The first of several cases of meningococcal meningitis was reported in April 2005, in New Delhi, India. Subsequent to this the Government declared an outbreak, which persisted for two periods, from April-July 2005 and January-March 2006. The National Institute of Communicable Diseases (NICD) recommended using WHO criteria for diagnosis of disease. During the outbreak 380 clinically suspected cases were investigated. Of 55 cases diagnosed as confirmed/probable the mortality rate was 14.6%. Meningitis was reported in 60% of cases and meningococcaemia in 40%. Microscopy of petechial rash was positive in 87.5%, CSF Gram stain positive in 68.3%, and latex agglutination test of CSF positive in 64.9% of samples. Neisseria meningitidis (serogroup A) was isolated from 37.7% of cases, 57.7% from CSF. Blood culture was positive in 10.4% of cases. CrgA polymerase chain reaction for N. meningitidis confirmed the isolates. All isolates were susceptible to third-generation cephalosporins, azithromycin and rifampicin, with increasing resistance to ceftriaxone. Penicillin resistance was encountered in 15.4% of strains. Resistance to quinolones was very high at 100% for levofloxacin, 84.6% for ofloxacin and 65.4% for ciprofloxacin. All patients with penicillin-resistant organisms (4) or intermediate sensitivity (4) succumbed to the disease. These patients also had a higher minimum inhibitory concentration to ceftriaxone.

The apolipoprotein A1 gene polymorphism (G-75A and C+83T) was studied in 100 subjects (50 patients diagnosed with myocardial infarction and 50 healthy subjects). Serum apolipoprotein (apo) A1 and apo B levels were estimated immunoturbidometrically. Extracted DNA from blood was amplified by polymerase chain reaction, digested with MspI restriction enzyme, run on 8% polyacrylamide gel, and restriction fragment length polymorphism was studied by using a gel documentation system. Serum (mean +/- SD) apo A1 levels were significantly higher in control subjects than the study group (100.80 +/- 7.06 mg/dL [1.0 +/- 0.07 g/L] and 72.56 +/- 9.86 mg/dL [0.73 +/- 0.1 g/L], respectively; P < .0001), whereas apo B levels were significantly lower (72.12 +/- 11.32 mg/dL [0.7 +/- 0.1 g/L] and 97.45 +/- 9.04 mg/dL [1.0 +/- 0.09 g/L], respectively; P < .0001). The G allele frequency at the -75-base-pair (bp) site was higher in the study group (79%) compared with the control group (58%). The T allele frequency at the +83-bp site was higher in the study group (56%) than in the control group (32%). G at -75 bp upstream from the start of transcription and T at +83 bp in the first intron may be susceptibility alleles for myocardial infarction.

Background MicroRNAs (miRNAs) represent a novel class of single-stranded RNA molecules of 18–22 nucleotides that serve as powerful tools in the regulation of gene expression. They are important regulatory molecules in several biological processes. Main body Alteration in the expression profiles of miRNAs have been found in several diseases. It is anticipated that miRNA expression profiling can become a novel diagnostic tool in the future. Hence, this review evaluates the implications of miRNAs in various diseases and the recent advances in miRNA expression level detection and their target identification. A systematic approach to review existing literature available on databases such as Medline, PubMed, and EMBASE was conducted to have a better understanding of mechanisms mediating miRNA-dependent gene regulation and their role as diagnostic markers and therapeutic agents. Conclusion A clear understanding of the complex multilevel regulation of miRNA expression is a prerequisite to explicate the origin of a wide variety of diseases. It is understandable that miRNAs offer potential targets both in diagnostics and therapeutics of a multitude of diseases. The inclusion of specific miRNA expression profiles as biomarkers may lead to crucial advancements in facilitating disease diagnosis and classification, monitoring its prognosis, and treatment. However, standardization of methods has a pivotal role in the success of extensive use of miRNA expression profiling in routine clinical settings.

Association of cholesteryl ester transfer protein (CETP) Gene -629C/A Polymorphism with angiographically proven atherosclerosis CETP gene has been linked to CAD risk via its role in HDL and LDL metabolism. There is no agreement of whether CETP is atherogenic or not. Furthermore, various genotypes of CETP gene have been associated with CETP levels and thus with atherosclerosis risk. Our aim was to study the association of CETP -629C/A gene polymorphism with CETP and HDL levels and their association if any with atherosclerosis. Study population consisted of angiographically documented 50 cases with coronary artery atherosclerosis and 50 controls negative for atherosclerosis of coronary artery. Serum lipid profile was measured on SYNCHRON CX-9 using standard kits. Serum CETP levels were measured by ELISA method. CETP -629C/A gene polymorphism was studied using PCR-RFLP method. There was no significant difference in lipid profile of the two groups. However, serum CETP level was significantly higher (46.44 ± 21.75 ng/ml) in cases than controls (37.10 ± 21.92 ng/ml) with value =0.035. The frequency of -629A allele was higher (0.85) in cases than that of controls (0.81). Homozygosity of A allele was more in subjects with atherosclerosis of coronary artery. We conclude that CETP is atherogenic and could be used as atherogenic risk predictor in angiographically proven atherosclerosis. Also A allele of -629C/A polymorphism is more prevalent in cases; indicating its effect on expression of CETP gene.

No abstract