Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The responses of type A atrial receptors to graded infusions of saline and large doses of propranolol were examined in anesthetized cats. Infusion of saline raised the mean atrial pressure, but usually the amplitude of the atrial a wave was reduced. In general the receptor discharge was unaffected. Propranolol reduced the discharge from the control level when it was injected in doses no less than 4 mg/kg. Infusions of saline after propranolol resulted in an increase in the discharge and the increase was related to the amplitude and/or initial pressure of the a wave. In one case the discharge after propranolol was less than that when the atrium was widely slit open. It is concluded that at least part of the effect of the drug is due to a direct depression of the receptor rendering it less sensitive to the stretch provided by atrial contraction. The demonstration of a stimulus-response relationship between the a wave and the receptor discharge at low levels of activity suggests that under normal conditiions the receptor operates on a plateau of maximum activity, thus making a response to small changes in stimulus strength obscure.
Arch Int Pharmacodyn Ther 1976 Sep
PMID:Effect of propranolol on the relationship between atrial systolic pressure and type A atrial receptor discharge in cats. 18 31

Twenty-four patients with small cell carcinoma of the lung were treated with a combination of vinblastine, 5 mg/m2 iv on Day 1; adriamycin, 40 mg/m2 iv on Day 1; and procarbazine, 100 mg/m2 orally on Days 1-7. The courses were repeated every 21 days. Tumor regression was noted in five of eight previously untreated patients, in two of six patients with previous chemotherapy, and in one of ten patients with previous chemotherapy and irradiation. The median duration of response was 130 days (range, 42-488+ days). The major toxic effects were bone marrow depression, gastrointestinal disturbances, and alopecia. This drug combination deserves consideration for inclusion into sequential combination chemotherapy regimens used in the treatment of this tumor type.
Cancer Treat Rep 1976 Sep
PMID:Phase II study of vinblastine, adriamycin, and procarbazine in small cell carcinoma of the lung. 18 21

Incubation of HeLa cells with the anticancer agent N-methyl-N-nitrosourea (MNU) results in: (a) depression of intracellular nicotinamide adenine dinucleotide levels; (b) stimulation of the chromatin-associated, chromosomal protein-modifying enzyme polyadenosine diphosphoribose [poly(ADP-ribose)] polymerase, which uses nicotinamide adenine dinucleotide as substrate; and (c) some fragmentation of cellular DNA. DNase treatment of HeLa nuclei in vitro also stimulates poly(ADP-ribose) polymerase activity, but not in nuclei derived from MNU-treated cells unless they have been subsequently incubated to allow for recovery from MNU damage. DNA polymerase activity is stimulated in vitro by poly(ADP) ribosylation of nuclear proteins. By using intact nuclei derived from MNU-treated HeLa cells, the repair via elongation of single-strand DNA breaks is demonstrated in vitro. This repair is dependent on DNA polymerase activity and is enhanced by adenosine diphosphate ribosylation of histones. Inhibition of poly(ADP-ribose) polymerase with nicotinamide results in extensive degradation of MNU-damaged DNA. Taken as a whole, these results suggest that poly(ADP-ribose) polymerase may play a role in the repair of alkylation damage to cellular DNA and that the inhibition of this enzyme in vivo might be exploited to potentiate the antitumor and carcinogenic activities of MNU.
Cancer Res 1977 Sep
PMID:A putative role for nicotinamide adenine dinucleotide-promoted nuclear protein modification in the antitumor activity of N-methyl-N-nitrosourea. 19 15

Neurophysiological experiments were conducted in vitro on 400 mu thick transverse hippocampal slices from aged and young rats. These slices exhibit neurophysiological responses similar to those of intact hippocampus. The aged rats have previously been found to exhibit impaired retention. Synaptic responses of the Schaffer collateral system were not found to be different between aged and young slices when elicited by very low frequency (0.3 Hz) electrical stimulation. However, the aged slices exhibited marked deficits in frequency and posttetanic potentiation in response to repetitive stimulation (15 Hz). This deficit was interpreted as resulting from an increased tendency to synaptic depression, rather than from impaired potentiation processes. The possibility of a relationship of these physiological deficits in hippocampal synaptic plasticity to the deficits in behavioral plasticity found in these aged animals is considered.
J Gerontol 1977 Sep
PMID:Impaired monosynaptic potentiation in in vitro hippocampal slices from aged, memory-deficient rats. 19 1

