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Artykuły w czasopismach na temat "Hypothalamic hormones"
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Crowley, W. R. "Toward Multifactorial Hypothalamic Regulation of Anterior Pituitary Hormone Secretion". Physiology 14, nr 2 (kwiecień 1999): 54–58. http://dx.doi.org/10.1152/physiologyonline.1999.14.2.54.
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The hypothalamus regulates the secretion of anterior pituitary hormones via release of releasing hormones into the hypophysial portal vasculature. Additional neuromessengers act at the pituitary to modulate responses to the hypothalamic hormones. For example, neuropeptide Y enhances the effect of gonadotropin-releasing hormone and the response to the prolactin-inhibiting hormone dopamine.
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Richalet, Jean-Paul, Murielle Letournel i Jean-Claude Souberbielle. "Effects of high-altitude hypoxia on the hormonal response to hypothalamic factors". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 299, nr 6 (grudzień 2010): R1685—R1692. http://dx.doi.org/10.1152/ajpregu.00484.2010.
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Acute and chronic exposure to high altitude induces various physiological changes, including activation or inhibition of various hormonal systems. In response to activation processes, a desensitization of several pathways has been described, especially in the adrenergic system. In the present study, we aimed to assess whether the hypophyseal hormones are also subjected to a hypoxia-induced decrease in their response to hypothalamic factors. Basal levels of hormones and the responses of TSH, thyroid hormones, prolactin, sex hormones, and growth hormone to the injection of TRH, gonadotropin-releasing hormone, and growth hormone-releasing hormone (GHRH) were studied in eight men in normoxia and on prolonged exposure (3–4 days) to an altitude of 4,350 m. Thyroid hormones were elevated at altitude (+16 to +21%), while TSH levels were unchanged, and follicle-stimulating hormone and prolactin decreased, while leutinizing hormone was unchanged. Norepinephrine and cortisol levels were elevated, while no change was observed in levels of epinephrine, dopamine, growth hormone (GH), IGF-1, and IGFBP-3. The mean response to hypothalamic factors was similar in both altitudes for all studied hormones, although total T4 was lower in hypoxia during 45 to 60 min after injection. The effect of hypoxia on the hypophyseal response to hypothalamic factors was similar among subjects, except for the GH response to GHRH administration. We conclude that prolonged exposure to high-altitude hypoxia induces contrasted changes in hormonal levels, but the hypophyseal response to hypothalamic factors does not appear to be blunted.
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Nikolayev, V. I., Ye Yu Gornushkina i A. A. Nikolayeva. "Effects of hypothalamic mediator systems on the hormonal changes in rabbit blood during prolonged electric stimulation of emotiogenic zones of the hypothalamus". Problems of Endocrinology 40, nr 6 (15.12.1994): 53–56. http://dx.doi.org/10.14341/probl12196.
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Changes in the blood hormonal levels were studied In 36 rabbits with electrodes implanted to the area of the dorsomedial nuclei of the hypothalamus in the course of a 5-cycle electrostimulation experiment. After each period blood hormonal levels were correlated to the activities of the hypothalamic catecholamino-, GABA-, and serotoninergic systems. The first two cycles of the experiment were associated with a high activity of the hypothalamic mediator systems and with increased levels of all hormones in the blood. The functional activity of the hypothalamus was reduced due to the predominance of stress-limiting systems. The initial reduction of GABA, and then of serotonin in the hypothalamus caused be the end of experiment a reduction of the blood levels of the tested hormones, except the Ca-regulating ones and active renin. Disturbances in the regulatory mechanisms of hypothalamic mediator systems leads to an increase in its excitability and to transformation of the adaptive pattern of hormonal changes into pathological mechanisms of prolonged emotional stress.
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Subramani, Ramadevi, Adriana Estrada, Madeline Dixon, Maria Parada, Sheryl Rodriguez, Diego A. Pedroza, Matthew D. Ramirez, Alexa Clift, Lilia Garcia i Rajkumar Lakshmanaswamy. "Pregnancy Inhibits Mammary Carcinogenesis by Persistently Altering the Hypothalamic–Pituitary Axis". Cancers 13, nr 13 (26.06.2021): 3207. http://dx.doi.org/10.3390/cancers13133207.
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Early full-term pregnancy is known to reduce the lifetime risk of breast cancer. Although the phenomenon of parity-induced protection is well-established, the physiological mechanisms involved in this protection are not clear. Earlier reports have shown that pregnancy results in alterations of hormone levels. How pregnancy affects hypothalamic hormones and how the change, if any, influences breast cancer is not well understood. Seven-week-old female Lewis rats were given N-methyl-N-nitrosourea. Two weeks post carcinogen exposure, a set of females were housed with males to generate the parous rats and another set of rats served as the nulliparous controls. Mammary tumorigenesis was assessed for 9 months. Hypothalamic and pituitary levels of hormones were measured at various timepoints. Further, animals were also challenged with growth hormone and prolactin secretagogues to test the effect of pregnancy on the hypothalamic–pituitary hormonal axis. Persistent alterations in the level of growth hormone-releasing hormone, thyrotropin releasing hormone, dopamine, and somatostatin in the hypothalamus of parous animals was observed. Further, we also observed that pregnancy had a significant effect on the pituitary gland and its response to growth hormone and prolactin secretagogues. Our studies using the rodent model system demonstrate that pregnancy could be reducing the risk of breast cancer by persistently altering the hypothalamic–pituitary axis, which could have implications for breast cancers in humans as well.
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Tena-Sempere, Manuel, i Ilpo Huhtaniemi. "Sex in the brain: How the brain regulates reproductive function". Biochemist 31, nr 2 (1.04.2009): 4–7. http://dx.doi.org/10.1042/bio03102004.
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Reproductive functions are maintained by a complex hormonal regulatory network called the hypothalamic–pituitary–gonadal (HPG) axis, which is under the hierarchical control of a network of neurohormones that ultimately modulate the synthesis and pulsatile release of the decapeptide gonadotropin-releasing hormone (GnRH) by specialized neural cells distributed along the mediobasal hypothalamus. This neuropeptide drives the production of the two gonadotropic hormones of the anterior pituitary gland, luteinizing hormone (LH) and folliclestimulating hormone (FSH), which are released into the circulation and regulate specific functions of the ovary and testis. In turn, hormones produced by the gonads feed back to the hypothalamic– pituitary level to maintain functional balance of the HPG axis, through negative and positive (only in females) regulatory loops. In this article, we review the main hormonal regulatory systems that are operative in the HPG axis with special emphasis on recent developments in our knowledge of the neuroendocrine pathways governing GnRH secretion, including the identification of kisspeptins and G-protein-coupled receptor 54 (GPR54) as major gatekeepers of puberty onset and fertility.
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Pekary, A. E., M. Knoble, N. H. Garcia, S. Bhasin i J. M. Hershman. "Testosterone regulates the secretion of thyrotrophin-releasing hormone (TRH) and TRH precursor in the rat hypothalamic-pituitary axis". Journal of Endocrinology 125, nr 2 (maj 1990): 263–70. http://dx.doi.org/10.1677/joe.0.1250263.
