Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.10.2 (focal adhesion kinase)
 44,029 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate whether the addition of epinephrine would enhance postoperative pain relief by intrathecal morphine, we studied 36 patients scheduled to have spinal anesthesia for gynecologic surgery. Patients were randomly allocated to one of three groups: the first received epinephrine 0.12 mg, morphine 0.2 mg, and hyperbaric tetracaine 12 mg intrathecally (EMT group, n = 11); the second received morphine 0.2 mg and hyperbaric tetracaine 12 mg intrathecally (MT group, n = 13); and the third received epinephrine 0.12 mg and hyperbaric tetracaine 12 mg intrathecally (ET group, n = 12). The time to the first request for supplemental analgesics was longest (2182 +/- 251 min, mean +/- SEM) and the injection number of supplemental analgesics was least in the EMT group (P < 0.05). The percentage of patients who received supplemental analgesics in the EMT group (45.5%) was less than the other two groups (P < 0.05). Six patients in the EMT group and one in the MT group needed no additional analgesics during 48 h (P < 0.05 versus the MT and ET groups). The visual analog scale (VAS) pain score was larger in the ET group than the EMT group (P < 0.05), but was similar in the EMT and MT groups. There were no differences among groups in the incidence of nausea and pruritus. Our data show that the addition of epinephrine enhances postoperative analgesia by intrathecal morphine without increasing the incidence of adverse effects as compared with intrathecal morphine alone.
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PMID:The addition of epinephrine enhances postoperative analgesia by intrathecal morphine. 765 13

The aim of this study was to evaluate the thermoregulatory changes induced by 27-h of sleep deprivation (SD) in men at rest both in a comfortable ambient temperature and in cold air. A group of 12 male subjects were placed in a comfortable ambient temperature (dry bulb temperature, Tdb = 25 degrees C, relative humidity, rh = 40%-50%, clothing insulation = 1 clo) for 1 h and then they were submitted to a standard cold air test in a climatic chamber for 2 h (Tdb = 1 degree C, rh = 40%-50%, wind speed = 0.8 m.s-1, nude), before and after 27 h of sleep deprivation. Thermoregulatory changes (rectal temperature, Tre; mean skin temperature. Tsk; metabolic heat production M) were monitored continuously. At comfortable ambient temperature, no significant change was observed after SD for Tre, Tsk and M. During the cold test, Tre did not change but Tsk and M were higher after SD (P < 0.05). Increased M (+ 6%, P < 0.05) was related to earlier and higher shivering, with a possible increase in the sensitivity of the thermoregulatory system as shown by the shorter time to onset of continuous shivering (d): 8.66 (SEM 1.33) min versus 28.20 (SEM 1.33) min (P < 0.001) and by a higher Tsk observed at d: 27.60 (SEM 1.40) degrees C versus 21.40 (SEM 0.60) degrees C (P < 0.001). These results were associated with higher cold sensations and shivering following SD. They also suggested that SD modified thermoregulatory responses at a central level especially in a cold environment.
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PMID:Cold thermoregulatory changes induced by sleep deprivation in men. 800 32

Energy substrate mobilization has been suggested as being a limiting factor for the rate of cold-induced thermogenesis (M), and consequently in delaying hypothermia. The evidence supporting this hypothesis in humans, however, is not convincing and the hypothesis has yet to be tested in a rigorous manner using a full heat balance analysis (partitional calorimetry). The goal of this study was therefore to re-investigate whether enhancing energy substrate mobilization by feeding cold-exposed subjects would improve M and affect heat debt (S; the minute-by-minute balance of M and heat losses) as well as rectal (Tre) and mean skin temperatures (Tsk). Nine healthy semi-nude fasted subjects were exposed to 5 degrees C (3 h at rest, 1 m.s-1 wind) on three occasions following the ingestion at min 0 and 90 of either: (1) a placebo, (2) 710 kJ of pure carbohydrates (100%-CHO), or (3) 710 kJ of a high-carbohydrate bar (High-CHO). As expected in the cold, Tre and Tsk decreased whereas M, S and heat losses increased (P < 0.01). However, there were no differences between treatments, including the final Tre [mean (SEM); 36.4 (0.2); 36.5 (0.3) and 36.5 (0.2) degrees C for the placebo, 100%-CHO and High-CHO tests, respectively]. During the 100%-CHO treatment, rates of carbohydrate oxidation were the highest and fat oxidation the lowest (P < 0.05), whereas the High-CHO treatment caused smaller changes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Is energy substrate mobilization a limiting factor for cold thermogenesis? 822 37

