Prevalence of H. pylori in Immune Thrombocytopenic Purpura (ITP) in a tertiary care center, South India

Introduction: Immune thrombocytopenic purpura (ITP) has been linked with Helicobacter Pylori infection. Objectives: The objective of the present study was to determine the prevalence of H pylori infection in adult ITP patients in a tertiary care center in South India. Methods: 50 adult patients with ITP in the Department Hematology, Madras Medical College were recruited for a cross -sectional study over a period of 6 months. Biopsy from the antrum was subjected to Rapid urease test to detect H. pylori. A total of 50 patients participated in the study. Result: The prevalence of H. pylori infection in ITP patients was 36%. The majority of patients were male (78%). Conclusion: The diagnosis of H. pylori in ITP patients may be considered in high prevalent areas.

Amlodipine Abridged Calcium Associated Complex-I Inhibition in 6-OHDA Lesioned Parkinson’s Rat.

Aims: The present study was carried out to evaluate Amlodipine, a L-type calcium channel blocker for alleviating or reducing the neurodegeneration in 6-OHDA lesioned rat models. Place and Duration of Study: Department of Pharmacology, JSS College of Pharmacy, Rocklands, Ooty, India between October 2011 and may 2012. Methodology: Male adult Wistar rats were given with intra-cerebroventricular injection of 6-hydroxydopamine (6-OHDA) into the median forebrain bundle and treated post 48 hours with Amlodipine (10 mg/kg and 20 mg/kg) per oral for 30 days. Motor coordination, striatal dopamine, mid brain calcium and complex-I activity were estimated. Data were statistically analyzed and p<0.05 was considered significant. Results: Amlodipine regained motor coordination, mid-brain dopamine content, and prevented calcium overload and complex I activity at both dose levels when compared with 6-OHDA control group. Alleviation of calcium overload and complex I inhibition with subsequent increase in dopamine level in Parkinson’s rats were observed at the end of treatment period. Conclusion: The experimental study gave light to a new therapeutic intervention of Amlodipine in preventing neuronal morbidity in Parkinson’s disease (PD). So, further neuro-molecular study with Amlodipine in experimental PD is warranted in future.

Characterization of foot-and-mouth disease virus types Ο and Asia 1 RNA.

Poly (A) RNA was isolated from foot-and-mouth disease virus-infected cells by oligo (dT)-cellulose chromatography. One-dimensional oligonucleotide mapping of virusinduced poly (A) RNA indicated major differences between virus types Ο and Asia 1. Base composition analysis of virus-induced RNA showed no significant differences between types O and Asia 1.

Effect of cupric-isonicotinic acid hydrazide complex on avian myeloblastosis virus reverse transcriptase and its associated enzyme activities.

Cupric complex of isonicotinic acid hydrazide inhibits DNA synthesis by avian myloblastosis virus reverse transcriptase. This inhibition occurs in the presence of either ribonucleotide or deoxyribonucleotide templates. The inhibition of reverse transcriptase by cupric-INH complex is considerably reduced when stored or proteolytically cleaved enzyme was used in the reaction. The complex also inhibits the reverse transciptase-associated RNase Η activity. The cupric-isonicotinic acid hydrazide complex cleaves pBR 322 from I DNA into smaller molecules in the presence or absence of reverse transcriptase-associated endonuclease. However, in the presence of the enzyme the DNA is cleaved to a greater extent.

Effect of cupric-isonicotinic acid hydrazide complex on normal and avian myeloblastosis virus-infected cells cultivated in vitro.

The cupric complex of isonicotinic acid hydrazide was found to be nontoxic to normal yolk sac macrophages upto a concentration of 100 μΜ. At this concentration the complex did not significantly inhibit DNA, RNA or protein synthesis in these cells. The complex inhibited the avian myeloblastosis virus multiplication in these cells when added 0–4 h post-infection as demonstrated by the inhibition of both focus formation and expression of viral specific antigens. This inhibition was not observed when the complex was added 8 and 16 h after avian myeloblastosis virus infection. The studies carried out on avian myeloblastosis virus-transformed myeloblasts indicated that the complex had no effect on the colony (focus) formation. The results suggest that the complex inhibits the virus multiplication by interfering in an early event of viral growth cycle, possibly the process of reverse transcription.

Characterisation of rinderpest virus RNA and the action of actinomycin D on its replication.

RNA extracted from purified rinderpest virus was characterised by sucrose gradient sedimentation and polyacrylamide gel electrophoresis. The predominant virion RNA species had a sedimentation constant of 46S and its estimated molecular weight was 4·8 × 106 daltons. Consistently high amounts of UMP and AMP were detected. The melting-temperature profile of the virion RNA suggested absence of secondary structure. The effect of actionomycin D on the replication of rinderpest virus in Vero cells was studied by following the viral RNA synthesis using labelled uridine as well as by infectivity titration. The viral RNA synthesis was not affected until 12 h following infection and was inhibited thereafter between 18 and 48 h to an extent of 25% at 5 and 10 μg levels of the drug. A 100 to 1000-fold reduction in the infectivity titres was observed in the presence of the drug. These results suggest that actinomycin D inhibits rinderpest viral RNA replication. Sedimentation analysis of viral RNA extracted from drug-treated cultures showed inhibition of the genome RNA of rinderpest virus.