Abnormal Male Internal Genitalia Morphology
Introduction
Section titled “Introduction”Abnormal male internal genitalia morphology refers to structural deviations from typical development within the internal reproductive organs of males. These crucial structures include the testes, epididymis, vas deferens, seminal vesicles, and prostate, all of which play vital roles in the production, maturation, storage, and transport of sperm. Variations in their formation or position can range from subtle alterations to significant malformations, impacting reproductive function and overall health.
Biological Basis
Section titled “Biological Basis”The development of male internal genitalia is a complex process orchestrated by a precise interplay of genetic programming and hormonal signaling during embryonic and fetal stages. Disruptions to this intricate process can arise from various factors, including chromosomal abnormalities, single gene mutations, and environmental influences such as endocrine disruptors. For instance, specific genes have been identified as candidates for male fertility, and mutations in these genes may contribute to unexplained infertility or subfertility. These include _USP8_, an enzyme involved in acrosome assembly; _UBD_ and _EPSTI1_, which may have roles in innate immunity; and _LRRC32_, encoding a receptor on regulatory T cells. [1]
Clinical Relevance
Section titled “Clinical Relevance”The clinical implications of abnormal male internal genitalia morphology are diverse. A primary concern is male infertility or subfertility, which affects a significant portion of couples, with male factors contributing nearly equally to female factors.[1] Conditions such as cryptorchidism (undescended testes), agenesis (absence), or hypoplasia (underdevelopment) of these structures can lead to impaired sperm production or transport. Beyond fertility, some morphological abnormalities may increase the risk of other health issues, including hormonal imbalances, testicular torsion, and an elevated risk of germ cell tumors. Early diagnosis and appropriate medical or surgical intervention are often critical for managing these conditions and improving long-term outcomes.
Social Importance
Section titled “Social Importance”The presence of abnormal male internal genitalia morphology can have substantial social and psychological impacts on affected individuals. It may influence self-identity, sexual health, and family planning aspirations. Coping with infertility or the need for medical interventions can be emotionally challenging and may sometimes carry a social stigma. Understanding these conditions, providing supportive care, and ensuring access to comprehensive medical information are important for addressing the full spectrum of challenges faced by individuals with abnormal male internal genitalia morphology.
Limitations
Section titled “Limitations”Methodological and Design Constraints
Section titled “Methodological and Design Constraints”Research into complex morphological traits often faces significant methodological and statistical challenges that can impact the reliability and generalizability of findings. Many studies, particularly initial genome-wide association studies (GWAS), operate with modest sample sizes, which inherently limits their statistical power to detect true genetic associations and can lead to an inflation of effect sizes for the associations that are identified. [2] Furthermore, the combination of data from multiple cohorts or the use of different genotyping platforms can introduce heterogeneity and potential biases, complicating downstream analyses and interpretation of results. [2] The assumption of an additive genetic model in statistical analyses may also oversimplify the true genetic architecture of complex traits, potentially overlooking non-additive effects like dominance or epistasis. [3]
Phenotypic measurement itself often presents a substantial limitation, especially for complex anatomical features. Differences in data collection methods, imaging modalities, and specific landmarking protocols can lead to a lack of directly comparable phenotypes across studies or even within different cohorts of the same study. [4] This variability in phenotypic assessment, coupled with considerable natural variation within the population, can obscure subtle genetic effects and reduce the power to detect significant associations. [1]Moreover, the reliance on imputation using reference panels, while a standard practice, means that the accuracy of imputed genotypes depends on the diversity and size of these panels, particularly affecting rare variants or those in populations underrepresented in the reference.[5]
Population Specificity and Generalizability
Section titled “Population Specificity and Generalizability”A major limitation in genetic studies is the common practice of sampling primarily from one ancestral group, typically those of European descent, which significantly restricts the generalizability of any discovered genetic associations to other populations. [2] Allele frequencies, linkage disequilibrium patterns, and the genetic architecture of traits can vary substantially across different ancestral backgrounds, meaning findings from one group may not be directly transferable or even relevant to others. Beyond ancestry, specific cohort biases can arise from recruitment strategies, such as focusing on individuals referred for particular clinical conditions like infertility, rather than a general population sample. [1] This selective sampling can lead to findings that are not representative of the broader population or applicable to individuals without the specific referral condition, thereby limiting the external validity and clinical utility of the research. [6]
Unaccounted Environmental and Genetic Complexity
Section titled “Unaccounted Environmental and Genetic Complexity”The etiology of complex morphological traits is rarely purely genetic; environmental factors and their interactions with genetic predispositions play a crucial role, yet these are frequently difficult to capture comprehensively in study designs. Factors such as maternal health conditions during development, like thyroid dysfunction during pregnancy, or lifestyle factors such as obesity, are known to influence various traits and can act as significant confounders if not adequately accounted for.[2]The absence of detailed clinical histories, comprehensive lifestyle data, or other relevant physiological measurements in many research cohorts further constrains the ability to identify nuanced associations or understand the full biological context of genetic findings.[1] Even for traits with a clear genetic component, a substantial portion of heritability often remains unexplained by common variants identified in GWAS, a phenomenon known as “missing heritability.” This gap suggests that undiscovered genetic factors, including rare variants, structural variations, or complex gene-environment interactions, contribute to the trait but are not adequately captured by current methodologies.
