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Background: Polycystic ovary syndrome (PCOS) is a unity of endocrine and metabolic disorders, associated with PI3K/AKT/mTOR, autophagy, and gut microbiota. Quinoa is a valuable food source, which contains rich minerals, unsaturated fatty acids, and has a positive modulating effect on metabolic diseases. However, its effects and potential mechanisms on PCOS have not been reported yet. Therefore, the purpose of this study is to investigate the effect of quinoa on PCOS rats by regulating PI3K/AKT/mTOR, autophagy, and gut microbiota. Methods: Ten–week-old female Sprague-Dawley (SD) rats have received letrozole for 24 days for induction of PCOS and subsequently were treated with a quinoa diet for 8 weeks. Vaginal smears were used to analyze the estrous cycle of rats. Hormone and biochemical indexes were analyzed by kit assays and glucometer. The pathological changes of ovary, pancreas, duodenum and colon were observed by HE staining. PI3K, AKT, mTOR and autophagy-related proteins in the ovary and colon were measured by western blot and immunohistochemistry staining. Tight junction proteins in colon were measured by immunohistochemistry staining. 16 s rDNA sequencing was used to detect the changes of intestinal microbiota in rats. Network pharmacology and molecular docking were used to study the possible targets and mechanisms of quinoa on PCOS. Spearman correlation analysis was used to study the relationship between intestinal microbial abundance and hormone levels of PCOS rats at the phylum and genus level. Results: Quinoa significantly improved estrous cycle and biochemical parameters of PCOS-like rats, and the pathological state of ovary, pancreas, duodenum and colon tissues. Especially, quinoa significantly regulated the expression of PI3K, AKT, mTOR and autophagy-related proteins in the ovary. Quinoa may repair the intestinal barrier by upregulating the expression of tight junction proteins in the colon, and regulate autophagy-related factors in colon. Additionally, quinoa increased the abundance of Lactobacillu, Bacteroides and Oscillospira, and decreased the Firmicutes/Bacteroidetes ratio and the Blautia, and Prevotella, reversing the dysregulation of the gut microbiota. Correlation analysis showed that there is a strong correlation between gut microbiota with significant changes in abundance and hormone related to PCOS. Conclusion: Our result indicated that effect of quinoa on PCOS maybe associated with activation of the PI3K/AKT/mTOR signaling pathway, inhibition of autophagy, and regulation of intestinal flora. [ABSTRACT FROM AUTHOR]

Background: Although sex hormones are recognized to induce immune variations, the effect of hormonal therapy use on immunity is only poorly understood. Here, we quantified how hormonal therapy use affects HIV‐1 immune markers in cis women (CW) and trans women and non‐binary people (TNBP) with HIV. Methods: We considered CD4, CD8 and lymphocyte measurements from cis men (CM), CW and TNBP in the Swiss HIV Cohort Study. We modelled HIV‐1 markers using linear mixed‐effects models with an interaction between 'gender' (CW, TNBP) and 'hormonal therapy use' (yes/no). Models were adjusted on age, ethnicity, education level, time since start of antiretroviral therapy and use of intravenous drugs. We assessed the inflammatory effect of hormonal therapy use in 31 TNBP using serum proteomics measurements of 92 inflammation markers. Results: We included 54 083 measurements from 3092 CW and 83 TNBP, and 147 230 measurements from 8611 CM. Hormonal therapy use increased CD4 count and CD4:CD8 ratio in TNBP more than in CW (pinteraction = 0.02 and 0.007, respectively). TNBP with hormonal therapy use had significantly higher CD4 counts [median = 772 cells/μL, interquartile range (IQR): 520–1006] than without (617 cells/μL, 426–892). This was similar to the effect of CW versus CM on CD4 T cells. Hormonal therapy use did not affect serum protein concentrations in TNBP. Conclusion: This study highlights the potential role of hormonal therapy use in modulating the immune system among other biological and social factors, especially in TNBP with HIV. [ABSTRACT FROM AUTHOR]

Hypopituitarism is a heterogenous disorder characterised by a deficiency in one or more anterior pituitary hormones. There are marked sex disparities in the morbidity and mortality experienced by patients with hypopituitarism. In women with hypopituitarism, the prevalence of many cardiovascular risk factors, myocardial infarction, stroke and mortality are significantly elevated compared to the general population, however in men, they approach that of the general population. The hypothalamic-pituitary-gonadal axis (HPG) is the most sexually dimorphic pituitary hormone axis. Gonadotropin deficiency is caused by a deficiency of either hypothalamic gonadotropin-releasing hormone (GnRH) or pituitary gonadotropins, namely follicle-stimulating hormone (FSH) and luteinising hormone (LH). HPG axis dysfunction results in oestrogen and testosterone deficiency in women and men, respectively. Replacement of deficient sex hormones is the mainstay of treatment in individuals not seeking fertility. Oestrogen and testosterone replacement in women and men, respectively, have numerous beneficial health impacts. These benefits include improved body composition, enhanced insulin sensitivity, improved atherogenic lipid profiles and increased bone mineral density. Oestrogen replacement in women also reduces the risk of developing type 2 diabetes mellitus. When women and men are considered together, untreated gonadotropin deficiency is independently associated with an increased mortality risk. However, treatment with sex hormone replacement reduces the mortality risk comparable to those with an intact gonadal axis. The reasons for the sex disparities in mortality remain poorly understood. Potential explanations include the reversal of women's natural survival advantage over men, premature loss of oestrogen's cardioprotective effect, less aggressive cardiovascular risk factor modification and inadequate oestrogen replacement in women with gonadotropin deficiency. Regrettably, historical inertia and unfounded concerns about the safety of oestrogen replacement in women of reproductive age have impeded the treatment of gonadotropin deficiency. [ABSTRACT FROM AUTHOR]

The objective of this study was to explore the effect of goserellin on the levels of serum vascular endothelial growth factor (VEGF), anti-endometrial antibody (EMAb) and sex hormone in patients with endometriosis. Participants in the study, 92 patients with endometriosis admitted from June 2016 to May 2017 to our hospital, randomly were divided into control group and study group (46 cases in each group). The control group was given routine treatment such as medroxyprogesterone acetate tablet, and the study group was given injection of goserellin on the basis of the control group. The changes of serum VEGF, EMAb, CA125 and sex hormones (FSH, LH, E2, P) were compared before and after treatment. Adverse reactions were recorded during the treatment The occurrence and recurrence were followed up for 1 year. After treatment, the total effective rate of the study group was 95.65%, which was significantly higher than the control group of 80.43% (P <0.05). After treatment, the VEGF level in the study group was significantly lower than the control group, and the EMAb, CA125 levels, and EMAb positive rates were significantly higher In the control group, the difference was statistically significant (P <0.05); after treatment, the levels of FSH, LH, E2, and P in the study group were significantly lower than those in the control group (P <0.05); there was no statistically significant difference in the incidence of adverse reactions between the two groups; After a 1-year follow-up, the relapse rate in the study group was 8.69%, which was significantly lower than the control group's 52.17%. It was concluded that Goserellin has a definite clinical effect in the treatment of endometriosis. It can significantly reduce the levels of VEGF, EMAb and CA125 in serum, regulate the level of sex hormone, inhibit the growth of endometriosis, reduce the recurrence rate, and have a high safety. [ABSTRACT FROM AUTHOR]

Purpose: This study aimed to investigate the effect of the MC and endogenous sex hormone concentrations on performance-determining variables in three distinctMC phases in endurance-trained females. Methods: Twenty-one eumenorrheic trained/highly trained endurance athletes completed a standardized test battery during the early follicular phase (EFP), ovulatory phase (OP), and midluteal phase (MLP) for either one (n = 7) or two test cycles (n = 14). MC phases were determined using calendar-based counting, urinary ovulation testing, and verified with serum hormone analysis. MCs were retrospectively classified as eumenorrheic or disturbed. Disturbed MCs were excluded from analysis. The test battery consisted of 4-6 x 5-min submaximal stages with stepwise speed increases, a 30-s all-out double-poling ski ergometer test, and a maximal incremental treadmill running test. Results: At a group level, there was no effect of MC phase or the serum concentrations of estrogen and progesterone on peak oxygen uptake (...), oxygen uptake at 4 mmol⋅L-1 blood lactate concentration, time to exhaustion, running economy, or mean 30-s power output (MPO30s). Serum testosterone concentration was positively associated with MPO30s (P = 0.016). Changes in ... from EFP to MLP were inconsistent between individuals and across cycles. Conclusions: None of the measured performance-determining variables were influenced by MC phase or serumestrogen or progesterone concentrations. Although some individual patterns could be observed, there was no indication that any single MC phase is consistently associated with improved or impaired ... on a group level. [ABSTRACT FROM AUTHOR]

Background: Females are considered to have an increased susceptibility to neuromyelitis optica spectrum disorder (NMOSD) than males, especially aquaporin-4 (AQP4) antibody positive NMOSD, indicating that sex hormones may be involved in the NMOSD pathogenesis. However, the causality between sex hormones and NMOSD still remains unclear. Methods: Based on the genome-wide association study (GWAS) data of three sex hormones (estradiol (E2), progesterone (PROG) and bioavailable testosterone (BAT)), sex hormone-binding globulin (SHBG), age of menarche, age of menopause, and NMOSD (total, AQP4 + and AQP4 −), we performed a two-sample bidirectional Mendelian randomization (MR) study. Sex-stratified GWAS data of E2, PROG, BAT, and SHBG was obtained for gender-specific MR analysis. Causal inferences were based on the inverse variance weighted method, MR-Egger regression, and weighted median method. The reverse MR analysis was also performed to assess the impact of NMOSD on hormone levels. Results: PROG in females had aggravative effects on NMOSD (P < 0.001), especially AQP4 − NMOSD (P < 0.001). In the reverse MR analysis, total NMOSD was found to decrease the level of BAT (P < 0.001) and increase the level of SHBG (P = 0.001) in females. Conclusion: Findings of this MR analysis revealed mutual causal associations between sex hormones and NMOSD, which provided novel perspectives about the gender-related pathogenesis of NMOSD. [ABSTRACT FROM AUTHOR]