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ABSTRACT Orchidectomy has been reported to decrease concentrations of thyrotrophin (TSH) in the circulation of male rats without affecting serum levels of thyroid hormones. To understand the mechanism underlying this observation, we have measured the effect of gonadal status on the in-vitro release of TSH-releasing hormone (TRH) by male rat hypothalamic fragments. Because hormone release rates can be affected by changes in the post-translational processing of the hormonal precursors, we have also studied the corresponding changes in the concentrations of TRH and TRH-Gly, a TRH precursor peptide in hypothalamus and pituitary, by radioimmunoassay. We observed a significant decline in the in-vitro release of TRH from incubated hypothalami 1 week after castration, which was quantitatively reversed by testosterone replacement. Concentrations of TRH and TRH-Gly in the posterior pituitary, on the other hand, which derive from neurones of hypothalamic origin, increased significantly with castration and were returned to the normal range by testosterone replacement. We conclude that the primary effect of testosterone is the stimulation of hypothalamic TRH release, resulting in the depletion of TRH and TRH precursors from TRH-containing neurones which project into the median eminence and posterior pituitary. Journal of Endocrinology (1990) 125, 263–270
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Mori, M., i M. Yamada. "Thyroid hormones regulate the amount of thyrotrophin-releasing hormone in the hypothalamic median eminence of the rat". Journal of Endocrinology 114, nr 3 (wrzesień 1987): 443–48. http://dx.doi.org/10.1677/joe.0.1140443.
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ABSTRACT The negative-feedback action of thyroid hormones on TRH in the hypothalamic median eminence was examined. Thyroidectomy caused a progressive decrease in TRH content of the median eminence, but not of the whole hypothalamus. In contrast, it did not affect the LHRH content of the median eminence. Administration of thyroid hormone prevented the decrease in TRH content of the median eminence after thyroidectomy. Destruction of the hypothalamic paraventricular nucleus (PVN) led to a significant reduction in TRH content of the median eminence in normal and thyroidectomized rats. These data provide evidence that thyroid hormones regulate directly the amount of median eminence TRH which is derived from the hypothalamic PVN in the rat. J. Endocr. (1987) 114, 443–448
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Guillemin, Roger. "Hypothalamic hormones a.k.a. hypothalamic releasing factors". Journal of Endocrinology 184, nr 1 (styczeń 2005): 11–28. http://dx.doi.org/10.1677/joe.1.05883.
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Originally searched for and eventually isolated as factors of hypothalamic origin controlling anterior pituitary secretions, these hypophysiotropic peptides are now a chapter of physiology and medical endocrinology of their own. Defying the concept of ‘neuropeptides’ they and their receptors are now known to be ubiquitous and to have subtle as well as profound effects on a large number of functions of both soma and psyche. This review will be composed of brief essays on current knowledge of each of the original ‘hypothalamic hormones’, TRH, GnRH, somatostatin, GHRH and corticotropin releasing hormone and will close on possible and probable futures.
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Yli-Mattila, Tapani, El-Refaie Kenawy, H. Rozsypal, N. F. Ismail, Izet Masić, Patrice Bouree i Kamal G Effat. "An Overview of the Hypothalamus: A Review of Hypothalamic–Pituitary Axis and Autoantibody Related Disorders". Endocrinology and Disorders 1, nr 3 (5.12.2017): 01–03. http://dx.doi.org/10.31579/2640-1045/095.
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The hypothalamus is a portion of the brain that contains a number of small nuclei with a variety of functions. One of the most important functions of the hypothalamus is to link the nervous system to the endocrine system via the pituitary gland. The hypothalamus is located below the thalamus and is part of the limbic system. In the terminology of neuroanatomy, it forms the ventral part of the diencephalon. All vertebrate brains contain a hypothalamus. In humans, it is the size of an almond. The hypothalamus is responsible for the regulation of certain metabolic processes and other activities of the autonomic nervous system. It synthesizes and secretes certain neurohormones, called releasing hormones or hypothalamic hormones, and these in turn stimulate or inhibit the secretion of hormones from the pituitary gland.
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Schally, Andrew V. "Hypothalamic hormones". Anti-Cancer Drugs 5, nr 2 (kwiecień 1994): 115–30. http://dx.doi.org/10.1097/00001813-199404000-00001.
Pełny tekst źródłaRozprawy doktorskie na temat "Hypothalamic hormones"
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Tam, Sau-ping. "Gene expression of hypothalamic somatostatin, growth hormone releasing factor, and their pituitary receptors in hypothyroidism /". Hong Kong : University of Hong Kong, 1996. http://sunzi.lib.hku.hk/hkuto/record.jsp?B17538865.
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譚秀萍 i Sau-ping Tam. "Gene expression of hypothalamic somatostatin, growth hormone releasingfactor, and their pituitary receptors in hypothyroidism". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1996. http://hub.hku.hk/bib/B31213637.
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Dromey, Jasmin Rachel. "Elucidating novel aspects of hypothalamic releasing hormone receptor regulation". University of Western Australia. School of Medicine and Pharmacology, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0133.
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[Truncated abstract] G-protein coupled receptors (GPCRs) form one of the largest superfamilies of cell-surface receptors and respond to a vast range of stimuli including light, hormones and neurotransmitters. Although structurally similar, GPCRs are regulated by many diverse proteins, which allow the specific functions of each receptor to be carried out. This thesis focussed on two well-documented GPCRs, the thyrotropin releasing hormone receptor (TRHR) and gonadotrophin-releasing hormone receptor (GnRHR), which control the thyroid and reproductive endocrine pathways respectively. Although each of these anterior pituitary receptors is responsible for distinct physiological responses, both are integral to normal development and homeostasis. This thesis focused on three areas of GPCR regulation: ?-arrestin recruitment, transcription factor regulation and receptor up-regulation. The role of the cytoplasmic protein, ?-arrestin, has perhaps been previously underestimated in GPCR regulation, but it is now increasingly apparent that ?-arrestins not only inhibit further G-protein activation and assist in GPCR internalisation but also act as complex scaffolding platforms to mediate and amplify downstream signalling networks for hours after initial GPCR activation. It is therefore becoming increasingly important to be able to monitor such complexes in live cells over longer time-frames. ... Members of the E2F transcription family have been previously identified by this laboratory as potential GnRHR interacting proteins, via a yeast-2-hybrid screen and BRET. This thesis further investigated the role of E2F family members and demonstrates that a range of GPCRs are able to activate E2F transcriptional activity when stimulated by agonist. However, despite GnRHR displaying robust E2F transcriptional activation upon agonist stimulation, this did not result in any conclusive evidence for functional regulation, although it is possible E2F may modulate and assist in GnRHR trafficking. Furthermore it is apparent that E2F family members are highly redundant, as small effects in GnRHR binding and cell growth were only observed when protein levels of both E2F4 and E2F5 were altered. During the course of the investigation into the effect of E2F transcription on GPCR function, it was evident that long-term agonist stimulation of GnRHR had a profound effect on its expression. As this was explored further, it became clear that this agonist-induced up-regulation was both dose- and time-dependent. Furthermore, altering levels of intracellular calcium and receptor recycling/synthesis could modulate GnRHR up-regulation. In addition, an extremely sensitive CCD camera has been used for the first time to visualise the luciferase activity attributed to GnRHR up-regulation. Overall, this thesis demonstrates the complex nature of GPCR regulation. For the first time, long-term BRET analysis on ?-arrestin interactions with both classes of GPCRs has been examined in a variety of cellular formats. This has given valuable insights into the roles of phosphorylation and internalisation on ?-arrestin interaction. Additionally, this thesis has revealed that prolonged agonist exposure increases receptor expression levels, which has major implications for drug therapy regimes in the treatment of endocrine-related disorders and tumours.
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Ladyman, Sharon Rachel, i n/a. "Characterisation of hypothalamic leptin resistance during pregnancy in the rat". University of Otago. Department of Pharmacology & Toxicology, 2006. http://adt.otago.ac.nz./public/adt-NZDU20070427.154329.
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Leptin is primarily an adipose-derived hormone that acts in the hypothalamus to regulate body fat levels by suppressing appetite and increasing metabolic rate. Pregnancy is characterised by increased food intake and fat mass to meet the metabolic demands of this physiological state. Leptin concentrations also increase during pregnancy, but this does not prevent the pregnancy-induced hyperphagia, suggesting a state of leptin resistance. The aims of this thesis were to measure hypothalamic leptin responsiveness during pregnancy and to investigate the potential mechanisms underlying pregnancy-induced leptin resistance.
