Objective:To analyze the trend of lipid changes in patients and individuals undergoing physical examination at Zhongshan Hospital of Fudan University from 2014 to 2024, providing evidence for the formulation of cardiovascular disease prevention and control strategies.Methods:A total of 2 657 835 individuals (general population) who underwent lipid testing during medical visits or physical examinations at Zhongshan Hospital of Fudan University from January 1, 2014, to December 31, 2024, were selected. Among them, 6 234 individuals who were tested consecutively for 11 years were considered as the fixed population. Lipid levels were analyzed across different genders and age groups. Total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) were analyzed. The trends in lipid changes and the abnormal rates of TC (≥5.18 mmol/L) and LDL-C (≥3.40 mmol/L) in both the general and fixed populations were statistically analyzed.Results:The median age of the general population was 53 (41, 63) years, with 1 498 533 males (56.4%); 1 149 662 individuals (43.3%) were from the physical examination group. The median age of the fixed population was 52 (39, 62) years, with 3 262 males (52.3%); 2 955 individuals (47.4%) were from the physical examination group. Over an 11-year period, the logarithmically transformed TG (lnTG) in the general population slightly increased from 1.35 mmol/L to 1.36 mmol/L (Sen slope=0.007 mmol·L -1·year -1; S=27, P=0.043). Although there were fluctuations in TC, LDL-C, and HDL-C, the trends were not statistically significant ( P>0.05). However, in the subset of the population undergoing regular health check-ups, TC showed a steady increase over time ( S=27, P=0.043). Within a fixed population over the same 11-year period, there were no statistically significant changes in lipid profiles ( P>0.05). Nevertheless, in the fixed subset undergoing regular health check-ups, both TC and lnTG exhibited an upward trend (TC: S=27, P=0.043; lnTG: S=31, P=0.020), while in the fixed subset seeking medical attention, TC and LDL-C demonstrated a downward trend (TC: S=-31, P=0.020; LDL-C: S=-27, P=0.043). Trends in lipid profiles varied among different genders and age groups. Specifically, both men and women aged 20-<40 years old showed an increase in TC, abnormal TC rates, and abnormal LDL-C rates ( P<0.05). Conversely, in the fixed population, women over 60 years old exhibited a decrease in TC, abnormal TC rates, and abnormal LDL-C rates ( P<0.05). Conclusion:During the period from 2014 to 2024, there were slight fluctuations in the average lipid levels of both the general and fixed populations. Notably, TC, abnormal TC rates, and abnormal LDL-C rates increased among men and women aged 20-<40 years old, while these parameters decreased among women over 60 years old in the fixed population.

Nature killer(NK)cells are lymphocytes of the innate immune that play a significant role in aging through direct cell killing and secretion of cytokines.NK cells can delay the occurrence of age-related diseases and prolong lifespan by eliminating senescencent cells.Significant progress has been achieved in the research utilizing NK cells to improve aging.This review aims to summarize that the recent research on the mechanism of NK cells in the context of senescence, as well as the progress made in anti-senescence interventions through animal and clinical studies.Nevertheless, substantial challenges remain for the clinical application of NK cell-based anti-senescence therapies.

