The origins of repetitive thought in rumination: separating cognitive style from deficits in inhibitory control over memory.

BACKGROUND AND OBJECTIVES: Rumination is a major contributor to the maintenance of affective disorders and has been linked to memory control deficits. However, ruminators often report intentionally engaging in repetitive thought due to its perceived benefits. Deliberate re-processing may lead to the appearance of a memory control deficit that is better explained as a difference in cognitive style. METHODS: Ninety-six undergraduate students volunteered to take part in a direct-suppression variant of the Think/No-Think paradigm after which they completed self-report measures of rumination and the degree to which they deliberately re-processed the to-be-suppressed items. RESULTS: We demonstrate a relation between rumination and impaired suppression-induced forgetting. This relation is robust even when controlling for deliberate re-processing of the to-be-suppressed items, a behavior itself related to both rumination and suppression. Therefore, whereas conscious fixation on to-be-suppressed items reduced memory suppression, it did not fully account for the relation between rumination and memory suppression. LIMITATIONS: The current experiment employed a retrospective measure of deliberate re-processing in the context of an unscreened university sample; future research might therefore generalize our findings using an online measure of deliberate re-processing or within a clinical population. CONCLUSIONS: We provide evidence that deliberate re-processing accounts for some--but not all--of the relation between rumination and suppression-induced forgetting. The present findings, observed in a paradigm known to engage top-down inhibitory modulation of mnemonic processing, provide the most theoretically focused evidence to date for the existence of a memory control deficit in rumination.

Analysis of interleukin-10 gene polymorphisms and hepatitis C susceptibility in Pakistan.

INTRODUCTION: Hepatitis C virus (HCV) commonly causes a chronic infection but few of patients are able to clear the virus naturally. Interleukin-10 (IL-10) is an anti-inflammatory cytokine that can suppress the immune response against HCV. Interindividual variations in IL-10 production are genetically contributed by polymorphisms within the IL-10 promoter region. This study aimed to investigate the association of the IL-10 gene promoter -1082 G/A, -819 C/T, and -592 C/A polymorphisms with HCV infection susceptibility in Pakistani individuals. METHODOLOGY: Eighty-nine chronically infected patients and 99 controls were enrolled in the study. IL-10 (-1,082 G/A, -819 C/T, -592 C/A) genotyping was performed by amplification refractory mutation system-polymerase chain reaction (ARMS-PCR). RESULTS: A suggestive evidence of association with hepatitis C was obtained for the IL-10 -819 C/T (-592 C/A) (p: 0.03) promoter polymorphism at the allele level  but not in genotype distribution. The IL-10 -1082 allele showed no association while positive association of GG (p: 0.001) gene and negative association for GA (0.001) gene were observed.  Higher frequencies were observed for GTA (p: 0.02), ACC (p: 0.01) haplotype and GCC/GTA (p: 0.005) diplotype in HCV patients than controls while diplotype GCC/ATA showed protective effect against HCV. CONCLUSIONS: Our findings suggest that different IL-10 gene polymorphisms may lead to an imbalance between the pro-inflammatory and anti-inflammatory cytokine responses which may in turn influence the susceptibility to HCV infection.

Comparative analysis of organophosphate degrading enzymes from diverse species.

Different types of organophosphorous compounds constitute most potent pesticides. These chemicals attack the nervous system of living organisms causing death. Different organisms produce enzymes to degrade these chemicals. These enzymes are present in simple microorganisms from archaea, bacteria to complex eukaryotes like humans. A comparison of representative eight shortlisted enzymes involved in the degradation and inactivation of organophosphates from a wide range of organisms was performed to infer the basis of their common functionality. There is little sequence homology in these enzymes which results in divergent tertiary structures. The only feature that these enzymes seem to share is their amino acid composition. However, structural analysis has shown no significant similarities among this functionally similar group of organophosphate degrading enzymes.

In silico comparative genome analysis of malaria parasite Plasmodium falciparum and Plasmodium vivax chromosome 4.

Malarial parasite has long been a subject of research for a large community of scientists and has yet to be conquered. One of the main obstacles to effectively control this disease is rapidly evolving genetic structure of Plasmodium parasite itself. In this study, we focused on chromosome 4 of the Plasmodium falciparum and Plasmodium vivax species and carried out comparative studies of genes that are responsible for antigenic variation in respective species. Comparative analysis of genes responsible for antigenic variation (var and vir genes in P. falciparum and P. vivax, respectively) showed significant difference in their respective nucleotide sequence lengths as well as amino acid composition. The possible association of exon's length on pathogenecity of respective Plasmodium species was also investigated, and analysis of gene structure showed that on the whole, exon lengths in P. falciparum are larger compared to P. vivax. Analysis of tandem repeats across the genome has shown that the size of repetitive sequences has a direct effect on chromosomes length, which can also be a potential reason for P. falciparum's greater variability and hence pathogenecity than P. vivax.