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Biomedical subjects

S Datta

Publications and source records attributed to S Datta.

At least 73 records · Page 4Linked to original sources

Hemodynamic effects of simultaneous administration of intravenous ephedrine and spinal anesthesia for cesarean delivery.

STUDY OBJECTIVE: To evaluate the hemodynamic effects of an intravenous (IV) ephedrine bolus given simultaneously with spinal anesthesia for cesarean delivery. DESIGN: Randomized, prospective, double-blind study. SETTING: Tertiary-care academic medical center. PATIENTS: 40 ASA physical status I and II nonlaboring women undergoing elective cesarean delivery of term, uncomplicated, singleton pregnancies. INTERVENTIONS: After a 10 mL/kg IV lactated Ringers bolus given over 15 minutes, patients simultaneously received an IV dose of 2 mL (10 mg) ephedrine or 2 mL saline, and an intrathecal dose of 12 mg (1.6 mL 0.75%) bupivacaine with 10 microg of fentanyl. Hypotension, defined as a 20% decrease in mean arterial pressure (MAP), was treated with 10-mg IV doses of ephedrine. MEASUREMENTS: Hemodynamic (heart rate and MAP) and non-invasive thoracic impedance (cardiac index, stroke index, and systemic vascular resistance index) measurements at baseline and at 1-minute intervals until the time of delivery. Total fluid, supplemental ephedrine, and Apgar scores were recorded. Data were evaluated using analysis of variance (ANOVA), ANOVA for repeated measures, and Mann-Whitney U-tests where appropriate, with p < 0.05 considered significant. MAIN RESULTS: Significant changes from baseline in MAP, systemic vascular resistance index, heart rate, and cardiac index were observed in both groups after spinal anesthesia. However, there were no differences between the ephedrine and saline groups in the incidence and severity of change from the baseline. The overall incidence of hypotension was 70% in both groups. No difference in total fluid or supplemental ephedrine use was observed. CONCLUSIONS: 10 mg of IV ephedrine given at the time of spinal anesthesia, and after a 10 mL/kg lactated Ringers fluid bolus, does not diminish the incidence or severity of hypotension in parturients undergoing cesarean delivery.

Adult↗

Expanding multiple antibiotic resistance among clinical strains of Vibrio cholerae isolated from 1992-7 in Calcutta, India.

Antimicrobial susceptibilities of Vibrio cholerae strains isolated from cholera patients admitted to the Infectious Diseases Hospital, Calcutta, India for 6 years were analysed to determine the changing trends; 840 V. cholerae strains isolated in 1992-1997 were included in this study. Among V. cholerae serogoup O1 and O139, ampicillin resistance increased from 1992 (35 and 70%, respectively) to 1997 (both serogroups 100%). Resistance to furazolidone and streptomycin was constantly high among V. cholerae O1 strains with gradual increase in resistance to other drugs such as ciprofloxacin, co-trimoxazole, neomycin and nalidixic acid. V. cholerae O139 strains exhibited susceptibilities to furazolidone and streptomycin comparable with those of O1 strains. However, after initial increase in resistance to chloramphenicol and co-trimoxazole, all the V. cholerae O139 strains became susceptible to these two drugs from 1995 onwards. Both V. cholerae O1 and O139 remained largely susceptible to gentamicin and tetracycline. V. cholerae non-O1, non-O139 strains, in contrast, exhibited high levels of resistance to virtually every class of antimicrobial agents tested in this study especially from 1995. Kruskal-Wallis one-way analysis showed that V. cholerae O1 Ogawa serogroup exhibited significant yearly increase in resistance to nine antibiotics followed by non-O1 non-O139 and O139 strains to six antibiotics and two antibiotics respectively. Interesting observation encountered in this study was the dissipation of some of the resistant patterns commonly found among V. cholerae non-O1 non-O139 or O1 serogroups to the O139 serogroup and vice versa during the succeeding years.

Cholera↗

The rat as an experimental model for sleep neurophysiology.

