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Biomedical subjects

S S Murthy

Publications and source records attributed to S S Murthy.

At least 19 recordsLinked to original sources
PubMed2004

The burden of diabetes and impaired fasting glucose in India using the ADA 1997 criteria: prevalence of diabetes in India study (PODIS).

This random multistage cross sectional population survey was undertaken to determine the prevalence of diabetes mellitus (DM) and impaired fasting glycemia/glucose (IFG) in subjects aged 25 years and above in India. The study was carried out in 108 centers (49 urban and 59 rural) to reflect the size and heterogeneity of the Indian population. 41,270 (20,534 males and 20,736 females) subjects were studied. 21,516 (10,865 males and 10,651 females) were from urban areas and 19,754 (9669 males and 10,085 females) from rural areas. Blood samples were taken after a fast of 10-12h and the subjects were categorized as having IFG or DM using the 1997 American Diabetes Association criteria. The age and gender standardized prevalence rate for DM and IFG in the total Indian population was 3.3 and 3.6% respectively (P < 0.001). The standardized prevalence of DM and IFG in urban areas was significantly higher than that for the rural population (urban DM prevalence 4.6% versus rural DM prevalence 1.9%, P < 0.001; urban IFG prevalence 4.8% versus rural IFG prevalence 2.5%, P < 0.001). There was no statistically significant difference in the prevalence between DM (4.6%) and IFG (4.8%) in the urban population. The rural prevalence of IFG (2.5%) was significantly (P <0.001) more than the rural prevalence of DM (1.9%). Type 2 diabetes is a major health problem is India.

Adult↗
PubMed2004

The burden of diabetes and impaired glucose tolerance in India using the WHO 1999 criteria: prevalence of diabetes in India study (PODIS).

This random multistage cross-sectional population survey was undertaken to determine the prevalence of diabetes mellitus (DM) and impaired glucose tolerance (IGT) in subjects aged 25 years and above in India. The study was carried out in 77 centers (40 urban and 37 rural). 18363 (9008 males and 9355 females) subjects were studied. 10617 (5379 males and 5238 females) were from urban areas and 7746 (3629 males and 4117 females) from rural areas. Blood samples were taken after a fast of 10-12 h and 2 h after 75 g of oral glucose. Subjects were categorized as having IGT or DM using the World Health Organisation (WHO) (1999) criteria. The standardized prevalence rate for DM in the total Indian, urban and rural populations was 4.3, 5.9 and 2.7%, respectively. The corresponding IGT rates in the three populations was 5.2, 6.3 and 3.7%, respectively. The urban prevalence of DM and IGT was significantly greater than in the rural population (P < 0.001 in both instances). The prevalence of DM was significantly, more than that of IGT (P < 0.001) within both the rural and urban populations. Type 2 diabetes is a major health problem is India.

Adult↗
PubMed2004

Comparing the ADA 1997 and the WHO 1999 criteria: Prevalence of Diabetes in India Study.

This random multistage cross-sectional population survey was undertaken to determine the prevalence of type 2 diabetes mellitus (DM) in subjects aged 25 years and above in India. The study was carried out in 77 centres (42 urban and 35 rural) to reflect the size and heterogeneity of the Indian population. 18,363 (9008 male and 9355 female) subjects were studied. 10,617 (5379 males and 5238 females) were from urban areas and 7746 (3629 males and 4117 females) from rural areas. Blood samples were taken after a fast of 10-12 and 2 h after 75 g of oral glucose. Subjects were categorized as having impaired fasting glycemia (IFG) or DM using the 1997 ADA or having impaired glucose tolerance (IGT) or DM using the 1999 WHO criteria. The age- and gender-standardized prevalence rate for DM using the ADA criteria was 3.6% whilst that using the WHO criteria was 4.3% (P < 0.001). The respective standardized prevalence of DM, using the two criteria was, 4.7 and 5.6%, respectively (P < 0.001) in the urban Indian population and 2.0 and 2.7% (P < 0.02) in the rural Indian population. Using the WHO criteria, 581 subjects were newly diagnosed whilst the ADA criteria newly diagnosed 437 subjects. The respective numbers for the urban population were 425 and 323, and for the rural population were 146 and 114, respectively. The ADA criteria could diagnose 75.2, 76.0 and 73.0% of the subjects who had DM as per the WHO criteria. Of 739 Indian subjects who had IFG, 106 (14.3%) were diagnosed as having DM by the WHO criteria whilst 505 (68.3%) had values compatible with a diagnosis of IGT. Of the 536 urban subjects with IFG, 74 (13.8%) had DM and 350 (65.3%) had IGT using the WHO criteria. Of the 302 rural subjects with IFG, 32 (15.8%) had DM and 155 (76.3%) had IGT using the WHO criteria. 505 (49.9%) of 1012 Indian subjects with IGT as per the WHO criteria had IFG. 350 (47.7%) of 733 urban subjects and 155 (55.5%) of 279 rural subjects with IGT had values compatible with IFG as per the ADA criteria. Type 2 diabetes is a major health problem is India. The use of the ADA criteria would underestimate the prevalence of DM by not diagnosing subjects showing a poor response to a glucose challenge. This along with the discrepancies between subjects showing IGF or IGT could be a challenge to any prevention program.

