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Biomedical subjects

G Singh

Publications and source records attributed to G Singh.

At least 181 records · Page 10Linked to original sources
PubMed2000

Enlarging single CT lesions can also spontaneously resolve.

Computed tomography in two patients, aged 9 and 14 years, with history of focal seizures, revealed single, small, enhancing CT lesions. These patients were treated with albendazole and anticonvulsants. Follow-up CT scans revealed an increase in the size of the solitary lesions. They were managed conservatively and further follow-up CT scans revealed complete resolution of the lesions. The report suggests that some enlarging CT lesions may also spontaneously resolve. The most likely cause of the enlarging lesions was albendazole therapy.

Adolescent↗
PubMed2000

Recent advances in chromosome breakage syndromes and their diagnosis.

Chromosome instability is a characteristic cytogenetic feature of a number of genetically determined disorders collectively called as the chromosome breakage syndromes or DNA-repair disorders. They are characterized by susceptibility to chromosomal breakages, increased frequency of breaks and interchanges occurring either spontaneously or following exposure to various DNA-damaging agents. These diseases are a group of genetic disorders sharing a number of features. They are all autosomal recessive, show an increased tendency for chromosomal aberrations and to develop malignancies. The principal diseases in this group having a diverse etiology and clinical manifestations include Fanconi anemia (FA), ataxia telangiectasia (AT), Nijmegen breakage syndrome (NBS), Bloom syndrome (BS), xeroderma pigementosum (XP), Cockayne syndrome (CS) and trichothiodystrophy (TTD). The underlying defect in these syndromes is the inability to repair a particular type of DNA damage. A number of repair disorder phenotypes are caused by more than one gene. The diagnosis of these syndromes is made by the characteristic clinical features specific to each disease, but the definitive diagnosis is achieved by laboratory investigations such as cytogenetic, biochemical and molecular methods. The importance of prenatal diagnosis and our experience are discussed in this article.

Ataxia Telangiectasia↗
PubMed2000

Effect of intraamniotic vitamin A on palatal closure of fetal rats.

On day 15 of gestation, intraamniotic vitamin A in a dose of 150 IU was administered to the fetal rats to examine its effect on palatal closure. Fetuses subjected to only amniocentesis acted as control for the study. The fetuses were recovered on day 19, 20 and 21, respectively. Vitamin A resulted in poor development of palatine shelves. There was no clear demarcation of the base and the free margins of the shelves were either rounded or blunted with poor attempt towards closure. In the vitamin A group, the incidence of cleft palate were similar in all three days while there was a gradual decline with increasing gestational age in the amniocentesis group. The results suggest that unlike amniocentesis, in vitamin A treated fetuses, there was no attempt towards a delayed closure of the palate.

Amniocentesis↗
PubMed2000

Serial neuro-electrophysiological studies in acute organophosphate poisoning--correlation with clinical findings, serum cholinesterase levels and atropine dosages.

OBJECTIVES AND METHODS: A prospective evaluation of the correlation between the serial clinical findings, serum cholinesterase levels, electrodiagnostic abnormalities and the daily atropine requirement was undertaken in 29 patients with confirmed acute organophosphate poisoning (OPP). RESULTS: Clinical weakness conforming to the pattern found in 'Intermediate Syndrome' was noted in 19 patients (65.55%). It was associated with all types of organophosphate compounds and occurred in all patients in whom the serum cholinesterase on admission was less than 200 units. Three types of electrodiagnostic abnormalities were noted: single supramaximal electrical stimulus induced repetitive response, a decrement--increment response to 30 Hz repetitive nerve stimulation (RNS) and a decremental responses to 30 Hz RNS. The 30 Hz decremental response correlated best with the presence of clinically detectable weakness (sensitivity = 61.72%; specificity = 81.54%; positive predictive value = 73.91%; negative predictive value = 71.62%). Time trends evaluation revealed that the peak daily atropine dosages were given at a mean of 1.76 +/- 0.83 days in comparison to a mean nadir of serum cholinesterase of 2.48 +/- 1.97 days and a mean nadir of 9:1 ratio of 2.65 +/- 1.76 days. The 2-tailed correlation coefficient analysis and simple regression analysis revealed a positive correlation between serum cholinesterase levels and the 9:1 ratios (correlation coefficient: 0.59). A negative correlation was observed between the 9:1 ratios and the daily atropine requirement (correlation coefficient: -0.57) and between serum cholinesterase levels and daily atropine requirement (correlation coefficient: -0.49). CONCLUSIONS: At admission, level of serum cholinesterase of less than 200 units is a predictor and the 30 Hz RNS decremental response could be a useful marker for the 'Intermediate Syndrome'.

