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Copper (Cu) is a component that performs a crucial role in the normal function and development of the human body. Nonetheless, it is still largely unclear how Cu consumption in the diet relates to the risk for all-cause and cardiovascular disease (CVD) mortality. Data from the National Health and Nutrition Examination Survey from 2001-2018 were used to conduct a prospective cohort study of individuals between the ages of 20 years and above. Regression coefficients and 95% confidence intervals for the link between dietary Cu consumption and all-cause and cardiovascular-related mortality were computed utilizing univariate and multivariate-adjusted Cox proportional hazards models. A total of 197.9 million non-institutionalized American citizens were represented by the NHANES's 39,784 participants. The link between Cu in the diet and all-cause mortality was discovered to be non-linear in our restricted cubic spline regression models. When comparing the highest with the lowest quartile of Cu consumption in the diet, the weighted multivariate hazard ratios for all-cause mortality were 0.91 (0.83-0.99) for Q2, 0.88 (0.80-0.97) for Q3, and 0.86 (0.76-0.98) for Q4 (P for trend = 0.017). An identical trend was observed for cardiovascular mortality, but the association is not significant. The most important discovery was that higher dietary Cu consumption was associated with a lower risk of all-cause mortality. This trend was also consistent with that of cardiovascular-related mortality, but the association is not significant.

Background Heart failure is frequently associated with hypoalbuminaemia and poor prognosis. Acute heart failure (AHF) patients are commonly treated with intravenous albumin to improve osmotic pressure and haemodynamics. However, the effects of exogenous albumin supplementation on the fatality rate of AHF patients have not yet been demonstrated. Therefore, the present study strived to examine the impacts of albumin injections on the mortality rate of patients with AHF. Methods This retrospective cohort study evaluated the clinical outcomes of all consecutive hospitalized patients. Data were collected from medical records. The primary end-point was a composite of intubation, emergency renal replacement, or mortality in a time-to-event analysis. An inverse probability-weighted multivariable Cox model was used to compare outcomes between patients who were treated with albumin and those who were not based on the propensity score. Results Among the 1420 consecutive patients hospitalized in our hospital with acute decompensated heart failure between 1 January 2017 and 27 February 2021, 382 were excluded, 337 (32.5%) were administered albumin (median treatment dose of 29.0 g), and 701 (67.5%) were not. The albumin exposure varied by body mass index, age group, previous diagnoses, clinical signs and symptoms, laboratory tests, and use of other drugs in the unmatched sample. The patients receiving albumin exhibited a lower serum albumin level at baseline in contrast with those who were not treated with albumin (median, 37.3 g/L vs. 31.7 g/L, respectively). Overall, primary end-point events occurred in 357 patients (34.4%) (79 died without being intubated or during an emergency renal replacement therapy, 118 were intubated and 160 had an emergency renal replacement therapy). In the inverse probability weighted multivariable analysis based on the propensity score, albumin use was not significantly associated with the composite primary end-point (hazard ratio, 1.05; 95% confidence interval, 0.75–1.47). Conclusion In this observational study of AHF patients hospitalized in our hospital, the administration of albumin did not show a relationship with either a greatly reduced or aggregated risk of the composite end-point of intubation, emergency renal replacement therapy, or death. Therefore, randomized controlled trials of albumin administration are needed for patients with AHF.

Paroxysmal means PAVB is more dangerous than persistent third-degree AVB, as patients may experience prolonged ventricular asystole without warning, increasing the risk of syncope or sudden death.4 Electrophysiology tests often have a low diagnostic yield in such cases, making prolonged monitoring crucial for diagnosis. Extended ECG monitoring, including implantable loop recorders, can improve the detection rate of PAVB.5 Besides, timely pacemaker implantation is essential to prevent sudden death. Ethics approval This study involves human participants and was approved by the Ethical Review Board of Peking University Aerospace School of Clinical Medicine (Aerospace Center Hospital) and was performed in accordance with the ethical standards laid down in the 1964 Declaration of Helsinki and its later amendments.

