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Altered glucoregulatory response to physiological infusions of epinephrine and glucagon in hyperthyroidism.
No full textTo study the mechanism of altered glucose homeostasis in hyperthyroidism, the effects of a 2-h physiological infusion of epinephrine (0.05 microgram/kg x min) or glucagon (3 ng/kg x min) on glucose kinetics and glucoregulatory hormones were determined in nine normal subjects and five untreated hyperthyroid patients. Under basal conditions, hyperthyroid patients exhibited increased glucose turnover (2.2 +/- 0.09 vs. 1.62 +/- 0.1 mg/kg x min in normals), a modest hyperglycemia, hyperglucagonemia, and normal levels of plasma insulin, cortisol, and GH. In normal subjects, epinephrine induced a sustained increase in plasma glucose (45 mg/dl), reflecting a transient 100% rise in glucose output, and a sustained 28% decrease in glucose clearance. In hyperthyroid patients, the rise in plasma glucose was significantly lower (22 mg/dl) due to a smaller but sustained increase in glucose output (45%) and the lack of a fall in glucose clearance. Plasma insulin rose to a peak 80% higher than baseline in hyperthyroid patients, whereas in normals it initially declined and then rose to levels 50% higher than basal. Plasma glucagon displayed only minor changes in both groups. Glucagon infusion induced similar increments in plasma glucagon levels in the two groups (120-150 pg/ml). Insulin, cortisol, and GH remained unchanged. Plasma glucose rose by 4 mg/dl in hyperthyroid patients and by 11 mg/dl in normal subjects. The net increments were significantly lower in the former group (P < 0.05-0.01). Glucose output increased by 40% in normals and returned to baseline by 75 min, whereas it increased by only 15% in hyperthyroid patients and remained above baseline until the end of the infusion. Glucagon had no appreciable effect on glucose clearance in either group. We conclude that hyperthyroidism is characterized by 1) increased glucose turnover and hyperglucagonemia in the basal state, 2) a reduced glucemic response to physiological infusions of epinephrine and glucagon, 3) a sustained response of glucose production to epinephrine and glucagon, and 4) the lack of epinephrine-induced suppression of glucose clearance, presumably due to an exaggerated response of insulin secretion to epinephrine
Plasma immunoreactive thyrotropin releasing hormone (TRH) values in normal newborns
No full textThe study reported here extends investigation on the pituitary thyroid axis in newborn infants, including the assay of plasma immunoreactive TSH levels at different intervals after delivery. Blood samples were collected at birth and after 30, 60, 120 minutes, 6, 24 and 48 hours. Plasma TRH levels were also estimated in normal adult subjects and pregnant women. No significant difference was observed with regard to sex, pregnancy or age, except for a marked increase in newborn infants after delivery. Plasma TRH values, already moderately high at birth (mean 46 pg/ml, range 34-57) reached rapidly a peak of 78 pg/ml (range 60-93) 30 minutes after delivery, decreased rapidly between 30 minutes and 2 hours post-partum, then fell gradually to normal range at 24 hours. A comparison of plasma TRH and TSH levels measured simultaneously suggests that the acute TSH surge at delivery is mediated by TRH secretion
Increased plasma prolactin levels induced in rats by d-fenfluramine: relation to central serotonergic stimulation
No full textSerum Bcl-2 concentrations in overweight-obese subjects with nonalcoholic fatty liver disease
No full textAIM:
To shed some light on the relationship between anti-apoptotic serum Bcl-2 concentrations and metabolic status, anthropometric parameters, inflammation indices, and non-alcoholic fatty liver disease severity were investigated in 43 young individuals with fatty liver (FL) and 41 with nonalcoholic steatohepatitis (NASH).
METHODS:
Circulating levels of Bcl-2 were detected in 84 patients with ultrasonographic findings of "bright liver" and/or hyper-transaminasemia of unknown origin and/or increase in γ-glutamyl-transpeptidase (γ-GT) strictly in the absence of other acute or chronic liver disease, whose age was not advanced, who gave consent to liver biopsy and were then divided on the basis of the histological results into two groups (43 with FL and 41 with NASH). Twenty lean subjects, apparently healthy and young, were chosen as controls.
