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Biomedical subjects

G Gustafson

Publications and source records attributed to G Gustafson.

51 records · Page 3Linked to original sources
PubMed1977

Disulfide crosslinks and the specificity of protein turnover in plants.

Studies of the protein metabolism of detached tomato leaves, hormonally induced to accumulate proteinase inhibitors, have indicated that the state of oxidation of protein-bound half-cystine residues may be a principal parameter affecting in vivo and in vitro stability of leaf proteins. Induced leaves exhibited a general specificity of intracellular protein degradation directed towards the preferential hydrolysis of proteins having free-sulfhydryl residues. Proteins having disulfide cross-linkages, including the proteinase inhibitors, were markedly stable to in vivo degradation, and as a result, accumulated. These results provide a precedence for a cellular protein selection process, resulting from a directed specificity of intracellular protein degradation, which is focused on a particular protein structural parameter.

Cysteine↗
PubMed1976

Specificity of protein turnover in tomato leaves. Accumulation of proteinase inhibitors, induced with the wound hormone, PIIF.

Detached tomato leaves, supplied with the proteinase inhibitor inducing factor (PIIF) and incubated with water under constant light, exhibited a specificity of intracellular protein turnover directed toward the selective accumulation of heat-stable proteins having disulfide corss-linkages. Approximately 70% of the accumulated proteins could be accounted for in two proteinase inhibitors rich in disulfide links. The accumulation of proteins containing disulfides was accompanied by a net loss in total leaf protein, mainly of heat-precipitable proteins having free sulfhydryl residues. Relative rates of synthesis of --S--S-- proteins and --SH proteins were assessed by comparing rates of incorporation of isotope into the inhibitor proteins and noninhibitor leaf proteins. Although the inhibitors represented about 12% of total leaf protein after 71 h of induction, only about 2% of total protein synthesis was directed toward inhibitor synthesis during incubation of induced leaves. The marked stability of inhibitors, and other disulfide proteins against degradation in vivo, appeared to be a major factor providing for their selective accumulation. It was concluded that the state of oxidation of protein-bound half-cystine residues may be a principle parameter influencing the susceptibility of leaf proteins to degradation in vivo.

Binding Sites↗
PubMed1975

Evidence for a physiologic role of pancreatic glucagon in human glucose homeostasis: studies with somatostatin.

To study the role of glucagon in human glucose homeostasis, experimental glucagon deficiency was produced by infusing somatostatin (i. v. 250 mug bolus, followed by infusion of 500 mug/hr) in six normal subjects and in two hypophysectomized patients-an insulin-dependent diabetic and a nondiabetic. In normal subjects, somatostatin lowered plasma glucagon from a mean (plus or minus SE) basal level of 85 plus or minus 15 to 33 plus or minus 10 pg/ml, p smaller than 0.001. Concurrently, plasma glucose fell from 90 plus or minus 2 to 73 plus or minus 3 mg/100 ml, p smaller than 0.001. Serum insulin and growth hormone fell slightly during somatostatin infusion, while plasma free fatty acids rose. In both hypophysectomized patients, somatostatin lowered plasma glucagon and glucose levels. In all subjects, after stopping somatostatin infusions, plasma glucagon and glucose returned promptly to control values, while serum growth hormone did not change. In additional in vitro studies, somatostatin (1 mug/ml) had no effect on muscle glucose uptake. Since it is known that somatostatin has no direct effect on hepatic glucose production, these results suggest that the fall in plasma glucose during somatostatin infusion resulted from inhibition of glucagon secretion, thus providing evidence that this hormone plays a physiologic role in the maintenance of fasting euglycemia in man.

Adult↗
PubMed1975

Normalization of fasting hyperglucagonemia and excessive glucagon responses to intravenous arginine in human diabetes mellitus by prolonged infusion of insulin.

Infusion of insulin (1 U/hr) for 14 hr suppressed basal glucagon levels and normalized previously excessive glucagon responses to arginine in juvenile-onset, insulin-dependent diabetic subjects, indicating that abnormal pancreatic alpha-cell function in human juvenile-onset diabetes mellitus may be a consequence of insulin lack.

Adult↗
PubMed1971

Effects of adenosine 3',5'-monophosphate and adenosine 5'-monophosphate on glycogen degradation and synthesis in Dictyostelium discoideum.

Data are presented demonstrating that the presence in vivo of adenosine 3',5'-monophosphate (3',5'-AMP) causes a rapid depletion of glycogen storage material in the cellular slime mold. The effect of adenosine 5'-monophosphate (5'-AMP) is twofold, stimulating both glycogen degradation and synthesis. In pseudoplasmodia, cell-free extracts appear to contain at least two species of glycogen phosphorylase, one of which is severely inhibited by glucose-1-phosphate and another which is only partially inhibited by this hexose-phosphate. In some cases, 5'-AMP partially overcomes the inhibition by glucose-1-phosphate. Data presented here also indicate the existence of two forms of glycogen synthetase, the total activity of which does not change during 10 hr of differentiation from aggregation to culmination. During this period there is a quantitative conversion of glucose-6-phosphate-independent enzyme activity to glucose-6-phosphate-dependent activity. It is suggested that one effect of 3',5'-AMP is closely related to enzymatic processes involved in the rapid conversion of glycogen to cell wall material and other end products accumulating during sorocarp construction.

Adenine Nucleotides↗
PubMedDate not supplied

Hospital CEOs, CFOs, and nurse executives: opportunities for a new alliance.

This article examines the involvement of Utah acute care hospital nurse executives (NEs) in financial management roles. The authors surveyed NEs and their career supporters and hinderers. Findings suggest that NFs: 1. lack financial management skills, support, involvement, and satisfaction; 2. recognize financial management's importance and desire to improve performance; and 3. consider chief executive officers (CEOs) as their major supporters and chief financial officers (CFOs) their major hinderers in financial management. These "supporters" and "hinderers" of NEs showed consensus regarding the primacy of NEs' leadership and patient advocacy roles. These findings contrast with major professional association policy directives and expert opinions that advocate expanded financial management roles for NEs that will enable them to fully realize their executive potential. CEOs are positioned to establish norms that balance the traditional leadership-patient advocacy roles of NEs with newer financial management roles. CEOs can offer NEs and CFOs opportunities to improve NEs' financial management participation and performance. CEOs can provide empowerment and encourage CFOs to offer NEs "power tools" (for example, information, expertise, resources, and support). The three groups, however, must negotiate reasonable expectations for NEs in financial management and adequate preparation for these consequent responsibilities. Together, CEOs, CFOs, and NEs can successfully take hospitals into the future by leading them in ongoing learning and change.

Chief Executive Officers, Hospital↗