Aucubin (AU) is one of the main components of the traditional Chinese medicine Eucommia ulmoides Oliv (EU). This study investigated the effects of AU on aging-related skeletal muscle atrophy in vitro and in vivo. The results of network pharmacology revealed the potential therapeutic effects of AU on muscle atrophy. In vitro, AU effectively attenuated D-gal-induced cellular damage, reduced the number of senescence-associated β-galactosidase (SA-β-Gal)-positive cells, down-regulated the expression levels of muscle atrophy-related proteins Atrogin-1 and MuRF1, and improved myotube differentiation, thereby mitigating myotube atrophy. Notably, AU was found to attenuate oxidative stress and apoptosis in skeletal muscle cells by reducing ROS production, regulating Cleaved caspase3 and BAX/Bcl-2 expression in apoptotic pathways, and enhancing Sirt1 and PGC-1α signaling pathways. In vivo studies demonstrated that AU treatment extended the average lifespan of Caenorhabditis elegans (C. elegans), increased locomotor activity, improved body wall muscle mitochondrial content, and alleviated oxidative damage in C. elegans. These findings suggested that AU can ameliorate aging-related muscle atrophy and show significant potential in preventing and treating muscle atrophy.

The antineoplastic effects of docosahexaenoic acid-containing phosphatidylcholine (DHA-PC) and eicosapentaenoic acid-containing phosphatidylcholine (EPA-PC) were explored, and their underlying mechanisms in the human lung carcinoma 95D cells (95D cells) were investigated. After treatment of 95D cells with DHA-PC or EPA-PC, cell biological behaviors such as growth, adhesion, migration, and invasion were studied. Immunofluorescence and western blotting were carried out to assess underlying molecular mechanisms. Results showed that 95D cells proliferation and adherence in the DHA-PC or EPA-PC group were drastically inhibited than the control group. DHA-PC and EPA-PC suppressed the migration and invasion of 95D cells by disrupting intracellular F-actin, which drives cell movement. The protein expression of PPARγ was induced versus the control group. Furthermore, critical factors related to invasion, including matrix metallopeptidase 9 (MMP9), heparanase (Hpa), and vascular endothelial growth factor (VEGF), were drastically downregulated through the PPARγ/NF-κB signaling pathway. C-X-C chemokine receptor type 4 (CXCR4) and cofilin were significantly suppressed via DHA-PC and EPA-PC through the PPARγ/phosphatase and tensin homolog (PTEN)/serine-threonine protein kinase (AKT) signaling pathway. DHA-PC and EPA-PC reversed the PPARγ antagonist GW9662-induced reduction of 95D cells in migration and invasion capacity, suggesting that PPARγ was directly involved in the anti-metastasis efficacy of DHA-PC and EPA-PC. In conclusion, DHA-PC and EPA-PC have great potential for cancer therapy, and the antineoplastic effects involve the activation of PPARγ. EPA-PC showed more pronounced antineoplastic effects than DHA-PC, possibly due to the more robust activation of PPARγ by EPA-PC.

Tilapia skin is a great source of collagen. Here, we aimed to isolate and identify the peptides responsible for combating dry eye disease (DED) in tilapia skin peptides (TSP). In vitro cell DED model was used to screen anti-DED peptides from TSP via Sephadex G-25 chromatography, LC/MS/MS, and in silico methods. The anti-DED activity of the screened peptide was further verified in the mice DED model. TSP was divided into five fractions (TSP-I, TSP-II, TSP-III, TSP-IV, and TSP-V), and TSP-II exerted an effective effect for anti-DED. A total of 131 peptides were identified using LC/MS/MS in TSP-II, and NGGPSGPR (NGG) was screened as a potential anti-DED fragment in TSP-II via in silico methods. In vitro, NGG restored cell viability and inhibited the expression level of Cyclooxygenase-2 (COX-2) protein in Human corneal epithelial cells (HCECs) induced by NaCl. In vivo, NGG increased tear production, decreased tear ferning score, prevented corneal epithelial thinning, alleviated conjunctival goblet cell loss, and inhibited the apoptosis of corneal epithelial cells in DED mice. Overall, NGG, as an anti-DED peptide, was successfully identified from TSP, and it may be devoted to functional food ingredients or medicine for DED.

