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)

Multinucleate cells are found frequently in rheumatoid synovium. In this study, polyethylene glycol was used to fuse rabbit synovial fibroblasts. Approximately 40% of the cells developed more than one nucleus in a 24 hour period, during which time cell membranes had increased permeability. In cultures containing multinucleate cells, 3H-thymidine incorporation was depressed for 24 hours although 3H-leucine incorporation into TCA precipitable material was unaffected; autoradiography showed that depression of 3H-thymidine continued for at least 4 days. Collagenase production by cultures containing fused cells was increased more than 10-fold over control cultures during a 28 day period.
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PMID:Collagen production by cultures containing multinucleated cells derived from synovial fibroblasts. 21 86

1. The velocity of shortening at zero load was studied during fused tetanic contractions and single twitches in isolated skeletal muscle fibres of Rana temporaria. 2. The technique used for determination of the speed of unloaded shortening consisted of a series of quick releases of different amplitudes applied at a given instant during activity. The time, delta t, needed for the fibre to take up the slack was plotted against the amplitude of release, delta L. The slope of the straight line relating delta t-delta L provided a measure of the velocity of shortening at zero load, V0. 3. V0 was compared with force-velocity data obtained at finite loads (load-clamp recordings). The predicted velocity of shortening at zero load, derived by hyperbolic extrapolation from velocities at low and intermediate loads, was not significantly different from V0. 4. The temperature dependence of isometric force and of shortening velocity was investigated between 2 and 12 degrees C in the same fibres. Q10 was 2.67 +/- 0.07 (S.E. of mean, n = 6) for V0 and 1.24 +/- 0.01 for tetanic force. 5. The velocity of unloaded shortening was determined at different sarcomere lengths in the range 1.4--3.1 microns. V0 was constant between 1.65 microns and approximately 2.7 microns. It decreased below 1.65 microns and increased above 2.7 microns. 6. The decrease in velocity at short sarcomere lengths probably reflects an increase of the passive resistance to shortening. The increase in velocity at long sarcomere lengths can be accounted for by the passive compressive force that is produced by the parallel elastic elements of the prestretched fibre. 7. V0 was determined at the peak of the twitch and during the plateau of the fused tetanus in the same fibre. Whereas the peak twitch force varied between 38 and 85% of the tetanic tension in the different fibres (mean: 71 +/- 5%, n = 8), V0 during the twitch was 99 +/- 2% of the value recorded during the tetanus. Depression of the isometric twitch amplitude to 10% of the control value by dantrolene did not cause any significant reduction of V0.
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PMID:The velocity of unloaded shortening and its relation to sarcomere length and isometric force in vertebrate muscle fibres. 31 10

1. The effect of active shortening on the time course and magnitude of isometric tension development during a single twitch and during an incompletely fused tetanus was studied at 0-2-1-2 degres C in isolated semitendinosus muscle fibres of the frog. 2. Active shortening caused a depression of the contractile force without markedly affecting the total duration of the twitch. The depressant effect increased with increasing amounts of sarcomere shortening. Sarcomere shortenings of 0-05 mum and 0-3 mum reduced the twitch force by approximately 5 and 20 percent of the maximal tetanic tension, respectively. 3. A given sarcomere shortening induced the same absolute amount of depression of the contractile strength when the movement was carried out at different times during the initial 200-250 msec after the stimulus. 4. The influence of load and velocity of shortening during the movement phase was studied. Differences in load ranging between zero and 1/3 of the maximal tetanic tension (with concomitant changes in speed of shortening from Vmax to approximately 1/5 of Vmax) did not affect the degree of depression markedly. Underthe conditions studied, the extent of movement appeared to be the only significant determinant of the depressant effect. 5. The reduction in force induced by active shortening persisted for 800-900 msec during an incompletely fused tetanus. 6. It is suggested that the depressant effect is based on a structural change in the myofilament system that is produced as the A and I filaments slide along each other during muscle activity.
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PMID:Mechanical deactivation induced by active shortening in isolated muscle fibres of the frog. 107 34

