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S Ray

Publications and source records attributed to S Ray.

At least 199 records · Page 11Linked to original sources
PubMed1994

1-beta-D-arabinofuranosylcytosine-, mitoxantrone-, and paclitaxel-induced apoptosis in HL-60 cells: improved method for detection of internucleosomal DNA fragmentation.

We investigated the ability of different doses and durations of exposure to the chemotherapeutic drugs 1-beta-D-arabinofuranosylcytosine (Ara-C), mitoxantrone (MTN), and paclitaxel (taxol, TXL) to induce internucleosomal DNA fragmentation and apoptosis in human acute myeloid leukemia (AML) HL-60 cells in suspension culture. At clinically achievable concentrations, all three drugs have been shown to induce apoptosis in HL-60 cells. An improved method was developed for the isolation of pure genomic DNA and the detection of drug-induced internucleosomal DNA fragmentation in < 1.0 microgram of DNA sample by agarose gel electrophoresis. Morphologic evidence for apoptosis was determined by light microscopy following Wright staining, and cell viability was assessed by trypan blue dye exclusion. Internucleosomal DNA fragmentation was observed following exposure to 1.0 microM Ara-C for 4 h, which increased with 10 and 50 microM Ara-C. Incubation with 100 microM Ara-C produced internucleosomal DNA fragmentation starting at 3 h, which increased with longer periods of exposure to Ara-C. Utilizing a schedule of 1-h exposure followed by 3-h suspension in drug-free medium, 0.25 microM MTN was found to initiate DNA fragmentation, which increased with exposure to 1.0 and 5.0 microM MTN. However, identical treatment with higher concentrations of MTN resulted in random DNA degradation. Alternatively, continuous exposure to 1.0 microM MTN for 3 h was necessary to initiate internucleosomal DNA fragmentation. This increased with exposure intervals of up to 6 h. Exposure to TXL concentrations as low as 0.01 microM for 24 h caused internucleosomal DNA fragmentation, which increased with dose escalation (0.05, 0.1, 0.5, and 1.0 microM) of TXL. Although continuous exposure to 1.0 microM TXL for a period as short as 8 h produced internucleosomal DNA fragmentation, this increased significantly with longer exposure intervals. In general there appears to be a threshold concentration and duration of exposure below which none of these three drugs activates endonucleolytic internucleosomal DNA fragmentation and apoptosis. This threshold is lower for the DNA-interactive drugs MTN and Ara-C but higher for the non-DNA-interactive drug TXL. Higher doses or prolonged treatments with the drugs produce random DNA fragmentation associated with necrotic cell death. These in vitro results may further improve our understanding of the antileukemic cytotoxic effects of these drugs, which may enable a more rational design of drug regimens for optimal treatment of AML.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1994

Infarct-related heart failure: the choice of ACE inhibitor does not matter.

Angiotensin converting enzyme (ACE) inhibitors are effective across the whole spectrum of heart failure from mild to severe but there are little data on the use of ACE inhibitors specifically in patients with postinfarct heart failure. Pharmacological properties that might potentially be relevant to the choice of drug after myocardial infarction include differences in metabolism, possession of a sulphydryl group, tissue binding, duration of action, and side effect profile. Of these duration of action is probably the most important, as longer acting drugs generally cause more prolonged first-dose hypotension that shorter acting agents and first-dose hypotension is a particular concern in the early postinfarct period. In the SAVE study captopril was effective in reducing mortality and delaying the onset of symptomatic heart failure after myocardial infarction. Similarly, ramipril reduced mortality in the AIRE study. In contrast, enalapril was largely ineffective in CONSENSUS II. These differences result largely from study design and do not indicate an inherent superiority of captopril or ramipril over enalapril. Nonetheless, a short-acting agent should probably be used for the initial dose in postinfarct heart failure to minimize the risks of prolonged hypotension. This aside, the choice of agent is far less important than appropriate patient selection and appropriate maintenance dosages.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1994

The effect of water on polymer matrix and composite wear.

