Sexual Development最新文献

{"title":"Cytogenomic Investigation of Individuals with Ovotesticular Difference of Sex Development.","authors":"Júlia Lima-Santos, Carolina Gama Nascimento-Vidoti, Gabriela Roldão Correia-Costa, Nilma Lúcia Viguetti Campos, Mara Sanches Guaragna, Flávia Marcorin de Oliveira, Beatriz Amstalden Barros, Marcio Lopes Miranda, Arthur Antolini Tavares, Gil Guerra-Junior, Andréa Trevas Maciel-Guerra, Helena Fabbri-Scallet, Társis Paiva Vieira","doi":"10.1159/000551594","DOIUrl":"https://doi.org/10.1159/000551594","url":null,"abstract":"<p><strong>Introduction: </strong>Ovotesticular Difference of Sex Development (OT-DSD) may result from chimerism, mosaicism, structural or sequence variants. However, even after investigating all known causes, many individuals still lack an established etiology. This study aimed to perform cytogenomic investigation of individuals with OT-DSD.</p><p><strong>Methods: </strong>The sample consisted of 15 individuals with OT-DSD. Methods included G-banding karyotype, Chromosomal Microarray Analysis (CMA), Optical Genome Mapping (OGM), and Whole-Genome Sequencing (WGS).</p><p><strong>Results: </strong>G-banding karyotype revealed chimerism in two individuals, mosaicism in one, and 47,XXY karyotype in another. One individual had a pericentric inversion at the X chromosome, with breakpoints mapped close to SOX3. Ten individuals had a normal karyotype, eight 46,XX, and two 46,XY. CMA, performed in 11, identified a duplication including the SOX3 gene in one 46,XX individual, and two duplications in a 46,XY individual, with breakpoints mapped by WGS, suggesting a complex rearrangement that could affect VAMP7 expression. OGM was performed in two individuals and WGS in nine individuals, which did not reveal additional relevant structural variants (SVs).</p><p><strong>Conclusion: </strong>Cytogenomic methods identified causative alterations in 5/15 (33.3%) individuals, underscoring the need to combine complementary approaches to detect and characterize SVs. In the remaining cases, the etiology was undetermined, emphasizing the need for further molecular investigations.</p>","PeriodicalId":49536,"journal":{"name":"Sexual Development","volume":" ","pages":"1-18"},"PeriodicalIF":2.4,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147787299","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A case of disorder of sex development in red deer (Cervus elaphus elaphus).","authors":"Maciej Zacharski, Katarzyna Pieczka, Stanisław Dzimira","doi":"10.1159/000551880","DOIUrl":"https://doi.org/10.1159/000551880","url":null,"abstract":"<p><p>We describe a hunted red deer (Cervus elaphus elaphus) with well-developed antlers and male-typical morphology, but female-like external genitalia characterized by a hypertrophic clitoris/penile-like protrusion and absence of a scrotum. Only external genital tissues were available for histopathology, which revealed penile-type structures, including cavernous tissue and urethral-like epithelium. Genetic sex was assessed using PCR amplification of SRY and ZFX/ZFY markers from formalin-fixed paraffin-embedded (FFPE) material. Due to the degraded DNA, we redesigned ZFY primers to yield a short amplicon suitable for compromised templates. PCR positive for SRY and ZFY indicated the presence of Y-linked sequences. However, in the absence of internal reproductive organs, karyotyping and hormonal analyses, the etiology and DSD category cannot be determined, and chromosomal mosaicism or other Y-chromosome anomalies cannot be excluded. This report documents an unusual phenotype in a free-ranging red deer and provides a practical short-amplicon ZFY assay for sex-marker detection in degraded samples.</p>","PeriodicalId":49536,"journal":{"name":"Sexual Development","volume":" ","pages":"1-13"},"PeriodicalIF":2.4,"publicationDate":"2026-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147655190","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"WT1 Deletion in 46,XY DSD: The Importance of Copy Number Variant Analysis.","authors":"Gabby Atlas, Katrina M Bell, Gorjana Robevska, Jocelyn van den Bergen, Peter I Hadiprajitno, Nurin Listyasari, Ardy Santosa, Achmad Zulfa Juniarto, David I Francis, Michele A O Apos Connell, Tiong Yang Tan, Elena Tucker, Sultana M H Faradz, Andrew Sinclair, Katie Ayers","doi":"10.1159/000551741","DOIUrl":"https://doi.org/10.1159/000551741","url":null,"abstract":"<p><strong>Introduction: </strong>Diagnostic copy number variants (CNVs) have been detected in up to 30% of individuals with DSD. Tools have been developed to detect CNVs from exome/genome sequencing.