Adult↗
PubMed2003

Bispectral index monitoring in patients undergoing cardiac surgery under cardiopulmonary bypass.

BACKGROUND AND OBJECTIVE: Monitoring the depth of anaesthesia by the bispectral index facilitates the titration of anaesthetic drugs during operation as well as assisting in early recovery. We planned to use this index to control the administration of anaesthetic agents in order to stabilize haemodynamics and promote recovery from anaesthesia in patients undergoing cardiac surgery with cardiopulmonary bypass. METHODS: Thirty adult patients undergoing valve replacement or coronary artery grafting under cardiopulmonary bypass were studied in a prospective, randomized, controlled study. Bispectral index monitoring was used in all patients. Patients received isoflurane anaesthesia and boluses of morphine: in the study group, anaesthetic depth was controlled using the bispectral index and clinical variables. In the control group, the bispectral index monitor could not be viewed by the anaesthesiologist. Bispectral index, mean arterial pressure and heart rate were noted every 5 min, and the incidence of hypotension, hypertension, tachycardia and bradycardia also noted. The time to recovery, when patients started obeying commands, was also recorded. RESULTS: Patients in the study group had significantly less hypertension and tachycardia (P < 0.05) than those in the control group. The time to recovery of consciousness was less in the study group than in the control group (n.s., P > 0.05). The bispectral index rose significantly in the control group at the time of institution and termination of cardiopulmonary bypass (P < 0.05). CONCLUSIONS: Anaesthesia controlled by bispectral index monitoring decreases the incidence of haemodynamic disturbances and facilitates titration of anaesthetic agents during cardiopulmonary bypass and thus may assist recovery from anaesthesia.

Adolescent↗
PubMed2001

Absence of post-transcriptional RNA modifications of BCL10 in human malignant mesothelioma and colorectal cancer.

The BCL10 gene, located at 1p22, has been implicated in a number of human malignancies, including malignant mesotheliomas (MMs) and colorectal carcinomas. Subsequent reports, however, have revealed an absence of BCL10 mutations in genomic DNA from such tumors. It has been proposed that some abnormalities of this gene may be found only in RNA and not in genomic DNA, suggesting that BCL10 may be mutated post-transcriptionally, rather than at the genomic level. To explore this possibility, we performed SSCP mutation analysis and direct sequencing of cDNA from 17 MM cell lines displaying LOH in 1p22, 12 MM tumor specimens, and 11 colon carcinoma cell lines. SSCP revealed several different band shifts in these samples. The nucleotide changes observed in the cDNA samples were also seen in matched genomic DNA and corresponded to known polymorphisms in the general population. Thus, we conclude the BCL10 mutations are absent at the cDNA level, and that this gene does not undergo "molecular misreading." Since BCL10 also does not possess mutations at the genomic DNA level, it can be ruled out as a gene involved in the pathogenesis of MM and colorectal cancer.

Adaptor Proteins, Signal Transducing↗
PubMed2000

Expression of GPC3, an X-linked recessive overgrowth gene, is silenced in malignant mesothelioma.

