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Most psychiatric disorders are associated with an elevated risk of suicide. Suicidal behavior is the product of the interaction of many risk factors, such as genetics and environmental factors. Hence, epigenetics research may help to understand the mechanisms leading to suicidal ideation and behavior. This review will discuss epigenetic studies in both suicidal ideation and behavior. Epigenetic modifications are likely to be important in both suicidal ideation and behavior. Most of the reviewed studies found significant epigenetic modifications linked with suicidal behavior rather than ideation. Although sizable research has been carried out on this topic, most studies have been done on small-scale samples, and future research is required in larger samples with better clinical characterization of suicide phenotypes to investigate these epigenetic modifications further.
Postpartum depression (PPD) is a multifactor disorder caused by psychological, social, and also biological factors. 5-HTTLPR polymorphism in the promoter region of serotonin transporter gene seems to influence PPD onset. In this study, we examined the effect of 5-HTTLPR polymorphism on prenatal and postnatal symptoms of depression and posttraumatic stress in women.

A longitudinal design with three points - time 1 (32-40 weeks gestation); time 2 (2 or 3 weeks after birth), and time 3 (3 months after birth) - was made. A total of 141 women were recruited during childbirth preparation courses. At time 1, women completed the Beck Depression Inventory (BDI) and the Los Angeles Symptoms Checklist (LASC). At time 2, they fulfilled BDI and Edinburgh Postnatal Depression Scale (EDPS), LASC and the Perinatal Posttraumatic stress disorder (PTSD) Questionnaire (PPQ); midwives and nurses collected biological test tubes by blood sampling for the genetic analysis. At time 3, the women were reassessed for BDI, LASC, EDPS, and PPQs. Analysis of variance and moderation analysis were used to correlate genotype and psychological investigations.

Results showed that, compared with LL/LS genotypes, SS genotype moderated cognitive depressive symptoms onset at T2 and T3. Moreover, this genotype correlated, directly or indirectly, with PTSD postpartum aspects (re-experience, avoidance, and hyperarousal).

Findings revealed that a lower expression of serotonin transporter gene, associated with SS genotype, seems to render women more vulnerable to depressive and PTSD symptoms after childbirth.
Findings revealed that a lower expression of serotonin transporter gene, associated with SS genotype, seems to render women more vulnerable to depressive and PTSD symptoms after childbirth.
Infertility may occur in women with Crohn's disease (CD) and ulcerative colitis (UC), especially after surgery such as ileal pouch-anal anastomosis (IPAA). Assisted reproductive technology (ART) may be an option, but the safety and efficacy in this setting has been based on small cohorts to date. We performed a systematic review and meta-analysis to address this data gap.

A systematic review and random-effects meta-analysis was performed until May 2020. The primary outcomes were pregnancy and live birth rates per cycle of ART.