The aim of this study was to develop a sleep-wake recording system for rats that would yield results more comparable to those obtained from cats than those that are usually reported. For 18 male Sprague-Dawley rats, the authors combined measures of cortical and hippocampal electroencephalogram (EEG) and neck muscle electromyogram with the electrooculogram and pontine EEG, so that the behavioral states could be identified with greater confidence with the use of polygraphic criteria developed in the cat and so that the distinctive phasic events of REM sleep could be more easily studied in the rat. The results suggest that for many neurophysiological studies, the rat is a suitable alternative to the cat.

Animals↗

Prenatal protein malnourished rats show changes in sleep/wake behavior as adults.

Prenatal protein malnutrition significantly elevates brain levels of serotonin in rats, and these levels remain elevated throughout their lives. This biogenic amine is involved in the regulation of many physiological functions, including the normal sleep/wake cycle. The present study examined the effects of prenatal protein malnutrition on the sleep/wake cycle of freely moving adult rats. Six prenatally protein malnourished (6% casein) and 10 well-nourished (25% casein) male rats (90-120-day-old) were chronically implanted with a standard set of electrodes (to record cortical electroencephalogram, neck muscle electromyogram, electrooculogram, and hippocampal theta wave) to objectively measure states of sleep and wakefulness. Six-hour polygraphic recordings were made between 10.00 and 16.00 h; a time when the rats normally sleep. Prenatally malnourished rats spent 20% more time in slow wave sleep (SWS) compared to the well-nourished rats. The total percentage of time spent in rapid eye movement (REM) sleep was 61% less in prenatally malnourished rats compared to well-nourished control rats. These findings demonstrate the adverse consequences of prenatal protein malnutrition on the quality and quantity of adult sleep in rats. These sleep changes are potentially detrimental to normal social behavior and cognitive functions. Prenatally malnourished rats are an excellent animal model to study the role of endogenous serotonin in the regulation of the normal sleep/wake cycle.

Aging↗

Arterial to end-tidal carbon dioxide pressure difference during laparoscopic surgery in pregnancy.

BACKGROUND: There is controversy about whether capnography is adequate to monitor pulmonary ventilation to reduce the risk of significant respiratory acidosis in pregnant patients undergoing laparoscopic surgery. In this prospective study, changes in arterial to end-tidal carbon dioxide pressure difference (PaCO2--PetCO2), induced by carbon dioxide pneumoperitoneum, were determined in pregnant patients undergoing laparoscopic cholecystectomy. METHODS: Eight pregnant women underwent general anesthesia at 17-30 weeks of gestation. Carbon dioxide pnueumoperitoneum was initiated after obtaining arterial blood for gas analysis. Pulmonary ventilation was adjusted to maintain PetCO2 around 32 mmHg during the procedure. Arterial blood gas analysis was performed during insufflation, after the termination of insufflation, after extubation, and in the postoperative period. RESULTS: The mean +/- SD for PaCO2--PetCO2 was 2.4 +/- 1.5 before carbon dioxide pneumoperitoneum, 2.6 +/- 1.2 during, and 1.9 +/- 1.4 mmHg after termination of pneumoperitoneum. PaCO2 and pH during pneumoperitoneum were 35 +/- 1.7 mmHg and 7.41 +/- 0.02, respectively. There were no significant differences in either mean PaCO2--PetCO2 or PaCO2 and pH during various phases of laparoscopy. CONCLUSIONS: Capnography is adequate to guide ventilation during laparoscopic surgery in pregnant patients. Respiratory acidosis did not occur when PetCO2 was maintained at 32 mmHg during carbon dioxide pneumoperitoneum.

Analysis of Variance↗

Nonparametric estimation for the three-stage irreversible illness-death model.

In this paper, we present new nonparametric estimators of the stage-occupation probabilities in the three-stage irreversible illness-death model. These estimators use a fractional risk set and a reweighting approach and are valid under stage-dependent censoring. Using a simulated data set, we compare the behavior of our estimators with previously proposed estimators. We also apply our estimators to data on time to Pneumocystis pneumonia and death obtained from an AIDS cohort study.

AIDS-Related Opportunistic Infections↗

Differences in genotypes of Helicobacter pylori from different human populations.

