Huiping Yuan

Background: Thyroid function differs between the oldest-old and younger adults, however, there is a lack of appropriate RIs for the serum FT4, T4, FT3, T3, and TSH concentrations for the oldest-old.

Increased entropy is a common cause of disease and aging. Lifespan entropy is the overall increase in disorder caused by a person over their lifetime. Aging leads to the excessive production of reactive oxygen species (ROS), which damage the antioxidant system and disrupt redox balance. Organ aging causes chronic inflammation, disrupting the balance of proinflammatory and anti-inflammatory factors. Inflammaging, which is a chronic low-grade inflammatory state, is activated by oxidative stress and can lead to immune system senescence. During this process, entropy increases significantly as the body transitions from a state of low order to high disorder. However, the connection among inflammation, aging, and immune system activity is still not fully understood. This review introduces the idea of the ROS-inflammation-immune balance for the first time and suggests that this balance may be connected to aging and the development of age-related diseases. We also explored how the balance of these three factors controls and affects age-related diseases. Moreover, imbalance in the relationship described above disrupts the regular structures of cells and alters their functions, leading to cellular damage and the emergence of a disorganized state marked by increased entropy. Maintaining a low entropy state is crucial for preventing and reversing aging processes. Consequently, we examined the current preclinical evidence for antiaging medications that target this balance. Ultimately, comprehending the intricate relationships between these three factors and the risk of age-related diseases in organisms will aid in the development of clinical interventions that promote long-term health.

Objective: To investigate the relationship between sleep duration and activities of daily living (ADL) disability, and to explore the optimal sleep duration among oldest-old Chinese individuals. Methods: In this cross-sectional study, 1,798 participants (73.2% female) were recruited from Dongxing and Shanglin in Guangxi Zhuang Autonomous Region, China in 2019. The restricted cubic spline function was used to assess the dose-response relationship between sleep duration and ADL disability, and the odds ratios (ORs) of the associations were estimated by logistic regression models. Results: The overall prevalence of ADL disability was 63% (64% in females and 58% in males). The prevalence was 71% in the Han population (72% in females and 68% in males), 60% in the Zhuang population (62% in females and 54% in males) and 53% in other ethnic population (53% in females and 53% in males). A nonlinear relationship between sleep duration and ADL disability was observed. Sleep duration of 8-10 hours was associated with the lowest risk of ADL disability. Sleep duration (≥12 hours) was associated with the risk of ADL disability among the oldest-old individuals after adjusting for confounding factors (OR = 1.47, 95% CI [1.02, 2.10], p < 0.05). Conclusion: Sleep duration more than 12 hours may be associated with an increased risk of ADL disability in the oldest-old individuals, and the optimal sleep duration among this population could be 8–10 h.

Background: The number of patients suffering from depression is continuously increasing in China. Demographic characteristics, physical health levels, and individual lifestyles/healthy behaviors are associated with the severity of depression. However, the major risk factor for depression remains unclear.Materials and methods: In this investigation, 16,512 patients were screened using the CHARLS (China Health and Retirement Longitudinal Study) database after being determined to be eligible based on the inclusion criteria. Depressive symptoms were evaluated through the CESD-10 (10-item Center for Epidemiological Studies Depression Scale). Consequently, various models were developed based on potential predictive factors, employing stepwise LR (Logistic Regression)/RF (Random Forests) models to examine the influence and weighting of candidate factors that affect depression.Results: Gender, residential address location, changes in health status following last interview, physical disabilities, chronic pain, childhood health status, ADL (activity of daily living), and social activity were all revealed to be independent risk factors for depression (p < 0.05) in this study. Depression has a synergic effect (across chronic pain and age groups). In comparison to other factors, RF results showed that chronic pain had a stronger impact on depression.Conclusion: This preliminary study reveals that chronic pain is a major risk factor for depression.

Background: Aging is characterized by a continuous loss of protein homeostasis. A closer examination of peripheral blood, which houses proteins from nearly all tissues and cells, helped identify several biomarkers and other aspects of aging biology. To further explore the general law of aging and identify key time nodes and associated aging biology, we collected 97 plasma samples from 253 healthy individuals aged 0-100 years without adverse outcomes to conduct nano-Ultra High Performance Liquid Chromatography-Mass Spectrometry/Mass Spectrometry (nano-UHPLC-MS/MS) and weighted gene co-expression network analysis (WGCNA). Results: Through biological processes and key biological pathways identified in discrete age group modules, our analyses highlighted a strong correlation between alterations in the immune system and aging process. We also identified hub genes associated with distinct age groups that revealed alterations not only in protein expression but also in signaling cascade. Among them, hub genes from age groups of 0-20 years old and 71-100 years old are mostly involved in infectious diseases and the immune system. In addition, CDC5L and HMGB2 were the key transcription factors (TFs) regulating genes expression in people aged between 51-60 and 71-100 years of age. They were shown to not only be independent but also mutually regulate certain hub gene expressions. Conclusions: This study reveals that the plasma proteome undergoes a complex alteration over the lifetime of a human. In this process, the immune system is crucial throughout the lifespan of a human being. However, the underlying mechanism(s) regulating differential protein expressions at distinct ages remains to be elucidated.

Glucotoxicity-induced pancreatic β-cell failure contributes to the development of type 2 diabetes mellitus (T2DM). Accumulating evidence reveals that miRNAs play a critical role in regulating pancreatic β-cell function and survival. In this study, we employed a self-assembled cell microarray (SAMcell)-based functional screening assay to identify miRNAs that are capable of regulating the dysfunction of β-cells induced by glucotoxicity. Among 62 conserved miRNAs we tested, miR-190 was identified as a candidate regulator that could effectively restore insulin expression in NIT-1 cells under high-glucose (HG) stimulation. Further analyses demonstrated that miR-190 was significantly down-regulated in HG-treated NIT-1 cells, as well as in the pancreas of diabetic mice. Mechanistic studies showed that Cybb is the direct target gene of miR-190, which encodes the gp91phox protein, a subunit of the NOX2 complex. Furthermore, both miR-190 overexpression and Cybb knockdown inhibited apoptosis and improved glucose-stimulated insulin secretion (GSIS) in HG-stimulated NIT-1 cells by attenuating the excessive production of reactive oxygen species (ROS). More importantly, a targeted delivery of mPEG-PCL-g-PDMAEMA nanoparticles/miR-190 complexes (PECgD NPs/miR-190) to the pancreas significantly ameliorated hyperglycemia, decreased fasting serum insulin levels, and improved glucose tolerance in diabetic mice. Taken together, our findings suggest that the miR-190/Cybb axis plays an important role in glucotoxicity-induced pancreatic β-cell failure. Restoring miR-190 expression levels may be a possible therapeutic strategy to protect β-cells in T2DM.