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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Requirements in terms of water activity (a(w)) for the growth, sporulation, and germination of Clostridium perfringens were determined. Strain A48 was used in all phases, and in addition either NCTC 8239 or NCTC 8797 was used for growth, sporulation, and germination studies. The desired a(w) of the test media was obtained by the addition of one of three solutes: glycerol, sucrose, or sodium chloride. The freezing point depression method was used to determine the a(w). The basal medium for growth and germination was Fluid Thioglycollate Medium. It had an a(w) of 0.995 and produced maximum growth and fastest growth rate among the six levels of a(w) tested. The lowest a(w) supporting growth and germination of C. perfringens was between 0.97 and 0.95 in the test media made with sucrose or sodium chloride and 0.93 or below in the test media adjusted with glycerol. Spore production by C. perfringens in Ellner's or modified medium required a higher a(w) than growth.
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PMID:Growth, sporulation, and germination of Clostridium perfringens in media of controlled water activity. 431 68

1. End-plate currents have been studied in glycerol-treated frog sartorius nerve-muscle preparations with the voltage clamp technique.2. End-plate currents follow a simple exponential time course over most of their declining phase.3. The rate constant alpha that characterizes this exponential decay depends upon membrane potential V according to the relationship alpha (V) = Be(AV), with A = 0.00795 +/- 0.00043 (S.E.) mV(-1) and B = 1.67 +/- 0.04 (S.E.) msec(-1).4. Voltage sensitivity decreases (that is, A in the above equation becomes smaller) as the recording and current-passing electrodes are moved away from the end-plate region.5. The voltage sensitivity of alpha is decreased by decreasing the gain of the voltage clamp amplifier.6. Changing the end-plate current amplitude by curare treatment, by increased calcium ion concentration, and by facilitation and depression has essentially no effect on end-plate current time course.7. When membrane potential is changed step-wise during the decaying phase of the end-plate conductance change, currents begin to decline with a rate constant alpha appropriate to the new membrane potential in less than 0.2 msec.8. Treatment with prostigmine methylsulphate in concentrations up to 50 mug/ml. slows end-plate current decay but has little effect on voltage sensitivity. That is, B in the above equation is decreased by prostigmine treatment, but A is relatively unaffected.
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PMID:The effect of voltage on the time course of end-plate currents. 453 43

Thrombin and poly-l-lysine alter the incorporation of acetate, glycerol, and fatty acids into the lipids of washed human platelets. Both aggregating agents decrease the incorporation of acetate into all lipid classes other than free fatty acids. Similarly, glycerol incorporation into complex lipids is impaired by both thrombin and polylysine. Thrombin caused marked depression of the incorporation of palmitic acid into both lecithin and triglycerides. By contrast it enhanced the incorporation of oleic acid into lecithin, but not into triglycerides. The data suggest that the process of primary platelet aggregation is associated with a defect in the assembly of complex lipids.
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PMID:Altered lipid metabolism in human platelets after primary aggregation. 468 85

1. After young men had exercised for approximately 2 hr at 70% maximum O(2) uptake, and taken 28 ml. ethanol by mouth, their mean blood glucose fell to 2.17 mM. It fell further to 1.77 mM during a 30 min exposure to air at 14.5 degrees C. Plasma lactate, glycerol, beta-hydroxybutyrate and free fatty acid concentrations increased.2. Rectal temperature fell to reach a mean level of 34.49 degrees C by the end of the cold exposure; oesophageal temperature fell to as low as 33.00 degrees C in one case.3. Virtually no increase in metabolic rate and no visible shivering occurred during the cold exposure.4. Administration of glucose (mean 60.4 g) prevented the falls in temperature, and restored metabolic response to the cold to the size found in control experiments without exercise or ethanol.5. Neither exercise without ethanol or ethanol without exercise significantly lowered the blood glucose or impaired the maintenance of body temperature in the cold.6. One obese subject showed almost as great a fall in blood glucose and depression of metabolic response to cold as the thinner men, but no fall in body temperature.
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PMID:Failure of thermoregulation in the cold during hypoglycaemia induced by exercise and ethanol. 468 95