The satiety response to intracerebroventricular (i.c.v) leptin was measured in fasted non-pregnant (diestrous), early pregnant (day 7), and mid-pregnant (day 14) rats. Serial blood samples collected from another group of rats demonstrated that despite initial elevated plasma leptin concentrations in pregnant rats, fasting significantly decreased leptin concentrations so that pregnant and non-pregnant groups had similar, low leptin concentrations. Leptin treatment significantly reduced food intake in non-pregnant and early pregnant rats but not in mid-pregnant rats. In addition, there was no post-fasting hyperphagic response in the pregnant rats. These results indicate that pregnant rats become resistant to the satiety action of leptin.
To investigate the mechanisms underlying pregnancy-induced leptin resistance, leptin-induced activation of hypothalamic leptin-target neurons was examined. Signal transducer and activator of transcription 3 (STAT3) phosphorylation was measured in non- pregnant and mid-pregnant rats following i.c.v. administration of leptin. Western blot and immunohistochemistry analysis indicated that leptin-induced STAT3 phosphorylation was significantly reduced in the ventromedial nucleus of the hypothalamus (VMH) during pregnancy. A suppression in the amount of leptin-induced STAT3 activation was observed in the arcuate nucleus during pregnancy, yet there was no overall change in the number of leptin responsive neurons compared to non-pregnant rats. This raises the possibility of a decrease in the degree of responsiveness of arcuate nucleus neurons to leptin during pregnancy. Using double-labelled immuno-histochemistry for alpha-melanocyte stimulating hormone (α-MSH) and leptin-induced pSTAT3 it was demonstrated that pro-opiomelanocortin (POMC) neurons remain responsive to leptin during pregnancy. In the VMH, consistent with the reduced pSTAT3, pregnancy also induced a 2-fold reduction in mRNA for the long form of the leptin receptor (Ob-Rb), the only isoform with full signal transduction capabilities. Expression of mRNA for one of the short forms of the leptin receptor (Ob-Ra) in the choroid plexus was decreased in early and late pregnancy, suggesting that reduced leptin transport into the brain may contribute to pregnancy-induced leptin resistance. CSF/plasma leptin concentration ratios did not differ between pregnant and non-pregnant rats however, suggesting unimpaired leptin transport during pregnancy.
These results indicate that pregnancy is a state of hypothalamic leptin resistance and is associated with impaired activation of the leptin-induced JAK/STAT3 signalling pathway in the VMH and arcuate nucleus, and reduced expression of Ob-Rb mRNA in the VMH. This state of leptin resistance represents an important adaptation of the maternal brain allowing increased food intake and fat mass so that the maternal body can meet the metabolic demands of pregnancy and prepare for the subsequent demands of lactation.
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Innala, Leyla. "Organizational effects of gonadal hormones on the hypothalamic-pituitary-adrenal axis and glucocorticoid receptor responses in male and female rats". Thesis, University of British Columbia, 2016. http://hdl.handle.net/2429/58874.
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Neonatal gonadal hormones during critical periods of development can irreversibly alter the adult hypothalamic-pituitary-adrenal (HPA) axis. The aims of this thesis were to investigate the role of neonatal gonadal hormones to 1. have direct organizational effects on the HPA axis or via indirect effects on corticosterone binding globulin that lead to compensatory changes in HPA output and 2. if changes in HPA output are met by changes in glucocorticoid receptor (GR) responses. To assesses these questions, the neonatal hormone milieu in Long Evan rats were manipulated in males by blocking the conversion of testosterone to estradiol with an aromatase blocker (ATD) and in females by administering testosterone propionate (TP). As adults, we assessed the influence of neonatal hormone manipulations on plasma corticosterone levels and GR activation in response to acute and repeated restraint exposure. GR responses were assessed using western blots to analyze GR translocation (nuclear/ nuclear and cytoplasm) and phosphorylation of GR at the serine 211 site (Ser211). We then assessed if changes in GR translocation and Ser211 followed restraint induced changes in total and estimated free CORT levels. Our results showed significant differences in corticosterone levels in neonatal ATD treated male and TP treated female rats compared to their same sex control groups under basal-naïve conditions and after restraint exposure, respectively. In both sexes, for GR translocation and Ser211, there was a main effect of restraint stress exposure, and overall significant positive correlations with CORT (total and estimated free) levels. GR translocation was lower in neonatal TP treated females, with no effect in Ser211. Differences between male neonatal ATD and Sham groups were observed compared to untouched controls in Ser211, indicating the effects of the neonatal ATD treatment appear to be due to effects of surgery and gonadal hormone milieu exposure. Adult gonadal hormone levels differed between female neonatal groups, which are likely due to organizational effects of the neonatal treatments. The current study demonstrates neonatal gonadal hormones have long lasting effects on adult corticosterone outputs and sequential GR responses.Medicine, Faculty of
Graduate
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Solomon, Matia B. "The Effect of Gonadal Hormones on Agonistic Behavior in Previously Defeated Female and Male Syrian Hamsters". Digital Archive @ GSU, 2006. http://digitalarchive.gsu.edu/psych_diss/13.
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Following social defeat, male hamsters exhibit behavioral changes characterized by a breakdown of normal territorial aggression and an increase in submissive/defensive behaviors in the presence of a non-aggressive intruder (NAI). We have termed this phenomenon conditioned defeat (CD). By contrast, only a small subset of defeated females exhibit submissive/defensive behavior in the presence of a NAI. We hypothesized that fluctuations in gonadal hormones might contribute to differences in the display of submissive behavior in intact female hamsters. Following social defeat, proestrous females (higher endogenous estradiol) were more likely to display conditioned defeat compared with diestrous 1 (lower endogenous estradiol) females. This finding suggests that there is an estrous cycle-dependent fluctuation in the display of CD in female hamsters and suggests that increased estradiol might contribute to increased submissive behavior. We then demonstrated that ovariectomized females given estradiol prior to CD testing exhibited significantly higher submissive behavior in the presence of a NAI suggesting that estradiol increases the expression of CD in female hamsters. We have also shown that castrated males that were singly housed for four weeks displayed significantly more submissive behavior than did their intact counterparts. Interestingly, castrated and intact males that were singly housed for 10 days prior to behavioral testing displayed similar behavior during CD testing. Together these data suggest that androgens and isolation modulate the display of CD in male hamsters. Finally, we examined brain activation following CD testing in defeated males and females (in diestrus 1 and proestrus). Defeated male and proestrous females exhibited increased Fos activation in the dorsal lateral septum and hypothalamic paraventricular nucleus relative to defeated diestrous 1 females. Diestrous 1 females exhibited increased Fos expression in the lateral bed nucleus of the stria terminalis compared with both defeated groups. Collectively, these data suggest that gonadal hormones and duration of individual housing modulate the display of CD in female and male hamsters and that those animals which display CD exhibit differences in patterns of neuronal activation than do those that do not display CD.
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Jean, Arnaud. "Plasticité moléculaire de l'aire pré-optique médiane de l'hypothalamus induite par l'expérience sexuelle chez la souris mâle". Thesis, Paris 6, 2017. http://www.theses.fr/2017PA066109/document.
