As a traditional Chinese medicinal herb with a long history, Codonopsis pilosula (CP) has attracted much attention from the medical community in recent years. This review summarizes the research progress of CP in the medical field in the past 5 years. By searching and analyzing the literature, and combining with Cytoscape software, we comprehensively examined the role and mechanism of action of CP in individual application, combination drug application, and the role and mechanism of action of codonopsis pilosula's active ingredients in a variety of diseases. It also analyzes the medicinal use of CP and its application value in medicine. This review found that CP mainly manifests important roles in several diseases, such as cardiovascular system, nervous system, digestive system, immune system, etc., and regulates the development of many diseases mainly through the mechanisms of inflammation regulation, oxidative stress, immunomodulation and apoptosis. Its rich pharmacological activities and diverse medicinal effects endow CP with broad prospects and application values. This review provides valuable reference and guidance for the further development of CP in traditional Chinese medicine.
Existing natural language processing (NLP) methods to convert free-text clinical notes into structured data often require problem-specific annotations and model training. This study aims to evaluate ChatGPT's capacity to extract information from free-text medical notes efficiently and comprehensively. We developed a large language model (LLM)-based workflow, utilizing systems engineering methodology and spiral "prompt engineering" process, leveraging OpenAI's API for batch querying ChatGPT. We evaluated the effectiveness of this method using a dataset of more than 1000 lung cancer pathology reports and a dataset of 191 pediatric osteosarcoma pathology reports, comparing the ChatGPT-3.5 (gpt-3.5-turbo-16k) outputs with expert-curated structured data. ChatGPT-3.5 demonstrated the ability to extract pathological classifications with an overall accuracy of 89%, in lung cancer dataset, outperforming the performance of two traditional NLP methods. The performance is influenced by the design of the instructive prompt. Our case analysis shows that most misclassifications were due to the lack of highly specialized pathology terminology, and erroneous interpretation of TNM staging rules. Reproducibility shows the relatively stable performance of ChatGPT-3.5 over time. In pediatric osteosarcoma dataset, ChatGPT-3.5 accurately classified both grades and margin status with accuracy of 98.6% and 100% respectively. Our study shows the feasibility of using ChatGPT to process large volumes of clinical notes for structured information extraction without requiring extensive task-specific human annotation and model training. The results underscore the potential role of LLMs in transforming unstructured healthcare data into structured formats, thereby supporting research and aiding clinical decision-making.
Chemokines, cytokines, and inflammatory cells mediate the onset and progression of many diseases through the induction of an inflammatory response. LncRNAs have emerged as important regulators of gene expression and signaling pathways. Increasing evidence suggests that lncRNAs are key players in the inflammatory response, making it a potential therapeutic target for various diseases. From the perspective of lncRNAs and inflammatory factors, we summarized the expression level and regulatory mechanisms of lncRNAs in human inflammatory diseases, such as cardiovascular disease, osteoarthritis, sepsis, chronic obstructive pulmonary disease, asthma, acute lung injury, diabetic retinopathy, and Parkinson's disease. We also summarized the functions of lncRNAs in the macrophages polarization and discussed the potential applications of lncRNAs in human inflammatory diseases. Although our understanding of lncRNAs is still in its infancy, these data will provide a theoretical basis for the clinical application of lncRNAs.
Background: Prior research has identified one's own education level as a risk factor for frailty. However, the association between spousal education and frailty in later life is uncertain. We aim to examine the longitudinal association between spousal education and frailty levels among Chinese older populations. Methods: 3856 participants aged 60 and older from the 2011-2018 China Health and Retirement Longitudinal Study were analyzed. A 54-item deficit cumulative frailty index was developed to evaluate frailty levels at each follow-up. Linear mixed-effects models were used to examine the longitudinal association of spousal education with frailty levels, and whether this association varied by sex and own education level. Results: Higher spouse education was associated with lower frailty levels, and this association decreased with age. Compared with older adults whose spouses had no formal education, older adults whose spouses had less than middle school education had an 8.82 lower level of frailty (95% CI: 15.05 to -2.58, P < 0.01); those with spouses with middle school education and above had a 23.44 lower level (95% CI: 31.43 to -15.44, P < 0.001). Stratified analysis showed that every additional year of spouse education was also associated with lower frailty levels in non-frail participants at baseline, but stronger among those already frail. The association between high spousal education and lower frailty did not vary by sex or own education. Conclusion: This study reveals a significant association between having a more educated spouse and lower later-life frailty levels for both older men and women, regardless of one's own educational background. It emphasizes the importance of leveraging educated spouses to prevent and manage frailty.
