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S Babu

Publications and source records attributed to S Babu.

At least 19 recordsLinked to original sources
PubMed2006

Flocculation and percolation in reversible cluster-cluster aggregation.

Off-lattice dynamic Monte-Carlo simulations were done of reversible cluster-cluster aggregation for spheres that form rigid bonds at contact. The equilibrium properties were found to be determined by the life time of encounters between two particles (te). te is a function not only of the probability to form or break a bond, but also of the elementary step size of the Brownian motion of the particles. In the flocculation regime the fractal dimension of the clusters is df=2.0 and the size distribution has a power law decay with exponent tau=1.5. At larger values of te transient gels are formed. Close to the percolation threshold the clusters have a fractal dimension df=2.7 and the power law exponent of the size distribution is tau=2.1. The transition between flocculation and percolation occurs at a characteristic weight average aggregation number that decreases with increasing volume fraction.

Journal Article↗
PubMed2006

Conserved cis-elements in the Xenopus red opsin promoter necessary for cone-specific expression.

The long-wavelength sensitive (red) opsin genes encode proteins which play a central role in daytime and color vision in vertebrates. We used transgenic Xenopus to identify 5' cis-elements in the red cone opsin promoter necessary for cone-specific expression. We found a highly conserved extended region (-725 to -173) that was required for restricting GFP transgene expression to cones. We further identified a short element (5'-CCAATTAAGAGAT-3') highly conserved amongst tetrapods, including humans, necessary to restrict expression to cones in the retina. These results identify novel conserved elements that regulate spatial expression of tetrapod red cone opsin genes.

5' Flanking Region↗
PubMed2006

Chromosome 22 microdeletion by F.I.S.H. in isolated congenital heart disease.

OBJECTIVE: To analyze the frequency of del22q11.2 in non-syndromic CHDs using classical cytogenetics and Fluorescence In Situ Hybridization (FISH) technique in Indian population. METHODS: 105 prospective cases which included 6 families with isolated, non-syndromic cardiac defects were analyzed clinically by a cardiologist and a geneticist. The cases were then subjected to karyotypic (classical cytogenetics) as well as FISH analysis. The efficacy of FISH technique was compared with inference drawn from classical cytogenetics. RESULTS: Karyotypic analysis of all the 105 patients revealed a normal chromosomal complement. Microdeletion 22q11.2 was observed in six patients (5.71%) by FISH studies. FISH studies were also performed on the parents of these six patients who revealed a normal chromosome 22. No correlation was found between clinical features (mild or unspecific) with 22q11.2 microdeletion. CONCLUSION: The testing for microdeletion 22q11.2 in isolated non-syndromic patients using FISH technique is mandatory even when mild/unspecific extracardiac abnormalities are seen in the patients.

Adolescent↗
PubMed2004

High frequency of abnormal glucose tolerance in DQA1*0102/DQB1*0602 relatives identified as part of the Diabetes Prevention Trial--Type 1 Diabetes.

AIMS/HYPOTHESIS: Immunological and genetic markers can be used to assess risk of developing type 1 diabetes prior to the onset of clinical symptoms. Autoantibody-positive relatives of patients with type 1 diabetes are at increased risk for disease, while the presence of HLA DQA1*0102/DQB1*0602 is thought to confer protection. Using the unique population identified by the Diabetes Prevention Trial--Type Diabetes (DPT-1), our aim was to determine if these individuals were protected from type 1 diabetes. METHODS: We described metabolic and immunological characteristics of islet cell cytoplasmic autoantibodies-positive relatives with DQB1*0602 identified as part of DPT-1. RESULTS: We found that 32% of DQB1*0602-positive relatives identified through the DPT-1 had abnormalities of glucose tolerance despite the fact that only 19% had multiple type 1 diabetes-associated autoantibodies and only 13% had abnormal insulin secretion, markers typically associated with the disease. In addition, these markers were not associated with abnormal glucose tolerance. In contrast, the DQB1*0602-positive relatives had elevated fasting insulin (117+/-10 pmol/l) and homeostasis model assessment of insulin resistance (HOMA-R) (4.90+/-0.5) values, which are more commonly associated with type 2 diabetes. The later marker of insulin resistance was associated with glucose tolerance status. CONCLUSIONS/INTERPRETATION: Our data indicate that DQA1*0102/DQB1*0602 relatives identified through DPT-1 have a high frequency of abnormal glucose tolerance and a disease phenotype with characteristics of type 1 and type 2 diabetes. Thus, multiple pathways to abnormal glucose tolerance are present within families of these type 1 patients.

Autoantibodies↗
PubMed2004

Clinical presentation of acute chest syndrome in sickle cell disease.