To explore the causal relationships between sex hormone levels and incidence of isolated REM sleep behavior disorder (iRBD). In our study, we utilized Genome-Wide Association Studies (GWAS) data for iRBD, including 9447 samples with 1061 cases of iRBD provided by the International RBD Study Group. Initially, we conducted a two-sample univariate MR analysis to explore the impact of sex hormone-related indicators on iRBD. This was followed by the application of multivariable MR methods to adjust for other hormone levels and potential confounders. Finally, we undertook a network MR analysis, employing brain structure Magnetic Resonance Imaging (MRI) characteristics as potential mediators, to examine whether sex hormones could indirectly influence the incidence of iRBD by affecting brain structure. Bioavailable testosterone (BioT) is an independent risk factor for iRBD (Odds Ratio [95 % Confidence Interval] = 2.437 [1.308, 4.539], P = 0.005, corrected-P = 0.020), a finding that remained consistent even after adjusting for other sex hormone levels and potential confounders. Additionally, BioT appears to indirectly increase the risk of iRBD by reducing axial diffusivity and increasing the orientation dispersion index in the left cingulum and cingulate gyrus. Our research reveals that elevated levels of BioT contribute to the development of iRBD. However, the specific impact of BioT on different sexes remains unclear. Furthermore, high BioT may indirectly lead to iRBD by impairing normal pathways in the left cingulum and cingulate gyrus and fostering abnormal pathway formation. [Display omitted] • Higher BioT levels increase iRBD risk, with sex-specific effects needing more study. • Elevated BioT levels may disrupt neural pathways in the left cingulum and cingulate gyrus. • Disrupted neural pathways may foster atypical pathways, indirectly triggering iRBD onset. [ABSTRACT FROM AUTHOR]

Background: The primary aim of this study was to explore whether sex hormones affect the occurrence of basal cell carcinoma (BCC) from a genetic perspective using a two-sample Mendelian randomization (MR) study. Methods: Exposure and outcome data for this MR analysis were derived from previously published GWAS studies. In this study, estradiol, sex hormone-binding globulin (SHBG), bioavailable testosterone, and total testosterone were used as exposures, and BCC was used as the outcome for the two-sample MR analysis. The random effects inverse variance weighted (IVW) model was the primary analytical model, and the simple mode, weighted median, MR-Egger, and weighted mode methods were applied as complementary approaches. Furthermore, the "leave-one-out" sensitivity analysis was performed to assess stability, Cochran's Q test to evaluate heterogeneity, and the MR-Egger intercept test to analyze horizontal multiplicity. Results: The two-sample MR analysis of the sex hormone and BCC showed that estradiol, sex hormone-binding globulin (SHBG), bioavailable testosterone, and total testosterone were not a causal factor in BCC (P> 0.05). The results of the heterogeneity test and horizontal pleiotropic analysis showed that no heterogeneity or horizontal pleiotropic existed in all MR analyses (Cochran's Q-P> 0.05, Egger intercept-P> 0.05). Conclusion: The two-sample MR analysis showed that estrogen and testosterone did not affect the occurrence and development of BCC at the genetic level. [ABSTRACT FROM AUTHOR]

Abstract Background Polycystic ovary syndrome (PCOS) is a unity of endocrine and metabolic disorders, associated with PI3K/AKT/mTOR, autophagy, and gut microbiota. Quinoa is a valuable food source, which contains rich minerals, unsaturated fatty acids, and has a positive modulating effect on metabolic diseases. However, its effects and potential mechanisms on PCOS have not been reported yet. Therefore, the purpose of this study is to investigate the effect of quinoa on PCOS rats by regulating PI3K/AKT/mTOR, autophagy, and gut microbiota. Methods Ten–week-old female Sprague-Dawley (SD) rats have received letrozole for 24 days for induction of PCOS and subsequently were treated with a quinoa diet for 8 weeks. Vaginal smears were used to analyze the estrous cycle of rats. Hormone and biochemical indexes were analyzed by kit assays and glucometer. The pathological changes of ovary, pancreas, duodenum and colon were observed by HE staining. PI3K, AKT, mTOR and autophagy-related proteins in the ovary and colon were measured by western blot and immunohistochemistry staining. Tight junction proteins in colon were measured by immunohistochemistry staining. 16 s rDNA sequencing was used to detect the changes of intestinal microbiota in rats. Network pharmacology and molecular docking were used to study the possible targets and mechanisms of quinoa on PCOS. Spearman correlation analysis was used to study the relationship between intestinal microbial abundance and hormone levels of PCOS rats at the phylum and genus level. Results Quinoa significantly improved estrous cycle and biochemical parameters of PCOS-like rats, and the pathological state of ovary, pancreas, duodenum and colon tissues. Especially, quinoa significantly regulated the expression of PI3K, AKT, mTOR and autophagy-related proteins in the ovary. Quinoa may repair the intestinal barrier by upregulating the expression of tight junction proteins in the colon, and regulate autophagy-related factors in colon. Additionally, quinoa increased the abundance of Lactobacillu, Bacteroides and Oscillospira, and decreased the Firmicutes/Bacteroidetes ratio and the Blautia, and Prevotella, reversing the dysregulation of the gut microbiota. Correlation analysis showed that there is a strong correlation between gut microbiota with significant changes in abundance and hormone related to PCOS. Conclusion Our result indicated that effect of quinoa on PCOS maybe associated with activation of the PI3K/AKT/mTOR signaling pathway, inhibition of autophagy, and regulation of intestinal flora.

Physical activity (PA) has beneficial effects on erectile dysfunction (ED). It has been proposed to affect ED physiologically via the vascular and nervous systems. This study aimed to evaluate the effect of physical activity on endothelial erectile function, sex hormones and sperm production in healthy males. Sixty-one healthy men aged 18–35 years were eligible to participate in this biochemical and questionnaire-based study. The participants were classified into two groups according to their physical activity level: a physically active group (PA = 38) and a physically inactive group (PINA = 23). PA was evaluated using the ACTi graph GT1M accelerometer. Erectile function was evaluated using the International Index of Erectile Function (IIEF-15) questionnaire. The levels of the sex hormones testosterone (T) and free testosterone (f-T), and the nitric oxide (NO) and E-selectin levels were measured by enzyme linked immuno sorbent assay (ELISA). In addition, a complete semen analysis was performed for all subjects. Better sperm production was reported in physically active subjects than in nonactive subjects. There was a significant increase (p = 0.001) in the IIEF-15 score, and the levels of T, f-T, NO and E-selectin were estimated in physically active subjects compared with those in nonactive subjects. Erectile function (IIEF-15 score) correlated positively with PA and with increased levels of T, f-T, NO and E-selectin, whereas the IIEF-15 score correlated negatively with age and adiposity. Seminological parameters such as the spermatozoa concentration, sperm viability, motility, morphology and normal forms were significantly improved in physically active subjects. Physical activity at mild to moderate levels is significantly associated with improved erectile function, increased endothelial function, increased sex hormone levels and better sperm production in healthy men aged 18–35 years. This study proposes that physical activity physiologically affects erectile function and spermatogenesis via cellular free radical-antioxidant mechanisms.

BACKGROUND: Exercise has been widely recognized in the prevention and treatment of diabetes. Aerobic exercise has become an important part of the treatment of type 1 diabetes. However, the effect of treadmill exercise on the metabolism and chronic neuroinflammation of type 1 diabetes in different sexes needs further discussion. OBJECTIVE: To study the effects of treadmill exercise on metabolism and chronic neuroinflammation in type 1 diabetes mice of different sexes. METHODS: Forty C57BL/6 mice were divided into male group and female group, with 20 mice in each group. Then, a diabetes model was established by continuous injection of streptozotocin at 80 mg/kg for 3 days. Ten rats from each group were randomly selected to perform 6-week treadmill exercise as the diabetes+exercise group and another 10 rats from each group were selected as the diabetes group. Serum sex hormones, liver tissue oxidative stress, brain tissue inflammatory factors, and liver pathology were detected, and Morris water maze was performed for the observation of behavioral changes in mice. RESULTS AND CONCLUSION: Compared with the diabetes group, the diabetes+exercise group delayed the rise of blood sugar in type 1 diabetes mice (P < 0.05) and showed a significant reduction in serum follicle-stimulating hormone, luteinizing hormone, liver superoxide dismutase, malondialdehyde, brain tumor necrosis factor α, interleukin-6 and interleukin-1β levels (P < 0.01), while serum estradiol, progesterone, estrogen, and liver glutathione peroxidase protein levels were significantly increased (P < 0.01, P < 0.05). Compared with male type 1 diabetes mice, female type 1 diabetes mice had significantly higher estradiol levels and lower luteinizing hormone levels (P < 0.05). Compared with the male diabetes+exercise group, the female diabetes+exercise group had lower liver glutathione peroxidase levels (P < 0.05). Compared with type 1 diabetes mice, the escape latency of exercise training mice was shorter (P < 0.01). In male mice, exercises significantly increased the time and platform crossing times of type 1 diabetes mice in the target quadrant (P < 0.01 or P < 0.05), while in female mice, exercises significantly increased the time of type 1 diabetes mice in the target quadrant (P < 0.05). Correlation analysis results showed that the levels of follicle-stimulating hormone, luteinizing hormone, progesterone, superoxide dismutase, malondialdehyde, tumor necrosis factor α, and interleukin-6 were positively correlated with the level of interleukin-1β (P < 0.05 or P < 0.01), whereas the levels of estradiol and progesterone were negatively correlated with the levels of superoxide dismutase, malondialdehyde, tumor necrosis factor α, interleukin-6 and interleukin-1β (P < 0.05 or P < 0.01). Overall, there are sex differences in the effects of treadmill exercise on metabolic indicators and chronic neuroinflammatory regulation in diabetes mice. Sex hormones are an important variable of treadmill exercise in the metabolic, inflammatory and cognitive responses in diabetes mice. [ABSTRACT FROM AUTHOR]

