Articoli di riviste sul tema "Hypothalmic diseases"

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1

Haug, R. H. "Recovery of the hypothalmic-pituitary adrenal (HPA) axis in patients with rheumatic diseases receiving low-dose prednisone". Journal of Oral and Maxillofacial Surgery 52, n. 2 (febbraio 1994): 203. http://dx.doi.org/10.1016/0278-2391(94)90422-7.

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2

Kim, Ye Jin, Thai Hien Tu, Sunggu Yang, Jae Kwang Kim e Jae Geun Kim. "Characterization of Fatty Acid Composition Underlying Hypothalamic Inflammation in Aged Mice". Molecules 25, n. 14 (11 luglio 2020): 3170. http://dx.doi.org/10.3390/molecules25143170.

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Abstract (sommario):
Degenerative diseases, which can develop during aging, are underlined by inflammatory processes. Hypothalamic inflammation triggered by elevation in circulating fatty acid levels is directly coupled to metabolic disorders. The present study aimed to investigate and characterize the hypothalamic inflammation and composition of fatty acids in the hypothalami of aged mice. We verified that inflammation and microglial activation occur in the hypothalami of aged mice by performing quantitative real-time PCR and using immunohistochemistry methods. In addition, we observed increased levels of various saturated fatty acids in the hypothalami of aged mice, whereas no major changes in the levels of circulating fatty acids were detected using gas chromatography with a flame ionization detector. Collectively, our current findings suggest that increases in saturated fatty acid levels are coupled to hypothalamic inflammation and thereby cause perturbations in energy metabolism during the aging process.
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Zapanti, Evangelia, Konstantinos Terzidis e George Chrousos. "Dysfunction of the Hypothalamic-Pituitary-Adrenal axis in HIV infection and disease". HORMONES 7, n. 3 (15 luglio 2008): 205–16. http://dx.doi.org/10.14310/horm.2002.1200.

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Mravec, Boris, e Alena Szelle Černáčková. "Hypothalamic inflammation and somatic diseases". Česká a slovenská neurologie a neurochirurgie 81/114, n. 3 (31 maggio 2018): 278–83. http://dx.doi.org/10.14735/amcsnn2018278.

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von Werder, K., e O. A. Müller. "Medical therapy of hypothalamic diseases". Acta Neurochirurgica 75, n. 1-4 (marzo 1985): 147–51. http://dx.doi.org/10.1007/bf01406335.

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Salvio, Gianmaria, Marianna Martino, Giulia Giancola, Giorgio Arnaldi e Giancarlo Balercia. "Hypothalamic–Pituitary Diseases and Erectile Dysfunction". Journal of Clinical Medicine 10, n. 12 (9 giugno 2021): 2551. http://dx.doi.org/10.3390/jcm10122551.

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Abstract (sommario):
Several hormones contribute to ensure penile erection, a neurovascular phenomenon in which nitric oxide plays a major role. Erectile dysfunction (ED), which is defined as the persistent inability to obtain or maintain penile erection sufficient for a satisfactory sexual performance, may be due to arteriogenic, neurogenic, iatrogenic, but also endocrinological causes. The hypothalamus–pituitary axis plays a central role in the endocrine system and represents a fundamental link between the brain and peripheral glands, including gonads. Therefore, the hormonal production of the hypothalamic–pituitary axis can control various aspects of sexual function and its dysregulation can compromise erectile function. In addition, excess and deficiency of pituitary hormones or metabolic alterations that are associated with some pituitary diseases (e.g., Cushing’s disease and acromegaly, hypopituitarism) can determine the development of ED with different mechanisms. Thus, the present review aimed to explore the relationship between hypothalamic and pituitary diseases based on the most recent clinical and experimental evidence.
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Swaab, Dick F. "Hypothalamic Peptides in Human Brain Diseases". Trends in Endocrinology & Metabolism 10, n. 6 (agosto 1999): 236–44. http://dx.doi.org/10.1016/s1043-2760(99)00158-7.

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Reimann, Hobart A. "HYPOTHALAMIC-HYPOPHYSEAL-NEURAL INFLUENCE IN PERIODIC DISEASES". Annals of the New York Academy of Sciences 117, n. 1 (16 dicembre 2006): 589–94. http://dx.doi.org/10.1111/j.1749-6632.1964.tb48210.x.

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Rychlik, A., M. Nowicki, A. Kolodziejska-Sawerska e M. Szweda. "The effect of orally administered Budesonide on the hypothalamic-pituitary-adrenal axis in dogs with inflammatory bowel disease". Veterinární Medicína 62, No. 5 (9 maggio 2017): 261–68. http://dx.doi.org/10.17221/130/2015-vetmed.

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The aim of this study was to evaluate the effect of Budesonide on the hypothalamic-pituitary-adrenal (HPA) axis in dogs with inflammatory bowel disease. The effect of orally administered Budesonide (Entocort) on the HPA axis was analysed in 21 dogs with inflammatory bowel disease. Biochemical analyses were carried out to evaluate the activity levels of alanine aminotransferase, asparagine aminotransferase, alkaline phosphatase, cortisol and endogenous adrenocorticotropic hormone. Urine samples were collected from each patient before the study and after 30 days of the experiment to determine the composition and the physical and chemical properties of urine sediments. Considerably lower serum concentrations of cortisol and endogenous adrenocorticotropic hormone were observed after 30 days of treatment. A significant increase in alkaline phosphatase levels was noted on Day 30. In the studied dogs, the drop in HPA axis activity was correlated with side effects associated with the administered glucocorticosteroid (polyuria, polydipsia). In conclusion, we have shown that oral administration of Budesonide to dogs diagnosed with inflammatory bowel disease significantly suppressed the activity of the HPA axis.
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10

Lapko, Inna V., Alla V. Zheglova, Kristina V. Klimkina e Inessa A. Bogatyreva. "Neurohumoral regulation under exposure to vibration and physical overloads". Hygiene and sanitation 101, n. 10 (23 ottobre 2022): 1200–1205. http://dx.doi.org/10.47470/0016-9900-2022-101-10-1200-1205.