In this study the records of 45 patients with sickle cell disease involved in 63 presentations of acute chest syndrome at the Princess Margaret Hospital in Nassau, the Bahamas, between 1997 and 2001 were examined. Patients were divided into three groups on the basis of age (<13 years, 13-18 years, >/=19 years) with a view to assessing clinical presentation. The incidence of symptoms, physical signs, and laboratory findings were enumerated and significant differences between age groups determined. The data were analysed using analysis of variance, t test, and chi(2) test and compared with existing knowledge on the subject. This study proposed to evaluate the clinical presentation of acute chest syndrome with emphasis on historical and physical findings, and to encourage the physician to maintain a high index of suspicion for the condition in susceptible patients. It was found that presentation varied significantly with age groups, children presenting most classically with fever and cough and adults, with chest pain. The 13-18 age group emerged as the group which presented most frequently with the typical symptoms of chest infection, thus potentially making diagnosis easier. Of note, the most frequent finding was a normal examination, while the second commonest physical finding was crepitations on auscultation of the chest.

Acute Disease↗
PubMed2002

Phylogenetic relationships and genetic polymorphisms in wild Indian mice.

Randomly amplified polymorphic DNA (RAPD) analysis was used to examine the extent of variability in 11 Indian wild derived commensal house mice (Mus musculus) populations and compared with inbred strains of musculus and domesticus subspecies as well as commonly used laboratory inbred strains C57BL/6J and DBA/2J. Arbitrary designed 10 mer oligonucleotide primers with 60-70% (G+C) content were used to amplify DNA template. Out of 52 primers screened initially on the laboratory strains, 20 were selected for analysis on the basis of amplification product in the size range of 200-1400 bp. Among 353 total polymorphic bands, 220 bands (64%) were found to be polymorphic in Indian wild mice, 85 bands (25%) in wild derived inbred strains and 37 bands (11%) in laboratory mice strains. The amplification patterns produced by primers were statistically analysed by Jaccard's similarity coefficient the value of which ranged from 0.56 to 0.80. High level of genetic diversity was seen in the Indian wild mice populations as compared to the controls. The UPGMA phenogram grouped mice population into two major clusters except Bikaner [BIK], Bilaspur [BIL] and Ranikhet [RK] populations which were placed outside the close-knit clusters. Inspite of low values of bootstrap estimates obtained by Wagner and Dollo parsimony analysis, the results were comparable with UPGMA phenogram when constitution of the populations in the major cluster was considered. Indian mice populations appeared to be diverse from laboratory inbred mice strains.

Animals↗
PubMed2002

MHC class I chain-related gene alleles 5 and 5.1 are transmitted more frequently to type 1 diabetes offspring in HBDI families.

Type 1 diabetes mellitus (T1DM) is an autoimmune disease characterized by autoimmune destruction of pancreatic beta cells. Genetic and environmental factors contribute in this disease. There is evidence that MHC class I chain-related gene (MIC-A) plays a role in the susceptibility to this and other autoimmune diseases. There are five alleles of the MIC-A gene, which consist of different repetitions of GCT. In particular, MIC-A alleles 5 and 5.1 (the former with five repetitions of GCT, the latter with five repetitions and one additional insertion of nucleotide G) have been found to be associated with susceptibility to and age at onset of T1DM. The aim of our study was to analyze the transmission of these MIC-A alleles to T1DM-affected offsprings in HBDI families. These are multiplex families with affected offsprings and unaffected parents. DNA samples were amplified for MIC-A using fluorescence-labeled primers and analyzed on an ABI prism DNA sequencer. The transmission of alleles was then analyzed using pedigrees of families also obtained from HBDI. We analyzed 78 families and found that MIC-A alleles 5 and 5.1 are present and transmitted more frequently than expected. Heterozygotic parents for MIC-A alleles 5 and 5.1 were excluded from the study. Our results suggest that MIC-A alleles 5 and 5.1 are associated with susceptibility to T1DM in family studies.

Alleles↗
PubMed2001

Course of Brugia malayi infection in C57BL/6J NOS2 +/+ and -/- mice.

Previous results from our laboratory using pharmacological approaches suggested a role for nitric oxide (NO) in the host defense against the human filarial parasite, Brugia malayi. We sought to determine whether a complementary genetic approach, using mice homozygous for a targeted mutation in the gene encoding inducible nitric oxide-synthase (NOS2), would confirm our observation. We hypothesized that such mice would exhibit some deficit in their ability to clear B. malayi. Our data show that the course of infection in NOS2-/- mice is the same as in wild-type mice. Thus, peritoneal cellular responses to infection are similar in NOS2-/- and wild-type mice, with the exception that T cells form a higher percentage of total peritoneal cells in the former. We find virtually no serum IgE in NOS2-/- mice, suggesting a less robust Th2 response. In contrast, NOS2-/- mice demonstrate an early rise in IgG2a titers compared to B6 +/+ mice. Our data suggest that NO is not an obligate requirement for the elimination of B. malayi from the peritoneal cavities of mice.

