OBJECTIVE To explore the efficacy of low temperature plasma(LTP)in treatment of the rats with Pseudomonas aeruginosa(PA)wound infection.METHODS Totally 20 SD rats were assigned to establish the PA wound infection models and were randomly divided into the LTP group with 10 rats and the air control group with 10 rats.The wound healing dynamics,bacterial loading capacity,histopathology,levels of cytokines and microen-vironment features were observed during the healing process.RESULTS LTP accelerates the healing of PA infec-tion wound,the wound area reduced after the treatment for 3 days,and the inflammatory reactions alleviated;the infection symptoms subsided after the treatment for 7 days,and the wounds became dry and scabbed;the wounds reduced in size by day 15,showing favorable healing trends.Repeated measurement analysis of variance(ANOVA)indicated that there was significant difference in the impact of LTP on the covering rate of wounds(Ftime=10.230,P＜0.001;Fbetween-group=11.340,P=0.001;Finteraction=2.890,P=0.042).The result of quantitative bacterial loads analysis showed that the bacterial loads of the LTP group were lower than those of the control group after the treatment for 3,7 and 15 days(P＜0.05).The result of histopathology indicated that the infiltra-ted wound inflammatory cells of the LTP group reduced,the collagen fibers were well-aligned,and the neovascu-larization and formation of granulation tissues were evident.In addition,the pH value of wound tissues and reac-tive oxygen species(ROS)level were improved after the treatment with LTP,which was matched with the process of wound healing.The result of cytokines test showed that LTP could upregulate the levels of VEGF and TGF-β1,downregulate the levels of IL-1β and TNF-α,and promote the wound healing,with statistically signifi-cant differences observed(P＜0.05).CONCLUSION LTP may facilitate the control of infections by reducing the bacterial colony counts,establish the effective microenvironment for tissue healing,and accelerate the healing of wounds with PA infection by regulating the release of healing-related cytokines.

OBJECTIVE To explore the efficacy of low temperature plasma(LTP)in treatment of the rats with Pseudomonas aeruginosa(PA)wound infection.METHODS Totally 20 SD rats were assigned to establish the PA wound infection models and were randomly divided into the LTP group with 10 rats and the air control group with 10 rats.The wound healing dynamics,bacterial loading capacity,histopathology,levels of cytokines and microen-vironment features were observed during the healing process.RESULTS LTP accelerates the healing of PA infec-tion wound,the wound area reduced after the treatment for 3 days,and the inflammatory reactions alleviated;the infection symptoms subsided after the treatment for 7 days,and the wounds became dry and scabbed;the wounds reduced in size by day 15,showing favorable healing trends.Repeated measurement analysis of variance(ANOVA)indicated that there was significant difference in the impact of LTP on the covering rate of wounds(Ftime=10.230,P＜0.001;Fbetween-group=11.340,P=0.001;Finteraction=2.890,P=0.042).The result of quantitative bacterial loads analysis showed that the bacterial loads of the LTP group were lower than those of the control group after the treatment for 3,7 and 15 days(P＜0.05).The result of histopathology indicated that the infiltra-ted wound inflammatory cells of the LTP group reduced,the collagen fibers were well-aligned,and the neovascu-larization and formation of granulation tissues were evident.In addition,the pH value of wound tissues and reac-tive oxygen species(ROS)level were improved after the treatment with LTP,which was matched with the process of wound healing.The result of cytokines test showed that LTP could upregulate the levels of VEGF and TGF-β1,downregulate the levels of IL-1β and TNF-α,and promote the wound healing,with statistically signifi-cant differences observed(P＜0.05).CONCLUSION LTP may facilitate the control of infections by reducing the bacterial colony counts,establish the effective microenvironment for tissue healing,and accelerate the healing of wounds with PA infection by regulating the release of healing-related cytokines.