DNA motifs at several informative loci in more than 500 strains of Helicobacter pylori from five continents were studied by PCR and sequencing to gain insights into the evolution of this gastric pathogen. Five types of deletion, insertion, and substitution motifs were found at the right end of the H. pylori cag pathogenicity island. Of the three most common motifs, type I predominated in Spaniards, native Peruvians, and Guatemalan Ladinos (mixed Amerindian-European ancestry) and also in native Africans and U.S. residents; type II predominated among Japanese and Chinese; and type III predominated in Indians from Calcutta. Sequences in the cagA gene and in vacAm1 type alleles of the vacuolating cytotoxin gene (vacA) of strains from native Peruvians were also more like those from Spaniards than those from Asians. These indications of relatedness of Latin American and Spanish strains, despite the closer genetic relatedness of Amerindian and Asian people themselves, lead us to suggest that H. pylori may have been brought to the New World by European conquerors and colonists about 500 years ago. This thinking, in turn, suggests that H. pylori infection might have become widespread in people quite recently in human evolution.

Amino Acid Isomerases↗

Distinctiveness of genotypes of Helicobacter pylori in Calcutta, India.

The genotypes of 78 strains of Helicobacter pylori from Calcutta, India (55 from ulcer patients and 23 from more-benign infections), were studied, with a focus on putative virulence genes and neutral DNA markers that were likely to be phylogenetically informative. PCR tests indicated that 80 to 90% of Calcutta strains carried the cag pathogenicity island (PAI) and potentially toxigenic vacAs1 alleles of the vacuolating cytotoxin gene (vacA), independent of disease status. This was higher than in the West (where cag PAI(+) vacAs1 genotypes are disease associated) but lower than in east Asia. The iceA2 gene was weakly disease associated in Calcutta, whereas in the West the alternative but unrelated iceA1 gene at the same locus is weakly disease associated. DNA sequence motifs of vacAm1 (middle region) alleles formed a cluster that was distinct from those of east Asia and the West, whereas the cagA sequences of Calcutta and Western strains were closely related. An internal deletion found in 20% of Calcutta iceA1 genes was not seen in any of approximately 200 strains studied from other geographic regions and thus seemed to be unique to this H. pylori population. Two mobile DNAs that were rare in east Asian strains were also common in Calcutta. About 90% of Calcutta strains were metronidazole resistant. These findings support the idea that H. pylori gene pools differ regionally and emphasize the potential importance of studies of Indian and other non-Western H. pylori populations in developing a global understanding of this gastric pathogen and associated disease.

Adult↗

The long terminal repeat of Jaagsiekte sheep retrovirus is preferentially active in differentiated epithelial cells of the lungs.

Jaagsiekte sheep retrovirus (JSRV) is the etiologic agent of a contagious bronchioloalveolar carcinoma of sheep known as sheep pulmonary adenomatosis (SPA; ovine pulmonary carcinoma). JSRV is unique among retroviruses because it transforms the alveolar type II cells and the nonciliated bronchiolar cells (Clara cells) of the lungs; these cells are where JSRV is specifically expressed in both naturally and experimentally SPA-affected sheep. In this study, we investigated the cell specificity of JSRV expression. By transient-transfection assays of 23 different cell lines with a reporter plasmid driven by the JSRV long terminal repeat (LTR), pJS21-luc, we found that the JSRV LTR is preferentially active in cell lines derived from type II pneumocytes and Clara cells (MLE-15 and mtCC1-2 mouse cell lines). Reporter assays using progressive 5' deletions of pJS21-luc allowed us to establish that the JSRV enhancers are able to activate the JSRV proximal promoter in MLE-15 and mtCC1-2 cells, but they have very low activity in mouse cells of other lineages (e.g., NIH 3T3). The JSRV enhancers are able to activate heterologous promoters in both MLE-15 and 3T3 cells, although optimal activity is achieved in MLE-15 cells only with the homologous JSRV promoter. Thus, JSRV cell-specific LTR activity appears to result from an interaction between the enhancer elements and the JSRV proximal promoter elements. By mutation analysis, we established that an upstream NF-kappaB-like element appears to be responsible for approximately 50% of the JSRV LTR transcriptional activity in MLE-15 cells. Electrophoretic mobility shift assays showed evidence of a factor(s) that binds to this sequence. Antibody supershift experiments indicated that the factor(s) is not related to NF-kappaB component p50 or p52. This factor also appeared to be present in cells that do not support a high level of JSRV expression. Finally the JSRV(21) LTR contains putative enhancer binding motifs for transcription factors such as hepatocyte nuclear factor 3 (HNF-3) that are involved in lung-specific gene expression. Cotransfection experiments demonstrated that exogenous HNF-3 is able to enhance the expression of pJS21-luc in NIH 3T3 cells, which normally show minimal enhancer activity for the JSRV LTR.

