Transcriptome analysis elucidates mating affects the expression of intra-/extra-ovarian factors, thereby influencing ovarian development in the mud crab Scylla paramamosain.

Prior to the pubertal molt and mating, the ovarian development of the mud crab Scylla paramamosain was primarily at stage II. However, immediately after mating, female crabs initiate vitellogenesis, and their ovaries quickly develop. The aim of this study was to identify differentially expressed genes associated with ovarian development in the mud crab before and after mating, in order to elucidate the influence of mating on ovarian development using comparative transcriptomics. The KEGG pathway analysis results indicated that ribosome and ribosome-related pathways were highly associated with ovarian development at stage II across both transcriptomes, likely to support the subsequent vitellogenesis by providing the necessary materials. Additionally, the neurodegeneration, MAPK, cAMP and PLD pathways were active in regulating oogonia differentiation, oocyte proliferation and vitellogenesis after mating. Meanwhile, certain intra-ovarian factors, such as the cell cycle-related genes cyclin B and APC, the forkhead box family genes Foxl2 and slp1, the SOX family gene SOX5-like, the hormone-related genes SULT1E1 and Eip74EF-like, the growth factor-related genes VEGFD-like and CUBE1-like, as well as HPS10 and tra1-like, have essential functions in regulating ovarian development after mating. Furthermore, the receptors of extra-ovarian hormones, such as RPCHR, HR4, and ILR1, as well as the neurotransmitter receptor 5-HTR4, were involved in ovarian development. It is believed that ovarian development is controlled by the coordinated action of both intrinsic and extrinsic endocrine factors, and these factors are influenced by mating. Finally, the analysis of epigenic modification-related genes, transcription factors, and target genes revealed the regulation of gene expression. Our study indicated that, those genes work in a coordinated manner to regulate the complex processes of follicle cell development, oogonia differentiation, oocyte proliferation, and vitellogenesis during ovarian development.

Targeting Hypertension: A Review on Pathophysiological Factors and Treatment Strategies.

Hypertension is one of the primary causes of cardiovascular diseases and death, with a higher prevalence in low- and middle-income countries. The pathophysiology of hypertension remains complex, with 2% to 5% of patients having underlying renal or adrenal disorders. The rest are referred to as essential hypertension, with derangements in various physiological mechanisms potentially contributing to the development of essential hypertension. Hypertension elevates the risk of cardiovascular disease (CVD) events (coronary heart disease, heart failure, and stroke) and mortality. First-line therapy for hypertension is lifestyle change, which includes weight loss, a balanced diet that includes low salt and high potassium intake, physical exercise, and limitation or elimination of alcohol use. Blood pressure-lowering effects of individual lifestyle components are partially additive, enhancing the efficacy of pharmaceutical treatment. The choice to begin antihypertensive medication should be based on the level of blood pressure and the existence of a high atherosclerotic CVD risk. First-line hypertension treatment includes a thiazide or thiazide-like diuretic, an angiotensin-converting enzyme inhibitor or angiotensin receptor blocker, and a calcium channel blocker. Addressing hypertension will require continued efforts to improve access to diagnosis, treatment, and lifestyle interventions.

The Biology of Chronic Pain and Its Implications for Pain Neuroscience Education: State of the Art.

Pain is an individualized experience for the person suffering from chronic pain. Significant strides have been made in the last few decades in understanding various biological changes that coincide with chronic pain. This state-of-the-art overview looks at the current evidence related to the biology of chronic pain and the implications these findings have on the delivery of pain neuroscience education (PNE). The paper summarizes the various (epi)genetic, neural, endocrine, and immune factors discovered and explored in the scientific literature concerning chronic pain. Each of these biological factors has various implications for the content and delivery of PNE. We discuss the future directions these biological factors have for the clinical implementation of PNE by linking the importance of behavior change, optimizing the learning environment, and using an individualized multimodal treatment approach with PNE. In addition, future directions for research of PNE based on these biological factors are provided with importance placed on individualized patient-centered care and how PNE can be used with traditional modes of care and growing trends with other care methods. PNE was originally and continues to be rooted in understanding chronic pain biology and how that understanding can improve patient care and outcomes.