BACKGROUND: Air pollution is a frailty risk factor, yet the frailty-related health benefits of China's air pollution control policy, the Clean Air Action (CCAA), are unclear. Frailty progression and transitions differ among robust, prefrail, and frail adults. This study aimed to evaluate the CCAA's effect on frailty levels among robust, prefrail, and frail Chinese adults. METHODS: Using propensity score matching with difference-in-differences analysis, we studied 9 788 adults aged ≥45 from the 2011 and 2018 China Health and Retirement Longitudinal Study. The Frailty Index (FI), summarizing 32 health deficits, quantifies frailty level (range: 0-1 scores). Frailty was defined as FIâ ≥â 0.25, prefrailty as FI 0.10-0.25, and robust as FIâ ≤â 0.10. We examined frailty transitions between these states (robust, prefrail, and frail) from 2011 to 2018. Based on provincial particulate matter reduction targets, participants were assigned to intervention (>10% reduction) or control (≤10%) groups and categorized as robust, prefrail, or frail pre-CCAA implementation. RESULTS: The CCAA significantly reduced FI scores among preimplementation robust individuals by 0.0205 and among prefrail individuals by 0.0114, with no significant changes in frail individuals. Frailty transition analyses confirmed specific benefits of the CCAA, which significantly reduced worsening from robust to prefrail or frail by 7.0% and prefrail to frail by 3.9%. However, it did not facilitate the improvement from frail to prefrail/robust or from prefrail back to robust. No significant subgroup differences were observed across age, gender, Hukou, education, and social participation. CONCLUSIONS: CCAA has been associated with a reduction in frailty deterioration in robust and prefrail populations.
Frailty , Aged , Humans , Middle Aged , Frailty/epidemiology , Frailty/prevention & control , Frail Elderly , Longitudinal Studies , Independent Living , Risk Factors , Geriatric Assessment
Background and Objectives: Evidence remains unclear on the impact of life-course socioeconomic position (SEP) mobility on frailty trajectories in later life. We aim to examine the longitudinal effects of social mobility on frailty trajectories among Chinese middle-aged and older populations. Research Design and Methods: A total of 13 239 participants aged 45 and older from the 2011-2018 China Health and Retirement Longitudinal Study were analyzed. Based on changes in SEP from childhood to adulthood, 5 patterns of social mobility were established. A 32-item deficit cumulative frailty index (FI) was developed to evaluate frailty trajectories at each follow-up. Linear mixed-effects models were used to examine the longitudinal association of the 5 social mobility patterns with the frailty trajectory. Results: The trajectory of late-life FI increased across all 5 social mobility groups during the follow-up. The FI trajectory had the largest disparity between stable high SEP and stable low SEP, with a faster increase in FI of 0.489 (95% confidence interval [CI]: 0.327-0.650, pâ <â .001) in the stable low versus stable high SEP group. The FI trajectories of individuals in the upward and downward mobility groups fall between those in the stable high SEP and low SEP groups. Specifically, compared to the stable high SEP group, the increase in FI was 0.229 (95% CI: 0.098-0.360, pâ =â .001) faster in the downward mobility group, and 0.145 (95% CI: 0.017-0.273, pâ =â .03) faster in the upward mobility group. The impact of social mobility on frailty trajectories was more pronounced among middle-aged adults and women. Discussion and Implications: These findings emphasize that policies to identify vulnerable populations and reduce frailty inequalities should focus on the socioeconomic environment across the life course, with particular attention paid to those with consistently low SEP and downward mobility.
Subarachnoid hemorrhage (SAH) is a stroke subtype with high mortality, and its severity is closely related to the short-term prognosis of SAH patients. S100 calcium-binding protein A9 (S100A9) has been shown to be associated with some neurological diseases. In this study, the concentration of S100A9 in clinical cerebrospinal fluid samples was detected by enzyme-linked immunosorbent assay (ELISA), and the relationship between S100A9 and the prognosis of patients was explored. In addition, WT mice and S100A9 knockout mice were used to establish an in vivo SAH model. Neurological scores, brain water content, and histopathological staining were performed after a specified time. A co-culture model of BV2 and HT22 cells was treated with heme chloride to establish an in vitro SAH model. Our study confirmed that the expression of S100A9 protein in the CSF of SAH patients is increased, and it is related to the short-term prognosis of SAH patients. S100A9 protein is highly expressed in microglia in the central nervous system. S100A9 gene knockout significantly improved neurological function scores and reduced neuronal apoptosis. S100A9 protein can activate TLR4 receptor, promote nuclear transcription of NF-κB, increase the activation of inflammatory body, and ultimately aggravate nerve injury.
