16 research outputs found
ON CERTAIN PECULIARITIES OF HYPERTENSION IN ITSENKO—CUSHING`S DISEASE AND PRIMARY (TUMOROUS) HYPERCORTICISM
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HYPOGLYCEMIC CONDITIONS PRESENTING DIAGNOSTICAL DIFFICULTIES IN A DIABETIC FEMALE PATIENT
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А COMBINATJON BEТWEEN DIABETES MELLIТUS AND IDIOPATHIC HYPERLIPEMIA
Get PDFDespite the fact that fat metabolism disturbances in diabetes mellitus аге known а long time since, the relationship between diabetes and hyperlipemia has been emphasized оnlу in the past several decades.The presence of hyperlipemia in diabetes mellitus has been reported as early as 1799 bу Mariet, Traill (1823), Lecann (1903). Тhе first рubliсаtiоn оn eruptive xanthoma in dliabetes mellitus was made by Addison and Gull (1851). Тhereafter а great numbеr of diabetes mellitus cases have bееn described with eruptive xanthoma, Hyperlipemia аnd hypercholesterolemia.On lhe other hand, il is known that in essential hyperlipemia in adults, disturbances are present in the carbohydrate metabolism as well.In 1955 Adlersberg and Wang made а description of five e patients with idiopathic hyperlipemia, slight dliabetes and severe vascular lesions. According to Chritlensen, Dollerup and Jensen up to 1958 the total number of cases reported with idiopathic hyprrlipemia amounts to 126. In one fifth of them, disturbances are noted in the caгbohydrate metabolism and merely in 16 - diabetic metabolic disorders. The same authors report а female patient with essential hyperlipemia, diabetes, severe arteriosclerosis with occlusion of the lower limb vessels and heavy neuropathy. They lay emphasis on the fact that diiabetes mellitus is encountered very often in the families of patients with essential hyperlipemia.In 1961 Вierman аnd Hamlin reported carbonhydrate induced hyperglyceridemia in 5 patients with diabetes mellitus.Actually, we have under observation at the Naval Hospital in Varпa а patient wilh diabetes mellitus and essentilal hyperlipemia
SUCCESSFUL RESUSCIТATION AND REHABILIТAТION OF А CHILD FROM ТНЕ STATE OF CLINICAL DEATH (CARDIAC ARREST), CAUSED ВУ NOVOCAIN INTOXICATION
Get PDFCases of cardiac death (cardiac arrest) caused by local anesthesia with novocain аrе rarity. According tо Waters Jimms - 1944, clinical death accidents during lосаl anesthesia аrе encountered in 0,106%. They аrе mostly casually related to hypersensibility and intolerance to novocain. Exceedingly rаrе аrе the instances of cardiac arrest, caused bу novocain intoxication.Recently, we had the possibility to observe resuscitation of а child from clinical death bу novocain intoxication, as well as its subsequent successful rehabilitation.Оn 12 September, 1964 in the Naval Hospital at Varna, the patient N. J. J., 9-year-old schoolboy (case history 845/12.IX.1963) was admitted for tonsillectomy. Erroneously, peritonsillar anesthesia was carried out with 10 % instead of 1 % Novocain solution, totaling a quantity of 40 ml. About 5 min, after the anesthesia the child sustains heavy epileptiform fits with loss of consciousness. Breathing is gradually delayed, becomes superficial and in 1-2 minutes it ceases completely. Several minutes later heart activity is also arrested. Dilatation of the pupils is established and reaction to light disappears. The eyeballs are softened. Full areflexia (absence of reflexes) occurs. Epinephrine, luminal, caffeine, cardiazol, plegomazin, nor-epinephrine and cortisone are administered by injection. On the 4-5th minute of cardiac arrest, the child is intubated, and after further 5 min, leftside thoracotomy and direct heart massage performed. On opening the chest cavity, the heart is found relaxed in diastole, filled up with blood. The wound is not bleeding. After nearly 40 compressions (pumping), independent cardiac activity is resumed. Blood pressure is increased up to 120/80mm of Mercury column, the pupilis are contracted. Pupillary reaction to light is restored. An hour later spontaneous breathing occurs, initially weaker and superficial (28-30 respitations per minute) and subsequently, though speeded up – with adequate depth and effectiveness. Twenty four hours later extubations is resorted to and tracheostomy applied. The operative wound of the thorax heals by first intention and no pulmonary complications occur
Loss of mTORC1 signaling alters pancreatic α cell mass and impairs glucagon secretion
Get PDFGlucagon plays a major role in the regulation of glucose homeostasis during fed and fasting states. However, the mechanisms responsible for the regulation of pancreatic α cell mass and function are not completely understood. In the current study, we identified mTOR complex 1 (mTORC1) as a major regulator of α cell mass and glucagon secretion. Using mice with tissue-specific deletion of the mTORC1 regulator Raptor in α cells (αRaptorKO), we showed that mTORC1 signaling is dispensable for α cell development, but essential for α cell maturation during the transition from a milk-based diet to a chow-based diet after weaning. Moreover, inhibition of mTORC1 signaling in αRaptorKO mice and in WT animals exposed to chronic rapamycin administration decreased glucagon content and glucagon secretion. In αRaptorKO mice, impaired glucagon secretion occurred in response to different secretagogues and was mediated by alterations in KATP channel subunit expression and activity. Additionally, our data identify the mTORC1/FoxA2 axis as a link between mTORC1 and transcriptional regulation of key genes responsible for α cell function. Thus, our results reveal a potential function of mTORC1 in nutrient-dependent regulation of glucagon secretion and identify a role for mTORC1 in controlling α cell-mass maintenance
