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The hypothalamic–pituitary axis is central to the functioning of the neuroendocrine system and essential for regulating physiological and behavioral homeostasis and coordinating fundamental body functions. The expanding line of evidence shows the indispensable role of the microRNA pathway in regulating the gene expression profile in the developing and adult hypothalamus and pituitary gland. Experiments provoking a depletion of miRNA maturation in the context of the hypothalamic–pituitary axis brought into focus a prominent involvement of miRNAs in neuroendocrine functions. There are also a few individual miRNAs and miRNA families that have been studied in depth revealing their crucial role in mediating the regulation of fundamental processes such as temporal precision of puberty timing, hormone production, fertility and reproduction capacity, and energy balance. Among these miRNAs, miR‐7 was shown to be hypothalamus‐enriched and the top one highly expressed in the pituitary gland, where it has a profound impact on gene expression regulation. Here, we review miRNA profiles, knockout phenotypes, and miRNA interaction (targets) in the hypothalamic–pituitary axis that advance our understanding of the roles of miRNAs in mammalian neurosecretion and related physiology. [ABSTRACT FROM AUTHOR]

Emotion suppression may be linked to poor health outcomes through elevated stress-related physiology. The current meta-analyses investigate the magnitude of the association between suppression and physiological responses to active psychological stress tasks administered in the laboratory. Relevant articles were identified through Medline, PsychINFO, PubMed, and ProQuest. Studies were eligible if they (a) used a sample of healthy, human subjects; (b) assessed physiology during a resting baseline and active psychological stress task; and (c) measured self-report or experimentally manipulated suppression. Twenty-four studies were identified and grouped within two separate random effects meta-analyses based on study methodology, namely, manipulated suppression (k = 12) and/or self-report (k = 14). Experimentally manipulated suppression was associated with greater physiological stress reactivity compared to controls (Hg = 0.20, 95% CI [0.08, 0.33]), primarily driven by cardiac, hemodynamic, and neuroendocrine parameters. Self-report trait suppression was not associated with overall physiological stress reactivity but was associated with greater neuroendocrine reactivity (r = 0.08, 95% CI [0.01, 0.14]). Significant moderator variables were identified (i.e., type/duration of stress task, nature of control instructions, type of physiology, and gender). This review suggests that suppression may exacerbate stress-induced physiological arousal; however, this may differ based upon the chosen methodological assessment of suppression. [ABSTRACT FROM AUTHOR]

Background: Esophageal neuroendocrine carcinomas (NECs) are extremely rare. Published information on their clinical features, pathological findings, and prognosis is lacking. The optimal treatment for esophageal NECs has not yet been determined because they appear extremely malignant histologically and have a poor prognosis. We here report on a patient with an esophageal NEC who was successfully treated with multidisciplinary therapies. Case presentation: The patient, a 47-year-old man, was admitted to our hospital with dysphagia and weight loss and an ECOG performance status of 3–4. Upper endoscopy showed a large circumferential neoplasm at the esophagogastric junction. Computed tomography showed lymph node metastases around the left gastric artery. Echocardiography raised a suspicion of invasion of the left atrium. Histopathological examination of biopsy tissue revealed diffuse proliferation of small atypical cells resembling naked nuclei with extensive necrosis and degeneration. The cells showed positive staining for CD56, chromogranin A, and synaptophysin on immunohistochemical analysis. Ki67 was positive in over 90% of cells. He was diagnosed with an esophageal NEC that had infiltrated the left atrium; his cancer was therefore inoperable. Because of his poor overall condition, palliative radiotherapy (30 Gy in 15 fractions) was administered, accompanied by nutritional management. This was followed by four courses of chemotherapy with carboplatin plus etoposide, after which the primary tumor and locoregional lymph node metastases were found to have shrunk. Thoracoscopic- and laparoscopic-assisted McKeown esophagectomy were performed. The postoperative pathological diagnosis was NEC pT3pN0M0 Stage II. The patient had a good postoperative course and received two courses of postoperative adjuvant chemotherapy (carboplatin plus etoposide). Currently, 3 years after commencing treatment, there is no evidence of recurrence. Conclusions: As mentioned above, there is no established treatment regime for esophageal NEC, and the benefits of conversion surgery are unknown. Our patient achieved long-term recurrence-free survival after radiation therapy, chemotherapy, and surgery for an esophageal NEC with left atrial invasion and multiple lymph node metastases. Conversion surgery for esophageal NECs that respond to chemotherapy may contribute to long-term survival. [ABSTRACT FROM AUTHOR]

Japanese eel (Anguilla japonica) is a commercially important fish species in Asia. Understanding factors like photoperiod, temperature, and lunar cycles is crucial for successful aquaculture and managing its reproduction. Melatonin and dopamine (DA) are essential for regulating reproduction in vertebrates, including fish. This study investigated the effects of melatonin and DA on the reproductive system of mature male Japanese eels to better understand reproductive regulation in fish. To clarify the effects of these hormones on sexual maturation in eels, a critical stage in the reproductive process, sexual maturation was induced by injecting human chorionic gonadotropin, which stimulates the production of sex hormones. To check the effect of melatonin and DA on sexual maturation, DA, melatonin, and DA + domperidone were intraperitoneally injected into fish from each group (six per treatment) at a dose of 1 mg/kg body weight. The fish were then examined using quantitative RT‐PCR by comparing the messenger RNA level of reproduction‐related genes (gonadotropin releasing hormone 1; gnrh1, gonadotropin releasing hormone 2; gnrh2, follicle stimulating hormone; fshβ, luteinizing hormone; lhβ and DA receptor 2b; d2b), involved in the gonadotropic axis in eels, to those that received a control injection. The results indicate significant differences in the expression levels of gnrh1, gnrh2 and d2b in the brain and d2b, fshβ, lhβ in the pituitary at different stages of sexual maturation. Melatonin appears to enhance the production of sex gonadotropins, whereas DA inhibits them. These findings suggest an interaction between melatonin and DA in regulating reproduction in Japanese eels. Research Highlights: Melatonin enhances gonadotropin genes, while dopamine inhibits it in Japanese eels, revealing a dynamic interplay in their reproductive regulation [ABSTRACT FROM AUTHOR]

Endocrine-disrupting chemicals (EDCs) may mimic the endogenous neuroendocrine and endocrine messengers and interfere with developmental, reproductive, immune, metabolic and other physiological functions. Modulation of basal metabolic rate, energy metabolism, food intake and engorgement by endocrine disruptors may lead to loss of metabolic equilibrium. EDC-induced loss of metabolic homeostasis and obesity gave rise to the concept of metabolic-disrupting chemicals (MDC) and environmental obesogens. Elevated oxidative stress, alterations in the circadian clock, and energy-sensing homeostasis are some of the major pathophysiological conditions implicated in promoting metabolic disruption. Reportedly, fish are the most vulnerable candidate due to their direct exposure to metabolic disruptors in aquatic habitats. Though limited, studies conducted using piscine models have helped to identify MDCs in the aquatic environment. Notably, the molecular mechanisms through which MDCs can negatively influence the metabolism of hormones, epigenetic alteration, gut dysbiosis, and changes in endocrine and metabolic receptor expression and functions have recently gained considerable attention. In this review, we provide an update on the impact of MDCs on the initiators, cellular mediators, and hormone receptors related to the maintenance of metabolic homeostasis, with particular emphasis on fish models. [ABSTRACT FROM AUTHOR]