Laryngeal squamous cell carcinoma (LSCC) is one of the common malignant tumors in the head and neck region, and its high migration and invasion seriously threaten the survival and health of patients. In cancer development, m6A RNA modification plays a crucial role in regulating gene expression and signaling. This study delved into the function and mechanism of the m6A reading protein YTHDF1 in LSCC. It was found that YTHDF1 was highly expressed in the GEO database and LSCC tissues. Cell function experiments confirmed that the downregulation of YTHDF1 significantly inhibited the proliferation, migration, and invasion ability of LSCC cells. Further studies revealed that EIF4A3 was a downstream target gene of YTHDF1, and knockdown of EIF4A3 similarly significantly inhibited the malignant progression of LSCC in both in vivo and in vitro experiments. The molecular mechanism studies suggested that YTHDF1-EIF4A3 may promote the malignant development of LSCC by activating the EMT signaling pathway. This study provides important clues for an in-depth understanding of the pathogenesis of LSCC and is a solid foundation for the discovery of new therapeutic targets and approaches.
Carcinoma, Squamous Cell , Head and Neck Neoplasms , Laryngeal Neoplasms , MicroRNAs , Humans , Squamous Cell Carcinoma of Head and Neck , Carcinoma, Squamous Cell/pathology , Laryngeal Neoplasms/genetics , Laryngeal Neoplasms/metabolism , Cell Proliferation/genetics , Cell Line, Tumor , Gene Expression Regulation, Neoplastic , MicroRNAs/metabolism , Eukaryotic Initiation Factor-4A/genetics , Eukaryotic Initiation Factor-4A/metabolism , DEAD-box RNA Helicases/metabolism , RNA-Binding Proteins/metabolism
Emodin was extracted from Rheum officinale Baill by ultrasound-assisted extraction (UAE), and ethanol was chosen as the suitable solvent through SEM and molecular dynamic simulation. Under the optimum conditions (power 541 W, time 23 min, liquid to material ratio 13:1 mL/g, ethanol concentration 83 %) predicted by RSM, the yield of emodin was 2.18 ± 0.11 mg/g. Moreover, ultrasound power and time displayed the significant effects on the extraction process. Extracting dynamics analysis indicated that the extraction process of emodin by UAE conformed to Fick's second diffusion law. The results of antibacterial experiments suggested that emodin can damage cell membrane and inhibit the expression of cps2A, sao, mrp, epf, neu and the hemolytic activity of S. suis. Biolayer interferometry and FT-IR multi-peak fitting assays demonstrated that emodin induced a secondary conformational shift in CcpA. Molecular docking and molecular dynamics confirmed that emodin bound to CcpA through hydrogen bonding (ALA248, GLU249, GLY129 and ASN196) and π-π T-shaped interaction (TYR225 and TYR130), and the mutation of amino acid residues affected the affinity of CcpA to emodin. Therefore, emodin inhibited the sugar utilization of S. suis through binding to CcpA, and CcpA may be a potential target to inhibit the growth of S. suis.
