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The brain-derived neurotrophic factor (BDNF) gene is a candidate gene in therapeutic responses to antidepressants. The aim of the study was to determine the effects of BDNF allelic variability on responses to escitalopram treatment at 3\xa0weeks after treatment initiation and at a 6-week endpoint.', 'We included 187 Caucasian subjects with depression; 153 completed the 6-week study. Clinical evaluation was performed using the Montgomery and Asberg Depression Rating Scale (MADRS) before and after 3-6 weeks of treatment.', 'After 3\xa0weeks of treatment, we saw significantly better treatment responses in the Met carriers and greater antidepressant resistance among the Val/Val homozygotes. Relative to Val/Val homozygous (59.78\xa0%), a significantly greater proportion of subjects Met-carriers (77.94\xa0%) responded to escitalopram treatment (χ (2)\u2009=\u20095.88, p\u2009=\u20090.015). After 6\xa0weeks, we found the same pattern of results but this effect did not reach statistical significance (χ (2)\u2009=\u20092.07, p\u2009=\u20090.15).
Is the BDNF Val ( 66 ) Met polymorphism associated with escitalopram response in depressed patients?

In vitamin K antagonist (VKA)-treated patients with severe hemorrhage, guidelines recommend prompt VKA reversal with prothrombin complex concentrate (PCC) and vitamin K. The aim of this observational cohort study was to evaluate the impact of guideline concordant administration of PCC and vitamin K on seven-day mortality.', 'Data from consecutive patients treated with PCC were prospectively collected in 44 emergency departments. Type of hemorrhage, coagulation parameters, type of treatment and seven-day mortality mortality were recorded. Guideline-concordant administration of PCC and vitamin K (GC-PCC-K) were defined by at least 20 IU/kg factor IX equivalent PCC and at least 5 mg of vitamin K performed within a predefined time frame of eight hours after admission. Multivariate analysis was used to assess the effect of appropriate reversal on seven-day mortality in all patients and in those with intracranial hemorrhage (ICH).', 'Data from 822 VKA-treated patients with severe hemorrhage were collected over 14 months. Bleeding was gastrointestinal (32%), intracranial (32%), muscular (13%), and "other" (23%). In the whole cohort, seven-day mortality was 13% and 33% in patients with ICH. GC-PCC-K was performed in 38% of all patients and 44% of ICH patients. Multivariate analysis showed a two-fold decrease in seven-day mortality in patients with GC-PCC-K (odds ratio (OR)\u2009=\u20092.15 (1.20 to 3.88); P\u2009=\u20090.011); this mortality reduction was also observed when only ICH was considered (OR\u2009=\u20093.23 (1.53 to 6.79); P\u2009=\u20090.002).
Is guideline-concordant administration of prothrombin complex concentrate and vitamin K associated with decreased mortality in patients with severe bleeding under vitamin K antagonist treatment ( EPAHK study )?

Stat6 signaling is active in cancer cells and IL-4-induced Stat6 activities or Stat6 activational phenotypes vary among cancer cells. This study aimed at investigating possible mechanism(s) involved in the formation of varying Stat6 activities/phenotypes.', "Stat6 regulatory genes, SOCS-1 and SHP-1, were examined for mRNA expression using RT-PCR, and their promoter DNA methylation was assayed by methylation-specific PCR in Stat6-phenotyped colon cancer cell lines. DNA methylation was then verified by sequencing. RT-PCR assay and Western blotting were used to detect the expression of SOCS-1 and SHP-1 after demethylation using 5-aza-2'-deoxycytidine.", "Compared with Stat6(null) Caco-2 cells, Stat6(high) HT-29 cells showed decreased constitutive expression of SOCS-1 and SHP-1, which correlated with DNA hypermethylation in these genes' promoters. Interestingly, demethylation in HT-29 cells recovered the constitutive expression of SOCS-1 and SHP-1.

Does dNA methylation regulate constitutive expression of Stat6 regulatory genes SOCS-1 and SHP-1 in colon cancer cells?