New Insights into the Mutual Promotion of Rosacea, Anxiety, and Depression from Neuroendocrine Immune Aspects.

Rosacea is a common chronic inflammatory skin disease with a complex etiology and undefined pathogenesis, and there is still a lack of targeted clinical treatment. Patients with rosacea are at a higher risk of anxiety and depression compared to the healthy population. Compared to skin conditions such as acne and psoriasis, rosacea has been much less studied in relation to multiple-etiology psychiatric disorders such as anxiety and depression. In contrast to the mainstream belief that the causal association between rosacea and psychiatric disorders is that rosacea increases the psychological burden of patients and thus triggers psychiatric disorders simply by altering their facial appearance, this review outlines the possible common mechanisms between rosacea and anxiety and depression disorders, starting from the pathophysiological mechanisms of transient receptor potential family cation channels, HPA axis, and Th1/Th17 cell polarization. It envisages the possibility of the neuroendocrine-immune interplay between rosacea and anxiety and depression, and new ideas on the complex causal relationship between rosacea and psychiatric disorders, offering more orientations to open up new therapeutic approaches for rosacea.

The epidemiology of obesity in reproduction.

Over the last decades, overweight and obesity rates have been rising exponentially and have now reached epidemic proportions. These are significantly higher in women than men, and indeed, data from 2022 show rates varying from the lowest (12%) in the South East Asian Region to the highest (82.8%) in the Western Pacific Region. This rise is mirrored by the increasing health cost of obesity and overweight. Recent estimates put the percentage of medical spending in various countries to vary from 3 to 21%. Obesity is associated with noncommunicable diseases, such as hypertension, diabetes mellitus, and cardiovascular disorders. It is associated with 13 cancers, among which are breast, endometrial, and ovarian. The reproductive consequences of obesity are variable and include but not exclusively menstrual disorders; fertility difficulties; recurrent miscarriages; gestational diabetes, hypertension, and pre-eclampsia; postpartum hemorrhage; and fetal macrosomia. Various factors are responsible for these increasing rates (which are more marked in middle- and low-income countries). These include genetic, epigenetic, environmental, physiologic, cultural, political, and socioeconomic factors that interact in most cases, making it challenging to develop effective interventions on both a local and global scale. In this article, we review the epidemiology of obesity and the factors which modify rates, as well as an overview of the reproductive consequences of obesity. We discuss approaches to reduce the rates and that these should be at three levels: individual, national, and international.

Endocrine and metabolic factors and the risk of idiopathic pulmonary fibrosis: a Mendelian randomization study.

Background: Previous observational studies have investigated the association between endocrine and metabolic factors and idiopathic pulmonary fibrosis (IPF), yet have produced inconsistent results. Therefore, it is imperative to employ the Mendelian randomization (MR) analysis method to conduct a more comprehensive investigation into the impact of endocrine and metabolic factors on IPF. Methods: The instrumental variables (IVs) for 53 endocrine and metabolic factors were sourced from publicly accessible genome-wide association study (GWAS) databases, with GWAS summary statistics pertaining to IPF employed as the dependent variables. Causal inference analysis encompassed the utilization of three methods: inverse-variance weighted (IVW), weighted median (WM), and MR-Egger. Sensitivity analysis incorporated the implementation of MR-PRESSO and leave-one-out techniques to identify potential pleiotropy and outliers. The presence of horizontal pleiotropy and heterogeneity was evaluated through the MR-Egger intercept and Cochran's Q statistic, respectively. Results: The IVW method results reveal correlations between 11 traits and IPF. After correcting for multiple comparisons, seven traits remain statistically significant. These factors include: "Weight" (OR= 1.44; 95% CI: 1.16, 1.78; P=8.71×10-4), "Body mass index (BMI)" (OR= 1.35; 95% CI: 1.13, 1.62; P=1×10-3), "Whole body fat mass" (OR= 1.40; 95% CI: 1.14, 1.74; P=1.72×10-3), "Waist circumference (WC)" (OR= 1.54; 95% CI: 1.16, 2.05; P=3.08×10-3), "Trunk fat mass (TFM)" (OR=1.35; 95% CI: 1.10,1.65; P=3.45×10-3), "Body fat percentage (BFP)" (OR= 1.55; 95% CI: 1.15,2.08; P=3.86×10-3), "Apoliprotein B (ApoB)" (OR= 0.78; 95% CI: 0.65,0.93; P=5.47×10-3). Additionally, the sensitivity analysis results confirmed the reliability of the MR results. Conclusion: The present study identified causal relationships between seven traits and IPF. Specifically, ApoB exhibited a negative impact on IPF, while the remaining six factors demonstrated a positive impact. These findings offer novel insights into the underlying etiopathological mechanisms associated with IPF.