Objective:To elucidate the expression of angiopoietin-like protein 4 (ANGPTL4) in LPS-induced septic cardiomyopathy tissue and cardiomyocyte, and to explore the mechanism of ANGPTL4 in septic cardiomyopathy.Methods:Fifty C57BL/6 mice, aged 8 weeks, were randomly(random number) divided into a treatment group (LPS) and a control group ( n = 25 each). The mice in the treatment group were intraperitoneally injected with LPS (10 mg/kg) to establish a sepsis model. After 24 h, the myocardial tissues of the mice in the sepsis group and the control group, which were caused by LPS, were collected for RNA sequencing to pick out the differentially expressed gene of ANGPTL4.Ventricular myocytes of neonatal mice were taken, and the silencing and overexpression vectors of ANGPTL4 were transfected. After 48 hours of transfection, the cells were collected for subsequent detection. Western blot method was used to detect the expression of apoptotic factors Bax, Bcl-2, and Caspase 3 in mouse ventricular myocytes; CCK8 method was used to detect the activity of ventricular myocytes; using the Annexin V-FITC and PI double staining method, the apoptosis of ventricular myocytes was detected. Results:RNA-seq analysis revealed a statistically significant upregulation of ANGPTL4 expression at both transcriptional and translational levels in the ventricular tissue of septic mice, as compared to the control group ( P<0.05). The results of qRT-PCR and Western blot indicated that the mRNA and protein levels of ANGPTL4 in the ventricular tissues and cardiomyocytes of mice treated with LPS were significantly increased ( P<0.05). After transfection of the silencing and overexpression vectors of ANGPTL4 in cardiomyocytes, it was found that compared with NC, the mRNA and protein expression levels of ANGPTL4 in the si-ANGPTL4 group significantly decreased ( P<0.05), the vitality of ventricular myocytes increased ( P<0.05), the expressions of apoptosis-related factors Bax and Caspase 3 significantly decreased ( P<0.05), and the expression of Bcl-2 significantly increased ( P<0.05), and the number of apoptotic cells significantly decreased ( P<0.05); while the transfection of the overexpression vector of ANGPTL4 showed an opposite trend. Conclusions:In septic myocardial tissue and cardiomyocyte, the expression of ANGPTL4 is elevated, resulting in the inhibition of ventricular myocyte viability and the promotion of cardiomyocyte apoptosis.

This study aimed to comprehensively examine the association of gallstones, cholecystectomy, and cancer risk. Multivariable logistic regressions were performed to estimate the observational associations of gallstones and cholecystectomy with cancer risk, using data from a nationwide cohort involving 239 799 participants. General and gender-specific two-sample Mendelian randomization (MR) analysis was further conducted to assess the causalities of the observed associations. Observationally, a history of gallstones without cholecystectomy was associated with a high risk of stomach cancer (adjusted odds ratio (aOR)=2.54, 95% confidence interval (CI) 1.50-4.28), liver and bile duct cancer (aOR=2.46, 95% CI 1.17-5.16), kidney cancer (aOR=2.04, 95% CI 1.05-3.94), and bladder cancer (aOR=2.23, 95% CI 1.01-5.13) in the general population, as well as cervical cancer (aOR=1.69, 95% CI 1.12-2.56) in women. Moreover, cholecystectomy was associated with high odds of stomach cancer (aOR=2.41, 95% CI 1.29-4.49), colorectal cancer (aOR=1.83, 95% CI 1.18-2.85), and cancer of liver and bile duct (aOR=2.58, 95% CI 1.11-6.02). MR analysis only supported the causal effect of gallstones on stomach, liver and bile duct, kidney, and bladder cancer. This study added evidence to the causal effect of gallstones on stomach, liver and bile duct, kidney, and bladder cancer, highlighting the importance of cancer screening in individuals with gallstones.
Humans ; Mendelian Randomization Analysis ; Gallstones/complications* ; Female ; Male ; Cholecystectomy/statistics & numerical data* ; Middle Aged ; Risk Factors ; Aged ; Adult ; Neoplasms/etiology* ; Stomach Neoplasms/epidemiology*

