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Background Oxidative stress and inflammation play important roles in the neuronal injury caused by intracerebral hemorrhage (ICH). Uric acid (UA), an important natural antioxidant, might reduce the neuronal injury caused by ICH. Delineating the relationship between UA and ICH will enhance our understanding of antioxidative mechanisms in recovery from ICH. Methods We conducted a retrospective study of 325 patients with acute supratentorial ICH to investigate the relationship between serum UA levels and hematoma volumes and prognosis. A hematoma volume of ≥30 mL was defined as a large hematoma. An unfavorable outcome was defined as a modified Rankin scale score of 4–6 on day 30. Results The serum UA level was significantly lower in the patients with a large hematoma volume (median, 306 μmol/L; 25th to 75th percentile, 243–411 μmol/L) than in those with a small hematoma volume (median, 357 μmol/L; 25th to 75th percentile, 271–442 μmol/L; P = 0.012). Similarly, the unfavorable outcome group had had lower serum UA levels (median, 309 vs. 363 μmol/L; P = 0.009) compared with the favorable outcome group. The results of the multivariate logistic analysis indicated that a lower serum UA level was associated with a larger hematoma volume (odds ratio, 0.996; P = 0.006) and an unfavorable outcome (odds ratio, 0.997; P = 0.030). Conclusions The results from the present study have indicated that in patients with acute supratentorial ICH, a low serum UA level might indicate that the patient has a large hematoma volume and might be a risk factor for a poor day 30 functional prognosis.

International audience; Zebrafish is broadly used as a model organism in gene loss-of-function studies in vivo, but its employment in vitro is greatly limited by the lack of efficient gene knockdown approaches in zebrafish cell lines such as ZF4. In this article, we attempted to induce silencing of telomere associated genes in ZF4 by applying the frequently-used siRNA transfection technology and a novel moiety-linked morpholino (vivo-MO). By proceeding with integrated optimization of siRNAs transfection and vivo-MOs treatment, we compared five transfection reagents and vivo-MOs simultaneously to evaluate the efficiency of terfa silencing in ZF4. 48 h after siRNAs transfection, Lipofectamine™ 3000 and X-tremeGENE™ HP leaded to knockdown in 35% and 43% of terfa transcription, respectively, while vivo-MO-terfa modulated 58% down-expression of zfTRF2 in contrast to vivo-MO-ctrl 72 h after treatment. Further siRNAs transfection targeting telomere associated genes by X-tremeGENE™ HP showed silencing in 40-68% of these genes without significant cytotoxicity and off-target effect. Our results confirmed the feasibility of gene loss-of-function studies in a zebrafish cell line, offered a systematic optimizing strategy to employ gene silencing experiments, and presented Lipofectamine™ 3000, X-tremeGENE™ HP and vivo-morpholinos as candidate gene silencing approaches for zebrafish in vitro gene loss-of-function studies. Successfully knockdown of shelterin genes further opened a new field for telomeric study in zebrafish.

To explore the necessity and feasibility of early anti-depressive therapies in acute stroke patients, we conducted a meta-analysis of currently available randomized control studies (RCTs). Literature search in six databases was done with keywords of cerebrovascular accident, depression and prevention. Only RCTs that met the inclusion criteria were enrolled for further analysis. Twelve eligible studies were included in this meta-analysis. Prophylactic anti-depressive therapies following acute stroke were shown to reduce the incidence of depression in the patients (RR = =0.33, 95% CI: 0.25 to 0.43, p 0.001), improve symptoms of depression (WMD: 5.73, 95% CI: 4.18 to 7.29, p 0.001), improve motor function (WMD: 12.56, 95%CI: 9.07 to 16.04, p 0.001) and neurological function (WMD: 1.13, 95%CI: 0.57 to 1.69, p 0.001). However, anti-depressive therapies showed no effects on mortality (RR = 1.63, 95%CI: 0.55 to 4.85, p = 0.377) and adverse events incidence (RR = 0.93, 95%CI: 0.53 to 1.64, p = 0.806). Anti-depressive therapies following acute stroke is effective thus deserves to be advocated.