1. Single fibres isolated from the anterior tibialis muscle of Rana temporaria (temperature, 2-5 degrees C; sarcomere length, 2.10 microns) were fatigued using two separate protocols that led to different degrees of depression of tetanic force. Under control conditions the fibre was stimulated to produce a 1 s fused isometric tetanus at 300 s intervals. A moderate degree of fatigue (tetanic force reduced to 70-80% of the control value) was produced by decreasing the intervals between tetani to 15 s ('fatiguing protocol 1'). A more pronounced depression of tetanic force (to 40-50% of the control value) was produced by evoking a single twitch at 1-2 s intervals ('fatiguing protocol 2'). 2. Fatiguing protocol 1 reduced the contracture response to submaximal and supramaximal concentrations of caffeine (3-15 mM) in proportion to the decrease in tetanic force. These results support the view that fatiguing stimulation according to protocol 1 leads to a true 'myofibrillar fatigue' with no failure of activation of the muscle fibre. 3. Fatiguing protocol 2 reduced the amplitudes of isometric twitch and tetanus to below 10 and 50% of the control values, respectively. By contrast, the maximal contracture response to caffeine (15 mM) was depressed by merely 2-3% of its prefatigue value. 4. Force and instantaneous fibre stiffness were recorded simultaneously during twitch and tetanus as fatigue was induced by protocol 2. During the initial part of fatigue (tetanic force reduced by 25% of control) stiffness was reduced by merely 9% in accordance with previous measurements during fatigue induced by protocol 1. However, with further depression of twitch and tetanus by protocol 2 there was a marked reduction of fibre stiffness. These results, together with the findings reported under point 3, strongly suggest that at an advanced state of fatigue induced by protocol 2 the decrease in active force is largely due to failure of activation of the contractile system. 5. Muscle fibres were quickly frozen for electron microscopical examination after shortening below slack length (to approximately 1.6 microns sarcomere spacing) during tetanic stimulation. In non-fatigued fibres, and in fibres fatigued according to protocol 1, the myofibrils exhibited a straight appearance throughout the preparation suggesting that the entire volume of the fibre was properly activated. In fibres fatigued by protocol 2, on the other hand, only the most peripheral layers of myofibrils remained straight after shortening, whereas the centre of the fibre showed marked waviness indicating failure of the inward spread of activation in this case.
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PMID:Myofibrillar fatigue versus failure of activation during repetitive stimulation of frog muscle fibres. 129 47

Experiments were conducted to determine the effect of an induced enteric disorder, stunting syndrome (SS), on young turkeys. One-day-old poults were dosed per os with tryptose-phosphate broth (control) or inoculum (inoc) prepared from intestines of SS-affected poults. Inoculation depressed gain (P less than .001) and feed consumption (P less than .001) and impaired (P less than .001) the utilization of feed for gain up to 9 days of age (utilization was 2.02, 2.62 in inoc and 1.27, 1.61 in control poults at 5 and 9 days of age, respectively). Inoculation impaired (P less than .05) retention of nutrients at 8 days of age (dry matter, fat, protein, and ash retentions were 82.5, 88.8, 81.3, and 77.8% in controls and 79.3, 85.6, 74.5, and 74.1% in inoc poults, respectively). Small intestinal weight per 100 g of body weight was greater (P less than .001) in inoc poults, but empty weights per length of jejunum and ileum were less (P less than .05). The jejunal mucosa in inoc poults was thinner, exhibited extensive erosion of villi tips, and had microvilli that seemed to be fused when observed by using scanning electron microscopy. Activities of disaccharidases in the jejunum and ileum of inoc poults were less (P less than .05) than in control poults. In a second experiment, two additional treatments were included, a pair-fed control and a negative control. Control poults pair-fed with the inoc poults grew more rapidly (P less than .01) than inoc poults. The depression in feed consumption due to inoculation accounted for only 54% of the growth depression. Poults inoculated with a suspension prepared from intestines obtained from healthy poults (negative control) performed similarly to controls. Thus, the adverse effects of the SS-inoculum were due to an agent(s) that was present int he intestines of SS-affected poults but not in intestines of healthy poults.
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PMID:Stunting syndrome in turkeys: physical and physiological changes. 208 51

New planar lipid bilayer technology enabled the pharmacologic study of single sodium channels from human brain, overcoming the limitations of tissue availability and the rapid loss of protein function in conventional experimental preparations. Synaptosomal vesicles prepared from human brain cortical tissue were fused with planar lipid bilayers. In the presence of batrachotoxin, sodium channels were incorporated into lipid bilayers and their single-channel properties studied. Pentobarbital was found to depress two major functions of the sodium channel, leading to a voltage-independent reduction of the fractional channel open-time (ED50 0.61-0.75 mM) and an interaction with the voltage-dependent steady-state activation. The steady-state activation curve was shifted to more negative potentials and had a reduced slope, i.e., negative membrane potentials became less effective at closing sodium channels. The results were consistent with a pentobarbital-induced increase in protein flexibility. The actions of the two optical stereoisomers of pentobarbital showed no significant differences, indicating that other ion channels must also be involved in the clinical actions of barbiturates. The pentobarbital effects on sodium channels occurred at concentrations thought to be relevant in general anesthesia and within the clinical range. This suggests that sodium channels could contribute to overall anesthetic depression, supporting our hypothesis that anesthesia results from the superposition and integration of several anesthetic actions at the molecular level.
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PMID:Molecular actions of pentobarbital isomers on sodium channels from human brain cortex. 215 52

In Escherichia coli synthesis of several proteins is transiently depressed upon heat shock treatment. A comparison of nucleotide sequences of the genes encoding these proteins revealed the occurrence of a consensus sequence, GAGGAA(N)3-6ATG, in their translation start signal region. To examine whether this sequence is involved in heat shock-induced depression of protein synthesis, DNA segments corresponding to this region of four of these genes, fusA, rpoB, glnS, and pheT, were synthesized, and each of them was fused in frame with the lacZ gene on the open reading frame vector pORF1. The effect of heat shock on the synthesis of beta-galactosidase encoded by these fused genes was then studied in E. coli. It was thus found that beta-galactosidase synthesis starting from the inserted translation start signal was arrested transiently upon temperature shift-up from 30 to 42 degrees C. I conclude that the heat shock-induced depression of gene expression is an event taking place at the initiation of translation.
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PMID:A nucleotide sequence in the translation start signal region is involved in heat shock-induced translation arrest in Escherichia coli. 218 26