The main neuroendocrine pathways of induction of reproductive behavior in fish are elucidated. 17α, 20β-dihydroxy-4-pregnen-3-one (17,20β-DHP), an oocyte maturation-inducing hormone, was found to act as a pheromone to induce male reproductive behavior. 17α, 20β-DHP-sulfate (17,20β-DHP-S), a derivative of 17,20β-DHP, was also identified as a later-acting pheromone. In addition, prostaglandin F2 alpha (PGF2α), which is synthesized during female ovulation, has been shown to also act as a pheromone, inducing the final ovipositioninducing behavior to make fertilization successful. It appears that these molecular events are initiated by stimuli from the brain. Numerous neuropeptides have been discovered that promote the initiation of reproductive behavior. Recently, with the proliferation of genome editing technology, a detailed analysis of the molecules involved in these pathways is underway. Analysis of gene knockout in zebrafish and medaka is actively underway. On the other hand, many research reports have shown that the induction pathways of male reproductive behavior are adversely affected by chemical substances. Knowledge of the adverse effects of chemical substances is not only useful as information to prevent their mixing from the viewpoint of protecting the natural environment and as a point of caution in fish farming, but also provides clues for elucidating the pathways of reproductive behavior induction. The elucidation of the pathways of reproductive behavior induction is also important from the point of view of breeding technology for fish farming and biodiversity conservation. In this review, we summarize recent research on the pathways of male reproductive behavior induction in fish and the possibility of developing new aquaculture techniques depending on the results. [ABSTRACT FROM AUTHOR]

This review highlights the recent developments regarding neuroendocrine mechanisms controlling teleost reproduction. In teleosts, the pituitary gland receives major neuronal innervations from Gnrh neurons as well as minor innervations from small population of neurons that will secrete neurotransmitters and/or neuropeptides. The diversity of Kiss/Kissr system in various teleost species and their actions in the context of HPG axis and reproduction has been extensively covered. In teleost model systems, zebrafish and medaka, mutant lines for key components of the HPG axis have been generated through targeted mutagenesis but surprisingly most of the mutants developed normally without major defects in reproduction; these mutant phenotypes are described. In the last decade, complex role of diverse neuropeptides in teleost reproduction is being revealed. A brief overview about the reproductive functions of neuropeptides is presented. Finally, the effects of environmental factors namely photoperiodism and temperature on the functions of HPG axis is summarised. [ABSTRACT FROM AUTHOR]

Reproduction is one of the most crucial physiological processes for the continuation of the generation of any species. Teleost are one of the most divergent aquatic species. The reproductive neuro-endocrine regulatory studies are limited to only few species. Neuroendocrine regulation is a finely tuned complex mechanistic pathways, involving mainly hypothalamic-pituitary-gonad (HPG) axis. Within the HPG axis, gonadotropin-releasing hormone (GnRH) modulates the synthesis and release of pituitary gonadotropins, which act on the gonads to stimulate steroidogenesis and gametogenesis. Very recently, several novel neuropeptides, associated with reproductive regulation, have been identified. Spexin (SPX), a novel neuropeptide coevolved with the galanin/kisspeptin family, has been identified as a regulator of the species-specific reproductive processes in teleost. Pituitary adenylate cyclase-activating polypeptide (PACAP) is another novel member of the secretin-glucagon peptide family that functions as a hypophysiotropic factor involved in regulating pituitary hormone secretion in fish. These two emerging neuropeptides have pleiotropic functions, but information regarding their exact roles in fish reproduction is very limited. An updated overview of the mechanistic reproductive functions of these two new neuropeptides are highlighted in this review. [ABSTRACT FROM AUTHOR]

L'obésité de l'enfant et de l'adolescent est une pathologie dont la compréhension a profondément évolué depuis quelques années grâce à l'identification des formes génétiques et à un accroissement exponentiel des connaissances en biologie. Le tissu adipeux est un organe endocrine en dialogue permanent avec les autres organes dont les centres de régulation de l'appétit cérébraux et la signalisation neuroendocrine du tube digestif. Face à un enfant ou un adolescent développant une obésité, une analyse rigoureuse de la dynamique de sa pathologie, des éventuelles anomalies et complications cliniques associées est requise. La coopération avec les centres de référence pédiatriques et de recherche en nutrigénomique permettant d'identifier les mutations associées permet de poser dans des cas encore rares mais probablement sous diagnostiqués l'indication de traitement spécifiques efficaces. Récemment un essai randomisé a montré qu'un analogue du Glucagon like peptide 1 (GLP1-R), molécule clé de régulation de l'appétit d'origine intestinale, avait un effet bénéfique majeur dans des obésités polygéniques. Des études sont encore nécessaires pour s'assurer des résultats à long terme et de l'absence de toxicité mais les résultats acquis font d'ores et déjà rediscuter la place de la chirurgie bariatrique. Si la prévention doit rester une priorité, de nombreuses autres molécules et d'autres voies thérapeutiques sont en cours d'investigation dans la plus fréquente des maladies métaboliques et chroniques de l'enfance. Child and adolescent obesity is definitely a pathology the understanding of which has faced dramatic changes in recent years thanks to the identification of the genetic background of some cases and an amazing increase in the knowledge of its biological background. The adipose tissue is an endocrine organ in permanent communication with other ones, including the appetite regulation centres of the brain and the neuroendocrine system of the digestive tract. A precise analysis of the trajectory of weight gain and its associated manifestations such as abnormal physical or developmental features and complications is mandatory while facing a child or adolescent with obesity. A close cooperation with reference centres for childhood obesity and nutrigenomics research units leading to the diagnosis of genetic forms, likely to be underdiagnosed, may allow the use of targeted and efficient drug treatment. A recent double-blind study has shown that a Glucagon like peptide 1 (GLP1) analogue, a key contributor of appetite regulation from intestinal origin, has a major beneficial impact on adolescents with obesity of polygenic origin. Further studies are still required to ensure the long-term effect and the lack of side effects of such a treatment. However, such results already challenge the indication of bariatric surgery. While prevention still must be a priority, many other molecules and therapeutic approaches are underway for the most frequent metabolic and chronic childhood disorder. [ABSTRACT FROM AUTHOR]

Introduction: Previous studies have shown that fetal hypoxia predisposes individuals to develop addictive disorders in adulthood. However, the specific impact of maternal stress, mediated through glucocorticoids and often coexisting with fetal hypoxia, is not yet fully comprehended. Methods: To delineate the potential effects of these pathological factors, we designed models of prenatal severe hypoxia (PSH) in conjunction with maternal stress and prenatal intrauterine ischemia (PII). We assessed the suitability of these models for our research objectives by measuring HIF1α levels and evaluating the glucocorticoid neuroendocrine system. To ascertain nicotine dependence, we employed the conditioned place aversion test and the startle response test. To identify the key factor implicated in nicotine addiction associated with PSH, we employed techniques such as Western blot, immunohistochemistry, and correlational analysis between chrna7 and nr3c1 genes across different brain structures. Results: In adult rats exposed to PSH and PII, we observed increased levels of HIF1α in the hippocampus (HPC). However, the PSH group alone exhibited reduced glucocorticoid receptor levels and disturbed circadian glucocorticoid rhythms. Additionally, they displayed signs of nicotine addiction in the conditioned place aversion and startle response tests. We also observed elevated levels of phosphorylated DARPP-32 protein in the nucleus accumbens (NAc) indicated compromised glutamatergic efferent signaling. Furthermore, there was reduced expression of α7 nAChR, which modulates glutamate release, in the medial prefrontal cortex (PFC) and HPC. Correlation analysis revealed strong associations between chrna7 and nr3c1 expression in both brain structures. Conclusion: Perturbations in the glucocorticoid neuroendocrine system and glucocorticoid-dependent gene expression of chrna7 associated with maternal stress response to hypoxia in prenatal period favor the development of nicotine addiction in adulthood. [ABSTRACT FROM AUTHOR]

Long-term intake of procyanidins has been suggested to reduce the risk of cardiovascular disease, dementia, and sensory function decline associated with aging. However, most of the ingested procyanidins are not absorbed and are excreted in the feces, so the mechanism of their beneficial impact is unknown. Procyanidins are the components of astringency in plant foods and their stimulation appears to be directly transmitted to the central nervous system via sensory nerves. Recent attention has been focused on the taste receptors expressed in the extra-oral gastrointestinal tract may regulate homeostasis via the neuroendocrine system. In this paper, we have reviewed recent findings on the relationship between the astringency of procyanidins and their bioregulatory effects. [ABSTRACT FROM AUTHOR]

