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Pregnancy and the postpartum period are characterized by physiological alterations in cortisol and cortisone levels. In the present study, we sought to explore the risk factors for postpartum depression (PPD) and self-remitting postpartum adjustment disorder (AD) and whether cortisol/cortisone metabolism might have any bearing on them. Hair samples from 196 participants (mean age = 31.44, SD = 4.71) were collected at two time points (1-6 days after childbirth and 12 weeks postpartum) to determine the cumulative hair cortisol (HCC) and hair cortisone (HCNC) exposure in the third trimester and during the 12 weeks postpartum. Compared to the non-depressed group (ND, n = 141), more women in the AD (n = 28) and PPD (n = 27) groups had a personal or family history of depression and more stressful life events. Compared to ND and PPD, more women in the AD group had birth-related complications with their children being more often transferred to a pediatric ward. The factors associated with PPD were found to include being unmarried and having a lower household income, less support at home, more subjectively perceived stress after childbirth and lower maternal sensitivity. The natural decrease in HCC concentration from the third trimester to 12 weeks postpartum was significant only in the ND and AD groups, but not in PPD. In summary, prolonged subjectively perceived postpartum stress associated with living situations may contribute to the development of PPD while birth- and child-related complications are likely to trigger brief episodes of AD. Only in ND and AD, the pregnancy-related physiological changes in glucocorticoid levels return to the pre-pregnancy baseline after 12 weeks. Our observations point to the difference between the ND and PPD groups in glucocorticoid metabolism-related postpartum adjustment, which may be a factor in the development of PPD.

We investigated the possible significance of rare genetic variants to response to valproic acid (VPA) and ethosuximide (ETX) in patients with absence epilepsy. Our primary hypothesis was that rare CACNA1H variants are more frequent in ETX-non-responsive patients compared to ETX-responsive. Our secondary hypothesis was that rare variants in GABA-receptor genes are more frequent in VPA-non-responsive patients compared to VPA-responsive.

We recruited patients with absence epilepsy treated with both VPA and ETX, and performed whole exome sequencing in order to investigate the potential role of rare variants in CACNA1H, other voltage-gated calcium channel (VGCC) genes, or GABA-receptor genes in predicting response to ETX or VPA.

Sixty-two patients were included; 12 were ETX-responsive, 14 VPA-responsive, and 36 did not have a clear positive response to either medication. We did not find significant enrichment inCACNA1H rare variants in ETX-responsive patients (odds ratio 3.43; 0.43-27.65; p = 0.20), nor was cient power. Increased GABA-receptor gene rare variant frequency in absence epilepsy patients who fail initial anti-seizure therapy suggests subtle GABA receptor dysfunction may contribute to the underlying pathophysiology.This study aimed at providing valid estimates for the risk of clinically relevant seizure aggravation by recommended anti-seizure medications in patients with Genetic Generalized Epilepsy (GGE). To this aim, treatment response, side effects and paradoxical reactions to anti-seizure treatment were retrospectively assessed in a near-population based cohort comprising 471 adult GGE patients. A total of 1046 treatment attempts were analyzed (lamotrigine 351, valproic acid 295, levetiracetam 249, primidone/phenobarbital 94, zonisamide 57). Under lamotrigine, seizure aggravation was observed in 15 patients (two patients during levetiracetam, one patient during zonisamide, none during phenobarbital and valproic acid). All but two patients with paradoxical reactions to lamotrigine were diagnosed with juvenile myoclonic epilepsy (JME), otherwise, the clinical and electroencephalographic characteristics of patients with paradoxical reactions did not differ. At treatment start, the estimated risk of a paradoxical reaction to lamotrigine was 7.9 % in JME patients (n = 190). Pexidartinib in vitro For all GGE patients (incl. JME), the estimated risk of clinically relevant seizure aggravation under treatment with lamotrigine was 3.7 % (1.8 % for zonisamide and 0.8 % for levetiracetam). In conclusion, clinical significant aggravation of seizure frequency is common in lamotrigine-treated JME patients but rare in patients with other GGE subsyndromes or under treatment with other recommended anti-seizure medication.Polyaromatic hydrocarbons (PAH) are persistent pollutants of great concern due to their potential toxicity, mutagenicity and carcinogenicity. A biotechnological approach to remove PAH from soil was evaluated in this work using a laccase mediator system. Initially, laccase was produced by fungal co-cultivation, using kiwi peels as substrate. The produced laccase was applied to PAH contaminated soil to evaluate its efficiency on enzymatic bioremediation. Results showed that laccase mediator system was effective in the degradation of pyrene, fluorene, chrysene and a lower extension anthracene. Mediators improved the PAH degradation and natural mediators (ferulic acid and p-coumaric acid) were as effective as the synthetic mediator ABTS. However, the process was not effective in the benzo[a]pyrene degradation, one of the most recalcitrant and toxic PAH. This low degradation rate could be related to the low activity of the laccase mediator system in an environment lacking water. To overcome this issue, a PAH contaminated soil degradation system was developed in packed bed reactor (PBR) fed with laccase/mediator. Continuous flow of laccase/mediator improved the PAH degradation, achieving 74.8 %, 71.9 %, 72.2 %, 81.8 % and 100 % degradation for fluorene, anthracene, phenanthrene, chrysene and pyrene, respectively. This system was able to degrade 96 % benzo[a]pyrene, which was 90 % higher than the degradation in batch system. Results indicated that the produced laccase as well as the fed-batch degradation system developed in PBR could be successfully applied in the degradation of soil PAH pollutants, with the advantage of achieving higher degradation rates than in simple batch, as well as being a faster and simpler process than microorganism bioremediation.