Abstract Background We aimed to examine sex-specific associations between sex- and thyroid-related hormones and the risk of metabolic dysfunction-associated fatty liver disease (MAFLD) in patients with type 2 diabetes mellitus (T2DM). Methods Cross-sectional analyses of baseline information from an ongoing cohort of 432 T2DM patients (185 women and 247 men) in Xiamen, China were conducted. Plasma sex-related hormones, including estradiol (E2), follicle-stimulating hormone (FSH), luteinizing hormone (LH), prolactin (PRL), progesterone, and total testosterone (TT), and thyroid-related hormones, including free triiodothyronine (FT3), free thyroxine (FT4), thyroid-stimulating hormone (TSH), and parathyroid hormone (PTH), were measured using chemiluminescent immunoassays. MAFLD was defined as the presence of hepatic steatosis (diagnosed by either hepatic ultrasonography scanning or fatty liver index (FLI) score > 60) since all subjects had T2DM in the present study. Results Prevalence of MAFLD was 65.6% in men and 61.1% in women with T2DM (P = 0.335). For men, those with MAFLD showed significantly decreased levels of FSH (median (interquartile range (IQR)):7.2 (4.9–11.1) vs. 9.8 (7.1–12.4) mIU/ml) and TT (13.2 (10.4–16.5) vs. 16.7 (12.8–21.6) nmol/L) as well as increased level of FT3 (mean ± standard deviation (SD):4.63 ± 0.68 vs. 4.39 ± 0.85 pmol/L) than those without MAFLD (all p-values

This study aimed to investigate the effects of prolonged inhalation of nature-derived odors indoors on humans. Twenty-six women participated in this study. Heart rate variability, heart rate, blood pressure, pulse rate, estradiol, testosterone, and cortisol were used as indicators of autonomic nervous system and endocrine system activities. Profile of mood state, state–trait anxiety inventory, menopause rating scale and general sleep disturbance scale were used as psychological indicators. The order was as follows: After the participants relaxed in a chair for 5 min, their heart rate variability and heart rate were measured for 3 min with their eyes closed. Subsequently, blood pressure and pulse rate were measured, salivary samples were collected for estradiol, testosterone, and cortisol analyses, and a subjective assessment was conducted. The participants received a diffuser containing fir essential oil and were instructed on its usage and precautions. Subsequently, they returned home and inhaled the fir oil for a week. After 7 days, participants revisited the laboratory for posttest measurements, conducted at the same time as the pretest. Prolonged inhalation of the fir essential oil resulted in increased estradiol concentration, decreased systolic and diastolic blood pressure, relief of menopausal symptoms, reduced anxiety levels, improved sleep quality and mood states. Prolonged inhalation of the fir essential oil induced physiological and psychological relaxation on menopausal women. [ABSTRACT FROM AUTHOR]

Purpose: The study aimed to investigate the correlation between the change of sex hormone levels and ocular surface parameters in girls with idiopathic central precocious puberty(ICPP). Methods: Eighteen girls with ICPP and 18 age-matched normal girls participated in this study, all of the participants had undergone physical measurements, laboratory tests, imaging examination and ocular surface assessments. Results: The Objective Scatter Index (OSI) in the ICPP group was significantly higher than in the control group (P = 0.031), girls with ICPP showed slightly lower MNITBUT compared to the normal control group, although this difference was not statistically significant. Bivariate analysis revealed a positive association between estradiol and OSI (r=0.383, P=0.021), Additionally, in the study population, both Luteinizing hormone (LH) and Follicle-stimulating hormone (FSH) were negatively correlated with Mean noninvasive tear breakup time (MNITBUT) (r=-0.359, P=0.031)(r=-0.357, P=0.032). Conclusion: In comparison with the normal control group, alterations in the OSI were observed in girls with ICPP. This alteration may be associated with an elevation in estrogen levels. Although there was a slight non-significant decrease in NITBUT in ICPP girls, the negative correlation between LH and FSH with MNITBUT suggests new perspective for further investigation. [ABSTRACT FROM AUTHOR]

Cardiovascular kidney metabolic (CKM) syndrome represents a complex interplay of cardiovascular disease (CVD), chronic kidney disease (CKD), and metabolic comorbidities, posing a significant public health challenge. Gender exerts a critical influence on CKM syndrome, affecting the disease severity and onset through intricate interactions involving sex hormones and key physiological pathways such as the renin–angiotensin system, oxidative stress, inflammation, vascular disease and insulin resistance. It is widely known that beyond the contribution of traditional risk factors, men and women exhibit significant differences in CKM syndrome and its components, with distinct patterns observed in premenopausal women and postmenopausal women compared to men. Despite women generally experiencing a lower incidence of CVD, their outcomes following cardiovascular events are often worse compared to men. The disparities also extend to the treatment approaches for kidney failure, with a higher prevalence of dialysis among men despite women exhibiting higher rates of CKD. The impact of endogenous sex hormones, the correlations between CKM and its components, as well as the long-term effects of treatment modalities using sex hormones, including hormone replacement therapies and gender-affirming therapies, have drawn attention to this topic. Current research on CKM syndrome is hindered by the scarcity of large-scale studies and insufficient integration of gender-specific considerations into treatment strategies. The underlying mechanisms driving the gender disparities in the pathogenesis of CKM syndrome, including the roles of estrogen, progesterone and testosterone derivatives, remain poorly understood, thus limiting their application in personalized therapeutic interventions. This review synthesizes existing knowledge to clarify the intricate relationship between sex hormones, gender disparities, and the progression of CVD within CKM syndrome. By addressing these knowledge gaps, this study aims to guide future research efforts and promote tailored approaches for effectively managing CKD syndrome. [ABSTRACT FROM AUTHOR]

Purpose: This study aimed to investigate the changes in serum Anti-Müllerian Hormone (AMH) levels, sex hormone levels, follicle-stimulating hormone (FSH)/luteinizing hormone (LH) ratio in patients with celiac disease (CeD), and their correlation with clinical characteristics and nutrient levels. Methods: This cross-sectional study collected clinical and biochemical data from a total of 67 females diagnosed with CeD and 67 healthy females within the reproductive age range of 18–44 years. The study was conducted at a tertiary hospital between September 2016 and January 2024. Both groups underwent comprehensive clinical and laboratory assessments. Serum levels of AMH and sex hormones were quantified using chemiluminescence immunoassay, and their associations with CeD clinical features and nutrient levels were thoroughly analyzed. Results: The study included 67 patients and 67 controls with a mean age of 36.7±7.6 years. No statistically significant differences were found between the two groups in mean age, BMI, FSH, LH, E2, P levels, FSH/LH, menstrual irregularities, abortions history, parity, and gravidity (all P>0.05). However, AMH, T, FER, FA, Zn, and Se levels were significantly lower, and PRL levels were higher in the CeD group (all P<0.05). Spearman's correlation analysis showed that AMH levels were negatively correlated with age, tTG level, disease duration, and Marsh grading (P<0.05). Conclusions: This study highlights the association between impaired ovarian function in CeD patients and disease severity and nutrient levels. Early detection and intervention for ovarian function abnormalities are imperative to enhance fertility potential in CeD patients. [ABSTRACT FROM AUTHOR]

In this study, feces samples were collected from 7 individuals in Hainan gibbon (Nomascus hainanus) family group C by through non-invasive methods, and the levels of progesterone and testosterone were analyzed by high-performance liquid chromatography mass spectrometry. The results showed that the menstrual cycle of adult females in Hainan gibbon group C was 32±3.6 days and the duration of the menstrual period was 10±2.4 days. There was no significant difference in progesterone levels between individuals of different age and sex classes, no significant periodicity in the change of testosterone in the feces samples of Hainan gibbon group C, and no significant difference in the level of testosterone between individuals of the same sex and age. However, there was a significant difference in testosterone levels between adult males and adult females. By comparing the levels of testosterone in different individuals, it could be hypothesized that both juveniles in group C may be males. The results show that the circadian cycle of adult females and the sex identification of juveniles in Hainan gibbons may be inferred from differences in fecal progesterone and testosterone levels. [ABSTRACT FROM AUTHOR]