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Introduction. In response to the action of various occupational factors, central regulatory mechanisms, including the hypothalamus, are involved. Clarification of the influence of the hypothalamus on the indicators of peripheral blood circulation, peripheral innervation and bone metabolism under the influence of vibration and physical overloads is relevant for the diagnosis and treatment of occupational diseases of a neurological profile. The aim of the study. To establish the relationship between hypothalamic disorders and functional indicators of occupational diseases of the peripheral nervous system under the influence of vibration and physical overloads. Material and methods. One hundred fifteen tunnellers and machinists of the drilling rig of JSC “KMAruda Combine”, 26 tunnellers of the drainage mine of JSC “Stoilensky Mining and Processing Plant”, 65 workers of auxiliary occupations were examined. Depending on the influencing factor, they were divided into four groups with occupational neurological pathology, the fifth group was control Examined cases were divided into subgroups: A - without hypothalamic disorders and B - with hypothalamic syndrome. The criteria for the diagnosis of hypothalamic syndrome are clinical. All the examined patients underwent rheovasography, stimulation electroneuromyography of the extremities, ultrasound densitometry. Results. It was found that in patients with vibration disease from the effects of local or general vibration, especially when combined with lumbosacral radiculopathy during rheovasography, there are decrements in pulse blood filling, changes in vascular tone in vessels of various calibers and venous dysfunction, which are aggravated against the background of hypothalamic disorders. Hypothalamic disorders contribute to the aggravation of peripheral nerve indices: a decrease in the amplitude of the M-response, the rate of propagation of excitation along sensory axons and an increase in the value of residual latency. Functional assessment of bone tissue revealed the greatest prevalence of osteopenia syndrome in patients with vibration disease and its combined forms with lumbosacral radiculopathy in subgroups with hypothalamic-pituitary dysfunction (up to 33.6%). The frequency of detected functional disorders was established to increase with the progression of occupational diseases. Limitations. The study was conducted in workers with neurological occupational diseases exposed to vibration and physical overloads. Conclusions. Neurohumoral disorders, manifested by hypothalamic syndrome caused by exposure to general and local vibration in combination with physical overloads, contribute to the development or aggravation of functional changes in the body of workers, aggravating the course of occupational diseases of the peripheral nervous system, which can be used to develop diagnostic and treatment methods, and study the pathogenesis of diseases.
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Mravec, Boris, Lubica Horvathova e Alena Cernackova. "Hypothalamic Inflammation at a Crossroad of Somatic Diseases". Cellular and Molecular Neurobiology 39, n. 1 (30 ottobre 2018): 11–29. http://dx.doi.org/10.1007/s10571-018-0631-4.

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Cai, Dongsheng, e Sinan Khor. "“Hypothalamic Microinflammation” Paradigm in Aging and Metabolic Diseases". Cell Metabolism 30, n. 1 (luglio 2019): 19–35. http://dx.doi.org/10.1016/j.cmet.2019.05.021.

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Karagiannis, Asterios, e Faidon Harsoulis. "Gonadal dysfunction in systemic diseases". European Journal of Endocrinology 152, n. 4 (aprile 2005): 501–13. http://dx.doi.org/10.1530/eje.1.01886.

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Gonadal function is significantly affected in many acute and chronic systemic diseases. As the function of the testes and the ovaries is determined by the integrity of the hypothalamic–pituitary–gonadal axis, it is obvious that a systemic disease may affect one or more levels of the axis in such a manner that the gonadal dysfunction may have various clinical and laboratory manifestations. In this brief review, the most common disturbances seen in the main systemic diseases will be discussed.
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Plakkot, Bhuvana, Ashley Di Agostino e Madhan Subramanian. "Implications of Hypothalamic Neural Stem Cells on Aging and Obesity-Associated Cardiovascular Diseases". Cells 12, n. 5 (28 febbraio 2023): 769. http://dx.doi.org/10.3390/cells12050769.

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The hypothalamus, one of the major regulatory centers in the brain, controls various homeostatic processes, and hypothalamic neural stem cells (htNSCs) have been observed to interfere with hypothalamic mechanisms regulating aging. NSCs play a pivotal role in the repair and regeneration of brain cells during neurodegenerative diseases and rejuvenate the brain tissue microenvironment. The hypothalamus was recently observed to be involved in neuroinflammation mediated by cellular senescence. Cellular senescence, or systemic aging, is characterized by a progressive irreversible state of cell cycle arrest that causes physiological dysregulation in the body and it is evident in many neuroinflammatory conditions, including obesity. Upregulation of neuroinflammation and oxidative stress due to senescence has the potential to alter the functioning of NSCs. Various studies have substantiated the chances of obesity inducing accelerated aging. Therefore, it is essential to explore the potential effects of htNSC dysregulation in obesity and underlying pathways to develop strategies to address obesity-induced comorbidities associated with brain aging. This review will summarize hypothalamic neurogenesis associated with obesity and prospective NSC-based regenerative therapy for the treatment of obesity-induced cardiovascular conditions.
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Cai, Dongsheng, e Tiewen Liu. "Hypothalamic inflammation: a double-edged sword to nutritional diseases". Annals of the New York Academy of Sciences 1243, n. 1 (dicembre 2011): E1—E39. http://dx.doi.org/10.1111/j.1749-6632.2011.06388.x.

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Kurup, R. K., e P. A. Kurup. "Hypothalamic digoxin and brain function". Acta Neuropsychiatrica 15, n. 2 (aprile 2003): 74–90. http://dx.doi.org/10.1034/j.1601-5215.2003.00012.x.

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Background and objectives:The study assessed the biochemical differences between right hemispheric-dominant and left hemispheric-dominant individuals. The chemical hemispheric-dominance in various systemic and neuropsychiatric diseases was also studied.Methods:The isoprenoid metabolites, digoxin, dolichol and ubiquinone, glycoconjugate metabolism, free radical metabolism and the RBC membrane composition, were studied in individuals with differing hemispheric-dominance. The digoxin levels and RBC membrane Na+-K+ATPase activity were also studied in systemic and neuropsychiatric diseases.Results:The results showed that right hemispheric-dominant individuals had elevated digoxin levels, increased free radical production and reduced scavenging, increased tryptophan catabolites and reduced tyrosine catabolites, increased glycoconjugate levels and increased cholesterol : phospholipid ratio of RBC membranes. Left hemispheric-dominant individuals had the opposite patterns. This patterns could be correlated with various systemic and neuropsychiatric diseases.Conclusion:Right hemispheric-dominance represents a hyperdigoxinaemic state with membrane sodium–potassium ATPase inhibition. Left hemispheric-dominance represents the reverse pattern with hypodigoxinaemia and membrane sodium–potassium ATPase stimulation. Hemispheric-dominance could predispose to various systemic and neuropsychiatric diseases.
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KURUP, RAVI KUMAR, e PARAMESWARA ACHUTHA KURUP. "HYPOTHALAMIC DIGOXIN, CEREBRAL CHEMICAL DOMINANCE, AND PATHOGENESIS OF PULMONARY DISEASES". International Journal of Neuroscience 113, n. 2 (1 gennaio 2003): 235–58. http://dx.doi.org/10.1080/00207450390162056.

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18

ABRAMSKY, O., E. WERTMAN, A. RECHES, T. BRENNER e H. OVADIA. "Effect of Hypothalamic Lesions on Experimental Autoimmune Diseases in Rats". Annals of the New York Academy of Sciences 496, n. 1 Neuroimmune I (maggio 1987): 360–65. http://dx.doi.org/10.1111/j.1749-6632.1987.tb35788.x.

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19

Müller, Hermann L. "RARE-04. Hypothalamic syndrome – severe sequelae due to different sellar and parasellar masses". Neuro-Oncology 24, Supplement_1 (1 giugno 2022): i9—i10. http://dx.doi.org/10.1093/neuonc/noac079.029.

