Influence of dynamic load and water on energy accumulation and dissipation in sandstone.

In various engineering projects such as mineral extraction, hydropower resource utilization, railway construction, and geological hazard mitigation, rock engineering is often encountered. Furthermore, dynamic loads and moisture content exert notable influence on the energy transformation processes within rocks. Yet, the specific interplay of dynamic loading and water's impact on the energy conversion mechanism within the sandstone remains unexplored. To address this gap, this study conducted impact loading experiments on sandstone, elucidating the rock's mechanical response under these conditions and unraveling the underlying energy conversion mechanisms. It was observed that the strength of sandstone exhibits a direct correlation with impact velocity. Moreover, employing energy calculation principles, we established a connection between moisture content and the sandstone's internal energy conversion properties. The study also delved into the microscopic fracture mechanisms within the sandstone, ultimately concluding that both water content and dynamic loading have a significant impact on these microscopic fracture mechanisms.

G-protein coupled receptor 30 attenuates myocardial hypertrophy by reducing oxidative stress and apoptosis in Ang II-treated mice.

G protein-coupled receptors (GPCRs) are the largest family of membrane receptors that mediate the effects of cardiac diseases. GPR30, also named G-protein-coupled estrogen receptor, shows beneficial effect on female patients with heart failure. This research aimed to probe the role and mechanism of GPR30 in myocardial hypertrophy. The model of cardiac hypertrophy was induced by infusion of angiotensin (Ang) II in mice, and was induced by Ang II treatment in neonatal rat cardiomyocyte (NRCM). The mouse model of myocardial hypertrophy was induced by angiotensin (Ang) Ⅱ, and the neonatal rat cardiomyocyte (NRCM) was induced by Ang Ⅱ treatment. GPR30 agonist G1 reduced cardiac hypertrophy induced by Ang II in mice, and reduced cardiac atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and ß-myosin heavy chain (ß-MHC) induced by Ang II. Ang Ⅱ treatment of myocardial fibrosis in mice was suppressed after administration of G1. GPR30 deficiency produced the opposite results. Oxidative stress and apoptosis were enhanced in the mice heart induced by Ang II, which were suppressed by G1 administration, but were further exacerbated after GPR30 deficiency. The outcomes demonstrated that GPR30 participated in the regulation of cardiac hypertrophy and fibrosis. Activation of GPR30 ameliorated cardiac hypertrophy and fibrosis by reducing oxidative stress and apoptosis.

Dysregulated thyroid hormones correlate with anxiety and depression risk in patients with autoimmune disease.

BACKGROUND: Autoimmune disease (AID) patients always present with increased risk of psychiatric disorders, and thyroid function or thyroid hormone may play a critical role in the development of anxiety and depression. Thus, this study aimed to assess the free triiodothyronine (FT3), free tetraiodothyronine (FT4), thyroid-stimulating hormone (TSH) levels, and their correlations with anxiety/depression in patients with AID. METHODS: Ninety-eight AID patients and 100 health controls (HCs) were recruited. Serum samples were obtained from all the participants to detect FT3, FT4, and TSH levels. Anxiety and depression were determined using the HADS assessment. RESULTS: HADS-Anxiety score, anxiety subject percentage, HADS-Depression score, and depression subject proportion were elevated in AID patients compared with HCs. FT3 and FT4 were downregulated while TSH was upregulated in AID patients compared with HCs. In AID patients, FT3 and FT4 negatively correlated with HADS-Anxiety score, and they were downregulated in patients with anxiety compared to patients without anxiety. Meanwhile, FT3 and FT4 were negatively associated while TSH level positively associated with HADS-Depression score. Besides, FT3 and FT4 reduced, but TSH level was of no difference in patients with depression compared to patients without depression. Additionally, increased FT4 independently correlated with both reduced anxiety risk and depression risk. CONCLUSIONS: FT3, FT4, and TSH are dysregulated, and FT4 has the potential to serve as an independent biomarker related to anxiety as well as depression in AID patients. These findings may provide some information on the values of thyroid hormones in facilitating the management of AID patients with anxiety/depression.