Gene expression changes in rat asbestos-induced malignant mesothelioma (MM) cells were investigated by differential mRNA display. A mRNA transcript identified by this approach was abundant in normal rat mesothelial cells but not expressed in rat MM cell lines. Northern blot analysis confirmed that this transcript is uniformly silenced in rat MM cell lines and primary tumors. Nucleotide sequence analysis revealed that this transcript is encoded by the rat glypican 3 gene (GPC3), whose human homolog is mutated in the Simpson-Golabi-Behmel overgrowth syndrome. Allelic loss at the GPC3 locus was infrequent (6.9%) in MM cell lines, and no mutations were found. GPC3 transcript levels were markedly decreased in 16 of 18 primary tumors and 17 of 22 human MM cell lines. Most of the cell lines were shown to have aberrant methylation of the GPC3 promoter region. In two of four human MM cell lines tested, GPC3 expression was restored after 2-deoxy 5-azacytidine (DAC)-mediated demethylation of its promoter region. Ectopic expression of GPC3 inhibited in vitro colony formation of human MM cells. Collectively, these data suggest that down-regulation of GPC3 is a common occurrence in MM and that GPC3, an X-linked recessive overgrowth gene, may encode a negative regulator of mesothelial cell growth.

Alleles↗
PubMed2000

Mapping of AKT3, encoding a member of the Akt/protein kinase B family, to human and rodent chromosomes by fluorescence in situ hybridization.

Previously, a rodent cDNA encoding the third member of the Akt/PKB family of serine/threonine kinases was cloned. We have now cloned the human homolog of this cDNA, and we have used this clone to map the AKT3 gene to human chromosome 1q44 by fluorescence in situ hybridization (FISH). We have also mapped the rodent homologs of AKT3 to rat chromosome 13q24-->q26 and mouse chromosome 1H4-6 by FISH.

Animals↗
PubMed1999

Asbestos, chromosomal deletions, and tumor suppressor gene alterations in human malignant mesothelioma.

Exposure to the carcinogen asbestos is considered to be a major factor contributing to the development of most malignant mesotheliomas (MMs). We highlight the role of asbestos in MM and summarize cytogenetic and molecular genetic findings in this malignancy. The accumulation of numerous clonal chromosomal deletions in most MMs suggests a multistep process of tumorigenesis, characterized by the loss and/or inactivation of multiple tumor suppressor genes (TSGs). Cytogenetic and loss of heterozygosity (LOH) analyses of MMs have demonstrated frequent deletions of specific sites within chromosome arms 1p, 3p, 6q, 9p, 13q, 15q, and 22q. Furthermore, TSGs within two of these regions, i.e., p16/CDKN2A-p14ARF at 9p21 and NF2 at 22q12, are frequently altered in MMs. Homozygous deletion appears to be the major mechanism affecting p16/CDKN2A-p14ARF, whereas inactivating mutations coupled with allelic loss occur at the NF2 locus. Finally, recent studies have demonstrated the presence and expression of simian virus 40 (SV40) in many MMs. SV40 large T antigen has been shown to inactivate the TSG products Rb and p53, suggesting the possibility that asbestos and SV40 could act as cocarcinogens in MM. The frequent occurrence of homozygous deletions of p16/CDKN2A-p14ARF and the ability of SV40 Tag to bind TSG products suggest that perturbations of both Rb- and p53-dependent growth-regulatory pathways are critically involved in the pathogenesis of MM.

Asbestos↗
PubMed1998

Some insight into the physical basis of the cryoprotective action of dimethyl sulfoxide and ethylene glycol.

In the determination of the solid-liquid phase equilibria in the aqueous mixtures of dimethyl sulfoxide (Me2SO) and ethylene glycol (EG) one often encounters the problem of equilibrium crystallization. In the present report the above aqueous solutions are equilibrated for crystallization in a dielectric cell during which the dielectric method is used for monitoring the extent of crystallization. The melting temperatures are then measured by using the dielectric technique in combination with the differential scanning calorimeter. The equilibrium phase diagram of Me2SO is found to be eutectic with two compounds formed of water and Me2SO in the ratio of 3:1 and 2:1. In the case of EG solutions it is eutectic with a 1:1 compound formation. It is suggested that the greater depression of the freezing point of water due to the complex formation and hence the attendant increase in the viscosity near the freezing point is the reason for the sluggish crystallization in these solutions. The variation of the glass transition temperature with composition is also examined in the above solutions along with the aqueous solutions of a number of other cryoprotectants. The glass-forming tendency of these solutions is discussed in terms of complex formation. An attempt is made to distinguish between good and bad glass-forming additives in terms of complex formation and ice clathrate formation.