Immune nutrition is currently used to enhance fish health by incorporating functional ingredients into aquafeeds. This study aimed to investigate the connections between tryptophan nutrition and the network that regulates the communication pathways between neuroendocrine and immune systems in European seabass (Dicentrarchus labrax). When tryptophan was supplemented in the diet of unstressed fish, it induced changes in the hypothalamic-pituitary-interrenal axis response to stress. Tryptophan-mediated effects were observed in the expression of anti-inflammatory cytokines and glucocorticoid receptors. Tryptophan supplementation decreased pro-opiomelanocortin b-like levels, that are related with adrenocorticotropic hormone and cortisol secretion. When stressed fish fed a tryptophan-supplemented diet were subjected to an inflammatory stimulus, plasma cortisol levels decreased and the expression of genes involved in the neuroendocrine response was altered. Modulatory effects of tryptophan dietary intervention on molecular patterns seem to be mediated by altered patterns in serotonergic activity. [ABSTRACT FROM AUTHOR]

Simple Summary: Cancer-related fatigue is a prevalent symptom, with a significant impact on the daily lives of those affected. While physical exercise has demonstrated effectiveness in reducing the intensity and duration of fatigue, the literature still lacks sufficient evidence on the physiological mechanisms explaining this impact. This conceptual review aimed to provide an overview of the evidence regarding the effect of acute exercise on peripheral and neuronal inflammation, immune function, and the neuroendocrine system in the context of cancer. We aim to integrate these pathways into a conceptual model that can serve as a starting point for further research into the physiological mechanisms linking exercise and cancer-related fatigue. Cancer-related fatigue (CRF) is a prevalent and persistent issue affecting cancer patients, with a broad impact on their quality of life even years after treatment completion. The precise mechanisms underlying CRF remain elusive, yet its multifaceted nature involves emotional, physical, and cognitive dimensions. The absence of effective medical treatments has prompted researchers to explore integrative models for potential insights. Notably, physical exercise emerges as a promising strategy for managing CRF and related symptoms, as studies showed a reduction in CRF ranging from 19% to 40%. Current recommendations highlight aerobic training at moderate intensity as beneficial, although questions about a dose–response relationship and the importance of exercise intensity persist. Despite the positive impact of exercise on CRF, the underlying mechanisms remain elusive. This review aims to provide a theoretical model explaining how aerobic exercise may alleviate CRF. Focusing on acute exercise effects, this review delves into the potential influence on peripheral and neural inflammation, immune function dysregulation, and neuroendocrine system disruptions. The objective is to enhance our understanding of the intricate relationship between exercise and CRF, ultimately paving the way for tailored interventions and potential pharmacological treatments for individuals unable to engage in physical exercise. [ABSTRACT FROM AUTHOR]

Background: Which patients benefit from the addition of immune checkpoint inhibitors (ICIs) to chemotherapy for small cell lung cancer (SCLC) remains unclear. There have been few reports on the efficacy of ICIs based on conventional immunohistochemical neuroendocrine (NE) markers (synaptophysin, chromogranin A, and neural cell adhesion molecule [NCAM]). In the present study, we aimed to analyze the relationship between the expression of immunohistochemical NE markers and the efficacy of ICIs in patients with extensive disease (ED)‐SCLC, to assess whether conventional NE markers are predictive of ICIs. Methods: Patients with untreated ED‐SCLC who received first‐line therapy at the Shizuoka Cancer Center between November 2002 and July 2021 were retrospectively reviewed. We evaluated the efficacy of first‐line chemotherapy according to the expression status of each immunohistochemical NE marker in patients treated with ICI plus chemotherapy (ICI‐chemo group) and with chemotherapy alone (chemo group). Results: A total of 227 patients were included in the ICI‐chemo and chemo groups, respectively. The progression‐free survival (PFS) tended to be better in patients in the ICI‐chemo group than those treated with chemotherapy alone in patients with NE marker‐positive SCLC. In particular, it was statistically significant in patients with chromogranin A‐positive SCLC (p = 0.036). In patients with NE marker‐negative SCLC, no significant differences were observed in PFS between the two groups. There were no significant differences in overall survival (OS), regardless of the expression of any conventional NE marker. Conclusion: Our study suggests that the efficacy of ICIs in addition to chemotherapy may be poor in patients with NE marker‐negative SCLC. [ABSTRACT FROM AUTHOR]

Recent studies have demonstrated that the interaction of dietary constituents with taste and olfactory receptors and nociceptors expressed in the oral cavity, nasal cavity and gastrointestinal tract regulate homeostasis through activation of the neuroendocrine system. Polyphenols, of which 8000 have been identified to date, represent the greatest diversity of secondary metabolites in plants, most of which are bitter and some of them astringent. Epidemiological studies have shown that polyphenol intake contributes to maintaining and improving cardiovascular, cognitive and sensory health. However, because polyphenols have very low bioavailability, the mechanisms of their beneficial effects are unknown. In this review, we focused on the taste of polyphenols from the perspective of sensory nutrition, summarized the results of previous studies on their relationship with bioregulation and discussed their future potential. [ABSTRACT FROM AUTHOR]

Dilatation of the main pancreatic duct (MPD) ˃50 mm is a rare phenomenon. We present the case of successful surgical treatment a 63-year-old female patient who presented epigastric pain and weight loss of 10 kg in 6 months. Based on preoperative examination, the dilatation of MPD was 75 mm. The preliminary diagnosis was main duct intraductal papillary mucinous neoplasm. Extended pylorus-preserving pancreatoduodenectomy with resection of the body of the pancreas was performed. According to the results of pathological and immunohistochemical studies, performed by independent experts, the final diagnosis of congenital anomaly of the ductal system and neuroendocrine tumor of the accessory pancreatic duct was made. [ABSTRACT FROM AUTHOR]

• Psychological stress is a crucial factor in the development of many skin diseases. • Psychological stress can worsen skin diseases and affect patients' quality of life. • Stress impacts skin diseases through the HPA axis, SNS, and neuropeptides. Psychological stress is a crucial factor in the development of many skin diseases, and the stigma caused by skin disorders may further increase the psychological burden, forming a vicious cycle of psychological stress leading to skin diseases. Therefore, understanding the relationship between stress and skin diseases is necessary. The skin, as the vital interface with the external environment, possesses its own complex immune system, and the neuroendocrine system plays a central role in the stress response of the body. Stress-induced alterations in the immune system can also disrupt the delicate balance of immune cells and inflammatory mediators in the skin, leading to immune dysregulation and increased susceptibility to various skin diseases. Stress can also affect the skin barrier function, impair wound healing, and promote the release of pro-inflammatory cytokines, thereby exacerbating existing skin diseases such as psoriasis, atopic dermatitis, acne, and urticaria. In the present review, we explored the intricate relationship between stress and skin diseases from a neuroendocrine-immune interaction perspective. We explored the occurrence and development of skin diseases in the context of stress, the stress models for skin diseases, the impact of stress on skin function and diseases, and relevant epidemiological studies and clinical trials. Understanding the relationship between stress and skin diseases from a neuroendocrine-immune interaction perspective provides a comprehensive framework for targeted interventions and new insights into the diagnosis and treatment of skin diseases. [ABSTRACT FROM AUTHOR]

The article discusses the strong connection between the brain and the endocrine system, highlighting how hormones can impact brain functions and behavior. It introduces the concept of endocrine disrupters, which are exogenous chemicals that interfere with hormone action and can have harmful effects on both humans and wildlife. The article emphasizes the need for further research and standardized testing to identify and understand the potential impacts of these disrupters. It also explores specific studies on the effects of various chemicals on neuroplasticity, neurogenesis, and behavior, as well as the importance of investigating the impact of disrupters on pregnant and lactating individuals. The article concludes by emphasizing the importance of standardized methodologies and validated tests to assess the risks associated with exposure to these chemicals. [Extracted from the article]

