Early-Life Factors and Multimorbidity Risk Later in Older Age: Evidence Based on CHARLS.

INTRODUCTION: Early-life factors were reported to exert influence on the health condition of individuals in the long-term. However, limited research explored the connection between early-life factors and multimorbidity in later years. METHODS: We utilized the data from the China Health and Retirement Longitudinal Study to assess this possible association in the present cross-sectional study. Multimorbidity was determined based on 14 common chronic diseases included in the study. Logistic regression was employed to examine the link between early-life factors and subsequent multimorbidity. RESULTS: Out of 7,578 participants who met the inclusion criteria for analysis, 3,765 (49.68%) were females. The mean age was 68.25 ± 6.70 years. Participants who rated their health during childhood as average (odds ratio [OR] 0.78, 95% confidence interval [CI] 0.63-0.96) or better [OR 0.72, 95% CI 0.57-0.91] were significantly less likely to experience multimorbidity in older life. By contrast, experiencing violence from two of the family members was significantly associated with future multimorbidity (OR [95% CI], 1.29 [1.04-1.60]). A superior family financial situation was also negatively associated with multimorbidity, with average (OR [95% CI], 0.72 [0.63-0.83]) and better off than average (OR [95% CI], 0.76 [0.62-0.93]). DISCUSSION: Individuals with poor health status, inferior family socioeconomic status, or experienced violence from family members in childhood were more likely to suffer from multimorbidity in later life. Enhanced social monitoring of potentially adverse conditions in youngsters and targeted interventions could help mitigate the progression of multimorbidity in later life.

The role of CNPY2 in endothelial injury and inflammation during the progress of atherosclerosis.

Vascular endothelial cells (VECs) injury is closely related to the occurrence and development of atherosclerosis. Canopy FGF signaling regulator 2 (CNPY2), a novel unfolded protein response promoter, has been reported to activate the PERK-CHOP pathway. This study aimed to explore whether CNPY2 is associated with atherosclerosis mediated by VEC injury. By establishing ApoE-/- mouse atherosclerosis model and oxidized low-density lipoprotein (ox-LDL) cell model, we found that CNPY2 was abnormally highly expressed in ApoE-/- mice and ox-LDL-induced mouse aortic endothelial cells (MAECs). Exogenous CNPY2 can significantly aggravate the activation, inflammation, and apoptosis of MAECs induced by ox-LDL and promote the activation of PERK/eIF2α/CHOP signal. The PERK inhibitor GSK2606414 can inhibit CNPY2-induced MAECs injury and PERK signal activation. In addition, in vivo animal experiments furtherly confirmed that CNPY2 could aggravate the process of atherosclerosis in ApoE-/- mice by activating PERK signaling. In conclusion, this study indicated that high level of CNPY2 induces VECs injury by activating PERK signaling and thus participating in the progress of atherosclerosis.

The function of LncRNA-H19 in cardiac hypertrophy.

Cardiac hypertrophy, characterized by the enlargement of cardiomyocytes, is initially an adaptive response to physiological and pathological stimuli. Decompensated cardiac hypertrophy is related to fibrosis, inflammatory cytokine, maladaptive remodeling, and heart failure. Although pathological myocardial hypertrophy is the main cause of hypertrophy-related morbidity and mortality, our understanding of its mechanism is still poor. Long noncoding RNAs (lncRNAs) are noncoding RNAs that regulate various physiological and pathological processes through multiple molecular mechanisms. Recently, accumulating evidence has indicated that lncRNA-H19 is a potent regulator of the progression of cardiac hypertrophy. For the first time, this review summarizes the current studies about the role of lncRNA-H19 in cardiac hypertrophy, including its pathophysiological processes and underlying pathological mechanism, including calcium regulation, fibrosis, apoptosis, angiogenesis, inflammation, and methylation. The context within which lncRNA-H19 might be developed as a target for cardiac hypertrophy treatment is then discussed to gain better insight into the possible biological functions of lncRNA-H19 in cardiac hypertrophy.

Demethylation of the NRF2 Promoter Protects Against Carcinogenesis Induced by Nano-SiO2.

