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However, more studies are needed to map the differential epigenetic effects of ER in different adipocyte subtypes, including those in subcutaneous and visceral adipose tissues. We here review recent discoveries of ER-mediated transcriptional and epigenetic regulation in adipocytes, which may explain sexual dimorphisms in body fat distribution and obesity-related disease risk.Previous studies have revealed that melatonin could play a role in anti-osteoporosis and promoting osteogenesis. However, the effects of melatonin treatment on osteoporotic bone defect and the mechanism underlying the effects of melatonin on angiogenesis are still unclear. Our study was aimed to investigate the potential effects of melatonin on angiogenesis and osteoporotic bone defect. Bone marrow mesenchymal stem cells (BMSCs) were isolated from the femur and tibia of rats. The BMSC osteogenic ability was assessed using alkaline phosphatase (ALP) staining, alizarin red S staining, qRT-PCR, western blot, and immunofluorescence. BMSC-mediated angiogenic potentials were determined using qRT-PCR, western blot, enzyme-linked immunosorbent assay, immunofluorescence, scratch wound assay, transwell migration assay, and tube formation assay. Ovariectomized (OVX) rats with tibia defect were used to establish an osteoporotic bone defect model and then treated with melatonin. The effects of melatonin treatment on osteogenesis-related markers (VEGF and CD31) in the melatonin-treated OVX rats. Then, it showed that melatonin treatment also increased the bone strength of tibia defect in OVX rats, with increased ultimate load and stiffness, as performed by three-point bending test. In conclusion, our study demonstrated that melatonin could promote BMSC-mediated angiogenesis and promote osteogenesis-angiogenesis coupling. We further found that melatonin could accelerate osteoporotic bone repair by promoting osteogenesis and angiogenesis in OVX rats. These findings may provide evidence for the potential application of melatonin in osteoporotic bone defect.

To reveal the characteristics of vaginal microbiota in premature ovarian insufficiency (POI) patients and their relationship with ovarian function.

In this case-control study, the vaginal bacterial composition of 30 POI patients and 26 healthy women of comparable age was assessed by 16S rRNA gene sequencing targeting the V3-V4 hypervariable regions. The metabolic functions of vaginal microflora were preliminarily predicted through the PICRUSt2 analysis. Redundancy analysis and Spearman's correlation analyzed the relationships between vaginal microbiota and ovarian function indicators.

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were significantly increased in POI patients. Their increments were significantly negatively correlated with anti-müllerian hormone (AMH) and inhibin B, and positively correlated with follicle-stimulating hormone (FSH) and luteinizing hormone (LH). While

was significantly decreased in POI patients. Its relative abundance was significantly positively correlated with AMH and negatively correlated with FSH andetween vaginal microbiota and ovarian function.

40) patients were also identified. These findings may provide new evidence for the relationship between vaginal microbiota and ovarian function.Continuous and intermittent intraoperative nerve monitoring (IONM) has become an important asset for endocrine surgeons over the past few decades. The ability to determine neurophysiologic integrity of the recurrent laryngeal nerve (RLN) and external branch of the superior laryngeal nerve (EBSLN) on top of identification and meticulous dissection of the nerve in the surgical field, has allowed for advances in technology and improved outcomes when it comes to prevention of vocal fold immobility. This article aims to compare in review continuous and intermittent nerve monitoring (CIONM, IIONM), as well as review the current paradigms of their use. Entinostat concentration This article will also discuss the future of intraoperative nerve monitoring technologies in scarless thyroid surgery and percutaneous approaches to thyroid pathology in form of radiofrequency ablation (RFA).

Triglyceride-glucose (TyG) index is a reliable and specific biomarker for insulin resistance and is associated with renal dysfunction. The present study sought to explore the relationship between TyG index and the incidence of contrast-induced nephropathy (CIN) in non-ST elevation acute coronary syndrome (NSTE-ACS) patients implanted with drug-eluting stents (DESs).

A total of 1108 participants were recruited to the study and assigned to two groups based on occurrence of CIN. TyG index was calculated as ln [fasting triglycerides (mg/dL) × fasting blood glucose (mg/dL)/2]. Baseline characteristics and incidence of CIN were compared between the two groups. Logistic regression analysis was performed to evaluate the relationship between TyG index and CIN.

The results showed that 167 participants (15.1%) developed CIN. Subjects in the CIN group had a significantly higher TyG index compared with subjects in the non-CIN group (8.9 ± 0.7 vs. 9.3 ± 0.7, P<0.001). TyG index was significantly correlated with intly and independently associated with incidence of CIN in NSTE-ACS patients firstly implanted with DESs. Routine preoperative assessment of TyG index can alleviate CIN and TyG index provides a potential target for intervention in prevention of CIN.

The effects of levothyroxine (LT4)/liothyronine (LT3) combination therapy on quality of life (QoL) in hypothyroid patients former on LT4 monotherapy have been disappointing. We therefore wanted to test the effects of LT3 monotherapy on QoL in hypothyroid patients with residual symptoms despite thyroid stimulating hormone (TSH) values within the reference range.

Female hypothyroid patients with residual symptoms on LT4 monotherapy or combination LT4/LT3 therapy received LT3 and LT4 monotherapy, respectively for 12 weeks in a non-blinded randomized crossover study.

