Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “EXERTION”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 595 records · Page 33Linked to original sources
PubMed1990

Cyclosporin A exerts a cytostatic effect in vivo on human and murine epithelial cells.

Cyclosporin A (CsA) is a potent immunosuppressant that may also affect nonlymphoid cells. Indeed, CsA exerts a growth inhibition in vitro of several human and animal, normal and neoplastic cell types. To assess a possible in vivo direct cytostatic activity of CsA, the authors evaluated the proportion of S-phase (5-bromo-2'-deoxyuridine incorporating) cells of epithelial origin (skin, tongue, esophagus) of congenitally athymic (nude) mice bearing xenografts of human skin and receiving a daily subcutaneous injection of 50 mg/kg of CsA for 3 weeks. As compared with control animals, CsA-treated mice showed a decreased labeling index (LI) of all the epithelial tissues studied, which was statistically significant in the case of epidermis (both human and murine) and the tongue. Because nude mice lack T-cell-mediated immunity, these results suggest that CsA also exerts an immunologically independent antiproliferative activity on epithelial cells in vivo and they also highlight the interest in pursuing studies on cyclosporins as cytostatic agents.

Animals↗
PubMed1985

Improvement in exercise capacity and associated changes in hemodynamics and left ventricular function after the addition of metoprolol to nifedipine in patients with stable exertional angina.

In 10 men with stable exertional angina, the changes in exercise capacity, hemodynamics, and left ventricular (LV) function were measured after 20 mg sublingual nifedipine (N) and again after adding 100 mg oral metoprolol (M). Nifedipine alone did not significantly improve exercise workloads (+18%) and duration (+21%), but the addition of metoprolol increased both parameters by a further 37 and 32%, respectively (both p less than 0.005 vs. N). After nifedipine the onset of angina was slightly delayed (5.14 +/- 2.41 min placebo (P), 6.00 +/- 2.31 min N, p less than 0.1) and occurred at higher workloads (36 +/- 17 W P, 43 +/- 8 W N, p less than 0.1). After the addition of metoprolol, the onset of angina was delayed substantially more (9.57 +/- 2.22 min, p less than 0.001 vs. P and N) and occurred at much higher workloads (62 +/- 20 W, p less than 0.001 vs. P and N). At rest (R) and during exercise (E), nifedipine decreased systemic vascular resistance (-36% R, -27% E, both p less than 0.001) and mean arterial pressure (-18% R, -21% E, both p less than 0.001), and increased heart rate (+15% R, +11% E, both p less than 0.001), Pulmonary artery wedge pressure on exercise increased less (22 +/- 7 mmHg P, 13 +/- 5 mmHg N, p less than 0.001). After adding metoprolol, the major change was a reduced heart rate (-25% vs. N at R and E, both p less than 0.001), and arterial pressure was unaltered. Pulmonary artery wedge pressure on exercise increased to 18 +/- 5 mmHg (p less than 0.05 vs. N). Exercise LV ejection fraction and volume did not change significantly after adding metoprolol despite marked improvement in angina. In this acute exercise study in patients with stable exertional angina, metoprolol added to nifedipine markedly improved exercise capacity by preventing the increase in heart rate seen with nifedipine. In our patients with relatively normal LV function at rest, the combination was safe and produced no deleterious effects on LV function.

Administration, Oral↗
PubMed1990

Subclavian stenosis presenting as progressive exertional angina pectoris.

Left subclavian stenosis is an uncommon cause of exertional left arm pain. In a patient who presented with exertional chest and left arm pain in an increasing pattern, clinical evaluation disclosed a discrepancy between right and left arm blood pressure. Exercise stress testing with thallium revealed normal myocardial perfusion. Aortic arch and selective angiography revealed a high-grade proximal left subclavian stenosis. Subclavian angioplasty was performed with complete resolution of symptoms. This case demonstrates that ischemic left arm pain due to subclavian stenosis can present as accelerated angina, and highlights the importance of determining blood pressure in both arms in routine evaluation of patients at risk for atherosclerosis.

Angina Pectoris↗
PubMed2002

Curcumin exerts multiple suppressive effects on human breast carcinoma cells.

