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Biomedical subjects

R Mehra

Publications and source records attributed to R Mehra.

121 records · Page 7Linked to original sources

Effects of hormones on the synthesis of alpha 1 (acute-phase) glycoprotein in isolated rat hepatocytes.

Hormone effects on the synthesis of alpha(1) (acute-phase) glycoprotein and of albumin by isolated rat hepatocytes in suspension were examined. Insulin, glucagon, cortisol, somatotropin (bovine growth hormone) and tri-iodothyronine were added to achieve physiological concentrations in the medium [Jeejeebhoy, Ho, Greenberg, Phillips, Bruce-Robertson & Sodtke (1975) Biochem. J.146, 141-155]. After periodic additions, there were increases (compared with values for non-hormone-treated suspensions) in the concurrent absolute syntheses of alpha(1) (acute-phase) glycoprotein and of albumin. Trends were detectable after 24h, and significant increases were demonstrated after 48h of incubation (219 and 119% respectively of control values). Manipulation of hormones, by omission from the mixture or by addition of only one or two hormones in various combinations, indicated that for alpha(1) (acute-phase) glycoprotein (which may be representative of some other acute-phase proteins), cortisol was one of the most important hormones involved in the stimulation of synthesis, with glucagon enhancing the effect of cortisol but not being stimulatory by itself. Addition of actinomycin D inhibited this stimulation, suggesting that cortisol might have acted through promotion of RNA synthesis. For albumin, cortisol alone did not stimulate synthesis, but its absence from a hormone mixture significantly decreased synthesis compared with that observed with the complete hormone mixture. Our findings support the possibility that following tissue injury, synthesis of alpha(1) (acute-phase) glycoprotein may be stimulated by the hormonal response to this injury (which response includes elevated blood concentrations of cortisol and glucagon).

Albumins↗

Cardiac pacing and pacemakers II. Serial electrophysiologic-pharmacologic testing for control of recurrent tachyarrhythmias.

The place of pacemakers in the treatment of tachyarrhythmias has expanded far beyond the initial role in the brady-tachy syndrome, of providing a "minimum guaranteed rate" while medications suppress the tachycardia. Techniques have been developed for prevention, termination, and duplication of a patient's spontaneous tachycardia under safe catheterization laboratory conditions. Combined with accumulating information about the normal responses to electrophysiologic stresses, these techniques have led to a new dimension in arrhythmia control. Most tachycardias previously felt to be refractory can be controlled after serial electrophysiologic-pharmacologic testing, during which sequential pharmacologic and pacer regimens are tested until a combination is found which prevents induction of tachycardias, and/or a pace mode is found which reliably terminates the tachycardia. Use of such an approach reduces hospital admissions and referral for surgery, and eliminates prolonged hospitalization for assessment of therapy in patients with infrequent but potentially lethal spontaneous tachycardias.

Adolescent↗

Vulnerability of the mildly ischemic ventricle to cathodal, anodal, and bipolar stimulation.

We studied the difference between myocardial vulnerability to arrhythmias caused by cathodal, anodal, and bipolar stimulation in 29 dogs with partial right coronary artery occlusion. We used 2-msec duration stimuli of up to 8 mA to determine the ventricular vulnerable periods, their relationship to the refractory periods, and the fibrillation or multiple response thresholds for unipolar anodal and cathodal stimulation after two premature ventricular contractions. The vulnerable period for arrhythmias began at the end of the respective refractory periods and terminated at a specific time within the cardiac cycle. Within this period the arrhythmia and excitation thresholds were equal. Because shorter refractory periods were obtained with anodal stimulation than cathodal, the vulnerable periods for anodal stimulation were longer. This indicated that the vulnerable periods for bipolar stimulation also would be longer than for unipolar cathodal stimulation since bipolar and anodal refractory periods are equal when the cathode and anode are of similar surface area. Results from seven of the experiments showed that a dual focus of excitation, which can only occur with bipolar stimulation, did not make the ventricle more vulnerable to arrhythmias than did unifocal stimulation. These results indicate that the difference between the arrhythmia vulnerability to unipolar cathodal, anodal, and bipolar stimulation is dependent on the relationship between their excitability characteristics, i.e., their strength-interval curves.

Animals↗

Trends in neonatal outcome with low Apgar scores.

Trends in incidence and neonatal outcome following low Apgar scores (1 min Apgar score < 6) were prospectively studied during the years (1981, 1983, 1986 and 1988. The incidence of birth asphyxia was 7.6% of live births during the study period; it was 5.8% in 1981, increased to highest of 8.9% in 1986 with slight reduction to 7.2% in 1988. Birth weight distribution of asphyxiated babies and 1 min Apgar score < 3 (severe asphyxia) remained unchanged. A significant decline in neonatal mortality with asphyxia was noted from 46.0% to 28.4% during 1981 and 1988 respectively. Aetiological factors for asphyxia could be identified in nearly 90% of infants during 1988, and all but 2 of 12 factors studied registered significant differences from control non-asphyxiated group.

Apgar Score↗

Chlorambucil in the treatment of iridocyclitis in juvenile rheumatoid arthritis.

A patient with chronic, progressive, iridocyclitis secondary to pauciarticular juvenile rheumatoid arthritis (JRA) is described. The patient's iridocyclitis was unresponsive to topical, systemic, and subtenon injections of corticosteroids, but did respond to low doses of chlorambucil. The use of immunosuppressives may be indicated in severe, unresponsive iridocyclitis secondary to JRA.

Arthritis, Juvenile↗