3T3 Cells↗

In vivo genomic footprinting of the human T-cell leukemia virus type 1 (HTLV-1) long terminal repeat enhancer sequences in HTLV-1-infected human T-cell lines with different levels of Tax I activity.

The Tax protein of human T-cell leukemia virus type 1 (HTLV-1) enhances viral gene expression through sequences in the U3 region of the viral long terminal repeat. These sequences consist of three imperfect 21-bp repeats (TRE-1s) and a region between the promoter-central and promoter-proximal 21-bp repeats (TRE-2). The TRE-1s contain a core cyclic AMP response element (CRE) motif and can be bound by CREB, ATF-1, ATF-2, and other members of the CREB-ATF superfamily of transcription factors. Tax enhances CREB binding to TRE-1 in vitro, and it promotes dimerization of CREB as well as other bZIP proteins. Using ligation-mediated PCR on in vivo dimethyl sulfate-treated HTLV-1-infected cell lines MT-2 and MT-4, we have compiled a profile of protein occupancy in the HTLV-1 enhancer sequences in the presence of high (MT-2) and low (MT-4) levels of biologically active Tax I. The in vivo footprinting showed that all three TRE-1s were bound by protein(s), but only in MT-2 cells. In MT-2 cells, all TRE-1s showed strong protection of the G residues in the central CRE, and the footprints extended to differing degrees into the GC-rich flanking sequences. This indicated Tax I-dependent loading of transcription factors onto the HTLV-1 TRE-1s in vivo. In vivo footprinting on TRE-2 indicated that this region was bound by proteins regardless of the Tax I status of the cell line. However, the presence of Tax I increased the extent and altered the profile of proteins binding TRE-2 in vivo.

Base Sequence↗

c-Jun-dependent inhibition of cutaneous procollagen transcription following ultraviolet irradiation is reversed by all-trans retinoic acid.

The aged appearance of skin following repeated exposure to solar ultraviolet (UV) irradiation stems largely from damage to cutaneous connective tissue, which is composed primarily of type I and type III collagens. We report here that a single exposure to UV irradiation causes significant loss of procollagen synthesis in human skin. Expression of type I and type III procollagens is substantially reduced within 24 hours after a single UV exposure, even at UV doses that cause only minimal skin reddening. Daily UV exposures over 4 days result in sustained reductions of both type I and type III procollagen protein levels for at least 24 hours after the final UV exposure. UV inhibition of type I procollagen synthesis is mediated in part by c-Jun, which is induced by UV irradiation and interferes with procollagen transcription. Pretreatment of human skin in vivo with all-trans retinoic acid inhibits UV induction of c-Jun and protects skin against loss of procollagen synthesis. We have reported previously that UV irradiation induces matrix-degrading metalloproteinases in human skin and that pretreatment of skin with all-trans retinoic acid inhibits this induction. UV irradiation, therefore, damages human skin connective tissue by simultaneously inhibiting procollagen synthesis and stimulating collagen breakdown. All-trans retinoic acid protects against both of these deleterious effects and may thereby retard premature skin aging.

Dose-Response Relationship, Radiation↗

Effect of a herbal protein, CI-1, isolated from Cajanus indicus on immune response of control and stressed mice.