In our study, we present experimental evidence suggesting that curcumin exerts multiple different suppressive effects on human breast carcinoma cells in vitro. Our experiments demonstrate that curcumin's antiproliferative effects are estrogen dependent in ER (estrogen receptor)-positive MCF-7 cells, being more pronounced in estrogen-containing media and in the presence of exogenous 17-beta estradiol. Curcumin inhibits the expression of ER downstream genes including pS2 and TGF-beta (transforming growth factor) in ER-positive MCF-7 cells, and this inhibition is also dependent on the presence of estrogen. Curcumin also decreases ERE (estrogen responsive element)-CAT activities induced by 17-beta estradiol. In addition, we demonstrate that curcumin exerts strong anti-invasive effects in vitro that are not estrogen dependent in the ER-negative MDA-MB-231 breast cancer cells. These anti-invasive effects appear to be mediated through the downregulation of MMP-2 (matrix metalloproteinase) and the upregulation of TIMP-1 (tissue inhibitor of metalloproteinase), 2 common effector molecules that have been implicated in regulating tumor cell invasion. Our study also demonstrates that curcumin inhibits the transcript levels of 2 major angiogenesis factors VEGF (vascular endothelial growth factor) and b-FGF (basic fibroblast growth factor) mainly in ER-negative MDA-MB-231 cells.

Antineoplastic Agents↗
PubMed2007

Corticotropin releasing factor receptor 1 (CRF1) and CRF2 agonists exert an anti-inflammatory effect during the early phase of inflammation suppressing LPS-induced TNF-alpha release from macrophages via induction of COX-2 and PGE2.

Corticotropin-releasing factor (CRF), the principal regulator of the hypothalamus-pituitary-adrenal (HPA) axis, also modulates the inflammatory response directly, via its effect on mast cells and macrophages. On macrophages, it augments production of lipopolysaccharide (LPS)-induced pro-inflammatory cytokines. CRF and its related peptides may also act as anti-inflammatory agents. Aim of the present work was to examine the role of macrophages on the anti-inflammatory effects of CRF-peptides and the mechanism involved. Thus, we examined if CRF receptor 1 (CRF1) and CRF2 agonists exert any anti-inflammatory effect on primary mouse macrophages. We have found that: (a) CRF, Urocortin (UCN)1 and UCN2 transiently suppressed the release of Tumor Necrosis Factor-alpha (TNF-alpha) in LPS-activated macrophages, an effect peaking at 4 h. This effect did not involve changes on TNF-alpha transcription. (b) CRF peptide-induced suppression of TNF-alpha release depended on induction of COX-2 and PGE2 synthesis. (c) Use of specific CRF1 and CRF2 antagonists suggested that this effect involved both CRF receptor types. (d) The effect of CRF-peptides on COX-2 was mediated via PI3K and p38MAPK. (e) Longer exposure of macrophages to CRF-peptides resulted in induction of TNF-alpha production via enhancement of its transcription. In conclusion, this is the first report suggesting that CRF1 and CRF2 agonists exert a biphasic effect on macrophages. During the early stages of the inflammatory response, they suppress TNF-alpha release via induction of COX-2/PGE2 while later on they induce TNF-alpha transcription. Hence, the reported anti-inflammatory effect of CRF-peptides appears to involve macrophages and is confined at the early stage of inflammation.

Animals↗
PubMed2001

Melittin exerts multiple effects on the release of free fatty acids from L1210 cells: lack of selective activation of phospholipase A2 by melittin.

Melittin is known as a phospholipase A2 (PLA2) activator, but the selectivity of its effect on PLA2 is uncertain. We examined the selectivity of melittin effect on the release of free fatty acids (FFAs) from L1210 cells using various inhibitors. A systemic lipid analysis by HPLC and GLC revealed that melittin induced release of various FFAs including saturated, monounsaturated, and polyunsaturated FFAs. Various PLA2 inhibitors examined exerted only minimal effects on the melittin-induced arachidonic acid (AA) and palmitic acid (PAL) releases. Specific inhibitors of phosphatidylinositol-phospholipase C (U73122) and diacylglycerol lipase (RHC80267) exerted significant inhibitory effects on both AA and PAL releases. These results suggest that melittin-induced FFA release is most likely due to multiple participations of various types of lipases. Since BAPTA/AM, an intracellular Ca2+ chelator, did not influence the FFA release, the Ca2+ influxed by melittin appeared not to be a key factor for the FFA release. The mimicking of the melittin-induced FFA release by digitonin, a membrane-permeabilizing agent, implies that the membrane-perturbing action of melittin is likely the cause of the FFA release. Melittin also induced release of multiple FFAs from other cell lines including P388D1 and HL60. The rapid melittin-stimulated phospholipase D (PLD) observed in L1210 cells appeared not directly related to the steady release of FFA, as indicated by the fact that the PLD was not blocked by RHC80267. In view of melittin's multiple effects on the composition of cellular lipids, we conclude that melittin does neither exclusively release any single FFA nor selectively activate PLA2 in L1210 cells. The problem of using melittin as a PLA2 activator is discussed.