Variants
Section titled “Variants”The LPIN1 gene, or Lipin 1, plays a critical role in lipid metabolism and acts as a transcriptional coactivator, influencing gene expression related to fat synthesis and breakdown. It is essential for maintaining energy balance and cellular membrane integrity throughout the body. Disruptions in LPIN1function can lead to a range of metabolic disorders, including issues with muscle development, insulin sensitivity, and fat accumulation . Given its broad involvement in metabolic pathways and cellular signaling,LPIN1 is crucial for proper tissue development and organogenesis, including the complex processes involved in the formation of male internal genitalia .
The variant rs555800956 is located within the LPIN1gene, and its presence can potentially influence the gene’s activity or the stability of the mRNA or protein. While the exact functional consequence of this specific single nucleotide polymorphism (SNP) may vary, variants within genes likeLPIN1 can affect the efficiency of gene transcription, mRNA processing, or even protein structure and function . Such alterations in LPIN1 activity could lead to subtle or significant changes in lipid signaling and transcriptional regulation, potentially impacting the delicate balance required for normal embryonic development, including the differentiation and formation of male reproductive structures .
Abnormal male internal genitalia morphology, such as conditions affecting the prostate, seminal vesicles, or vas deferens, can arise from complex genetic and environmental interactions. GivenLPIN1’s fundamental role in lipid metabolism and gene regulation, a variant like rs555800956 could contribute to these developmental anomalies by altering crucial metabolic pathways or by disrupting the precise timing and expression of genes necessary for reproductive organ formation . For instance, altered lipid environments can affect cell proliferation, migration, and hormone synthesis, all of which are vital for the proper development of male internal genitalia. Therefore, even subtle changes inLPIN1 function due to rs555800956 may have implications for the normal development and morphology of these structures .
The provided research context does not contain sufficient information to generate a Classification, Definition, and Terminology section for ‘abnormal male internal genitalia morphology’ as per the specific requirements for precise definitions, classification systems, terminology, and diagnostic criteria related to morphology.
Key Variants
Section titled “Key Variants”| RS ID | Gene | Related Traits |
|---|---|---|
| rs555800956 | LPIN1 | abnormal male internal genitalia morphology |
Causes of Abnormal Male Internal Genitalia Morphology
Section titled “Causes of Abnormal Male Internal Genitalia Morphology”Genetic Predisposition and Chromosomal Aberrations
Section titled “Genetic Predisposition and Chromosomal Aberrations”Genetic factors play a significant role in the development of abnormal male internal genitalia morphology, influencing both complex and monogenic forms of reproductive tract defects. Studies on male fertility traits, which can be indicative of underlying morphological integrity and function, have identified various genetic components. Genome-wide association studies (GWAS) aim to uncover candidate genes that influence parameters such as sperm concentration, total count, and motility, all of which exhibit significant heritability.[1] While specific overall morphological abnormalities are not directly detailed by these studies, the genetic predispositions they uncover contribute to a spectrum of male reproductive health outcomes, suggesting a polygenic influence on the structures and functions involved in fertility.
