brain edema/carbohydrate

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[Isothiobarbamine prevention of disorders of carbohydrate and oxygen metabolism and of the development of brain edema in the early period after an intracerebral hemorrhage].

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In experiments on cats after injection of isothiobarbamine intravenously (50 mg/kg) at 30 min, intracerebral hemorrhage prevented activation of brain glucose utilization, depression of brain oxygen utilization, surplus lactate accumulation in brain, early development of brain edema and death of

Brain edema and carbohydrate metabolism in the early stages of thermal injury and burn shock.

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Three cases of adult-onset type II citrullinemia treated with different therapies: Efficacy of sodium pyruvate and low-carbohydrate diet.

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We report three cases of adult-onset type II citrullinemia (CTLN2) treated with different therapies including one case successfully treated with p.o. administration of sodium pyruvate and low-carbohydrate diet. Although recent advances in liver transplantation have enabled successful treatment of

Effect of chronic hypernatremic dehydration and rapid rehydration on brain carbohydrate, energy, and amino acid metabolism in weanling mice.

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This is a study of the effects of chronic hypernatremic dehydration and rehydration on carbohydrate, energy, and amino acid metabolism in the brains of weanling mice. Chronic hypernatremic dehydration induced by 4 days of water deprivation and salt loading was associated with severe weight loss (no

Carbohydrate source influences gelatinase production by mouse astrocytes in vitro.

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Molecular mediators of ischemic brain injury include intercellular adhesion molecule-1 (ICAM-1) and matrix metalloproteinase-9 (MMP-9), involved in the alteration of blood-brain barrier permeability and induced in astroglial cultures by tumor necrosis factor-alpha (TNF-alpha). Hyperglycemia is known

Medium-chain triglyceride supplementation under a low-carbohydrate formula is a promising therapy for adult-onset type II citrullinemia.

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BACKGROUND Citrin, encoded by SLC25A13, is a component of the malate-aspartate shuttle, which is the main NADH-transporting system in the liver. Citrin deficiency causes neonatal intrahepatic cholestasis (NICCD), which usually resolves within the first year of life. However, small numbers of adults

Fatal cerebral edema from late-onset ornithine transcarbamylase deficiency in a juvenile male patient receiving valproic acid.

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OBJECTIVE The aims of this report are to 1) present a rare case of fatal cerebral edema associated with late-onset ornithine transcarbamylase (OTC) deficiency in a juvenile male patient receiving valproic acid and 2) review the neuropathologic changes associated with the hyperammonemia. METHODS Case

Adaptive decreases in amino acids (taurine in particular), creatine, and electrolytes prevent cerebral edema in chronically hyponatremic mice: rapid correction (experimental model of central pontine myelinolysis) causes dehydration and shrinkage of brain.

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The experimental model of central pontine myelinolysis--chronic (4-day) hyponatremia induced by daily injections of hypotonic dextrose solutions and vasopressin followed by rapid correction with saline--was used in young fasted and thirsted mice. In normal controls chronic fasting and thirsting

[The protective effect of mannitol, vitamin E, and glucocorticoid in experimental cerebral ischemia--influence on lipid peroxidation, energy metabolism and brain edema].

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At present we apply the three-drug-combination therapy consisting of mannitol, vitamin E and glucocorticoid (betamethasone) in the treatment of cerebral infarction at acute stage with favorable results. However, much of the action mechanism of these drugs remains unelucidated. For the purpose to

Hyponatremia and antidiuresis syndrome.

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Antidiuretic hormone (ADH), or arginine vasopressin (AVP), is primarily regulated through plasma osmolarity, as well as non-osmotic stimuli including blood volume and stress. Links between water-electrolyte and carbohydrate metabolism have also been recently demonstrated. AVP acts via the

[Diabetic ketoacidosis in children: review of pathophysiology and treatment with the use of the "two bags system"]

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OBJECTIVES: To review diabetic ketoacidosis, including the "two bags system", a method of administering liquids in order to provide a smoother correction of the hyperglycemic and ketotic states. METHODS: Review of recent publications (last 7 years) from a Medline search and chapters published in

Arginase Deficiency

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Clinical characteristics: Arginase deficiency in untreated individuals is characterized by episodic hyperammonemia of variable degree that is infrequently severe enough to be life threatening or to cause death. Most commonly, birth and early childhood are normal.

A trek to the top: a review of acute mountain sickness.

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Acute mountain sickness (AMS) affects, to varying degrees, all travelers to high altitudes (elevations greater than 5280 feet). In a small percentage of patients, AMS can lead to high-altitude pulmonary edema (HAPE) or high-altitude cerebral edema (HACE). Symptoms of AMS range from a combination of

Alcohol induced diabetic ketoacidosis exacerbated by an acute respiratory infection with Klebsiella pneumoniae.

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Ketoacidosis is a metabolic condition that occurs as a result of an insufficient amount of insulin. The lack of insulin results in an increased release of glucose from the liver and an excess of ketone bodies as a result of the breakdown of adipose tissue. This occurs when carbohydrates are unable

[Severely increased serum lipid levels in diabetic ketoacidosis - case report].

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Severe hypertriglyceridemia is a known, but uncommon complication of diabetic ketoacidosis. We discuss the case of a 23-year-old, previously healthy, woman who initially presented to the emergency department with abdominal pain. Grossly lipemic serum due to extremely high triglyceride (38.6 mmol/L)

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