Animals↗
PubMed1999

Evidence that physiological levels of circulating leptin exert a stimulatory effect on luteinizing hormone and prolactin surges in rats.

Increasing evidence suggests that leptin, an adipocyte-derived hormone, may positively regulate the reproductive axis, and serve as a critical metabolic signal linking nutrition and the reproductive function. However, along this line there remains an as-of-yet unresolved important issue whether physiological levels of circulating leptin exert a stimulatory effect on the reproductive axis. It is also unknown whether hyperleptinemia affects the reproductive function. In this study, we attempted to examine these unexplored issues, employing as an indicator the estradiol/progesterone-induced luteinizing hormone (LH) and prolactin (PRL) surges in ovariectomized female rats. Experiments were performed on normally fed, 3-day starved, 3-day starved + murine leptin (100 microg/kg/day), and normally fed + murine leptin (300 microg/kg/day) groups. Leptin was administered utilizing osmotic minipumps during 3 days immediately before experimentation. From 11:00 to 18:00 h, blood was collected every 30 min to measure LH and PRL. The 3-day starvation completely abolished both LH and PRL surges, but 3-day starved + leptin (100 microg/kg/day) group, whose plasma leptin levels (3.7 +/- 0.4 ng/ml) were similar to those in normally fed group (3.4 +/- 0.5 ng/ml), showed a significant recovery of the hormonal surges. On the other hand, the magnitudes of LH and PRL surges in normally fed + leptin (300 microg/kg/day) group, whose leptin levels were 10.8 +/- 1.5 ng/ml, were statistically the same as those in normally fed group. These results indicate for the first time that physiological concentrations of circulating leptin exert a stimulatory effect on the steroid-induced LH and PRL surges in the rat. It was also suggested that mild hyperleptinemia of 3 days' duration may not significantly affect the hormonal surges.

Animals↗
PubMed2002

TNFalpha and IL-1beta exert no direct vasoactivity in human isolated resistance arteries.

The proinflammatory cytokines TNFalpha and IL-1beta are thought to play a role in the mechanism of septic vasodilatory shock. Most evidence indicate that the vascular effects these cytokines are mediated through increased expression of inducible nitric oxide synthase, whereas several animal studies report a more rapid vasorelaxant effect. We studied the direct vascular effects of TNFalpha and IL-1beta in human isolated resistance arteries (n=9) using a microvascular myograph. After precontraction with noradrenaline or a depolarising high potassium solution, TNFalpha and IL-1beta (up to 10(-8) M, alone or in combination) did not exert any relevant vasoactive effect. We conclude that, in contrast with some animal experiments, these cytokines exert no direct vasoactivity in human resistance arteries.

Arteries↗
PubMed1998

The human myoepithelial cell exerts antiproliferative effects on breast carcinoma cells characterized by p21WAF1/CIP1 induction, G2/M arrest, and apoptosis.

Ductal carcinoma in situ of the breast (DCIS) is surrounded by a layer of myoepithelial cells. Our previous studies have suggested that these myoepithelial cells exert paracrine tumor-suppressive effects on invasion of breast carcinoma cells. Conditioned medium (CM), concentrated 10-100x of HMS-1, HMS-3, and HMS-4, human myoepithelial cell lines, block Matrigel invasion of a series of carcinoma cell lines. Immunoprecipitation of maspin, a recently described serpin, from these CM abolishes this anti-invasive effect. Both CM and maspin-immunoprecipitated CM, however, exert equal antiproliferative effects on a series of ER+ and ER- cell lines including MCF-7, T47D, MDA-MB-231, and MDA-MB-468. These antiproliferative effects are characterized by induction of a G2/M arrest, a twofold increase in p21(WAF1/CIP1) transcription and expression, and a threefold increase in apoptosis in the breast carcinoma lines examined. The antiproliferative effects mediated by myoepithelial cell CM do not manifest themselves in an autocrine manner, are not mediated by TGF-beta1, nor involve ER- or p53-dependent pathways. Neither the antiproliferative nor the anti-invasive effects of myoepithelial cell CM is observed with nonmyoepithelial cell CM. The in vitro observations of our present study may have relevance in explaining the increased degree of apoptosis exhibited by DCIS cells in vivo. Our findings illustrate another way myoepithelial cells function as natural paracrine tumor suppressors.

Apoptosis↗
PubMed1994

Forces exerted by locomoting cells.

The movement of cells along substrata is a complex phenomenon involving cell extension and retraction, and cell-substratum adhesion. Knowledge is beginning to accumulate about the forces required for cell protrusion and retraction. Both of these processes also require traction to be exerted on the substratum, and new assays for these forces are under development. This review briefly discusses the forces that locomotory cells exert, in terms of both recent force measurements and possible mechanisms for their generation.