OBJECTIVE: To investigate the variability of bone metabolism levels among different populations and its association with knee osteoarthritis (KOA) pain. METHODS: A total of 50 people (control group) who participated in physical examination from January 2023 to June 2023 were selected, including 26 males and 24 females, wtih a mean aged of (52.14±9.04) years old ranging 41 to 65 years old. The other 50 patients with knee osteoarthritis(case group) who attended the outpatient clinic of the Orthopedics and Traumatology Department in the same time period, including 19 males and 31 females, with a mean age of (53.60±7.76) years old ranging 40 to 65 years. The two groups of Western Ontario and McMaster Universities Osteoarthritis Index(WOMAC) and bone metabolism markers, such as 25-hydroxy-cholecalciferol[25(OH)D], β-isomerized typeⅠcollagen C-telopeptide breakdown products (β-CTX), total typeⅠprocollagen N-terminal propeptide (t-PINP), osteocalcin (OC), parathormone (PTH) levels were compared. Pearson correlation analysis was used to compare the correlation between two groups of bone metabolism related markers and WOMAC. RESULTS: The WOMAC score of the case group (39.90±2.34) was higher than that of the control group (3.60±0.57), with significant difference (P<0.05). There was no significant difference between the two groups of 25 (OH)D, β-CTX and PTH (P>0.05). The t-PINP and OC of the case group were (62.90±52.40) and (19.88±10.15) ng·ml-1, respectively, and those of the control group were (38.86±10.82) and (14.90±3.62) ng·ml^-1, respectively;the t-PINP and OC of the case group were higher than those of the control group, with significant difference (P<0.05). Pearson correlation analysis showed that t-PINP was positively correlated with WOMAC pain score in the case group (r²=0.045, P<0.01). CONCLUSION Bone metabolism levels in the serum of patients with knee osteoarthritis are different from those of healthy people, and the difference between OC and t-PINP is the most obvious, and the concentration of t-PINP levels is positively correlated with pain symptoms in patients with KOA. However, the specific mechanism of correlation between the bone metabolism levels of patients with KOA and their pain symptoms needs to be further elucidated by basic experimental research as well as by enlarging the samples.
Humans ; Female ; Male ; Middle Aged ; Osteoarthritis, Knee/metabolism* ; Aged ; Adult ; Bone and Bones/metabolism* ; Pain/etiology* ; Biomarkers/metabolism*

Peripheral nerve injury (PNI) encompasses damage to nerves located outside the central nervous system, adversely affecting both motor and sensory functions. Although peripheral nerves possess an intrinsic capacity for self-repair, severe injuries frequently result in significant tissue loss and erroneous axonal junctions, thereby impeding complete recovery and potentially causing neuropathic pain. Various therapeutic strategies, including surgical interventions, biomaterials, and pharmacological agents, have been developed to enhance nerve repair processes. While preclinical studies in animal models have demonstrated the efficacy of certain pharmacological agents in promoting nerve regeneration and mitigating inflammation, only a limited number of these agents have been translated into clinical practice to expedite nerve regeneration. Chinese herb medicine (CHM) possesses a longstanding history in the treatment of various ailments and demonstrates potential efficacy in addressing PNI through its distinctive, cost-effective, and multifaceted methodologies. This review critically examines the advancements in the application of CHM for PNI treatment and nerve regeneration. In particular, we have summarized the most commonly employed and rigorously investigated CHM prescriptions, individual herbs, and natural products, elucidating their respective functions and underlying mechanisms in the context of PNI treatment. Furthermore, we have deliberated on the prospective development of CHM in both clinical practice and fundamental research.
Drugs, Chinese Herbal/pharmacology* ; Humans ; Peripheral Nerve Injuries/drug therapy* ; Animals ; Nerve Regeneration/drug effects* ; Medicine, Chinese Traditional

Hypercholesterolemia is a significant risk factor for the development of atherosclerosis. 2',3',5'-Tri-O-acetyl-N ⁶-(3-hydroxyphenyl) adenosine (IMM-H007), a novel AMPK agonist, has shown protective effects in metabolic diseases. However, its impact on cholesterol and triglyceride metabolism in hypercholesterolemia remains unclear. In this study, we aimed to elucidate the effects and specific mechanisms by which IMM-H007 regulates cholesterol and triglyceride metabolism. To achieve this goal, we used Apoe ^-/- and Ldlr ^-/- mice to establish a hypercholesterolemia/atherosclerosis model. Additionally, hepatocyte-specific Ampka1/2 knockout mice were subjected to a 5-week high-cholesterol diet to establish hypercholesterolemia, while atherosclerosis was induced via AAV-PCSK9 injection combined with a 16-week high-cholesterol diet. Our results demonstrated that IMM-H007 improved cholesterol and triglyceride metabolism in mice with hypercholesterolemia. Mechanistically, IMM-H007 modulated the AMPKα1/2-LDLR signaling pathway, increasing cholesterol uptake in the liver. Furthermore, IMM-H007 activated the AMPKα1-FXR pathway, promoting the conversion of hepatic cholesterol to bile acids. Additionally, IMM-H007 prevented hepatic steatosis by activating the AMPKα1/2-ATGL pathway. In conclusion, our study suggests that IMM-H007 is a promising therapeutic agent for improving hypercholesterolemia and atherosclerosis through the activation of AMPKα.