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Les mâles sexuellement expérimentés présentent des modifications à long terme de l'arborisation dendritique, de modifications épigénétiques ainsi qu'une augmentation des niveaux d'expression de protéines associées à la neurotransmission glutamatergique et à la microglie dans l'aire pré-optique médiane (mPOA). En revanche, les concentrations plasmatiques et hypothalamiques en hormones stéroïdes ainsi que les propriétés du système nitrergique, connues pour être modulés par l'expérience sexuelle chez le rat, ne sont pas modifiées. Dans un second temps, l'implication de la voie de signalisation ERK1/2 dans la réponse comportementale associée à l'expérience sexuelle a été étudiée. Nous avons montré que cette voie de signalisation, activée dans la mPOA lors de l'accouplement, est potentialisée par l'expérience sexuelle. Nous avons ensuite démontré que son activation est possible par une action rapide (30 minutes) des stéroïdes. Enfin, nous avons montré que l'inhibition de la voie ERK1/2 avant un premier accouplement n'altère pas la mise en place de l'expérience sexuelle mais diminue de façon réversible la motivation sexuelle des mâles. Ainsi, l'expérience sexuelle est à l'origine de modifications structurales et biochimiques à long terme de la mPOA. Ces modifications, différentes de celles connues chez le rat, sont associées à une potentialisation de la voie de signalisation ERK1/2 activée de façon transitoires durant l'accouplement. Ces résultats mettent en évidence la nécessité d'élaborer un nouveau modèle, différent de celui établi chez le rat, permettant d'expliquer l'amélioration comportementale associée à l'expérience sexuelle chez la souris mâleSexually experimented males exhibit long term modifications of the dendritic arborization, epigenetic modifications and increased levels of microglia and glutamate associated protein within the hypothalamic medial preoptic area (mPOA). However, hypothalamic and plasmatic concentration of steroid hormones and the nitrergic system are not impacted, contrary to data obtained in rat.The involvement of the ERK1/2 signaling pathway in the induction of sexual experience has also been studied. We showed that ERK1/2 pathway was activated within the mPOA during mating. This activation was increased in sexually experienced males. Furthermore, we showed ex vivo on hypothalamic slices that sex steroids were capable of rapidly (30 min) activate this pathway. Finally, the inhibition of ERK1/2 phosphorylation before the first mating did not disrupt the induction of sexual experience but decreased sexual motivation in a reversible manner.Taken together, these results indicate that long lasting and transitory plasticity mechanisms leading to sexual experience are different between rat and mouse. This indicate the necessity to elaborate a new molecular model associated with the behavioral improvement induced by sexual experience in male mouse
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Darzy, Ken H. K. "Pharmacological and physiological studies of anterior·pituitary hormones secretion (GH, ACTH and TSH) in cranially irradiated adult cancer survivors with radiation-induced hypothalamic- pituitary dysfunction". Thesis, University of Manchester, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.490184.
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THE UNIVERSITY OF MANCHESTER ABSTRACT OF THESIS submitted by Ken Darzy for the Degree of M.D. and entitled 'Pharmacological and physiological studies of anterior pituitary hormones secretion (GH, ACTH and TSH) in cranially irradiated adult cancer survivors with radiation-induced hypothalamic-pituitary dysfunction'. Month and Year of submission: June 2008. This thesis describes the dynamics of GH, ACTH/Cortisol and TSH/T4 secretion in adult cancer survivors irradiated for non-pituitary brain tumours or leukaemia. Stimulated and physiological hormonal secretions were studied simultaneously. It was shown that, in patients with severe radiation-induced GH deficiency diagnosed by failure to pass both the ITT and the GHRH + AST, pulsatile GH secretion and diurnal rhythm are preserved, yet with severe amplitude attenuation and an overall feminised pattern of GH secretion characterized by relatively higher inter-peak levels (tonic secretion) and increased secretory disorderliness, as measured by ApEn. Patients with normal individual peak GH responses to the ITT and the GHRH+AST still showed evidence of damage to the h-p axis, as the overall mean GH responses were reduced by 50%. However, spontaneous fed and fasting GH secretion in this group was fully maintained both individually and at a group level compared with a matched control group. This finding argues against the previously held belief that somatotroph dysfunction is primarily due to radiation-induced GHRH deficiency, as the combined effect of reduced GHRH and secondary somatotroph atrophy would be expected to result in reduced spontaneous GH secretion. It was, therefore, concluded that radiation causes direct pituitary damage and that endogenous hyperstimulation of the h-p axis mediated by a compensatory increase in GHRH release restores normality of GH secretion in these patients with partially damaged somatotrophic axis (compensated GHD). Based on the findings in some patients, it was also suggested that 'near maximal' endogenous hyper-stimulation and GHRH release may limit further stimulation with the ITT, so much so, that a failed ITT response can occur in the presence of normal GHRH+AST response and normal spontaneous GH secretion. . These findings in adults has lead to the suggestion that failure of the hyperstimulated partially damaged h-p axis to increase GH secretion during periods of increased demand, such as growth and puberty may explain what has previously been described as radiation-induced GH neurosecretory dysfunction. It was reasonable to conclude that unlike the ITT, a failed response to the GHRH+AST almost always indicated GHD in the irradiated adult. On the contrary, failure to pass the ITT reflects 'a potential failure of the h-p axis to respond to increased demands and therefore it should remain the gold standard guide for the need for GH replacement therapy in children. Adult cancer survivors with normal ACTH reserve indicated by normal cortisol responses to the ITT have showed parallel and significant increases in fed and fasting 24-hour integrated cortisol concentrations and secretion rates with no change in half-life. This has been attributed to a pro-active h-p-adrenal axis with increased CRH-ACTH release mediated by the direct effects of radiation on the axis or perhaps the higher level of chronic stress in cancer survivors. In addition, euthyroid adult cancer survivors have significantly increased stimulated and integrated 24-hour TSH levels, especially in spinally irradiated patients with severe GHD. There was no change in the TSH bioactivity and the increase in TSH levels could be attributed to subclinical thyroidal damage, GHD-induced reduction in somatostatin tone and/or radiation-induced reduction in somatostatin and dopamine tone. The maximum TSH surge in the. 24-hour profile was slightly but significantly reduced. The subnormal nocturnal TSH surge seen in some patients reflected a shift in the timing of the peak and/or nadir TSH levels rather than a genuine loss of the TSH diurnal rhythm, as similarly seen in some normal individuals. This finding argues against the existence of so-called hidden central hypothyroidism. In summary, this thesis has provided novel insights into the pathophysilogy and site of radiation damage and its relevance to the clinical application ofthe diagnostic tests currently in use.
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Christian, Mark. "Investigation of the influence of sex steroid hormones and potential endocrine disrupting chemicals on developing rat hypothalamic dopaminergic neurones in vitro and in vivo". Thesis, Imperial College London, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.327047.
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Brischoux, Frédéric. "Etude ontogénétique du système à hormone de mélano-concentration (MCH) chez le rat et régionalisation de l'hypothalamus". Besançon, 2002. http://www.theses.fr/2002BESA0006.
Pełny tekst źródłaKsiążki na temat "Hypothalamic hormones"
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Kenkyūjo, Gunma Daigaku Naibunpi, i Gunma Symposium on Endocrinology (22nd : 1984 : Maebashi-shi, Japan), red. Hypothalamic peptides in endocrinology: Morphological and physiological aspects. Tokyo: Center for Academic Publications Japan, 1985.
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Shennan, Kathleen I. J. Regulation of hypothalamic neurotensin by thyroid hormones. Birmingham: University of Birmingham, 1985.
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P, Beck-Peccoz, red. Syndromes of hormone resistance on the hypothalamic-pituitary-thyroid axis. Boston: Kluwer Academic Publishers, 2004.
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Liposits, Zsolt. Ultrastructural immunocytochemistry of the hypothalamic corticotropin releasing hormone synthesizing system: Anatomical basis of neuronal and humoral regulatory mechanisms. Stuttgart: Gustav Fischer Verlag, 1990.
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Rasmussen, Jane Elliott. The trophic effects of estradiol on virally transformed hypothalamic cell lines. [New Haven: s.n.], 1990.
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International Symposium on Protirelin Tartrate (TRH-T) (1988 Taormina, Italy). Protirelin tartrate (TRH-T): Pharmacological and clinical studies : recent advances and perspectives. London: Libbey, 1988.