Actins↗
PubMed1993

Isometric tension exerted by a myofibril of the frog at 0 degree C: geometrical considerations.

For a number of years, the isometric force per myosin head has been taken as 1 pN by the authors who studied in vitro movement. This value was deduced from the value of the isometric tension exerted by a living or a skinned fibre at approximately 0 degree C and for the frog (1-3 kg cm-2). Starting from an isometric tension exerted by a single unit cell of approximately 10 kg cm-2, it has been shown that the isometric force per myosin head is (8 +/- 1)pN. The value of approximately 10 kg cm-2 was deduced from theoretical and semi-empirical reasonings independent of the mechanical roles of the crossbridges. Here, we discuss this latest value by using simple geometrical considerations.

Animals↗
PubMed1994

Platelet-derived growth factor exerts trophic effects on rat striatal DARPP-32-containing neurons in culture.

The objective of the present study was to determine if either of the two isoforms of platelet-derived growth factor (PDGF), PDGF-AA and PDGF-BB, exerts trophic effects in vitro on developing rat strial neurons. Striatal neurons were identified using immunocytochemistry for dopamine- and adenosine 3':5'-monophosphate-regulated phosphoprotein with a molecular weight of 32 kilodalton (DARPP-32). In control cultures without PDGF, the mean number of DARPP-32-positive neurons decreased by 47% at days 3 to 5 in vitro. PDGF-BB, but not PDGF-AA, significantly increased the number of DARPP-32-positive neurons both at day 3 (by 42%) and day 5 (by 149%). Total cell number was similar in control and PDGF-BB-treated cultures, suggesting that, in striatal cultures, the action of PDGF-BB is relatively specific for DARPP-32-positive neurons. The DARPP-32-positive neurons in PDGF-BB-treated cultures had longer neurites and larger soma areas than those in control and in PDGF-AA-treated cultures. Our data provide evidence that PDGF-BB exerts a trophic action on striatal DARPP-32-positive neurons in vitro by promoting cell survival and morphological differentiation, although a stimulatory effect on intraneuronal DARPP-32 levels also is possible. The findings raise the possibility that PDGF-BB might also be involved in the development and maintenance of striatal neurons in vivo, and could be used to counteract striatal degeneration in models of Huntington's disease.

Animals↗
PubMed1996

Perceived exertion and blood lactate concentration during graded treadmill running.

The purpose of this study was to investigate the influences of treadmill gradients on the rating of perceived exertion (RPE) at two fixed blood lactate concentrations ([La-]b). Ten subjects performed three different incremental treadmill protocols by running either uphill (concentrically-biased), downhill (eccentrically-biased), or on the flat (non-biased). Individual data of each protocol were interpolated to reflect [La-]b corresponding to 2.0 and 4.0 mmol.l-1. At 2.0 mmol.l-1 [La-]b, RPE and treadmill speed during downhill running were greater than during level running which was greater than during uphill running (p < 0.05). Also, the downhill heart rate (HR) was greater than the uphill HR, and downhill minute ventilation (VE) was greater than the level VE. Treadmill speed was the only measure at 4.0 mmol.l-1 [La-]b to differ between gradients. There was a moderate correlation of RPE with HR at both [La-]b (r = 0.73 at 2.0 mmol.l-1; r = 0.48 at 4.0 mmol.l-1) while treadmill speed was moderately correlated with RPE only at 2.0 mmol.l-1 [La-]b (r = 0.70). The results of this study demonstrated that the degree of eccentric-bias during running exercise is an influence of perceived exertion at a moderate but not at a high exercise intensity.

Adult↗
PubMed1991

Cynical hostility, attempts to exert social control, and cardiovascular reactivity in married couples.

Chronically hostile persons may be at greater risk of cardiovascular illness, perhaps because of their more pronounced physiologic responses to interpersonal stressors. The present study of married couples examined the association between Cook and Medley Hostility (Ho) Scale scores and cardiovascular reactivity while couples were engaged in a discussion task with or without an incentive to exert control over their partner. Cynical hostility was associated with greater heart rate (HR) reactivity among husbands in both conditions and with greater systolic blood pressure (SBP) reactivity among husbands attempting to influence their wives. Further, husbands' cynical hostility was associated with greater SBP reactivity in their wives. Wives' cynical hostility was unrelated to their own or their husbands' reactivity. These results underscore the importance of social contexts in the association between hostility and psychophysiologic processes and suggest that the motive to exert social control may be important for hostile persons.

Adult↗
PubMed1995

Specific delta-opioid antagonists exert an agonist-independent inhibitory effect, similar to the agonist, on the release of GnRH in vitro.