There is considerable evidence to suggest that macrophages participate in host resistance to the development and spread of cancer. We have, therefore, studied monocytemacrophage function in humans and animals with neoplasms. Approximately 60% of patients with various types of cancer were found to have abnormal monocyte chemotactic responsiveness in vitro, and abnormal chemotaxis was an indicator of poor prognosis in patients with melanoma. By studying patients before and after surgery, it was found that abnormal chemotactic responses normalized within weeks after removal of malignant tumors, indicating that a neoplasm itself might affect the host's monocyte chemotactic responsiveness. Subsequent studies using transplantable neoplasms in mice substantiated this hypothesis in that macrophage accumulation in vivo as well as macrophage chemotactic responsiveness in vitro was depressed in animals during the early phases of tumor growth. This depression of macrophage function could be attributed to a low-molecular-weight factor contained in murine neoplasms, which when given to normal mice was extremely potent in depressing peritoneal macrophage accumulation and chemotaxis but, paradoxically, enhanced phagocytosis. The serum of tumor-bearing mice also contained potent inhibitory activity for macrophage accumulation. In contrast to the effects on macrophages, granulocyte accumulation in vivo and chemotaxis in vitro was not depressed by the presence of a neoplasm or the administration of the factor from neoplasms. By releasing factors which depress macrophage migratory function, neoplasms may protect themselves from immunologically mediated host destruction during the early phases of tumor growth.
Am J Pathol 1977 Sep
PMID:Macrophage migratory dysfunction in cancer. A mechanism for subversion of surveillance. 19 6

Post-tetanic potentiation (PTP) of monosynaptic reflex was estimated in spinal cords in the drug-free state after the administration of a convulsant dose of penicillin and after the administration of phenytoin. There was no apparent correlation between the degree of depression of PTP and the efficacy of controlling seizure activity by phenytoin. Extracellular potassium levels were measured with ion-selective microelectrodes. The post-stimulation clearing of [K+]0 was not accelerated by phenytoin, and frequently it was slowed. Post-stimulus undershooting of [K+]0 was diminished. Oxidation of NADH in cortex and of cytochrome a, a3 in spinal cord were measured by optical methods. Stimulus-evoked transient oxidation responses evoked by electrical stimulation were depressed by phenytoin. It is concluded that systemic administration of phenytoin in therapeutic doses does not stimulate Na+-K+-activated membrane ATPase in cortex and spinal cord. Unlike other depressants, phenytoin did not cause a reduction of "resting" redox levels of respiratory enzymes. The local regulation of blood flow remained unaltered after phenytoin administration. Phenytoin caused a moderate but consistent depression of the stimulus-evoked responses of potassium activity, electric potential, and oxidative enzymes, consistent with diminished outflow of potassium from cells, owing either to lesser activation of cells or to a lesser exchange of ions.
Epilepsia 1977 Sep
PMID:Phenytoin, electric, ionic, and metabolic responses in cortex and spinal cord. 19 41

Hand radiographs in 10 male patients (eight white, two black) with isolated growth hormone deficiency were studied before and after treatment. The length of the second metacarpal was the most significantly depressed measurement when considered by chronologic age and responded most to treatment with human growth hormone. All patients had osteoporosis even when evaluated by height age. The bone mass improved with treatment by subperiosteal new bone apposition. Skeletal maturation was retarded with the carpals showing more severe retardation than the tubular bones and responding more dramatically to treatment. The depression in height age and carpal age was very similar, indicating that the carpal age may have the greatest correlation with height. The greater sensitivity of the carpal age deficiency of growth hormone and its greater response to treatment suggest that the carpal age and the phalangeal-metacarpal age should be considered independently during evaluation of skeletal maturation.
AJR Am J Roentgenol 1977 Sep
PMID:Hand radiographic measurements in growth hormone deficiency before and after treatment. 19 44

