Background Organ confined prostate cancer (PCa) can be cured by radical retropubic prostatectomy (RRP); however, some tumors will still recur. Current tools fail to identify patients at risk of recurrence. Glutathione-S-Transferases (GSTs) are involved in the metabolism of carcinogens, hormones and drugs. Thus, genetic polymorphisms that modify the GSTs activities may modify the risk of PCa recurrence. Methods We retrospectively recruited Argentine PCa patients treated with RRP to study the association between GSTs polymorphisms and PCa biochemical relapse after RRP. We genotyped germline DNA in 105 patients for: GSTP1 c.313 A>G (p.105 Ile>Val, rs1695) by PCR-RFLP; and GSTT1 null and GSTM1 null polymorphisms by multiplex-PCR. Kaplan-Meier curves and Cox proportional hazard models were used to evaluate these associations. Results Patients with GSTP1 c.313 GG genotype showed shorter biochemical relapse-free survival (BRFS) (p=0.003) and higher risk for recurrence in unadjusted (Hazard Ratio (HR)=3.16, 95% Confidence Interval (95% CI)=1.41–7.06, p=0.005) and multivariate models (HR=3.01, 95% CI=1.13–8.02, p=0.028). We did not find significant associations for GSTT1 and GSTM1 genotypes. In addition, we found shorter BRFS (p=0.010) and increased risk for recurrence for patients having 2 or more risk alleles when we combined the genotypes of the three GSTs in multivariate models (HR=3.06, 95% CI=1.20–7.80, p=0.019). Conclusions Our results give support to the implementation of GSTs genotyping for personalized therapies as a novel alternative for PCa management for patients who undergo RRP. This is the first study that examined GST polymorphisms in PCa progression in Argentine men. Replication of our findings in larger cohort is warranted.

Reduced expression of nestin-IR in granular cells layers of epileptic's dentate gyrus may reflect changes in dentate gyrus neuroplasticity associated to chronic temporal epilepsy with hippocampal sclerosis. Further studies are required to determine the clinical implications on memory an emotional alterations such as depression.

The consequences of perinatal asphyxia (PA) include alterations which may manifest as schizophrenia. Characteristic features of this disease include a decrease in specific subpopulations of GABAergic cells and deterioration of social interaction. The purpose of this study is to assess if a deep and short‐hypothermic treatment can ameliorate this damage in a model of PA. Rats offsprings were exposed to 19 min of asphyxia by immersing the uterus horns in water at 37 °C followed by 30 min in air at 10 °C that resulted in 15 °C body temperature. At postnatal day 36–38, the rats were tested in the open field and social interaction paradigms and processed for immunostaining of calbindin and reelin. A brief exposure to deep hypothermia reversed the deterioration produced by PA in play soliciting. PA decreased the density of calbindin neurons in layer II of the Anterior Insular Cortex, while deep hypothermia reversed this effect. Paradoxically, in AIC, there was a significant increase in the number of reelin‐secreting neurons in layers II and III generated by PA and this increase was reversed by hypothermia. This suggests a compensatory mechanism, where reelin neurons trend to compensate for the loss of calbindin neurons, at least within Anterior Insular Cortex. Finally, the deep hypothermic shock might represent a valuable therapeutic alternative to treat PA.