Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serial investigations of electrolytes, osmolality and nutritional status were undertaken in 28 babies less than 33 weeks gestation. 6 died with intraventricular haemorrhage, 9 died without intraventricular haemorrhage, and 13 survived. Significant hypersomality was detected in the babies who died with intraventricular haemorrhage, whereas babies who died without intraventricular haemorrhage and survivors had values within normal limits. No relation was found between hyperosmolality and sodium concentrations. Total fluid intake and caloric intake were comparable in the three groups, but protein intake was much reduced in babies with intraventricular haemorrhage due to a lower milk intake. The hyperosmolality could have resulted from tissue breakdown following protein starvation and may be a factor in the occurrence of intraventricular haemorrhage. In premature babies an osmolality of over 320 mOsm/l carried a grave prognostic implication.
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PMID:Hyperosmolality and intraventricular haemorrhage in premature babies. 93 96

Hyperosmolar infusions of the inert pentose sugar, xylose (MW 150), were used to induce hyperosmolar states in non-starved and starved rats. Using 51Cr EDTA and RIHSA the extracellular fluid (ECF) and plasma fluid volumes (PV) were determined before and after infusions. The cause of weight loss after 24-30 h starvation was also examined. Equal osmolar provocation in starved and non-starved animals caused the same degree of hyperosmolality. The greater the osmolality increase the larger the volume of intracellular fluid mobilised. Despite the total ECF volume increments being large relative to PV, this fluid compartment remained hardly effected by the fluid released from the cells. No evidence could be found to support 24-30 h starvation as causing a measurable fluid balance defect, a finding of considerable importance when considering short term problems arising out of starvation. The strict control of PV in normovolemic rats has again been confirmed.
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PMID:Mobilised fluid volumes after induced hyperosmolality in the rat. 688 May 43

Elevated pCO(2) inhibits cell growth. This growth inhibition is accompanied by a decrease in intracellular pH (pHi), as well as a decrease in glycolysis. Elevated concentrations (mM) of some amino acids have been shown by others to protect cells exposed to two very different environmental stresses: nutrient starvation and hyperosmolality. The fact that many of the amino acids shown to have protective effects against other stresses are transported into the cell through a pHi-sensitive transporter led us to study the possibility of using these amino acids as protective agents under elevated pCO(2). Screening experiments using 5, 15, and 25 mM of each amino acid showed that not all amino acids that protect cells from hyperosmolality protect them from elevated pCO(2). Glycine betaine and glycine were chosen for further characterization in both hybridoma and CHO cells. Asparagine and threonine were also tested in hybridoma and CHO cells, respectively. All amino acids tested under 195 mm Hg pCO(2)/435 mOsm/kg (50% growth inhibition) restored the specific growth rate (mu) in hybridoma cells to that observed under control conditions (40 mm Hg/320 mOsm/kg). Addition of each amino acid resulted in an increase in the consumption rate and intracellular accumulation of that amino acid. In CHO cells, glycine betaine also restored mu to control values, while glycine and threonine partially restored mu. In hybridoma cells, the higher specific antibody productivity obtained at elevated pCO(2) was maintained with the lowest amino acid concentration (5 mM). Productivity decreased toward control values with increasing amino acid concentrations. Elevated pCO(2) decreased the specific tPA productivity in the CHO cell line studied. Only glycine betaine resulted in a 20% increase in productivity at 195 mm Hg/435 mOsm/kg. With the exception of glycine betaine in hybridoma cells, amino acids did not mitigate the associated pHi decrease of at least 0.2 pH units at 195 mm Hg/435 mOsm/kg. pHi in hybridoma cells under elevated pCO(2) in the presence of glycine betaine was about 0.1 pH units below that of control. Amino acids had no effect on the cell size response of hybridoma cells, while they partially offset the increase in CHO cell size at elevated pCO(2). Glycine betaine, asparagine, and glycine increased the specific glucose consumption rate observed at 195 mm Hg/435 mOsm/kg (50% of control) to values greater than 70% of control in hybridoma cells. In CHO cells, only glycine betaine increased q(glc) (by 20%) under elevated pCO(2). All amino acids tested improved the cell yield from glutamine at 195 mm Hg/435 mOsm/kg in both cell lines.
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PMID:Selected amino acids protect hybridoma and CHO cells from elevated carbon dioxide and osmolality. 1200 Nov 66