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Ferring Symposium on Brain and Pituitary Peptides (3rd 1985 Noordwijk, Netherlands). Pulsatile GnRH 1985: Proceedings of the 3rd Ferring Symposium, Noordwijk, September 11-13, 1985. Redaktor Coelingh Bennink, Herman Jan Tymen, 1943-. Haarlem: Ferring, 1985.
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B, Bercu Barry, Walker Richard F. 1939- i International Symposium on Growth Hormone Secretagogues (1994 : Saint Petersburg Beach, Fla.), red. Growth hormone secretagogues. New York: Springer, 1996.
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Beck-Peccoz, Paolo, red. Syndromes of Hormone Resistance on the Hypothalamic-Pituitary-Thyroid Axis. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4020-7852-1.
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F, Schatzberg Alan, Nemeroff Charles B i American College of Neuropsychopharmacology. Meeting, red. The Hypothalamic-pituitary-adrenal axis: Physiology, pathophysiology, and psychiatric implications. New York: Raven Press, 1988.
Znajdź pełny tekst źródłaCzęści książek na temat "Hypothalamic hormones"
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Sandow, Jürgen. "Hypothalamic Hormones". W Drug Discovery and Evaluation: Pharmacological Assays, 3627–90. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-05392-9_83.
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Stratakis, Constantine A., i George P. Chrousos. "Hypothalamic Hormones". W Endocrinology, 185–209. Totowa, NJ: Humana Press, 1997. http://dx.doi.org/10.1007/978-1-59259-641-6_13.
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Arimura, Akira. "Hypothalamic Hormones". W Neuroendocrinology in Physiology and Medicine, 41–58. Totowa, NJ: Humana Press, 2000. http://dx.doi.org/10.1007/978-1-59259-707-9_3.
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Sandow, Jürgen. "Hypothalamic Hormones". W Drug Discovery and Evaluation: Pharmacological Assays, 1–76. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27728-3_83-1.
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Bhandari, Prasan. "Hypothalamic and pituitary hormones". W Pharmacology Mind Maps for Medical Students and Allied Health Professionals, 432–38. Boca Raton, FL : CRC Press/Taylor & Francis, 2020.: CRC Press, 2019. http://dx.doi.org/10.1201/9780429023859-48.
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Subramanian, Umamaheswari. "Hypothalamic and Pituitary Hormones". W Introduction to Basics of Pharmacology and Toxicology, 633–52. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-33-6009-9_42.
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Purnell, Jonathan Q., Mary Samuels i Maria Fleseriu. "Hypothalamic–Pituitary Hormones and Obesity". W Handbook of Obesity - Volume 1, 241–49. Wyd. 4. Boca Raton: CRC Press, 2023. http://dx.doi.org/10.1201/9781003437673-26.
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Purnell, Jonathan Q., Mary Samuels i Maria Fleseriu. "Hypothalamic–Pituitary Hormones and Obesity". W Handbook of Obesity, Two-Volume Set, Vol1:241—Vol1:249. Wyd. 5. Boca Raton: CRC Press, 2024. http://dx.doi.org/10.1201/9781003437734-26.
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Wuarin, Jean-Pierre, i F. Edward Dudek. "Neuromodulatory Action of Opioid Peptides on Hypothalamic Neurons". W Alcohol and Hormones, 295–305. Totowa, NJ: Humana Press, 1995. http://dx.doi.org/10.1007/978-1-4612-0243-1_16.
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Cocchi, D. "Radioimmunoassay of Pituitary and Hypothalamic Hormones". W Radioimmunoassay in Basic and Clinical Pharmacology, 255–90. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71809-0_11.
Pełny tekst źródłaStreszczenia konferencji na temat "Hypothalamic hormones"
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RAVIZZA, L., R. G. MASERA, P. PROLO, A. H. STAURENGHI, E. ZANALDA, M. L. SARTORI i A. ANGELI. "MODULATION OF NATURAL KILLER (NK) CELL ACTIVITY BY HORMONES OF THE HYPOTHALAMIC-PITUITARY-ADRENAL AXIS IN ANOREXIA NERVOSA". W IX World Congress of Psychiatry. WORLD SCIENTIFIC, 1994. http://dx.doi.org/10.1142/9789814440912_0012.
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Perov, S. Yu, i S. A. Askerova. "THE NEUROENDOCRINE SYSTEM RESPONSE OF 2-5 G COMMUNICATION ELECTROMAGNETIC FIELD ANIMAL EXPOSURE". W The 16th «OCCUPATION and HEALTH» Russian National Congress with International Participation (OHRNC-2021). FSBSI “IRIOH”, 2021. http://dx.doi.org/10.31089/978-5-6042929-2-1-2021-1-398-402.
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Abstract: Background. The neuroendocrine effect on the hypothalamus-pituitary-adrenal cortex axis is significant example stressor of electromagnetic exposure for biological object. Aim. The neuroendocrine effect investigation of multi-frequency electromagnetic field laboratory animals’ exposure from 2-5 generations cellular base stations Methods. The neuroendocrine status evaluated by corticosterone and adrenocorticotropic hormone (ACTH) concentrations in blood exposed and sham rats. ACTH and corticosterone rat blood assessed by immunoenzyme method. Results. The results of the multi-frequency electromagnetic field laboratory animals’ exposure from 2-5 generations cellular base stations in a chronic experiment showed wave-like changes in the hypothalamic-pituitary-adrenal function. These changes are manifested in an immediate increase in corticosteroids secretion and depression of the corticosteroid response to normal or subnormal levels. After 3 month chronic exposure there was a secondary rise in hormonal secretion.
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Steiger, A., J. Weeger, M. Ising, M. Uhr i U. Schmidt. "Influence of corticotropin releasing hormone receptor type 1 genotype on changes of hypothalamo-pituitary-adrenocortical hormones and sleep after Trier social stress test". W Abstracts of the 1st Symposium of the Arbeitsgemeinschaft für Neuropsychopharmakologie und Pharmakopsychiatrie (AGNP) and Deutsche Gesellschaft für Biologische Psychiatrie (DGBP). Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1679154.
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Oliveira, Jefferson Borges de, Caroline Berthier Zanin, Gustavo Carreira Henriques, Maiévi Liston, Rafael Glória Zatta, Rodrigo de Faria Martins i Tatiana Pizzolotto Bruch. "Pallister-Hall Syndrome - case report". W XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.575.