</p><p><strong>Methods: </strong>Sequencing data from a cohort of individuals with DSD was re-analysed through a CNV-caller (Ximmer) after no diagnostic single nucleotide variants were identified through traditional sequencing analysis.</p><p><strong>Results: </strong>A deletion was identified for an individual with gonadal dysgenesis that encompassed all exons of the gene WT1.</p><p><strong>Conclusion: </strong>This case reinforces the role of CNV analysis as part of genomic analysis, which holds exciting potential for improving diagnostic rates in the future.</p>","PeriodicalId":49536,"journal":{"name":"Sexual Development","volume":" ","pages":"1-12"},"PeriodicalIF":2.4,"publicationDate":"2026-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147534158","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"XX/XY chimerism in tortoiseshell tomcats - a new case and review of the literature.","authors":"Izabela Szczerbal, Joanna Nowacka-Woszuk, Marek Switonski","doi":"10.1159/000551472","DOIUrl":"https://doi.org/10.1159/000551472","url":null,"abstract":"<p><strong>Introduction: </strong>Tortoiseshell coat color in cats typically occurs in females due to random X-chromosome inactivation, which affects the expression of the orange coat color gene. The presence of a tortoiseshell phenotype in male cats usually indicates an unusual sex chromosome constitution.</p><p><strong>Case presentation: </strong>A young Maine Coon tomcat with a normally developed penis was referred for genetic examination because of its tortoiseshell coat. At the age of 11 months, he successfully mated with a queen, which subsequently gave birth to five healthy kittens.</p><p><strong>Results: </strong>Cytogenetic analysis of chromosome preparations obtained from leukocyte cultures revealed the presence of two cell lines - XX and XY. Molecular studies were performed on DNA extracted from blood, hair follicles, and saliva using a ddPCR approach to estimate the ratio of Y- to X-chromosome copy numbers. These analyses confirmed the presence of both XX and XY cell lines in the tested tissues, with the highest proportion of the XX line detected in hair follicles.</p><p><strong>Conclusion: </strong>This study demonstrates that tortoiseshell tomcats with XX/XY chimerism can be fertile. Therefore, cytogenetic and molecular analyses of tri-colored male cats are recommended before making decisions regarding their use in breeding.</p>","PeriodicalId":49536,"journal":{"name":"Sexual Development","volume":" ","pages":"1-12"},"PeriodicalIF":2.4,"publicationDate":"2026-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147445733","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic, endocrine and epigenetic mechanisms underlying sexual size dimorphism in fish.","authors":"Silvia Beato, Gabriel Ecker-Eckhofen, Changwei Shao, Francesc Piferrer","doi":"10.1159/000550574","DOIUrl":"https://doi.org/10.1159/000550574","url":null,"abstract":"<p><p>Background Sexual size dimorphism (SSD), i.e., size difference between sexes, is common in fishes and spans from negligible to extreme body size differences, with both female‑ and male‑biased directions. While evolutionary drivers behind SSD such as sexual selection, fecundity selection and natural selection are increasingly well understood, our understanding of the underlying mechanisms of how sex‑specific growth trajectories develop is less clear. Summary Here we review recent findings of such mechanisms in fishes and reveal that SSD arises from an interplay of sex-linked and autosomal genetic factors. In teleosts, master sex-determining genes and growth regulators such as dmrt1/dmY, sdY, amhr2by, gdf6Y and gsdfY play key roles, while quantitative trait loci (QTL) influence growth and maturation, further contributing to SSD. Essential sex-specific regulation of hormones across brain, pituitary, liver and gonad determines SSD directionality. Epigenetic mechanisms, such as DNA methylation and non-coding RNA further modulate gene expression in growth and reproductive pathways. We identify the basic mechanisms, highlight knowledge gaps, and propose that multi-omics approaches can disentangle sex effects from dimorphism-specific regulation, linking together endocrine, genetic and epigenetic drivers. Key Messages 1. At the mechanistic level, SSD results from an interplay of genetic, endocrine and environmental influences. 