1. In in vitro studies with adult male rats we have recently shown that the delta-opioid agonist DTLET inhibits the release of the Gonadotropin-Releasing Hormone (GnRH) from hypothalamic fragments containing the arcuate nucleus and the median eminence. This effect is receptor mediated and eicosanoid dependent (Gerozissis et al., 1993). 2. In the present study we report that the delta-opioid antagonists with negative intrinsic activity, Diallyl-G and ICI 174864, applied under the same experimental conditions (30 min static incubations at 37 degrees C, in a potassium rich milieu), in the absence of the agonist DTLET, also exert a similar to the agonist inhibitory effect on the release of GnRH. 3. The dose-dependent inhibitory effect of Diallyl-G on GnRH release is reversed by increasing concentrations of DTLET. The mu and delta opioid antagonist, naloxone is without effect in the absence of DTLET. However, naloxone acts as an antagonist on the Diallyl-G-induced inhibition of GnRH release. 4. Diallyl-G also inhibits the release of prostaglandin E2 (PGE2). In the presence of indomethacin or nordihydroguaiaretic acid, Diallyl-G is ineffective to further inhibit the release of GnRH. These latter observations taken together with the results of eicosanoid estimation suggest that PGE2 but not leukotrienes participate in the agonist-independent effects of Diallyl-G on GnRH release. 5. Therefore these results support the hypothesis that delta-opioid antagonists with negative intrinsic activity exert agonist-independent biological responses similar to those of the agonists.

Animals↗
PubMed1991

Static dynamometer for the measurement of multidirectional forces exerted by the thumb.

The functioning of a static dynamometer designed to measure simultaneous forces exerted by the thumb in the vertical and horizontal axes is described. The analysis of the output signals by a desktop computer program provides information regarding the forces generated in eight directions covering a plane transverse to the thumb by 45 degree increments. In 12 normal female subjects, the maximum voluntary torques exerted at the trapezo-metacarpal joint of the thumb were examined and the muscle activation patterns of the interosseus, flexor pollicis brevis and adductor pollicis brevis muscles were recorded in one subject. Torques and muscle activation patterns were depicted using polar plots. Dynamometric data indicate that strength varies with direction and that higher torques are obtained in directions that bring the thumb towards the palm, i.e. flexion, adduction, combined flexion-adduction and extension-adduction. Patterns of muscle activity vary according to the direction evaluated suggesting that strength depends on the number of activated muscles as well as the relative force contribution of each muscle.

Calibration↗
PubMed1998

Device for measuring the forces exerted on the shaft of an endoscope during colonoscopy.

Colonoscopy involves advancing a flexible endoscope into and along the entire length of the colon. The procedure can be painful and carries the risk of perforating the organ, yet very little is known of the forces involved. A device to measure the forces exerted on the endoscope during colonoscopy is described. The device features a handle designed in the shape of a hinged split cylinder that locks around the endoscope, gripping it tightly. The handle has two parts, an inner part that grips the endoscope, and an outer part that is gripped by the endoscopist. The two parts are joined together by members that transmit the forces through to the endoscope. One of the members incorporates strain gauges that measure the torque applied to the endoscope, as well as the push and pull forces. The handle can easily be unlocked and moved along the endoscope as the colonoscopy proceeds. The device is used to measure the forces applied to the endoscope during 11 routine colonoscopies, and summary results are presented. These are believed to be the first accurate measurements of the forces exerted during colonoscopy.

Colonoscopes↗
PubMed2001

[Exertion-related heat stroke. Lethal multiorgan failure from accidental hyperthermia in a 23 year old athlete].

We report the case of a 23-year-old rower who suffered from an exertional heatstroke while trying to lose 2 kg in weight by jogging before a competition. The development of this illness was favoured by clothes that were inappropriate for the environmental conditions and which the sportsman wore intentionally to enhance sweating. The maximum core temperature was over 43 degrees C. As a consequence the comatose patient developed a fulminant multi-organ failure with the liver ceasing its function, renal failure, massive rhabdomyolysis, and disseminated intravascular coagulation. In addition, he suffered from pericardial effusion and acute pulmonary failure (ARDS). In spite of maximum intensive care with an extensive substitution of blood products, continuous hemodiafiltration, and inhalative administration of nitrous oxide the young sportsman died 48 h after his admission to the intensive care unit. This tragic course demonstrates the danger of the widespread habit of losing weight by vigorously exercising with inappropriate clothes. In this article, potential risk factors, symptomatology, therapy, and methods of preventing an exertional heatstroke are shown and discussed.

Adult↗