The hypothalamus is a brain structure that is deputed to maintain organism homeostasis by regulating autonomic function and hormonal production as part of the neuroendocrine system. Dysfunction in hypothalamic activity results in behavioral alterations, depression, metabolic syndromes, fatigue, and infertility. Remarkably, many of these symptoms are associated with multiple sclerosis (MS), a chronic autoimmune disorder of the central nervous system (CNS) characterized by focal demyelination, immune cell infiltration into the brain parenchyma, and neurodegeneration. Furthermore, altered hormonal levels have been documented in MS patients, suggesting the putative involvement of hypothalamic deficits in MS clinical manifestations. Yet, a systematic analysis of hypothalamic function in response to neuroinflammatory stress is still lacking. To fill this gap, here we performed a longitudinal profiling of the hypothalamic transcriptome upon experimental autoimmune encephalomyelitis (EAE)—a murine disease model recapitulating key MS phenotypes at both histopathological and molecular levels. We show that changes in gene expression connected with an anti-inflammatory response start already at pre-onset and persist along EAE progression. Altered levels of hypothalamic neuropeptides were also detected, which possibly underlie homeostatic responses to stress and aberrant feeding behaviors. Last, a thorough investigation of the principal endocrine glands highlighted defects in the main steroidogenic pathways upon disease. Collectively, our findings corroborate the central role of hypothalamic dysfunction in CNS autoimmunity. [ABSTRACT FROM AUTHOR]

The brain-gut axis refers to the communication between the central nervous system and the gastrointestinal tract, with the gut microbiome playing a crucial role. While our understanding of the interaction between the gut microbiome and the host's physiology is still in its nascent stage, evidence suggests that the gut microbiota can indeed modulate host behavior. Understanding the specific mechanisms by which the gut microbiota community modulates the host's behavior remains the focus of present and future neuro-gastroenterology studies. This paper reviews several pieces of evidence from the literature on the impact of gut microbiota on host behavior across animal taxa. We explore the different pathways through which this modulation occurs, with the aim of deepening our understanding of the fascinating relationship between the gut microbiome and the central nervous system. [ABSTRACT FROM AUTHOR]

The adrenal gland is paired peripheral end organs of the neuroendocrine system and is responsible for producing crucial stress hormones from its two functional compartments, the adrenal cortex, and the adrenal medulla under stimuli. Left–right asymmetry in vertebrates exists from the central nervous system to peripheral paired endocrine glands. The sided difference in the cerebral cortex is extensively investigated, while the knowledge of asymmetry of paired endocrine glands is still poor. The present study aims to investigate the asymmetries of bilateral adrenal glands, which play important roles in stress adaptation and energy homeostasis via steroid hormones produced from the distinct functional zones. Left and right adrenal glands from male C57BL/6J mice were initially histologically analyzed, and high-throughput RNA sequencing was then used to detect the gene transcriptional difference between left and right adrenal glands. Subsequently, the enrichment of functional pathways and ceRNA regulatory work was validated. The results demonstrated that the left adrenal gland had higher tissue mass and levels of energy expenditure, whereas the right adrenal gland appeared to be more potent in glucocorticoid secretion. Further analysis of adrenal stem/progenitor cell markers predicted that Shh signaling might play an important role in the left–right asymmetry of adrenal glands. Of the hub miRNAs, miRNA-466i-5p was identified in the left–right differential innervation of the adrenal glands. Therefore, the present study provides evidence that there are asymmetries between the left and right adrenal glands in glucocorticoid production and neural innervation, in which Shh signaling and miRNA-466i-5p play an important role. [ABSTRACT FROM AUTHOR]

Aim: Primary neuroendocrine tumors in the ovary are rare. These tumors arise from the neuroendocrine cell system of ovarian stroma and surface epithelium, and may also arise from teratoma. We present four primary ovarian neuroendocrine tumors and discuss clinical, histomorphological, and immunohistochemical findings. Methods: Four primary ovarian neuroendocrine tumors were identified from our 4-year departmental archives. H and E slides and immunostains were reviewed. Clinical history, imaging studies, and follow-up data were obtained from medical records. Results: Patients' age ranged from 37 to 45 years. All the patients presented with abdominal discomfort, abnormal uterine bleeding, and unilateral or bilateral ovarian masses. Two of the cases were primary ovarian carcinoid tumors, one being the pure primary ovarian carcinoid tumor (PPOCT), and the other being associated with mature cystic teratoma, while the other two cases were neuroendocrine carcinoma. All the cases showed expression of neuroendocrine markers, namely, synaptophysin, chromogranin, and NSE. Conclusions: Primary neuroendocrine tumors in the ovary are rare and consist of a group of heterogeneous tumors that express similar immunohistochemical markers. [ABSTRACT FROM AUTHOR]

Seasonal mammals register photoperiodic changes through the photoneuroendocrine system enabling them to time seasonal changes in growth, metabolism, and reproduction. To a varying extent, proximate environmental factors like ambient temperature (Ta) modulate timing of seasonal changes in physiology, conferring adaptive flexibility. While the molecular photoneuroendocrine pathway governing the seasonal responses is well defined, the mechanistic integration of nonphotoperiodic modulatory cues is poorly understood. Here, we explored the interaction between Ta and photoperiod in tundra voles, Microtus oeconomus, a boreal species in which the main impact of photoperiod is on postnatal somatic growth. We demonstrate that postweaning growth potential depends on both gestational and postweaning patterns of photoperiodic exposure, with the highest growth potential seen in voles experiencing short (8 h) gestational and long (16 h) postweaning photoperiods—corresponding to a spring growth program. Modulation by Ta was asymmetric: low Ta (10 °C) enhanced the growth potential of voles gestated on short photoperiods independent of postweaning photoperiod exposure, whereas in voles gestated on long photoperiods, showing a lower autumn-programmed growth potential, the effect of Ta was highly dependent on postweaning photoperiod. Analysis of the primary molecular elements involved in the expression of a neuroendocrine response to photoperiod, thyrotropin beta subunit (tshβ) in the pars tuberalis, somatostatin (srif) in the arcuate nucleus, and type 2/3 deiodinase (dio2 / dio3) in the mediobasal hypothalamus identified dio2 as the most Ta-sensitive gene across the study, showing increased expression at higher Ta, while higher Ta reduced somatostatin expression. Contrastingly dio3 and tshβ were largely insensitive to Ta. Overall, these observations reveal a complex interplay between Ta and photoperiodic control of postnatal growth in M. oeconomus, and suggest that integration of Ta into the control of growth occurs downstream of the primary photoperiodic response cascade revealing potential adaptivity of small herbivores facing rising temperatures at high latitudes. [ABSTRACT FROM AUTHOR]

The gut–brain axis augments the bidirectional communication between the gut and brain and modulates gut homeostasis and the central nervous system through the hypothalamic–pituitary–adrenal axis, enteroendocrine system, neuroendocrine system, inflammatory and immune pathways. Preclinical and clinical reports showed that gut dysbiosis might play a major regulatory role in neurological diseases such as epilepsy, Parkinson's, multiple sclerosis, and Alzheimer's disease. Epilepsy is a chronic neurological disease that causes recurrent and unprovoked seizures, and numerous risk factors are implicated in developing epilepsy. Advanced consideration of the gut–microbiota–brain axis can reduce ambiguity about epilepsy pathology, antiepileptic drugs, and effective therapeutic targets. Gut microbiota sequencing analysis reported that the level of Proteobacteria, Verrucomicrobia, Fusobacteria, and Firmicutes was increased and the level of Actinobacteria and Bacteroidetes was decreased in epilepsy patients. Clinical and preclinical studies also indicated that probiotics, ketogenic diet, faecal microbiota transplantation, and antibiotics can improve gut dysbiosis and alleviate seizure by enhancing the abundance of healthy biota. This study aims to give an overview of the connection between gut microbiota, and epilepsy, how gut microbiome changes may cause epilepsy, and whether gut microbiome restoration could be used as a treatment for epilepsy. [ABSTRACT FROM AUTHOR]