2. Sex chromosomes and autosomal loci form the genetic architecture that shapes growth differences between males and females. 3. The somatotropic axis, involving GH/IGF signaling, together with the actions of sex steroids, serves as a central effector system underlying SSD in fish. 4. Epigenetic mechanisms help establish and maintain sex-specific gene expression programs, but integrative multi‑omic approaches are needed to uncover causal relationships and phenotypic plasticity in SSD.</p>","PeriodicalId":49536,"journal":{"name":"Sexual Development","volume":" ","pages":"1-20"},"PeriodicalIF":2.4,"publicationDate":"2026-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146031483","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Functional Validation of a Novel <italic>PBX1</italic> Missense Variant in a 46,XY Girl.","authors":"Meng-Che Tsai, Yun-Han Weng, Yi-Chieh Wang, Yen-Yin Chou, Kung-Chao Chang, Peng-Chieh Chen","doi":"10.1159/000550575","DOIUrl":"10.1159/000550575","url":null,"abstract":"<p><strong>Introduction: </strong>The pre-B-cell leukemia transcription factor encoded by PBX1 is expressed throughout human embryonic stages. Accumulating cases with differences of sex development (DSDs) have been reported harboring PBX1 variants, suggesting a yet elusive role of PBX1 in the gonadal differentiation and sexual development processes.</p><p><strong>Methods: </strong>We report a syndromic case of 46,XY DSD presenting severely undervirilized genitalia and gonadal dysgenesis with mixed ovarian and testicular differentiation, where whole-exome sequencing analysis identified a novel missense variant c.710G>C (p.R237T) in the highly conserved nuclear localization sequence in the three-amino acid loop extension domain of PBX1.</p><p><strong>Results: </strong>Compared with wild-type (WT) PBX1, PBX1 p.R237T reduced protein stability and hampered nuclear translocation of PBX1 in the inducible Flp-In TREx HEK293 cells. Induction with tetracycline significantly decreased cell proliferation in both Flp-In HEK293 PBX1 WT and p.R237T cells compared to untransfected HEK293 cells, while adhesive ability was not different. RNA sequencing identified differentially expressed genes in DSD-related genes, including MAP3K4, EMX2, KISS1R, and HOXA13 in cells expressing PBX1 p.R237T when compared to cells expressing WT PBX1.</p><p><strong>Conclusion: </strong>Altogether, our results demonstrated the deleterious functional consequences of the rare PBX1 p.R237T variant identified in a Taiwanese proband with 46,XY DSD.</p>","PeriodicalId":49536,"journal":{"name":"Sexual Development","volume":" ","pages":"45-57"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13043130/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147311962","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ovarian-Specific FOXL2 Protein Expression in Testes from Patients with Complete Androgen Insensitivity Syndrome and Undescended Testes.","authors":"Katja P Wolffenbuttel, Hans Stoop, Remko Hersmus, Marij Dinkelman-Smit, Sabine E Hannema, Geert J H L van Leenders","doi":"10.1159/000550740","DOIUrl":"10.1159/000550740","url":null,"abstract":"<p><strong>Introduction: </strong>The transcription factors Forkhead box L2 (FOXL2) and SRY-box transcription factor 9 (SOX9), among others, are required for embryonic ovarian and testicular differentiation, respectively. In patients with complete androgen insensitivity syndrome (CAIS), the testes are usually undescended and may show histological changes similar to those sometimes seen in patients with undescended testes (UDT). The aim of this study was to explore the expression of FOXL2 and SOX9 in testes from patients with CAIS and UDT.