer, Web Developer (MCPD), Microsoft Certified Technology Specialist, .NET Framework 2.0 Web (MCTS). 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