Knowledge of circadian rhythm clock gene expression outside the suprachiasmatic nucleus is increasing. The purpose of this study was to determine whether expression of circadian clock genes differed within or among the bovine stress axis tissues (e.g., amygdala, hypothalamus, pituitary, adrenal cortex, and adrenal medulla). Tissues were obtained at an abattoir from eight mature nonpregnant Brahman cows that had been maintained in the same pasture and nutritional conditions. Sample tissues were stored in RNase-free sterile cryovials at −80 °C until the total RNA was extracted, quantified, assessed, and sequenced (NovaSeq 6000 system; paired-end 150 bp cycles). The trimmed reads were then mapped to a Bos taurus (B. taurus) reference genome (Umd3.1). Further analysis used the edgeR package. Raw gene count tables were read into RStudio, and low-expression genes were filtered out using the criteria of three minimum reads per gene in at least five samples. Normalization factors were then calculated using the trimmed mean of M values method to produce normalized gene counts within each sample tissue. The normalized gene counts important for a circadian rhythm were analyzed within and between each tissue of the stress axis using the GLM and CORR procedures of the Statistical Analysis System (SAS). The relative expression profiles of circadian clock genes differed (p < 0.01) within each tissue, with neuronal PAS domain protein 2 (NPAS2) having greater expression in the amygdala (p < 0.01) and period circadian regulator (PER1) having greater expression in all other tissues (p < 0.01). The expression among tissues also differed (p < 0.01) for individual circadian clock genes, with circadian locomotor output cycles protein kaput (CLOCK) expression being greater within the adrenal tissues and nuclear receptor subfamily 1 group D member 1 (NR1D1) expression being greater within the other tissues (p < 0.01). Overall, the results indicate that within each tissue, the various circadian clock genes were differentially expressed, in addition to being differentially expressed among the stress tissues of mature Brahman cows. Future use of these findings may assist in improving livestock husbandry and welfare by understanding interactions of the environment, stress responsiveness, and peripheral circadian rhythms. [ABSTRACT FROM AUTHOR]

Insects from high latitudes spend the winter in a state of overwintering diapause, which is characterized by arrested reproduction, reduced food intake and metabolism, and increased life span. The main trigger to enter diapause is the decreasing day length in summer–autumn. It is thus assumed that the circadian clock acts as an internal sensor for measuring photoperiod and orchestrates appropriate seasonal changes in physiology and metabolism through various neurohormones. However, little is known about the neuronal organization of the circadian clock network and the neurosecretory system that controls diapause in high‐latitude insects. We addressed this here by mapping the expression of clock proteins and neuropeptides/neurohormones in the high‐latitude fly Drosophila littoralis. We found that the principal organization of both systems is similar to that in Drosophila melanogaster, but with some striking differences in neuropeptide expression levels and patterns. The small ventrolateral clock neurons that express pigment‐dispersing factor (PDF) and short neuropeptide F (sNPF) and are most important for robust circadian rhythmicity in D. melanogaster virtually lack PDF and sNPF expression in D. littoralis. In contrast, dorsolateral clock neurons that express ion transport peptide in D. melanogaster additionally express allatostatin‐C and appear suited to transfer day‐length information to the neurosecretory system of D. littoralis. The lateral neurosecretory cells of D. littoralis contain more neuropeptides than D. melanogaster. Among them, the cells that coexpress corazonin, PDF, and diuretic hormone 44 appear most suited to control diapause. Our work sets the stage to investigate the roles of these diverse neuropeptides in regulating insect diapause. [ABSTRACT FROM AUTHOR]

Neuroendocrine cancer, often known as a neuroendocrine tumor (NET) or neuroendocrine neoplasm, originates from the specialized cells of the neuroendocrine system. These cells have characteristics that are indicative of both endocrine cells and nerve cells. Neuroendocrine tumors mostly arise inside the gastrointestinal tract, with the large intestine accounting for 20% of cases, followed by the small intestine (19%) and the appendix (4%). In order to provide a comprehensive literature review of neuroendocrine tumors that start from the small bowel, the used methodology included performing a thorough investigation of the primary attributes of NETs by using renowned academic databases, such as PubMed, Scopus and Academic Oxford Journals. The findings were classified into four distinct groups: a) genetics, epidemiology and pathology; b) clinical aspects; c) paraclinical aspects; d) treatment and prognosis. Although there is a possibility of encountering both local and systemic complications, nevertheless, it is important to note that neuroendocrine tumors are associated with rather positive survival rates in the long run (five-year and ten-year survival, respectively). [ABSTRACT FROM AUTHOR]

Aim: Primary neuroendocrine tumors in the ovary are rare. These tumors arise from the neuroendocrine cell system of ovarian stroma and surface epithelium, and may also arise from teratoma. We present four primary ovarian neuroendocrine tumors and discuss clinical, histomorphological, and immunohistochemical findings. Methods: Four primary ovarian neuroendocrine tumors were identified from our 4-year departmental archives. H and E slides and immunostains were reviewed. Clinical history, imaging studies, and follow-up data were obtained from medical records. Results: Patients' age ranged from 37 to 45 years. All the patients presented with abdominal discomfort, abnormal uterine bleeding, and unilateral or bilateral ovarian masses. Two of the cases were primary ovarian carcinoid tumors, one being the pure primary ovarian carcinoid tumor (PPOCT), and the other being associated with mature cystic teratoma, while the other two cases were neuroendocrine carcinoma. All the cases showed expression of neuroendocrine markers, namely, synaptophysin, chromogranin, and NSE. Conclusions: Primary neuroendocrine tumors in the ovary are rare and consist of a group of heterogeneous tumors that express similar immunohistochemical markers. [ABSTRACT FROM AUTHOR]

Postpartum depression (PPD) is a common complication of pregnancy in women, and its pathogenesis mainly involves disturbances of the neuroendocrine regulation, immune system, neurotransmitters, hormone secretion, and the gut microbiome. Gut microbes play essential physiological and pathological roles in the gut-brain axis' pathways which are involved in various central nervous system (CNS) and psychiatric disorders, including PPD. Numerous studies have identified the fundamental role of the gut-brain axis in the pathogenesis and treatment of PPD patients and also correlates with other pathogenic mechanisms of PPD. Disturbances in gut microbes are associated with the disruption of multiple signaling pathways and systems that ultimately lead to PPD development. This review aimed to elucidate the potential connections between gut microbes and the established PPD network, and this might serve as a guide for the development of new efficient diagnostic, therapeutic, and prognostic strategies in the management of PPD. [ABSTRACT FROM AUTHOR]

Neuroendocrine neoplasms (NENs) are a group of lesions originating from cells of the diffuse neuroendocrine system. NENs may involve different sites, including the gastrointestinal tract (GEP-NENs). The incidence and prevalence of GEP-NENs has been constantly rising thanks to the increased diagnostic power of imaging and immuno–histochemistry. Despite the plethora of biochemical markers and imaging techniques, the prognosis and therapeutic choice in GEP-NENs still represents a challenge, mainly due to the great heterogeneity in terms of tumor lesions and clinical behavior. The concept that biomedical images contain information about tissue heterogeneity and pathological processes invisible to the human eye is now well established. From this substrate comes the idea of radiomics. Computational analysis has achieved promising results in several oncological settings, and the use of radiomics in different types of GEP-NENs is growing in the field of research, yet with conflicting results. The aim of this narrative review is to provide a comprehensive update on the role of radiomics on GEP-NEN management, focusing on the main clinical aspects analyzed by most existing reports: predicting tumor grade, distinguishing NET from other tumors, and prognosis assessment. [ABSTRACT FROM AUTHOR]

• Opioid use disorder (OUD) is a major current cause of morbidity and mortality. • Neuroimmune and neuroinflammatory mechanisms are changed in OUD. • These mechanisms can include peripheral components (cytokines and leukocytes). • Glia, neurons and blood–brain barrier can also be affected by inflammation in OUD. • Longitudinal multiomic biomarker/neuroimaging studies are necessary in OUD. Opioid use disorder (OUD) is a major current cause of morbidity and mortality. Long-term exposure to short-acting opioids (MOP-r agonists such as heroin or fentanyl) results in complex pathophysiological changes to neuroimmune and neuroinflammatory functions, affected in part by peripheral mechanisms (e.g., cytokines in blood), and by neuroendocrine systems such as the hypothalamic–pituitary–adrenal (HPA) stress axis. There are important findings from preclinical models, but their role in the trajectory and outcomes of OUD in humans is not well understood. The goal of this narrative review is to examine available data on immune and inflammatory functions in persons with OUD, and to identify major areas for future research. Peripheral blood biomarker studies revealed a pro-inflammatory state in persons with OUD in withdrawal or early abstinence, consistent with available postmortem brain studies (which show glial activation) and diffusion tensor imaging studies (indicating white matter disruptions), with gradual abstinence-associated recovery. The mechanistic roles of these neuroimmune and neuroinflammatory changes in the trajectory of OUD (including recovery and medication management) cannot be examined practically with postmortem data. Collection of longitudinal data in larger-scale human cohorts would allow examination of these mechanisms associated with OUD stage and progression. Given the heterogeneity in presentation of OUD, a precision medicine approach integrating multi-omic peripheral biomarkers and comprehensive phenotyping, including neuroimaging, can be beneficial in risk stratification, and individually optimized selection of interventions for individuals who will benefit, and assessments under refractory therapy. [ABSTRACT FROM AUTHOR]