Beyond polygenic factors, specific genetic and chromosomal anomalies are recognized causes of male infertility, often manifesting as internal genitalia morphology issues. For instance, current diagnostic approaches for male infertility include cytogenetic studies and the detection of Y chromosome deletions, which can lead to testicular dysgenesis or other structural defects. [1] Additionally, CFTR gene mutation analysis is a standard test, as mutations in this gene are strongly associated with congenital bilateral absence of the vas deferens, a clear morphological abnormality of the internal reproductive tract. [1] These examples highlight how precise genetic alterations can directly underpin developmental abnormalities in male internal genitalia.
Biological Background
Section titled “Biological Background”Genetic and Developmental Foundations of Male Internal Genitalia
Section titled “Genetic and Developmental Foundations of Male Internal Genitalia”The development of male internal genitalia is a highly regulated process influenced by a complex interplay of genetic factors and hormonal signaling from early embryonic stages. While the specific genes directly dictating the precise morphology of internal male genitalia are subjects of ongoing research, studies have identified genetic underpinnings for male fertility traits, which are often indicative of underlying structural or functional integrity of these organs. Genome-wide association studies (GWAS), for instance, have been instrumental in pinpointing candidate genes associated with conditions such as azoospermia (absence of sperm) and severe oligozoospermia (low sperm count), both of which can stem from developmental or functional anomalies within the male reproductive system. [1] This genetic regulation establishes the foundational blueprint for the tissues and organs that comprise the male internal reproductive tract.
The general principle of hormonal control over sexual characteristic development is evident in female biology, where sex steroid hormones like estrogen and progesterone govern the development of mammary glands and the menstrual cycle.[7] This highlights the crucial role of a precisely timed hormonal environment during development, suggesting a similar, albeit male-specific, hormonal orchestration for the formation of male internal genitalia. The proper differentiation and growth of these structures are critically dependent on these early genetic and hormonal cues, ensuring the correct anatomical arrangement necessary for subsequent reproductive function.
Molecular Pathways and Hormonal Regulation
Section titled “Molecular Pathways and Hormonal Regulation”Hormonal signaling constitutes a pivotal molecular pathway that profoundly influences the development and subsequent function of male internal genitalia. The intricate balance and action of various hormones, alongside their specific receptors, drive cellular differentiation and tissue patterning. Research indicates that hormonal signaling is a likely candidate for the shared biological pathways influencing diverse traits, emphasizing its fundamental role in reproductive physiology and morphology. [8] This suggests that the precise activation and regulation of these molecular cascades are essential for the proper formation and maturation of gonadal tissues and other internal reproductive organs.
Furthermore, the broader hormonal environment during critical developmental windows can have significant implications. For example, thyroid dysfunction during pregnancy has been explored for its potential connection to aspects of male sexual development, indicating that a stable endocrine milieu is vital for normal developmental trajectories. [2] These molecular and cellular events, mediated by specific hormones and their receptors, orchestrate the complex processes of cell proliferation, migration, and differentiation that are required for the normal morphology and function of internal male genitalia.
Tissue-Level Biology and Pathophysiological Consequences
Section titled “Tissue-Level Biology and Pathophysiological Consequences”The appropriate functioning of male internal genitalia relies on the coordinated development and interaction of various tissues and organs, including the testes, epididymis, vas deferens, and accessory glands. Abnormalities in the morphology or function of these organs can lead to significant pathophysiological consequences, predominantly manifesting as male infertility. Conditions such as severe motility defects, oligozoospermia, and azoospermia are direct indicators of compromised reproductive function, often originating from structural or functional issues within these internal reproductive structures. [1] These disruptions signify a failure in the homeostatic processes essential for spermatogenesis (sperm production) and efficient sperm transport.
The integrity of these tissues and their complex interactions are paramount for maintaining reproductive health. For instance, the seminal analysis, a key diagnostic tool, evaluates the output of these organs, providing insights into their functional status and highlighting how deviations from normal morphology or physiology can lead to impaired fertility. [9] Thus, understanding the precise tissue and organ-level biology is crucial for deciphering how developmental errors or acquired disruptions can lead to abnormal internal genitalia morphology and its associated clinical outcomes.