Animals↗
PubMed2001

Purification and characterization of an extracellular alpha-glucosidase protein from Trichoderma viride which degrades a phytotoxin associated with sheath blight disease in rice.

AIMS: To purify and characterize an extracellular alpha-glucosidase from Trichoderma viride capable of inactivating a host-specific phytotoxin, designated RS toxin, produced by the rice sheath blight pathogen, Rhizoctonia solani Kühn. METHODS AND RESULTS: The host-specific RS toxin was purified from both culture filtrates (culture filtrate toxin, CFTox) and R. solani-inoculated rice sheaths (sheath blight toxin, SBTox). Sodium dodecyl sulphate-polyacrylamide gel electrophoresis analyses of extracellular proteins, purified from a biocontrol fungus T. viride (TvMNT7) grown on SBTox and CFTox separately, were carried out. The antifungal activity of the purified high molecular weight protein (110 kDa) was studied against RS toxin as well as on the sclerotial germination and mycelial growth of R. solani. Enzyme assay and Western blot analysis with the antirabbit TvMNT7 110-kDa protein indicated that the protein was an alpha-glucosidase. The 110-kDa protein was highly specific to RS toxin and its Michaelis-Menten constant value was 0.40 mmol l-1 when p-nitrophenyl alpha-D-glucopyranoside was used as the substrate. The isoelectric point of the protein was 5.2. N-terminal sequencing of the alpha-glucosidase protein showed that its amino acid sequence showed no homology with other known alpha-glucosidases. CONCLUSION: This appears to be the first report of the purification and characterization of an alpha-glucosidase capable of inactivating a host-specific toxin of fungal origin. The alpha-glucosidase is specific to RS toxin and is different from the known alpha-glucosidases. SIGNIFICANCE AND IMPACT OF THE STUDY: As RS toxin could be inactivated by the microbial alpha-glucosidase enzyme, isolation of the gene that codes for the enzyme from T. viride and transfer of the gene to rice plants would lead to enhanced resistance against sheath blight pathogen by inactivation of RS toxin.

Amino Acid Sequence↗
PubMed2001

Acid-labile subunit regulation during the early stages of liver regeneration: implications for glucoregulation.

The initiation of liver regeneration is regulated by endogenously produced growth factors and cytokines and is accompanied by suppression of growth hormone (GH) binding to hepatocytes. We have demonstrated some of these factors, particularly GH, which modulate acid-labile subunit (ALS) expression in vitro. Consequently, we investigated ALS hepatic mRNA and serum levels in rats for 24 h after partial hepatectomy (PHx). There was a significant suppression of ALS gene expression (approximately 50%, P < 0.005) and serum levels (approximately 30%, P < 0.02) by 12 h in PHx rats relative to controls. Relative to intact animals, hepatic mRNA and serum levels of ALS were suppressed by approximately 60% at 24 h. Similarly, hepatic GH receptor mRNA levels were significantly reduced in PHx animals. Moreover, hepatocytes isolated from PHx animals were less responsive to GH than those from controls. Overall, our results demonstrate that suppression of ALS gene expression and serum levels during liver regeneration relates to lowered hepatic GH sensitivity. Suppressed circulating ALS may alter insulin-like growth factor bioavailability and constitute a mechanism to maintain relatively normal glucoregulation after loss of liver mass.

Animals↗
PubMed2000

Development of a serum-free system for the in vitro cultivation of Brugia malayi infective-stage larvae.

Over the past several years, numerous attempts have been made to culture the infective-stage (L3) larvae of the human filarial parasite Brugia malayi in an in vitro system that promotes molting to the fourth larval stage (L4). Although there have been reports in the literature of successful L3 to L4 development in vitro, all of these systems have required serum supplementation. The complexity of serum as a culture supplement has made reproducibility of results and identification of specific factors necessary for L3 development problematic. We have developed a serum-free in vitro system consisting of RPMI 1640 supplemented with one of three fatty acids (arachidonic, linoleic, or linolenic) that supports consistent and reproducible molting to the fourth larval stage in the presence of a basidiomycetous yeast, Rhodotorula minuta. Coculture with this yeast, initially isolated as a culture contaminant, is required for successful molting. In serum-free cultures lacking R. minuta, L3 larvae survive for upward of 2 weeks, but do not molt successfully. The L4 larvae generated in cultures containing R. minuta are well formed, as seen by light and electron microscopy, and are capable of further development upon transfer to a permissive host. This culture system is inexpensive and easily reproducible, thus making it a useful tool for studying the requirements for the development of B. malayi L3.

Animals↗
PubMed2000

Inactivation of phytotoxin produced by the rice sheath blight pathogen Rhizoctonia solani.

