Thyroid Density in CT Imaging as a Potential Marker of Lung Involvement in COVID-19: A Retrospective Analysis.

Background The SARS-CoV-2 pandemic has underscored the multifaceted impact of the virus on human health, extending beyond the respiratory system to involve other organ systems, including the endocrine system. Emerging evidence suggests a notable interaction between COVID-19 and thyroid function, characterized by alterations in thyroid hormone levels and structural changes within the gland. This study aims to explore the association between thyroid density on CT imaging and lung involvement in patients with COVID-19, potentially offering new insights into the systemic effects of the virus.

Exploring the Correlation Between Splenomegaly and Lung Involvement in COVID-19: A Retrospective Study.

Background Coronavirus disease 2019 (COVID-19), resulting from the severe acute respiratory syndrome corona virus 2 (SARS-CoV-2), has not only shown substantial effects on the respiratory system but also on extrapulmonary systems, including cardiovascular, gastrointestinal, hematological, and immune responses, notably spleen enlargement. The connection between the enlargement of the spleen and pulmonary complications in individuals with COVID-19 is still not well elucidated, with current studies offering divergent conclusions. Objective This study aims to elucidate the correlation between splenomegaly, as assessed by computed tomography (CT) imaging, and the extent of lung involvement (LI) in COVID-19 patients, thereby offering insights into potential prognostic indicators.

Lung Involvement Patterns in COVID-19: CT Scan Insights and Prognostic Implications From a Tertiary Care Center in Southern India.

Background COVID-19, caused by the SARS-CoV-2 virus, has presented an unparalleled challenge and a profound learning curve globally. Among the myriad of investigative tools, CT scans of the chest have become instrumental in assessing the magnitude of lung involvement in the pathogenesis of this disease. Objectives This study aimed to evaluate the distribution and patterns of lung involvement depicted in the CT chest scans of COVID-19 patients admitted to a specialized tertiary care center located in a southern state of India.

3T proton MR Spectroscopy evaluation of spinal cord lesions.

Objective: The objective of this study was to evaluate intramedullary spinal cord lesions using magnetic resonance spectroscopy and correlate the results with histo-pathological examination (HPE).

Materials And Methods: Approval for this study was obtained from our institute ethical committee. , with a maximum age of 53 years and minimum age of 7 years.

Basal insulin, glucagon, and growth hormone replacement.

Conclusions drawn from the pancreatic (or islet) clamp technique (suppression of endogenous insulin, glucagon, and growth hormone secretion with somatostatin and replacement of basal hormone levels by intravenous infusion) are critically dependent on the biological appropriateness of the selected doses of the replaced hormones. To assess the appropriateness of representative doses we infused saline alone, insulin (initially 0.20 mU.

Nocturnal hypoglycemia in type 1 diabetes: an assessment of preventive bedtime treatments.

Objective: We assessed four putative bedtime treatments in the prevention of nocturnal hypoglycemia in type 1 diabetes.

Research Design And Methods: Plasma glucose concentrations were measured every 15 min from 2200 h through 0700 h in 21 patients with type 1 diabetes (mean +/- sd HbA(1C) = 7.1 +/- 1.

Maintenance of the postabsorptive plasma glucose concentration: insulin or insulin plus glucagon?

The prevalent view is that the postabsorptive plasma glucose concentration is maintained within the physiological range by the interplay of the glucose-lowering action of insulin and the glucose-raising action of glucagon. It is supported by a body of evidence derived from studies of suppression of glucagon (and insulin, among other effects) with somatostatin in animals and humans, immunoneutralization of glucagon, defective glucagon synthesis, diverse mutations, and absent or reduced glucagon receptors in animals and glucagon antagonists in cells, animals, and humans. Many of these studies are open to alternative interpretations, and some lead to seemingly contradictory conclusions.

Loss of the decrement in intraislet insulin plausibly explains loss of the glucagon response to hypoglycemia in insulin-deficient diabetes: documentation of the intraislet insulin hypothesis in humans.

The intraislet insulin hypothesis for the signaling of the glucagon secretory response to hypoglycemia states that a decrease in arterial glucose --> a decrease in beta-cell insulin secretion --> a decrease in tonic alpha-cell inhibition by insulin --> an increase in alpha-cell glucagon secretion. To test this hypothesis in humans, a hyperinsulinemic- euglycemic ( approximately 5.0 mmol/l [90 mg/dl] x 2 h) and then a hypoglycemic ( approximately 3.

Mechanism, temporal patterns, and magnitudes of the metabolic responses to the KATP channel agonist diazoxide.

To assess the mechanism, temporal patterns, and magnitudes of the metabolic responses to the ATP-dependent potassium channel agonist diazoxide, neuroendocrine and metabolic responses to intravenous diazoxide (saline, 1.0 and 2.0 mg/kg) and oral diazoxide (placebo, 4.

Cortisol elevations comparable to those that occur during hypoglycemia do not cause hypoglycemia-associated autonomic failure.

The concept of hypoglycemia-associated autonomic failure (HAAF) in diabetes posits that recent antecedent iatrogenic hypoglycemia causes both defective glucose counterregulation (by reducing the epinephrine response in the setting of an absent glucagon response) and hypoglycemia unawareness (by reducing the autonomic-sympathetic neural and adrenomedullary response and the resulting neurogenic [autonomic] symptom responses) and thus causes a vicious cycle of recurrent hypoglycemia. To assess the suggestion that it is the cortisol response to antecedent hypoglycemia that mediates HAAF, we tested the hypothesis that plasma cortisol elevations during euglycemia that are comparable to those that occur during hypoglycemia reduce sympathoadrenal and neurogenic symptom responses to subsequent hypoglycemia. To do this, 12 healthy subjects were studied with hyperinsulinemic-stepped hypoglycemic clamps the day after saline or cortisol (1.