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Abstract Hypothalamic syndrome is a rare disorder caused by disease- and/or treatment-related injury to the hypothalamus, most commonly associated with rare, noncancerous parasellar masses such as craniopharyngioma, germ cell tumours, gliomas, cysts of Rathke’s pouch and Langerhans cell histiocytosis as well as genetic neurodevelopmental syndromes such as Prader-Willi syndrome and septo-optic dysplasia. Hypothalamic syndrome is characterized by intractable weight gain associated with severe morbid obesity and memory impairment, attention deficit, reduced impulse control as well as increased risk of cardiovascular and metabolic disorders. Currently, there is no cure for this condition. Treatments used for general obesity such as surgery, medication and counselling are often tried in hypothalamic syndrome, but are mostly ineffective, and there are no medications specifically approved for hypothalamic syndrome. The most important aspects of presentation and outcome of hypothalamic syndrome due to different neuro oncological diseases, its risk factors and an overview of currently available therapeutic interventions aiming to decrease and ameliorate the consequences of hypothalamic dysfunction will be presented. Furthermore, novel aspects and perspectives for future research will be discussed.
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Ulisse, Salvatore, Enke Baldini, Daniele Pironi, Federica Gagliardi, Domenico Tripodi, Augusto Lauro, Sabino Carbotta et al. "Is Melanoma Progression Affected by Thyroid Diseases?" International Journal of Molecular Sciences 23, n. 17 (2 settembre 2022): 10036. http://dx.doi.org/10.3390/ijms231710036.

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Clinical and epidemiological evidence indicate a relationship between thyroid diseases and melanoma. In particular, the hypothyroidism condition appears to promote melanoma spread, which suggests a protective role of thyroid hormones against disease progression. In addition, experimental data suggest that, in addition to thyroid hormones, other hormonal players of the hypothalamic–pituitary–thyroid (HPT) axis, namely the thyrotropin releasing hormone and the thyrotropin, are likely to affect melanoma cells behavior. This information warrants further clinical and experimental studies in order to build a precise pattern of action of the HPT hormones on melanoma cells. An improved knowledge of the involved molecular mechanism(s) could lead to a better and possibly personalized clinical management of these patients.
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Melnichenko, G. A., V. A. Chernogolov e M. G. Pavlova. "General data on the hypothalamic-pituitary disorders (guidelines for patients)". Problems of Endocrinology 42, n. 4 (15 agosto 1996): 31–32. http://dx.doi.org/10.14341/probl12072.

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Most diseases of the hypothalamus and pituitary gland are relatively rare, and therefore not only patients, but many doctors are new to their manifestations, diagnostic methods, treatment tactics, and most importantly, rehabilitation methods (including psychological). The low incidence of such diseases, however, does not detract from the importance of the problems faced by a particular patient. Currently, schools for teaching methods of self-monitoring of patients with diabetes mellitus and a number of other chronic diseases have been created and are actively functioning. There is a need to create such schools for patients with hypothalamic-pituitary diseases, since competent replacement therapy, which the vast majority of patients need after various interventions on the pituitary gland, significantly improves their quality of life. And if we take into account that the age of most patients does not exceed 40 years, then the importance of such schools, as well as the need to create a comprehensive rehabilitation system for these patients, become obvious. Schools for patients with hypothalamic-pituitary diseases have already been established and are successfully functioning in Western Europe, in particular in the UK. These schools help patients with Itsenko-Cushing's disease, prolactinomas, acromegaly, diabetes insipidus, pituitary dwarfism, panhypopituitarism. During classes, patients get acquainted with the anatomical and physiological features of the hypothalamic-pituitary system, its relationship with peripheral endocrine glands, they explain the main clinical manifestations of their disease, methods for its diagnosis and treatment. Patients are told about the meaning of certain terms used by attending physicians to describe their disease, as well as the possible side effects of the medications they take.
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Mukhopadhyay, Debasmita, e Bashair M. Mussa. "Identification of Novel Hypothalamic MicroRNAs as Promising Therapeutics for SARS-CoV-2 by Regulating ACE2 and TMPRSS2 Expression: An In Silico Analysis". Brain Sciences 10, n. 10 (25 settembre 2020): 666. http://dx.doi.org/10.3390/brainsci10100666.

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Background: Neuroinvasion of severe acute respiratory syndrome coronavirus (SARS-CoV) is well documented and, given the similarities between this virus and SARS-CoV-2, it seems that the neurological impairment that is associated with coronavirus disease 2019 (COVID-19) is due to SARS-CoV-2 neuroinvasion. Hypothalamic circuits are exposed to the entry of the virus via the olfactory bulb and interact centrally with crucial respiratory nuclei. Hypothalamic microRNAs are considered as potential biomarkers and modulators for various diseases and future therapeutic targets. The present study aims to investigate the microRNAs that regulate the expression of hypothalamic angiotensin-converting enzyme 2 (ACE2) and transmembrane serine protease 2 (TMPRSS2), essential elements for SARS-CoV-2 cell entry. Methods: To determine potential hypothalamic miRNAs that can directly bind to ACE2 and TMPRSS2, multiple target bioinformatics prediction algorithms were used, including miRBase, Target scan, and miRWalk2.029. Results: Our in silico analysis has revealed that, although there are over 5000 hypothalamic miRNAs, around 31 miRNAs and 29 miRNAs have shown binding sites and strong binding capacity against ACE2 and TMPRSS2, respectively. Conclusion: These novel potential hypothalamic miRNAs can be used to identify new therapeutic targets to treat neurological symptoms in COVID-19 patients via regulation of ACE2 and TMPRSS2 expression.
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Schaefer, S., N. Boegershausen, S. Meyer, D. Ivan, K. Schepelmann e P. H. Kann. "Hypothalamic–pituitary insufficiency following infectious diseases of the central nervous system". European Journal of Endocrinology 158, n. 1 (gennaio 2008): 3–9. http://dx.doi.org/10.1530/eje-07-0484.

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ObjectiveHypothalamic–pituitary insufficiency may have diverse causes. The aim of this study was to determine the incidence of hypothalamic–pituitary insufficiency in patients with previous infectious diseases of the central nervous system (CNS) of different etiologies and mild-to-moderate clinical course.DesignPatient series. Basal and stimulated (insulin tolerance test) pituitary function testing was performed in 19 patients with previous neuroborreliosis, encephalitis, or meningitis following an interval of between 10 and 56 months (mean 26.1±13.1 months) after the acute event.ResultsFour patients (21%; two males, two females) showed an isolated corticotropic insufficiency (peak cortisol <181.25 μg/l during the insulin tolerance test). Two patients (11%, males) showed borderline gonadotropic insufficiency (basal testosterone between 2.4 and 3.0 μg/l). No patient had somatotropic or thyrotropic insufficiency or evidence for diabetes insipidus; all had prolactin concentrations within the reference range.ConclusionsHypothalamic–pituitary dysfunction and especially isolated corticotropic insufficiency may develop in a relevant proportion of patients after infectious diseases of the CNS.
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Crofford, Leslie J. "The hypothalamic–pituitary–adrenal axis in the pathogenesis of rheumatic diseases". Endocrinology and Metabolism Clinics of North America 31, n. 1 (marzo 2002): 1–13. http://dx.doi.org/10.1016/s0889-8529(01)00004-4.

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HARBUZ, M. S., D. S. JESSOP, H. S. CHOWDREY, J. M. BLACKWELL, P. J. LARSEN e S. L. LIGHTMAN. "Evidence for Altered Control of Hypothalamic CRF in Immune-Mediated Diseases". Annals of the New York Academy of Sciences 771, n. 1 Stress (dicembre 1995): 449–58. http://dx.doi.org/10.1111/j.1749-6632.1995.tb44701.x.

