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Biomedical subjects

G Das

Publications and source records attributed to G Das.

At least 127 records · Page 7Linked to original sources
PubMed1985

Characterization of a surrogate TATA box promoter that regulates in vitro transcription of the simian virus 40 major late gene.

The presence of a surrogate TATA box sequence located ca. 30 nucleotides upstream of the major late RNA start site at nucleotide position (np) 325 (Brady et al., Cell 31:625-633, 1982) has been confirmed, and its structural specificity has been determined by the generation of additional base substitution mutations at the KpnI restriction site (np 294) in cloned simian virus 40 DNA. Two mutants generated new RNA initiation sites upstream of the np 325 start site and continued to utilize the authentic start site, but with decreased efficiency. The replacement of either one or both cytosines by thymines at np 298 and np 299 specifically enhanced in vitro transcription from the np 325 start site by 430 and 800%, respectively. This enhancement was due to conversion of the simian virus 40 late promoter present in the wild-type virus to a sequence that is similar to the TATA box present in the simian virus 40 early promoter.

Base Sequence↗
PubMed1984

Reduction of digoxin effect during the digoxin-quinidine interaction.

The effects of the digoxin-quinidine interaction on cardiac function was examined in healthy subjects. Our results indicate that while serum digoxin levels were elevated, the improved cardiac function due to digoxin declined during combined therapy. Our data also provide an alternate explanation for the changes previously interpreted as "enhanced digitalis effects" during the interaction.

Adult↗
PubMed1984

Pacemaker headaches.

A symptom complex (pacemaker syndrome) consisting of hypotension, dizziness, or near-syncope in patients with functioning ventricular pacemakers has been previously described. Whereas, the effects of synchronized ventriculo-atrial contraction on forward systemic circulation are known, the effects of increased venous dynamics on systemic function are not known. We describe a patient who developed severe headaches during periods of ventricular pacing with retrograde ventriculo-atrial conduction. These headaches occurred in the absence of symptoms of Pacemaker syndrome or of changes in systemic blood pressure. We believe that the headaches were caused by alterations in intracranial pressure from exaggerated pulsatile venous dynamics. Conversion of the pacing system from VVI to AV sequential pacing completely relieved the headaches.

Adult↗
PubMed1984

Simian virus 40 major late promoter: an upstream DNA sequence required for efficient in vitro transcription.

We have previously identified an 11-base DNA sequence, 5'-G-G-T-A-C-C-T-A-A-C-C-3' (simian virus 40 [SV40] map position 294 to 304), which is important in the control of SV40 late RNA expression in vitro and in vivo (Brady et al., Cell 31:625-633, 1982). We report here the identification of another domain of the SV40 late promoter. A series of mutants with deletions extending from SV40 map position 0 to 300 was prepared by nuclease BAL 31 treatment. The cloned templates were then analyzed for efficiency and accuracy of late SV40 RNA expression in the Manley in vitro transcription system. Our studies showed that, in addition to the promoter domain near map position 300, there are essential DNA sequences between nucleotide positions 74 and 95 that are required for efficient expression of late SV40 RNA. Included in this SV40 DNA sequence were two of the six GGGCGG SV40 repeat sequences and an 11-nucleotide segment which showed strong homology with the upstream sequences required for the efficient in vitro and in vivo expression of the histone H2A gene. This upstream promoter sequence supported transcription with the same efficiency even when it was moved 72 nucleotides closer to the major late cap site. In vitro promoter competition analysis demonstrated that the upstream promoter sequence, independent of the 294 to 304 promoter element, is capable of binding polymerase-transcription factors required for SV40 late gene transcription. Finally, we show that DNA sequences which control the specificity of RNA initiation at nucleotide 325 lie downstream of map position 294.

Base Sequence↗
PubMed1983

Radiation-sensitive mutant of hypertoxinogenic strain 569B of Vibrio cholerae.

A radiation-sensitive mutant of the hypertoxinogenic strain 569B of Vibrio cholerae was isolated and characterized. The mutant, designated V. cholerae 569Bs, lacks both excision- and medium-dependent dark-repair mechanisms of UV-induced DNA damage while retaining the wild-type photoreactivating capability. Analysis of the UV-irradiated cell DNA by velocity sedimentation in alkaline sucrose gradient suggests that UV-induced pyrimidine dimers may not be incised in these cells. In contrast to the wild-type cells, the mutant cell DNA was degraded after treatment with nalidixic acid. The mutant cells failed to produce any detectable amount of cholera toxin as measured by ileal-loop assay.

