Gene fusions involving the structural gene of B. licheniformis coding for a thermostable alpha-amylase.
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Biomedical subjects
Publications and source records attributed to D Levin.
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Spontaneous pneumothorax is a rare complication of pneumonia. Three cases of spontaneous pneumothorax in patients with Pneumocystis carinii pneumonia and acquired immunodeficiency syndrome are described. Two patients had bronchopleural fistulas. Local subpleural necrosis was felt to be the cause of the pneumothorax. Pneumothorax should be considered in patients with P carinii pneumonia who experience respiratory deterioration.
In an in vitro poliovirus replication system, purified viral polymerase, plus sense virion RNA, and a host factor have been previously shown to be necessary for the transcription of minus strands. We have found that a partially purified eukaryotic initiation factor-2 (eIF-2) fraction from rabbit reticulocytes can replace HeLa host factor in the replicase reaction. This enzyme preparation contains eIF-2 and two other major proteins. In addition to eIF-2 activity, which does not appear to play a role in the replicase reaction, we find that the fraction contains terminal uridylyl transferase activity. The enzyme adds UMP moieties to the 3' end of primer RNA molecules. The number of UMP residues added depends on the primer. Although long tails of heterogeneous lengths (50 to 100 nucleotides) can be polymerized on the 3' end of oligo(U), a poly(A) primer accepts only four U's. The terminal uridylyl transferase activity requires only UTP, Mg2+, a sulfhydryl reagent, and an RNA primer for activity. It is partially associated with ribosomes. We provide preliminary evidence that it may be responsible for host factor-like activity. We present a model for minus strand synthesis by poliovirus replicase, based on the hypothesis that a terminal uridylyl transferase can participate in initiation.
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We evaluated 48 patients with chronic obstructive pulmonary disease by means of pulmonary-function and exercise testing to determine whether any tests of pulmonary function could predict the development of arterial desaturation during exercise. We found that only two indexes--diffusing capacity and forced expiratory volume in one second (FEV1)--were predictive of desaturation. The diffusing capacity was more specific and sensitive than FEV1. A diffusing capacity above 55 per cent of predicted was 100 per cent specific in excluding desaturation, as compared with an 82 per cent specificity for an FEV1 above 55 per cent of predicted. With this cutoff point, the sensitivity of the diffusing capacity was 68 per cent, as compared with 46 per cent for the FEV1. Both the frequency and the magnitude of arterial desaturation increased substantially when the diffusing capacity was below 55 per cent of predicted. Testing the diffusing capacity should be useful in identifying which patients with chronic obstructive lung disease are likely to become desaturated during exercise and may therefore benefit from oxygen therapy.
Secondary components of visual evoked potentials (slow negative wave-SNW, and photically-evoked sensory after discharge-SAD) are known to be precursors of experimentally activated wave-spike discharges, similar to wave-spikes of petit mal epilepsy. Both SNW and SAD may be potently suppressed either by amphetamine or GABAergic compounds such as diazepam and sodium valproate. A hypothesis was tested in the present study, that amphetamine-induced suppression of wave-spike discharges may require GABA-benzodiazepine activity for its expression. Electrocortical activity was recorded and averaged in unrestrained albino rats with chronically implanted epicortical electrodes. SNW and SAD obtained in habituated rats in the predrug state were potently suppressed by amphetamine (1 mg/kg, i.p.). Fifteen minutes after amphetamine injection, a challenging drug (metrazol, picrotoxin, convulsant benzodiazepine, Ro 5-3663, or imidazodiazepine, Ro 15-1788) was administered intraperitoneally. Subconvulsive doses of metrazol (10 mg/kg) reversed amphetamine suppression; imidazodiazepine (20 mg/kg) and picrotoxin (1.5 mg/kg) reliably opposed the SNW suppression; convulsant benzodiazepine, Ro 5-3663 (2 mg/kg), showed modest and nonsignificant effect in the same direction. It is proposed that the antiepileptic potency of amphetamine may be associated with its ability, apparently via modulatory effect of norepinephrine, to facilitate the activation of benzodiazepine-GABA receptors.
Heme-deficiency and double-stranded RNA (dsRNA) activate distinct cyclic 3':5'-AMP independent protein kinases (HRI and dsI, respectively) in rabbit reticulocyte lysates. These kinases inhibit protein synthesis by phosphorylating the 38,000 daltons (38K) subunit of the initiation factor eIF-2 (eIF-2 alpha). Using separation techniques to obtain a reticulocyte enriched fraction and reticulocyte-free erythrocytes, we have prepared lysates of these fractions from normal human whole blood. Human reticulocyte-enriched lysates contain the hemin-regulated and dsRNA-dependent protein kinases which inhibit protein synthesis and which phosphorylate rabbit eIF-2 alpha. An endogenous 38K polypeptide which co-migrates with rabbit eIF-2 alpha is also phosphorylated. In contrast, human mature erythrocytes contain little or no heme-regulated or dsRNA-dependent eIF-2 alpha kinase activities which are inhibitory of protein synthesis.