Objective To investigate the protective effect of paravertebral nerve block combined with general anesthesia on liver injury after laparoscopic hepatectomy(LH).Methods A randomized controlled trial was conducted on 51 patients undergoing LH in our hospital between April and August 2024.They were randomly divided into control group(n=25,general anesthesia)and paravertebral block group(n=26,paravertebral nerve block before general anesthesia induction).Beside anesthesia,they received same other medical treatment.The following indicators were compared between the 2 groups,that is,serum levels of alanine aminotransferase(ALT),aspartate aminotransferase(AST),total bilirubin(TBIL)and albumin(ALB),and systemic-immune inflammation(SII)index within 7 d before and on the 1st and 2nd days after surgery;heart rate and mean arterial pressure(MAP)before anesthesia induction(T1),before pneumoperitoneum establishment(T2),pneumoperitoneum establishment(T3),and at the first hilar occlusion(T4);usages of intraoperative norepinephrine,sevoflurane,and analgesic drugs 24 h postoperatively;as well as operation time,extubation time,and lengths of postanesthesia care unit(PACU)stay and hospital stay.Results The paravertebral block group had significantly lower ALT on the 1st day after surgery[178.40(126.55,325.86)vs 292.20(197.20,468.95)U/L],SII on the 2nd day after surgery[704.13(486.61,1 078.59)vs 1 075.09(753.80,1 614.38)],and amount of analgesic drugs in 24 h after surgery[29.70(27.37,32.07)vs 31.99(28.92,40.81)mg],and decreased MAP level at T3 and T4,early extubation,and shorter lengths of PACU stay and hospital stay when compared with the control group(all P<0.05).Conclusion Paravertebral nerve block combined with general anesthesia can reduce inflammatory responses,relieve postoperative pain,stabilize hemodynamics for patients undergoing LH,and thereby alleviate postoperative liver injury in them.

Objective:To investigate the pathogen distribution characteristics and related risk factors for postoperative infection in liver transplant recipients.Method:A retrospective analysis was conducted on the clinical data of 153 recipients who underwent liver transplantation and received postoperative treatment in the intensive care unit (ICU) of China-Japan Friendship Hospital from January 2019 to December 2023. According to whether postoperative infection occurred, the recipients were divided into the infection group (33 cases) and the non-infection group (120 cases). Pathogen-related data were collected from multiple postoperative body fluid sites of liver transplant recipients. Univariate analysis and multivariate logistic regression analysis were performed to identify independent risk factors.Result:Among the 153 recipients, 105 were male and 48 were female, with a mean age of (52.2 ± 9.5) years. During the ICU stay after liver transplantation, 33 recipients developed infections, including 15 cases of single-pathogen infection and 18 cases of mixed-pathogen infection. The most common site of infection was the lung, accounting for 22 cases (66.67%). Eleven recipients (33.33%) in the infection group died, with septic shock being the leading cause of death (7 cases, 63.63%), and the median survival time was 14 days. Infected recipients had Gram-negative bacteria (171 strains), mainly Stenotrophomonas maltophilia[54 strains (31.57%)] and Pseudomonas aeruginosa[52 strains (30.41%)]. Gram-positive bacteria (47 strains) were dominated by Enterococcus faecalis[25 strains (53.19%)]. Multivariate regression analysis showed that postoperative mechanical ventilation for more than 48 hours was an independent risk factor for infection in liver transplant recipients ( OR=10.878, 95% CI: 3.632-32.580, P<0.001). Conclusion:It is necessary to prevent ventilator-associated pneumonia in liver transplant recipients. Early removal of the tracheal tube and strengthening hospital infection prevention and control are of great significance in reducing the risk of postoperative infection in liver transplant recipients.