RESULTS:
Serum Bcl-2 concentrations were significantly higher in the FL group than in the NASH group. Insulin resistance and γ-GT activity were significantly higher in NASH subjects. Apoptotic hepatocytes were significantly more numerous in NASH patients. NASH patients presented with larger spleens and augmented C-reactive protein (CRP) concentrations than healthy subjects. Steatosis grade at histology was similar in both NASH and FL populations. The number of apoptotic cells was significantly related to anti-apoptotic Bcl-2 protein values in FL patients. Bcl-2 serum levels positively correlated to body mass index (BMI) values (P ≤ 0.0001) but not to age of the population. Triglycerides/HDL ratio correlated well to waist circumference in males (P = 0.0008). γ-GT activity was associated with homeostatic metabolic assessment (HOMA) (P = 0.0003) and with serum ferritin (P = 0.02). Bcl-2 concentrations were not related to either spleen size or CRP values. NASH patients presented a weak negative correlation between lobular inflammation and Bcl-2 levels. A prediction by low values of serum Bcl-2 towards a greater presence of metabolically unhealthy overweight/obese patients (MUOs) was evidenced. HOMA, BMI and uric acid, in that sequence, best predicted serum Bcl-2 concentrations.
CONCLUSION:
MUOs could be detected by Bcl-2 levels. By favoring the life span of hepatocytes, and enhancing triglyceride formation, the anti-apoptotic process inhibits free fatty acids toxicity in FL
Myeloperoxidase, but not C-reactive protein, predicts cardiovascular risk in peripheral arterial disease.
No full textAIMS: The prognostic role of inflammation in peripheral arterial disease (PAD) remains to be conclusively established. Accordingly, in these patients we investigated the impact of myeloperoxidase (MPOx) and C-reactive protein on the
incidence of myocardial infarction and stroke. METHODS AND RESULTS: Of 156 PAD patients, 10 had a myocardial infarction and seven a stroke, during follow-up. We used the receiver operating characteristic curve analysis and the bootstrap
approach to identify the MPOx, C-reactive protein, and ankle brachial index (ABI) threshold levels that provided the best cut-off to predict the outcome. For MPOx a cut-off > or =183.7 pM was independently associated with a poor outcome (HR =
6.80, 95% CI 1.20-38.69, P = 0.031). The result remained unmodified when MPOx was used as a continuous variable (HR = 1.03, 95% CI 1.01-1.05, P = 0.031). Conversely, C-reactive protein was not a prognostic determinant in our series (HR
= 0.88, 95% CI 0.60-1.29, P = 0.514). Kaplan-Meier curves for the four groups of patients delineated according to ABI and MPOx values identified using the bootstrap approach showed that the addition of MPOx measurement to ABI improved the ability to identify patients at risk for myocardial infarction and stroke. CONCLUSION: In PAD, MPOx, but not C-reactive protein, predicts an increased risk of major cardiovascular events, and adds to the prognostic value of ABI, currently the most powerful prognostic indicator in these patients
[Degenerative nuclear changes in the cells of oral mucosa in congenital adrenal gland hyperplasia and their interference with the frequency of nuclear chromatin]
No full text
The role of central noradrenergic neurons in the control of thyrotropin secretion in the rat.