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Vorontsov, A. V., T. V. Semicheva e V. A. Peterkova. "Magnetic resonance imaging in the diagnosis of hypothalamopituitary diseases in patients with true premature sexual development". Problems of Endocrinology 49, n. 1 (15 febbraio 2003): 32–36. http://dx.doi.org/10.14341/probl11438.

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То evaluate the incidence of different types of organic abnormal­ities occurring in premature sexual development (PSD) of central genesis and to study a role of magnetic resonance imaging (MRI) in the diagnosis of PSD, MRI was used in 33 patients with a clin­ically established diagnosis of true (gonadotropin-dependent) PSD of central genesis. Among the examined children with PSD, hypothalamic hamartoma was detected in 27.3%) of the patients; there were no MRI data suggesting hypothalamopituitary abnor­malities in 72.7%o. On the MRI images, a hypothalamic hamar­toma appeared as a round or oval mass having a well -defined outlines, a homogeneous structure, 3 to 15 mm in size, which is located in the projection of mamillary bodies or retrochiasmally. Patients with PSD were found to have an increased volume of the adenohypophysis mainly due to the vertical size as compared with a group of healthy children of the same age.
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Lencu, Codruţa, Teodora Alexescu, Mirela Petrulea e Monica Lencu. "RESPIRATORY MANIFESTATIONS IN ENDOCRINE DISEASES". Medicine and Pharmacy Reports 89, n. 4 (28 ottobre 2016): 459–63. http://dx.doi.org/10.15386/cjmed-671.

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The control mechanisms of respiration as a vital function are complex: voluntary – cortical, and involuntary – metabolic, neural, emotional and endocrine. Hormones and hypothalamic neuropeptides (that act as neurotrasmitters and neuromodulators in the central nervous system) play a role in the regulation of respiration and in bronchopulmonary morphology. This article presents respiratory manifestations in adult endocrine diseases that evolve with hormone deficit or hypersecretion. In hyperthyroidism, patients develop ventilation disorders, obstructive and central sleep apnea, and pleural collection. The respiratory abnormalities in hyperthyroidism as a result of the hypermetabolic action of thyroid hormones are hyperventilation, myopathy and cardiovascular involvement; recent studies have reported pulmonary arterial hypertension in Graves’ disease, as a result of the association of several mechanisms. Thyroid hypertrophy can induce through compression of the upper airways dyspnea, stridor, wheezing and cough. The respiratory disorders in acromegaly are ventilatory dysfunction and sleep apnea, which contribute to an unfavorable evolution of the disease. Respiratory changes in parathyroid, adrenal and reproductive system diseases have been described. Respiratory disorders should be recognized, investigated and monitored by medical practitioners of various specialties (family physicians, internists, endocrinologists, pneumologists, cardiologists). They are frequently severe, causing an unfavorable evolution of the associated endocrine and respiratory disease.
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Lee, Hannah, Thai Hien Tu, Byong Seo Park, Sunggu Yang e Jae Geun Kim. "Adiponectin Reverses the Hypothalamic Microglial Inflammation during Short-Term Exposure to Fat-Rich Diet". International Journal of Molecular Sciences 20, n. 22 (15 novembre 2019): 5738. http://dx.doi.org/10.3390/ijms20225738.

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Adiponectin, an adipokine derived from the adipose tissue, manifests anti-inflammatory effects in the metabolically active organs and is, therefore, beneficial in various metabolic diseases associated with inflammation. However, the role of adiponectin in alleviating the hypothalamic inflammation connected to the pathogenesis of obesity has not yet been clearly interrogated. Here, we identified that the systemic administration of adiponectin suppresses the activation of microglia and thereby reverses the hypothalamic inflammation during short-term exposure to a high-fat diet. Additionally, we show that adiponectin induces anti-inflammatory effects in the microglial cell line subjected to an exogenous treatment with a saturated free fatty acid. In conclusion, the current study suggests that adiponectin suppresses the saturated free fatty acid-triggered the hypothalamic inflammation by modulating the microglial activation and thus maintains energy homeostasis.
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Kõks, Sulev, Ursel Soomets, Mario Plaas, Anton Terasmaa, Klari Noormets, Vallo Tillmann, Eero Vasar, Cathy Fernandes e Leonard C. Schalkwyk. "Hypothalamic gene expression profile indicates a reduction in G protein signaling in the Wfs1 mutant mice". Physiological Genomics 43, n. 24 (dicembre 2011): 1351–58. http://dx.doi.org/10.1152/physiolgenomics.00117.2011.

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The Wfs1 gene codes for a protein with unknown function, but deficiency in this protein results in a range of neuropsychiatric and neuroendocrine syndromes. In the present study we aimed to find the functional networks influenced by Wfs1 in the hypothalamus. We performed gene expression profiling (Mouse Gene 1.0 ST Arrays) in Wfs1-deficient mice; 305 genes were differentially expressed with nominal P value < 0.01. FDR (false discovery rate)-adjusted P values were significant (0.007) only for two genes: C4b (t=9.66) and Wfs1 ( t = −9.03). However, several genes related to G protein signaling were very close to the FDR-adjusted significance level, such as Rgs4 (regulator of G protein signaling 4) that was downregulated (−0.34, t = −5.4) in Wfs1-deficient mice. Changes in Rgs4 and C4b expression were confirmed by QRT-PCR. In humans, Rgs4 is in the locus for bipolar disease (BPD), and its expression is downregulated in BPD. C4b is a gene related to the neurodegenerative diseases. Functional analysis including the entire data set revealed significant alterations in the canonical pathway “G protein-coupled receptor signaling.” The gene expression profile in the hypothalami of the Wfs1 mutant mice was significantly similar to the profiles of following biological functions: psychological disorders, bipolar disorder, mood disorder. In conclusion, hypothalamic gene expression profile resembles with some molecular pathways functionally related to the clinical syndromes in the Wolfram syndrome patients.
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Ryzhov, J. R., e A. O. Shpakov. "ADIPONECTIN AS AN ENDOGENOUS REGULATOR OF THE HYPOTHALAMIC-PITUITARY-GONADAL AXIS". Translational Medicine 5, n. 5 (21 dicembre 2018): 26–36. http://dx.doi.org/10.18705/2311-4495-2018-5-5-.

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Abstract (sommario):
Adiponectin is the most important adipokine controlling the food behavior and energy homeostasis. At present, there is much evidence that adiponectin also regulates the functions of the reproductive system, and its targets are hypothalamic neurons responsible for the synthesis and secretion of gonadoliberin, the pituitary gonadotrophs producing the luteinizing hormone, and the gonads. In the target tissues, which are blocks of the hypothalamic-pituitary-gonadal axis, all the main components of adiponectin-regulated signaling system, including adiponectin and both types of adiponectin receptors, are detected. The impairments in the adiponectin signaling pathways lead to the development of reproductive dysfunctions, as a result of which this pathways in the future can become one of the most important targets of therapy of diseases of the male and female reproductive systems. In the review, the current state of the problem of the participation of adiponectin in the functioning of the hypothalamic-pituitary-gonadal axis, and the relationship between the functional status of the reproductive system and the activity of the adiponectin system in hypothalamic neurons, gonadotrophs and gonads are considered.
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Ryzhov, J. R., e A. O. Shpakov. "ADIPONECTIN AS AN ENDOGENOUS REGULATOR OF THE HYPOTHALAMIC-PITUITARY-GONADAL AXIS". Translational Medicine 5, n. 5 (21 dicembre 2018): 26–36. http://dx.doi.org/10.18705/2311-4495-2018-5-5-26-36.