Control of (pre)-analytical aspects in immunoassay measurements of metabolic hormones in rodents.

The measurement of circulating hormones by immunoassay remains a cornerstone in preclinical endocrine research. For scientists conducting and interpreting immunoassay measurements of rodent samples, the paramount aim usually is to obtain reliable and meaningful measurement data in order to draw conclusions on biological processes. However, the biological variability between samples is not the only variable affecting the readout of an immunoassay measurement and a considerable amount of unwanted or unintended variability can be quickly introduced during the pre-analytical and analytical phase. This review aims to increase the awareness for the factors 'pre-analytical' and 'analytical' variability particularly in the context of immunoassay measurement of circulating metabolic hormones in rodent samples. In addition, guidance is provided how to gain control over these variables and how to avoid common pitfalls associated with sample collection, processing, storage and measurement. Furthermore, recommendations are given on how to perform a basic validation of novel single and multiplex immunoassays for the measurement of metabolic hormones in rodents. Finally, practical examples from immunoassay measurements of plasma insulin in mice address the factors 'sampling site and inhalation anesthesia' as frequent sources of introducing an unwanted variability during the pre-analytical phase. The knowledge about the influence of both types of variability on the immunoassay measurement of circulating hormones as well as strategies to control these variables are crucial, on the one hand, for planning and realization of metabolic rodent studies and, on the other hand, for the generation and interpretation of meaningful immunoassay data from rodent samples.

Understanding the pathophysiology of depression: From monoamines to the neurogenesis hypothesis model - are we there yet?

A number of factors (biogenic amine deficiency, genetic, environmental, immunologic, endocrine factors and neurogenesis) have been identified as mechanisms which provide unitary explanations for the pathophysiology of depression. Rather than a unitary construct, the combination and linkage of these factors have been implicated in the pathogenesis of depression. That is, environmental stressors and heritable genetic factors acting through immunologic and endocrine responses initiate structural and functional changes in many brain regions, resulting in dysfunctional neurogenesis and neurotransmission which then manifest as a constellation of symptoms which present as depression.

Lung carcinoma progression and survival versus amino- and carboxyl-parathyroid hormone-related protein expression.

PURPOSE: Expression of the carboxyl PTHrP region of parathyroid hormone-related protein (PTHrP) is a positive prognostic indicator in women with lung cancer, but amino PTHrP is a negative indicator in other lung cancer patients. This project investigated whether PTHrP could be expressed as predominantly amino PTHrP or carboxyl PTHrP in individual lung carcinomas. It also assessed domain-specific effects on cancer progression and patient survival. METHODS: PTHrP immunoreactivities were analyzed versus survival in a human lung cancer tissue microarray (TMA). Growth was compared in athymic mice for isogenic lung carcinoma xenografts differing in expression of amino and carboxyl PTHrP domains. RESULTS: In the TMA, 33 of 99 patient tumors expressed only one PTHrP domain, while 54 expressed both. By Cox regression, the hazard ratio for cancer-specific mortality (95% confidence interval) was 2.6 (1.28-5.44) for amino PTHrP (P = 0.008) and 0.6 (0-2.58) for carboxyl PTHrP (P = 0.092). Xenografts of H358 lung adenocarcinoma cells that overexpressed amino PTHrP grew twice as fast as isogenic low PTHrP tumors in athymic mice, but growth of tumors expressing amino plus carboxyl PTHrP was not significantly different than growth of the control tumors. In summary, the presence of amino PTHrP signifies worse prognosis in lung cancer patients. In mouse xenografts, this effect was abrogated if carboxyl PTHrP was also present. CONCLUSION: Amino PTHrP and carboxyl PTHrP can vary independently in different lung carcinomas. Carboxyl PTHrP may temper the stimulatory effect of amino PTHrP on cancer progression.