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In 1980, Hall et all described a syndrome characterized by “hamartoblastoma”, hypopituitarism, unperfurated anus, polydactyly postaxial and numerous visceral anomalies, today known as Pallister-Hall Syndrome. On the study, Hall et all reported six cases of children with that malformation syndrome - lethal on neonatal period. None of the newborns had anterior hypophysis and the hypothalamic tumor was apparent in the inferior part of the brain, going from the optic chiasm to the interpeduncular fossa. Besides, other anomalies were found, such as: laryngeal split, abnormal pulmonary lobation, renal agenesis or dysplasia, shorts fourth metacarpals, nail dysplasia, multiple mouth frenulum, hypoadrenalism, congenital cardiomyopathy and intrauterine growth retardation. Every case was sporadic, the chromosome were apparently normal, without consaguinity relations. Several similar, milder and even asymptomatic cases were described later on. Kletter and Biesecker (1992), Topf et all (1993) and Penman Splitt et all (1994), define the disease as dominant autosomal inheritance. Kettler and Biesecker (1992) stated that most cases as sporadic as a result of a gene mutation with variable expressiveness. According to Biesecker et al (1996), an international workshop determined diagnostic criteria to the Syndrome: Hypothalamic Hamartroma and Central Polydactyly; First degree relative with hypothalamic hamartroma and polydactyly; Dominant autosomal parrent inheritance or in a consistent form with germaine mosaicism. The radiological changes are important for differential diagnosis between Pallister-Hall Syndrome and other hamartroma-present diseases. The hypothalamic hamartroma isolated has phenotypical features and causes hormonal disorders such as early puberty. On the MRI (Magnetic resonance imaging) it shows hyperintese sign on attenuated fluid. On the other hand, the Pallister-Hall Syndrome the hamartroma shows itself as a isointense signs along with other deformities as polydactyly, for example. According to Kuo et al (1999), on MRI, the classic hypothalamic hamartroma isn’t calcified, is homogenous and isointense to the grey matter on weight images in T1, and isointense and often hyperintense on weight images in T2. Those findings are pretty distinctive and help distinguish the hypothalamic hamartroma from ordinary lesions, as craniopharyngioma and hypothalamic/opticalchiasmic glioma, observed in children. Case report: The patient ALDV, male, born in 30/12/1995, was referred to evaluation on the Medical Genetic Service from HCPA. At the time, aged one year and 8 months, he was the only son of a young, healthy couple with no consanguinity. The family history of similar cases or other genetic pathologies are unknown. The prenatal happened with no intercurrences, unless the smoking mother. It was a natural birth; Birth Weight: 2kg; High: 42cm; PC: 32cm. APGAR 9. At 8 months, starts an investigation for precocious puberty, and a karyotype was performed in her hometown: 46, XY (normal). He presents convulsive crises since one year old. DNPM: cephalic support when he had 8 months, sat without support at the age of one. Physical examination: Head circumference in the 97th percentile, length above the 97th percentile. Good general condition, dysmorphic, facies with fusion of eyebrows (sinofre), epicanthus, small nose, dysplastic ears with a broad shield, three café-au-lait spots on the body. Presence of pubic hair. Increase in length and diameter of the penis, as well as of the testicles, in relation to chronological age. In the hands, significant brachydactyly with bitateral hexadactyly. In the feet, bilateral hexadactyly. Proximal cutaneous syndactyly between the 2nd and 3rd bilateral arthroids, mainly on the right. Additional exams: Rx of hands and wrists for bone age: 7 years; Chronological Age: 1 year and 10 months. Normal abdominal ultrasound; Computed Tomography of Skull/Magnetic Resonance of Skull: hypothalamic expansive lesion (3 cm), compatible with hamartoma; triventricular hydrocephalus; Cavum septum pellucidum. Endocrinological Evaluation: compatible with precocious puberty of central cause. High resolution karyotype: 46, XY (normal). Computed tomography of the brain: Examination for neurological control, performed on 10/12/2014, 18-year-old patient. It was observed solid nodular formation in the hypothalamic region, hypodense, with well-defined limits, in close contact with the mesencephalon, without impregnation by contrast medium administered intravenously, measuring about 2.9 X 2.4 X 3.0 cm, in the respective laterolateral, anteroposterior and craniocaudal planes, which in correlation with the patient’s clinical history may be related to hypothalamic Hamartoma.
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Yan, Bin. "Role of Anti-Müllerian Hormone (AMH) in Regulating Hypothalamus-Pituitary Function". W ICBBE '20: 2020 7th International Conference on Biomedical and Bioinformatics Engineering. New York, NY, USA: ACM, 2020. http://dx.doi.org/10.1145/3444884.3444899.
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Aflahiyah, Shiva, Didik Gunawan Tamtomo i Hanung Prasetya. "A Meta-Analysis on the Effectiveness of Prenatal Yoga in Reducing Cortisol Hormone in Pregnancy". W The 7th International Conference on Public Health 2020. Masters Program in Public Health, Universitas Sebelas Maret, 2020. http://dx.doi.org/10.26911/the7thicph.05.47.
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ABSTRACT Backgrund: A growing body of evidence suggests that activity of the stress-responsive hypothalamic-pituitary-adrenal axis and its end-product cortisol also may be associated with perinatal emotional well-being. A number of preventive interventions, such as Yoga, targeting psychosocial and physiological risk factors for perinatal depression have utilized mind-body practices, which embody the idea that the mind interacts with the body to influence physical functioning, improve symptoms, and promote health. This study aimed to investigate effectiveness of prenatal yoga in reducing cortisol hormone in pregnancy Subjects and Method: This was a meta-analysis and systematic review. This study collected published articles during 2000 to 2020 from PubMed, Science Direct, Springer, Proquest, and Chocrane electronic databases. The inclusion criteria were full text, randomized controlled trial, and prenatal yoga intervention. The study subjects were pregnant women who received prenatal yoga for 8 to 20 weeks. Outcome was cortisol hormone reduction during pregnancy. The selected articles were analyzed by PRISMA flow chart and RevMan 5.3. Results: 5 articles from America and Asia were met the inclusion criteria. This study had high heterogeneity (I2=88%; p<0.001). Therefore, this study used random effect model (REM). Prenatal yoga reduced cortisol level 0.59 times in pregnancy (Mean Difference= -0.59; 95% CI= 1.18 to 0.01; p= 0.050). Conclusion: Prenatal yoga is effective to reduce cortisol level in pregnant women. Keywords: prenatal yoga, cortisol hormone, pregnant women Correspondence: Shiva Aflahiyah. Masters Program in Public Health, Universitas Sebelas Maret. Jl. Ir. Sutami 36 A, Surakarta 57126, Central Java. Email: shivaafla@gmail.com. DOI: https://doi.org/10.26911/the7thicph.05.47
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Seprina, Dina, Adelina Fitri i M. Dody Izhar. "Relationship amoung Body Mass Index, History of Maternal Menarche and Exposure of Pornographic Media with Menarche Age in Elementary School Students, Jambi". W The 7th International Conference on Public Health 2020. Masters Program in Public Health, Universitas Sebelas Maret, 2020. http://dx.doi.org/10.26911/the7thicph.03.46.
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ABSTRACT Background: Menstruation is the cyclic, orderly sloughing of the uterine lining, in response to the interactions of hormones produced by the hypothalamus, pituitary, and ovaries. Many factors influence the age of menarche, such as body mass index, history of maternal menarche and exposure to pornographic media. This study aimed to determine the relationship between body mass index, history of maternal and exposure to pornographic media with menarche age in elementary school students in Jambi City. Subject and Methods: This was a cross sectional study conducted at elementary school 207/ IV Jambi City, Indonesia. A sample of 74 students was purposively sampled. The dependent variable was age of menarche. The independent variables were body mass index (BMI), history of maternal menarche, and exposure to pornographic media. The data were collected by questionnaires, digital scales, and microtoise. Bivariate analysis was performed by Chi-Square. Results: Large body mass index (PR= 4.50; 95% CI= 0.40 to 51.29), history of early menarche (PR= 9.75; 95% CI= 3.35 to 28.36), and exposure to pornographic media (PR= 4.81; 95% CI= 1.74 to 13.29), accelerated age of menarche. Conclusion: Large body mass index, history of early menarche, and exposure to pornographic media, accelerate age of menarche. Keywords: Menarche, BMI, Pornography Media Correspondence: Adelina Fitri. Universitas Jambi. Jl. Lintas Jambi – Muara Bulian No. Km. 15, Mendalo Darat, Muaro Jambi Regency, Jambi, Indonesia. Email: adelinafitri@unja.ac.id. 081272030308. DOI: https://doi.org/10.26911/the7thicph.03.46
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Durães, Jullyana Almeida, i Samara Atanielly Rocha. "Sleep deprivation in the puerperal period: Experience report". W III SEVEN INTERNATIONAL MULTIDISCIPLINARY CONGRESS. Seven Congress, 2023. http://dx.doi.org/10.56238/seveniiimulti2023-119.