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Abstract (sommario):
Adiponectin is the most important adipokine controlling the food behavior and energy homeostasis. At present, there is much evidence that adiponectin also regulates the functions of the reproductive system, and its targets are hypothalamic neurons responsible for the synthesis and secretion of gonadoliberin, the pituitary gonadotrophs producing the luteinizing hormone, and the gonads. In the target tissues, which are blocks of the hypothalamic-pituitary-gonadal axis, all the main components of adiponectin-regulated signaling system, including adiponectin and both types of adiponectin receptors, are detected. The impairments in the adiponectin signaling pathways lead to the development of reproductive dysfunctions, as a result of which this pathways in the future can become one of the most important targets of therapy of diseases of the male and female reproductive systems. In the review, the current state of the problem of the participation of adiponectin in the functioning of the hypothalamic-pituitary-gonadal axis, and the relationship between the functional status of the reproductive system and the activity of the adiponectin system in hypothalamic neurons, gonadotrophs and gonads are considered.
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32

Van Drunen, Rachel, e Kristin Eckel-Mahan. "Circadian Rhythms of the Hypothalamus: From Function to Physiology". Clocks & Sleep 3, n. 1 (25 febbraio 2021): 189–226. http://dx.doi.org/10.3390/clockssleep3010012.

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Abstract (sommario):
The nearly ubiquitous expression of endogenous 24 h oscillations known as circadian rhythms regulate the timing of physiological functions in the body. These intrinsic rhythms are sensitive to external cues, known as zeitgebers, which entrain the internal biological processes to the daily environmental changes in light, temperature, and food availability. Light directly entrains the master clock, the suprachiasmatic nucleus (SCN) which lies in the hypothalamus of the brain and is responsible for synchronizing internal rhythms. However, recent evidence underscores the importance of other hypothalamic nuclei in regulating several essential rhythmic biological functions. These extra-SCN hypothalamic nuclei also express circadian rhythms, suggesting distinct regions that oscillate either semi-autonomously or independent of SCN innervation. Concurrently, the extra-SCN hypothalamic nuclei are also sensitized to fluctuations in nutrient and hormonal signals. Thus, food intake acts as another powerful entrainer for the hypothalamic oscillators’ mediation of energy homeostasis. Ablation studies and genetic mouse models with perturbed extra-SCN hypothalamic nuclei function reveal their critical downstream involvement in an array of functions including metabolism, thermogenesis, food consumption, thirst, mood and sleep. Large epidemiological studies of individuals whose internal circadian cycle is chronically disrupted reveal that disruption of our internal clock is associated with an increased risk of obesity and several neurological diseases and disorders. In this review, we discuss the profound role of the extra-SCN hypothalamic nuclei in rhythmically regulating and coordinating body wide functions.
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33

Hosseinifard, Elaheh-Sadat, Khadijeh Bavafa-Valenlia, Maryam Saghafi-Asl e Mohammad Morshedi. "Antioxidative and Metabolic Effects of Lactobacillus plantarum, Inulin, and Their Synbiotic on the Hypothalamus and Serum of Healthy Rats". Nutrition and Metabolic Insights 13 (gennaio 2020): 117863882092509. http://dx.doi.org/10.1177/1178638820925092.

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Abstract (sommario):
Nowadays, much attention has been paid to the link between gut microbiota and brain. The beneficial metabolic effects of probiotics and prebiotics in several diseases such as diabetes and obesity have been reported. However, studies bridging the association of gut microbiome with brain function in healthy states are rare. Therefore, it was hypothesized that the administration of Lactobacillus plantarum ( L plantarum) and inulin may affect serum and hypothalamic metabolic parameters as well as oxidative markers in healthy male rats. Daily L plantarum (107 CFU/mL) and inulin (5% of daily food weight) or their combination (synbiotic) was given to healthy rats. Then, serum and hypothalamic levels of leptin, insulin, and oxidative markers were measured. Administration of synbiotic for 8 weeks led to significant changes in serum levels of high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, very low-density lipoprotein cholesterol, low-density lipoprotein/high-density lipoprotein ratio, triglyceride, and total cholesterol. The intake of synbiotic also resulted in a significantly reduced hypothalamic level of malondialdehyde and increased hypothalamic superoxide dismutase (SOD). Also, L plantarum could significantly increase hypothalamic SOD level. Furthermore, synbiotic administration insignificantly increased the hypothalamic and serum levels of insulin and leptin. These findings suggest that the synbiotic could significantly improve oxidative markers and lipid profile in healthy rats. Therefore, simultaneous intake of L plantarum and inulin appears to be more effective in the amelioration of metabolic and oxidative parameters.
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34

Laviano, Alessandro, Akio Inui, Daniel L. Marks, Michael M. Meguid, Claude Pichard, Filippo Rossi Fanelli e Marilia Seelaender. "Neural control of the anorexia-cachexia syndrome". American Journal of Physiology-Endocrinology and Metabolism 295, n. 5 (novembre 2008): E1000—E1008. http://dx.doi.org/10.1152/ajpendo.90252.2008.

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Abstract (sommario):
The anorexia-cachexia syndrome is a debilitating clinical condition characterizing the course of chronic diseases, which heavily impacts on patients' morbidity and quality of life, ultimately accelerating death. The pathogenesis is multifactorial and reflects the complexity and redundancy of the mechanisms controlling energy homeostasis under physiological conditions. Accumulating evidence indicates that, during disease, disturbances of the hypothalamic pathways controlling energy homeostasis occur, leading to profound metabolic changes in peripheral tissues. In particular, the hypothalamic melanocortin system does not respond appropriately to peripheral inputs, and its activity is diverted largely toward the promotion of catabolic stimuli (i.e., reduced energy intake, increased energy expenditure, possibly increased muscle proteolysis, and adipose tissue loss). Hypothalamic proinflammatory cytokines and serotonin, among other factors, are key in triggering hypothalamic resistance. These catabolic effects represent the central response to peripheral challenges (i.e., growing tumor, renal, cardiac failure, disrupted hepatic metabolism) that are likely sensed by the brain through the vagus nerve. Also, disease-induced changes in fatty acid oxidation within hypothalamic neurons may contribute to the dysfunction of the hypothalamic melanocortin system. Ultimately, sympathetic outflow mediates, at least in part, the metabolic changes in peripheral tissues. Other factors are likely involved in the pathogenesis of the anorexia-cachexia syndrome, and their role is currently being elucidated. However, available evidence shows that the constellation of symptoms characterizing this syndrome should be considered, at least in part, as different phenotypes of common neurochemical/metabolic alterations in the presence of a chronic inflammatory state.
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35

Panaro, Maria Antonietta, Tarek Benameur e Chiara Porro. "Hypothalamic Neuropeptide Brain Protection: Focus on Oxytocin". Journal of Clinical Medicine 9, n. 5 (19 maggio 2020): 1534. http://dx.doi.org/10.3390/jcm9051534.