Bacteriophages↗
PubMed1983

Repair of ultraviolet light-induced DNA damage in cholera bacteriophages.

DNA repair-proficient and -deficient strains of Vibrio cholerae were used to examine host cell reactivation, Weigle reactivation and photoreactivation of u.v.-irradiated cholera bacteriophages. U.v. light-induced DNA damage in phages of different morphological and serological groups could be efficiently photoreactivated. Host cell reactivation of irradiated phages of different groups was different on the same indicator host. Phage phi 149 was the most sensitive, and phi 138 the most resistant to u.v. irradiation. While phi 138 showed appreciable host cell reactivation, this was minimal for phi 149. Attempts to demonstrate Weigle reactivation of u.v.-irradiated cholera phages were not successful, although u.v.-induced filamentation of host cells was observed.

Bacteriophages↗
PubMed1982

Site-specific base substitution and deletion mutations that enhance or suppress transcription of the SV40 major late RNA.

Transcriptional analysis of SV40 late promoter mutants indicates that the DNA sequence 5'-GGTACCTAACC-3' (map positions 294-304) is important in the control of SV40 late RNA expression. C to T base substitutions at map positions 298, 299 and 304 increased initiation of late RNA synthesis at map position 325 five to ten fold. G to A base substitutions at map positions 294 and 295 decreased RNA initiation by a factor of 2 to 3. Deletion of nucleotides 295-298 reduced RNA initiation by a factor of 4 to 5. S1 analysis of in vivo RNA, isolated 24-36 hr after infection, demonstrated that the four base deletion not only decreased RNA initiation at nucleotide 325, but also increased RNA initiation at three alternate sites located approximately 125 nucleotides upstream from the major late RNA initiation site.

Base Sequence↗
PubMed1982

Digoxin-quinidine interaction in unanesthetized guinea pigs.

The clinically relevant interaction between quinidine (3 mg/kg) and digoxin (0.6 mg/kg plus 20 microCi 3H-digoxin) was investigated using unanesthetized and unrestrained guinea pigs for in vivo pharmacokinetic and tissue disposition studies. Quinidine caused a significant elevation of plasma levels of digoxin as early as 5 min after injection, and the increase persisted for at least 8 h. A significant decrease in the volume of distribution for digoxin from 3.6 to 2.7 liters/kg (20%) was observed in quinidine-treated animals. No change was noted in the dominant elimination half-life of digoxin in quinidine-treated animals. The decreased volume of distribution appeared to be due to displacement of digoxin from tissue stores by quinidine as evidenced by decreased tissue to plasma ratios for kidney (41%), intestine (41%), fat (33%), lung (31%), left ventricle (27%), liver (24%), left atrium (22%), right ventricle (21%), right atrium (18%), pancreas (12%), and bladder (-4%) samples.

Animals↗
PubMed1981

Repair of ultraviolet-light-induced DNA damage in vibrio cholerae.

Repair of ultraviolet-light-induced DNA damage in a highly pathogenic Gram-negative bacterium, Vibrio cholerae, has been examined. All three strains of V. cholerae belonging to two serotypes, Inaba and Ogawa, are very sensitive to ultraviolet irradiation, having inactivation cross-sections ranging from 0.18 to 0.24 m2/J. Although these cells are proficient in repairing the DNA damage by a photoreactivation mechanism, they do not possess efficient dark repair systems. The mild toxinogenic strain 154 of classical Vibrios presumably lacks any excision repair mechanism and studies of irradiated cell DNA indicate that the ultraviolet-induced pyrimidine dimers may not be excised. Ultraviolet-irradiated cells after saturation of dark repair can be further photoreactivated.

DNA Repair↗
PubMed1981

Natural history of electrical interventricular septal force in the course of left ventricular hypertrophy in man.