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Introduction: Sleep is characterized as a biological rhythm, endogenously generated and controlled by a neural structure located in the hypothalamus, regulated by homeostatic S and circadian C processes. Sleep has an important role for cognitive functioning, skills such as memory, reasoning, psychomotor vigilance and visual perception. The deprivation of this active event of such necessity for the organism causes all systems to be altered and leads to a decline in cognitive functions, with worsening quality of life and productivity. Objective: To discuss the experience lived by the health professional about sleep deprivation in the puerperal period and its impacts on the mother's life as a human being. Methodology: This is an experience report lived by a Nurse from the city, from December 11, 2022 to January 26, 2023 with women living in the city of Januária - MG, using the conversation wheel, sharing experiences and research on social networks. Results: Through the evaluation made, it is possible to identify that sleep interferes with the quality of life of these women. Bringing with it, an exacerbation of anxiety, feelings of anger, depression, suffering, emotional reactivity, fatigue, extreme tiredness, besides the guilt for not being productive as in the period before pregnancy. Conclusion: With this, it is possible to verify that sleep deprivation in the puerperal period is treated as something common, and many women in this period of regulation of pregnancy hormones wear out to the point of collapse. And it is up to the public authorities, together with the support network, community and health services to offer means of support so that they are treated as the situation requires. This experience adds great value for patients and health professionals, as the puerperal woman is treated in a holistic, empathetic and humanized way.
Raporty organizacyjne na temat "Hypothalamic hormones"
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Gothilf, Yoav, Yonathan Zohar, Susan Wray i Hanna Rosenfeld. Inducing sterility in farmed fish by disrupting the development of the GnRH System. United States Department of Agriculture, październik 2007. http://dx.doi.org/10.32747/2007.7696512.bard.
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Hypothalamic gonadotropinreleasing hormone (GnRH1) is the key hormone in the control of gametogenesis and gonadal growth in vertebrates. Developmentally, hypothalamic GnRHproducing neurons originate from the olfactory placode, migrate along olfactory axons into the forebrain, and continue to the preoptic area and hypothalamus where they function to stimulate gonadotropin secretion from the pituitary gland. An appropriate location of GnRH neurons within the hypothalamus is necessary for normal reproductive function in the adult; abnormal migration and targeting of GnRH neurons during embryogenesis results in hypogonadism and infertility. The developmental migration of GnRH neurons and axonal pathfinding in mammals are modulated by a plethora of factors, including receptors, secreted molecules, adhesion molecules, etc. Yet the exact mechanism that controls these developmental events is still unknown. We investigated these developmental events and the underlying mechanisms using a transgenic zebrafish model, Tg(gnrh1: EGFP), in which GnRH1 neurons and axons are fluorescently labeled. The role of factors that potentially affect the development of this system was investigated by testing the effect of their knockdown and mutation on the development of the GnRH1 system. In addition, their localization in relation to GnRH1 was described during development. These studies are expected to generate the scientific foundation that will lead to developing innovative technologies, based on the disruption of the early establishment of the GnRH system, for inducing sterility in farmed fish, which is highly desirable for economical and environmental reasons.
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Ori, Naomi, i Sarah Hake. Similarities and differences in KNOX function. United States Department of Agriculture, marzec 2008. http://dx.doi.org/10.32747/2008.7696516.bard.
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Hypothalamic gonadotropinreleasing hormone (GnRH1) is the key hormone in the control of gametogenesis and gonadal growth in vertebrates. Developmentally, hypothalamic GnRHproducing neurons originate from the olfactory placode, migrate along olfactory axons into the forebrain, and continue to the preoptic area and hypothalamus where they function to stimulate gonadotropin secretion from the pituitary gland. An appropriate location of GnRH neurons within the hypothalamus is necessary for normal reproductive function in the adult; abnormal migration and targeting of GnRH neurons during embryogenesis results in hypogonadism and infertility. The developmental migration of GnRH neurons and axonal pathfinding in mammals are modulated by a plethora of factors, including receptors, secreted molecules, adhesion molecules, etc. Yet the exact mechanism that controls these developmental events is still unknown. We investigated these developmental events and the underlying mechanisms using a transgenic zebrafish model, Tg(gnrh1: EGFP), in which GnRH1 neurons and axons are fluorescently labeled. The role of factors that potentially affect the development of this system was investigated by testing the effect of their knockdown and mutation on the development of the GnRH1 system. In addition, their localization in relation to GnRH1 was described during development. These studies are expected to generate the scientific foundation that will lead to developing innovative technologies, based on the disruption of the early establishment of the GnRH system, for inducing sterility in farmed fish, which is highly desirable for economical and environmental reasons.
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Gothilf, Yoav, Roger Cone, Berta Levavi-Sivan i Sheenan Harpaz. Genetic manipulations of MC4R for increased growth and feed efficiency in fish. United States Department of Agriculture, styczeń 2016. http://dx.doi.org/10.32747/2016.7600043.bard.
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The hypothalamic melanocortin system plays a central role in the regulation of food consumption and energy homeostasis in mammals. Accordingly, our working hypothesis in this project was that genetic editing of the mc4r gene, encoding Melanocortin Receptor 4 (MC4R), will enhance food consumption, feed efficiency and growth in fish. To test this hypothesis and to assess the utility of mc4r editing for the enhancement of feed efficiency and growth in fish, the following objectives were set: Test the effect of the mc4r-null allele on feeding behavior, growth, metabolism and survival in zebrafish. Generate mc4r-null alleles in tilapia and examine the consequences for growth and survival, feed efficiency and body composition. Generate and examine the effect of naturally-occurring mc4r alleles found in swordfish on feeding behavior, growth and survival in zebrafish. Define the MC4R-mediated and MC4R-independent effects of AgRP by crossing mc4r- null strains with fish lacking AgRP neurons or the agrpgene. Our results in zebrafish did not support our hypothesis. While knockout of the agrpgene or genetic ablation of hypothalamic AgRP neurons led to reduced food intake in zebrafish larvae, knockout (KO) of the mc4r gene not only did not increase the rate of food intake but even reduced it. Since Melanocortin Receptor 3 (MC3R) has also been proposed to be involved in hypothalamic control of food intake, we also tested the effectofmc3r gene KO. Again, contrary to our hypothesis, the rate of food intake decreased. The next step was to generate a double mutant lucking both functional MC3R and MC4R. Again, the double KO exhibited reduced food intake. Thus, the only manipulation within the melanocortin system that affected food intake in consistent with the expected role of the system was seen in zebrafish larvae upon agrpKO. Interestingly, despite the apparent reduced food intake in the larval stage, these fish grow to be of the same size as wildtype fish at the adult stage. Altogether, it seems that there is a compensatory mechanism that overrides the effect of genetic manipulations of the melanocortin system in zebrafish. Under Aim 3, we introduced the Xna1, XnB1l, and XnB2A mutations from the Xiphophorus MC4R alleles into the zebrafish MC4R gene. We hypothesized that these MC4R mutations would act as dominant negative alleles to increase growth by suppressing endogenous MC4R activity. When we examined the activity of the three mutant alleles, we were unable to document any inhibition of a co-transfected wild type MC4R allele, hence we did not introduce these alleles into zebrafish. Since teleost fish possess two agrpgenes we also tested the effect of KO of the agrp2 gene and ablation of the AgRP2 cells. We found that the AgRP2 system does not affect food consumption but may rather be involved in modulating the stress response. To try to apply genetic editing in farmed fish species we turned to tilapia. Injection of exogenous AgRP in adult tilapia induced significant changes in the expression of pituitary hormones. Genetic editing in tilapia is far more complicated than in zebrafish. Nevertheless, we managed to generate one mutant fish carrying a mutation in mc4r. That individual died before reaching sexual maturity. Thus, our attempt to generate an mc4r-mutant tilapia line was almost successful and indicate out non-obvious capability to generate mutant tilapia.