Tail flick latencies (TFL) were examined in order to distinguish between rats from genetically high (HI) and low (LO) self-stimulation lines (LC2-HI and LC2-LO). In addition, slow secondary negative wave (SNW) of the visual evoked potential, which is considered to be a sensitive index of normal and pharmacologically-induced behavioral arousal, was analysed. Small, albeit statistically significant enhancement of SNW was obtained in LO rats. Unlike LO animals, HI rats gained in SNW amplitude during repeated photic stimulation. The difference between the lines was highly significant. TFL assessment yielded slightly reduced (NS) values for HI rats. However, when TFL and SNW data were compared it appeared that TFL vary as a function of SNW amplitude in LO but not in HI rats, (r = 0.9). SNW may be employed as a predictor of the nociceptive threshold in rats.
Visual evoked potentials (VEPs) were analyzed in order to distinguish between rats from genetically high (HI) and low (LO) self-stimulation lines (LC2-HI and LC2-LO). Secondary VEP components - slow secondary negative wave (SNW) and sensory afterdischarge (SAD) - which are considered to be most sensitive indices of normal and pharmacologically-induced behavioral changes, were used for the comparison. Small, albeit statistically significant enhancement of SNW and SAD was obtained in LO rats. Unlike LO animals, HI rats gained in SNW amplitude and SAD area during repeated photic stimulation. The difference being highly significant. D,L-Amphetamine (1 mg/kg, i.p.) suppressed SAD and reduced the SNW amplitude in both HI and LO animals, although the predrug difference in their values remained practically unaltered. Apomorphine (0.25, 2.75, 5.25 mg/kg i.p.) had no measurable effect on VEP parameters even though it caused a regular picture of dose-related enhancement of locomotion and stereotypy. The effect of amphetamine can, therefore, be attributed to the activation of the norepinephrinergic system. Correspondingly, VEP variance in the two lines of rats is interpreted as related to the peculiarities of norepinephrine modulation of neocortical activity.
Past research has attempted to delineate personality differences between insomniacs and good sleepers but has failed to control for type of insomnia or severity of the disorder. The purpose of this study was to compare MMPI scores of mild and severe sleep onset insomniacs with a control group of noninsomniacs . Results demonstrated that sleep onset insomniacs, regardless of degree of severity, differed significantly from noninsomniacs ; and that mild and severe insomniacs differed from each other on only one MMPI scale.
Measures of quality of life were obtained on 985 patients with mild hypoxemia and chronic obstructive pulmonary disease (COPD). A subsample of 100 patients were also given extensive neuropsychological and personality tests. Mildly hypoxemic COPD patients showed impairment in quality-of-life activities. They showed less impairment in physical function, compared with previous studies on COPD patients with hypoxemia, but about equal impairment in psychosocial function and dysphoric mood. Nonrelated health changes in life do not seem to account for these findings. Degree of self-reported tension-anxiety was the single greatest predictor of both physical and psychosocial measures of quality of life. Level of exercise completed, forced expiratory volume in 1 s, and neuropsychological status were significantly related to physical limitations, but not psychosocial functioning. The Pao2 was not significantly related to quality-of-life measures in this patient group.
The potential "anxiogenic" effects of convulsant benzodiazepine and GABA-antagonist, Ro 5-3663 and specific antagonist of benzodiazepine receptors, Ro 15-1788 were compared in the Geller-Seifter conflict paradigm. Chlordiazepoxide (CDP) (5 mg/kg) was used as a "positive" control. Both Ro 5-3663 (1 mg/kg) and Ro 15-1788 (10 mg/kg) antagonized the anticonflict effect of CDP. However, while Ro 15-1788 had a modest anticonflict potency. Ro 5-3663 had an anxiogenic effect in its own right.
The day-hospital concept had its beginning in the 1930s and has gained greater impact in recent years because of changes in public-health policy and in traditional psychiatric attitudes. The main therapeutic medium of day hospitals is based on an original concept combining treatment and readaptation in a specially designed therapeutic milieu. A therapeutic milieu is built according to a given theoretical approach. At the Geha Psychiatric Hospital in Petah Tiqva, Israel, the day-care department for adolescents is built according to a combination of the behaviorist and psychoanalytical approaches.
Whether hypertrophied cardiac muscle functions normally or abnormally is a point of controversy in the literature. Most animal studies showing depressed performance of hypertrophied cardiac muscle have used experimental methods in which hypertrophy was produced by acutely imposing a pressure overload on the left or right ventricle, which may cause myocardial injury. To assess the possibility that chronic, slowly developing hypertrophy is associated with normal myocardial function, we developed an experimental model in which increased afterload is imposed gradually on the left ventricle in the dog. A snug band was placed around the aorta beneath the left coronary artery in puppies without producing a stenosis. As the puppies grew, relative aortic stenosis developed as increased cardiac output flowed across that fixed outflow area. One group (group A) of six puppies was banded early, whereas a second group (group B, five puppies) was banded late and served as controls. Left ventricular weight (g) to body weight (kg) ratio remained normal in group B animals (3.9 +/- 0.14), whereas this ratio was increased to 5.3 +/- 0.24 (P < 0.001) in group A animals indicating development of moderate cardiac hypertrophy. Ejection fraction, dP/dt, Vcf, and stroke work per gram of myocardium were virtually identical in both groups. We conclude that moderate, gradually developing cardiac hypertrophy as produced by this model is associated with normal myocardial contractile performance.
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