Emodin , Rheum , Streptococcus suis , Emodin/pharmacology , Emodin/chemistry , Rheum/chemistry , Streptococcus suis/genetics , Streptococcus suis/metabolism , Molecular Docking Simulation , Spectroscopy, Fourier Transform Infrared , Anti-Bacterial Agents/pharmacology , Ethanol/metabolism
Background: The occurrence rate of distal anterior cerebral artery (DACA) aneurysms is relatively low, primarily due to their deep-seated location, which makes surgical clamping challenging. The objective of this study was to investigate the efficacy and safety of computed tomography (CT) navigation-assisted clipping of DACA aneurysms compared to traditional clipping without navigation. Methods: A retrospective cohort study involving retrospective data collection was performed. The retrospective analysis was conducted on 139 patients with ruptured DACA aneurysms who underwent clipping. From January 2013 to November 2021, 164 patients were retrieved at the Department of Neurosurgery, Renmin Hospital of Wuhan University. The inclusion criteria were patients diagnosed with DACA aneurysms via CT angiography (CTA) or digital subtraction angiography (DSA), those with complete clinical data, and those who underwent craniotomy for aneurysm clipping. Meanwhile, the exclusion criteria were as follows: aneurysm recurrence, traumatic brain injury or surgery history, blood disorders or recent anticoagulant use, and severe organ dysfunction. Data on gender, age, Hunt-Hess grade, Fisher grade, modified Rankin Scale (mRS) score, aneurysm location, hospitalization time, aneurysm found time (the duration from incision to aneurysm discovery), and intraoperative bleeding volume were collected from medical records and neurosurgical databases. Patients were followed up in the clinic or by telephone in May 2022. All patients were divided into a navigation group or a traditional group for statistical analysis. Results: No statistically significant differences were observed in age, sex, Fisher grade, Hunt-Hess grade, hospitalization time, or aneurysm site between the navigation group and traditional group (P>0.05). Intraoperative blood loss was lower in the navigation group than in the traditional group {370 [280-460] vs. 430 [310-610] mL, P=0.045}. Patients in the traditional group had a shorter aneurysm found time than did those in the navigation group {49 [42-53] vs. 79 [63-84] min, P<0.001}. There was no significant difference in the mRS score at hospital discharge (P=0.336) or follow-up (P=0.157) between the two groups. Conclusions: CT neuronavigation-assisted microsurgery for clipping DACA aneurysms may improve surgical accuracy, shorten the time to locate aneurysms, and reduce intraoperative blood loss. Although no significant difference in prognosis was observed, this technique shows promise as a safe and effective alternative to traditional clipping without navigation.
BACKGROUND AND PURPOSE: Neuroinflammation is an important mechanism underlying brain injury caused by subarachnoid hemorrhage (SAH). C-C chemokine receptor type 1 (CCR1)-mediated inflammation is involved in the pathology of many central nervous system diseases. Herein, we investigated whether inhibition of CCR1 alleviated neuroinflammation after experimental SAH and aimed to elucidate the mechanisms of its potential protective effects. METHODS: To analyze SAH transcriptome data R studio was used, and a mouse model of SAH was established using endovascular perforations. In this model, the selective CCR1 antagonist Met-RANTES (Met-R) and the CCR1 agonist recombinant CCL5 (rCCL5) were administered 1 h after SAH induction. To investigate the possible downstream mechanisms of CCR1, the JAK2 inhibitor AG490 and the JAK2 activator coumermycin A1 (C-A1) were administered 1 h after SAH induction. Furthermore, post-SAH evaluation, including SAH grading, neurological function tests, Western blot, the terminal deoxynucleotidyl transferase dUTP nick end labeling assay, and Fluoro-Jade B and fluorescent immunohistochemical staining were performed. Cerebrospinal fluid (CSF) samples were detected by ELISA. RESULTS: CCL5 and CCR1 expression levels increased significantly following SAH. Met-R significantly improved neurological deficits in mice, decreased apoptosis and degeneration of ipsilateral cerebral cortex neurons, reduced infiltrating neutrophils, and promoted microglial activation after SAH induction. Furthermore, Met-R inhibited the expression of p-JAK2, p-STAT3, interleukin-1ß, and tumor necrosis factor-α. However, the protective effects of Met-R were abolished by C-A1 treatment. Furthermore, rCCL5 injection aggravated neurological dysfunction and increased the expression of p-JAK2, p-STAT3, interleukin-1ß, and tumor necrosis factor-α in SAH mice, all of which were reversed by the administration of AG490. Finally, the levels of CCL5 and CCR1 were elevate in the CSF of SAH patient and high level of CCL5 and CCR1 levels were associated with poor outcome. CONCLUSION: The present results suggested that inhibition of CCR1 attenuates neuroinflammation after SAH via the JAK2/STAT3 signaling pathway, which may provide a new target for the treatment of SAH.
