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Articles by P Xie
Total Records ( 2 ) for P Xie
  Z Lu , P Xie and Z. Qin

The standard gene disruption and replacement to delete the actinorhodin biosynthetic gene cluster (Act) in Streptomyces coelicolor was inefficient, and the polymerase chain reaction-targeting of the cosmid could efficiently delete the Act, but still was a time-consuming procedure for markerless gene replacement. By using optimal Streptomyces codons, we synthesized a sceS gene encoding identical amino acid sequence as the chromosome rare-cutting meganuclease I-sce I of the Saccharomyces cerevisiae mitochondria. Expression of sceS gene in S. coelicolor resulted in promotion of homologous recombination and subsequently, successful achieved markerless deletion of the Act. The sceS system may be useful for the sequential markerless deletions of chromosomal segments in Streptomyces.

  P Xie , H. R Kranzler , J Poling , M. B Stein , R. F Anton , K Brady , R. D Weiss , L Farrer and J. Gelernter

Context  The 5-HTTLPR polymorphism in the promoter region of the serotonin transporter gene (SLC6A4) has been found to moderate several categories of emotional response after stressful life events. Previous studies generally focused on its effect on depressive symptoms; little is known about its moderation of the development of posttraumatic stress disorder (PTSD).

Objective  To examine the effects of childhood adversity, adult traumatic events, 5-HTTLPR genotypes, and gene x environment interactions on the etiology of PTSD.

Design  A cross-sectional study in which participants in several studies investigating the genetics of substance dependence were also screened for lifetime PTSD. The triallelic system of 5-HTTLPR was genotyped. Logistic regression modeling was used in the analyses.

Setting  General community.

Participants  Five hundred eighty-two European American and 670 African American individuals who reported experiences of childhood adversity, adult traumatic events, or both.

Main Outcome Measure  Diagnosis of PTSD, defined by DSM-IV diagnostic criteria and assessed through the Semi-Structured Assessment for Drug Dependence and Alcoholism interview.

Results  Childhood adversity and adult traumatic events both predicted PTSD. Although the 5-HTTLPR genotype alone did not predict the onset of PTSD, it interacted with adult traumatic events and childhood adversity to increase the risk for PTSD, especially for those with high rates of both types of trauma exposure (European American: odds ratio [OR], 2.86; 95% confidence interval [CI], 1.50-5.45; P = .002; African American: OR, 1.88; 95% CI, 1.04-3.40; P = .04; pooled: OR, 2.31; 95% CI, 1.50-3.56; P < .001).

Conclusions  Participants who had both childhood adversity and adult traumatic events were more likely to develop lifetime PTSD compared with those who experienced either type of adverse event. The risk was increased in individuals with 1 or 2 copies of the S’ (S) allele compared with the L’ (L) homozygotes. Our study provides additional direct evidence that PTSD is influenced by the interactive effect of environmental and genetic factors.

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