Biomedical subjects

G Welk

Publications and source records attributed to G Welk.

8 recordsLinked to original sources

PubMed2005

Physical activity staging distribution: establishing a heuristic using multiple studies.

The purpose of this study was to identify the population prevalence across the stages of change (SoC) for regular physical activity and to establish the prevalence of people at risk. With support from the National Institutes of Health, the American Heart Association, and the Robert Wood Johnson Foundation, nine Behavior Change Consortium studies with a common physical activity SoC measure agreed to collaborate and share data. The distribution pattern identified in these predominantly reactively recruited studies was Precontemplation (PC) = 5% (+/- 10), Contemplation (C) = 10% (+/- 10), Preparation (P) = 40% (+/- 10), Action = 10% (+/- 10), and Maintenance = 35% (+/- 10). With reactively recruited studies, it can be anticipated that there will be a higher percentage of the sample that is ready to change and a greater percentage of currently active people compared to random representative samples. The at-risk stage distribution (i.e., those not at criteria or PC, C, and P) was approximately 10% PC, 20% C, and 70% P in specific samples and approximately 20% PC, 10% C, and 70% P in the clinical samples. Knowing SoC heuristics can inform public health practitioners and policymakers about the population's motivation for physical activity, help track changes over time, and assist in the allocation of resources.

Behavioral Research↗

PubMed1992

Epidermal growth factor induces glucose transport in primary cell cultures derived from human astrocytic glioma biopsies.

The gene for the epidermal growth factor (EGF) receptor is amplified in a variety of neoplastic tissues, including malignant gliomas. To reveal whether increased sensitivity to EGF has significance for the supply of metabolic substrate to tumor cells, the rate of glucose transport was determined in cells exposed to EGF for up to six hours. In the epidermoid carcinoma line A431, and in primary cultures from 7/12 human glioma biopsies, EGF (10 ng/ml) induced an increase (two-fold) in glucose transport. This effect was transient and independent of protein synthesis.

Astrocytoma↗

PubMed1992

Anaerobic and aerobic power in arms and legs of elite senior wrestlers.

UNLABELLED: The purpose of this study was to characterize anaerobic power and aerobic power (power at peak oxygen uptake, or peak VO2) of elite senior (post-collegiate) wrestlers. Subjects (n = 14) from the U.S. national senior freestyle and Greco Roman wrestling teams were evaluated at separate tests using cycle ergometry for peak VO2 of the arms, peak VO2 of the legs, arm anaerobic peak power, and leg anaerobic peak power. Power output at peak VO2 was recorded for each test and compared to the anaerobic power of the appropriate body segment. The results (mean +/- SD) showed that wrestlers produced 2.3 +/- 0.4 W.kg body weight-1 at arm peak VO2 (43.7 +/- 4.6 ml.kg body weight-1. min-1), 4.2 +/- 0.5 W.kg body weight-1 at leg peak VO2 (50.9 +/- 5.1 ml.kg body weight-1.min-1), arm PP of 7.7 +/- 1.0 W.kg body weight-1, and leg PP of 10.5 +/- 1.7 W.kg body weight-1. Comparing power output during anaerobic and aerobic tests, the subjects performed at 3.4 +/- 0.6 times their peak oxygen uptake during arm anaerobic ergometry, whereas leg anaerobic peak power was 2.7 +/- 0.4 times the power at peak oxygen uptake for the legs (p < 0.05 for difference between ratios). CONCLUSION: relative to aerobic power, elite senior wrestlers may produce power anaerobically in the upper body at significantly higher levels than in the lower body.

Adult↗

PubMed1990

Hydrolysis of polyphosphoinositides in astrocytes by platelet-activating factor.

In primary astrocyte cultures, picomolar concentrations of platelet-activating factor (1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine, PAF) evoked the formation of inositol phosphates (InsP), including inositol trisphosphate. This effect was not observed with the biologically inert lyso-PAF, nor in cells pretreated with phorbol myristate acetate to downregulate receptors. PAF at concentrations greater than or equal to 10(-9) M did not elevate InsP, suggesting some form of uncoupling of the receptor from phospholipase C. The responsiveness of astrocytes to PAF is further evidence for the role of these cells in the central nervous system response to trauma.