Endogenous ways to stimulate brown adipose tissue in humans.

Obesity is the result of disequilibrium between energy intake and energy expenditure (EE). Successful long-term weight loss is difficult to achieve with current strategies for the correction of this caloric imbalance. Non-shivering thermogenesis (NST) in brown adipose tissue (BAT) is a possible therapeutic target for the prevention and treatment of obesity and associated metabolic diseases. In recent years, more knowledge about the function and stimulation of bat has been obtained. The sympathetic nervous system (SNS) is currently seen as the main effector for brown fat function. Also, interplay between the thyroid axis and SNS plays an important role in BAT thermogenesis. Almost daily new pathways for the induction of BAT thermogenesis and 'browning' of white adipose tissue (WAT) are identified. Especially the activation of BAT via endogenous pathways has received strong scientific attention. Here we will discuss the relevance of several pathways in activating BAT and their implications for the treatment of obesity. In this review we will focus on the discussion of the most promising endocrine and paracrine pathways to stimulate BAT, by factors and pathways that naturally occur in the human body.

Adverse effects of 4-tert-octylphenol on the production of oxytocin and hCG in pregnant rats.

Endocrine-disrupting chemicals (EDCs) are exogenous substances that alter the structure or function of the endocrine system. 4-Tert-octylphenol (OP) is one of the most representative EDCs and has estrogenic effects. In this study, we examined the effects of ethinyl estradiol (EE) and OP on the pituitary gland, placenta, and uterus of pregnant rats. Expression levels of human chorionic gonadotropin (hCG), oxytocin (OT), and contraction-associated proteins (CAPs) were determined, and uterine contractile activity was measured by uterine contraction assay. EE and OP both increased mRNA expression of OT and hCG in the pituitary gland but not the placenta. Since OT and hCG control uterine contraction, we next examined CAP expression in the uterus. Expression of 15-hydroxyprostaglandin-dehydrogenase (PGDH) was upregulated by OP, whereas expression of other CAPs was unaffected. To clarify the effect of OP on uterine contraction in pregnant rats, uterine contraction assay was performed. The 17ß-Estradiol (E2) did not affect contraction of primary uterine cells harvested from pregnant rats in a 3D collagen gel model. However, OP showed different effects from E2 by significantly reducing contraction activity. In summary, we demonstrated that OP interferes with regulation of OT and hCG in the pituitary gland as well as PGDH in the uterus, thereby reducing uterine contraction activity. This result differs from the action of endogenous E2. Collectively, these findings suggest that exposure to EDCs such as OP during pregnancycan reduce uterine contractile ability, which may result in contraction-associated adverse effects such as metratonia, bradytocia, and uterine leiomyomata.

Lead exposure is a risk for worsening bone mineral density in middle-aged male workers.

OBJECTIVE: Lead exposure linked to osteoporosis in women. However, there is no direct evidence whether lead exposure has effects on bone metabolism in middle-aged male subjects. Therefore, the present study investigated the relationship between bone mineral densitometry measurements, bone markers, endocrine hormones and blood lead levels. MATERIAL AND METHODS: The present study included lead exposure patients (n: 30) and control subjects (n: 32). We recorded information on patient demographics and risk factors of osteoporosis. Blood lead levels were evaluated using Varian AA 240Z atomic absorption spectrophotometry. Bone mineral density measurements were measured using dual-energy X-ray absorptiometry. RESULTS: Each lumbar T and Z scores in the lead exposure group were lower than the control group. There were no significant differences in femur neck and femur total T and Z scores between two groups. Blood lead levels were also negatively correlated with lumbar 2-4 T score, total lumbar T score, lumbar 2-4 Z score and total lumbar Z score. Urinary hydroxyproline and urinary deoxypyridinoline levels in the lead exposure group were significantly higher compared to controls. Blood lead levels were strong, positively correlated with urinary deoxypyridinoline. Endocrine hormone levels and 1,25-dihydroxy-vitamin D3 levels were comparable between lead exposure and control group. CONCLUSION: Lead exposure in male workers is an important factor for deterioration in bone mineral density. We should be screening blood lead levels and history of lead exposure in male osteoporosis.