The effect of a herbal protein, CI-1, purified from the leaves of Cajanus indicus was evaluated as a probable immunomodulator on immune response in control and stressed mice. In mice, sensitized with sheep red blood cells (SRBC), CI-1 enhanced IgG level by 28% over control (P < 0.05). Primary and secondary antibody response to SRBC and bovine serum albumin (BSA) were significantly increased in CI-1 treated group. Furthermore CI-1 facilitated the delayed type of hypersensitivity (DTH) response to SRBC in sensitized mice and also enhanced leucocyte and macrophage migration inhibition response in immunized mice. A fewer mice displayed symptoms of anaphylactic shock after CI-1 administration at a dose of 6.0 mg/kg body wt. in BSA sensitized mice. The immediate effect of CI-1 on anaphylactic shock was not seen when 150 microg of CI-1 was injected in combination with BSA in the shocking injection. These results suggest that CI-1 influences both humoral and cell-mediated immune response.

Adjuvants, Immunologic↗

Characterization of the dimer interface of transcription factor NFkappaB p50 homodimer.

Dimers of the Rel/NFkappaB transcription factor family form with differential stabilities through the combinatorial association of five polypeptides: p50, p52, p65, cRel, and RelB. Here, we have characterized the nature of the monomer-dimer equilibrium of the p50 homodimer. Sedimentation equilibrium studies show that the equilibrium constant for p50 dimer dissociation is in the low micromolar range. Using the X-ray crystal structure of the p50 homodimer as a guide, we have created site-directed alanine mutations at ten dimer-forming residues in p50 and measured their effects on p50 homodimerization. Characterization of these alanine mutants by a series of chemical crosslinking, size-exclusion chromatography, and sedimentation equilibrium experiments shows that the most critical residue in stabilizing the p50 dimer interface is Y267. Sedimentation equilibrium experiments show that an alanine substitution at position 267 destabilizes the dimer interface by 2.0 kcal/mol. Alanine substitutions at two other positions, L269 and V310, significantly destabilize the p50 dimer interface. These two residues are observed to mediate critical interactions in the crystal structure. Together, these three residues constitute the "hot-spot" of protein-protein interaction in p50 dimerization. Of the four charged residues in the dimer interface, R252, D254, E265, and D302, only D302 contributes significantly to p50 dimer stability. D254 appears to slightly destabilize the subunit interface. Although residues H304, R305, and F307 occupy positions at the hydrophobic core of the interface and appear to be involved in multiple interactions in the X-ray crystal structure, alanine substitutions at these positions do not significantly reduce the affinity for p50 dimerization. Upon evaluating the roles of these amino acid residues at the p50 dimer interface, we propose that differential contributions of a few key residues dictate the selectivity of dimer formation within the Rel/NFkappaB family.

Amino Acid Sequence↗

Activation of neuroblast proliferation in explant culture of the Drosophila larval CNS.

The developmental control of neuroblast proliferation is absolutely required for the assembly and function of the central nervous system. A lethal mutation in trol results in the failure of quiescent neuroblasts to begin division at the appropriate time. I have established a culture system in which quiescent neuroblasts in explants of Drosophila larval CNSs initiate cell division in vitro to normal in vivo levels. This activation requires removal of the CNS for culture after a specific developmental stage and the presence of fetal calf serum or a larval extract in the medium. Either supplement is effective when heat-treated. Substitution of the steroid hormone ecdysone or the non-steroidal ecdysone analog RH5992 for either fetal calf serum or larval extract also results in activation of neuroblast proliferation. Culture of trolsd CNSs with wildtype larval extract or ecdysone results in the defective neuroblast proliferation phenotype observed in trol mutants in vivo, while culture of wildtype CNSs with trolsd extract produces normal neuroblast proliferation.

Animals↗

Hepatoprotective activity of a herbal protein CI-1, purified from Cajanus indicus against beta-galactosamine HCl toxicity in isolated rat hepatocytes.

A herbal protein, CI-1 purified from a leguminous plant Cajanus indicus, showed dose dependent-(1.5-6.0 mg/kg x 7 days) protective activity on isolated hepatocytes (ex vivo) against beta-galactosamine-HCl induced hepatic damage in rats. It enhanced the percent viability of the hepatocytes following beta--galactosamine treatment. CI-1 was also effective in counteracting the toxic effects of beta-galactosamine, as shown by reversed levels of the altered enzymes, glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transminase (GPT) and alkaline phosphatase (ALP) both in isolated hepatic cells as well as in serum. In comparison silymarin, a known hepatoprotective agent, produced dose related protection at-relatively much higher doses than CI-1.