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Yahav, Shlomo, John McMurtry i Isaac Plavnik. Thermotolerance Acquisition in Broiler Chickens by Temperature Conditioning Early in Life. United States Department of Agriculture, 1998. http://dx.doi.org/10.32747/1998.7580676.bard.
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The research on thermotolerance acquisition in broiler chickens by temperature conditioning early in life was focused on the following objectives: a. To determine the optimal timing and temperature for inducing the thermotolerance, conditioning processes and to define its duration during the first week of life in the broiler chick. b. To investigate the response of skeletal muscle tissue and the gastrointestinal tract to thermal conditioning. This objective was added during the research, to understand the mechanisms related to compensatory growth. c. To evaluate the effect of early thermo conditioning on thermoregulation (heat production and heat dissipation) during 3 phases: (1) conditioning, (2) compensatory growth, (3) heat challenge. d. To investigate how induction of improved thermotolerance impacts on metabolic fuel and the hormones regulating growth and metabolism. Recent decades have seen significant development in the genetic selection of the meat-type fowl (i.e., broiler chickens); leading to rapid growth and increased feed efficiency, providing the poultry industry with heavy chickens in relatively short growth periods. Such development necessitates parallel increases in the size of visceral systems such as the cardiovascular and the respiratory ones. However, inferior development of such major systems has led to a relatively low capability to balance energy expenditure under extreme conditions. Thus, acute exposure of chickens to extreme conditions (i.e., heat spells) has resulted in major economic losses. Birds are homeotherms, and as such, they are able to maintain their body temperature within a narrow range. To sustain thermal tolerance and avoid the deleterious consequences of thermal stresses, a direct response is elicited: the rapid thermal shock response - thermal conditioning. This technique of temperature conditioning takes advantage of the immaturity of the temperature regulation mechanism in young chicks during their first week of life. Development of this mechanism involves sympathetic neural activity, integration of thermal infom1ation in the hypothalamus, and buildup of the body-to-brain temperature difference, so that the potential for thermotolerance can be incorporated into the developing thermoregulation mechanisms. Thermal conditioning is a unique management tool, which most likely involves hypothalamic them1oregulatory threshold changes that enable chickens, within certain limits, to cope with acute exposure to unexpected hot spells. Short-tem1 exposure to heat stress during the first week of life (37.5+1°C; 70-80% rh; for 24 h at 3 days of age) resulted in growth retardation followed immediately by compensatory growth" which resulted in complete compensation for the loss of weight gain, so that the conditioned chickens achieved higher body weight than that of the controls at 42 days of age. The compensatory growth was partially explained by its dramatic positive effect on the proliferation of muscle satellite cells which are necessary for further muscle hypertrophy. By its significant effect of the morphology and functioning of the gastrointestinal tract during and after using thermal conditioning. The significant effect of thermal conditioning on the chicken thermoregulation was found to be associated with a reduction in heat production and evaporative heat loss, and with an increase in sensible heat loss. It was further accompanied by changes in hormones regulating growth and metabolism These physiological responses may result from possible alterations in PO/AH gene expression patterns (14-3-3e), suggesting a more efficient mechanism to cope with heat stress. Understanding the physiological mechanisms behind thermal conditioning step us forward to elucidate the molecular mechanism behind the PO/AH response, and response of other major organs. The thermal conditioning technique is used now in many countries including Israel, South Korea, Australia, France" Ecuador, China and some places in the USA. The improvement in growth perfom1ance (50-190 g/chicken) and thermotolerance as a result of postnatal thermal conditioning, may initiate a dramatic improvement in the economy of broiler's production.
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Gong, Xuan, Zhou Chen, Kui Yang, Chuntao Li, Songshan Feng, Mingyu Zhang, Zhixiong Liu, Hongshu Zhou i Zhenyan Li. Endoscopic Transsphenoidal Surgery for Infra-Diaphragmatic Craniopharyngiomas: Impact of Diaphragm Sellae Competence on Hypothalamic Injury. International Journal of Surgery, maj 2024. http://dx.doi.org/10.60122/j.ijs.2024.20.03.
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Objective: Investigate the impact of diaphragm sellae competence on surgical outcomes and risk factors for postoperative hypothalamic injury (HI) in patients undergoing endoscopic transsphenoidal surgery (ETS) for infra-diaphragmatic craniopharyngiomas (ICs). Methods: A retrospective analysis of 54 consecutive patients (2016-2023) with ICs treated by ETS was conducted. All tumors originated from the sellar region inferior to the diaphragm sellae and were classified into two subtypes in terms of diaphragm sellae competence: IC with competent diaphragm sellae (IC-CDS) and IC with incompetent diaphragm sellae (IC-IDS). Clinical features, intraoperative findings, and follow-up data were compared between subtypes. Postoperative HI was assessed using a magnetic resonance imaging-based scoring system. Results: Fifty-four patients (29 males, 25 females) were included in this study, with 12 (22.2%) under 18 years old. Overall, 35 cases were IC-CDS, while 19 were IC-IDS. Compared with IC-CDS, patients with IC-IDS tended to have hormone hypofunction before surgery (p = 0.03). Tumor volume in IC-IDS group (9.0 ± 8.6 cm3) was also higher than that in IC-CDS group (3.3 ±3.4 cm, p = 0.011). Thirty-seven patients underwent standard endoscopic transsphenoidal approach (SEA) and 17 underwent an extended endoscopic transsphenoidal approach (EEA). Gross total resection (GTR) was achieved in 50 cases (92.6%). Postoperative CSF leak was observed in four patients (7.4%). Permanent diabetes insipidus (DI) occurred in 13 patients (27.7%), six in IC-CDS and seven in IC-IDS. Postoperative HI occurred in 38.9% of patients. Univariate analysis revealed that large tumor size (p = 0.014), prior hypopituitarism (p = 0.048) and IC-IDS (p < 0.001) were significantly associated with postoperative HI. Multivariate analysis revealed that IC- IDS was the sole predictor of postoperative HI. Conclusion: To our knowledge, this is the largest case series in the literature to describe IC resected by endoscopic surgery in a single institution. Classification based on diaphragm sellae competence highlights distinct clinical features and surgical outcomes between IC-CDS and IC-IDS subtypes. Notably, IC-IDS is an independent risk factor for postoperative HI. Preoperative identification of subtype can guide surgical strategy and potentially minimize complications.
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He, zhe, liwei Xing, ming He, yuhuan Sun, jinlong Xu i rong Zhao. Effect of Acupuncture on Mammary Gland Hyperplasia (MGH): a Bayesian network meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, wrzesień 2022. http://dx.doi.org/10.37766/inplasy2022.9.0058.
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Review question / Objective: This review aims at conducting a network meta-analysis to assess the potential therapeutic effectiveness and safety of acupuncture therapy for the treatment of MGH. Condition being studied: MGH is a benign breast disease caused by excessive growth of mammary duct epithelial cells and interstitial fibers. Its prevalence rate among women of childbearing age is about 13.5-42%, accounting for 99.3% of the total number of patients with breast related diseases, and its possibility of developing breast cancer can reach 5-10%. Breast hyperplasia can cause clinical symptoms such as breast pain, breast lump, nipple pigmentation and mood fluctuation, which brings severe physical and mental burden to patients. Modern medicine believes that the pathogenesis of MGH is related to sexual hormone disorder secondary to hypothalamus pituitary ovary axis dysfunction.At present, the treatment options of MGH are limited and not completely effective. The commonly used drugs in clinical practice, such as tamoxifen, danazol and goserelin, are expensive, which may lead to breast pain, swelling and increase of interstitial fibrous nodules, and the long-term use of MGH has huge side effects. The clinical guidelines recommend that the use time should be 2 to 6 months. Therefore, it is necessary to seek a treatment method of MGH that is effective, stable and safe.