1. A method is described by which a selective lesion can be made in vitro in the transverse tubules of frog skeletal muscle.2. The method consists of exposing the muscle for 1 hr or more to a buffered salt solution made hypertonic by the inclusion of 400 mM glycerol and then returning the muscle to an isotonic salt solution. The lesion is induced during the washout of the glycerol.3. Electron micrographs reveal that the lesion consists of a rearrangement of the T-system membranes in such a way that the continuity of the tubules is lost. The membranes appear to coalesce into large vesicles scattered irregularly throughout the sarcoplasm.4. The glycerol treatment results in a depression of the resting potential of up to 30 mV. The treated fibres are depolarized by high concentrations of K as are normal muscle fibres.5. T-tubule lesioned fibres are unable to respond mechanically either to electrical stimulation or to elevated K but they do contract in the presence of caffeine and relax when the caffeine is removed.6. Problems concerning the variability of the procedure are presented and certain considerations concerning the mechanism of the effect are discussed.
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PMID:A lesion of the transverse tubules of skeletal muscle. 576 80

Catalase in extracts of the extreme halophile Halobacterium cutirubrum exhibits up to threefold stimulation by 0.5 to 1.5 m monovalent salts and by 0.1 m divalent salts. Above these concentrations, inhibition of enzyme activity is observed. The inhibitory effect, and to some extent the stimulation, is salt-specific; the effectiveness of a salt in inhibiting enzyme activity depends on both cation and anion. Thus, the order of effectiveness is MgCl(2) > LiCl > NaCl > KCl > NH(4)Cl, and LiCl > LiNO(3) > Li(2)SO(4). The magnitude of enzyme inhibition for the salts tested is positively correlated with their molar vapor pressure depression in aqueous solution. Stimulation of enzyme activity was observed when one salt was added at its optimal concentration in the presence of inhibiting concentrations of another salt, indicating that the effect on the enzyme is not due to changing water activity but probably to enzyme-salt interaction. Aqueous solutions of ethylene glycol, glycerol, and dimethyl sulfoxide containing no ions influence enzyme activity in the same manner as do salts.
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PMID:Effect of salts and organic solvents on the activity of Halobacterium cutirubrum catalase. 578 14

The metabolic and hormonal responses to exhaustive short-term supramaximal exercise were studied in 10 male physical education students. The exercise task was a single bout of running on the treadmill at 22 km X h-1 and 7.5% slope. It was performed with single oral doses of 100 mg Bupranolol (non-selective beta-blockade), 100 mg Metoprolol (beta-1-selective blockade), and placebo. Arterialized capillary and venous blood were sampled until 30 min post exercise. Time to exhaustion was 52.0 +/- 2.6, 47.6 +/- 2.0, and 46.0 +/- 1.9 s in the control, Metroprolol, and Bupranolol experiments. At cessation of exercise, adrenaline and noradrenaline were grossly elevated in all three conditions. Lactate and glucose increased markedly, this being accompanied by increasing insulin in the control and Metoprolol, but not the Bupranolol trials. Glycerol increased moderately, while FFA were depressed. Growth hormone showed a delayed increase at 15 and 30 min post exercise. Cortisol was unaffected by exercise. beta-blockade reduced the increases of lactate, glucose, glycerol, insulin, and growth hormone, exaggerated the depression of FFA and had no effect on cortisol. The results demonstrate that the strong sympatho-adrenal response to exercise of this nature is a major determinant of the increase of glucose at cessation of exercise. The hyperglycemia in concert with beta-2-adrenergic stimulation leads to elevation of insulin. Furthermore, lipolysis is controlled by beta-adrenergic stimulation. The delayed increase of growth hormone seems to be triggered by the declining glucose level during recovery.
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PMID:Metabolic and hormonal responses to exhaustive supramaximal running with and without beta-adrenergic blockade. 614 64