Cryopreservation↗
PubMed1996

Stability of revex, nalmefene hydrochloride injection, in injectable solutions.

The short-term stability of Revex, nalmefene hydrochloride injection, was determined in a number of diluents commonly employed for intravenous use. An HPLC method was used to follow the potency of the diluted solutions, and was fully validated for its intended concentration range prior to its use. Dilutions of Revex were prepared separately in 0.9% sodium chloride injection, 0.45% sodium chloride injection, 5% dextrose injection, 5% dextrose and 0.45% sodium chloride injection, lactated Ringer's injection, 5% dextrose and lactated Ringer's injection and 5% sodium hydrogencarbonate injection. Each admixture was stored at 4 degrees C, room temperature (21 degrees C) and 40 degrees C, with samples being tested after storage at each temperature for 0, 24, 48 and 72 h. Defining stability as the retention of at least 95% of the initial drug concentration at the end of the storage period, it was concluded that the diluted solutions of Revex were uniformly stable for up to 72 h in all of the injectable solutions maintained at either 4, 21 or 40 degrees C.

Chromatography, High Pressure Liquid↗
PubMed1996

Disposition of the opioid antagonist, nalmefene, in rat and dog.

1. The disposition of nalmefene in rat and dog was studied using in vitro and in vivo methodology. In vitro metabolite profiles were obtained following incubation of nalmefene with liver microsomes and biological fluids were assayed to profile in vivo metabolites. Characterization of metabolites was accomplished using hplc, co-chromatography with synthetic standards, or LC/MS. 2. In rat, tissue distribution and metabolite plasma concentration-time data were obtained following intravenous bolus dosing of nalmefene. 3. The results indicate that the primary phase I metabolite of nalmefene from liver microsome incubations was the N-dealkylated metabolite, nornalmefene. Quantitative metabolite production was rat >> dog. In vivo, nornalmefene glucuronide was the major metabolite in rat urine, whereas nalmefene glucuronide(s) were predominant in dog urine. 4. More than 90% of the radioactive dose was recovered in the rat excreta and tissues 24 h after an intravenous bolus dose of 14C-nalmefene, with no apparent organ-specific retention of radioactivity. 5. Pharmacokinetic analysis of the rat plasma metabolite data indicated that terminal half-lives for nalmefene and nornalmefene were comparable (approximately 1 h). However, Cmax and AUC of nornalmefene were < or = 7% that of corresponding nalmefene values.

Animals↗
PubMed1994

Molecular cloning and characterization of a cDNA encoding pea monodehydroascorbate reductase.

Monodehydroascorbate radicals are generated in plant cells enzymatically by the hydrogen peroxide scavenging enzyme, ascorbate peroxidase, and nonenzymatically via the univalent oxidation of ascorbate by superoxide, hydroxyl, and various organic radicals. Regeneration of ascorbate is achieved by monodehydroascorbate reductase (EC 1.6.5.4) using NAD(P)H as an electron donor or, alternatively, by a set of two coupled reactions requiring dehydroascorbate reductase, glutathione reductase, glutathione, and NAD(P)H. As monodehydroascorbate reductase is a key enzyme in maintaining reduced pools of ascorbate, an important antioxidant, we undertook this study to learn more about its structure, function, and regulation. Herein we report the molecular cloning and characterization of a cDNA encoding monodehydroascorbate reductase of pea (Pisum sativum L.). The cDNA encodes a 433-amino acid polypeptide that shows, respectively, 73 and 87% identity with peptide fragments from soybean and cucumber monodehydroascorbate reductase. Monodehydroascorbate reductase contains the NAD(P)H and FAD binding domains of other flavin oxidoreductases. The cloned enzyme lacks a transit peptide, but the sequence of the carboxyl terminus is Ser-Lys-Ile, similar to the targeting motif found in peroxisomal proteins. When expressed in Escherichia coli fused to maltose-binding protein, monodehydroascorbate reductase has enzymatic properties comparable with purified soybean and cucumber monodehydroascorbate reductase. Northern blot analysis shows that the monodehydroascorbate reductase transcript is 1.6 kilobase in size and is expressed at relatively low levels in all plant tissues examined.