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Abstract (sommario):
Oxytocin (OXT) is hypothalamic neuropeptide synthetized in the brain by magnocellular and parvo cellular neurons of the paraventricular (PVN), supraoptic (SON) and accessory nuclei (AN) of the hypothalamus. OXT acts in the central and peripheral nervous systems via G-protein-coupled receptors. The classical physiological functions of OXT are uterine contractions, the milk ejection reflex during lactation, penile erection and sexual arousal, but recent studies have demonstrated that OXT may have anti-inflammatory and anti-oxidant properties and regulate immune and anti-inflammatory responses. In the pathogenesis of various neurodegenerative diseases, microglia are present in an active form and release high levels of pro-inflammatory cytokines and chemokines that are implicated in the process of neural injury. A promising treatment for neurodegenerative diseases involves new therapeutic approaches targeting activated microglia. Recent studies have reported that OXT exerts neuroprotective effects through the inhibition of production of pro-inflammatory mediators, and in the development of correct neural circuitry. The focus of this review is to attribute a new important role of OXT in neuroprotection through the microglia–OXT interaction of immature and adult brains. In addition, we analyzed the strategies that could enhance the delivery of OXT in the brain and amplify its positive effects.
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36

Chiurazzi, Martina, Martina Di Maro, Mauro Cozzolino e Antonio Colantuoni. "Mitochondrial Dynamics and Microglia as New Targets in Metabolism Regulation". International Journal of Molecular Sciences 21, n. 10 (13 maggio 2020): 3450. http://dx.doi.org/10.3390/ijms21103450.

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Abstract (sommario):
Energy homeostasis regulation is essential for the maintenance of life. Neuronal hypothalamic populations are involved in the regulation of energy balance. In order play this role, they require energy: mitochondria, indeed, have a key role in ensuring a constant energy supply to neurons. Mitochondria are cellular organelles that are involved in dynamic processes; their dysfunction has been associated with many diseases, such as obesity and type 2 diabetes, indicating their importance in cellular metabolism and bioenergetics. Food intake excess can induce mitochondrial dysfunction with consequent production of reactive oxygen species (ROS) and oxidative stress. Several studies have shown the involvement of mitochondrial dynamics in the modulation of releasing agouti-related protein (AgRP) and proopiomelanocortin (POMC) neuronal activity, although the mechanisms are still unclear. However, recent studies have shown that changes in mitochondrial metabolism, such as in inflammation, can contribute also to the activation of the microglial system in several diseases, especially degenerative diseases. This review is aimed to summarize the link between mitochondrial dynamics and hypothalamic neurons in the regulation of glucose and energy homeostasis. Furthermore, we focus on the importance of microglia activation in the pathogenesis of many diseases, such as obesity, and on the relationship with mitochondrial dynamics, although this process is still largely unknown.
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37

KAUPPILA, MARJUT, PERTTI KOSKINEN, KARI REMES, JORMA VIIKARI e KERTTU IRJALA. "Hypothalamic-Pituitary Axis Remains Intact After Interferon-α Treatment in Hematologic Diseases". Journal of Interferon & Cytokine Research 17, n. 9 (settembre 1997): 543–50. http://dx.doi.org/10.1089/jir.1997.17.543.

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38

Salahuddin, Mohammed F., Fakhri Mahdi, Suresh P. Sulochana e Jason J. Paris. "HIV-1 Tat Protein Promotes Neuroendocrine Dysfunction Concurrent with the Potentiation of Oxycodone’s Psychomotor Effects in Female Mice". Viruses 13, n. 5 (30 aprile 2021): 813. http://dx.doi.org/10.3390/v13050813.

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Abstract (sommario):
Human immunodeficiency virus (HIV) is associated with neuroendocrine dysfunction which may contribute to co-morbid stress-sensitive disorders. The hypothalamic-pituitary-adrenal (HPA) or -gonadal (HPG) axes are perturbed in up to 50% of HIV patients. The mechanisms are not known, but we have found the HIV-1 trans-activator of transcription (Tat) protein to recapitulate the clinical phenotype in male mice. We hypothesized that HPA and/or HPG dysregulation contributes to Tat-mediated interactions with oxycodone, an opioid often prescribed to HIV patients, in females. Female mice that conditionally-expressed the Tat1–86 protein [Tat(+) mice] or their counterparts that did not [Tat(−) control mice] were exposed to forced swim stress (or not) and behaviorally-assessed for motor and anxiety-like behavior. Some mice had glucocorticoid receptors (GR) or corticotropin-releasing factor receptors (CRF-R) pharmacologically inhibited. Some mice were ovariectomized (OVX). As seen previously in males, Tat elevated basal corticosterone levels and potentiated oxycodone’s psychomotor activity in females. Unlike males, females did not demonstrate adrenal insufficiency and oxycodone potentiation was not regulated by GRs or CRF-Rs. Rather OVX attenuated Tat/oxycodone interactions. Either Tat or oxycodone increased anxiety-like behavior and their combination increased hypothalamic allopregnanolone. OVX increased basal hypothalamic allopregnanolone and obviated Tat or oxycodone-mediated fluctuations. Together, these data provide further evidence for Tat-mediated dysregulation of the HPA axis and reveal the importance of HPG axis regulation in females. HPA/HPG disruption may contribute vulnerability to affective and substance use disorders.
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39

Gilyazutdinov, I. A., M. K. Mikhailov e F. Z. Mindubaeva. "Importance of craniography in the diagnosis of neuroendocrinal syndromes and central genesis diseases". Kazan medical journal 74, n. 4 (15 agosto 1993): 288–90. http://dx.doi.org/10.17816/kazmj71446.

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Abstract (sommario):
As many as 681 patients with syndromes of scleropolycystosis of ovaries, amenorrhea, galactorrhea, oligonorrhea, lutein phase deficiency, climacteric, hypothalamic genesis obesity and sterility, precancer and cancer of endometrium, and body of the womb are observed. Calcium metabolism is examined in some patients. The frequency of the changes of bones of the vault and base of the skull in the above mentioned states (signs of endocraniosis, en docrinopathy, intracranial hypertension as well as calcification of the pineal gland) is given,, It is stated that patients with ncuroendocrii. Syndromes manifest phosphoric-calcium metabolism violation and structural changes of bones of the skull.
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40

Zenkova, T. S., e I. A. Fedin. "The use of magnetic resonance imaging in the diagnosis of diseases of the hypothalamic-pituitary system". Problems of Endocrinology 39, n. 6 (15 dicembre 1993): 57–62. http://dx.doi.org/10.14341/probl11955.

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Abstract (sommario):
In recent years, it has become apparent that the incidence of diseases of the hypothalamic-pituitary system is extremely high. The clinical manifestations of diseases such as acromegaly, Itsenko Cushing's disease, primary hyperprolactinemic hypogonadism are considered to be well known [8, 9, 32, 45]. However, to select the optimal method of treatment in each specific clinical situation, it is imperative for the clinician to obtain information about the state of the main structural link of the pathological process - the pituitary gland
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41

Molfino, Alessio, Gianfranco Gioia, Filippo Rossi Fanelli e Alessandro Laviano. "Contribution of Neuroinflammation to the Pathogenesis of Cancer Cachexia". Mediators of Inflammation 2015 (2015): 1–7. http://dx.doi.org/10.1155/2015/801685.

