Rejuvenation research最新文献

Exploring the causal relationship between sarcopenia and neoplasm of bone and articular cartilage (NBAC) by bidirectional Mendelian randomization (MR). Genome-wide association study (GWAS) data on sarcopenia-associated traits including appendicular lean mass, low handgrip strength (including criteria from the European Working Group on Sarcopenia in Older People and the Foundation for the National Institutes of Health), and usual walking speeds were obtained from the UK Biobank. GWAS data for NBAC (benign and malignant) were provided by the Finnish Genetic Database. Three different methods of MR analysis, including inverse-variance weighted, Mendelian randomized Egger regression, and weighted median methods, were utilized. MR analysis showed that high appendicular lean mass was positively associated with the risk of developing benign NBAC (odds ratio and 95% confidence interval = 1.236 (1.026,1.489), p = 0.025). At the same time, there is no statistically significant association was found between traits related to sarcopenia and malignant neoplasm of bone and articular cartilage. There was also no reverse causal correlation between NBAC and traits related to sarcopenia. In European populations, better appendicular lean body mass is positively associated with the risk of benign neoplasm of bone and articular cartilage, representing the possibility that sarcopenia may be a protective factor against neoplasm of bone and articular cartilage.

In-stent restenosis (ISR) commonly occurs in elderly patients with coronary artery disease (CAD) after percutaneous coronary intervention. Atherosclerosis in elderly patients may be the leading cause of ISR. Therefore, we aim to explore the relationship between vascular calcification-associated factors and ISR occurrence. Elderly patients were enrolled according to standard inclusion and exclusion criteria. The serum fibroblast growth factor 23 (FGF23), hypoxia-inducible factor-1α (HIF-1α), and Klotho levels were determined using an enzyme-linked immunosorbent assay. The degree of coronary artery stenosis of the patients with CAD before operation was assessed using the Gensini score. The correlation was analyzed using Pearson analysis. The prediction value was evaluated using receiver operating characteristic (ROC) curve analysis. The patients with CAD were classified into the ISR group with 97 cases and the non-ISR (NISR) group with 349 cases. The Gensini score, serum FGF23, and HIF-1α levels increased while Klotho levels decreased in patients with CAD of the ISR group compared with those of the NISR group. Pearson analysis showed that FGF23 and HIF-1α positively correlated while Klotho negatively correlated to the Gensini score. ROC analysis showed all three factors could effectively predict the occurrence of ISR. Furthermore, the joint had a more effective prediction value for ISR occurrence. The dynamic analysis presented that the serum FGF23 and HIF-1α levels dramatically increased while Klotho levels decreased in patients with CAD after 1-year follow-up. Serum FGF23 and HIF-1α positively correlated while serum Klotho negatively correlated to ISR. Conclusively, these three factors effectively predicted the occurrence of ISR.

Elderly individuals represent a significant demographic undergoing total hip arthroplasty, with distinct risks and complications. The study aimed to determine whether predictive nursing, guided by risk assessment, could reduce these risks and improve patient outcomes. A total of 191 elderly patients undergoing total hip arthroplasty were included in the study, with 142 patients randomly assigned to either the control or observation groups. The control group received routine care, while the observation group received predictive nursing based on comprehensive risk assessment. Various assessment tools were employed to evaluate risks such as venous thrombosis, pressure injuries, falls, joint dislocation, infections, and psychological factors. The primary outcomes included functional improvement measured by the Harris Hip Score, Activities of Daily Living (ADL), anxiety levels, and patient satisfaction. Our study demonstrated that predictive nursing interventions, guided by comprehensive risk assessment, yielded significant reductions in postoperative complications, particularly deep vein thrombosis, in elderly patients undergoing total hip arthroplasty. In addition, patients who received predictive nursing care experienced notable benefits, including shorter hospital stays, heightened satisfaction levels, enhanced hip function, improved ADL scores, and reduced anxiety levels compared with those receiving standard care. The study underscores the substantial benefits of predictive nursing interventions guided by risk assessment in improving outcomes for elderly patients undergoing total hip arthroplasty, highlighting the potential of individualized nursing care to optimize postoperative recovery and enhance patient well-being.