Purpose: The purpose of this study was to determine if aging would lead to greater decline in neuromuscular function during a fatiguing task under severe whole‐body hyperthermia conditions. Methods: Twelve young (aged 19–21 years) and 11 older (aged 65–80 years) males were enrolled in the study, which comprised a randomized control trial under a thermoneutral condition at an ambient temperature of 23°C (CON) and an experimental trial with passive lower body heating in 43°C water (HWI‐43°C). Changes in neuromuscular function and fatigability, and physical performance‐influencing factors such as psychological, thermoregulatory, neuroendocrine, and immune responses to whole‐body hyperthermia were measured. Results: A slower increase in rectal temperature, and a lower heart rate, thermal sensation, and sweating rate were observed in older males than young males in response to HWI‐43°C trial (p < 0.05). Nevertheless, prolactin increased more in response to hyperthermia in young males, while interleukin‐6 and cortisol levels increased more in older males (p < 0.05). Peripheral dopamine levels decreased in older males and increased in young males in response to hyperthermia (p < 0.05). Surprisingly, older males demonstrated greater neuromuscular fatigability resistance and faster maximal voluntary contraction (MVC) torque recovery after a 2‐min sustained isometric MVC task under thermoneutral and severe hyperthermic conditions (p < 0.05). Conclusion: Neuromuscular performance during fatigue‐provoking sustained isometric exercise under severe whole‐body hyperthermia conditions appears to decline in both age groups, but a lower relative decline in torque production for older males may relate to lower psychological and thermophysiological strain along with a diminished dopamine response and prolactin release. [ABSTRACT FROM AUTHOR]

The hypothalamus regulates fundamental aspects of physiological homeostasis and behavior, including stress response, reproduction, growth, sleep, and feeding, several of which are affected in patients with Prader–Willi (PWS) and Schaaf–Yang syndrome (SYS). PWS is caused by paternal deletion, maternal uniparental disomy, or imprinting defects that lead to loss of expression of a maternally imprinted region of chromosome 15 encompassing non-coding RNAs and five protein-coding genes; SYS patients have a mutation in one of them, MAGEL2. Throughout life, PWS and SYS patients suffer from musculoskeletal deficiencies, intellectual disabilities, and hormonal abnormalities, which lead to compulsive behaviors like hyperphagia and temper outbursts. Management of PWS and SYS is mostly symptomatic and cures for these debilitating disorders do not exist, highlighting a clear, unmet medical need. Research over several decades into the molecular and cellular roles of PWS genes has uncovered that several impinge on the neuroendocrine system. In this review, we will discuss the expression and molecular functions of PWS genes, connecting them with hormonal imbalances in patients and animal models. Besides the observed hormonal imbalances, we will describe the recent findings about how the loss of individual genes, particularly MAGEL2, affects the molecular mechanisms of hormone secretion. These results suggest that MAGEL2 evolved as a mammalian-specific regulator of hypothalamic neuroendocrine function. [ABSTRACT FROM AUTHOR]

Allostatic load (AL) is a comprehensive index reflecting the cumulative wear status of multiple physiological systems, which can significantly predict the physical and mental healtli of individuals. The evaluation of AL includes quantitative and qualitative methods, with quantitative approaches being more commonly utilized. However, there exists considerable heterogeneity in the selection and calculation methods of biomarkers when determining the allostatic load index (ALI). Some AL studies do not contain biomarkers of neuroendocrine system, which is not consistent with its original conceptual framework. Currently, numerous ALI calculation methods are employed, with the high-risk quartile method being the most prevalent, yet this restricts the comparability of cross-sample research outcomes. Each calculation method has its own advantages and disadvantages. Therefore, the purpose of this paper is to review the selection of bio markers and ALI calculation methods in the evaluation of AL and its influence on the research results. The purpose of this study is to provide a reference for the selection of biomarkers and index calculation methods in future AL research. [ABSTRACT FROM AUTHOR]

Background: The neuroendocrine system and the hypot halam ic--pi tuita ry--ad renal axis are among the possible neurobiological factors that may be involved in the emergence and persistence of post-traumatic stress disorder. Here, we determined the levels of vasopressin and oxytocin in the peripheral blood of people with post-traumatic stress disorder, investigating their correlation with post-traumatic stress disorder symptoms. Methods: The study included patients with post-traumatic stress disorder according to the Diagnostic and Statistical Manual of Mental Disorders Version 4 and healthy controls. People who accepted to participate in the study, who did not have any additional diseases, who had the ability to understand the questionnaires, and who did not use medications during the 3 months preceding the study onset were enrolled. The levels of vasopressin and oxytocin were measured using the enzyme-linked immunosorbent assay. Results: Twenty-eight subjects with post-traumatic stress disorder and 19 healthy controls were included. The 2 groups were not significantly different in terms of oxytocin blood levels (P = .481). However, subjects with post-traumatic stress disorder had a significantly lower vasopressin level than controls (P < .001). We found no significant correlations of trauma duration and scale scores with oxytocin or vasopressin levels. Conclusion: The findings of this study show that blood vasopressin may play a role in post-traumatic stress disorder. Prospective studies based on a larger number of participants are warranted to clarify how neuromodulators may affect the pathogenesis of posttraumatic stress disorder. [ABSTRACT FROM AUTHOR]

The fitness benefits of social life depend on the ability of animals to affiliate with others and form groups, on dominance hierarchies within groups that determine resource distribution, and on cognitive capacities for recognition, learning and information transfer. The evolution of these phenotypes is coupled with that of neuroendocrine mechanisms, but the causal link between the two remains underexplored. Growing evidence from our research group and others demonstrates that the tools available in zebrafish, Danio rerio, can markedly facilitate progress in this field. Here, we review this evidence and provide a synthesis of the state‐of‐the‐art in this model system. We discuss the involvement of generalized motivation and cognitive components, neuroplasticity and functional connectivity across social decision‐making brain areas, and how these are modulated chiefly by the oxytocin‐vasopressin neuroendocrine system, but also by reward‐pathway monoamine signaling and the effects of sex‐hormones and stress physiology. [ABSTRACT FROM AUTHOR]

Background: Alcohol binge drinking may compromise the functioning of the nucleus accumbens (NAc), i.e. the neural hub for processing reward and aversive responses. Methods: As socially stressful events pose particular challenges at developmental stages, this research applied the resident–intruder paradigm as a model of social stress, to highlight behavioural neuroendocrine and molecular maladaptive plasticity in rats at withdrawal from binge-like alcohol exposure in adolescence. In search of a rescue agent, cannabidiol (CBD) was selected due to its favourable effects on alcohol- and stress-related harms. Results: Binge-like alcohol exposed intruder rats displayed a compromised defensive behaviour against the resident and a blunted response of the stress system, in addition to indexes of abnormal dopamine (DA)/glutamate plasticity and dysfunctional spine dynamics in the NAc. CBD administration (60 mg/kg) was able to: (1) increase social exploration in the binge-like alcohol exposed intruder rats, at the expenses of freezing time, and in control rats, which received less aggressive attacks from the resident; (2) reduce corticosterone levels independently on alcohol previous exposure; (3) restore DA transmission and (4) facilitate excitatory postsynaptic strength and remodelling. Conclusions: Overall, the maladaptive behavioural and synaptic plasticity promoted by the intersection between binge-like alcohol withdrawal and exposure to adverse social stress can be rescued by a CBD détente effect that results in a successful defensive strategy, supported by a functional endocrine and synaptic plasticity. The current data highlight CBD's relevant therapeutic potential in alcohol- and stress-related harms, and prompt further investigation on its molecular targets. [ABSTRACT FROM AUTHOR]