The prediction of the mechanical properties of hot-rolled strips is a very complex, highly dimensional and nonlinear problem, and the published models might lack reliability, practicability and generalization. Thus, a new model was proposed for predicting the mechanical properties of hot-rolled strips by deep learning. First, the one-dimensional numerical data were transformed into two-dimensional data for expressing the complex interaction between the influencing factors. Subsequently, a new convolutional network was proposed to establish the prediction model of tensile strength of hot-rolled strips, and an improved inception module was introduced into this network to abstract features from different scales. Many comparative experiments were carried out to find the optimal network structure and its hyperparameters. Finally, the prediction experiments were carried out on different models to evaluate the performance of the new convolutional network, which includes the stepwise regression, ridge regression, support vector machine, random forest, shallow neural network, Bayesian neural network, deep feed-forward network and improved LeNet-5 convolutional neural network. The results show that the proposed convolutional network has better prediction accuracy of the mechanical properties of hot-rolled strips compared with other models.

Background De Winter pattern is associated with acute occlusion in the left anterior descending coronary artery combined with upsloping ST-segment depression at the J point in leads V 1 through V 6 without ST-segment elevation. The ECG changes in this case were illustrated by an up-sloping ST-segment depression in the V 1 to V 6 leads, followed by tall and symmetrical T waves. Changes from de Winter to ST-segment elevation myocardial infarction (STEMI) are rare. Case presentation Our case illustrated an evolutionary de Winter sign that changed to STEMI; the patient underwent cardiac catheterization in time. Conclusions Patients who have an electrocardiogram showing de Winter changes may require primary percutaneous coronary intervention. Emergency physicians and cardiologists should not ignore these changes.

Bidirectional ventricular tachycardia (BVT) is a rare ventricular tachyarrhythmia. It is usually regular, demonstrating a beat-to-beat alternation in the QRS frontal axis that varies between −20° to −30° and +110°. The tachycardia rate is typically between 140 and 180 beats/min and the QRS is relatively narrow, with a duration of 120 to 150 ms. The etiology of published BVT cases is most commonly digitalis toxicity and, rarely, herbal aconitine poisoning, hypokalemic periodic paralysis, catecholaminergic polymorphic ventricular tachycardia (CPVT), myocarditis, and Andersen-Tawil syndrome. We report a case of accelerated idioventricular rhythm (AIVR) degenerating into BVT following acute myocardial infarction, and briefly discuss the proposed mechanisms underlying BVT.

The extract of Broussonetia papyrifera has been proved to have antitumor activity. However, the underlying mechanism remains unclear. This study aimed to elucidate the mechanism of apoptosis of HepG2 cells induced by polyphenols from Broussonetia papyrifera (PBPs). The results revealed that PBPs inhibited the proliferation of HepG2 cells in a dose-dependent and time-dependent manner. Flow cytometry analysis showed that PBPs increased the apoptosis ratio of HepG2 cells significantly. PBPs increased intracellular reactive oxygen species (ROS) production and decreased intracellular superoxide dismutase (SOD) level of HepG2 cells. PBPs induced cell cycle arrest at G1 phase. Western blotting showed that PBPs upregulated the ratio of Bax/Bcl-2 and the expression level of Caspase-3, and activated p53 in HepG2 cells. The inhibition of proliferative relative signals (protein kinase B, PKB/AKT) and survival relative signals (extracellular signal-regulated kinase, ERK) were also observed in PBP-treated HepG2 cells. Our findings suggest that apoptosis of HepG2 cells induced by PBPs is mitochondria-mediated via inactivation of ERK and AKT signaling pathways.