Pathways and Mechanisms
Section titled “Pathways and Mechanisms”Hormonal Regulation and Androgen Sensitivity
Section titled “Hormonal Regulation and Androgen Sensitivity”The proper development and function of male internal genitalia are intricately tied to hormonal signaling pathways, particularly those involving androgens and thyroid hormones. Androgen receptor activation is a critical component, orchestrating gene expression patterns essential for the differentiation and maturation of male reproductive structures. Dysregulation within this pathway, such as altered receptor sensitivity or hormone levels, can lead to morphological abnormalities, as suggested by studies linking hormonal signaling to traits like male pattern baldness, which is androgen-dependent.[8]Furthermore, thyroid function during pregnancy has been suggestively connected to male sexual orientation[2] implying a broader systemic hormonal influence on male development that could extend to internal genitalia morphology. These feedback loops ensure homeostatic balance, but perturbations can cascade into developmental defects.
Core Developmental Signaling Pathways
Section titled “Core Developmental Signaling Pathways”Embryonic development of internal genitalia relies on highly conserved signaling cascades that guide cell proliferation, differentiation, and migration. Key pathways such as Hedgehog and WNT signaling are fundamental, with their interactions being critical for proper organogenesis, as seen in their role in craniofacial development. [10] Genes like GLI3, PAX1, and RUNX2, identified in studies of facial morphology[6] are transcription factors within these pathways, regulating downstream gene expression. For example, RUNX2 induces osteoblast and chondrocyte differentiation and enhances cell migration by coupling with PI3K-Akt signaling [11] and also regulates limb growth through Indian hedgehog [12] demonstrating pleiotropic effects across developmental systems that could impact internal genitalia. Abnormalities in these pathways, through gene mutations or altered signaling, can lead to significant morphological defects.
Transcriptional and Epigenetic Control
Section titled “Transcriptional and Epigenetic Control”Precise gene regulation at transcriptional and post-translational levels is vital for normal male internal genitalia development. Transcription factors like RUNX2, GLI3, and PAX1 serve as master regulators, controlling the expression of numerous genes involved in developmental processes. [6] Beyond sequence-level variation, epigenetic mechanisms, such as biased X chromosome inactivation, can also play a role in developmental outcomes. [2] Protein modifications and the activity of enzymes like histone deacetylases, such as HDAC9 which has been implicated in male-pattern baldness [13] can alter chromatin structure and gene accessibility, thereby influencing the developmental trajectory of cells and tissues. These regulatory layers provide intricate control over cell fate decisions and tissue patterning.
Systems-Level Integration and Metabolic Influences
Section titled “Systems-Level Integration and Metabolic Influences”Developmental pathways do not operate in isolation but are part of an integrated biological network where crosstalk and hierarchical regulation are common. Systemic factors, including metabolic state and overall hormonal balance, can influence these networks, leading to emergent properties that affect morphology. For instance, shared genetic influences have been observed between male pattern baldness and traits like BMI and height, suggesting an underlying connection through hormonal signaling pathways. [8]The potential connection between thyroid function and male development also highlights how broader metabolic regulation can impact specific organ systems[2] underscoring the importance of flux control and energy metabolism in supporting complex developmental processes.
Genetic Variation and Disease Mechanisms
Section titled “Genetic Variation and Disease Mechanisms”Genetic variants, including single nucleotide polymorphisms (_SNP_s), contribute to the spectrum of normal variation and can also predispose individuals to abnormal male internal genitalia morphology. Genome-wide association studies have identified _SNP_s associated with conditions like azoospermia and severe oligozoospermia, directly linking genetic variations to functional and morphological defects in the male reproductive system.[14] These variants can affect receptor activation, alter intracellular signaling cascades, or modify transcription factor binding, leading to pathway dysregulation. While compensatory mechanisms may exist, significant disruptions can result in overt abnormalities, offering potential therapeutic targets for intervention.
Clinical Relevance of Abnormal Male Internal Genitalia Morphology
Section titled “Clinical Relevance of Abnormal Male Internal Genitalia Morphology”Genetic Insights into Male Infertility and Reproductive Function
Section titled “Genetic Insights into Male Infertility and Reproductive Function”Understanding the genetic underpinnings of conditions such as azoospermia and severe oligozoospermia offers significant diagnostic utility in evaluating male infertility. Genome-wide association studies (GWAS) have identified single-nucleotide polymorphisms (SNPs) associated with these conditions, providing molecular markers that can help pinpoint specific etiologies beyond traditional clinical assessments.[14] This genetic characterization allows for more precise diagnostic classification, potentially differentiating between obstructive and non-obstructive forms or identifying specific developmental defects in internal reproductive structures. Such insights are crucial for guiding further diagnostic workup and patient counseling regarding the causes of their infertility.