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Abstract (sommario):
Inflammation characterizes the course of acute and chronic diseases and is largely responsible for the metabolic and behavioral changes occurring during the clinical journey of patients. Robust data indicate that, during cancer, functional modifications within brain areas regulating energy homeostasis contribute to the onset of anorexia, reduced food intake, and increased catabolism of muscle mass and adipose tissue. In particular, functional changes are associated with increased hypothalamic concentration of proinflammatory cytokines, which suggests that neuroinflammation may represent the adaptive response of the brain to peripheral challenges, including tumor growth. Within this conceptual framework, the vagus nerve appears to be involved in conveying alert signals to the hypothalamus, whereas hypothalamic serotonin appears to contribute to triggering catabolic signals.
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42

Pigarova, E. A., L. K. Dzeranova e L. Ya Rozhinskaya. "Klinicheskiy sluchay narusheniyavodno-elektrolitnogo obmena kak pervogosimptoma rasprostranennogo metastaticheskogoprotsessa: osobennosti diagnostiki i lecheniyapreparatom sinteticheskogo analogavazopressina (Presayneks)". Obesity and metabolism 8, n. 3 (15 settembre 2011): 67–70. http://dx.doi.org/10.14341/2071-8713-4840.

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Abstract (sommario):
The main manifestations of central diabetes insipidus (CDI), a disease of absolute deficiency of hypothalamic hormone vasopressin, are severe thirst and polyuria, which severely interferes with normal life of patients. In some cases CDI may be the first sign of wide spread metastatic process, appearing many years after successful treatment of oncological diseases.
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43

Muir, Andrew, e Noel K. Maclaren. "Autoimmune Diseases of the Adrenal Glands, Parathyroid Glands, Gonads, and Hypothalamic-Pituitary Axis". Endocrinology and Metabolism Clinics of North America 20, n. 3 (settembre 1991): 619–44. http://dx.doi.org/10.1016/s0889-8529(18)30261-5.

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44

Jiang, Wei, Xueyong Wang, Xiaodong Duan, Shan Li, Nan Li e Jiatai Dou. "Review of the Relationship between Mental Stress and Inflammatory Skin Diseases". International Journal of Social Sciences and Public Administration 3, n. 2 (26 giugno 2024): 308–14. http://dx.doi.org/10.62051/ijsspa.v3n2.38.

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Abstract (sommario):
Inflammatory skin diseases have a major impact on the psychological state and quality of life of patients, and can lead to an increased burden on the patient's mental state and cause psychological problems such as anxiety and depression. In addition, psychological stress can aggravate the condition of inflammatory skin diseases. Nowadays, the relationship between psychological stress and inflammatory skin diseases has received much attention. Therefore, a review of the relationship between the two is necessary. In this review, we discuss the close relationship between the neurobiological mechanisms of psychological stress and the secretion of proinflammatory cytokines induced by brain-gut-skin communication. We also discuss the mechanisms by which psychological stress may exacerbate inflammatory skin diseases through descending pathways (central and peripheral hypothalamic-pituitary-adrenal axes, peripheral nerves, and skin barrier function).
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45

Igaz, Péter, Károly >Rácz, Miklós Tóth, Edit Gláz e Zsolt Tulassay. "Treatment of iatrogenic Cushing’s syndrome: questions of glucocorticoid withdrawal". Orvosi Hetilap 148, n. 5 (febbraio 2007): 195–202. http://dx.doi.org/10.1556/oh.2007.27964.

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Abstract (sommario):
Iatrogenic Cushing’s syndrome is the most common form of hypercortisolism. Glucocorticoids are widely used for the treatment of various diseases, often in high doses that may lead to the development of severe hypercortisolism. Iatrogenic hypercortisolism is unique, as the application of exogenous glucocorticoids leads to the simultaneous presence of symptoms specific for hypercortisolism and the suppression of the endogenous hypothalamic-pituitary-adrenal axis. The principal question of its therapy is related to the problem of glucocorticoid withdrawal. There is considerable interindividual variability in the suppression and recovery of the hypothalamic-pituitary-adrenal axis, therefore, glucocorticoid withdrawal and substitution can only be conducted in a stepwise manner with careful clinical follow-up and regular laboratory examinations regarding endogenous hypothalamic-pituitary-adrenal axis activity. Three major complications which can be associated with glucocorticoid withdrawal are: i. reactivation of the underlying disease, ii. secondary adrenal insufficiency, iii. steroid withdrawal syndrome. Here, the authors summarize the most important aspects of this area based on their clinical experience and the available literature data.
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46

During, Matthew J., Xianglan Liu, Wei Huang, Daniel Magee, Andrew Slater, Travis McMurphy, Chuansong Wang e Lei Cao. "Adipose VEGF Links the White-to-Brown Fat Switch With Environmental, Genetic, and Pharmacological Stimuli in Male Mice". Endocrinology 156, n. 6 (1 giugno 2015): 2059–73. http://dx.doi.org/10.1210/en.2014-1905.

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Abstract (sommario):
Abstract Living in an enriched environment (EE) decreases adiposity, increases energy expenditure, causes resistance to diet induced obesity, and induces brown-like (beige) cells in white fat via activating a hypothalamic-adipocyte axis. Here we report that EE stimulated vascular endothelial growth factor (VEGF) expression in a fat depot-specific manner prior to the emergence of beige cells. The VEGF up-regulation was independent of hypoxia but required intact sympathetic tone to the adipose tissue. Targeted adipose overexpression of VEGF reproduced the browning effect of EE. Adipose-specific VEGF knockout or pharmacological VEGF blockade with antibodies abolished the induction of beige cell by EE. Hypothalamic brain-derived neurotrophic factor stimulated by EE regulated the adipose VEGF expression, and VEGF signaling was essential to the hypothalamic brain-derived neurotrophic factor-induced white adipose tissue browning. Furthermore, VEGF signaling was essential to the beige cells induction by exercise, a β3-adrenergic agonist, and a peroxisome proliferator-activated receptor-γ ligand, suggesting a common downstream pathway integrating diverse upstream mechanisms. Exploiting this pathway may offer potential therapeutic interventions to obesity and metabolic diseases.
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47

Tsertsvadze, Lana K., Marina V. Avdeeva, Larisa V. Scheglova e Vladimir S. Vasilenko. "Markers of endothelial dysfunction in adolescent and young patients with hypothalamic syndrome". Obesity and metabolism 17, n. 3 (6 dicembre 2020): 257–68. http://dx.doi.org/10.14341/omet12354.