Eleven studies met inclusion criteria for the systematic review and 4 for the meta-analysis. Compared with the general population, women with CD (with and without previous surgery) had no difference in pregnancy rates (odds ratio [OR] = 0.69, 95% confidence interval [CI] 0.45-1.05) but had reduced live births (OR = 0.67, 95% CI 0.53-0.85) per cycle of ART. ART live birth rates are not reduced in women with medically managed CD; however, they are 49%-71% lower after CD-related surgCD-related surgery and IPAA failure. Greater gastroenterologist awareness of ART is needed to facilitate timely fertility therapy referral when indicated, particularly in CD.
GLP-1(7-36), a major active form of GLP-1 hormone, is rapidly cleaved by dipeptidyl peptidase-4 to generate a truncated metabolite, GLP-1(9-36) which has a low affinity for GLP-1 receptor (GLP-1R). GLP-1(7-36) has been shown to have protective effects on cardiovascular system through GLP-1R-dependent pathway. Nevertheless, the cardioprotective effects of GLP-1(9-36) have not fully understood. The present study investigated the effects of GLP-1(9-36), including its underlying mechanisms against oxidative stress and apoptosis in H9c2 cells. Here, we reported that GLP-1(9-36) protects H9c2 cardiomyoblasts from hydrogen peroxide (H2O2)-induced oxidative stress by promoting the synthesis of antioxidant enzymes, glutathione peroxidase-1, catalase, and heme oxygenase-1. In addition, treatment with GLP-1(9-36) suppressed H2O2-induced apoptosis by attenuating caspase-3 activity and upregulating proapoptotic proteins, Bcl-2 and Bcl-xL. These protective effects of GLP-1(9-36) are attenuated by blockade of PI3K-mediateygenase-1. In addition, treatment with GLP-1(9-36) suppressed H2O2-induced apoptosis by attenuating caspase-3 activity and upregulating proapoptotic proteins, Bcl-2 and Bcl-xL. These protective effects of GLP-1(9-36) are attenuated by blockade of PI3K-mediated Akt phosphorylation and prevention of nitric oxide synthase (NOS)-induced nitric oxide production. Thus, GLP-1(9-36) represents the potential therapeutic target for prevention of oxidative stress and apoptosis in the heart via PI3K/Akt/NOS signaling pathway.
ZIP12, a plasmalemmal zinc transporter, reportedly promotes pulmonary vascular remodeling (PVR) by enhancing proliferation of pulmonary artery smooth muscle cells (PASMCs). However, the mechanisms of ZIP12 facilitating PASMCs proliferation remain incompletely appreciated. It has been acknowledged that proliferation-predisposing phenotypic switching of PASMCs leads to PVR. Given that hypoxia triggers phenotypic switching of PASMCs and ZIP12 mediates PVR, this study aims to explore whether ZIP12-mediated phenotypic switching of PASMCs contributes to hypoxia-induced PVR. Rats were exposed to hypoxia (10% O2) for 3 weeks to induce PVR, and primary rat PASMCs were cultured under hypoxic condition (3% O2) for 48 hours to induce proliferation. Immunofluorescence, quantitative RT-PCR and Western blot analysis were performed to detect the expression of target mRNAs and proteins. EdU incorporation and MTS assay were conducted to measure the proliferation of PASMCs. As revealed, hypoxia up-regulated ZIP12 expression (t PASMCs were cultured under hypoxic condition (3% O2) for 48 hours to induce proliferation. Immunofluorescence, quantitative RT-PCR and Western blot analysis were performed to detect the expression of target mRNAs and proteins. EdU incorporation and MTS assay were conducted to measure the proliferation of PASMCs. As revealed, hypoxia up-regulated ZIP12 expression (both mRNA and protein) in pulmonary arteries and PASMCs; knockdown of ZIP12 inhibited phenotypic switching of PASMCs induced by hypoxia. We propose that HIF-1α/ZIP12/pERK pathway could represent a novel mechanism underlying hypoxia-induced phenotypic switching of PASMCs. Therapeutic targeting of ZIP12 could be exploited to treat PVR in hypoxic pulmonary hypertension.
Lipoprotein(a) or lipoprotein "little a" is an under-recognized causal risk factor for cardiovascular (CV) disease (CVD), including coronary atherosclerosis, aortic valvular stenosis, ischemic stroke, heart failure and peripheral arterial disease. Elevated plasma Lp(a) (≥50 mg/dL or ≥100 nmol/L) is commonly encountered in almost 1 in 5 individuals and confers a higher CV risk compared to those with normal Lp(a) levels, although such normal levels have not been generally agreed upon. Elevated Lp(a) is considered a cause of premature and accelerated atherosclerotic CVD. Thus, in patients with a positive family or personal history of premature coronary artery disease (CAD), Lp(a) should be measured. However, elevated Lp(a) may confer increased risk for incident CAD even in the absence of a family history of CAD, and even in those who have guideline-lowered LDL-cholesterol (<70 mg/dl) and continue to have a persisting CV residual risk. Thus, measurement of Lp(a) will have a significant clinical impact on theent modalities, such as gene silencing via RNA interference with use of antisense oligonucleotide(s) or small interfering RNA molecules targeting Lp(a) seem very promising. These issues are herein reviewed, accumulated data are scrutinized, meta-analyses and current guidelines are tabulated and Lp(a)-related CVDs and newer therapeutic modalities are pictorially illustrated.
We aimed to assess the efficacy of hibiscus sabdariffa in patients with mild to moderate hypertension or metabolic syndrome (MetS) by comparing it against placebo, antihypertensive drugs, or other herbal products.Four databases were searched for randomized clinical trials (RCTs) examining the efficacy of hibiscus sabdariffa in patients with mild to moderate hypertension or hypertension associated with MetS. Data on the change in systolic blood pressure (SBP) and diastolic blood pressure (DBP) were extracted and analyzed using Review Manager Version 5.3.A total of 13 RCTs (1205 participants) were analyzed. Hibiscus sabdariffa significantly reduced both SBP and DBP compared to placebo (MD -6.67, P=0.004 and -4.35 mmHg, P=0.02). Subgroup analysis showed that change in SBP and DBP was statistically significant in patients with only hypertension while not significant in patients with hypertension associated with MetS. When hibiscus sabdariffa was compared to active controls (antihypertensive drugs or other herbals), the change in SBP and DBP was not statistically significant (all P>0.05).Hibiscus sabdariffa is effective in reducing the SBP and DBP in patients with mild to moderate hypertension but was neither effective in those with MetS nor superior to antihypertensive drugs. Further RCTs are required to determine the long-term efficacy of hibiscus sabdariffa and to describe patients who would benefit most from this treatment.
0.05).Hibiscus sabdariffa is effective in reducing the SBP and DBP in patients with mild to moderate hypertension but was neither effective in those with MetS nor superior to antihypertensive drugs. Further RCTs are required to determine the long-term efficacy of hibiscus sabdariffa and to describe patients who would benefit most from this treatment.
Noninvasive respiratory support has been widely applied during the COVID-19 pandemic. We provide a narrative review on the benefits and possible harms of noninvasive respiratory support for COVID-19 respiratory failure.

Maintenance of spontaneous breathing by means of noninvasive respiratory support in hypoxemic patients with vigorous spontaneous effort carries the risk of patient self-induced lung injury the benefit of averting intubation in successful patients should be balanced with the harms of a worse outcome in patients who are intubated after failing a trial of noninvasive support.The risk of noninvasive treatment failure is greater in patients with the most severe oxygenation impairment (PaO2/FiO2 < 200 mmHg).High-flow nasal oxygen (HFNO) is the most widely applied intervention in COVID-19 patients with hypoxemic respiratory failure. Also, noninvasive ventilation (NIV) and continuous positive airway pressure delivered with different interfaces have been used with variable success rates. A single randomized trial showed lower need for intubation in patients receiving helmet NIV with specific settings, compared to HFNO alone.
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