Prevalence and Risk Factors of Depression and Anxiety among Women in the Last Trimester of Pregnancy: A Cross-Sectional Study.

Pregnancy represents a psychologically and emotionally vulnerable period, and research indicates that pregnant women have a higher prevalence of symptoms of anxiety and depression, debunking the myth that hormonal changes associated with pregnancy protect the mother. In recent years, several researchers have focused on the study of prenatal anxiety/depression-emotional disorders manifested by mood lability and low interest in activities-with a high prevalence. The main objective of this research was to conduct an antenatal screening in a cohort of pregnant women hospitalized for delivery in order to assess the prevalence of anxiety and depression. The secondary objective was to identify the risk factors associated with depression and anxiety in women in the third trimester of pregnancy. We carried out a prospective study in which we evaluated 215 pregnant women in the third trimester of pregnancy hospitalized for childbirth at the Obstetrics and Gynecology Clinic of the Târgu-Mureș County Clinical Hospital. The research was carried out between December 2019 and December 2021. The results showed that age and the environment of origin are the strongest predictors of mental health during pregnancy (OR = 0.904, 95%CI: 0.826-0.991; p = 0.029). For women from urban areas, there is an increased probability of falling at a higher level on the dependent variable (moderate depression) (OR = 2.454, 95%CI: 1.086-5.545; p = 0.032). In terms of health behaviors, none of the variables were statistically significant predictors of the outcome variable. The study highlights the importance of monitoring mental health during pregnancy and identifying relevant risk factors to provide appropriate care to pregnant women and the need for interventions to support the mental health of pregnant women. Especially in Romania, where there is no antenatal or postnatal screening for depression or other mental health conditions, these results could be used to encourage the implementation of such screening programs and appropriate interventions.

Inflammatory Markers Used as Predictors of Subclinical Atherosclerosis in Patients with Diabetic Polyneuropathy.

BACKGROUND: peripheral arterial disease (PAD) is identified late in diabetic patients because, in the majority of cases, it is associated with diabetic peripheral neuropathy, resulting in little or no symptoms, or symptoms that are completely neglected. METHODS: In this study were enrolled all patients over 18 years of age, with diabetes mellitus type II for more than a year with poor glycemic control, diagnosed with diabetic polyneuropathy admitted to the Diabetology Department, Emergency County Hospital of Targu Mures, Romania between January 2020 and March 2023. We divided the patients into two groups, based on the presence or absence of subclinical atherosclerosis in the lower limb, named "SA" and "non-SA". RESULTS: Patients in the SA group were older (p = 0.01) and had a higher incidence of IHD (p = 0.03), history of MI (p = 0.02), and diabetic nephropathy (p = 0.01). Moreover, patients with subclinical atherosclerosis had a higher BMI (p < 0.0001) and a longer duration of diabetes (p < 0.0001). Among all patients, the systemic inflammatory markers, MLR (r = 0.331, p < 0.001), NLR (r = 0.517, p < 0.001), PLR (r = 0.296, p < 0.001), SII (r = 0.413, p < 0.001), as well as BMI (r = 0.241, p < 0.001) and HbA1C (r = 0.489, p < 0.001), demonstrated a strong positive correlation with the diabetes duration. The multivariate logistic regression analysis showed that older patients (OR: 2.58, p < 0.001), the male gender (OR: 2.30, p = 0.006), a higher baseline levels of BMI (OR: 7.71, p < 0.001), and the duration of diabetes (OR: 8.65, p < 0.001) are predictors of subclinical atherosclerosis in DN patients. Additionally, the high baseline levels of all systemic inflammatory markers (for all: p < 0.001) and poor diabetes management (OR: 10.4, p < 0.001 for HbA1C; OR: 10.78, p < 0.001 for admission glucose) are independent predictors of SA. CONCLUSIONS: the inflammatory markers, NLR, MLR, PLR, and SII, being cheap and easy to collect in routine medical practice from the standard blood tests, could be an important step in predicting vascular outcomes in diabetic patients and the disease's progression, playing a key role in follow-up visits in type-2 diabetic patients and PAD patients.

Selective increase of cardiomyocyte derived extracellular vesicles after experimental myocardial infarction and functional effects on the endothelium.

INTRODUCTION: Wound healing after myocardial infarction (MI) is mediated by different cell types, secreted proteins, components of the extracellular matrix (ECM) and, as increasing evidences suggest, extracellular vesicles (EVs). We aim to determine the dynamics of release and origin of EVs after MI, as well as their biological activity on endothelial cells (ECs). METHODS: MI was induced in WT mice and blood and tissues collected at baseline, 3, 15 and 30 days post-ligation for cardiac function (echocardiography) and histological evaluation. Circulating EVs subpopulations were measured by flow cytometry in mouse, and in a small cohort of patients with ST-segment elevation MI (STEMI, n = 6). In vitro, EVs were isolated from a cardiomyocyte cell line (HL1) and their function assayed on ECs. RESULTS: Leukocyte and endothelial EVs increased concomitant to inflammatory and angiogenic processes triggered by ischemia. More strikingly, cardiomyocyte EVs (connexin43+) were detected in STEMI patients and in murine MI, where a significant increase in their levels was reported at day 15 post-ischemia (p < 0.05 vs baseline). In vitro, HL1EVs induced ECs migration (p = 0.05) and proliferation (p < 0.05), but impaired tube formation. These apparent contradictory results could be partially explained by the upregulation of MMP3, and the apoptosis and senescence genes, p53 and p16, induced by HL1EVs on ECs (p < 0.05). CONCLUSIONS: MI induces the release of different EVs subpopulations, including those of cardiac origin, in a preclinical model of MI and STEMI patients. In vitro, cardiomyocyte derived EVs are able to modulate endothelial function, suggesting their active role in heart repair after ischemia.