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N Ramesh

Publications and source records attributed to N Ramesh.

87 records · Page 5Linked to original sources
PubMed1989

Type I C1 inhibitor deficiency with a small messenger RNA resulting from deletion of one exon.

The molecular genetic basis of C1 inhibitor (C1 INH) deficiency in a patient with type I hereditary angioneurotic edema was studied. This patient was found to have an abnormally short C1 INH mRNA together with a normal message. Restriction fragment length polymorphism of the C1 INH gene was detected by Southern blot analysis of the patient's DNA after digestion with Pst I or Sac I, and hybridization with a full-length C1 INH cDNA. Hybridization of the same blot with three different fragments of the full-length cDNA suggested that exon VII and portions of both flanking introns were deleted in the C1 INH gene. Northern blot analysis of RNA from cultured monocytes, using a probe corresponding to exon VII, also indicated that the abnormal C1 INH mRNA had a deletion of these nucleotides. To confirm the hypothesis that the short C1 INH mRNA contained a deletion, the involved segment of the patient's C1 INH mRNA was amplified using the polymerase chain reaction (PCR). PCR amplification yielded two C1 INH DNA fragments of different lengths (380 and 160 bp). Southern blot and sequence analysis of both DNA fragments clearly revealed that the smaller 160-bp DNA was derived from the abnormal message and had a deletion of nucleotides corresponding to exon VII.

Angioedema↗
PubMed1988

Purification and characterization of two trypsin inhibitors from the hemolymph of Manduca sexta larvae.

Trypsin inhibitory activity from the hemolymph of the tobacco hornworm (Manduca sexta) was purified by affinity chromatography on immobilized trypsin and resolved into two fractions with molecular weights of 14,000 (M. sexta hemolymph trypsin inhibitor (HLTI) A) and 8,000 (HLTI B) by molecular sieve chromatography on Sephadex G-75. Electrophoresis of these inhibitors under reducing conditions on polyacrylamide gels gave molecular weight estimates of 8,300 for HLTI A and 9,100 for HLTI B, suggesting that HLTI A is a dimer and HLTI B is a monomer. Isoelectrofocusing on polyacrylamide gels focused HLTI A as a single band with pI 5.7, whereas HLTI B was resolved into two components with pI values of 5.3 and 7.1. Both inhibitors were stable at 100 degrees C and pH 1.0 for at least 30 min. HLTIs A and B inhibited serine proteases such as trypsin, chymotrypsin, and plasmin, but did not inhibit elastase, papain, pepsin, subtilisin BPN', and thermolysin. In fact, subtilisin BPN' completely inactivated both inhibitors. Both inhibitors formed low-dissociation complexes with trypsin in a 1:1 molar ratio. The inhibition constant for trypsin inhibition by HLTI A was estimated to be 1.45 x 10(-8) M. The HLTI A-chymotrypsin complex did not inhibit trypsin; similarly, the HLTI A-trypsin complex did not inhibit chymotrypsin, indicating that HLTI A has a common binding site for both trypsin and chymotrypsin. The amino-terminal amino acid sequences of HLTIs A and B revealed that both these inhibitors are homologous to bovine pancreatic trypsin inhibitor (Kunitz).

Animals↗
PubMed1988

Molecular basis of ornithine aminotransferase deficiency in B-6-responsive and -nonresponsive forms of gyrate atrophy.

Gyrate atrophy (GA), a recessive eye disease involving progressive loss of vision due to chorioretinal degeneration, is associated with a deficiency of the mitochondrial enzyme ornithine aminotransferase (OATase; ornithine-oxo-acid aminotransferase; L-ornithine:2-oxo-acid aminotransferase, EC 2.6.1.13) with consequent hyperornithinemia. Genetic heterogeneity of GA has been suggested by the demonstration that administration of pyridoxine to increase the level of pyridoxal phosphate, a cofactor of OATase, reduces hyperornithinemia in a subset of patients. We have cloned and sequenced cDNAs for OATase from two GA patients, one responsive and one nonresponsive to pyridoxine treatment. The respective cDNAs contained different single missense mutations, which were sufficient to eliminate OATase activity when each cDNA was tested in a eukaryotic expression system. However, like the enzyme in fibroblasts from the pyridoxine-responsive patient, OATase encoded by the corresponding cDNA from this individual showed a significant increase in activity when assayed in the presence of an increased pyridoxal phosphate concentration. These data firmly establish that both pyridoxine responsive and nonresponsive forms of GA result from mutations in the OATase structural gene. Moreover, they provide a molecular characterization of the primary lesion in a pyridoxine-responsive genetic disorder.

