Rejuvenation research最新文献

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.

Chronic inflammation (inflammaging) is one of the important reasons for the development of age-related diseases and aging. Carrying out aging research and mining inflammatory markers can develop antiaging intervention targets, thus promoting healthy aging. By comparing the levels of inflammatory proteome in the serum of Chinese long-living people over 90 years and elderly aged 60∼79 which was detected by Olink platform, this study found that some pro-inflammatory or pro-aging proteins increased significantly in the long-living people, such as c-x-c motif chemokine ligand 9, accompanied by a significant increase in the levels of several anti-inflammatory or antiaging proteins, including fibroblast growth factor 19 and fibroblast growth factor 23, which confirmed that compared with elderly people, pro-inflammatory and anti-inflammatory (pro-aging and antiaging) tend to be balanced in long-living people, thus reducing the risk of age-related diseases and prolonging the lifespan of the elderly. These differently expressed proteins could serve as therapeutic targets and monitoring indicators for antiaging. At the same time, a few inflammatory protein markers, especially c-x-c motif chemokine ligand 9 and osteoprotegerin, could distinguish long-living and elderly correctly, which could be used to predict lifespan combined with other antiaging markers.

Geroscience, or longevity biotechnology, has made impressive advances in recent years that have led to the founding of dozens of start-ups, nonprofits and advocacy organizations, and the formation of a global movement to defeat aging. The community envisions changes at the regulatory and policy levels and calls for increased funding for research. Nevertheless, progress in the field has not been matched by discussions about ethical, legal, and social implications, as longevity advocates assume that seeking to expand lifespan or health span is inherently desirable and permissible. In this article, I make the case for the importance of putting ethics and society back into geroscience, along with three considerations for the longevity community. First, it should seek to understand the needs and attitudes of the public. Second, the community needs to define whether the field is primarily striving for healthy aging (increasing health span) or for extending years of life (lifespan). Third, it needs to define the role of investors and tech millionaires in shaping the field's priorities and direction. This last point raises the question of who is setting the direction of a field that can reshape the meaning of being human.

This study aimed to explore the effects of the cluster nursing strategy applied to traumatic brain injury (TBI) patients. Ninety-eight TBI patients admitted to the hospital were selected as the study subjects. They were randomized into two groups, the control group and the cluster group, with 49 cases in each group. The control group received routine nursing methods, while the cluster group received cluster nursing strategy. The intervention effects were compared between the two groups. After 3 months, the total occurrence of complications in the cluster group was significantly lower than that in the control group. Postintervention, the cluster group had a significantly lower National Institutes of Health Stroke Scale score and significantly higher Fugl-Meyer score and Loewenstein Occupational Therapy Cognitive Assessment score compared with the control group. The serum level of glial fibrillary acidic protein in the control group was significantly higher than that in the cluster group, while the serum level of brain-derived neurotrophic factor was significantly lower. The application of the cluster nursing strategy in the care of patients with TBI could effectively reduce the risk of complications and improve neurological, motor, and cognitive functions.

This study aims to investigate the expression differences of peripheral blood mononuclear cells (PBMCs) in patients with elderly rheumatoid arthritis (ERA). Differentially expressed genes (DEGs) of PBMCs between young patients with RA (RA_Y) and elderly patients with RA (RA_A) were identified by RNA sequencing using the DESeq2 package, followed by bioinformatics analysis. The overlapped targets of the current DEGs and proteomic differentially expressed proteins (another set of unpublished data) were identified and further validated. The bioinformatics analysis revealed significant transcriptomic heterogeneity between RA_A and RA_Y. A total of 348 upregulated and 363 downregulated DEGs were identified. Gene functional enrichment analysis indicated that the DEGs, which represented senescence phenotype for patients with ERA, were enriched in pathways such as Phosphatidylinositol3 kinase/AKT serine-threonine protein kinase (PI3K/Akt) signaling, Mitogen-activated protein kinases (MAPK) signaling, toll-like receptor family, neutrophil degranulation, and immune-related pathways. Gene set enrichment analysis further confirmed the activation of humoral immune response pathways in RA_A. Quantitative polymerase chain reaction validated the expression of five representative DEGs such as SPTA1, SPTB, VNN1, TNXB, and KRT1 in PBMCs of patients with ERA. Patients with ERA have significant senescence phenotype differences versus the young patients. The DEGs identified may facilitate exploring the biomarkers of senescence in RA.

Total hip arthroplasty (THA) is a highly effective intervention for addressing hip joint issues, yet managing perioperative pain remains a significant challenge. In this study, we aimed to investigate the impact of supplementing ropivacaine with dexmedetomidine in ultrasound-guided continuous pericapsular nerve group block (PENGB) among elderly patients undergoing THA. We conducted a retrospective analysis involving 112 elderly patients who underwent THA. These patients were divided into two groups: the Control group, receiving ropivacaine alone, and the DEX group, receiving ropivacaine combined with dexmedetomidine. We evaluated various parameters including hemodynamic data, postoperative pain levels assessed using the Visual Analog Scale, cognitive status measured with the Montreal Cognitive Assessment, and serum markers (S100β and GFAP). Our findings revealed that the DEX group exhibited improved stability in blood pressure and oxygen saturation following surgery. Moreover, patients in the DEX group reported significantly lower levels of pain at 6 and 12 hours postsurgery, with a prolonged duration of pain relief. Furthermore, dexmedetomidine administration was associated with preserved cognitive function during the early postoperative period. Analysis of serum markers suggested potential cognitive protection conferred by the addition of dexmedetomidine. Overall, our study underscores the multifaceted benefits of incorporating dexmedetomidine into ropivacaine-based PENGB for elderly THA patients.

Oxidative stress (OS) causes biochemical and morphological alterations in erythrocytes. The primary factors contributing to OS are aging and storage. Antioxidants significantly alleviate OS. Therefore, this study aimed to investigate the response of young and old erythrocytes to vitamin C and vitamin E during storage. Erythrocytes were separated into young and old by the Percoll method. Each erythrocyte subpopulation was categorized into the i) Control (additive solution-7 [AS-7]) and ii) vitamin C and vitamin E in AS-7 (VC+VE) groups and stored for 21 days at 4°C. OS, antioxidant, and aging markers were analyzed on days 1, 14, and 21. The activity of antioxidant enzymes was similar throughout storage in young cells. However, superoxide dismutase activity elevated in old cells (Control and VC+VE) on days 1 and 21. Catalase (CAT) activity increased on days 14 and 21, whereas glutathione peroxidase (GPX) increased on days 1 and 14 in old Controls. However, in old VC+VE, CAT increased on day 21 and GPX increased on day 1. Advanced oxidation protein products, superoxides, glutathione, and uric acid increased in old cells throughout storage. Malondialdehyde decreased in old VC+VE compared with old Control on days 14 and 21. Sialic acids and glutamate oxaloacetate transaminase activity were higher in young cells compared to old cells. Young cells exhibited lower oxidative changes throughout storage. Vitamin C and vitamin E were effective in maintaining the redox balance in old cells. These findings emphasize the need for specific approaches for different subpopulations during erythrocyte banking.