In different organisms, histamine (HA) is related to biological rhythms, moderating the circadian rhythm of the neuroendocrine system. Nevertheless, no work has been done on the putative pacemaker of the endemic crayfish, Cambarellus montezumae, wich threatened by anthropocentric modifications of its habitat. The aims of the present work were to evaluate the daily presence and localization of HA in two structures proposed as putative pacemakers of the crayfish, the eyestalk and the brain in females and males. We also evaluated whether there are changes in the F0 generation with respect to the F1 generation. Adult crayfish were used, euthanized at different times of day, to excise the eyestalk and brain and process them through immunohistochemical techniques. The results obtained showed that the immunopositivity to HA in the eyestalk and brain of the crayfish undergoes daily variations in both females and males, as well as between the F0 and F1 generations. [ABSTRACT FROM AUTHOR]

Non-enzymatic activation of renin via its interaction with prorenin receptor (PRR) has been proposed as a key mechanism of local renin–angiotensin system (RAS) activation. The presence of renin and angiotensinogen has been reported in the rostral ventrolateral medulla (RVLM). Overactivation of bulbospinal neurons in the RVLM is linked to hypertension (HTN). Previous studies have shown that the brain RAS plays a role in the pathogenesis of the deoxycorticosterone (DOCA)-salt HTN model. Thus, we hypothesized that PRR in the RVLM is involved in the local activation of the RAS, facilitating the development of DOCA-salt HTN. Selective PRR ablation targeting the RVLM (PRRRVLM-Null mice) resulted in an unexpected sex-dependent and biphasic phenotype in DOCA-salt HTN. That is, PRRRVLM-Null females (but not males) exhibited a significant delay in achieving maximal pressor responses during the initial stage of DOCA-salt HTN. Female PRRRVLM-Null subsequently showed exacerbated DOCA-salt-induced pressor responses during the "maintenance" phase with a maximal peak at 13 d on DOCA-salt. This exacerbated response was associated with an increased sympathetic drive to the resistance arterioles and the kidney, exacerbated fluid and sodium intake and output in response to DOCA-salt, and induced mobilization of fluids from the intracellular to extracellular space concomitant with elevated vasopressin. Ablation of PRR suppressed genes involved in RAS activation and catecholamine synthesis in the RVLM but also induced expression of genes involved in inflammatory responses. This study illustrates complex and sex-dependent roles of PRR in the neural control of BP and hydromineral balance through autonomic and neuroendocrine systems. Graphical abstract Graphical Abstract [ABSTRACT FROM AUTHOR]

Three-dimensional (3D) printing of manufactured goods has increased in the last 10 years. The increased use of this technology has resulted in questions regarding the influence of inhaling emissions generated during printing. The goal of this study was to determine if inhalation of particulate and/or toxic chemicals generated during printing with polycarbonate (PC) plastic affected the neuroendocrine system. Male rats were exposed to 3D-printer emissions (592 µg particulate/m3 air) or filtered air for 4 h/day (d), 4 days/week and total exposures lengths were 1, 4, 8, 15 or 30 days. The effects of these exposures on hormone concentrations, and markers of function and/or injury in the olfactory bulb, hypothalamus and testes were measured after 1, 8 and 30 days exposure. Thirty days of exposure to 3D printer emissions resulted in reductions in thyroid stimulating hormone, follicle stimulating hormone and prolactin. These changes were accompanied by (1) elevation in markers of cell injury; (2) reductions in active mitochondria in the olfactory bulb, diminished gonadotropin releasing hormone cells and fibers as well as less tyrosine hydroxylase immunolabeled fibers in the arcuate nucleus; and (3) decrease in spermatogonium. Polycarbonate plastics may contain bisphenol A, and the effects of exposure to these 3D printer-generated emissions on neuroendocrine function are similar to those noted following exposure to bisphenol A. [ABSTRACT FROM AUTHOR]

Although very common, the precise mechanisms that explain the symptomatology of neuroendocrine syncope (NES) remain poorly understood. This disease, which can be very incapacitating, manifests itself as a drop in blood pressure secondary to vasodilation and/or extreme slowing of heart rate. As studies continue, the involvement of the adenosinergic system is becoming increasingly evident. Adenosine, which is an ATP derivative, may be involved in a large number of cases. Adenosine acts on G protein-coupled receptors with seven transmembrane domains. A1 and A2A adenosine receptor dysfunction seem to be particularly implicated since the activation leads to severe bradycardia or vasodilation, respectively, two cardinal symptoms of NES. This mini-review aims to shed light on the links between dysfunction of the adenosinergic system and NHS. In particular, signal transduction pathways through the modulation of cAMP production and ion channels in relation to effects on the cardiovascular system are addressed. A better understanding of these mechanisms could guide the pharmacological development of new therapeutic approaches. [ABSTRACT FROM AUTHOR]

Individual features of age-related changes in the function of the neuroendocrine systems are an important problem as the basic component of a personalized approach to predicting and treating age-related pathologies. We studied the age-related features of the function of the hypothalamic—pituitary—thyroid axis in laboratory primates with depression- and anxiety-like behavior (DAB). It was found that in young female rhesus monkeys with DAB, the basal and thyrotropin-releasing hormone-stimulated levels of thyroid-stimulating hormone were significantly lower than in young animals with standard behavior (control). During aging, the levels of thyroid-stimulating hormone increased in DAB animals and free thyroxine concentrations decreased both at baseline (fasting) and in response to the thyrotropin-releasing hormone test, while in animals with standard behavior, only a trend towards similar hormonal changes was revealed. [ABSTRACT FROM AUTHOR]

Lactation is an important physiological stage of dairy cows, which affects milk yield, reestrus and actual service life of dairy cows. Good feeding management measures will improve the service life of cows and increase the economic benefits of feedlots. In summer, when the temperature of the external environment exceeds the upper limit that the cow can adjust, the body will produce heat stress, resulting in the decrease of feed intake, milk yield and milk quality of the cow, and in severe cases, shock or death. When heat stress occurs, the intestinal tract, neuroendocrine and immune systems of dairy cows all produce stress responses, and the secreted hormones and neurotransmitters regulate each other. The article reviewed the effects of heat stress on blood physiological and biochemical indexes, production performance, immune function, antioxidant capacity and intestinal tract of lactating cows and its mechanism, and proposed prevention and control measures in terms of physical, nutritional regulation, drugs and additives, in order to provide references for reducing the harm of heat stress on lactating cows and improving milk yield. [ABSTRACT FROM AUTHOR]

Finasteride and dutasteride are 5-alpha reductase selective inhibitors (5ARIs). They were introduced as therapeutic agents for the treatment of benign prostatic hyperplasia in 1992 and 2002, respectively; finasteride has also been approved for the treatment of androgenetic alopecia since early 2000. These agents inhibit the conversion of testosterone (T) to 5α-dihydrotestosterone (5α-DHT), limiting steroidogenesis and playing a crucial role in the physiological function of the neuroendocrine system. Therefore, it has been proposed that blocking androgen synthesis with the use of 5ARIs would be beneficial in the treatment of various diseases related to states of hyperandrogenism. This review describes the dermatological pathologies in which 5ARIs have been used as part of the treatment, evaluation of the efficacy, and knowledge of the safety profile. Specifically, we discuss the application of 5ARIs in androgenetic alopecia, acne, frontal fibrosing alopecia, hirsutism, and the implications of adverse events associated with its use to inform about the applications of 5ARIs in general dermatology practice. [ABSTRACT FROM AUTHOR]

Obesity has become a global health concern. it increases the risk of several diseases, such as type 2 diabetes mellitus, nonalcoholic fatty liver disease, and certain cancers, which threatens human health and increases social economic burden. As one of the most consumed beverages, tea contains various phytochemicals with potent bioactive properties and health-promoting effects, such as antioxidant, immune-regulation, cardiovascular protection and anticancer. Tea and its components are also considered as potential candidates for anti-obesity. epidemiological studies indicate that regular consumption of tea is beneficial for reducing body fat. in addition, the experimental studies demonstrate that the potential anti-obesity mechanisms of tea are mainly involved in increasing energy expenditure and lipid catabolism, decreasing nutrient digestion and absorption as well as lipid synthesis, and regulating adipocytes, neuroendocrine system and gut microbiota. Moreover, most of clinical studies illustrate that the intake of green tea could reduce body weight and alleviate the obesity. in this review, we focus on the effect of tea and its components on obesity from epidemiological, experimental, and clinical studies, and discuss their potential mechanisms. [ABSTRACT FROM AUTHOR]