Fifty-nine patients aged 18-65 years were included. QoL was assessed using one disease-specific questionnaire (ThyPRO) and two generic questionnaires (Fatigue Questionnaire and SF-36) at baseline and at the end of the two treatment periods. Clinical indices of cardiovascular health (resting heart rate and blood pressure), as well as thyroid tests, were assessed at baseline and at the end of the two treatment periods.

After 12 weeks of LT3 tre to only one on LT4.

LT3 treatment improved QoL in women with residual hypothyroid symptoms on LT4 monotherapy or LT4/LT3 combination therapy. Short-term LT3 treatment did not induce biochemical or clinical hyperthyroidism, and no cardiovascular adverse effects were recorded. Further studies are needed to assess the long-term safety and efficacy of LT3 monotherapy.

ClinicalTrials.gov, identifier NCT03627611.

ClinicalTrials.gov, identifier NCT03627611.Acromegaly is a rare condition typically caused by benign pituitary adenomas, resulting in excessive production of growth hormone. Clinical manifestations of acromegaly are diverse, varying from the overgrowth of body tissue to cardiovascular, metabolic, and osteoarticular disorders. Symptoms may emerge slowly, overlapping with other diseases and often involve many different healthcare specialists. In the last decade, efforts to provide an accurate and timely diagnosis of acromegaly have improved disease management and clinical experience. Despite this progress, marked differences in the diagnosis, treatment, and management of acromegaly exist from country-to-country. To address these inconsistencies in the region comprising Central and Eastern Europe, Israel, and Kazakhstan, a panel of acromegaly experts from 13 of these countries was convened. Acromegaly experts from each country provided available information on the approaches from their country, including regional treatment centers and multidisciplinary teams, treatment access, reimbursement and availability, and physician education, disease awareness, and patient advocacy. Across several areas of acromegaly management, divergent approaches were identified and discussed, including the provision of multidisciplinary care, approved and available treatments, and disease awareness programs. These were recognized as areas of potential improvement in the management of acromegaly, in addition to participation in national and regional acromegaly registries. Further experience exchange will facilitate the identification of specific strategies that can be adapted in each country, and widespread participation in acromegaly registries will enable their evaluation. It is anticipated that this approach will support the optimization of acromegaly patient care across this region.Sex steroid hormones have been implicated as disease modifiers in the neurodegenerative disorder amyotrophic lateral sclerosis (ALS). Androgens, signalling via the androgen receptor (AR), predominate in males, and have widespread actions in the periphery and the central nervous system (CNS). AR translocates to the cell nucleus when activated upon binding androgens, whereby it regulates transcription of target genes via the classical genomic signalling pathway. We previously reported that AR protein is decreased in the lumbar spinal cord tissue of symptomatic male SOD1G93A mice. Here, we further explored the changes in AR within motor neurons (MN) of the CNS, assessing their nuclear AR content and propensity to degenerate by endstage disease in male SOD1G93A mice. We observed that almost all motor neuron populations had undergone significant loss in nuclear AR in SOD1G93A mice. Interestingly, loss of nuclear AR was evident in lumbar spinal MNs as early as the pre-symptomatic age of 60 days. Several MN populations with high AR content were identified which did not degenerate in SOD1G93A mice. These included the brainstem ambiguus and vagus nuclei, and the sexually dimorphic spinal MNs cremaster, dorsolateral nucleus (DLN) and spinal nucleus of bulbocavernosus (SNB). In conclusion, we demonstrate that AR loss directly associates with MN vulnerability and disease progression in the SOD1G93A mouse model of ALS.

Although within the normal range, thyroid stimulating hormone (TSH) levels are associated with cardio-metabolic disorders and have an effect on the cardiovascular system. The aim of our study was to assess the prognostic value of normal TSH on long-term mortality in patients with ST-segment elevation myocardial infarction (STEMI).

Consecutive STEMI patients who had a TSH level within the normal range (0.55-4.78 μIU/ml) were enrolled from November 2013 to December 2018. Patients were stratified into three groups depending on the tertile of TSH level, and all-cause mortality and cardiac death were compared. TSH concentrations associated with risk of all-cause mortality were evaluated in a continuous scale (restricted cubic splines) and the Cox proportional hazards regression model.

A total of 1,203 patients with STEMI were eligible for analysis. During a median follow-up of 39 months, patients in the 3rd tertile group had higher all-cause mortality (20.1% vs. 12.2% and 14.3%, p = 0.006) and cardiac death (15.4% vs. 7.7% and 12.3%, p = 0.001) as compared to the 1st and 2nd tertile groups. The Cox proportional hazards model showed that TSH was an independent predictor on long-term all-cause mortality (HR 1.248, 95% CI 1.046-1.490, p = 0.014). However, subgroup analysis indicated that TSH (HR 1.313, 95% CI 1.063-1.623, p = 0.012) was only significantly associated with long-term all-cause mortality in the patients without emergency reperfusion therapy. Restricted cubic spline analyses showed a linear relationship between TSH concentrations and all-cause mortality (P for non-linearity = 0.659).

A Higher TSH level - even in a normal range is associated with long-term mortality in patients with STEMI, proposing an additional indication to identify STEMI patients with poor prognosis.

A Higher TSH level - even in a normal range is associated with long-term mortality in patients with STEMI, proposing an additional indication to identify STEMI patients with poor prognosis.