OBJECTIVES: Previous studies have demonstrated increased in vitro wear of composite after long-term water exposure. The increased wear effect was not clearly related to debonding of the filler from the matrix, resulting in accelerated loss of filler particles. The hypothesis tested in this experiment was that the changes in in vitro three-body wear of a composite following water storage are caused by changes in the wear resistance of the polymer matrix. METHODS: In the in vitro wear test used, a specimen wheel was rotated against an antagonist wheel in a slurry of millet seed and water. Specimens were fabricated of composite and polymer matrix only. Specimens were wear tested after 1 wk of ambient temperature dry storage and after 14, 20, and 26 mon of water storage at 37 degrees C. RESULTS: The wear of the composite significantly increased (23%) during the 26 mon of water storage. The wear of the polymer specimens increased slightly; however, the increase was not statistically significant. SIGNIFICANCE: Analyses of the data using a series model for the wear of a composite indicated that the increase in wear of the composite was not due to changes in the wear resistance of the polymer matrix. Instead, the increased composite wear was more likely due to increases in the dislodgment rate of filler particles and the wear rate of the filler itself.

Analysis of Variance↗
PubMed1994

The association of tuberculosis and HIV infection in Harare, Zimbabwe.

SETTING: The tuberculosis (TB) service responsible for all TB treatment in Harare, Zimbabwe. OBJECTIVES: (1) To determine HIV seroprevalence among TB patients and controls. (2) To compare clinical and demographic characteristics of HIV-infected and uninfected TB patients. DESIGN: Cohort study. Entry criterion: TB diagnosed during the 18 month study period. Assessment included HIV serology. Matched community controls were HIV serotested. RESULTS: In 1434 TB patients tested, HIV seroprevalence was 48% in men and 44% in women, peaked in the 25-34 year age group and was higher than in controls (relative risk [RR] = 3.1, 95% confidence interval [CI] = 2.6-3.7). In adults, seroprevalence was 34%, 49% and 58% in successive 6 month periods. A history of entry of prior TB treatment was less common in the HIV-seropositive (RR = 0.57, CI = 0.37-0.88). In adults, tuberculin negativity, TB at 2 sites, lymph node, pericardial and miliary TB, hilar adenopathy and pleural effusion were significantly more common in HIV-seropositive patients; cavitation and upper lobe involvement were significantly less frequent. Pulmonary TB and sputum smear positivity had similar frequencies in the 2 groups. CONCLUSION: HIV was strongly and increasingly associated with TB in Harare and altered the clinical and radiologic features of TB. Failed standard TB treatment in HIV-infected individuals contributed minimally to new cases of TB.

AIDS-Related Opportunistic Infections↗
PubMed1994

sin 1, a mutation affecting female fertility in Arabidopsis, interacts with mod 1, its recessive modifier.

In Arabidopsis thaliana, a mutation in the SIN 1 gene causes aberrant ovule development and female-specific sterility. The effect of the sin 1 mutation is polymorphic and pleiotropic in different genetic backgrounds. The polymorphism concerns morphology of the mutant ovules. The pleiotropism involves internodal distance and inflorescence initiation time. The particular ovule phenotype and the length of internodes are dependent on an interaction of sin 1 with a second recessive gene, which we term mod 1. The recessive mod 1 allele in a homozygous sin 1 mutant plant reduces internode length and ovule integument size. The mutation sin 1, but not mod 1, has a demonstrable effect on ovule morphology when acting independently. In our crosses mod 1 was inseparably linked to the well known mutation erecta that is known to cause a reduction in internode and pedicle lengths.

Arabidopsis↗
PubMed1994

Combined antileukemic activity of pIXY 321 and Ara-C against human acute myeloid leukemia cells.

Prolonged administration of conventional (100 mg/m2/day) or low dose Ara-C (20 mg/m2/day) has been associated with significant clinical antileukemic effects in AML and myelodysplastic syndromes. These doses and schedules of Ara-C yield plasma Ara-C concentrations in the range of 10 to 100 nM. Utilizing concentrations and a schedule of Ara-C treatment, representative of Ara-C exposures in these clinical situations, we performed in vitro studies to examine the effects of co-treatment with pIXY 321 on Ara-C induced apoptosis and Ara-C-mediated colony growth inhibition of human myeloid leukemia HL-60 cells. Significantly greater internucleosomal DNA fragmentation, higher percentage of morphologically recognizable apoptotic cells and increased colony growth inhibition were observed following treatment with 100 versus 10 nM Ara-C for 5 days. Simultaneous exposure to 10 ng/ml pIXY 321 resulted in significantly increased colony growth inhibition as well as DNA fragmentation and apoptosis due to 10 nM but not 100 nM Ara-C. These concentrations of Ara-C inhibited c-myc and did not induce c-jun mRNA expression. These effects of Ara-C on c-myc and c-jun expressions were not influenced by co-treatment with pIXY 321. Neither treatment with pIXY 321 or Ara-C alone, nor co-treatment with pIXY 321 and Ara-C, significantly altered the intracellular p26BCL-2 levels in HL-60 cells. These results indicate that co-treatment with pIXY 321 significantly increases low dose Ara-C-induced apoptosis and thereby its antileukemic activity.