Low-intensity pulsed ultrasound（LIPUS），with its remarkable advantages of higher safety and better penetrability，has gradually become a novel method of physical adjuvant therapy. Previous studies have verified that LIPUS can modulate the immune response of different immune cells such as macrophage，T lymphocyte，and neutrophil by reducing the level of pro-inflammatory cytokines. Therefore，it plays a crucial role on acceleration of fracture healing，expedition of wound repair，and repairation of myocardial injury. The review summarizes the regulatory effects and potential mechanisms of LIPUS on abnormal immune cell responses triggered by various diseases.

BACKGROUND: The mechanisms distinguishing metabolically healthy from unhealthy phenotypes within the same BMI categories remain unclear. This study aimed to investigate the associations between regional fat distribution and metabolically unhealthy phenotypes in Chinese adults across different BMI categories. METHODS: This cross-sectional study involving 11833 Chinese adults aged 20 years and older. Covariance analysis, adjusted for age, compared the percentage of regional fat (trunk, leg, or arm fat divided by whole-body fat) between metabolically healthy and unhealthy participants. Trends in regional fat percentage with the number of metabolic abnormalities were assessed by the Jonckheere-Terpstra test. Odds ratios (ORs) and their 95% confidence intervals (CIs) were estimated by logistic regression models. All analyses were performed separately by sex. RESULTS: In non-obese individuals, metabolically unhealthy participants exhibited higher percent trunk fat and lower percent leg fat compared to healthy participants. Additionally, percent trunk fat increased and percent leg fat decreased with the number of metabolic abnormalities. After adjustment for demographic and lifestyle factors, as well as BMI, higher percent trunk fat was associated with increased odds of being metabolically unhealthy [highest vs. lowest quartile: ORs (95%CI) of 1.64 (1.35, 2.00) for men and 2.00 (1.63, 2.46) for women]. Conversely, compared with the lowest quartile, the ORs (95%CI) of metabolically unhealthy phenotype in the highest quartile for percent arm and leg fat were 0.64 (0.53, 0.78) and 0.60 (0.49, 0.74) for men, and 0.72 (0.56, 0.93) and 0.46 (0.36, 0.59) for women, respectively. Significant interactions between BMI and percentage of trunk and leg fat were observed in both sexes, with stronger associations found in individuals with normal weight and overweight. CONCLUSIONS Trunk fat is associated with a higher risk of metabolically unhealthy phenotype, while leg and arm fat are protective factors. Regional fat distribution assessments are crucial for identifying metabolically unhealthy phenotypes, particularly in non-obese individuals.
Adult ; Aged ; Female ; Humans ; Male ; Middle Aged ; Young Adult ; Adipose Tissue ; Body Fat Distribution ; Body Mass Index ; China/epidemiology* ; Cross-Sectional Studies ; Health Surveys ; Phenotype

[This corrects the article DOI: 10.1016/j.apsb.2021.07.004.].

Body weight abnormalities, including overweight, obesity, and underweight, have become a dual public health challenge in Chinese adults: overweight and obesity lead to a variety of chronic complications, while underweight increases the risks of malnutrition, sarcopenia, and organ dysfunction. To systematically address these issues, multidisciplinary experts in endocrinology, sports science, nutrition, and psychiatry from various regions have held multiple weight management seminars. Based on the latest epidemiological data and clinical evidence, they expanded the guideline to include assessment and intervention strategies for underweight, in addition to the core content of obesity management. This guideline outlines the etiological mechanisms, evaluation methods, and multidimensional management strategies for overweight and obesity, covering key areas such as diagnosis and assessment, medical nutrition therapy, exercise prescription, pharmacological intervention, and psychological support. It is intended to provide a scientific and standardized approach to weight management across the adult population, aiming to curb the rising prevalence of obesity, mitigate complications associated with abnormal body weight, and improve nutritional status and overall quality of life.