Polycystic ovary syndrome (PCOS) is a common gynecological endocrine disorder characterized by anovulation or oligo-ovulation. Its etiology is associated with hyperandrogenism insulin resistance.and lipid metabolism abnormalities, but the exact mechanism is not yet clear. Vitamin D is a steroid hormone involved in calcium metabolism and bone structure. Reports indicate that vitamin D receptors can be detected in granulosa cells and theca cells of animal and human ovarian tissues, and vitamin D deficiency is a common complication of PCOS, with vitamin D levels being associated with the fertility. metabolic changes, and psychological health of PCOS patients. Some studies have found that the degree of vitamin D deficiency is related to the severity of PCOS. Although the etiology of PCOS is not yet clear, drug treatments are often ineffective, and relapse is common after discontinuation. However, in recent years, research has suggested that combined treatment with vitamin D and hormonal drugs can significantly improve clinical symptoms of PCOS, particularly benefiting follicular development and restoration of ovulation. Nevertheless, there are also some conflicting views in the literature. Therefore, it is necessary to comprehensively review vitamin D and its potentially related calcium ion channels. [ABSTRACT FROM AUTHOR]

Perigonadal adipose tissue is a homogeneous white adipose tissue (WAT) in adult male mice without any brown adipose tissue (BAT). However, there are congenital differences in the gonads between male and female mice. Whether heterogeneity existed in perigonadal adipose tissues (ATs) in female mice remains unknown. This study reported a perigonadal brown-like AT located between abdominal lymph nodes and the uterine cervix in female mice, termed lymph node-cervical adipose tissue (LNCAT). Its counterpart, lymph node-prostatic adipose tissue (LNPAT), exhibited white phenotype in adult virgin male mice. When exposed to cold, LNCAT/LNPAT increased uncoupling protein 1 (UCP1) expression via activation of tyrosine hydroxylase (TH), in which abdominal lymph nodes were involved. Interestingly, the UCP1 expression in LNCAT/LNPAT varied under different reproductive stages. The UCP1 expression in LNCAT was upregulated at early pregnancy, declined at midlate pregnancy, and reverted in weaning dams. Mating behavior stimulated LNPAT browning in male mice. We found that androgen but not estrogen or progesterone inhibited UCP1 expression in LNCAT. Androgen administration reversed the castration-induced LNPAT browning. Our results identified a perigonadal brown-like AT in female mice and characterized its UCP1 expression patterns under various conditions. NEW & NOTEWORTHY A novel perigonadal brown-like AT (LNCAT) of female mice was identified. Abdominal lymph nodes were involved in cold-induced browning in this newly discovered adipose tissue. The UCP1 expression in LNCAT/LNPAT was also related to ages, sexes, and reproductive stages, in which androgen acted as an inhibitor role. [ABSTRACT FROM AUTHOR]

This review systematically examines gender differences in hepatocellular carcinoma (HCC), identifying the influence of sex hormones, genetic variance, and environmental factors on the disease's epidemiology and treatment outcomes. Recognizing the liver as a sexually dimorphic organ, we highlight how gender-specific risk factors, such as alcohol consumption and obesity, contribute differently to hepatocarcinogenesis in men and women. We explore molecular mechanisms, including the differential expression of androgen and estrogen receptors, which mediate diverse pathways in tumor biology such as cell proliferation, apoptosis, and DNA repair. Our analysis underscores the critical need for gender-specific research in liver cancer, from molecular studies to clinical trials, to improve diagnostic accuracy and therapeutic effectiveness. By incorporating a gender perspective into all facets of liver cancer research, we advocate for a more precise and personalized approach to cancer treatment that acknowledges gender as a significant factor in both the progression of HCC and its response to treatment. This review aims to foster a deeper understanding of the biological and molecular bases of gender differences in HCC and to promote the development of tailored interventions that enhance outcomes for all patients. [ABSTRACT FROM AUTHOR]

Objective: People vaccinated with the coronavirus disease 2019 (COVID-19) (severe acute respiratory syndrome coronavirus-2 [SARS-CoV-2]) mRNA vaccine have reported experiencing various adverse effects. For instance, reproductive-age women have presented with complaints of abnormal uterine bleeding or menstrual cycle changes. We speculated that differences in basal sex hormone levels before and after vaccination may be present in women who experienced irregular bleeding or menstrual cycle changes; thus, this study aimed to investigate the differences in basal sex hormone levels of women before and after two doses of SARS-CoV-2 mRNA vaccination. Methods: This retrospective study included patients who received SARS-CoV-2 mRNA vaccines between January 2021 and February 2022 at a single center. In an outpatient setting, patients were queried regarding their menstrual cycle, the date of SARS-CoV-2 mRNA vaccination, vaccination type, and vaccination side effects. Differences in basal hormone levels (menstrual cycle days 2–3, follicle-stimulating hormone [FSH], luteinizing hormone [LH], and estradiol) before and after vaccination were compared. Results: Among the 326 patients, patients with no laboratory records of the hormones were excluded. The median time interval between SARS-CoV-2 mRNA vaccination and the laboratory test day was 79 days (interquartile range, 44 to 127). A comparative analysis of these hormones before and after vaccination revealed no significant differences. Subgroup analyses based on age and reported adverse events also found no statistically significant differences. Conclusion: This study showed no significant differences in basal hormone levels (FSH, LH, and estradiol) before and after SARS-CoV-2 mRNA vaccination. [ABSTRACT FROM AUTHOR]

Copper is an indispensable trace element in metabolism. This study aimed to investigate the relationship between copper and reproductive health, and possibly provide new insights for diagnosis and treatment. This study was based on data extracted from the NHANES database (2013–2014 and 2015–2016). The t-test, ANOVA, Chi-square test, multiple linear regression, and restricted cubic spline analysis were used. Serum copper levels were significantly higher in women with gestational diabetes than in those without gestational diabetes (P = 0.0150). Women with higher copper levels and smoking habits tended to deliver overweight babies (P = 0.028). Women with diabetes had higher serum copper and were prone to deliver overweight babies (P = 0.024). Serum copper levels showed a positive relationship with sex hormone-binding globulin (SHBG) levels (P < 0.0001). In this study, serum copper levels were found to be associated with reproductive health in women. Further studies are required to draw causal inferences. [ABSTRACT FROM AUTHOR]

Males and females exhibit intrinsic differences in the structure and function of the heart, while the prevalence and severity of cardiovascular disease vary in the two sexes. However, the mechanisms of this sex-based dimorphism are yet to be elucidated. Sex chromosomes and sex hormones are the main contributors to sex-based differences in cardiac physiology and pathophysiology. In recent years, the advances in induced pluripotent stem cell-derived cardiac models and multi-omic approaches have enabled a more comprehensive understanding of the sex-specific differences in the human heart. Here, we provide an overview of the roles of these two factors throughout cardiac development and explore the sex hormone signaling pathways involved. We will also discuss how the employment of stem cell-based cardiac models and single-cell RNA sequencing help us further investigate sex differences in healthy and diseased hearts. [ABSTRACT FROM AUTHOR]

Purpose: To evaluate the possible effects of novel coronavirus disease 2019 (2019-NCOV) on male sex hormones and reproductive ability, and analyze its incidence and risk factors. Methods: We retrieved from PubMed, Embase, The Cochrane Library, Web of Science, Clinical Trails, CNKI, CBM, Wan Fang Database and VIP to collect research on the effects of COVID-19 on the male sex hormone. Our literature search was conducted until April 2022, and two investigators independently screened articles based on inclusion and exclusion criteria. In strict accordance with the inclusion and exclusion criteria, two researchers independently screened the literature and comprehensively analyzed 8 cohort studies on the impact of COVID-19 on male sex hormone. And We used RevMan5.4.1 and Stata15.0 for statistical analysis. Finally, there were eight cohort studies on the effects of COVID-19 on male sex hormones. Results: T(RR = − 3.94; 95% CI − 6.22, − 1.66; P = 0.0007), testosterone in the COVID-19 group decreased by 3.94 nmol/L compared with the control group, and the difference was statistically significant. LH (RR = 0.85; 95% CI − 0.26, 1.96; P = 0.13), the LH in COVID-19 group was 0.85 mlU/ml higher than that in control group, but the difference was not statistically significant. FSH (RR = 0.25; 95% CI − 0.72, 1.23; P = 0.61), the FSH of COVID-19 group was 0.25 mlU/ml higher than that of the control group, but the difference was not statistically significant. PRL (RR = 2.42; 95% CI 0.52, 4.31; P = 0.01), the PRL in the COVID-19 group was 2.42 ng/ml higher than that in the control group, and the difference was statistically significant. E2(RR = 11.88; 95% CI 9.90, 13.86; P < 0.00001), The level of E2 in the COVID-19 group was 11.88 pg/ml higher than that in the control group, and the difference was statistically significant. T:LH (RR = − 0.39; 95% CI − 076, − 0.02; P = 0.04), the ratio of T:LH in COVID-19 group was lower than that in control group, and the difference was statistically significant. FSH:LH (RR = − 0.38; 95% CI − 0.86, 0.11; P = 0.13), the ratio of FSH:LH decreased in COVID-19 group compared with control group, but the difference was not statistically significant. Conclusions: COVID-19 can affect the level of sex hormones, especially T, which may further affect male fertility. Due to the limitations of this study, this conclusion needs to be further verified by large-sample, high-quality prospective cohort studies on the long-term effects of COVID-19 on male sex hormones and fertility. [ABSTRACT FROM AUTHOR]