The effect of pyridostigmine (60 mg orally), arginine (0.5 g/kg iv) and propranolol (PROP, 40 mg orally) on GHRH (1 microgram/kg iv)-induced GH release was studied in seven short children. Pyridostigmine and arginine induced a similar potentiating effect on GHRH-induced GH rise (Peak, mean +/- SEM: 56.9 +/- 12.8 and 48.6 +/- 8.5 micrograms/L, respectively vs 12.3 +/- 1.6 micrograms/L; p < 0.05). Combination of GHRH with propranolol induced an increase of GH that was significant only with regard to peak (28.9 +/- 8.4 micrograms/L) but not to AUC. However, GH rises observed after GHRH combined with PD or ARG did not significantly differ from that recorded after coadministration of GHRH and PROP both for peak and AUC. Our results confirm that pyridostigmine and arginine have a striking potentiating effect on the GHRH-induced GH rise in children and show that the tests with GHRH + PD and GH + H + ARG are ore reliable than that with GHRH + PROP to explore the secretory capacity of somatotroph cells.
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PMID:Comparison of the potentiating effect of pyridostigmine, arginine and propranolol on the GHRH-induced GH release in short children. 831 97

Thermoregulatory sweating [total body (msw,b), chest (msw,c) and thigh (msw,t) sweating], body temperatures [oesophageal (T(oes)) and mean skin temperature (Tsk)] and heart rate were investigated in five sleep-deprived subjects (kept awake for 27 h) while exercising on a cycle (45 min at approximately 50% maximal oxygen consumption) in moderate heat (T(air) and T(wall) at 35 degrees C). The msw,c and msw,t were measured under local thermal clamp (Tsk,l), set at 35.5 degrees C. After sleep deprivation, neither the levels of body temperatures (T(oes), Tsk) nor the levels of msw,b, msw,c or msw,t differed from control at rest or during exercise steady state. During the transient phase of exercise (when Tsk and Tsk,l were unvarying), the msw,c and msw,t changes were positively correlated with those of T(oes). The slopes of the msw,c versus T(oes) or msw,t versus T(oes) relationships remained unchanged between control and sleep-loss experiments. Thus the slopes of the local sweating versus T(oes) relationships (msw,c and msw,t sweating data pooled which reached 1.05 (SEM 0.14) mg.cm-2.min-1.degree C-1 and 1.14 (SEM 0.18) mg.cm-2.min-1.degree C-1 before and after sleep deprivation) respectively did not differ. However, in our experiment, sleep deprivation significantly increased the T(oes) threshold for the onset of both msw,c and msw,t (+0.3 degrees C, P < 0.001). From our investigations it would seem that the delayed core temperature for sweating onset in sleep-deprived humans, while exercising moderately in the heat, is likely to have been due to alterations occurring at the central level.
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PMID:Regulation of local sweating in sleep-deprived exercising humans. 835 55

During calorimetric experiments with forced cooling and rewarming, changes in rectal temperature (Tre) and mean skin temperature (Tsk) allowed calculations of Burton's (1935) weighting coefficient "a", which relates body temperature change to change in mean body temperature (delta Tb). Calculating delta Tb from change in body heat content (delta Hb), which was determined from direct and indirect calorimetry, included individualized values for body specific heat based on body fat content. In five different cooling procedures there were two with cooling by exposure to cold water and three with cooling in a tubing suit; two of the procedures included mild exercise. The delta Hb ranged from -335 to -1600 kJ; rewarming restored body heat content. The mean (SEM) value of "a" in 119 determinations was 0.75 (0.01). This small variability in the coefficient probably came from the large values of delta Hb and from the use of maximal changes in Tsk and Tre, including afterdrop. Change in Tre by itself correlated with delta Tb, but with much variability. In forced body cooling and rewarming, 0.75 (delta Tre) + 0.25 (delta Tsk) gives an accurate estimate of delta Tb, hence change in body heat storage.
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PMID:Heat storage and body temperature during cooling and rewarming. 842 8