ATP-Binding Cassette Transporters↗
PubMed1991

Enantioselective and diastereoselective hydroxylation of bufuralol. Absolute configuration of the 7-(1-hydroxyethyl)-2-[1-hydroxy-2-(tert-butylamino)ethyl]benzofurans, the benzylic hydroxylation metabolites.

Asymmetric synthesis of the diastereomeric 7-(1-hydroxyethyl)-2-[1-hydroxy-2-(tert-butylamino)ethyl]benzofurans (2), the benzylic hydroxylation metabolites of bufuralol (1), is described, and the absolute configurations of these diastereomers are assigned. 1"-Oxobufuralol (3) was reduced with a complex of (2S)-(-)-2-amino-3-methyl-1,1-diphenylbutan-1-ol and borane, yielding 2, which had a 95:5 ratio of the possible 1"R and 1"S isomers as determined by HPLC. Separation of the resulting diastereomers was facilitated by derivatization with the enantiomers of 1-phenethyl isocyanate (PEIC). The absolute configurations 1'S,1"R and 1'R,1"R were assigned to the diastereomers formed in excess, 2c and 2b, on the basis of the known stereochemistry of reduction of closely related alkyl phenyl ketones to R alcohols by using this chiral borane reagent. The circular dichroism spectra of the four isomeric benzylic alcohols were in agreement with these assignments. In the presence of the rat liver microsomal fraction, benzylic hydroxylation of bufuralol was significantly product stereoselective favoring formation of diastereomers with the 1"R absolute stereochemistry at the new chiral center in products from (1'R)-1 by a ratio of 4.5:1 [(1'R,1"R)-2:(1'R,1"S)-2] and by nearly 8:1 [(1'S,1"R)-2:(1'S,1"S)-2] from (1'S)-1. (1'R)-Bufuralol was more rapidly hydroxylated than was (1'S)-1, by about 3-fold. In the presence of human liver microsomes, (1'R)-bufuralol was also more rapidly hydroxylated than was (1'S)-1, by ca. 2.5-fold. However, product stereoselectivity from the 1'R enantiomer was reversed from that observed in the rat liver microsomal oxidation, with more (1"S)-carbinol being formed than 1"R isomer by nearly 4-fold. From (1'S)-1, about equal amounts of the two possible hydroxybufuralol diastereomers were formed. The results from the human liver microsomal studies are consistent with observed enantioselectivity of hydroxylation of bufuralol in vivo in humans.

Adrenergic beta-Antagonists↗
PubMed1990

Enantioselective and diastereoselective aspects of the oxidative metabolism of metoprolol.

Enantio- and diastereoselective aspects of oxidative metabolism of metoprolol (1) were examined in the presence of rat liver and human liver microsomes using a pseudoracemate of 1, made up of equal molar (2R)-1-d0 and (2S)-1-d2, as substrate. Both O-demethylation and alpha-hydroxylation showed only slight enantioselectivity, 2R/2S ratios being 1.18 and 0.93 for these pathways in rat liver microsomes and 1.09 and 0.92 in human liver microsomes. In the presence of the rat liver microsomal fraction, alpha-hydroxylation yielded predominantly the 1'R-hydroxy product, 1'R/1'S ratio greater than 12, regardless of the stereochemistry of the side chain. In humans (extensive metabolizers) administered a single 50 mg oral dose of pseudoracemic metoprolol tartrate, urinary alpha-hydroxymetoprolol (2) accounted for 9.3 +/- 2.4% of the dose, 2R/2S ratio 0.85 +/- 0.14, and the carboxylic acid metabolite 4, accounted for 52.7 +/- 6.8% of the dose, 2R/2S ratio 1.15 +/- 0.09. The data suggested that preferential O-demethylation of the (2R)-enantiomer of 1 could contribute to the 2S greater than 2R plasma ratio of metoprolol enantiomers observed in this population.

Animals↗