</p><p><strong>Methods: </strong>Immunohistochemical staining with FOXL2 and SOX9 was performed on samples from 13 patients with CAIS and 20 with UDT.</p><p><strong>Results: </strong>In addition to nuclear SOX9 expression in intratubular Sertoli cells, FOXL2 expression was present in stromal cells in 8 of 9 patients with CAIS and in 1 of 20 with UDT. Moreover, FOXL2 expression was found in the rete testis in three of nine samples that included this region.</p><p><strong>Conclusion: </strong>Expression of the ovarian-specific marker FOXL2 in regions of the testes of patients with CAIS and UDT has not previously been documented and suggests partial activation of the female pathway within these testes. Further research is needed, including FOXL2 protein expression studies in larger series and molecular studies, e.g., transcriptome analysis, to understand the pathophysiology and clinical significance of these novel findings.</p>","PeriodicalId":49536,"journal":{"name":"Sexual Development","volume":" ","pages":"36-44"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13004611/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146114628","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of Novel and Known Variants in Epigenetic Genes Associated with Syndromic 46,XY Differences of Sex Development among Moroccan Patients.","authors":"Imane Cherkaoui, Saida Lhousni, Manal Elidrissi Errahhali, Majida Charif, Rim Amrani, Aziza Elouali, Sanae Allaoui, Mounia Elidrissi Errahhali, Meryem Ouarzane, Guy Lenaers, Adnane Sellam, Mohammed Bellaoui, Redouane Boulouiz","doi":"10.1159/000549398","DOIUrl":"https://doi.org/10.1159/000549398","url":null,"abstract":"<p><strong>Introduction: </strong>46,XY differences of sex development (DSD) are conditions with extreme phenotypic and genetic heterogeneity. Therefore, their diagnosis remains a major challenge for both clinicians and geneticists. In this study, we aimed to identify the underlying genetic causes of DSD in a series of 3 Moroccan patients with syndromic 46,XY DSD recruited in the BRO Biobank.</p><p><strong>Case presentations: </strong>Methods: Karyotyping analysis was performed on peripheral blood samples using standard R banding techniques. SRY gene was analyzed using PCR amplification followed by Sanger sequencing. Whole exome sequencing (WES) was performed after unsuccessful conventional genetic analyses. Candidate variants were evaluated by segregation analysis and molecular modeling.</p><p><strong>Results: </strong>WES identified three pathogenic variants in genes encoding various components of the epigenetic machinery: in patient 1, a novel heterozygous frameshift variant c.4072dup (p.Glu1358GlyfsTer29) in the KAT6B gene associated with two clinically distinct syndromes (genitopatellar syndrome and Say-Barber-Biesecker-Young-Simpson syndrome) was detected; in patient 2, we identified a previously reported de novo heterozygous nonsense variant c.12943C>T (p.Gln4315Ter) in KMT2D responsible for Kabuki syndrome; in patient 3, WES revealed a novel heterozygous missense variant c.4056C>G (p.Phe1352Leu) in CHD7 responsible for CHARGE syndrome. We discuss the genotype-phenotype correlation in these syndromic 46,XY DSD and discuss the relevance of the epigenetic genes in sexual development.</p><p><strong>Conclusion: </strong>Our findings highlight the utility of WES in discriminating clinically overlapping syndromic 46,XY DSD to provide an accurate diagnosis, thus allowing better follow-up and appropriate patient management. In addition, our study enriched the mutational spectrum of syndromic 46,XY DSD and confirmed the genotype-phenotype correlations.