Seventy-eight unfused patients with idiopathic scoliosis were followed from skeletal maturity over a mean period of 17 years (range 10 to 27 years) with a mean age at follow up of 33.7 years. The following aspects were investigated: curve deterioration, back pain incidence, and psychosocial details. There was considerable variation in the progression rate of similar deformities but on average significant deterioration occurred when the Cobb angle was over 55 degrees with a maximum deterioration approaching 1.5 degrees per year in the thoracic curves between 90 degrees and 100 degrees mature Cobb angle. Thoracolumbar and lumbar curves were slightly more benign with a maximum progression rate of about 1 degree when the mature angle was 80 degrees to 90 degrees. The thoracic component of double curves progressed least. Rotation increased in proportion to the Cobb angle progression except in some lumbar curves where lateral subluxation occurred with a disproportionate amount of rotation. The incidence of back pain in relation to pain in the general population and in fused patients remains uncertain. Eighty-two percent of patients had married and 87% had job satisfaction; 10% received treatment for depression.
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PMID:The natural history of unfused scoliosis. 295 82

We have investigated the mechanism of the inhibition of phagosome-lysosome (P-L) fusion in macrophages known to occur after infection by Mycobacterium tuberculosis and by the mouse pathogen Mycobacterium microti. We have used an M. microti infection and have studied, first, the saltatory movements of periphagosomal secondary lysosomes by means of visual phase-contrast microscopy (a similar use of the method having been previously supported by computer analyses). The movements became slow or static after ingestion of live but not of heat-killed M. microti. They were unaffected by a fusiogenic mycobacterium M. lepraemurium. Second, we studied the behavior of a normally fusiogenic unrelated organism, Saccharomyces cerevisiae, after its phagocytosis by cells already containing live M. microti ingested 18 h previously. We observed, using a fluorescent assay of fusion, that many of these yeast phagosomes now also failed to fuse with the lysosomes; in contrast, when the host M. microti had been heat killed the yeast phagosomes fused normally. These observations were extended by ultrastructural quantitative analyses of P-L fusion, which confirmed the nonfusion of phagosomes of live M. microti and, more particularly, the change to nonfusion from the normal fusion behavior of the separate phagosomes of accompanying yeasts. Third, we have assembled evidence against the likelihood that these M. microti-induced phenomena are nonspecific, i.e., secondary to a general depression of activity of heavily infected host cells. The evidence includes the feasibility of adjusting the degree of infection so as to facilitate visual assessment of organelle movements without the presence of detectable damage to the cells studied; the absence of lysosomal stasis after comparable infection with another mycobacterium of comparable virulence (M. lepraemurium); and the reversibility of the stasis. We conclude that inhibition of lysosome saltatory movements (and consequently its secondary effect on the associated yeasts) is a significant, specifically induced phenomenon. From these observations and considerations, therefore, in conjunction with the analogous inhibition of lysosomal movements in normal macrophages by some chemical inhibitors of P-L fusion, and our suggestion that this association is causally related, we now suggest that M. microti-induced focal lysosomal stasis is also the main means by which the inhibition of P-L fusion is brought about by this organism. This concept is strengthened by the observations on S. cerevisiae, which provide strong evidence that stasis can cause suppression of fusion.
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PMID:Inhibition of phagosome-lysosome fusion in macrophages by certain mycobacteria can be explained by inhibition of lysosomal movements observed after phagocytosis. 330 28

Four male and two female Holstein-Friesian calves with segmental aplasia of the spinal cord were examined macroscopically and radiographically, and in some cases also histologically. External symptoms included inability to stand, deep depression of the body near the middle of the back but without any blemish in the skin, and slight reduction of the body length. Both hind limbs were almost normal. In every case segmental aplasia of the spinal cord was observed between the caudal thoracic and the cranial lumbar region. Owing to this defect, the vertebrae of that limited area consisted only of the body and the ribs fused on both sides. The sternum showed abnormal ossification at its caudal part. Other defects were observed such as kyphoscoliosis (six cases), polycystic kidney (one case), cryptorchidism (one case), and XX/XY chimerism (one case). From these findings it was apparent that this anomaly was uniquely different from the other two main spinal cord anomalies, spina bifida and perosomus elumbis. One conceivable pathogenesis of this rare anomaly, it was conjectured, is as follows: This anomaly results primarily from a segmental disorder of the neural tube, probably due to vascular problems, whereby a part of the spinal cord fails to develop properly from its normal genesis. Anomalous shapes of the vertebral column and ribs are perhaps secondary defects caused by aplasia of the spinal cord.
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PMID:Anatomical observation of six calves affected with segmental aplasia of the spinal cord. 344 55


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