Objective:To investigate the effect of chlorogenic acid on atherosclerosis (AS) in a mouse model.Methods:Twenty-four specific pathogen-free male ApoE-/- mice were adaptively fed for 1 week and then randomly divided into three groups ( n=8 per group): The model group, the atorvastatin group, and the chlorogenic acid group. All three groups were fed with a high-fat diet. Eight male C57BL/6N wild-type mice served as the control group and were fed with a standard diet. After 8 weeks, the atorvastatin group received intragastric administration of a solution containing 0.9% sodium chloride +2.6 mg/kg atorvastatin at 10 mL/kg, while the chlorogenic acid group received 0.9% sodium chloride +200 mg/kg chlorogenic acid at 10 mL/kg. The control and model groups were given an equal volume of 0.9% sodium chloride once a day. After 9 weeks of continuous treatment, the mice were anesthetized, and the aortas were collected for Oil Red O staining. Image J was used to measure plaque area and total vascular area, and the percentage was calculated. Liver tissues were subjected to hematoxylin-eosin (H&E) staining to observe pathological changes. Blood samples from the abdominal aorta were collected to measure lipid profiles [total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C)], liver function markers [aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP)], and inflammatory cytokines [interleukin-6 (IL-6), IL-1β, tumor necrosis factor-α (TNF-α)]. Non-HDL-C levels were calculated as TC minus HDL-C. Results:Aortic lipid plaque area: The model group exhibited a significantly higher plaque area than the control group [(44.91±1.91)% vs. (0.21±0.11)%]. Both the atorvastatin group [(15.00±1.29)%] and the chlorogenic acid group [(26.13±2.16)%] showed reduced plaque areas compared to the model group ( P<0.05). Liver pathology: The control group displayed intact hepatocyte structure with regular morphology, whereas the model group exhibited significant steatosis. Both the atorvastatin and chlorogenic acid groups showed alleviated liver damage compared to the model group. Blood lipid levels: The model group had higher TC, TG, HDL-C, LDL-C, and non-HDL-C levels than the control group [(30.3±4.0) mmol/L vs. (2.8±0.3) mmol/L, (1.26±0.32) mmol/L vs. (0.52±0.12) mmol/L, (3.02±0.39) mmol/L vs. (2.00±0.17) mmol/L, (14.87±5.23) mmol/L vs. (0.39±0.09) mmol/L, (27.3±4.0) mmol/L vs. (0.8±0.3) mmol/L, respectively]. Both the atorvastatin group [(24.0±3.1), (0.64±0.08), (2.04±0.41), (8.55±1.15), (22.0±3.2) mmol/L] and the chlorogenic acid group [(23.3±2.5), (0.88±0.14), (2.28±0.18), (8.90±0.29), (21.0±2.5) mmol/L] showed lower levels than the model group ( P<0.05). The model group had higher ALT, AST, and ALP levels than the control group [(274±43) U/L vs. (99±14) U/L, (130±66) U/L vs. (38±4) U/L, (86±15) U/L vs. (60±5) U/L, respectively]. Both the atorvastatin group [(139±12), (58±16), (69±5) U/L] and the chlorogenic acid group [(138±11), (55±16), (54±5) U/L] exhibited lower levels than the model group ( P<0.05). Inflammatory cytokines: The model group had higher IL-6, IL-1β, and TNF-α levels than the control group [(238±15) ng/L vs. (202±7) ng/L, (211±6) ng/L vs. (174±6) ng/L, (1 325±75) ng/L vs. (1 036±75) ng/L, respectively]. Both the atorvastatin group [(215±9), (191±4), (1 163±78) ng/L] and the chlorogenic acid group [(220±13), (195±7), (1 197±53) ng/L] showed reduced levels compared to the model group (all P<0.05). Conclusion:Chlorogenic acid may inhibit aortic lipid plaque deposition and ameliorate AS in mice by improving lipid metabolism and suppressing inflammatory responses.