This study investigated the effects of a roasted soybean (RSB)-supplemented diet and an estrogen implant (SYN; Synovex-S ear implant, 20 mg estradiol benzoate plus 200 mg progesterone) in young crossbred beef steers on their performance and plasma growth hormone (GH) response to challenge injections of thyrotropin-releasing hormone (TRH) + GH-releasing hormone (GHRH). Twenty individually fed steers (body weight 255 +/- 5 kg) were assigned to the following treatments: 1) no SYN and fed a soybean meal-supplemented diet, 2) no SYN and fed the RSB-supplemented diet, 3) plus SYN and soybean meal, and 4) plus SYN and RSB. Steers were fed 1.13 MJ metabolizable energy/kg metabolic body weight daily of an 18% protein diet. After a 5-wk growth period, all steers were challenged (intravenous injection) over a 3-wk period with three levels of a combination of TRH + GHRH (0.1 + 0.01, 1.0 + 0.1, 2.5 + 0.25 microg/kg body weight, respectively). After an additional 3 wk, steers were reimplanted and a second 5-wk growth period was followed by a single challenge of the 1.0 + 0.1 TRH + GHRH dose level. Plasma nonesterified fatty acid concentration was greater when steers were fed the RSB compared with soybean meal (265 vs. 205 micromol/L; P < 0.01; SEM = 9.5). Body weight gains for treatments 1, 2, 3 and 4 were 1.35, 1.21, 1.47 and 1.38 kg/d, respectively (RSB, P < 0.10; SYN, P < 0.07; SEM = 0.06). Gain/dry matter intake (g/kg) means were 184, 167, 197 and 184 (RSB, P< 0.04; SYN, P < 0.07; SEM = 7.5). Feeding roasted soybeans results in depressed area under the GH response curve [907, 555, 827 and 989 microg/(L*min) (SYN x RSB, P < 0.03; SEM = 117)] and depressed peak response (37.2, 26.6, 33.5 and 41.1 microg/L [SYN x RSB, P < 0.05; SEM = 4.5]), an effect alleviated by estrogen for young growing steers (Period 1) but not for heavier steers (Period 2).
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PMID:Roasted soybeans and an estrogenic growth promoter affect growth hormone status and performance of beef steers. 891 61

The effect of the blockade of the renin angiotensin system (RAS) on thermoregulatory, cardiovascular and renal function during moderate exercise in a hot [mean (SEM) 34.4 (0.1) degrees C] environment was evaluated. Six men and three women cycled at 60% peak oxygen uptake for 45 min following acute administration of a placebo (PLAC) or enalapril (ENAL), an angiotensin converting enzyme inhibitor (ACE-I). Resting mean arterial pressure (MAP) was reduced by ENAL, but the pressor response to exercise was unaffected [delta MAP = 7.8 (1.4)mmHg for both trials (P > 0.05)]. Peak esophageal temperature [T(es) = 38.7 (1.0) degrees C (PLAC) vs 38.4 (0.2) degrees C (ENAL)] and mean skin temperatures [Tsk = 36.5 (0.1) degrees C (PLAC) vs 36.6 (0.1) degrees C (ENAL)] were similar for both drug treatments during the exercise. Both aldosterone and plasma renin activity (PRA) increased five fold above resting values during exercise; however, only the PRA response [16.7 (3.2) ng angiotensin I (Ang I).ml-1.h-1 (ENAL) vs 7.4 (1.2)ng Ang I.ml-1.h-1 (PLAC)] was significantly altered by ENAL treatment (P < 0.05). Urine flow, sodium excretion and glomerular filtration rates, determined from creatinine clearance, were similarly reduced following exercise for both ENAL and PLAC treatments. These results suggest acute administration (5 mg) of ACE-I does not impair thermoregulatory, cardiovascular or renal responses during moderate exercise in the heat.
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PMID:Influence of angiotensin II blockade during exercise in the heat. 892 29