Initial electrical forces emanating from interventricular septal depolarization, being directed to the right and anteriorly, normally produce an initial negative deflection or Q wave in leads I, aVL and V6 and an initial positive deflection or R wave in leads V1 and V2. The observations of hypertrophied interventricular septum, an integral part of the left ventricle, in patients with left ventricular hypertrophy would predict an increase in these septal electrical forces similar to the total left ventricular (QRS) forces in these subjects. Contrary to this expectation, several studies document an actual decrease or absence of the normally oriented initial forces in ECGs of patients with the criteria of left ventricular hypertrophy. In order to clarify the nature of this paradox, this study was initiated. Our observations suggest that the normal initial septal forces indeed increase as expected, during the initial four to six years, and subsequently show a progressive decline in patients with left ventricular hypertrophy. Although the precise mechanism for the bimodal change in the septal forces during the period of the constancy of the total QRS forces is not clear, a hypothesis based on the current knowledge is advanced to explain these observations.

Adult↗
PubMed1981

Pacemaker malfunction following transthoracic countershock.

Electrical cardioversion or defibrillation may be necessary in patients with implanted artificial cardiac pacemakers. Sudden discharge of high electrical energy employed in DC transthoracic countershock procedures may damage the sensitive pacemaker circuitry and result in malfunction. We report a case in which, following synchronized DC countershock, a non-programmable demand pacemaker functioned in the R-wave triggered mode rather than the R-wave inhibited mode as designed. Further, the pacemaker output voltage was reduced to about half its specified output. Such a malfunction may not be readily apparent, and requires careful analysis following electric shock.

Aged↗
PubMed1978

Atrial pacing for cardioversion of atrial flutter in digitalized patients.

To test the safety and reliability of atrial pacing as a conversion technique in patients with atrial flutter who are receiving digitalis therapy, atrial pacing conversion was attempted for 49 episodes of atrial flutter in 32 consecutive patients. All patients except one were receiving digitalis. To control ventricular rates most patients had received larger than usual therapeutic doses of digitalis glycoside before pacing. Fourteen of the 25 patients whose serum levels were measured had glycoside concentrations greater than 2 ng/ml. Before atrial pacing the mean atrial and ventricular rates were, respectively, 290 +/- 20.6 and 134 +/- 27.9/min (mean +/- standard deviation). Successful rhythm conversion was achieved on 48 occasions (98%) in 31 patients. One patient required transthoracic direct current synchronized countershock cardioversion. With atrial pacing, the atrial flutter rhythm reverted immediately to sinus mechanism in 23 instances, and there were 25 episodes of atrial fibrillation. Among those who experienced atrial fibrillation, the rhythm spontaneously reverted to sinus mechanism within 24 hours on 14 occasions; on 11 occasions; the rhythm reverted to atrial flutter and repeat pacing was required. Sinus mechanism was eventually established in all 31 patients.

Adult↗
PubMed1977

Can angiography stage renal carcinoma?

We have compared the staging of renal carcinomas in 36 patients as judged preoperatively by angiography (T stage) and postoperatively by histopathology (P stage). Using the standard abdominal aortogram and selective renal arteriogram we found a considerable error rate in T staging (40%). The commonest error was preoperative overstaging, and this is probably determined by the behaviour of renal carcinoma, rather than by inadequate angiography. We conclude that whilst renal arteriography remains a useful diagnostic aid, it cannot answer questions on tumour extent with any accuracy. Staging by histopathology is essential for proper assessment and management of these patients.

Angiography↗
PubMed1977

Echocardiographic manifestations of ruptured aortic valvular leaflets in the absence of valvular vegetations.

The diagnosis of ruptured (perforated or torn) aortic valvular leaflets due to various causes has been made primarily at surgery or postmortem examination. Although angiocardiographic studies readily reveal aortic regurgitation, they rarely establish the presence of a ruptured aortic cusp as the cause of the aortic leak. Recent echocardiographic experience has brought to our attention seven patients with ruptured aortic valvular leaflets in whom the absenc of valvular vegetations was confirmed at surgery in six and at autopsy in one. The echocardiogram of the aortic root in these subjects revealed little or no increment in the diameter of the aortic root. In systole the usual box-like configuration of the leaflets, similar to that observed in normal subjects, was seen; however, in diastole the normal thin midaortic linear echoes were replaced by a thick band of echoes which often revealed high-frequency oscillations. In addition, high-frequency fibrations of the anterior mitral leaflet in diastole and increased systolic excursion of the interventricular septum and left ventricular posterior wall were observed.

Adult↗