The aim of this study is to elucidate the pharmacological mechanism underlying the effects of Ginseng Radix et Rhizoma (ginseng) in heart failure (HF), providing a theoretical foundation for its clinical application. The potential mechanism of ginseng in the context of HF was investigated using systems pharmacology that combined network pharmacology, Gene Expression Omnibus (GEO) analysis, molecular docking, and experimental verification. Network pharmacology was employed to identify drug-disease targets. Core gene targets were subsequently subjected to enrichment analysis by integrating network pharmacology with GEO. Molecular docking was utilized to predict the binding affinities between identified targets and ginseng compounds. Furthermore, the therapeutic efficacy of ginseng was validated in an isoproterenol (ISO)-induced rat model of HF. The modulation of key signaling pathways by ginseng was confirmed through Western blot analysis. A total of 154 potential targets of ginseng in the treatment of HF were identified through network pharmacology analysis. The analysis of GSE71613 revealed that the PI3K-Akt pathway, reactive oxygen species, oxidative phosphorylation, MAPK signaling, and Ras signaling pathways are predominantly associated with patients with HF. By integrating the findings from network pharmacology and GEO analysis, ginsenoside Rg1 and ginsenoside Rb3 were identified as the potential components in ginseng, while FN1 and PRKAA2 were recognized as key targets involved in the PI3K-AKT and AMPK pathways, respectively. Molecular docking analysis revealed a strong affinity between the potential components and the identified core targets. In vivo experiments indicated that the extract of ginseng (EPG) significantly ameliorated ISO-induced cardiac dysfunction by improving cardiac parameters such as cardiac left ventricular internal systolic diameter, left ventricular end-diastolic volume, left ventricular end systolic volume, and left ventricular ejection fraction, while also reducing malondialdehyde production. In addition, EPG was found to enhance superoxide dismutase activity and ATP levels, while concurrently reducing the levels of interleukin (IL)-1β, IL-6, and TNF-α. The extract also reduced myocardial oxygen consumption, inflammatory cell infiltration, and the number of damaged myocardial fibers. Moreover, EPG was observed to upregulate the expression of p-PI3K, p-AKT, p-AMPK, and Bcl-2, while downregulating the expression of p-NFκB, TGF-β, and Bax. The therapeutic effects of ginseng on HF are primarily mediated through the PI3K-Akt and AMPK pathways. Ginsenoside Rg1 and ginsenoside Rb3 have been identified as potential therapeutic agents for HF.

Parkinson's disease (PD) is a multifactorial degenerative disease in the elder. Given the involvement of mammalian sterile 20-like kinase 1 (MST1) in PD, this article was to illustrate the mechanism of MST1 in 1-methyl-4-phenylpyridinium ion (MPP⁺)-induced PD cell model. Cells were treated with different concentrations of MPP⁺ to establish a PD cell model. Reverse transcription-quantitative polymerase chain reaction and Western blot revealed that MST1 expression and iron ion concentration increased, but cellular viability decreased with MPP⁺ concentration. Inhibition of MST1 decreased ferroptosis; increased cellular viability, iron ion content, and levels of glutathione peroxidase 4; and decreased reactive oxygen species and lactate dehydrogenase release. Upregulation of ferroptosis levels using ferroptosis agonist Erastin reduced the protective effect of MST1 inhibition on PD cells. Mechanistically, dual-luciferase analysis identified that miR-23b-3p targeted MST1 and inhibited its expression. Overexpression of miR-23b-3p inhibited MST1 levels, thereby reducing cellular ferroptosis and attenuating MPP⁺-induced cell injury. Collectively, MST1 expression increased with increasing MPP⁺ concentration, and miR-23b-3p targeted MST1 to reduce ferroptosis and MPP⁺-induced cell injury.

Lipofuscin is indigestible garbage that accumulates in the autophagic vesicles and cytosol of postmitotic cells with age. Drs. Brunk and Terman postulated that lipofuscin accumulation is the main or at least a major driving factor in aging. They even posited that the evolution of memory is the reason why we get lipofuscin at all, as stable synaptic connections must be maintained over time, meaning that the somas of neurons must also remain in the same locale. In other words, they cannot dilute out their garbage over time through cell division. Mechanistically, their position certainly makes sense given that rendering a large percentage of a postmitotic cell's lysosomes useless must almost certainly negatively affect that cell and the surrounding microenvironment. It may be the case that lipofuscin accumulation is the main issue with regard to current age-related disease. Degradation in situ may be an insurmountable task currently. However, a method of systemic lipofuscin removal is discussed herein.

NQO1 disruption enhances susceptibility to oxidative stress during hyperglycemia and is a significant contributor to the development and progression of diabetes. Oxidative stress has been linked to several symptoms, including hyperglycemia, reactive oxygen species buildup, high blood pressure, and the expression of inflammatory markers. Therefore, the present research aimed to evaluate the genetic abnormality of NQO1 (rs1800566, C609T) gene polymorphism, expression, and vitamin-D level assessment among Type 2 diabetes mellitus (T2DM) patients. The study included 100 newly diagnosed T2DM cases and 100 healthy individuals as healthy controls. Total RNA was extracted from the whole blood using the TRIzol method, and further cDNA was synthesized, and expression was evaluated. There is a significant difference in NQO1 (rs1800566, C609T) genotype distribution among the T2DM patients and healthy controls (p = 0.04). Compared with the NQO1 CC wild-type genotype, the NQO1 CT heterozygous genotype had an odds ratio of 1.96 (1.08-3.55), and the NQO1 TT mutant type genotype had an odds ratio of 3.31 (0.61-17.77). Significantly decreased expression of NQO1 mRNA was observed with heterozygous CT (p < 0.0001) and homozygous mutant TT genotype (p = 0.0004), compared with homozygous wild-type CC genotype. NQO1 mRNA expression level was also compared with vitamin D levels among the T2DM patients. T2DM patients with vitamin D deficiency had 1.83-fold NQO1 mRNA expression, while vitamin D insufficient and sufficient T2DM cases had 3.31-fold (p < 0.0001) and 3.70-fold (p < 0.0001) NQO1 mRNA expression. It was concluded that NQO1 (rs1800566, C609T) CT and TT genotypes played a significant role in the worseness of type II diabetes mellitus, and decreased expression of NQO1 mRNA expression could be an essential factor for disease worseness as well as hypermethylation could be a factor for reduced expression leading to disease severity. The decreased NQO1 mRNA expression with heterozygous CT and mutant TT genotype associated with vitamin D deficiency may contribute to disease progression.