Tag: nevin manimala

Northwest Med Surg J. 1856 Jan;5(1):47-53.

NO ABSTRACT

PMID:37320580 | PMC:PMC9970425

Northwest Med Surg J. 1855 Mar;4(3):139-141.

NO ABSTRACT

PMID:37320302 | PMC:PMC9956402

Northwest Med Surg J. 1854 Mar;3(3):140-141.

NO ABSTRACT

PMID:37320266 | PMC:PMC9946641

Northwest Med Surg J. 1851 May;4(1):84-85.

NO ABSTRACT

PMID:37320133 | PMC:PMC9943205

Northwest Med Surg J. 1852 May;1(1):47.

NO ABSTRACT

PMID:37320019 | PMC:PMC9937401

Northwest Med Surg J. 1850 May;3(1):87.

NO ABSTRACT

PMID:37319754 | PMC:PMC9934192

Northwest Med Surg J. 1849 Apr-May;2(1):90.

NO ABSTRACT

PMID:37319675 | PMC:PMC9928371

Northwest Med Surg J. 1849 Jan;1(5):430-436.

NO ABSTRACT

PMID:37319531 | PMC:PMC9904673

Northwest Med Surg J. 1848 Apr-May;1(1):80-84.

NO ABSTRACT

PMID:37319455 | PMC:PMC9904560

Schizophr Bull. 2023 Jun 15:sbad082. doi: 10.1093/schbul/sbad082. Online ahead of print.

ABSTRACT

BACKGROUND: Immune mechanisms are indicated in schizophrenia (SCZ). Recent genome-wide association studies (GWAS) have identified genetic variants associated with SCZ and immune-related phenotypes. Here, we use cutting edge statistical tools to identify shared genetic variants between SCZ and white blood cell (WBC) counts and further understand the role of the immune system in SCZ.

STUDY DESIGN: GWAS results from SCZ (patients, n = 53 386; controls, n = 77 258) and WBC counts (n = 56 3085) were analyzed. We applied linkage disequilibrium score regression, the conditional false discovery rate method and the bivariate causal mixture model for analyses of genetic associations and overlap, and 2 sample Mendelian randomization to estimate causal effects.

STUDY RESULTS: The polygenicity for SCZ was 7.5 times higher than for WBC count and constituted 32%-59% of WBC count genetic loci. While there was a significant but weak positive genetic correlation between SCZ and lymphocytes (rg = 0.05), the conditional false discovery rate method identified 383 shared genetic loci (53% concordant effect directions), with shared variants encompassing all investigated WBC subtypes: lymphocytes, n = 215 (56% concordant); neutrophils, n = 158 (49% concordant); monocytes, n = 146 (47% concordant); eosinophils, n = 135 (56% concordant); and basophils, n = 64 (53% concordant). A few causal effects were suggested, but consensus was lacking across different Mendelian randomization methods. Functional analyses indicated cellular functioning and regulation of translation as overlapping mechanisms.

CONCLUSIONS: Our results suggest that genetic factors involved in WBC counts are associated with the risk of SCZ, indicating a role of immune mechanisms in subgroups of SCZ with potential for stratification of patients for immune targeted treatment.

PMID:37319439 | DOI:10.1093/schbul/sbad082