Abstract Background The incidence of male reproductive dysfunction is increasing annually, and many studies have shown that obesity can cause severe harm to male reproductive function. The mechanism of male reproductive dysfunction caused by obesity is unclear, and there is no ideal treatment. Identification of effective therapeutic drugs and elucidation of the molecular mechanism involved in male reproductive health are meaningful. In this study, we investigated the effects of the GLP-1 receptor agonist liraglutide on sex hormones, semen quality, and testicular AC3/cAMP/PKA levels in high-fat-diet-induced obese mice. Methods Obese mice and their lean littermates were treated with liraglutide or saline for 12 weeks. Body weight was measured weekly. Fasting blood glucose (FBG) was measured using a blood glucose test strip. The serum levels of insulin (INS), luteinizing hormone (LH), follicle stimulating hormone (FSH), testosterone (T), free testosterone (F-TESTO), estradiol (E2), and sex hormone binding globulin (SHBG) were detected using ELISA. The sperm morphology and sperm count were observed after Pap staining. The mRNA and protein expression levels of testicular GLP-1R and AC3 were measured by RT-qPCR and Western blot, respectively. Testicular cAMP levels and PKA activity were detected using ELISA. Results Liraglutide treatment can decrease body weight, FBG, INS, HOMA-IR, E2 and SHBG levels; increase LH, FSH, T, and F-TESTO levels; increase sperm count; decrease the sperm abnormality rate; and increase GLP-1R and AC3 expression levels and cAMP levels and PKA activity in testicular tissue. Conclusions Liraglutide can improve the sex hormone levels and semen quality of obese male mice. In addition to its weight loss effect, liraglutide can improve the reproductive function of obese male mice, which may also be related to the upregulation of AC3/cAMP/PKA pathway in the testis. This work lays the groundwork for future clinical studies.

Objective To investigate the effects of subcutaneous injection of glucagon-like peptide-1 (GLP-1) receptor agonist liraglutide on serum sex hormone levels in obese male mice. Methods Eighteen male C57BL/6J mice were randomly divided into the normal group (n = 6) model group (n = 6), and intervention group (n = 6) Mice in the nor- mal group were fed with normal diet, and mice in the model group and intervention group were fed with high-fat diet to establish the obesity models. After 10 weeks, mice in the intervention group were subcutaneously injected with liraglutide at 100 µg/(kg.d), and mice in the normal group and model group were subcutaneously injected with the equal volume of nor- mal saline for 12 weeks. Body weight was measured weekly. Fasting blood glucose (FBG) was measured using a blood glucose test strip. The serum levels of insulin (INS), luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone (T), free testosterone (FT), estradiol (E2), and sex hormone binding globulin (SHBG) were detected using ELI-SA. The homeostasis model assessment of insulin resistance (HOMA-IR) was calculated. Results Compared with the normal group, the body weight of the model group increased at 0, 4, 8, and 12 weeks (all P < 0.01 ) ; compared with the model group, the body weight of the intervention group decreased at 4, 8, and 12 weeks (all P<0.01); there was no statistically significant difference in body weight between the intervention group and the normal group at 12 weeks (P > 0.05). After administration, compared with the normal group, the serum FBG, INS, and HOMA-IR levels increased in the model group (all P < 0.01 ) ; compared with the model group, the serum FBG, INS, and HOMA-IR levels decreased in the intervention group (all P < 0 ). Compared with the normal group, the levels of LH, FSH, T, and FT decreased and the levels of E2, and SHBG increased in the model group (all P < 0.05 ) ; compared with the model group, the levels of LH, FSH, T, and FT in the intervention group increased, and the levels of E, and SHBG decreased (all P < 0.05 ) . Conclusion The sex hormone levels of obese male mice are abnormal; liraglutide can improve the sex hormone levels of obese male mice, and its mechanism may be related to its significant effects of reducing blood glucose and body mass. [ABSTRACT FROM AUTHOR]

Globally, ~8%-12% of couples confront infertility issues, male-related issues being accountable for 50%. This review focuses on the influence of gut microbiota and their metabolites on the male reproductive system from five perspectives: sperm quality, testicular structure, sex hormones, sexual behavior, and probiotic supplementation. To improve sperm quality, gut microbiota can secrete metabolites by themselves or regulate host metabolites. Endotoxemia is a key factor in testicular structure damage that causes orchitis and disrupts the blood-testis barrier (BTB). In addition, the gut microbiota can regulate sex hormone levels by participating in the synthesis of sex hormone-related enzymes directly and participating in the enterohepatic circulation of sex hormones, and affect the hypothalamic-pituitary-testis (HPT) axis. They can also activate areas of the brain that control sexual arousal and behavior throughmetabolites. Probiotic supplementation can improve male reproductive function. Therefore, the gut microbiotamay affectmale reproductive function and behavior; however, further research is needed to better understand themechanisms underlyingmicrobiota-mediated male infertility. [ABSTRACT FROM AUTHOR]

Intracranial dural arteriovenous fistulae (DAVFs) represent a subset of cerebral vascular malformations associated with significant morbidity and mortality. In Japan, DAVF exhibits sex-based differences in anatomical distribution, with female predominance in the cavernous sinus (CS) and male predominance in the transverse sinus (TS). Nevertheless, the pathophysiology of DAVF is not fully understood, and hormonal influences are hypothesized to play a role in its development. This study aimed to investigate changes in the concentrations of sex steroid hormones between intracranial and peripheral sampling sites in patients with CS- and TS-DAVF. We recruited 19 patients with CS-DAVF (n = 12) and TS-DAVF (n = 7) in this study. Blood hormone measurements were obtained from peripheral and jugular bulb samples during endovascular intervention. Hormone concentrations were analyzed using enzyme-linked immunosorbent assay kits, and statistical analyses were performed. Our study revealed a higher prevalence of CS-DAVF in females and TS-DAVF in males, which is consistent with previous studies. Estradiol concentration was significantly lower in the jugular bulb compared with in the periphery in both patients with CS- and TS-DAVF. This decrease in estradiol was observed irrespective of the patient's sex and independent of follicle-stimulating hormone levels. These findings indicate a local decrease in estradiol levels within the intracranial vasculature of patients with DAVF. This suggests a potential multifactorial role of estradiol in the pathomechanism of DAVFs, warranting further investigation to understand its influence on DAVF formation and potential targeted therapies, thereby enhancing patient outcomes. [ABSTRACT FROM AUTHOR]

It is widely known that all-female fish production holds economic value for aquaculture. Sebastes schlegelii, a preeminent economic species, exhibits a sex dimorphism, with females surpassing males in growth. In this regard, achieving all-female black rockfish production could significantly enhance breeding profitability. In this study, we utilized the widely used male sex-regulating hormone, 17α-methyltestosterone (MT) at three different concentrations (20, 40, and 60 ppm), to produce pseudomales of S. schlegelii for subsequent all-female offspring breeding. Long-term MT administration severely inhibits the growth of S. schlegelii, while short term had no significant impact. Histological analysis confirmed sex reversal at all MT concentrations; however, both medium and higher MT concentrations impaired testis development. MT also influenced sex steroid hormone levels in pseudomales, suppressing E2 while increasing T and 11-KT levels. In addition, a transcriptome analysis revealed that MT down-regulated ovarian-related genes (cyp19a1a and foxl2) while up-regulating male-related genes (amh) in pseudomales. Furthermore, MT modulated the TGF-β signaling and steroid hormone biosynthesis pathways, indicating its crucial role in S. schlegelii sex differentiation. Therefore, the current study provides a method for achieving sexual reversal using MT in S. schlegelii and offers an initial insight into the underlying mechanism of sexual reversal in this species. [ABSTRACT FROM AUTHOR]

Background: Gender differences existed in inflammatory bowel disease (IBD), including Crohn's disease (CD) and ulcerative colitis (UC). Observational studies have revealed associations between sex hormones and IBD, such as estrogen and testosterone. However, the exact relationship between these sex hormones and IBD is unclear. Method: Based on the genome-wide association studies data of eight sex hormones, two sex hormone receptors, sex hormone-binding globulin (SHBG), total IBD and its two subtypes, we performed a two-sample Mendelian randomization (MR) study to analyze their mutual relationship. For estradiol (E2), progesterone (PROG), bioavailable testosterone (BAT), total testosterone (TT) and SHBG, sex-stratified MR analyses were also performed. Inverse variance weighted method, MR-Egger regression and Weighted median method were used for causal analyses. Sensitivity analyses were conducted to test the stability of causal relationships. Besides, a reverse MR analysis was performed to estimate the reverse causation. Results: E2 (P=0.028) and TT (P=0.034) had protective effects on CD. Sexstratified analyses revealed protective roles of E2 in males on total IBD (P=0.038) and CD (P=0.020). TT in females had protective effects on total IBD (P=0.025) and CD (P=0.029), and BAT in females decreased the risk of developing CD (P=0.047) and UC (P=0.036). Moreover, SHBG in males was also associated with a decreased risk of CD (P=0.021). The reversed MR analysis showed that CD was negatively correlated with estrogen receptor (P=0.046). UC was negatively correlated with PROG in females (P=0.015) and positively correlated with SHBG levels in males (P=0.046). Conclusion: Findings of this study revealed the mutual causal associations between sex hormones and the risk of developing IBD. [ABSTRACT FROM AUTHOR]