Receptors, Chemokine , Subarachnoid Hemorrhage , Animals , Mice , Apoptosis , Interleukin-1beta/metabolism , Janus Kinase 2/metabolism , Neuroinflammatory Diseases , Receptors, CCR1/metabolism , Receptors, Chemokine/metabolism , Signal Transduction , STAT3 Transcription Factor/metabolism , Subarachnoid Hemorrhage/complications , Subarachnoid Hemorrhage/drug therapy , Subarachnoid Hemorrhage/metabolism , Tumor Necrosis Factor-alpha/metabolism
BACKGROUND AND PURPOSE: Neurogenic pulmonary edema (NPE) frequently arises as a complication subsequent to subarachnoid hemorrhage (SAH). Heterodimers of S100A8 and S100A9 are commonly formed, thereby initiating an inflammatory reaction through receptor binding on the cell surface. Paquinimod serves as a specific inhibitor of S100A9. The objective of this investigation is to assess the impact of Paquinimod administration and S100A9 knockout on NPE following SAH. METHODS: In this study, SAH models of C57BL/6J wild-type (WT) and S100A9 knockout mice were established through intravascular perforation. These models were then divided into several groups, including the WT-sham group, S100A9-KO-sham group, WT-SAH group, WT-SAH + Paquinimod group, and S100A9-KO-SAH group. After 24 h of SAH induction, pulmonary edema was assessed using the lung wet-dry weight method and Hematoxylin and eosin (HE) staining. Additionally, the expression levels of various proteins, such as interleukin-1ß (IL-1ß), tumor necrosis factor α (TNF-α), occludin, claudin-3, Bax, Bcl-2, TLR4, MYD88, and pNF-κB, in lung tissue were analyzed using western blot and immunofluorescence staining. Lung tissue apoptosis was detected by TUNEL staining. RESULTS: Firstly, our findings indicate that the knockout of S100A9 has a protective effect on early brain injury following subarachnoid hemorrhage (SAH). Additionally, the reduction of brain injury after SAH can also alleviate neurogenic pulmonary edema (NPE). Immunofluorescence staining and western blot analysis revealed that compared to SAH mice with wild-type S100A9 expression (WT-SAH), the lungs of S100A9 knockout SAH mice (S100A9-KO-SAH) and mice treated with Paquinimod exhibited decreased levels of inflammatory molecules (IL-1ß and TNF-α) and increased levels of tight junction proteins. Furthermore, the knockout of S100A9 resulted in upregulated expression of the apoptotic-associated protein Bax and down-regulated expression of Bcl-2. Furthermore, a decrease in TLR4, MYD88, and phosphorylated pNF-κB was noted in S100A9-KO-SAH and Paquinimod treated mice, indicating the potential involvement of the TLR4/MYD88/NF-κB signaling pathway in the inhibition of the protective effect of S100A9 on NPE following SAH. CONCLUSION: The knockout of S100A9 not only ameliorated initial cerebral injury following subarachnoid hemorrhage (SAH), but also mitigated SAH-associated neurogenic pulmonary edema (NPE). Additionally, Paquinimod was found to diminish NPE. These findings imply a correlation between the central nervous system and peripheral organs, highlighting the potential of safeguarding the brain to mitigate harm to peripheral organs.
Brain Injuries , Pulmonary Edema , Subarachnoid Hemorrhage , Animals , Mice , bcl-2-Associated X Protein/metabolism , Brain Injuries/pathology , Calgranulin B , Mice, Inbred C57BL , Myeloid Differentiation Factor 88/genetics , Myeloid Differentiation Factor 88/metabolism , Pulmonary Edema/drug therapy , Pulmonary Edema/etiology , Pulmonary Edema/prevention & control , Subarachnoid Hemorrhage/complications , Subarachnoid Hemorrhage/drug therapy , Subarachnoid Hemorrhage/metabolism , Toll-Like Receptor 4/genetics , Toll-Like Receptor 4/metabolism , Tumor Necrosis Factor-alpha/metabolism
C-X-C chemokine receptor type 4 (CXCR4) is critical for homeostasis of the adaptive and innate immune system in some CNS diseases. Bruton's tyrosine kinase (BTK) is an essential kinase that regulates inflammation in immune cells through multiple signaling pathways. This study aims to explore the effect of CXCR4 and BTK on neuroinflammation in the pathogenesis of early brain injury (EBI) after subarachnoid hemorrhage (SAH). Our results showed that the expression of CXCR4 and p-BTK increased significantly at 24 h after SAH in vivo and in vitro. Ibrutinib improved neurological impairment, BBB disruption, cerebral edema, lipid peroxidation, neuroinflammation and neuronal death at 24 h after SAH. Inhibition of BTK phosphorylation promoted the in vitro transition of hemin-treated proinflammatory microglia to the anti-inflammatory state, inhibited the p-P65 expression and microglial pyroptosis. NLRP3 deficiency can significantly reduce pyroptosis in SAH mice. Moreover, CXCR4 inhibition can suppress NLRP3-mediated pyroptosis, NF-κB activation and NOX2 expression in vitro, and ibrutinib can abolish CXCR4-aggravated BBB damage and pyroptosis in EBI after SAH. The levels of CXCR4 in CSF of SAH patients is significantly increased, and it is positively correlated with GSDMD and IL-1ß levels, and have a moderate diagnostic value for outcome at 6-month follow-up. Our findings revealed the effect of CXCR4 and P-BTK on NLRP3-mediated pyroptosis and lipid peroxidation after SAH in vivo and in vitro, and the potential diagnostic role of CXCR4 in CSF of SAH patients. Inhibition of CXCR4-BTK axis can significantly attenuate NLRP3-mediated pyroptosis and lipid peroxidation by regulating NF-κB activation in EBI after SAH.