Acetylcholinesterase↗
PubMed2000

Profile of hypertension in elderly subjects.

OBJECTIVE: To study clinical profile of hypertension in elderly subjects. METHODS: Two hundred and five consecutive subjects aged 60 years and above reporting to preventive cardiology clinic with cardiovascular disorders were studied. One hundred fifty six subjects (76.09%) were found to have essential hypertension (HTN). Newly detected hypertensives were classified as per JNC-VI classification. Detailed clinical examination and laboratory investigations were carried out to find evidence of associated ailments with HTN. RESULTS: Most of the patients belonged to 60-70 years age group. Mean age was 67.36 +/- 6.23 years (range 60 to 90 years) and male to female ratio was 1.44:1. Out of hypertensives 99 (63.46%) had HTN for long period, while 28 (17.94%), 17 (10.89%) and 12 (7.67%) belonged to mild, moderate and severe HTN categories, respectively. Out of newly detected hypertensives 14 (24.56%) were having isolated systolic HTN. Associated clinical conditions in hypertensives were coronary artery disease (CAD), non-insulin dependent diabetes mellitus (NIDDM), cerebrovascular disease (CVD), left ventricular hypertrophy (LVH) and chronic obstructive pulmonary disease (COPD) in 69 (57.05%), 49 (31.41%), 37 (23.71%), 20 (12.80%) and 10 (6.4%) subjects, respectively. HTN alone was found in 31 (19.87%) subjects only. Since most of these patients had other concomitant illnesses such as CAD. NIDDM etc. therapy was initiated accordingly. Four (20%) patients with LVH died within short period of 1 to 12 weeks. CONCLUSION: HTN is the commonest cardiovascular disorder in elderly subjects. CAD, NIDDM and CVD are commonly associated clinical conditions. Patients with associated LVH have very high short term mortality.

Age Distribution↗
PubMed1999

A validated stable isotope dilution liquid chromatography tandem mass spectrometry assay for the trace analysis of cocaine and its major metabolites in plasma.

A validated method has been developed for the simultaneous quantitation of cocaine and its major metabolites (ecgonine methyl ester, benzoylecgonine, and norcocaine) in rat plasma. The method is based upon the use of stable isotope dilution liquid chromatography/atmospheric pressure chemical ionization/tandem mass spectrometry. Previously reported methods do not have the sensitivity and specificity that can be attained with this method. Plasma samples required no cleanup apart from protein precipitation, and no derivatization was required. Selected reaction monitoring was performed on the transitions of m/z 200 to m/z 182 (ecgonine methyl ester), m/z 290 to m/z 168 (benzoylecgonine), m/z 304 to m/z 182 (cocaine), and m/z 290 to m/z 168 (norcocaine). The standard curves were linear over the range from 2 ng/mL (benzoylecgonine, cocaine, and norcocaine) or 5 ng/mL (ecgonine methyl ester) to 1000 ng/mL in rat plasma. The lower limit of quantitation (LLQ) for benzoylecgonine, cocaine, and norcocaine was 2 ng/mL, and for ecgonine methyl ester, the LLQ was 5 ng/mL for plasma. This simple, rapid, reliable, and sensitive method of quantitation had excellent accuracy and precision for the four analytes. The method was sensitive enough to permit a detailed study of the pharmacokinetics of cocaine and its metabolites after administration of a bolus intravenous dose to rats.