Nano silicon dioxide (Nano-SiO2) has been widely used in industries such as the field of biomedical engineering. Despite the existing evidence that Nano-SiO2 exposure could induce oxidative stress and inflammatory responses in multiple organ systems, the carcinogenicity of Nano-SiO2 exposure has rarely been investigated. Thus in this study, two types of human bronchial epithelial cell lines (16HBE and BEAS-2B) were selected as in vitro models to investigate the carcinogenicity of Nano-SiO2. Our results revealed that Nano-SiO2 induces a malignant cellular transformation in human bronchial epithelial cells according to the soft agar colony formation assay. The carcinogenesis induced by Nano-SiO2 was also confirmed in nude mice. By using immunofluorescence assay and high-performance capillary electrophoresis (HPCE), we observed a genome-wide DNA hypomethylation induced by Nano-SiO2. Besides the reduced enzyme activity of total DNMTs upon Nano-SiO2 treatment, altered expression of DNMTs and methyl-CpG binding proteins were observed. Besides, we found that the expression of NRF2 was activated by demethylation of CpG islands within the NRF2 promoter region and the overexpression of NRF2 could alleviate the carcinogenesis induced by Nano-SiO2. Taken together, our results suggested that Nano-SiO2 induces malignant cellular transformation with a global DNA hypomethylation, and the demethylation of NRF2 promoter activates the expression of NRF2, which plays an important role in protecting against the carcinogenesis induced by Nano-SiO2.

Isolated right ventricular noncompaction caused ventricular tachycardia and pulmonary embolism.

Isolated ventricular noncompaction is an unclassified cardiomyopathy due to intrauterine arrest of compaction of the loose interwoven meshwork. Its mortality and morbidity are high, including heart failure, thromboembolic events, and ventricular arrhythmias. Isolated right ventricular noncompaction was reported rarely, especially that causes pulmonary embolism and ventricular tachycardia. We describe a case of isolated noncompaction of the right ventricular causing pulmonary embolism and ventricular tachycardia.

Crackled nanocapsules: the "imperfect" structure for enzyme immobilization.

Herein, the first example of crackled organosilica nanocapsules (CONs) is reported to directly immobilize enzymes without any further chemical modification. Enzymes are adsorbed on both the exterior and interior surfaces of CONs, integrating the merits of adsorption and encapsulation. When used for Candida rugosa lipase (CRL) immobilization, the CONs displayed higher enzyme loading, lower enzyme leaching, and elevated enzyme activity, compared to the conventional non-crackled nanocapsules/particles.

Textiles/Metal-Organic Frameworks Composites as Flexible Air Filters for Efficient Particulate Matter Removal.

The health-threatening air pollution, especially from particulate matter (PM), has triggered increasing demands for developing low-cost and long-service-life air-cleaning technologies. In the present contribution, a range of high-efficiency textiles/metal-organic framework (MOF) composites (MOFs@textiles) air filters with excellent washable reusability is presented. By processing MOFs onto textile substrates via an eco-friendly solvent-free method to enable the microporous feature and also strong PM adhesion, we develop flexible, highly effective air filters with >95.00% PM removal efficiency (e.g., MiL-53(Al)@Aramid, PM2.5: 95.30%, PM10: 96.11%) under harmful air quality conditions (average PM2.5 mass concentration > 280 µg m-3 and PM10 > 360 µg m-3). Therefore, these MOFs@textiles are promising composites for producing efficient and recyclable out-/indoor air purifiers.

Acute Myocardial Infarction in a Young Girl with Nephrotic Syndrome: A Case Report and Literature Review.

Acute myocardial infarction is not a very rare complication of nephrotic syndrome. The pathogenesis of ischemic heart disease among patients with nephrosis is commonly thrombosis, whereas atherosclerosis is rare, especially in young individuals. In this case report, we present a 15-year-old girl with nephrotic syndrome who had acute non-ST-elevation myocardial infarction secondary to atherosclerosis of the 3 coronary arteries.

Effects of Angiotensin Inhibitor Valsartan on the Expression of the Angiotensin II 1 Receptor, Matrix Metalloproteinases -2 and -9 in Human Bladder Cancer Cell Lines.

BACKGROUND: In order to investigate how valsartan-the angiotensin II 1 receptor (AT1R) antagonist-affects the expressions of AT1R antigen, matrix metalloproteinases (MMPs) -2 and -9 in carcinoma of urinary bladder (CUB) cell lines with different invasive abilities. METHODS: Three cell lines, EJ-M3, EJ, and BIU-87, with different invasive abilities were cultured and treated with valsartan. Cell proliferation states were determined by the methyl thiazolyl tetrazolium (MTT) method. The expressions at protein level and gene level were determined by Western blot and real-time fluorescence reverse transcription polymerase chain reaction (RT-PCR), respectively. The invasive abilities and migratory abilities of the three cell lines were determined by Transwell in vitro cell invasion assay and wound healing assay, respectively. RESULTS: MTT results show that valsartan can inhibit the proliferation of CUB cells, and the inhibition effect is enhanced with the increase of concentration. CONCLUSIONS: AngII promotes the MMP2 and MMP9 expressions (both protein and gene levels) in CUB cells through AT1R, but their expressions can be effectively inhibited by valsartan, the AngII inhibitor. AngII inhibitor may become a novel drug that can inhibit CUB metastasis and prolong the survival of CUB patients.