Brain Injuries , Subarachnoid Hemorrhage , Rats , Humans , Mice , Animals , NF-kappa B/metabolism , Inflammasomes/metabolism , NLR Family, Pyrin Domain-Containing 3 Protein/genetics , NLR Family, Pyrin Domain-Containing 3 Protein/metabolism , Pyroptosis , Agammaglobulinaemia Tyrosine Kinase/metabolism , Lipid Peroxidation , Subarachnoid Hemorrhage/metabolism , Neuroinflammatory Diseases , Rats, Sprague-Dawley , Brain Injuries/etiology , Receptors, CXCR4/genetics , Receptors, CXCR4/metabolism
The aim of this study was to describe the effects of adropin deficiency on the distribution, phenotype and pathological phenotype of macrophages in colonic and mesenteric tissues of AdrKO (Enho-/-) mice, so as to explore the mechanism of adropin deficiency in spontaneous and experimental colitis. In this study, RNA-seq and metabonomics were used to screen the regulatory mechanism of adropin on the phenotypic transformation of macrophages. We found that adropin levels in active UC patients were significantly lower than those in normal subjects and remission UC patients, and at the same time, a large number of proinflammatory M1-type macrophages were infiltrated in the mesenteric tissue of colonic tissues from UC and CD patients. At the same time, spontaneous colitis occurred in Enho-/- (adropin-deficient)C57BL/6 mice, and there was an imbalance of M2 â M1 polarization of macrophages in colon and mesentery of Enho-/- mice. In vivo, it has showed that adropin deficiency could exacerbate the pathological phenotype of colitis induced by TNBS. In vitro, adropin was used to intervene RAW264.7 macrophages, and then combined analysis of RNA-seq and metabolomics demonstrated that adropin regulated lipid metabolism of macrophages through PPARγ, thus promoting the repolarization of macrophages from M1 to M2. Adropin deficiency led to an imbalance in the phenotypic distribution of macrophages infiltrating the colon and mesenteric tissues, namely, an increase in M1 type, which led to the occurrence and development of colitis.
OBJECTIVES: This study examines the association between workforce participation and mortality among Chinese older adults. METHODS: 6,138 participants aged 60 and older from the 2011 to 2018 China Health and Retirement Longitudinal Study were studied and 79.5% of the sample were rural Hukou. Cox proportional hazard models were used to estimate hazard ratios (HRs) for the associations of work status, work types, and changes in work status with all-cause mortality. Cox models with penalized splines were performed to explore the dose-response relationship for hours worked per week and mortality. RESULTS: 37,235.3 person-years observed 1,165 deaths (19.0%). Working reduced the mortality risk in older adults by 41% compared with those who did not work (HR: 0.59, 95% confidence interval: 0.50-0.69). This effect was consistent across subgroups. The mortality risk was lowest among self-employed older adults, followed by nonagricultural employment and then agricultural work, with adjusted HRs of (0.38, 0.21-0.70), (0.58, 0.36-0.93), and (0.61, 0.51-0.72), respectively. The mortality risk decreased with increasing hours of work per week and appeared to reach a threshold of about 45 hr of work per week. Compared with the older adults who continuously did not work, those who started and kept working had 28% (0.72, 0.53-0.97) and 48% (0.52, 0.41-0.65) lower mortality risks, respectively. When older adults transitioned from working to not working, the mortality risk would no longer be significantly different from that of older adults who were continuously not working (0.86, 0.65-1.12, p = 0.3). DISCUSSION: Workforce participation was associated with survival benefits among older adults in China.