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Abstract (sommario):
Background: Endothelial dysfunction is the first but reversible stage of atherosclerosis. A change in the functional state of the vascular endothelium, especially of a growing organism, can be the basis for the development of many diseases in adulthood. The study of the structural and functional state of peripheral vessels of adolescents with hypothalamic syndrome is extremely important for understanding of the mechanisms of formation of cardiometabolic risks.Aims: to compare the structural and functional state of the vascular wall of young men with hypothalamic syndrome and constitutionally exogenous obesity.Methods: During the study 360 males were examined (average age 21.27±2.44 years) and divided into 3 groups: group 1 -with hypothalamic syndrome (n=242); group 2 - with constitutionally exogenous obesity (n=98); control group - practically healthy individuals (n=20). Hypothalamic syndrome was verified in the presence of a symptom complex, including obesity and pink striae. Cross-group comparative analysis of results of clinical, laboratory and instrumental examination was carried out.Results: In the group of patients with hypothalamic syndrome, endothelium-dependent vasodilatation (9.44±1.26 versus 10.37±1.21%; p=0.001) and endothelium-independent vasodilatation (10.29±1.28 versus 11.29±1.14%; p=0.001) is worse than in the group of patients with constitutionally exogenous obesity, and the rate of endothelium-dependent vasodilatation is lower than the generally accepted norm. In addition, among patients with hypothalamic syndrome, the stiffness of the vascular wall is higher than among patients with constitutionally exogenous obesity (15.47±2.58 versus 13.24±3.84%; p=0.001). Statistically significant correlations were revealed between the structural and functional state of peripheral arteries and hemodynamic, hormonal, metabolic changes, and the level of C-reactive protein (p<0.05).Conclusions: The obtained data indicate a deterioration of endothelial function and an increase in vascular wall stiffness in obese patients, regardless of its etiology. The patients with hypothalamic syndrome have more pronounced structural and functional changes in the vascular wall are observed than patients with constitutionally exogenous obesity.
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48

Wannes, Selmen, Monique Elmaleh-Bergès, Dominique Simon, Delphine Zénaty, Laetitia Martinerie, Caroline Storey, Georges Gelwane et al. "High prevalence of syndromic disorders in patients with non-isolated central precocious puberty". European Journal of Endocrinology 179, n. 6 (dicembre 2018): 373–80. http://dx.doi.org/10.1530/eje-18-0613.

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Abstract (sommario):
Objective Non-idiopathic CPP is caused by acquired or congenital hypothalamic lesions visible on MRI or is associated with various complex genetic and/or syndromic disorders. This study investigated the different types and prevalence of non-isolated CPP phenotypes. Design and Methods This observational cohort study included all patients identified as having non-idiopathic CPP in the database of a single academic pediatric care center over a period of 11.5 years. Patients were classified on the basis of MRI findings for the CNS as having either hypothalamic lesions or complex syndromic phenotypes without structural lesions of the hypothalamus. Results In total, 63 consecutive children (42 girls and 21 boys) with non-isolated CPP were identified. Diverse diseases were detected, and the hypothalamic lesions visible on MRI (n = 28, 45% of cases) included hamartomas (n = 17; either isolated or with an associated syndromic phenotype), optic gliomas (n = 8; with or without neurofibromatosis type 1), malformations (n = 3) with interhypothalamic adhesions (n = 2; isolated or associated with syndromic CNS midline abnormalities, such as optic nerve hypoplasia, ectopic posterior pituitary) or arachnoid cysts (n = 1). The patients with non-structural hypothalamic lesions (n = 35, 55% of cases) had narcolepsy (n = 9), RASopathies (n = 4), encephalopathy or autism spectrum disorders with or without chromosomal abnormalities (n = 15) and other complex syndromic disorders (n = 7). Conclusion Our findings suggest that a large proportion (55%) of patients with non-isolated probable non-idiopathic CPP may have complex disorders without structural hypothalamic lesions on MRI. Future studies should explore the pathophysiological relevance of the mechanisms underlying CPP in these disorders.
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49

Ishido, Hideaki, Shigeru Chiba, Hana Takahashi, Megumi Isa, Yasuhiro Ogawa, Hiroki Kubota, Aya Imanishi et al. "Characteristics of hypersomnia due to inflammatory demyelinating diseases of the central nervous system". BMJ Neurology Open 5, n. 1 (giugno 2023): e000428. http://dx.doi.org/10.1136/bmjno-2023-000428.

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Abstract (sommario):
BackgroundNeuromyelitis optica spectrum disorder (NMOSD) diagnostic criteria for inflammatory demyelinating central nervous system diseases included symptomatic narcolepsy; however, no relevant case‐control studies exist. We aimed to examine the relationship among cerebrospinal fluid orexin‐A (CSF‐OX) levels, cataplexy and diencephalic syndrome; determine risk factors for low-and-intermediate CSF‐OX levels (≤200 pg/mL) and quantify hypothalamic intensity using MRI.MethodsThis ancillary retrospective case‐control study included 50 patients with hypersomnia and 68 controls (among 3000 patients) from Akita University, the University of Tsukuba and community hospitals (200 facilities). Outcomes were CSF‐OX level and MRI hypothalamus‐to‐caudate‐nucleus‐intensity ratio. Risk factors were age, sex, hypersomnolence and MRI hypothalamus‐to‐caudate‐nucleus‐intensity ratio >130%. Logistic regression was performed for the association between the risk factors and CSF‐OX levels ≤200 pg/mL.ResultsThe hypersomnia group (n=50) had significantly more cases of NMOSD (p<0.001), diencephalic syndrome (p=0.006), corticosteroid use (p=0.011), hypothalamic lesions (p<0.023) and early treatment (p<0.001). No cataplexy occurred. In the hypersomnia group, the median CSF-OX level was 160.5 (IQR 108.4–236.5) pg/mL and median MRI hypothalamus-to-caudate-nucleus-intensity ratio was 127.6% (IQR 115.3–149.1). Significant risk factors were hypersomnolence (adjusted OR (AOR) 6.95; 95% CI 2.64 to 18.29; p<0.001) and MRI hypothalamus‐to‐caudate‐nucleus‐intensity ratio >130% (AOR 6.33; 95% CI 1.18 to 34.09; p=0.032). The latter was less sensitive in predicting CSF-OX levels ≤200 pg/mL. Cases with MRI hypothalamus-to-caudate-nucleus-intensity ratio >130% had a higher rate of diencephalic syndrome (p<0.001, V=0.59).ConclusionsConsidering orexin as reflected by CSF‐OX levels and MRI hypothalamus‐to‐caudate‐nucleus‐intensity ratio may help diagnose hypersomnia with diencephalic syndrome.
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50

Fujitani, Masashi, Yoshinori Otani e Hisao Miyajima. "Do Neurotrophins Connect Neurological Disorders and Heart Diseases?" Biomolecules 11, n. 11 (19 novembre 2021): 1730. http://dx.doi.org/10.3390/biom11111730.

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Abstract (sommario):
Neurotrophins (NTs) are one of the most characterized neurotrophic factor family members and consist of four members in mammals. Growing evidence suggests that there is a complex inter- and bi-directional relationship between central nervous system (CNS) disorders and cardiac dysfunction, so-called “brain–heart axis”. Recent studies suggest that CNS disorders, including neurodegenerative diseases, stroke, and depression, affect cardiovascular function via various mechanisms, such as hypothalamic–pituitary–adrenal axis augmentation. Although this brain–heart axis has been well studied in humans and mice, the involvement of NT signaling in the axis has not been fully investigated. In the first half of this review, we emphasize the importance of NTs not only in the nervous system, but also in the cardiovascular system from the embryonic stage to the adult state. In the second half, we discuss the involvement of NTs in the pathogenesis of cardiovascular diseases, and then examine whether an alteration in NTs could serve as the mediator between neurological disorders and heart dysfunction. The further investigation we propose herein could contribute to finding direct evidence for the involvement of NTs in the axis and new treatment for cardiovascular diseases.
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