Furthermore, these genetic findings hold substantial prognostic value, influencing predictions of reproductive outcomes. Identifying specific genetic variants linked to azoospermia or severe oligozoospermia can inform the likelihood of successful sperm retrieval techniques, such as microdissection testicular sperm extraction (TESE), or the potential for natural conception in less severe cases. [14] This information enables clinicians to provide more accurate prognoses, manage patient expectations, and discuss long-term implications for reproductive potential and overall male reproductive health, including potential genetic counseling for familial risks.
Informing Personalized Treatment and Risk Management
Section titled “Informing Personalized Treatment and Risk Management”Genetic associations with abnormal male internal genitalia morphology, as manifested in conditions like azoospermia and severe oligozoospermia, facilitate enhanced risk stratification for male infertility. By identifying specific genetic markers, clinicians can better assess an individual’s predisposition to these conditions, allowing for targeted screening and earlier intervention strategies.[14] This proactive approach supports personalized medicine by identifying high-risk individuals who may benefit from specialized monitoring or preventative measures before significant reproductive compromise occurs.
The integration of genetic information into clinical practice also enables more precise treatment selection and tailored management strategies. For patients diagnosed with azoospermia or severe oligozoospermia, understanding the specific genetic basis can guide decisions on the most appropriate assisted reproductive technologies or medical interventions, optimizing treatment efficacy and reducing trial-and-error approaches. [14] This personalized approach to patient care, informed by genetic insights, aims to improve success rates in overcoming male infertility and enhance overall patient outcomes by aligning interventions with the underlying genetic etiology.
Frequently Asked Questions About Abnormal Male Internal Genitalia Morphology
Section titled “Frequently Asked Questions About Abnormal Male Internal Genitalia Morphology”These questions address the most important and specific aspects of abnormal male internal genitalia morphology based on current genetic research.
1. If I have fertility issues, will my son also struggle?
Section titled “1. If I have fertility issues, will my son also struggle?”Yes, there’s a chance. Many internal genital abnormalities have a genetic basis, meaning they can be passed down. However, it’s a complex interplay of multiple genes and sometimes environmental factors, so it’s not always a direct or simple inheritance pattern.
2. Can problems with my internal organs cause other health issues?
Section titled “2. Can problems with my internal organs cause other health issues?”Absolutely. Beyond fertility, these issues can lead to hormonal imbalances, increase your risk of painful testicular torsion, or even elevate your chances of developing certain germ cell tumors later in life. Early diagnosis helps manage these risks and improve long-term outcomes.
3. Did something I did growing up cause my internal issues?
Section titled “3. Did something I did growing up cause my internal issues?”No, it’s highly unlikely. These conditions typically arise from complex genetic programming and hormonal signaling disruptions during embryonic and fetal development, long before you had any control. While environmental factors like endocrine disruptors during pregnancy can play a role, it’s not due to anything you did as a child or adult.
4. Why can some men have kids easily, but I can’t?
Section titled “4. Why can some men have kids easily, but I can’t?”Male fertility is influenced by a complex mix of genetic factors and environmental exposures. Some men might have subtle genetic variations, like in genes such as USP8 or UBD, that impact sperm production or transport, while others may not. Lifestyle and environmental factors also contribute to individual differences.
5. Can chemicals in my daily life affect my internal reproductive organs?
Section titled “5. Can chemicals in my daily life affect my internal reproductive organs?”Yes, they can. Exposure to certain environmental endocrine disruptors during critical developmental stages can interfere with the hormonal signaling necessary for typical internal genitalia formation, potentially leading to abnormalities. This is an area of ongoing research.
6. Would a genetic test explain why I have these problems?
Section titled “6. Would a genetic test explain why I have these problems?”It might, but not always definitively. While specific gene mutations are linked to some conditions, the full genetic picture for complex traits is still being uncovered. Genetic tests can identify known contributing genes, but often other factors, including undiscovered genes or environmental interactions, are also at play.
7. Does my ethnic background affect my risk for these issues?
Section titled “7. Does my ethnic background affect my risk for these issues?”It can. Genetic variations and their frequencies differ across populations. Research has shown that genetic risk factors identified in one ancestral group, often of European descent, might not fully apply or be as prevalent in others, suggesting your background could influence your specific risk profile.