Animals↗
PubMed1999

Comparison of the effectiveness of adenovirus vectors expressing cyclin kinase inhibitors p16INK4A, p18INK4C, p19INK4D, p21(WAF1/CIP1) and p27KIP1 in inducing cell cycle arrest, apoptosis and inhibition of tumorigenicity.

Cell cycle regulatory proteins are important candidates for therapeutic tumour suppressors. Adenovirus vectors were constructed to overexpress cyclin kinase inhibitors p16INK4A, p18INK4C, p19INK4D, p21(WAF1/CIP1) and p27KIP1 under the control of the murine cytomegalovirus immediate early gene promoter. These vectors directed the efficient expression of each of the cyclin kinase inhibitors and induced growth arrest, inhibited DNA synthesis, and prevented phosphorylation of the retinoblastoma protein (pRb) in cell lines expressing functional pRb. In pRb-deficient cells, expression of the cyclin kinase inhibitors was not effective in inhibiting DNA replication or growth arrest. Interestingly, three of the cyclin kinase inhibitors, p16, p18 and p27 were found to induce apoptotic death in transduced HeLa and A549 cells. When the vectors were tested for their ability to inhibit tumorigenicity in a polyomavirus middle T antigen model of murine breast carcinoma, expression of the cyclin kinase inhibitors resulted in a delay in tumour formation that varied from several weeks for the p19 expressing vector to greater than 25 weeks for the p27 expressing vector. When tumours were injected directly with the adenovirus vectors expressing the cyclin kinase inhibitors, only treatment with the vector expressing p16 resulted in a delay in tumour growth.

Adenocarcinoma↗
PubMed1999

Metallothionein expression and nuclear size in benign, borderline, and malignant serous ovarian tumours.

Metallothioneins (MTs) are low-molecular-weight proteins involved in metalloregulatory functions such as cell proliferation, growth, and differentiation. In recent years, MT expression has been linked with carcinogenesis, resistance to cancer therapy, and tumour progression. However, the significance of MT expression in ovarian cancers is at present inadequately documented. In this study, MT immunohistochemistry was performed in 12 benign, 14 borderline, and eight malignant serous tumours of the ovary. The intensity of the immunostaining was evaluated by image analysis. There was a significantly higher number of MT-immunopositive cells in the multilayered epithelial cells of borderline serous tumours (atypical proliferative serous tumours) than in the single layered epithelial cells within the same tumour, and in the single cell layer of benign serous tumours. There was no difference in the expression of MTs in the single layered tumour cells of benign and borderline serous tumours. Significantly higher numbers of MT-immunopositive cells were observed in both the single and the multilayered epithelial cells of serous carcinomas, the highest number being observed in the multiple layers of serous carcinomas. The positively stained malignant tumour cells in both single and multiple layers were larger than the negatively stained cells in benign, borderline, and malignant serous ovarian tumours. There was moderate to intense staining. These findings indicate that there is increased expression of MTs in the progression of malignancy, which could be used as a marker in grading the three groups of ovarian serous tumours and for determining prognosis.

Adult↗
PubMed1999

Neuromuscular transmission failure due to common krait (Bungarus caeruleus) envenomation.

