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Yuminova, Nataliya Alexandrovna - One of the best experts on this subject based on the ideXlab platform.
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INFLUENCE OF HYDROCHLORINE MORPHINE ON MORPHOFUNCTIONAL STATE OF THYROID GLAND AND SOME LINKS ITS REGULATION AMONG RATS
1996Co-Authors: Yuminova, Nataliya AlexandrovnaAbstract:The investigation objects are the thyroid gland, blood plasma, adenoHypophysis and Hypothalamus of the non-breed albino rats. The aim is to perform the comparative analysis of the morphological non-functional changes in the thyroid gland and Hypothalamus-Hypophysis System of the rats at chronic morphine intoxication. The complex analysis of the structural-functional state in thyroid gland permitted to reveal the dose-depended activation of the thyrocytes and parafollicular cells of the compensatory-adaptation character on the background of introducing hydrochloride morphine in different doses (1 - 40 mg/kg) with courses of different duration (2 - 3 - 4 weeks) in different periods of the preparation abolition has been made firstly. The conclusion that at chronic morphine activation the activation of the thyroid epithelium can be stipulated with both the functional stress of the neurosecretory cells of the thyrotropic hypathalamus centre and beta-basophilic adenoHypophysis thyrotropocytes and organic specifics of the thyroid gland has been made. The investigation results have been put into the educational process at the departments of physiology and biology of the Izhevsk State Medical Academy, can be used in the following researches on the study of influencing morphine and morphine-similar preparations on the organism and also in the medical practiceAvailable from VNTIC / VNTIC - Scientific & Technical Information Centre of RussiaSIGLERURussian Federatio
ΓΕΩΡΓΑΚΟΠΟΥΛΟΣ ΚΡΙΣΤΟΦ - One of the best experts on this subject based on the ideXlab platform.
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ALTERATIONS OF ATRIAL NATRIURETIC PEPTIDE AFTER ADRENALECTOMY
'National Documentation Centre (EKT)', 1995Co-Authors: ΓΕΩΡΓΑΚΟΠΟΥΛΟΣ ΚΡΙΣΤΟΦAbstract:ΣΚΟΠΟΣ ΤΗΣ ΜΕΛΕΤΗΣ ΗΤΑΝ ΝΑ ΔΙΕΡΕΥΝΗΘΕΙ, ΕΑΝ Η ΕΚΚΡΙΣΗ ΤΟΥ ANP ΒΡΙΣΚΕΡΤΑΙ ΥΠΟ ΤΟΝ ΕΛΕΓΧΟ ΤΟΥ ΥΠΟΘΑΛΑΜΟΥΠΟΦΥΣΙΑΚΟΥ ΣΥΣΤΗΜΑΤΟΣ ΜΕΣΩ ΤΗΣ ACTH. ΧΡΗΣΙΜΟΠΟΙΗΘΗΚΑΝ ΕΞΙ ΧΟΙΡΟΙ ΜΕΣΟΥ ΒΑΡΟΥΣ: 25,58 +- 0,95 KG. ΜΕ ΓΕΝΙΚΗ ΑΝΑΙΣΘΗΣΙΑ ΑΦΑΙΡΕΘΗΚΑΝ ΤΑ ΕΠΙΝΕΦΡΙΔΙΑ ΑΜΦΟΤΕΡΟΠΛΕΥΡΑ. ΕΛΗΦΘΗΣΑΝ ΔΕΙΓΜΑΤΑ ΑΙΜΑΤΟΣ ΑΠΟ ΤΗΝ ΠΝΕΥΜΟΝΙΚΗ ΑΡΤΗΡΙΑ ΠΡΟ ΚΑΙ 30, 45, 60, 90 ΚΑΙ 120 MIN ΜΕΤΑ ΤΗΝ ΕΠΙΝΕΦΡΙΔΕΚΤΟΜΗ ΓΙΑ ΤΟΝ ΠΡΟΣΔΙΟΡΙΣΜΟ ΤΩΝ ΕΠΙΠΕΔΩΝ ΤΩΝ: ANP, ΡΕΝΙΝΗΣ, ACTH, ΚΟΡΤΙΖΟΛΗ, ΑΛΔΟΣΤΕΡΟΝΗΣ, ΑΙΜΑΤΟΚΡΙΤΗ, ΝΑΤΡΙΟΥ, ΚΑΛΙΟΥ ΜΕ ΤΑΥΤΟΧΡΟΝΗ ΜΕΤΡΗΣΗ ΤΩΝ: ΜΕΣΗ ΠΙΕΣΗ ΕΝΣΦΗΝΩΣΕΩΣ ΠΝΕΥΜΟΝΙΚΩΝ ΤΡΙΧΟΕΙΔΩΝ, ΠΙΕΣΗ ΑΟΡΤΗΣ, ΜΕΣΗ ΠΙΕΣΗ ΔΕΞΙΟΥ ΚΟΛΠΟΥ, ΚΑΡΔΙΑΚΗ ΣΥΧΝΟΤΗΣ ΚΑΙ ΚΑΡΔΙΑΚΗ ΠΑΡΟΧΗ. ΑΠΟΤΕΛΕΣΜΑΤΑ: Ο ΚΑΡΔΙΑΚΟΣ ΔΕΙΚΤΗΣ ΠΑΡΟΥΣΙΑΣΕ ΣΤΑΤΙΣΤΙΚΑ ΣΗΜΑΝΤΙΚΗ ΜΕΙΩΣΗ ΣΤΑ 90 MIN ΜΕΤΑ ΤΗΝ ΕΠΙΝΕΦΡΙΔΙΕΚΤΟΜΗ, Η ΚΑΡΔΙΑΚΗ ΣΥΧΝΟΤΗΤΑ ΣΤΑΤΙΣΤΙΚΑ ΣΗΜΑΝΤΙΚΗ ΑΥΞΗΣΗ ΣΤΑ 120 MIN ΜΕΤΑ ΤΗΝ ΕΠΙΝΕΦΡΙΔΙΕΚΤΟΜΗ, ΕΝΩ ΟΙ ΥΠΟΛΟΙΠΕΣ ΑΙΜΟΔΥΝΑΜΙΚΕΣ ΠΑΡΑΜΕΤΡΟΙ ΔΕΝ ΠΑΡΟΥΣΙΑΣΑΝ ΜΕΤΑΒΟΛΕΣ. ΤΑ ΕΠΙΠΕΔΑ ΤΟΥ ANP ΔΕΝ ΜΕΤΑΒΛΗΘΗΚΑΝ ΣΗΜΑΝΤΙΚΑ, ΑΝ ΚΑΙ ΤΑ ΕΠΙΠΕΔΑ ΤΗΣ ACTH ΠΑΡΟΥΣΙΑΣΑΝ ΣΤΑΤΙΣΤΙΚΑ ΣΗΜΑΝΤΙΚΗ ΑΥΞΗΣΗ ΣΤΑ 90 MIN ΜΕΤΑ ΤΗΝ ΕΠΙΝΕΦΡΙΔΙΕΚΤΟΜΗ. ΤΑ ΕΠΙΠΕΔΑ ΚΟΡΤΙΖΟΛΗΣ, ΑΛΔΟΣΤΕΡΟΝΗΣ ΚΑΙ ΝΑΤΡΙΟΥ ΟΡΟΥ ΥΠΟΧΩΡΗΣΑΝ ΣΗΜΑΝΤΙΚΑ, ΕΝΩ ΤΑ ΕΠΙΠΕΔΑ ΡΕΝΙΝΗΣ ΠΑΡΟΥΣΙΑΣΑΝ ΣΤΑΤΙΣΤΙΚΑ ΣΗΜΑΝΤΙΚΗ ΑΥΞΗΣΗ Σ'ΟΛΟΥΣ ΤΟΥΣ ΧΡΟΝΟΥΣ ΜΕΤΑ ΤΗΝ ΕΠΙΝΕΦΡΙΔΙΕΚΤΟΜΗ. ΟΙ ΤΙΜΕΣ ΑΙΜΑΤΟΚΡΙΤΗ ΚΑΙ ΚΑΛΙΟΥ ΟΡΟΥ ΜΕΙΩΘΗΚΑΝ ΣΕ ΣΤΑΤΙΣΤΙΚΑ ΣΗΜΑΝΤΙΚΟ ΒΑΘΜΟ ΜΟΝΟ ΣΤΑ 60 ΚΑΙ 90 MIN ΜΕΤΑ ΤΗΝ ΕΠΙΝΕΦΡΙΔΙΕΚΤΟΜΗ. (ΠΕΡΙΚΟΠΗ ΠΕΡΙΛΗΨΗΣ)THE AIM OF OUR STUDY WAS TO INVESTIGATE, IF THE SECRETION OF ANP IS UNDER THE CONTROL OF THE System "Hypothalamus-Hypophysis" THROUGH ACTH. SIX PIGS WERE USED WITH MEAN BODY WEIGHT: 25,58 +- 0,95 KG. UNDERAL GENERAL ANAESTHESIA BILATERAL ADRENALECTOMY WAS PERFORMED. BLOOD SAMPLES WERE DRAWN FROM THE PULMONARY ARTERY BEFORE AND AT 30, 45, 60, 90 AND 120 MIN AFTER ADRENALECTOMY FOR THE ESTIMATION OF ANP, RENIN, ACTH, CORTIZOL, ALDOSTERONE, HAEMATOCRIT, NATRIUM, POTASSIUM LEVELS WHILE AT THE SAME TIME RECORDINGS WERE MADE OF: MEAN PULMONARY CAPILLARY WEDGE PRESSURE, AORTIC PRESSURE, MEAN RIGHT ATRIAL PRESSURE, HEART RATE AND CARDIAC OUTPUT. CARDIAC INDEX SHOWED SIGNIFICANT DECREASE AT 90 MIN FOLLOWING ADRENALECTOMY, HEART RATE INCREASED SIGNIFICANTLY AT 120 MIN AFTER ADRENALECTOMY, WHILE THE OTHER HAEMODYNAMIC PARAMETERS DID NOT SHOW ANY ALTERATION. ANP LEVELS DID NOT CHANGE SIGNIFICANTLY, ALTHOUGH ACTH LEVELS INCREASED SIGNIFICANTLY AT 90 MIN AFTER ADRENALECTOMY. CORTIZOL, ALDOSTERONE AND NATRIUM LEVELS FELL SIGNIFICANTLY, WHILE RENIN LEVELS INCREASED SIGNIFICANTLY AT 30 MIN AFTER ADRENALECTOMY. HAEMATOCRIT AND POTASSIUM LEVELS DECREASED SIGNIFICANTLY AT 60 AND 90 MIN AFTER ADRENALECTOMY. IT WAS CONCLUDED, THAT THE SECRETION OFANP IS UNDER THE INDIRECT CONTROL OF "Hypothalamus-Hypophysis" System: STIMULATION OF THE System CAUSES INCREASED SECRETION OF ACTH, WHICH CAUSES INCREASEDSECRETION OF GLUCOCORTICOIDS, WHICH INCREASES ANP LEVELS
Schnell, Matthias J. - One of the best experts on this subject based on the ideXlab platform.