Acute Disease↗
PubMed1994

Our biggest challenge.

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Acquired Immunodeficiency Syndrome↗
PubMed1994

High levels of p26BCL-2 oncoprotein retard taxol-induced apoptosis in human pre-B leukemia cells.

In human leukemic cells clinically relevant concentrations of taxol have been demonstrated to induce the biochemical and morphologic hallmarks of apoptosis (Leukemia 1993;7:563-568). Since overexpression of the bcl-2 gene has been reported to retard apoptosis due to a variety of anticancer agents, we examined and compared taxol-induced intracellular microtubular bundling and apoptosis in pre-B human leukemia 697 cells and their counterparts which have been transfected with and overexpress cDNA derived from the bcl-2 gene. Treatment with 0.1 or 1.0 mumol/l taxol for 24 h resulted in internucleosomal DNA fragmentation and morphologic features of apoptosis in 697 cells, but not in 697/BCL-2 cells. However, indirect immunofluorescent staining with anti-tubulin antibody revealed that taxol treatment produces stable microtubule bundles resistant to calcium-mediated disassembly in 697, as well as 697/BCL-2 cells. In addition, taxol-induced microtubule bundling was associated with a marked accumulation of the two cell types in the G2/M phase of the cell cycle. Following exposure to taxol, when 697 cells were washed and kept in drug-free medium, they showed rapid onset of apoptosis followed by loss of cell viability and a decline in cell numbers. In contrast, identically treated 697/BCL-2 cells kept in drug-free medium remained in a growth arrested state, but showed little evidence of apoptosis for up to 4 days. They eventually demonstrated features of apoptotic cell death and loss of viability between 5 and 7 days. This was not accompanied by a decrease in p26BCL-2 levels. Anti-phosphotyrosine or anti-MAP kinase immunoblot analyses of proteins isolated from taxol-treated 697 and 697/BCL-2 cells failed to show any difference in tyrosine phosphorylation of cellular proteins. Therefore, our findings indicate that in 697/BCL-2 cells, high levels of p26BCL-2 significantly delay taxol-induced endonucleolytic internucleosomal DNA fragmentation and apoptosis, but do not affect taxol-induced microtubule bundling or cell cycle growth arrest. The delayed onset of taxol-induced DNA fragmentation and apoptosis in 697/BCL-2 cells without down-regulation of p26BCL-2 levels suggests that an alternative mechanism of taxol-mediated apoptosis might be triggered which is unimpeded by high p26BCL-2 levels, or taxol-induced prolongation of mitotic arrest may lead to the inactivation or inhibition of that mechanism by which p26BCL-2 is able to block apoptosis.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1994

Condom use and the risk of HIV infection: who is being protected?

Descriptive baseline data at enrollment into a cohort of male factory workers who were tested for HIV serology and monitored for sero-conversion over time, were analysed for condom use. At recruitment, the 1,146 men were asked about their sexual behaviour, history of sexually transmitted diseases (STDs), condom use and circumstances under which condoms were used. HIV seroprevalence in the cohort was 18.2 pc. Self reported use of condoms was low, with only 5 pc of the men reporting using them all the time. Forty four pc reported that they had never used a condom, 11.5 pc tried a condom only once, and 30.5 pc used condoms less than half the time. HIV positive men were more likely (Odds Ratio [OR] = 2.2 95 pc CI: 1.3-3.3) to use condoms than those who tested negative. Men using a condom more than once were younger and had more education (p values < 0.0005). Univariate analysis showed that men with self reported risk factors for HIV infection were more likely to use condoms. Significantly more condom users reported paying for sex, multiple sex partners or (for married men) a girlfriend (p < 0.005). Condom users also more often had a history of genital ulcers, urethral discharge or other STDs. Few married men (24 pc) reported using a condom with their wives. Condom use was more commonly reported with commercial sex workers (44 pc) or other extramarital partners (36 pc). Some risk factors for HIV infection were also present amongst men who reported that they did not use condoms.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1994

Effect of intravenous streptokinase on left ventricular function following acute myocardial infarction--an echocardiographic study.