The rice sheath blight pathogen, Rhizoctonia solani, produces a toxin designated as RS-toxin, a carbohydrate compound containing mainly alpha-glucose and mannose. Different microflora were tested for RS-toxin inactivation. Isolates of Trichoderma viride inactivated this toxin when it was provided as the sole food source, and these isolates reduced the severity of toxin-induced symptoms and electrolyte leakage from rice cells. The best-performing isolate, TvMNT7, produced two extracellular proteins of 110 and 17 kDa. The high molecular mass protein was shown to have alpha-glucosidase activity. The purified 110 kDa protein was able to reduce RS-toxin activity.

Blotting, Western↗
PubMed2000

Common susceptibility and transmission pattern of human leukocyte antigen DRB1-DQB1 haplotypes to Korean and Caucasian patients with type 1 diabetes.

The incidence of type 1 diabetes in Korea is less than 1/10th of that in the United States, and it has been suggested that human leukocyte antigen (HLA) alleles of Asian patients associated with diabetes differ from those of Caucasians. In this study we analyzed the common susceptibility and transmission pattern of a series of HLA DRB1-DQB1 haplotypes to Korean and Caucasian patients with type 1 diabetes. We performed HLA DR and DQ typing of 158 type 1 diabetic patients in a case control study, 140 nondiabetic subjects from the same geographical area, 49 simplex families from Seoul, and 283 families from the Human Biological Data Interchange. Although the haplotype frequencies in the two populations are quite different, when identical haplotypes are compared, their odds ratios are nearly the same. For all parental haplotypes, the transmission to diabetic offspring was similar for Korean and Caucasian families (r = 0.8; P: < 10(-)(4)). Allowing for ethnic differences in allelic associations due to different frequencies of DRB1 and DQB1 haplotypes (linkage disequilibrium), these data show, not only by case-control comparison but also by transmission analyses of the haplotypes, that the susceptibility effects of DRB1-DQB1 haplotypes are consistent in Koreans and Caucasians. Thus, the influence of class II susceptibility and resistance alleles appears to transcend ethnic and geographic diversity of type 1 diabetes.

Adolescent↗
PubMed1999

T cells facilitate Brugia malayi development in TCRalpha(null) mice.

The host-parasite interactions of Brugia malayi in mice are complex and multifactorial. In order to study the role of T cells in early B. malayi development, we infected TCRalpha(null) mice, which retain a population of CD4+ TCRbeta+ cells and TCRbeta(null) mice, which lack all TCRalphabeta(+) T cells. TCRalpha(null) mice were permissive to L4 larval and adult worm development but TCRbeta(null) mice were not. Depletion of the CD4(+) T cells in the former abrogated the permissive phenotype. It appears that the CD4(+) TCRbeta(+) T cells that have been described in TCRalpha(null) mice may facilitate early B. malayi development. These data are similar to our earlier demonstration of the role of NK cells in facilitating worm growth in SCID mice.

Animals↗
PubMed1999

One third of HLA DQ2 homozygous patients with type 1 diabetes express celiac disease-associated transglutaminase autoantibodies.

Type 1 diabetes and celiac disease are both immunologic disorders where specific HLA alleles are associated with disease risk. We have developed a radioassay for autoantibodies to tissue transglutaminase (tTG) following the report that this enzyme is 'the' endomysial autoantigen (EMA) of celiac disease. The radioassay for transglutaminase autoantibodies is similar to that utilized for detecting anti-islet autoantibodies. The 'cut-off' for the IgA autoantibody assay was established as 3 x 100th percentile of 184 healthy control subjects at an index of 0.05. Ninety-eight of 847 patients with type 1 diabetes (11.6%) had tissue transglutaminase autoantibodies (tTG). All EMA-positive patients were positive (49/49) for transglutaminase autoantibodies, as were 49/540 EMA-negative patients. Twenty transglutaminase-positive patients consented to intestinal biopsy and 15 biopsies were positive for celiac disease. All patients with a transglutaminase level greater than 0.70 (13/13) had a positive biopsy, while none (0/3) with a level <0.3 had a positive biopsy. The prevalence of transglutaminase autoantibodies was higher in diabetic patients with HLA DQ2 or DQ8. One third of DQ2 homozygous patients (22/68) expressed transglutaminase autoantibodies vs. less than 2% of patients lacking DQ2 or DQ8. A simple radioassay for IgA transglutaminase autoantibodies detects all endomysial antibody positive patients and detects transglutaminase autoantibodies in 5% of endomysial autoantibody negative patients. The prevalence of transglutaminase autoantibodies is associated with DQ2 and DQ8 and in particular DQ2 homozygosity. Autoimmunity to transglutaminase is remarkably prevalent amongst patients with type 1 diabetes expressing certain class II HLA alleles.

Adolescent↗