Cloning, Molecular↗
PubMed1986

Recognition of B and Z forms of DNA by Escherichia coli DNA polymerase I.

Since the substrate binding domain of the large proteolytic fragment of Escherichia coli DNA polymerase I has been shown to interact with the B forms of DNA, we have studied the ability of this enzyme to recognize structures other than the B form. The polymerase activity has been used to evaluate the degree of recognition of the B and Z forms of DNA. The Z form was found to promote less activity, indicating the probable inability of the polymerase to move along the conformationally rigid form of the template. The present study indicates that the Z-DNA found in vivo may have a role in the control of replication.

DNA Polymerase I↗
PubMed1985

Endogenous protease inhibitors prevent undesired activation of prophenolase in insect hemolymph.

Phenoloxidase activation in the whole hemolymph of Sarcophaga bullata and Manduca sexta larvae is shown to be achieved by proteolytic cleavage of the proenzyme. This process is inhibited by the serine protease inactivator, Diisopropyl phosphofluoridate. Endogenous protease inhibitors isolated from the larvae inhibit alpha-chymotrypsin mediated prophenoloxidase activation in the hemolymph. These observations suggest that the endogenous protease inhibitors prevent undesired activation of prophenol oxidase in the hemolymph by inhibiting the serine protease involved in the activation process.

Animals↗
PubMed1985

Poly(dG-dC) in the Z-form inhibits E. coli DNA polymerase I and AMV DNA polymerase activity.

The effect of Z-conformation of DNA on its template activity in DNA synthesis reactions in vitro has been studied. Normal poly(dG-dC) in the B-form, brominated and unbrominated in the Z-form have been compared for their template activity in DNA synthesis reactions mediated by AMV DNA polymerase and E. coli DNA polymerase I. The results indicate that poly(dG-dC) in the Z-form is totally inactive as a template for DNA synthesis and further that it is a strong competitive inhibitor of copying of the B-form DNA.

Avian Leukosis Virus↗
PubMed1983

Critical cation balance in B leads to Z transition: role of Li+.

The sodium salt of poly(dG-dC) is known to exhibit a B leads to Z transition in the presence of various cations and 60% alcohol. We here show that the lithium salt of poly(dG-dC) does not undergo B leads to Z transition in the presence of 60% alcohol since Li+ with its large hydration shell cannot stabilize the Z-form. On the other hand, high concentrations of Mg2+ or micromolar concentrations of the cobalt hexamine complex which are known to stabilize the Z-form can compete with Li+ for charge neutralization and hence bring about a B leads to Z transition in the same polymer. From the model building studies the mode of action of the cobalt-hexamine complex in stabilizing the Z-form is postulated.

Cations, Monovalent↗
PubMedDate not supplied

CD40 ligand/CD40 deficiency.

CD40 is a surface antigen expressed on B cells. The CD40 ligand (CD40L) is expressed on activated T cells. Interaction between CD40 and CD40L is critical for proliferation and isotype switching in the context of a response to a T-cell-dependent antigen. Patients with X-linked hyper-IgM syndrome (HIGMX-1) in their CD40L gene are unable to switch from IgM to IgG, IgA and IgE. Mice with a disrupted CD40 gene fail to undergo isotype switching to T-cell-dependent antigens but respond normally to T-independent antigens.

Animals↗
PubMedDate not supplied

Prevalence of periodontal disease in endemically flourosed areas of Davangere Taluk, India.

Success of fluoride in combating dental caries led to study of fluoride on periodontal disease, but studies are less reported in literature and results are varied in nature. To address this issue, the study was conducted to assess severity of periodontal disease among (n = 283) 36-45 years old adults residing in area of different concentration of fluoride in drinking water. The villages selected were having fluoride concentration in their drinking water are Shamnur (0.5 PPMF), Kundawada (1.1 ppmF) and Halebathi (3.17 ppm). Ion Selective Electrode Method (OrionUSA) estimated fluoride in drinking water. Community Periodontal Index (WHO, 1997) and Plaque Index (Silness and Loe, 1967) was used to assess periodontal status. There was consistent decrease in mean plaque score from 1.45+ _0.024 at 0.51 ppm, 1.21+ _0.009 at 1.1 ppm, and 1.12+ _0.08 at 3.17 ppm fluoride area. This difference was significant statistically (P < 0.001). As the fluoride concentration in drinking water increased there was decrease in severity of prevalence of periodontitis. This difference in observation was significant statistically (P < 0.05). There were no effects of fluoride on calculus, since little variability was found in three different fluoride areas. Thus it was concluded from the study results that the increase in fluoride concentration decreased the plaque accumulation. decreased the shallow and deep pockets. Hence lower prevalence and severity of periodontal disease.

Adult↗