8. If I have an internal issue, does it mean I’m less of a man?
Section titled “8. If I have an internal issue, does it mean I’m less of a man?”Absolutely not. Having an internal morphological abnormality has no bearing on your masculinity or self-identity. It’s a medical condition that many individuals face, and understanding it, along with seeking supportive care, is crucial for your well-being.
9. Why is it hard for doctors to pinpoint my specific problem sometimes?
Section titled “9. Why is it hard for doctors to pinpoint my specific problem sometimes?”The development of internal genitalia is incredibly complex, involving many genes and environmental factors. Diagnosing these conditions can be challenging due to the subtle nature of some abnormalities, the variability in how they present, and the complex genetic architecture that isn’t always fully understood or easily detectable with current methods.
10. Is there anything my parents could have done to prevent this for me?
Section titled “10. Is there anything my parents could have done to prevent this for me?”In most cases, probably not. Many of these conditions stem from spontaneous genetic variations or complex developmental processes that are beyond anyone’s control. While severe maternal health issues or certain environmental exposures during pregnancy can play a role, specific prevention is often not possible due to the intricate nature of human development.
This FAQ was automatically generated based on current genetic research and may be updated as new information becomes available.
Disclaimer: This information is for educational purposes only and should not be used as a substitute for professional medical advice. Always consult with a healthcare provider for personalized medical guidance.
References
Section titled “References”[1] Kosova, G et al. “Genome-wide association study identifies candidate genes for male fertility traits in humans.” Am J Hum Genet, vol. 90, no. 6, 2012, pp. 950-61.
[2] Sanders, A. R. et al. “Genome-Wide Association Study of Male Sexual Orientation.” Sci Rep. PMID: 29217827.
[3] Roosenboom, J et al. “Mapping genetic variants for cranial vault shape in humans.” PLoS One, vol. 13, no. 4, 2018, e0196245.
[4] Shaffer, John R., et al. “Genome-Wide Association Study Reveals Multiple Loci Influencing Normal Human Facial Morphology.”PLoS Genet, vol. 12, no. 8, 2016.
[5] Lee, M. K. et al. “Genome-wide association study of facial morphology reveals novel associations with FREM1 and PARK2.” PLoS One, vol. 11, no. 4, 25 Apr. 2016, p. e0154234. PMID: 28441456.
[6] Adhikari, K et al. “A genome-wide association study identifies multiple loci for variation in human ear morphology.” Nat Commun, vol. 6, 2015, 7500.
[7] Hirata, T et al. “Japanese GWAS identifies variants for bust-size, dysmenorrhea, and menstrual fever that are eQTLs for relevant protein-coding or long non-coding RNAs.”Sci Rep, vol. 8, no. 1, 2018, 8565.
[8] Pickrell, J. K. et al. “Detection and interpretation of shared genetic influences on 42 human traits.” Nat Genet. PMID: 27182965.
[9] Kim, H. H., P. N. Schlegel, and M. Goldstein. “Infertility: Principles Gender-Specific.” Infertility: Principles Gender-Specific, 2nd ed., edited by M. J. Legato, Academic Press, 2009, pp. 366–380.
[10] Napierala, D. et al. “Disrupting hedgehog and WNT signaling interactions promotes cleft lip pathogenesis.” J. Clin. Invest., vol. 124, 2014, pp. 1660–1671.
[11] Fujita, T. et al. “Runx2 induces osteoblast and chondrocyte differentiation and enhances their migration by coupling with PI3K-Akt signaling.” J. Cell Biol., vol. 166, 2004, pp. 85–95.
[12] Yoshida, C. A. et al. “Runx2 and Runx3 are essential for chondrocyte maturation, and Runx2 regulates limb growth through induction of Indian hedgehog.” Genes Dev., vol. 18, 2004, pp. 952–963.
[13] Brockschmidt, F. F. et al. “Susceptibility variants on chromosome 7p21.1 suggest HDAC9 as a new candidate gene for male-pattern baldness.”
[14] Aston, K. I. et al. “Genome-wide study of single-nucleotide polymorphisms associated with azoospermia and severe oligozoospermia.”J Androl, vol. 30, no. 6, Nov.-Dec. 2009, pp. 711-25. PMID: 19478329.