Objective:To investigate the effect of chlorogenic acid on atherosclerosis (AS) in a mouse model.Methods:Twenty-four specific pathogen-free male ApoE-/- mice were adaptively fed for 1 week and then randomly divided into three groups ( n=8 per group): The model group, the atorvastatin group, and the chlorogenic acid group. All three groups were fed with a high-fat diet. Eight male C57BL/6N wild-type mice served as the control group and were fed with a standard diet. After 8 weeks, the atorvastatin group received intragastric administration of a solution containing 0.9% sodium chloride +2.6 mg/kg atorvastatin at 10 mL/kg, while the chlorogenic acid group received 0.9% sodium chloride +200 mg/kg chlorogenic acid at 10 mL/kg. The control and model groups were given an equal volume of 0.9% sodium chloride once a day. After 9 weeks of continuous treatment, the mice were anesthetized, and the aortas were collected for Oil Red O staining. Image J was used to measure plaque area and total vascular area, and the percentage was calculated. Liver tissues were subjected to hematoxylin-eosin (H&E) staining to observe pathological changes. Blood samples from the abdominal aorta were collected to measure lipid profiles [total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C)], liver function markers [aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP)], and inflammatory cytokines [interleukin-6 (IL-6), IL-1β, tumor necrosis factor-α (TNF-α)]. Non-HDL-C levels were calculated as TC minus HDL-C. Results:Aortic lipid plaque area: The model group exhibited a significantly higher plaque area than the control group [(44.91±1.91)% vs. (0.21±0.11)%]. Both the atorvastatin group [(15.00±1.29)%] and the chlorogenic acid group [(26.13±2.16)%] showed reduced plaque areas compared to the model group ( P<0.05). Liver pathology: The control group displayed intact hepatocyte structure with regular morphology, whereas the model group exhibited significant steatosis. Both the atorvastatin and chlorogenic acid groups showed alleviated liver damage compared to the model group. Blood lipid levels: The model group had higher TC, TG, HDL-C, LDL-C, and non-HDL-C levels than the control group [(30.3±4.0) mmol/L vs. (2.8±0.3) mmol/L, (1.26±0.32) mmol/L vs. (0.52±0.12) mmol/L, (3.02±0.39) mmol/L vs. (2.00±0.17) mmol/L, (14.87±5.23) mmol/L vs. (0.39±0.09) mmol/L, (27.3±4.0) mmol/L vs. (0.8±0.3) mmol/L, respectively]. Both the atorvastatin group [(24.0±3.1), (0.64±0.08), (2.04±0.41), (8.55±1.15), (22.0±3.2) mmol/L] and the chlorogenic acid group [(23.3±2.5), (0.88±0.14), (2.28±0.18), (8.90±0.29), (21.0±2.5) mmol/L] showed lower levels than the model group ( P<0.05). The model group had higher ALT, AST, and ALP levels than the control group [(274±43) U/L vs. (99±14) U/L, (130±66) U/L vs. (38±4) U/L, (86±15) U/L vs. (60±5) U/L, respectively]. Both the atorvastatin group [(139±12), (58±16), (69±5) U/L] and the chlorogenic acid group [(138±11), (55±16), (54±5) U/L] exhibited lower levels than the model group ( P<0.05). Inflammatory cytokines: The model group had higher IL-6, IL-1β, and TNF-α levels than the control group [(238±15) ng/L vs. (202±7) ng/L, (211±6) ng/L vs. (174±6) ng/L, (1 325±75) ng/L vs. (1 036±75) ng/L, respectively]. Both the atorvastatin group [(215±9), (191±4), (1 163±78) ng/L] and the chlorogenic acid group [(220±13), (195±7), (1 197±53) ng/L] showed reduced levels compared to the model group (all P<0.05). Conclusion:Chlorogenic acid may inhibit aortic lipid plaque deposition and ameliorate AS in mice by improving lipid metabolism and suppressing inflammatory responses.