Mesenchymal stem cells(MSCs)play a crucial role in tissue repair and regeneration,and the extracellular vesicle(EV)released by them holds great promise for applications in clinical biomarkers,vaccines,and drug delivery.However,MSCs-derived EV(MSCs-EV)face challenges such as low pro-duction yield,poor retention,and targeted delivery issues.There-fore,engineering MSCs-EV to enhance their performance and en-able visual research has become a hot topic.Curcumin(CUR),an active component in traditional chinese medicine,exhibits pharmacological effects but has limited bioavailability.Using MSCs-EV as a carrier for CUR delivery can address its solubility and bioavailability challenges.This article reviews the drug loading methods,engineering strategies of MSCs-EV,and their important applications in the delivery and treatment of CUR for cartilage injury diseases.It provides a basis for the clinical ap-plication of engineered MSCs-EV in CUR delivery for cartilage repair,offering potential solutions to the challenges in cartilage tissue repair.

Aim To investigate the role of corylin in angiotensin Ⅱ(Ang Ⅱ)-induced cardiomyocyte hy-pertrophy and its underlying mechanisms.Methods An Ang Ⅱ-induced cardiomyocyte hypertrophy model was established and treated with corylin.Real-time PCR was employed to assess hypertrophic gene mRNA expression,and immunofluorescence was used to meas-ure cardiomyocyte surface area.Western blot and en-zyme activity assay kits were used to evaluate SIRT1 expression and activity.Results Corylin markedly mitigated Ang Ⅱ-induced hypertrophic gene expression and cardiomyocyte surface area enlargement.Moreo-ver,it prevented the Ang Ⅱ-mediated decline in SIRT1 protein levels and deacetylase activity.Further investi-gation indicated that corylin inhibited Ang Ⅱ-driven NF-κB transcriptional activity and the expression of its downstream target genes,such as TNF-α,IL-6,and IL-1β.Notably,SIRT1 silencing abolished the protective effects of corylin against cardiomyocyte hypertrophy,as well as its regulation of the SIRT1/NF-κB signaling pathway.Conclusion Corylin suppresses cardiomyo-cyte hypertrophy by modulating the SIRT1-dependent NF-κB signaling pathway.

Aim To investigate the role of corylin in angiotensin Ⅱ(Ang Ⅱ)-induced cardiomyocyte hy-pertrophy and its underlying mechanisms.Methods An Ang Ⅱ-induced cardiomyocyte hypertrophy model was established and treated with corylin.Real-time PCR was employed to assess hypertrophic gene mRNA expression,and immunofluorescence was used to meas-ure cardiomyocyte surface area.Western blot and en-zyme activity assay kits were used to evaluate SIRT1 expression and activity.Results Corylin markedly mitigated Ang Ⅱ-induced hypertrophic gene expression and cardiomyocyte surface area enlargement.Moreo-ver,it prevented the Ang Ⅱ-mediated decline in SIRT1 protein levels and deacetylase activity.Further investi-gation indicated that corylin inhibited Ang Ⅱ-driven NF-κB transcriptional activity and the expression of its downstream target genes,such as TNF-α,IL-6,and IL-1β.Notably,SIRT1 silencing abolished the protective effects of corylin against cardiomyocyte hypertrophy,as well as its regulation of the SIRT1/NF-κB signaling pathway.Conclusion Corylin suppresses cardiomyo-cyte hypertrophy by modulating the SIRT1-dependent NF-κB signaling pathway.