No full textTo investigate the role played by hypothalamic noradrenaline (NE) in the regulation of TRH-TSH release during tonic and cold activated conditions, drugs and surgical procedures able to interfere with central NE tonus were utilized. The time course of the effect of alpha-methyl-para-tyrosine (alpha-MpT) on basal TSH secretion was followed. The tyrosine hydroxylase (TH) inhibitor was unable to modify TSH plasma levels, whereas NE hypothalamic content decreased beginning with the third hour. The acute release of TSH evoked by cold exposure (CE) was prevented by pretreatment with alpha-MpT 1 h before; when alpha-MpT was followed 40 min later by clonidine, a central noradrenergic stimulating agent, TSH response to cold, previously blocked by the TH inhibitor was restored. Intraventricular injection of 10 micrograms of clonidine hydrochloride in unstimulated rats caused a significant rise of basal TSH levels 3, but not 10 min after the administration. Complex deafferentation of the medial basal hypothalamus (MBH), which destroys all the NE fibers afferent to this area, caused no change of thyrotropin secretion in basal conditions. Deafferented animals did not show any acute increase of TSH in response to CE. The results of this study provide evidence that NE may be the catecholamine (CA) mediating the rise in TSH following CE and that the direct stimulation of central NE receptors can evoke a massive TSH release from the anterior pituitary gland also in basal conditions
Ramipril in post-renal transplant erythrocytosis
No full textBACKGROUND: Posttransplant erythrocytosis (PTE; i.e., hematocrit [Ht] >=51%) may be responsible for cardiovascular events. Angiotensin-converting enzyme inhibitors (ACEIs) are increasingly employed in PTE treatment. Diverse ACEIs have been administered at variable doses and with erratic follow-up. In addition, guidelines recommend the administration of ACEIs as first-line therapy for PTE but do not give information on dosage. In this study the dose-response of a single ACEI was assessed, and patients were followed up for 1 year. The role of ACE gene polymorphism in both prevalence of PTE and successful response to ACEI therapy was also tested. METHODS: At study entry, blood chemistry and ACE-gene polymorphism were measured. ACEI (ramipril) was initiated at 1.25 mg/day; if Ht was still >=51%, ramipril was increased every 6 weeks to ensuing greater dosages. Scheduled dosages were 1.25, 2.5, 5.0, 7.5 and 10 mg/day. Blood chemistry was repeated every 6 weeks. Serum erythropoietin (EPO) concentration was assayed at the start and end of the study. Follow-up was extended for 1 year. RESULTS: PTE developed 12.6 +/- 16.0 months after transplantation in 40 out of 400 patients; 27 patients completed the study. Initial Ht was not correlated with any variable. Final Ht appeared normalized in 26 out of 27 patients. Mean dose (+/- SD) of ramipril was 4.6 +/- 3.6 mg. Mean time for correction of PTE was 135 days, and was not dependent on baseline Ht, hemoglobin or EPO. PTE relapsed in 4 patients. Prevalence of PTE and successful response to ramipril was not dependent on ACE-gene polymorphism. CONCLUSION: Ramipril was effective in PTE; low doses normalized Ht in most patients. No clinical characteristics or biochemical variables predicted the response to ramipril. PTE may relapse; thus long-term follow-up is mandator
Automated determination of neutrophil volume as screening test for late-onset sepsis in very low birth infants.
No full textThe diagnosis of sepsis is often a difficult issue for the neonatologist. Clinical signs and symptoms are poorly specific, and the quest for the optimal laboratory assay is still open. C-reactive protein (CRP) requires serial determinations to be of practical value,1 interleukins have not yet entered the routine clinical use, total white blood cells or absolute neutrophil counts alone have not enough sensitivity or specificity. Current hematology analyzers can determine white blood cell subpopulations based on their physical characteristics (eg, volume and granularity). In particular, mean neutrophil volume (MNeV) and its standard deviation (neutrophil distribution width) have been previously used to diagnose sepsis in an adult population with encouraging results.We investigated these same parameters in screening for late-onset neonatal sepsis, defined as a systemic infection, validated by a positive blood culture, diagnosed beyond the third day of life. When taken together, CRP and MNeV represent a powerful rapid combination both to suspect or exclude late onset sepsis. Neutrophil distribution width did not prove to be of any practical help in our neonatal series, possibly because the resting neutrophil population in the newborn is already more heterogeneous in size and shape than in the adult
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