</p>","PeriodicalId":49536,"journal":{"name":"Sexual Development","volume":"20 1-6","pages":"26-35"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146159046","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular Diagnosis of 46,XY Disorders of Sex Development: An Efficient Initial Molecular Analysis Using a Custom-Designed Targeted Gene Panel in a Single-Center Study.","authors":"Sukran Poyrazoglu, Agharza Aghayev, Guven Toksoy, Birsen Karaman, Ayca Dilruba Aslanger, Sahin Avci, Umut Altunoglu, Volkan Karaman, Melek Yildiz, Zehra Yavas Abali, Firdevs Bas, Seher Basaran, Feyza Darendeliler, Zehra Oya Uyguner","doi":"10.1159/000550371","DOIUrl":"10.1159/000550371","url":null,"abstract":"<p><strong>Background: </strong>The management of 46,XY disorders of sex development (DSD) is challenging due to genetic heterogeneity and phenotypic variability. This study aimed to characterize the clinical and genetic findings in patients with 46,XY DSD, using a targeted next-generation sequencing (NGS) panel for molecular evaluation.</p><p><strong>Methods: </strong>A targeted DSD gene panel covering 31 genes was applied in 112 patients with nonsyndromic 46,XY DSD. Forty-six patients had previously tested negative for AR and SRD5A2 by Sanger sequencing. Patients were clinically categorized into disorders of gonadal development, androgen synthesis or action. Variant classification was performed according to the ACMG criteria.</p><p><strong>Results: </strong>Among the 38 variants detected, 32 were pathogenic or likely pathogenic. Nineteen (50%) variants were novel. A molecular diagnosis was established in 31 (27.7%) patients and inclusion of previously diagnosed cases would have increased the overall diagnostic yield to 43.8%. The HSD17B3 variants were the most common, followed by NR5A1 and LHCGR. In 8 patients, the genetic findings led to reclassification of their clinical diagnosis, particularly in those initially suspected to have a disorder of androgen action.</p><p><strong>Conclusion: </strong>NGS is a valuable diagnostic tool in the evaluation of 46,XY DSD, offering improved diagnostic yield. For patients without molecular diagnosis, more comprehensive genomic analyses, including noncoding regions, are required.</p>","PeriodicalId":49536,"journal":{"name":"Sexual Development","volume":" ","pages":"15-25"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12890263/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145913559","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Testicular Volume of 4 mL Is Not an Appropriate Marker of Pubertal Onset in a Subset of Boys Born Small for Gestational Age.","authors":"Sofia Suco, Patricia Bedecarrás, María Gabriela Ballerini, María Gabriela Ropelato, Débora Braslavsky, María Eugenia Rodriguez, Ana Keselman, Rodolfo A Rey, Romina P Grinspon","doi":"10.1159/000551056","DOIUrl":"10.1159/000551056","url":null,"abstract":"<p><strong>Introduction: </strong>Considering that testicular volume (TV) is probably not an adequate marker of pubertal onset in boys born small for gestational age (SGA), we aimed to describe the progression of pubertal clinical and biochemical characteristics, comparing the trajectory of TV with other parameters as markers of pubertal onset in boys born SGA.</p><p><strong>Methods: </strong>We performed a retrospective, descriptive study of a cohort of boys born SGA with longitudinal follow-up. We determined the TV at the time when serum AMH decreased ≥30% or LH attained 0.35 IU/L.</p><p><strong>Results: </strong>Thirty boys born SGA were included: 16 of 30 (53.3%) had LH ≥0.35 IU/L and 7 of 24 boys (29.2%) had a decline ≥30% in serum AMH with a TV <4 mL. LH ≥0.35 IU/L and AMH decrease ≥30% were observed at least 1 year before TV 4-5 mL in 11 of 22 (50%) and 3 of 19 (15.8%) boys, respectively. During follow-up, higher serum LH, FSH, and testosterone and lower AMH levels than those expected for TV were observed, indicating that some boys born SGA have a more advanced stage of puberty than their TV suggests.</p><p><strong>Conclusion: </strong>We identified a subgroup of boys born SGA in whom hormonal changes typical of initial puberty (serum LH ≥0.35 IU/L and AMH decline ≥30%) occurred before a clinical diagnosis of pubertal onset (TV ≥4 mL) was evident. These results indicate that TV 4 mL is not a reliable clinical sign of pubertal onset in all boys born SGA and that other biomarkers, such as serum LH and AMH, may need to be assessed.</p>","PeriodicalId":49536,"journal":{"name":"Sexual Development","volume":" ","pages":"58-67"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13095185/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147311978","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}