The goal of the present investigation was to examine effects of a cognitive-behavioral group intervention for pregnant women with subclinically elevated stress, anxiety and/or depression on perceived stress and salivary cortisol levels. Expectant mothers were recruited in gynaecologist practices. They participated in a screening, a standardized diagnostic interview (Munich-Composite Diagnostic Interview, M-CIDI), and were randomly assigned to an intervention (N = 21) and treatment as usual control group (N = 40). The intervention consisted of a manualized cognitive-behavioral group program for expectant mothers with subclinically elevated stress, depression, and/or anxiety symptoms. Stress questionnaire (prenatal distress (PDQ), perceived stress (PSS)) as well as diurnal salivary cortisol assessment took place at T1 (antenatal, preintervention), at T2 (antenatal, post-intervention) and T3 (3-month postpartum). Subjects that participated in the intervention exhibited a significant post-treatment change in morning cortisol (cortisol awakening response, CAR) in contrast to control subjects, F(8,51) = 2.300, p = 0.047. Intervention participants showed a smaller CAR subsequent to the intervention, displaying a lessened stress reaction. This effect was not observed in the control group. In contrast, we failed in discovering a significant difference between the research groups regarding the cortisol area under curve parameter (AUC) and the applied subjective stress questionnaires. Evaluation results were thus heterogeneous. Nevertheless, intervention effects on the CAR are promising. Our results suggest that a cognitive-behavioral intervention might lead to an improvement in the biological stress response of pregnant women with subclinically elevated stress, anxiety, or depressive symptoms.
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http://dx.doi.org/10.3109/0167482X.2012.729111 | DOI Listing |
Drug Des Devel Ther
January 2025
Department of Anesthesiology, The Affiliated Hospital of Qingdao University, Qingdao, People's Republic of China.
Introduction: The mechanism of remimazolam, a benzodiazepine that activates γ-aminobutyric acid a (GABAa) receptors, in cerebral ischemia/reperfusion (I/R) injury is not well understood. Therefore, we explored whether remimazolam activates protein kinase B (AKT)/glycogen synthase kinase-3β (GSK-3β)/nuclear factor erythroid 2-related factor 2 (NRF2) to attenuate brain I/R injury in transcerebral I/R-injured rats and transoxygenic glucose deprivation/reperfusion (OGD/R)-injured SY5Y cells.
Material And Methods: Remimazolam was added at the beginning of cell and rat reperfusion, and the PI3K/AKT inhibitor LY294002 was added to inhibit the AKT/GSK-3β/NRF2 pathway 24 h before cellular OGD/R treatment and 30 min before rat brain I/R treatment.
Acta Pharm Sin B
December 2024
Metabolic Disease Research Center, Zhengzhou Central Hospital Affiliated to Zhengzhou University, Zhengzhou 450052, China.
Reductive stress, characterized by rising level of NADH (nicotinamide adenine dinucleotide) for a status of NADH/NAD ratio elevation, has been reported in obesity and cancer. However, the mechanism and significance of reductive stress remain to be established in obesity. This perspective is prepared to address the issue with new insights published recently.
View Article and Find Full Text PDFNat Commun
January 2025
Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain.
Obesity poses a global health challenge, demanding a deeper understanding of adipose tissue (AT) and its mitochondria. This study describes the role of the mitochondrial protein Methylation-controlled J protein (MCJ/DnaJC15) in orchestrating brown adipose tissue (BAT) thermogenesis. Here we show how MCJ expression decreases during obesity, as evident in human and mouse adipose tissue samples.
View Article and Find Full Text PDFZhongguo Zhong Yao Za Zhi
December 2024
School of Medicine, Jianghan University Wuhan 430056, China.
This study aims to investigate the mechanism of tanshinone Ⅱ_A(Tan Ⅱ_A) in protecting mice from diethylinitrosamine(DEN)/carbon tetrachloride(CCl_4)/ethanol(C_2H_5OH)-induced hepatocellular carcinoma(HCC) and HepG2 cells from hydrogen peroxide(H_2O_2)-induced oxidative damage via the phosphoinositide 3-kinase(PI3K)/protein kinase B(Akt) and nuclear factor E2-related factor 2(Nrf2)/heme oxygenase 1(HO-1) signaling pathways. Sixty male C57BL/6J mice were grouped as follows: control, model, low, medium, and high-dose(10, 20, 40 mg·kg~(-1), respectively) Tan Ⅱ_A, and colchicine(0.2 mg·kg~(-1)), with 10 mice in each group.
View Article and Find Full Text PDFMetabolism
January 2025
Department of Molecular and Cellular Endocrinology, Arthur Riggs Diabetes and Metabolism Research Institute, Beckman Research Institute of City of Hope, Duarte, CA, USA. Electronic address:
Introduction: Type 1 diabetic human islet β-cells are deficient in double C 2 like domain beta (DOC2b) protein. Further, DOC2b protects against cytokine-induced pancreatic islet β-cell stress and apoptosis. However, the mechanisms underpinning the protective effects of DOC2b remain unknown.
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