Animals↗

PubMed1990

Serotonin inhibits ATP-induced mobilization of arachidonic acid but not phosphoinositide turnover in astrocytes.

In response to ATP, astrocytes accumulate inositol phosphates and release arachidonic acid (AA) from phospholipid stores, events which may be linked through intracellular calcium mobilization and activation of phospholipase A2. When cells were exposed to ATP in the presence of serotonin there was a dose-dependent inhibition of AA release, an effect which was reversed by methysergide. However, the accumulation of inositol phosphates due to ATP was elevated in the presence of serotonin, and this effect was again reversed by methysergide. The mechanism by which serotonin inhibits ATP-induced arachidonate mobilization does not, therefore, involve the purinergic receptor or its coupling to inositol phospholipid pools. The hydrolysis of polyphosphoinositides by serotonin and subsequent generation of inositol trisphosphate may deplete a specific intracellular calcium store normally available to ATP, the mobilization of which stimulates phospholipase A2 and thus AA release.

Adenosine Triphosphate↗

PubMed1990

Stimulation of thromboxane release from primary cell cultures derived from human astrocytic glioma biopsies.

Stimulation of primary cultures of rat astrocytes with appropriate agents results in the mobilization of arachidonic acid from intracellular lipid pools and the synthesis of eicosanoids. Thromboxane A2 is one of the major prostanoids released upon stimulation with calcium ionophore, phorbol esters, and ATP; but a number of other predicted effectors are inactive. In an attempt to understand the pathophysiological significance of eicosanoid release from astrocytes, primary cultures have been derived from human astrocytic glioma biopsies. The majority of cells in the cultures expressed glial fibrillary acidic protein (GFAP), frequently in conjunction with vimentin and fibronectin. Cell sorting revealed that a significant proportion of cells in the cultures from the high-grade (malignant) tumors expressed epidermal growth factor receptor, indicative of neoplastic cells. Both effective and ineffective agents in rat cultures were tested for their ability to stimulate release of thromboxane from these gliomas, and also from cultures of medulloblastoma and ependymoma which contained significant numbers of GFAP-positive cells. Only cells from the high-grade tumors released thromboxane in response to the known effective stimuli. While the muscarinic agonist carbachol was ineffective, norepinephrine evoked thromboxane release from malignant astrocytomas. These data show that cells derived from malignant human gliomas retain the ability to release thromboxane upon stimulation and suggest that a transformation in receptor coupling might accompany neoplasia, such that the cells now respond to a previously ineffective agonist.

Astrocytes↗

PubMed1990

Evidence for an astrocyte-derived vasorelaxing factor with properties similar to nitric oxide.

To determine whether astrocytes release nonprostanoid vasodilators, cells on microcarrier beads were superfused with various agents in the presence of indomethacin, and the effluent was bioassayed and also analyzed for nitric oxide by a chemiluminescence technique. Bradykinin and A23187 induced release of a factor that relaxed arterial rings, an effect that was blocked by hemoglobin. The effluent contained either nitric oxide or a related compound that could be reduced to nitric oxide. Production of this factor was competitively inhibited by the arginine analogs NG-nitro-L-arginine and NG-methyl-L-arginine and could be restored with L-arginine. Quisqualate and norepinephrine were also effective in causing the release of nitric oxide from astroglial cells. Thus, astrocyte-derived relaxing factor has properties similar to those of an endothelium- and neuron-derived relaxing factor.

Animals↗

PubMed1989

Arachidonic acid evokes inositol phospholipid hydrolysis in astrocytes.

Astrocyte cultures prelabelled with [3H]inositol were exposed to arachidonic acid (AA) in the presence and absence of various agonists. AA alone evoked a dose-dependent increase in the accumulation of inositol phosphates (IP), an effect not secondary to eicosanoid synthesis and release but which was abolished by EGTA. Separation of the IP revealed that AA stimulated increases in inositol tris-, bis- and monophosphates. IP formation evoked by carbachol or norepinephrine was additive with AA, whereas IP formation by platelet activating factor (PAF) or ATP was non-additive with AA. These results suggest that AA released upon stimulation of astrocytes or other cells in the CNS could initiate and/or amplify intercellular signalling.

Animals↗