Simple Summary: In this review paper, we explore the role of chronic inflammation in the pathogenesis of prostatic diseases, such as chronic prostatitis, benign prostatic hyperplasia (BPH), and prostate cancer. Chronic inflammation is a significant risk factor for these diseases, but the molecular mechanisms behind it are not yet fully understood. Previous attempts to investigate, link, and target inflammatory signaling molecules in men with these conditions have been clinically ambiguous and inconclusive. As a result, we proposed a paradigm shift in which less-explored molecules in the inflammatory signaling cascade are investigated as possible therapeutic targets for prostate diseases. In addition, we comprehensively discuss how aberrant signaling of these molecules may cause prostate cancer stemness, neuroendocrine differentiation, castration resistance, metabolic reprogramming, and immunosuppression. In conclusion, we forecast that targeting the interleukin-1 receptor-associated kinases (IRAKs) signaling pathway may provide a far more effective therapeutic or prophylactic strategy for the management of chronic inflammation-driven prostatic diseases. Chronic inflammation is now recognized as one of the major risk factors and molecular hallmarks of chronic prostatitis, benign prostatic hyperplasia (BPH), and prostate tumorigenesis. However, the molecular mechanisms by which chronic inflammation signaling contributes to the pathogenesis of these prostate diseases are poorly understood. Previous efforts to therapeutically target the upstream (e.g., TLRs and IL1-Rs) and downstream (e.g., NF-κB subunits and cytokines) inflammatory signaling molecules in people with these conditions have been clinically ambiguous and unsatisfactory, hence fostering the recent paradigm shift towards unraveling and understanding the functional roles and clinical significance of the novel and relatively underexplored inflammatory molecules and pathways that could become potential therapeutic targets in managing prostatic diseases. In this review article, we exclusively discuss the causal and molecular drivers of prostatitis, BPH, and prostate tumorigenesis, as well as the potential impacts of microbiome dysbiosis and chronic inflammation in promoting prostate pathologies. We specifically focus on the importance of some of the underexplored druggable inflammatory molecules, by discussing how their aberrant signaling could promote prostate cancer (PCa) stemness, neuroendocrine differentiation, castration resistance, metabolic reprogramming, and immunosuppression. The potential contribution of the IL1R-TLR-IRAK-NF-κBs signaling molecules and NLR/inflammasomes in prostate pathologies, as well as the prospective benefits of selectively targeting the midstream molecules in the various inflammatory cascades, are also discussed. Though this review concentrates more on PCa, we envision that the information could be applied to other prostate diseases. In conclusion, we have underlined the molecular mechanisms and signaling pathways that may need to be targeted and/or further investigated to better understand the association between chronic inflammation and prostate diseases. [ABSTRACT FROM AUTHOR]

Transport stress is commonly suffered by animals with gastrointestinal dysfunction a common symptom. Currently, the mechanisms of transport stress-induced intestine impairment are largely unknown. The aim of this study was to investigate the effects of transport stress on the expression of neuronal nitric oxide synthase (nNOS) and the distribution of nNOS-positive neurons of the intestines in rats and to explore the neuroendocrine mechanism of transport stress. In this study, Sprague Dawley rats (n = 6) were subjected on a constant temperature shaker for 1 (S1d) or 3 d (S3d). Rats exhibited increased serum glucose and diminished total number of leukocytes, in which lymphocytes level was also decreased in the S1d group (P < 0.05). Also, normal intestinal morphology was disrupted in the S1d rats, and the thickness of muscle layers was decreased in duodenum, jejunum and colon of S3d rats. In addition, it was found that nNOS expression, as well as the number of Nnos-positive neurons in the myenteric plexus were downregulated in duodenum, jejunum and colon of S3d rats compared with that of unstressed rats (P < 0.05). These data reveals that transport stress induced intestinal damage and uncovers potential action mechanisms that nNOS-positive neurons and nNOS expression might be involved in modulating this process. [ABSTRACT FROM AUTHOR]

BACKGROUND: Shrimp is one of the most popular marine foods consumed throughout the world and its freshness is a crucial indicator for consumers. However, the flesh quality degradation of shrimp during waterless live transport has been observed and the underlying mechanism remains unknown. RESULTS: The present study aimed to clarify the biochemistry mechanisms of flesh degradation with integration of quality evaluation, metabolic profiling and histopathological analysis. The flesh quality indicators such as water holding capacity, protein and lipid contents, amino acid composition and myofiber components degraded with the prolongation of combined stress. In addition, the metabolites including gamma‐aminobutyric acid, Val‐Ala, Trh and derivatives of carnitine, phosphocholine and prostaglandin all reduced significantly under combined stress (P < 0.05). Furthermore, Kyoto Encyclopedia of Genes and Genomes (https://www.genome.jp/kegg) analysis revealed the enrichment of neuroactive ligand–receptor interaction and estrogen signaling pathways, indicating the involvement of neuroendocrine in stress response. Moreover, architecture impairment in hepatopancreas tissue verified the accumulation of metabolic disturbance. CONCLUSION: Taken together, the findings of the present study indicate that neuroendocrine system mediates the flesh degradation of L. vannamei during waterless transport by disturbing the biochemical metabolic pathways and inducing architecture impairment of myofibril components. © 2022 Society of Chemical Industry. [ABSTRACT FROM AUTHOR]

Activational effects of the reproductive neuroendocrine system may explain why some youths with ADHD are at greater risk for exacerbated ADHD symptoms (hyperactivity, inattention, impulsivity) during adolescence. For youths diagnosed with ADHD, first signs of ADHD symptoms become noticeable by multiple reporters (e.g., teachers, parents) when children enter schools, typically around kindergarten. The current study examined possible sex differences in ADHD, impairment, and comorbidity due to pubertal effects, as the role of pubertal development in ADHD is understudied. ADHD symptoms, depressive symptoms, impairment, and pubertal stage were assessed annually by multiple reporters in a well-characterized community sample of 849 children over-recruited for ADHD over eight years. Ages ranged from 7 to 13 years (38.16% female) at wave 1. Multilevel models indicated that males had higher levels of hyperactivity, impulsivity, and inattention than females, but that females had higher levels of impairment than males. Inattention symptoms did not show marked maturation changes. Hyperactivity and impulsivity declined as youth aged and impairment increased as youth aged. Lastly, depressive symptoms largely increased as youth aged and were higher amongst youth at later pubertal stages. Put together, aging and pubertal development are associated with improved ADHD symptoms but not for youth with high impairment. Findings from this study contributes to understanding the role that aging, pubertal status, and pubertal development plays in ADHD, impairment, and comorbidity in children and adolescents. [ABSTRACT FROM AUTHOR]

Obesity derives from impaired central control of body weight, implying interaction between environment and an individual genetic predisposition. Genetic obesities, including monogenic and syndromic obesities, are rare and complex neuro-endocrine pathologies where the genetic contribution is predominant. Severe and early-onset obesity with eating disorders associated with frequent comorbidities make these diseases challenging. Their current estimated prevalence of 5-10% in severely obese children is probably underestimated due to the limited access to genetic diagnosis. A central alteration of hypothalamic regulation of weight implies that the leptin-melanocortin pathway is responsible for the symptoms. The management of genetic obesity has so far been only based, above all, on lifestyle intervention, especially regarding nutrition and physical activity. New therapeutic options have emerged in the last years for these patients, raising great hope to manage their complex situation and improve quality of life. Implementation of genetic diagnosis in clinical practice is thus of paramount importance to allow individualized care. This review describes the current clinical management of genetic obesity and the evidence on which it is based. Some insights will also be provided into new therapies under evaluation. [ABSTRACT FROM AUTHOR]