Alanine Transaminase↗

Evidence for organochlorine contamination in tissues of salmonids in Lake Tahoe.

To evaluate the extent of organochlorine pollution in the Sierra Nevada ecosystem, residues of certain organochlorines in lake trout and Kokanee fish from Lake Tahoe, an alpine lake located between the Sierra Nevada Mountain Range and the Carson Range of California and Nevada, were analyzed. Multiresidue analysis in fish muscle revealed wet weight concentrations of total polychlorinated biphenyls (PCBs) in the range 18 to 430 ppb and of p,p'-DDE in the range 5 to 85 ppb in the two fish species studied. In one large lake trout sample (6.6 kg), which was studied in more detail as compared with others, residue levels of PCB (267 ppb), toxaphene (154 ppb), a chlordane mixture (78 ppb), and a DDT mixture (154 ppb) were found in muscle. Full spectra of specific PCB congeners and p,p'-DDE were obtained from fish fat tissues and their identities were confirmed using gas chromatography/mass spectrometry (GC-MS). The results of total PCB analysis indicated that residues found in fish consisted mostly of moderately (tri- to tetrachloro-) to highly (penta- to heptachloro-) chlorinated biphenyls. For all fish residues analyzed, the best match to PCB residue profiles was with Aroclor 1260 or 1262.

Adipose Tissue↗

Efficacy of a potentized homoeopathic drug (Arsenicum Album-30) in reducing genotoxic effects produced by arsenic trioxide in mice: comparative studies of pre-, post- and combined pre- and post-oral administration and comparative efficacy of two microdoses.

OBJECTIVE: To examine the comparative efficacies of Arsenicum Album 30C and 200C and three administrative modes in protecting against the genotoxic effects produced by Arsenic trioxide injection in mice. DESIGN: Healthy mice, Mus musculus, were intraperitoneally injected with a 0.004% solution of As2O3 @1 ml/100 gms of body weight. Genotoxic effects were assessed through chromosome aberrations (CA), micronucleated erythrocytes (MNE), mitotic index (MI) and sperm head anomaly (SHA) studies, keeping suitable succussed alcohol fed (positive) and As2O3 untreated normal (negative) controls. The As2O3 treated mice were divided into three subgroups, which were orally administered with the drug a) prior to, b) after and c) both prior to and after injection of As2O3 at specific fixation intervals. RESULTS: While the CA, MNE and SHA were reduced in the drug fed series as compared to respective controls, the MI showed an apparent increase. The combined pre- and post-feeding of Arsenicum album was found to be most effective in reducing the genotoxic effects of As2O3 i200C was more effective than 30C. CONCLUSION: Arsenicum Album reduces the genotoxic effect of arsenic poisoning.

Administration, Oral↗

Efficacy of a potentized homoeopathic drug (Arsenicum Album-30) in reducing genotoxic effects produced by arsenic trioxide in mice: II. Comparative efficacy of an antibiotic, actinomycin D alone and in combination with either of two microdoses.

OBJECTIVE: To determine whether actinomycin-D (AMD), an antibiotic, alters the reported efficacy of a potentized homoeopathic drug, Arsenicum Album, in reducing genotoxic effects produced in arsenic-trioxide-injected mice. DESIGN: Mice were separately injected with AMD, As2O3, and conjointly with AMD plus As2O3, AMD plus homoeopathic drug, AMD plus As2O3 plus homoepathic drug, and As2O3 plus homoeopathic drug in separate sets. METHODS: Several standard cytogenetical endpoints were assessed at different fixation intervals by adopting conventional techniques. RESULTS: Both Ars Alb-30 and Ars Alb-200 showed protective ability against AMD and As2O3 when injected individually, but this ability was reduced considerably in mice injected with AMD and As2O3 together. AMD itself had genotoxic effects, but also apparently reduced genotoxic effects of arsenic to some extent. CONCLUSION: AMD reduced the protective efficacy of the homoeopathic drug against arsenic. This result suggests a mechanism of action for homoeopathy, as AMD is a known transcription-blocker.

Animals↗