To investigate the effects of a short-term high altitude residence (2 weeks between 4150 m and 6885 m in the Andes) on the general and local cold responses after descent, 11 subjects were submitted both to a whole body standard cold air test (SCAT, dry bulb temperature = 1 degree C, 2 h, nude, at rest) and to a local cold water test of the right upper limb (CWT, 5 degrees C, 5 min) both before and after the expedition. Compared to before the expedition, a lower systolic blood pressure was observed after the high altitude residence [130.00 (SEM 3.35) mm Hg vs 140.40 (SEM 4.74) mm Hg at the end of CWT, P < 0.05] whereas no significant change either in diastolic blood pressure or in heart rate was found. All skin temperatures of the right upper limb were lowered (P < 0.05). During SCAT, body temperatures were unchanged (rectal and mean skin temperature, Tsk) but metabolic heat production was slightly but significantly diminished [110 (SEM 4) W.m-2 vs 125 (SEM 3) W.m-2, P < 0.05] and heat debt increased [11.37 (SEM 1.11) kJ.kg-1 vs 9.30 (SEM 2.30) kJ.kg-1, P < 0.05]. Moreover, the time of onset of continuous shivering (d) was shortened [8.20 (SEM 1.90) min vs 17.30 (SEM 3.60) min, P < 0.05] and the level of Tsk observed at (d) was higher [25.70 (SEM 0.80) degrees C vs 23.57 (SEM 0.78) degrees C, P < 0.05] suggesting an increase in the sensitivity of the thermoregulatory system despite the slight decreased shivering activity observed. It was concluded that general and local cold tolerance were modified by a short-term residence at altitude and that the changes observed were not in accordance with general or (and) local cold adaptation. In contrast, high altitude sojourn could be a risk factor for frostbite of the extremities.
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PMID:General and local cold responses in humans after 2 weeks at high altitude. 900 54

Chronic injection of an anti-c-KIT receptor tyrosine kinase monoclonal antibody (ACK2) results in the disruption of the normal motility patterns of young BALB/c mice intestine. This effect is accompanied by a drastic decrease in the number of intestinal c-kit-expressing (c-kit+) cells when studied immunohistochemically with the fluorescence-labelled antibody. In order to clarify the mechanism underlying the ACK2 action and the physiological roles of intestinal c-kit+ cells, we studied the excitability of intestinal c-kit+ cells in primary culture by use of the nystatin perforated-patch-clamp technique. Under voltage-clamp at -40 mV, the majority of c-kit+ cells tested (59/70) elicited rhythmic current waves with an amplitude and frequency of 263 +/- 24 pA and 2.30 +/- 0.25 cycles/min (mean +/- SEM), respectively. Intracellular perfusion of the c-kit+ cells with ethylenebis (okonitrilo) tetraacetate (EGTA) as well as a nominally Ca(2+)-free external solution or low holding voltage (< -60 mV) prevented the rhythmic current. The reversal potential of the rhythmic current was close to the equilibrium potential for Cl-(ECl). Moreover the rhythmic current was depressed by a Cl- channel blocker, 4-acetoamido-4-isothiocyanat-ostilbene-2,2'-disulphoni c acid (SITS). The smooth muscle cells freshly dissociated from the same intestinal specimen revealed a Ca(2+)-activated K+ current, as has been described in a variety of smooth muscle cells. Cultured smooth muscle cells from the ileum preparation lacked neither the Ca(2+)-activated K+ nor rhythmic Cl- currents. Smooth muscle cells freshly dissociated from the same ileum preparation and those in culture showed no immunoreactivity with the labelled ACK2, which was consistent with our previous in situ study. Results provided direct evidence that the intestinal c-kit+ cells, but not the smooth muscle cells, possess a rhythmic Cl- current oscillation, suggesting their participation in pacemaker activity for the peristaltic gut movement.
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PMID:Rhythmic Cl- current and physiological roles of the intestinal c-kit-positive cells. 902 76


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