East Asian People , Employment , Mortality , Aged , Humans , Middle Aged , China/epidemiology , Longitudinal Studies , Prospective Studies , Risk Factors
Corona Virus Disease 2019 (COVID-19) is an acute respiratory infection and a global public health event. The level of aß2GPI is significantly up-regulated in COVID-19 patients. The impact of inactivated vaccination against COVID-19 on aß2GPI and in vitro fertilization and embryo transfer (IVF-ET) remains unknown amidst the universal administration of COVID-19 vaccines. We conducted a retrospective study to assess the impact of COVID-19 inactivated vaccination on aß2GPI levels and its effect on superovulation and pregnancy outcomes. We found aß2GPI level is significantly up-regulated after vaccination. There was no statistical difference in mature egg rate, 2PN fertilization rate, day 3 high-quality embryo rate, blastocyst formation rate, embryo implantation rate and miscarriage rate between the vaccine group and control group. Our findings showed vaccination with COVID-19 inactivated vaccine can elevate the level of aß2GPI in peripheral blood but have no effect on the outcomes of controlled ovarian hyperstimulation and pregnancy in IVF-ET.
COVID-19 Vaccines , COVID-19 , Pregnancy , Female , Humans , Retrospective Studies , beta 2-Glycoprotein I , COVID-19/prevention & control , Fertilization in Vitro , Embryo Transfer , Vaccines, Inactivated
Purpose: To explore the mechanisms by which abnormal female BMI affects oocyte quality, particularly whether it involves the alteration of gene expression patterns and how these patterns may impact clinical outcomes. Methods: In Part 1, we performed a retrospective study to compare the clinical outcomes between the female BMI ≥25 kg/m2 and female BMI ≤20 kg/m2 groups. In Part 2, we performed the transcriptome analyses based on the GSE87201 dataset. Results: In Part 1, among the clinical outcomes, only the grade 1-2 embryo rate at day 3 of ICSI cycles was significantly different between the two BMI groups; the other outcomes were not. In Part 2, compared with the BMI ≤20 kg/m2 group, the oocyte gene expression pattern of the BMI ≥25 kg/m2 group seemed to result in better oocyte tolerance to exogenous stress, such as intracytoplasmic sperm injection (ICSI). It seemed to explain the result of Part 1 that the BMI ≥25 kg/m2 group had better day-3 embryo quality after ICSI than the BMI ≤20 kg/m2 group. Conclusions: Abnormal female BMI affects oocyte quality by altering the gene expression patterns of oocytes. While a female BMI ≥25 kg/m2 is known to have certain detrimental effects on ART, our findings suggest that it can also confer some benefits to oocytes.
Human dental pulp stem cells (hDPSCs) promote recovery after ischemic stroke; however, the therapeutic efficacy is limited by the poor survival of transplanted cells. For in vitro experiments in the present study, we used oxygen-glucose deprivation/reoxygenation in hDPSCs to mimic cell damage induced by ischemia/reperfusion. We found that miRNA-34a-5p (miR-34a) was elevated under oxygen-glucose deprivation/reoxygenation conditions in hDPSCs. Inhibition of miR-34a facilitated the proliferation and antioxidant capacity and reduced the apoptosis of hDPSCs. Moreover, dual-luciferase reporter gene assay showed WNT1 and SIRT1 as the targets of miR-34a. In miR-34a knockdown cell lines, WNT1 suppression reduced cell proliferation, and SIRT1 suppression decreased the antioxidant capacity. Together, these results indicated that miR-34a regulates cell proliferation and antioxidant stress via targeting WNT1 and SIRT1, respectively. For in vivo experiments, we injected genetically modified hDPSCs (anti34a-hDPSCs) into the brains of mice. We found that anti34a-hDPSCs significantly inhibited apoptosis, reduced cerebral edema and cerebral infarct volume, and improved motor function in mice. This study provides new insights into the molecular mechanism of the cell proliferation and antioxidant capacity of hDPSCs, and suggests a potential gene that can be targeted to improve the survival rate and efficacy of transplanted hDPSCs in brain after ischemic stroke.