Neurophysiological studies were performed in 12 patients with neuromuscular paralysis due to envenomation by the common krait (Bungarus caeruleus). All patients presented with an acute, reversible, oculofaciobulbar paresis. In addition, 7 patients had weakness of the limb muscles and 4 required assisted mechanical ventilation. Neurophysiological abnormalities included: (1) a reduction in the amplitude of the median-elicited compound muscle action potential (CMAP) in 4 patients; and (2) a decremental response (>10%) to 3-Hz repetitive nerve stimulation (RNS) in 4 patients. With 1 exception, these abnormalities were noted only in clinically weak muscles. The administration of edrophonium to 6 patients produced an insignificant increase in CMAP amplitudes as well as partial (not significant) improvement in the decremental response to 3-Hz RNS. Neurophysiological studies were performed in 2 patients before and after the administration of 20 mL of polyvalent antivenom. A decrease in amplitude of the median-elicited CMAP amplitude occurred after the administration of antivenom. In 1 patient, administered 100 mL of antivenom, the median-elicited CMAP amplitude increased and the decrement to 3-Hz RNS decreased. Neurophysiological studies can provide useful information regarding the nature, severity, and therapy of the neuroparalytic syndrome of krait envenomation.

Adolescent↗
PubMed1999

Changes in mitochondrial mass, membrane potential, and cellular adenosine triphosphate content during the cell cycle of human leukemic (HL-60) cells.

Oxidative phosphorylation within the inner mitochondrial membrane generates the majority of cellular adenosine triphosphate (ATP) required for normal physiological functions (including regulation of cell volume and solute concentration, maintenance of cellular architecture, and synthesis of essential macromolecules). Its efficient functioning depends on the maintenance of an electrochemical gradient and is tightly coupled to the energetic demands of the cell and/or tissue. Commitment to and completion of the cell division cycle are sensitive to changes in the availability of mitochondrially derived ATP, although the relationship between cell cycle and mitochondrial physiology is poorly understood. Using vital, mitochondrial-specific fluorochromes to differentiate between mitochondrial mass (10-N-nonyl acridine orange) and mitochondrial membrane potential (Rhodamine 123), together with a quantification of total cellular ATP levels, it was possible to generate profiles of these mitochondrial characteristics in HL-60 cells at different stages of their cell cycle. The data suggest that the availability of ATP changes in a cell cycle-specific manner and cannot be predicted by changes in mitochondrial mass or membrane potential. Furthermore, transition points in the cell cycle where ATP availability is low with respect to the amount of functional inner mitochondrial membrane have been observed. We suggest that these cell cycle phase transitions are sensitive to inhibition of mitochondrial activity because the basal levels of available ATP at these points are nearer to a theoretical "minimal threshold" below which cell cycle progression is inhibited.

Adenosine Triphosphate↗
PubMed1999

Regulation of prostate cancer cell division by glucose.

Previous studies have shown that rapid cell proliferation is associated with elevated glucose consumption. However, those studies did not establish whether glucose is required for prostate cancer cell proliferation or define the molecular mechanisms by which glucose regulates cell division. We addressed these issues by studying two metastatic human prostate cancer cell lines: DU145, which is androgen independent and highly proliferative; and LNCaP, which is androgen dependent and relatively slow growing. We found that proliferation of DU145 cells was significantly inhibited by reduction of glucose in the medium to 0.5 g/L, which is half the physiologic concentration, whereas LNCaP cells grew at control rates even in the presence of only 0.05 g/L glucose. Glucose deprivation of DU145 cells caused a 90% reduction in DNA synthesis; a 10-20-fold reduction in cyclins D and E and CDK4 levels; and cell cycle arrest in G0-G1. However, glucose deprivation did not cause global inhibition of protein synthesis, since mutant p53 levels increased in glucose-deprived DU145 cells. This observed increase in mutant p53 levels was not associated with a rise in p21 levels. Glucose deprivation of DU145 cells also led to apparent dephosphorylation of mutant retinoblastoma (RB) protein. We conclude that: 1) high levels of glucose consumption are required for rapid proliferation of androgen-independent prostate cancer cells, 2) glucose may not be required for slow growth of androgen-dependent prostate cancer cells, and 3) glucose promotes passage of cells through early G1 by increasing the expression of several key cell cycle regulatory proteins that normally inhibit RB function.

Adenosine Triphosphate↗