160 patients with first attack of acute myocardial infarction (AMI), admitted within 6 hours after onset of chest pain, were divided into two groups--80 receiving intravenous streptokinase (IVSK, Gr. I) an 80 being treated without IVSK (GR. II). They were studied for pre-discharge (12.5 +/- 2.5 days-post admission) echocardiographic LV function. Gr. I pts received 1.5 million units of IVSK within 6 hrs of onset of chest pain, alongwith beta-blockers, aspirin and heparin unless contraindicated. Gr. II received all these except IVSK alongwith conventional therapy. Highly significant (P < 0.001) improvement was noted in the end-diastolic volume (EDV), end-systolic volume (ESV), Ejection fraction (EF) and regional wall motion score (RWMS) in the anterior wall (AW) AMI group when treated early with IVSK. In the inferior wall (IW) AMI group significant decrease was observed in the EDV and ESV (P < 0.001) and RWMS (P < 0.05), but the difference was not statistically significant for EF. Early high-dose short term IVSK infusion is thus associated with highly significant improvement in LV functions--regional as well as global--especially in AW AMI; in IWAMI the improvement is less marked.

Echocardiography↗
PubMed1994

Development of a mutant strain of Aspergillus niger and optimization of some physical factors for improved calcium gluconate production.

In the course of mutation studies of Aspergillus niger strain AB with ethylene imine (1:4000), a mutant A. niger AB 501, produced greater amount of calcium gluconate in the culture broth (88.0 g/lit) as against the parent strain (36.0 g/lit) by the surface culture method of fermentation. This mutant was then exposed to UV-rays and a mutant, A.niger AB 1801, was found to produce high calcium gluconate in the culture broth (120 g/lit). The optimum cultural conditions for the production of calcium gluconate by A.niger AB 1801 were pH, 6.5; period of incubation, 9 days; volume of medium in 1 litre flask, 150 ml; temperature, 30 degrees C, volume of inoculum, 7.5 ml of cell suspension containing 2.6 x 10(7) spores and age of inoculum, 6 days old spores of A. niger AB 1801. The maximum yield of calcium gluconate to the above conditions was 168 g/lit. The cultural conditions that support maximum cultural growth did not, however, give optimal yield of calcium gluconate because after having yielded the maximum of calcium gluconate the growth of organism continued to increase further.

Aspergillus niger↗
PubMed1994

Characterization of a human myeloid leukemia cell line highly resistant to taxol.

Taxol-resistant sublines of HL-60 myeloid leukemia cells (HL-60/TAX100 and HL-60/TAX1000) have been isolated in vitro by subculturing in progressively higher concentrations of taxol. HL-60/TAX100 and HL-60/TAX1000 cells are capable of continuous growth in the presence of 0.1 microM and 1.0 microM taxol, respectively, and the IC50 (50% growth inhibitory dose) values for taxol for the two sublines are 0.34 and 2.44 microM as compared to 3.1 nM for the parent HL-60 cells. HL-60/TAX100 and HL-60/TAX1000 cells display a variable degree of cross-resistance to taxotere, vincristine and doxorubicin, but are sensitive to the antimetabolite Ara-C. Both HL-60/TAX100 and HL-60/TAX1000 cells over-express MDR-1 m-RNA and the membrane efflux multidrug transporter P-glycoprotein (PGP), as determined by Western blot and immunofluorescence labeling with anti-PGP antibodies. Consequently, exposure of the taxol-resistant cells to [3H]taxol or daunomycin results in the accumulation of significantly lower levels of the two drugs. Co-treatment with cyclosporine (0.5 microgram/ml) or verapamil (10 microM) partially overcomes taxol resistance in HL-60/TAX1000 cells. Following treatment with clinically relevant concentration of taxol (1.0 microM for 24 h), HL-60 but not HL-60/TAX1000 cells display intracellular microtubular bundling, markedly enhanced accumulation of the cells in G2/M phase of cell-cycle and internucleosomal DNA fragmentation associated with apoptosis which is independent of bcl-2 gene expression. These taxol-resistant myeloid leukemia cells may serve as in vitro experimental models for examinating strategies which may have potential applicability for overcoming taxol resistance.

ATP Binding Cassette Transporter, Subfamily B, Mem↗