Obejective: To investigate the effects of allylestradiol tablets combined with ritodrine in the treatment of threatened abortion and its effects on endocrine indexes, symptoms and signs. Methods: 92 patients with threatened abortion ranging from May 2023 to October 2023 were selected as the study subjects. All patients are randomly divided into two groups (control group and observation group), the control group LiTuoJun treatment, observation group on the control of the group with acrylic oestradiol tablets, compare the treatment effect, compare the two groups of vaginal bleeding, abdominal pain, contractions disappear time, compare the two groups of serum hormone levels, uterine blood flow state, compare the two groups of adverse reactions during the treatment of the success rate. Results: The effective rate in the observation group was higher (P<0.05). The disappearance time of abdominal pain, vaginal bleedingand uterine contraction in observation group was significantly lower (P<0.05). After treatment, the levels of human chorionic gonadotropin and progesterone were increased, and the levels of serum fibrinogen, uterine artery pulsation index and blood flow resistance index were significantly decreased in both groups, and the change range of observation group was significantly higher (P<0.05). During treatment, there was no statistical significance in adverse reactions between the two groups (P>0.05). The success rate of the observation group was higher, while there was no statistical significance (P>0.05). Conclusion: Allylestradiol tablets combined with ritodrine can obviously shorten the improvement time of clinical signs of threatened abortion, improve the level of endocrine indicators and uterine blood flow, improve the therapeutic effect and the success rate of fetal protection, and the application is safe, worthy of clinical application and promotion. [ABSTRACT FROM AUTHOR]

Obejective: To investigate the effect of the combination therapy of gestrinone and Sanjie analgesic capsule on sex hormone, uterine artery hemodynamics, and serum matrix metalloproteinases (MMPs) in patients with endometriosis (EMT). Methods: 195 patients with EMT admitted to the Central Theater Command General Hospital of the Chinese People's Liberation Army from January 2021 to December 2022 were selected, and patients were divided into the control group (gestrinone treatment, n=97) and the observation group (Sanjie analgesic capsule combined with gestrinone treatment, n=98) by the dual color sphere method. The efficacy, sex hormone indexes, uterine arterial hemodynamics and serum MMP-2, MMP-3 and MMP-9/tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) levels were compared between the two groups, and simultaneously observed the incidence of adverse reactions in both groups.Results: Compared with the control group, the clinical total effective rate of observation group was higher (P<0. 05). After treatment, the follicle stimulating hormone (FSH), luteinizing hormone (LH), and estradiol (E2) of the observation group were lower than those of the control group (P<0.05). After treatment, the pulsatile index (PI) and resistance index (RI) of the observation group were lower than those of the control group, while the peak systolic velocity (PSV) and end-diastolic velocity (EDV) were higher than those of the control group (P<0.05). After treatment, the MMP-2, MMP-3, MMP-9/TIMP-1 of the observation group were lower than those of the control group (P<0.05). There was no statistically significant difference in the incidence of adverse reactions between the two groups (P>0.05). Conclusion: Sanjie analgesic capsule combined with gestrinone could effectively improve sex hormones, uterine artery hemodynamics, and serum MMP-2, MMP-3, MMP-9/TIMP-1 levels in patients with EMT, and which had good safety. [ABSTRACT FROM AUTHOR]

Background: Polycystic ovary syndrome (PCOS) is a prevalent endocrine disease in women, intricately linked to hormonal imbalances. The microbiota composition plays a pivotal role in influencing hormonal levels within the body. In this study, we utilized a murine model to investigate how intestinal and vaginal microbiota interact with hormones in the development of PCOS. Methods: Twenty female mice were randomly assigned to the normal group (N) and the model group (P), where the latter received daily subcutaneous injections of 0.1 mL DHEA (6 mg/100 g). Throughout the experiment, we evaluated the PCOS mouse model by estrus cycle, serum total testosterone (T), prolactin (PRL) and luteinizing hormone (LH) levels, and ovarian pathological morphology. The microbial composition in both intestinal content and vaginal microbiota were studied by 16S rRNA gene high-throughput sequencing. Results: Compared with the N group, the P group showed significant increases in body weight, T, and PRL, with significant decrease in LH. Ovaries exhibited polycystic changes, and the estrous cycle was disrupted. The intestinal microbiota result shows that Chao1, ACE, Shannon and Simpson indexes were decreased, Desulfobacterota and Acidobacteriota were increased, and Muribaculaceae, Limosilactobacillus and Lactobacillus were decreased in the P group. T was significantly positively correlated with Enterorhabdus, and LH was significantly positively correlated with Lactobacillus. The analysis of vaginal microbiota revealed no significant changes in Chao1, ACE, Shannon, and Simpson indices. However, there were increased in Firmicutes, Bacteroidota, Actinobacteriota, Streptococcus, and Muribaculaceae. Particularly, Rodentibacter displayed a robust negative correlation with other components of the vaginal microbiota. Conclusion: Therefore, the response of the intestinal microbiota to PCOS is more significant than that of the vaginal microbiota. The intestinal microbiota is likely involved in the development of PCOS through its participation in hormonal regulation. [ABSTRACT FROM AUTHOR]

Objective: Sjögren's disease (SjD) has a strong sex bias, suggesting an association with sex hormones. Male SjD represents a distinct subset of the disease, but the pathogenic mechanisms of male SjD is poorly characterized. The aim of this study is to identify initiating events related to the development of gland hypofunction and autoimmunity in male SjD patients. Materials and methods: Human minor salivary glands were transcriptomically analyzed with microarrays to detect differentially expressed genes in male SjD patients. Identified genes were tested on their involvement in the disease using conditional transgenic mice and gene‐overexpressing cells. Results: GPR78, an orphan G protein–coupled receptor, was overexpressed in the salivary glands of male SjD patients compared with male healthy controls and female SjD patients. Male GPR78 transgenic mice developed salivary gland hypofunction with increased epithelial apoptosis, which was not seen in control or female transgenic mice. In cell culture, GPR78 overexpression decreased lysosomal integrity, leading to caspase‐dependent apoptotic cell death. GPR78‐induced cell death in vitro was inhibited by treatment with estradiol. Conclusion: GPR78 overexpression can induce apoptosis and salivary gland hypofunction in male mice through lysosomal dysfunction and increased caspase‐dependent apoptosis in salivary gland epithelium, which may drive disease in humans. [ABSTRACT FROM AUTHOR]

Purpose: Sex hormones are thought to be responsible for the unique gender differences in papillary thyroid cancer(PTC). Most previous studies on these have focused on the expression of estrogen receptors, or have been limited to animal studies. The aim of our study was to explore the relationship between serum sex hormones and the pathological features of PTC in the clinical setting, as further evidence of the role of sex hormones in PTC. Methods: Retrospective data analysis of patients who underwent thyroid surgery at the Department of Thyroid Surgery, Nanjing Drum Tower Hospital from January 2022 to September 2022 Correlation between serum sex hormone and pathological features was analyzed in male patients and in menopausal female patients. Serum sex hormones include luteinizing hormone(LH), follicle stimulating hormone(FSH), estradiol(E2), total testosterone(TT), progesterone(P), and prolactin(PRL). Tumor pathological characteristics include the number and size of tumor, presence of extrathyroidal extension(ETE), presence of lymph node metastasis(LNM). Results: Preoperative serum E2 in male patients was positively correlated with tumor size in PTC, LH was negatively correlated with LNM, while TT and P were negatively correlated with ETE. Similar findings were not observed in menopausal female patients. Conclusion: We observed that serum sex hormones correlate with the pathological features of PTC in male patients, for the first time in a clinical study. High serum estrogens may be a risk factor for PTC, while androgens are the opposite. This somewhat corroborates previous research and provides new variables for future PTC prediction models. [ABSTRACT FROM AUTHOR]

Summary: Huntington's disease is a rare autosomal dominant disorder presenting with chorea, rigidity, hypo-/akinesia, cognitive decline, and psychiatric disturbances. Numerous risk factors have been defined in the onset of this disease. However, the number of CAG repeats in the genes are the most crucial factor rendering patients susceptible to the disease. Studies have shown significant differences in onset and disease presentation among the sexes, which prompts analysis of the impact of different sexes on disease etiology and progression. This article therefore discusses the evidence-based role of sex in aspects of symptomatology, pathogenesis, biomarkers, progression, and prognosis of Huntington's disease, with a secondary review of sex-linked differences in Alzheimer's and Parkinson's disease. [ABSTRACT FROM AUTHOR]

AbstractObjectiveMethodResultsConclusionsIndividuals with opioid use disorder (OUD) have reduced life expectancy and inferior outcomes when treated for depression, diabetes, and fractures. Their elevated risk of testosterone deficiency may contribute to all of these relationships, however few individuals prescribed opioids are evaluated with testosterone assays. The purpose of this study is to determine whether patients with opioid use disorder are evaluated for testosterone deficiency after development of a symptom that may merit investigation, such as erectile dysfunction (ED).We conducted a retrospective longitudinal cohort study that utilized data from a national database called TriNetX. Patients were eligible for inclusion if they were 20 to 90 years of age, male, and diagnosed with erectile dysfunction. We utilized descriptive statistics and logistic regression to address study aims.Testosterone testing was uncommon for all patients with ED. Among 20,658 patients, it was assessed in 11.2% with OUD and 15.1% without OUD. Among those screened, 40% individuals with OUD and ED had testosterone deficiency. Odds of screening those with OUD were lower than matched controls (RR 0.74).Individuals with OUD are at increased risk of testosterone deficiency than the general population, but nearly 90% are not evaluated for this condition even after development symptoms. That 40% of individuals assessed were classified as testosterone deficient suggests endocrine disorders may be contributing to increased fracture risk, chronic pain, and severe depression commonly encountered in patients with OUD. Addressing this care gap may reduce morbidity and mortality associated with opioid use disorder. [ABSTRACT FROM AUTHOR]