Cardiovascular status and reactivity have been investigated in spontaneously hypertensive rats (SHR) with glycerol-induced acute renal failure. SHR with acute renal failure had significantly lower mean arterial blood pressures and heart rates. The pressor responses to noradrenaline and the chronotropic responses to right cervical sympathetic and vagal nerve stimulation were diminished in uraemic SHR compared to control SHR. The cardiovascular depression observed in SHR with acute renal failure was similar to that previously noted in normotensive rats with acute renal impairment.
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PMID:Cardiovascular responses in spontaneously hypertensive rats with acute renal failure. 614 56

Effects of the sodium ionophore, monensin, were examined on the passage from neuronal cell body to axon of materials undergoing fast intracellular transport. In vitro exposure of bullfrog dorsal root ganglia to concentrations of drug less than 1.0 micron led to a dose-dependent depression in the amount of fast-transported [3H]leucine- or [3H]glycerol-labeled material appearing in the nerve trunk. Incorporation of either precursor was unaffected. Exposure of a desheathed nerve trunk to similar concentrations of monensin, while ganglia were incubated in drug-free medium, had no effect on transport. With [3H]fucose as precursor, fast transport of labeled glycoproteins was depressed to the same extent as with [3H]leucine; synthesis, again, was unaffected. By contrast, with [3H]galactose as precursor, an apparent reduction in transport of labeled glycoproteins was accounted for by a marked depression in incorporation. The inference from these findings, that monensin acts to block fast transport at the level of the Golgi apparatus, was supported by ultrastructural examination of the drug-treated neurons. An extensive and selective disruption of Golgi saccules was observed, accompanied by an accumulation of clumped smooth membranous cisternae. Quantitative analyses of 48 individual fast-transported protein species, after separation by two-dimensional gel electrophoresis, revealed that monensin depresses all proteins to a similar extent. These results indicate that passage through the Golgi apparatus is an obligatory step in the intracellular routing of materials destined for fast axonal transport.
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PMID:Evidence that all newly synthesized proteins destined for fast axonal transport pass through the Golgi apparatus. 618 Oct 72

The effect of a single dose (50 mg/kg body weight) of 3-methylcholanthrene on de novo phosphatidylcholine biosynthetic activities in rat liver was studied both in a cell-free system and with slice experiments. 3-Methylcholanthrene caused a significant depression of either [methyl-14C]choline or [2-(3)H]glycerol incorporation into phosphatidylcholine when the precursor was incubated with liver slices. At the same time, there occurred a significant accumulation of radioactivity in either cholinephosphate or diacylglycerol molecule from [14C]choline or [3H]glycerol, respectively, suggesting that 3-methylcholanthrene could cause an inhibitory effect on hepatic phosphatidylcholine synthesis at the cholinephosphotransferase or/and cholinephosphate cytidylyltransferase step. Subsequent studies, where the activities of the three enzymes involved in de novo phosphatidylcholine synthesis were compared between control and 3-methylcholanthrene-pretreated rat liver subcellular fractions, demonstrated that the cholinephosphotransferase step could be the site of inhibition by 3-methylcholanthrene. On the other hand, 3-methylcholanthrene caused a significant induction of choline kinase activity in a time-dependent manner and, at the same time, the cholinephosphate pool size in liver cytosol was enlarged 2-3-fold when compared to the respective control. The overall results suggested strongly that 3-methylcholanthrene causes the counteractive effects on the de novo phosphatidylcholine biosynthesis, induction of choline kinase activity and inhibition of cholinephosphotransferase activity, both of which could participate in a concomitant increase in cholinephosphate pool size in rat liver.
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PMID:Induction of choline kinase by polycyclic aromatic hydrocarbons in rat liver. II. Its relation to net phosphatidylcholine biosynthesis. 629 18


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