The stathmokinetic technique was used to study quantitatively the proliferative response of cells comprising the alveolar wall of inbred mice which had inhaled coal or quartz. The exposures occupied 4 weeks and the observations continued over an extended period thereafter. Control observations suggested that mitotic inhibition was induced solely by residence in the exposure chamber, since cessation of exposure was quickly followed by a temporary rise of proliferative activity. This feature was not apparent when dust was inhaled, though with comparable exposure to both coal and quartz there was an elevation in mitotoic incidence of alveolar wall cells in dust-free areas of lung at a later interval. In dust-laden areas the rise was less in evidence, a situation that persisted throughout the post-exposure survival. The difference in mitotic incidence between dust-free and dust-containing areas was more evident after coal than after quartz inhalation, whilst in higher concentration a quartz aerosol induced a continued depression of mitotic activity. The proliferative response seen in the alveolar walls of control and dusted mice is most likely to be contributed by the interstitial precursors of alveolar macrophages, cells which are recognized to be marrow derived. The changes observed in mitotic incidence are interpreted in terms of demand for alveolar macrophages according to the nature of the dust and the inintensity of the exposure.
Inhaled Part 1975 Sep
PMID:A cell kinetic study of the alveolar wall following dust deposition. 19 64

1.beta-Bungarotoxin, crotoxin and taipoxin, presynaptic neurotoxins of snake venom origin, have about the same phospholipid-splitting activities as a much less toxic cobra phospholipase A2 in the presence of Ca2+ and deoxycholate. 2. Sr2+ was a much less effective activator of the enzymes than is Ca2+, the activation by Sr2+ being only 3-6% for beta-bungarotoxin and crotoxin and 12% for taipoxin. 3. Sr2+ also inhibited the Ca2+ -activated enzymes by 80% in the cases of beta-bungarotoxin and crotoxin, but only 16% in the case of taipoxin. 4. Mg2" had no significant effect on beta-bungarotoxin or crotoxin, but activated taipoxin in the presence or absence of Ca2". 5. In Sr2+ -Tyrode lacking Ca2+ all three toxins exhibited the same immediate depression followed by facilitation in the rat and mouse diaphragms, but the final blocking activity was only 3-10% with beta-bungarotoxin and crotoxin and was 30% with taipoxin. 6. In Sr2+ -Tyrode, increasing in the rate of nerve stimulation had less accelerating effect on the development of neuromuscular block than in Ca2+ -Tyrode for any of the toxins. 7. Removal of Mg2+ from Sr2+ -Tyrode did not diminish the potency of taipoxin in blocking neuromuscular transmission, suggesting that enzyme activity at the outer surface of the axolemma does not contribute to the neuromuscular blocking action. 8. All of the results indicate that there are close correlations between the presynaptic activities of these toxins and their phospholipid-splitting activities in the cationic environment prevailing in the axoplasm. Apparently the final blocking effect of these toxins is due to phospholipase A action within the nerve terminal.
Naunyn Schmiedebergs Arch Pharmacol 1977 Sep
PMID:Effects of Sr2+ and Mg2+ on the phospholipase A and the presynaptic neuromuscular blocking actions of beta-bungarotoxin, crotoxin and taipoxin. 19 83

Crude mediators from stimulated rabbit peritoneal leukocytes (LEM) engender numerous physiologic alterations in rats, which are similar to those observed during infection. One hour after the intraperitoneal injection of crude LEM, plasma insulin and glucagon concentrations are elevated; at 2 h the hormonal alterations are manifested by a 30% increase in hepatic cyclic adenosine 3',5'-monophosphate (cAMP), glycogen depression, and uptake of 14C-labeled nonmetabolizable amino acid analogues (AA). Plasma hormone concentrations reach maximum levels by 5 h and decline by 24 h. The hepatic concentrations of AA parallel the insulin and glucagon responses and correlate with the inverse of insulin/glucagon molar ratio. In spite of mobilization of hepatic glycogen evident at 5 h, plasma glucose concentrations were transiently depressed. Plasma insulin, glucagon, and hepatic AA concentrations were dose dependent. Plasma insulin and glucagon responses to crude LEM may explain increases in hepatic cAMP, uptake of AA, and glycogenolysis as well as hypoglycemia. These data partially characterize the role of crude LEM, provide an explanation for the stimuli-inducing hyperglucagonemia and hyperinsulinemia during infection. They implicate the endocrine pancreas as a factor regulating the host's metabolic response to infection.
Am J Physiol 1977 Sep
PMID:Effect of leukocytic endogenous mediators on endocrine pancreas secretory responses. 19 70


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