Background: The incidence of male reproductive dysfunction is increasing annually, and many studies have shown that obesity can cause severe harm to male reproductive function. The mechanism of male reproductive dysfunction caused by obesity is unclear, and there is no ideal treatment. Identification of effective therapeutic drugs and elucidation of the molecular mechanism involved in male reproductive health are meaningful. In this study, we investigated the effects of the GLP-1 receptor agonist liraglutide on sex hormones, semen quality, and testicular AC3/cAMP/PKA levels in high-fat-diet-induced obese mice. Methods: Obese mice and their lean littermates were treated with liraglutide or saline for 12 weeks. Body weight was measured weekly. Fasting blood glucose (FBG) was measured using a blood glucose test strip. The serum levels of insulin (INS), luteinizing hormone (LH), follicle stimulating hormone (FSH), testosterone (T), free testosterone (F-TESTO), estradiol (E2), and sex hormone binding globulin (SHBG) were detected using ELISA. The sperm morphology and sperm count were observed after Pap staining. The mRNA and protein expression levels of testicular GLP-1R and AC3 were measured by RT-qPCR and Western blot, respectively. Testicular cAMP levels and PKA activity were detected using ELISA. Results: Liraglutide treatment can decrease body weight, FBG, INS, HOMA-IR, E2 and SHBG levels; increase LH, FSH, T, and F-TESTO levels; increase sperm count; decrease the sperm abnormality rate; and increase GLP-1R and AC3 expression levels and cAMP levels and PKA activity in testicular tissue. Conclusions: Liraglutide can improve the sex hormone levels and semen quality of obese male mice. In addition to its weight loss effect, liraglutide can improve the reproductive function of obese male mice, which may also be related to the upregulation of AC3/cAMP/PKA pathway in the testis. This work lays the groundwork for future clinical studies. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To probe into the effects of kidney-tonifying, phlegm-eliminating and blood-activating formula on ovulation induction and anti-Müllerian hormone(AMH), sex hormones levels in patients with polycystic ovary syndrome (PCOS). METHODS: A total of 124 patients with PCOS admitted into Hebei Cangzhou Hospital of Integrated Traditional Chinese and Western Medicine from Jun. 2020 to Jun. 2022 were selected and prospectively randomized at 1 ∶1 ratio. Totally 62 cases in the control group was given clomiphene, while 62 patients in observation group was treated with clomiphene combined with kidney-tonifying, phlegm-eliminating and blood-activating formula. Efficacy, changes in traditional Chinese medicine syndrome scores and incidences of adverse drug reactions were compared between two groups, the number of follicles, ovarian volume, endometrial thickness, recovery of ovulation and pregnancy were observed, the serum estradiol (E2), testosterone (T), luteinizing hormone (LH), folliclestimulating hormone (FSH) and AMH were detected. RESULTS: The comprehensive curative effect rate and overall efficacy of the observation group were respectively 85. 48% (53/62) and 100. 00% (62/62), which were significantly higher than 72. 58% (45/62) and 90. 32% (56/62) of the control group, with statistically significant differences (P<0. 05). Compared with the control group, the traditional Chinese medicine syndrome score, follicles number and ovarian volume of the observation group decreased significantly after treatment, while the endometrial thickness of the observation group increased significantly, with statistically significant differences (P < 0. 05). Compared with the control group, the serum E2 of the observation group increased significantly after treatment, while the levels of T, LH, LH/ FSH and AMH in the observation group decreased significantly, with statistically significant differences (P < 0. 05). The recovery rate of ovulation and pregnancy rate of 1-year follow-up were respectively 87. 10% (54/62) and 43. 55% (27/62) in the observation group, significantly higher than 74. 19% (46/62) and 29. 03% (18/62) in the control group, with statistically significant differences (P<0. 05). The difference in the incidences of adverse drug reactions between two groups was not statistically significant (P > 0. 05), and no severe adverse drug reactions occurred. CONCLUSIONS: Kidney-tonifying, phlegm-eliminating and blood-activating formula in the treatment of PCOS can improve patients’ clinical symptoms, enhance therapeutic effect, promote ovulation, regulate AMH and sex hormones levels, protect ovarian function and increase the chance of pregnancy. [ABSTRACT FROM AUTHOR]

Objective Childhood cancer survivors are at risk for hypogonadism. The impact of hypogonadism on neurocognitive impairment and emotional distress in the non-cancer population has been shown; however, the relationship among the childhood cancer survivor population is unknown. We aimed to evaluate the contribution of hypogonadism to neurocognitive impairment and emotional distress among survivors. Design Cross-sectional study using retrospective cohort. Methods In total, 3628 survivors who completed standard neurocognitive tests (six domains: processing speed, memory, executive function, attention, academics, and global cognition) and self-reported emotional distress were included in our study. Participants were stratified by sex and gonadal status. Outcomes were compared between hypogonadal and eugonadal groups by multivariable analysis, adjusting for established predictors, and mediation analyses to determine the direct/indirect effects of hypogonadism on outcomes. Results The hypogonadal group exhibited a higher prevalence of neurocognitive impairment across domains, but no difference in emotional distress. Hypogonadal females exhibited higher relative risk (1.7, 95% CI, 1.2–2.5) for impaired visual processing speed, compared to eugonadal females after adjusting for cancer-related variables. In mediation models, hypogonadism had a significant direct (P <.01) and indirect (from P <.01) impact on impairment in visual processing speed among females. Males demonstrated direct (P =.03) and indirect (P =.04) impact of hypogonadism on motor processing speed. Conclusion Processing speed may be the most vulnerable neurocognitive domain associated with hypogonadism in survivors, while other domains were mainly impacted by cancer-related variables. Our findings support the need for further evaluation of the impact of sex hormone replacement therapy on neurocognitive function. [ABSTRACT FROM AUTHOR]

Objective: To observe the effects of xiaonang tiaojing decoction combined with diane-35 on sex hormones, lipid metabolism and ovarian stromal blood flow in patients with polycystic ovary syndrome (PCOS). Methods: 117 patients with PCOS who were admitted to Henan Provincial Hospital of Traditional Chinese Medicine from July 2020 to December 2022 were selected. Patients were divided into control group (diane-35, 58 cases) and study group (xiaonang tiaojing decoction combined with diane-35, 59 cases) according to the random number table method. The sex hormone indexes [luteinizing hormone (LH), estradiol (E2), follicle stimulating hormone (FSH), testosterone (T)], chinese medicine syndrome scores, lipid metabolism [high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), triglyceride (TG), total cholesterol (TC)] and ovarian stromal blood flow [uterine artery pulsation index (PI), uterine artery resistance index (RI)] were compared between two groups. Results: The main symptom score, secondary symptom score and total score in study group were lower than those in control group after treatment (P<0.05). LH, E2, FSH and T in study group were lower than those in control group after treatment (P<0.05). HDL-C in study group was higher than that in control group; TC, TG and LDL-C were lower than those in control group after treatment (P<0.05). PI and RI in study group were lower than those in control group after treatment (P<0.05). Conclusion: Xiaonang tiaojing decoction combined with diane-35 in the treatment of PCOS patients, which can improve the clinical symptoms of patients, regulate the body's sex hormones, lipid metabolism and ovarian stromal blood flow, and the curative effect is good. [ABSTRACT FROM AUTHOR]

Osteoporosis (OP) is a kind of metabolic disease characterized by reduced bone mass and damaged bone microstructure, which leads to increased bone brittleness and easy fracture. Recent studies have found that sleep deprivation affects the progression of OP in terms of hormone levels. Especially, the changes of growth hormone, sex hormone, and thyroid hormone are particularly obvious under sleep deprivation. Therefore, this paper summarizes the correlation between the changes of growth hormone, sex hormone, and thyroid hormone levels and OP under sleep deprivation, and further defines the relationship among sleep deprivation-hormone levels-osteoporosis, in order to provide theoretical basis for clinical prevention and treatment of OP from the perspective of sleep. [ABSTRACT FROM AUTHOR]

Nonalcoholic steatohepatitis (NASH) is a progressive form of nonalcoholic fatty liver disease (NAFLD) that is characterized by hepatic inflammation and steatosis. Currently, limited data exist regarding the risk of NASH in transgender women and the treatment options for this particular population. The use of testosterone supplementation is unfavorable for transgender women, and estrogen supplementation is linked to an increased risk of breast cancer; thus, an isoflavone derivative compound known as "genistein" could serve as a viable substitute for a hormone supplement in this context. The purpose of this study was to investigate the treatment effects and mechanisms of actions of genistein and sex hormones in orchidectomized (ORX) rats with nonalcoholic steatohepatitis induced via a high-fat high-fructose diet (HFHF) model. Male Sprague-Dawley rats (n = 42) were randomly assigned into seven groups; control, ORX + standard diet, HFHF, ORX + HFHF, ORX + HFHF diet + testosterone (50 mg/kg body weight (BW) once weekly), ORX + HFHF diet + estradiol (1.6 mg/kg BW daily), and ORX + HFHF diet + genistein (16 mg/kg BW daily). The duration of the study was 6 weeks. Some parts of liver tissue were used for histological examination by H&E staining. The determination of fat accumulation was performed using Oil Red O staining. SREBP1c and FAS gene expression were quantified using real-time PCR technique. The levels of all types of peroxisome proliferator-activated receptors (PPARs; α, δ, γ), proteins, and signal transducer and activator of transcription 1 (STAT1) signaling pathway were determined by both immunoblotting and immunohistochemistry. Rats in the ORX + HFHF group had the highest degree of hepatic steatosis, lobular inflammation, and hepatocyte ballooning, and showed higher levels of genes related to de novo lipogenesis, including SREBP1c and FAS. The expression of PPARγ and STAT1 were upregulated, while the expression of PPARα and PPARδ were downregulated in the ORX + HFHF group. Testosterone, estradiol and genistein treatments improved NASH histopathology together with the reversal of all types of PPAR protein expressions. Interestingly, genistein decreased the levels of STAT1 protein expression more than those of testosterone and estradiol treatment. Genistein and sex hormone treatment could ameliorate NASH through the upregulation of PPARα, and PPARδ, and the suppression of PPARγ and STAT1 expression. [ABSTRACT FROM AUTHOR]