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Intravenous Inoculation of a Bat-Associated Rabies Virus Causes Lethal Encephalopathy in Mice through Invasion of the Brain via Neurosecretory Hypothalamic Fibers
Public Library of Science, 2026Co-Authors: Preuss, Mirjam A. R., Faber Marie-luise, Tan, Gene S., Bette Michael, Dietzschold Bernhard, Weihe Eberhard, Schnell, Matthias J.Abstract:The majority of rabies virus (RV) infections are caused by bites or scratches from rabid carnivores or bats. Usually, RV utilizes the retrograde transport within the neuronal network to spread from the infection site to the central nervous System (CNS) where it replicates in neuronal somata and infects other neurons via trans-synaptic spread. We speculate that in addition to the neuronal transport of the virus, hematogenous spread from the site of infection directly to the brain after accidental spill over into the vascular System might represent an alternative way for RV to invade the CNS. So far, it is unknown whether hematogenous spread has any relevance in RV pathogenesis. To determine whether certain RV variants might have the capacity to invade the CNS from the periphery via hematogenous spread, we infected mice either intramuscularly (i.m.) or intravenously (i.v.) with the dog-associated RV DOG4 or the silver-haired bat-associated RV SB. In addition to monitoring the progression of clinical signs of rabies we used immunohistochemistry and quantitative reverse transcription polymerase chain reaction (qRT-PCR) to follow the spread of the virus from the infection site to the brain. In contrast to i.m. infection where both variants caused a lethal encephalopathy, only i.v. infection with SB resulted in the development of a lethal infection. While qRT-PCR did not reveal major differences in virus loads in spinal cord or brain at different times after i.m. or i.v. infection of SB, immunohistochemical analysis showed that only i.v. administered SB directly infected the forebrain. The earliest affected regions were those hypothalamic nuclei, which are connected by neurosecretory fibers to the circumventricular organs neuroHypophysis and median eminence. Our data suggest that hematogenous spread of SB can lead to a fatal encephalopathy through direct retrograde invasion of the CNS at the neurovascular interface of the Hypothalamus-Hypophysis System. This alternative mode of virus spread has implications for the post exposure prophylaxis of rabies, particularly with silver-haired bat-associated RV
Preuss, Mirjam A. R. - One of the best experts on this subject based on the ideXlab platform.
