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D N Das

Publications and source records attributed to D N Das.

9 recordsLinked to original sources
PubMed1995

Postmortem tissue samples: an alternative to urine and blood for drug analysis in racehorses.

Although urine is the sample of choice for drug tests in racehorses, it is rarely obtained following the sudden death of a racehorse on the track while racing. The purpose of this study was to demonstrate the significance of postmortem tissue samples as an alternative to urine and blood samples in equine drug analysis following the sudden death of a racehorse on the track while participating in a competitive race. Postmortem tissue samples were frozen (-80 degrees C) until analyzed. A 30-40-g portion of each organ was homogenized in a 0.1 M phosphate buffer (pH 7.4), deproteinized, hydrolyzed with beta-glucuronidase, extracted, and screened by thin-layer chromatography and immunoassay. Samples that initially tested positive for drug(s) were then extracted using high-flow, solid-phase extraction cartridges. The eluates were analyzed by gas chromatography-mass spectrometry. The presence of butorphanol in horses HB355 and CD387, pentobarbital in horse HO940, and ergotamine in horses HO940 and CD387 was detected and confirmed. Thus, in the absence of urine and blood samples following sudden death, postmortem tissue samples are equally useful for forensic toxicological investigations of racehorses.

Animals↗
PubMed1990

Age-associated changes in the components of atrioventricular conduction in apparently healthy volunteers.

The mechanism for the prolongation of P-R interval associated with advancing age is undefined. Using a high-resolution ECG (Marquette MAC-1) to signal average 512 cardiac cycles, we examined 185 healthy volunteers aged 20-83 years from the Baltimore Longitudinal Study of Aging with normal rest and exercise ECGs and a resting P-R interval less than 210 ms. Among the 161 subjects with visible His bundle activity, P-R interval increased with age (p less than .001). This increase was due entirely to prolongation of the interval between the P wave onset and His bundle potential, i.e., the P-H interval, (p less than .001) with no age-associated change in the H-V interval, p = NS. The P-H interval prolongation with age was localized to the P-R segment proximal to His bundle activation (p less than .001). In a separate group of 7 asymptomatic older men (mean age = 71 yr), with first-degree atrioventricular (A-V) block on standard ECG (mean PR = 238 +/- 14 ms), the P-H interval (193 +/- 21, vs 136 +/- 18 ms, p less than .001) and proximal P-R segment (82 +/- 19) vs 33 +/- 15 ms, p less than .001) but not the H-V interval (45 +/- 11 vs 40 +/- 9 ms, p = NS) were longer than in 25 age-matched men without A-V block. Thus, the modest age-associated prolongation of the P-R interval is localized to the proximal P-R segment, probably reflecting delay within the atrioventricular junction. A similar but more striking delay in the proximal P-R segment is responsible for first degree A-V block in apparently healthy older men.

Adult↗
PubMed1983

Right bundle branch block: long-term prognosis in apparently healthy men.

The long-term cardiac prognosis of 24 clinically healthy men with complete right bundle branch block, identified from the 1,142 men constituting the population of the Baltimore Longitudinal Study on Aging, was assessed over a follow-up period averaging 8.4 years. When compared with a control group matched for age at which right bundle branch block appeared (mean +/- standard deviation 64.0 +/- 13.5 years), men with right bundle branch block showed no difference in the prevalence of antecedent coronary risk factors or obstructive lung disease. The incidence of angina pectoris, myocardial infarction, valvular heart disease, cardiomegaly, congestive heart failure, advanced heart block or cardiac death in these men did not differ from that of the control group over the observation period. Furthermore, at the latest follow-up study, maximal aerobic exercise tolerance and chronotropic response to maximal exercise were not impaired in men with right bundle branch block relative to control men (9.1 +/- 2.2 versus 7.3 +/- 3.0 minutes and 150.3 +/- 23.5 versus 147.7 +/- 20.7 beats/minute, respectively). However, axis deviation leftward of -30 degrees was present in 46% of men with right bundle branch block but in only 15% of control subjects at latest follow-up (probability [p] less than 0.01). Although the PR interval lengthened by 40 ms or more developed in only 6% of control subjects over the observation period, such prolongation occurred in 29% of men with right bundle branch block (p less than 0.05). These results support the concept that right bundle branch block in these asymptomatic men is a manifestation of a primary abnormality of the cardiac conduction system but has no demonstrable adverse effect on long-term cardiac morbidity or mortality.

Aged↗
PubMed1969

Relations between coenzyme A and presumptive acyl carrier protein in different conditions of streptococcal growth.

Exploration of the specific role of cystine in the postexponential growth of Streptococcus faecalis led to an inquiry into the fate of cellular coenzyme A (CoA) and acyl carrier protein (ACP), both of which depend for their biosynthesis on cystine and pantothenate as precursors. In S. faecalis cells labeled by growth in the presence of (14)C-pantothenate, the label could be separated on the basis of solubility at pH 2.1 into two fractions of sharply differing metabolic characteristics. The fractions were not purified, but the soluble (14)C behaved analytically like CoA, and the insoluble (14)C was considered to represent an ACP-like entity on the basis of circumstantial evidence. The fate of these two fractions under various conditions of growth was studied. When the medium contained an excess of the needed precursors, the cellular content of CoA and ACP appeared to remain constant during exponential growth, and in a molar ratio of about 4 CoA to 1 ACP. Cellular ACP, once formed, appeared to be stable under these conditions, but CoA was degraded and replaced at the rate of approximately 20% per division period. With restrictive levels of pantothenate in the medium, initially formed CoA disappeared during growth, as a result, apparently of being converted to ACP. However, when the resulting CoA-depleted cells were returned to a medium containing enough pantothenate, resumption of normal growth was preceded by a lag period, during which rapid conversion of ACP to CoA appeared to take place.

Bacterial Proteins↗
PubMed1966

Pantothenate and coenzyme A in bacterial growth.

Toennies, G. (Temple University School of Medicine, Philadelphia, Pa.), D. N. Das, and F. Feng. Pantothenate and coenzyme A in bacterial growth. J. Bacteriol. 92:707-713. 1966.-The effect of environmental pantothenate levels on the growth of Streptococcus faecalis 9790 was studied in terms of growth rate, depletion phenomena, cellular coenzyme A (CoA) content, and differential rates of wall and membrane synthesis. Low concentrations of pantothenate yielded normal exponential growth curves up to peak turbidities which are a function of pantothenate concentration. Attainment of these peaks was followed by lysis. Under such conditions, bacterial CoA increased initially in proportion with cell substance, but attained a peak level much earlier than cell substance, and then gradually decreased down to vanishing amounts. With higher pantothenate concentrations, cellular CoA levels increased to a maximum, and, under these conditions, the CoA content remained constant during exponential growth. Four-fifths of the pantothenate requirement of growing cells was eliminated by environmental oleate and palmitate. When CoA disappeared during growth on low pantothenate levels, cell wall synthesis seemed to continue at nearly normal rates, but membrane synthesis was severely curtailed. The data suggest that in fermentative organisms pantothenate action might be confined to wall and membrane synthesis, that these two processes differ in their quantitative dependence on pantothenate, and that pantothenate might occur in the form of acyl carrier protein as well as CoA.

Cell Wall↗