Context: It is very necessary to delay ovarian aging and prevent age-related health problems. The active ingredient in Honghua Xiaoyao tablet (HHXYT) has the effects of anti-oxidation, anti-inflammation, immune regulation and so on.Objective: To explore the effect and mechanism of Honghua Xiaoyao tablet on aging model mice.Materials and methods: The aging model was established by intraperitoneal injection of D-galactose in model mice. The mice in the HHXYT-L,M,H group were given 0.3 g/kg, 0.6 g/kg and 1.2 g/kg Honghua Xiaoyao tablet suspension respectively, and the HHXYT-M + E2 group was given 0.6 g/kg HHXYT +0.13 mg/kg estradiol valerate for 30 days. In this study, ELISA, HE, Western blot, IH and TUNEL were used.Results: HHXYT + E2 can improve the gonadal index, estrous cycle of aging mice. In HHXYT-M + E2 group, the level of FSH and LH decreased, while E2 and AMH increased significantly. The number of growing follicles in HHXYT-M + E2 group increased, which was better than that of HHXYT alone. Western blot results showed that HHXYT-M + E2 group decreased the expression of Bax, cleaved-Parp, cleaved-Casp-3 and CytC molecules and increased the expression of Bcl-2 in ovarian tissue. FSHR expression decreased in model group and increased in HHXYT group. TUNEL staining showed that the number of apoptotic cells in HHXYT group was reduced, and the HHXYT-M + E2 group was the most significantly.Discussion and conclusion: HHXYT can improve the level of sex hormones and increase the number of growing follicles in aging mice. HHXYT-M + E2 group has the best effect, and its mechanism may be related to reducing ovarian granulosa cell apoptosis.

Abstract Purpose To evaluate the possible effects of novel coronavirus disease 2019 (2019-NCOV) on male sex hormones and reproductive ability, and analyze its incidence and risk factors. Methods We retrieved from PubMed, Embase, The Cochrane Library, Web of Science, Clinical Trails, CNKI, CBM, Wan Fang Database and VIP to collect research on the effects of COVID-19 on the male sex hormone. Our literature search was conducted until April 2022, and two investigators independently screened articles based on inclusion and exclusion criteria. In strict accordance with the inclusion and exclusion criteria, two researchers independently screened the literature and comprehensively analyzed 8 cohort studies on the impact of COVID-19 on male sex hormone. And We used RevMan5.4.1 and Stata15.0 for statistical analysis. Finally, there were eight cohort studies on the effects of COVID-19 on male sex hormones. Results T(RR = − 3.94; 95% CI − 6.22, − 1.66; P = 0.0007), testosterone in the COVID-19 group decreased by 3.94 nmol/L compared with the control group, and the difference was statistically significant. LH (RR = 0.85; 95% CI − 0.26, 1.96; P = 0.13), the LH in COVID-19 group was 0.85 mlU/ml higher than that in control group, but the difference was not statistically significant. FSH (RR = 0.25; 95% CI − 0.72, 1.23; P = 0.61), the FSH of COVID-19 group was 0.25 mlU/ml higher than that of the control group, but the difference was not statistically significant. PRL (RR = 2.42; 95% CI 0.52, 4.31; P = 0.01), the PRL in the COVID-19 group was 2.42 ng/ml higher than that in the control group, and the difference was statistically significant. E2(RR = 11.88; 95% CI 9.90, 13.86; P

Objective: The effect of hypolipidemic drugs on male erectile function is still controversial. This Mendelian randomization (MR) study aimed to explore the potential impact of lipid-lowering drug targets on ED. Methods: We collected seven genetic variants encoding lipid-lowering drug targets (LDLR, HMGCR, NPC1L1, PCSK9, APOB, APOC3 and LPL) from published genome-wide association study (GWAS) statistics, and performed drug target MR analysis. The risk of ED was defined as the primary outcome, sex hormone levels and other diseases as the secondary outcomes. Mediation analyses were performed to explore potential mediating factors. Results: The results showed that LDLR, LPL agonists and APOC3 inhibitors were significantly associated with a reduced risk of ED occurrence. APOB inhibitors were associated with an increased risk of ED occurrence. In terms of sex hormone levels, LDLR and LPL agonists were significantly associated with increased TT levels, and HMGCR was associated with decreased TT and BT levels significantly. In terms of male-related disease, MR results showed that LDLR agonists and PCSK9 inhibitors were significantly associated with an elevated risk of PH; HMGCR, NPC1L1 inhibitors were associated with a reduced risk of PCa; and LDLR agonists were significantly associated with a reduced risk of AS and MI; in addition, HMGCR inhibitors were associated with a reduced risk of PCa. Conclusion: After performing drug-targeted MR analysis, we found that that there was a causal relationship between lipid-lowering drug targets and ED. APOC3, APOB, LDLR and LPL may be new candidate drug targets for the treatment of ED. [ABSTRACT FROM AUTHOR]

Sex hormones play a pivotal role in modulating various physiological processes, with emerging evidence underscoring their influence on cancer progression and treatment outcomes. This review delves into the intricate relationship between sex hormones and cancer, elucidating the underlying biological mechanisms and their clinical implications. We explore the multifaceted roles of estrogen, androgens, and progesterone, highlighting their respective influence on specific cancers such as breast, ovarian, endometrial, and prostate. Special attention is given to estrogen receptor-positive (ER+) and estrogen receptornegative (ER-) tumors, androgen receptor signaling, and the dual role of progesterone in both promoting and inhibiting cancer progression. Clinical observations reveal varied treatment responses contingent upon hormonal levels, with certain therapies like tamoxifen, aromatase inhibitors, and antiandrogens demonstrating notable success. However, disparities in treatment outcomes between males and females in hormone-sensitive cancers necessitate further exploration. Therapeutically, the utilization of hormone replacement therapy (HRT) during cancer treatments presents both potential risks and benefits. The promise of personalized therapies, tailored to an individual's hormonal profile, offers a novel approach to optimizing therapeutic outcomes. Concurrently, the burgeoning exploration of new drugs and interventions targeting hormonal pathways heralds a future of more effective and precise treatments for hormone-sensitive cancers. This review underscores the pressing need for a deeper understanding of sex hormones in cancer therapy and the ensuing implications for future therapeutic innovations. [ABSTRACT FROM AUTHOR]

This article provides information on the management of hepatocellular adenomas (HCAs) in different populations, specifically focusing on polycystic ovary syndrome (PCOS), exogenous testosterone use, and transgender women. HCAs are benign liver tumors that are more commonly seen in women and are associated with hormonal factors. The article emphasizes the need for clinical management guidelines in these populations and suggests strategies such as discontinuing contraceptive use, weight loss, and surgical resection. It also highlights the increased risk of malignant transformation in men and transgender women with HCAs. The text discusses the importance of weight management for overweight/obese patients, including those undergoing gender-affirming hormone therapy, and addresses the management of endometrial hyperplasia in postmenopausal women. The article emphasizes the need for further research on the natural history of HCAs in different populations and suggests tailored management approaches based on hormone-related risks and the use of exogenous hormones and hormone-modifying therapies. [Extracted from the article]

This study investigates the role of lysosomal acid lipase (LIPA) in sex hormone regulation and gonadal development in Macrobrachium nipponense. The full-length Mn-LIPA cDNA was cloned, and its expression patterns were analyzed using quantitative real-time PCR (qPCR) in various tissues and developmental stages. Higher expression levels were observed in the hepatopancreas, cerebral ganglion, and testes, indicating the potential involvement of Mn-LIPA in sex differentiation and gonadal development. In situ hybridization experiments revealed strong Mn-LIPA signaling in the spermatheca and hepatopancreas, suggesting their potential role in steroid synthesis (such as cholesterol, fatty acids, cholesteryl ester, and triglycerides) and sperm maturation. Increased expression levels of male-specific genes, such as insulin-like androgenic gland hormone (IAG), sperm gelatinase (SG), and mab-3-related transcription factor (Dmrt11E), were observed after dsMn-LIPA (double-stranded LIPA) injection, and significant inhibition of sperm development and maturation was observed histologically. Additionally, the relationship between Mn-LIPA and sex-related genes (IAG, SG, and Dmrt11E) and hormones (17β-estradiol and 17α-methyltestosterone) was explored by administering sex hormones to male prawns, indicating that Mn-LIPA does not directly control the production of sex hormones but rather utilizes the property of hydrolyzing triglycerides and cholesterol to provide energy while influencing the synthesis and secretion of self-sex hormones. These findings provide valuable insights into the function of Mn-LIPA in M. nipponense and its potential implications for understanding sex differentiation and gonadal development in crustaceans. It provides an important theoretical basis for the realization of a monosex culture of M. nipponense. [ABSTRACT FROM AUTHOR]