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Intravenous Inoculation of a Bat-Associated Rabies Virus Causes Lethal Encephalopathy in Mice through Invasion of the Brain via Neurosecretory Hypothalamic Fibers
Public Library of Science, 2026Co-Authors: Preuss, Mirjam A. R., Faber Marie-luise, Tan, Gene S., Bette Michael, Dietzschold Bernhard, Weihe Eberhard, Schnell, Matthias J.Abstract:The majority of rabies virus (RV) infections are caused by bites or scratches from rabid carnivores or bats. Usually, RV utilizes the retrograde transport within the neuronal network to spread from the infection site to the central nervous System (CNS) where it replicates in neuronal somata and infects other neurons via trans-synaptic spread. We speculate that in addition to the neuronal transport of the virus, hematogenous spread from the site of infection directly to the brain after accidental spill over into the vascular System might represent an alternative way for RV to invade the CNS. So far, it is unknown whether hematogenous spread has any relevance in RV pathogenesis. To determine whether certain RV variants might have the capacity to invade the CNS from the periphery via hematogenous spread, we infected mice either intramuscularly (i.m.) or intravenously (i.v.) with the dog-associated RV DOG4 or the silver-haired bat-associated RV SB. In addition to monitoring the progression of clinical signs of rabies we used immunohistochemistry and quantitative reverse transcription polymerase chain reaction (qRT-PCR) to follow the spread of the virus from the infection site to the brain. In contrast to i.m. infection where both variants caused a lethal encephalopathy, only i.v. infection with SB resulted in the development of a lethal infection. While qRT-PCR did not reveal major differences in virus loads in spinal cord or brain at different times after i.m. or i.v. infection of SB, immunohistochemical analysis showed that only i.v. administered SB directly infected the forebrain. The earliest affected regions were those hypothalamic nuclei, which are connected by neurosecretory fibers to the circumventricular organs neuroHypophysis and median eminence. Our data suggest that hematogenous spread of SB can lead to a fatal encephalopathy through direct retrograde invasion of the CNS at the neurovascular interface of the Hypothalamus-Hypophysis System. This alternative mode of virus spread has implications for the post exposure prophylaxis of rabies, particularly with silver-haired bat-associated RV
Faber Marie-luise - One of the best experts on this subject based on the ideXlab platform.
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Intravenous Inoculation of a Bat-Associated Rabies Virus Causes Lethal Encephalopathy in Mice through Invasion of the Brain via Neurosecretory Hypothalamic Fibers
Public Library of Science, 2026Co-Authors: Preuss, Mirjam A. R., Faber Marie-luise, Tan, Gene S., Bette Michael, Dietzschold Bernhard, Weihe Eberhard, Schnell, Matthias J.Abstract:The majority of rabies virus (RV) infections are caused by bites or scratches from rabid carnivores or bats. Usually, RV utilizes the retrograde transport within the neuronal network to spread from the infection site to the central nervous System (CNS) where it replicates in neuronal somata and infects other neurons via trans-synaptic spread. We speculate that in addition to the neuronal transport of the virus, hematogenous spread from the site of infection directly to the brain after accidental spill over into the vascular System might represent an alternative way for RV to invade the CNS. So far, it is unknown whether hematogenous spread has any relevance in RV pathogenesis. To determine whether certain RV variants might have the capacity to invade the CNS from the periphery via hematogenous spread, we infected mice either intramuscularly (i.m.) or intravenously (i.v.) with the dog-associated RV DOG4 or the silver-haired bat-associated RV SB. In addition to monitoring the progression of clinical signs of rabies we used immunohistochemistry and quantitative reverse transcription polymerase chain reaction (qRT-PCR) to follow the spread of the virus from the infection site to the brain. In contrast to i.m. infection where both variants caused a lethal encephalopathy, only i.v. infection with SB resulted in the development of a lethal infection. While qRT-PCR did not reveal major differences in virus loads in spinal cord or brain at different times after i.m. or i.v. infection of SB, immunohistochemical analysis showed that only i.v. administered SB directly infected the forebrain. The earliest affected regions were those hypothalamic nuclei, which are connected by neurosecretory fibers to the circumventricular organs neuroHypophysis and median eminence. Our data suggest that hematogenous spread of SB can lead to a fatal encephalopathy through direct retrograde invasion of the CNS at the neurovascular interface of the Hypothalamus-Hypophysis System. This alternative mode of virus spread has implications for the post exposure prophylaxis of rabies, particularly with silver-haired bat-associated RV