The associated factors for physical activity-related injuries among first-year university students in southern China from a biopsychosocial perspective.

Background: Understanding the diverse factors influencing physical activity-related injuries is crucial for developing effective interventions that enable individuals to participate in physical activity (PA) while minimizing injury risk. Currently, research evidence on the multiple factors associated with PA-related injuries is inadequate. This study aimed to examine the associations between PA-related injuries and various biological, psychological, and social factors among first-year university students in China. Methods: We recruited first-year university students from Shantou University in Guangdong Province, China, to participate in our study. Data collection employed a structured self-administered questionnaire, gathering information on PA-related injuries, as well as relevant biological, psychological, and social factors. Binary logistic regression, using a stepwise modeling approach, was employed for the data analysis. Results: Among 1,051 first-year university students, 28.16% reported having experienced PA-related injuries in the past year. Most of the injuries reported were minor, with the knee or lower leg being the most frequently injured part of the body. Improper posture, environmental conditions, and excessive physical load were the leading causes of PA-related injuries. Multiple logistic regression analysis revealed that female students (OR = 0.67, 95% CI: 0.47-0.94, p = 0.022) had reduced odds of PA-related injuries. Conversely, high neuroticism (OR = 1.61, 95% CI: 1.07-2.41, p = 0.022), being a member of a sports team (OR = 2.09, 95% CI: 1.34-3.27, p < 0.001), PA on the wet ground (OR = 1.73, 95% CI: 1.18-2.54, p = 0.005) increased the odds of PA-related injuries. Conclusion: Our findings underscore the intricate interplay of various factors contributing to PA-related injuries. Identifying high-risk individuals based on physiological and psychological characteristics, coupled with targeted interventions addressing modifiable risk factors, is crucial for effective prevention.

Development and validation of a predictive model for acute kidney injury in patients with moderately severe and severe acute pancreatitis.

BACKGROUND: Acute kidney injury is a serious complication of moderately severe and severe acute pancreatitis, which significantly increases mortality. There are currently no reliable tools for early identification of AKI especially severe AKI in these patients. We aim to develop a predictive model so that physicians can assess the risk of AKI and severe AKI, thus take further preventive measures. METHODS: Patients with a diagnosis of MSAP and SAP admitted to our hospital from January 2018 to December 2021 were retrospectively included in the study. The participants were divided into the training and validation cohorts randomly, in a 2:1 ratio. A clinical signature was built based on reproducible features, using the least absolute shrinkage and selection operator method and machine learning. Multivariate logistic regression analysis was used to develop the prediction model. Nomogram performance was determined by its discrimination, calibration, and clinical usefulness. RESULTS: A total of 996 eligible patients were enrolled. 698 patients were allocated in the training cohort and 298 in the validation cohort. AKI occurred in 148 patients (21%) in the training cohort and 54 (18%) in the validation cohort, respectively. The clinical features, including C-reactive protein, intra-abdominal pressure and serum cysC, were significantly associated with AKI as well as severe AKI. The nomogram showed favorable discrimination, calibration and clinical usefulness. CONCLUSIONS: The novel risk score model has good performance for predicting AKI and severe AKI in MSAP and SAP patients. Application of this model can help clinicians stratify patients for primary prevention, surveillance and early therapeutic intervention to improve care and prognosis.

Epicatechin alleviates inflammation in lipopolysaccharide-induced acute lung injury in mice by inhibiting the p38 MAPK signaling pathway.

The p38 MAPK signaling pathway plays a key role in lung inflammation and the development of acute lung injury (ALI). We previously reported that the phenolic compound procyanidin B1 inhibits inflammation by suppressing the p38 MAPK signaling pathway. Here, we asked whether the monomer of procyanidin B1, epicatechin (EC), can alleviate LPS-induced ALI in mice, and if so, whether EC acts by inhibiting p38 MAPK. C57BL/6 mice were randomly divided into four groups (n = 8) and received EC alone, vehicle (sham group), LPS alone, or LPS and EC. LPS was administered via intraperitoneal injection and EC via nasogastric feeding. Lung histopathology, alveolocapillary membrane permeability, inflammation, and p38 MAPK pathway activation were assessed by immunohistochemistry, tissue wet/dry weight analysis, quantitative PCR, protein assays, ELISA, and western blot analysis using lung tissue and/or bronchoalveolar fluid. We also performed molecular modeling and in vitro enzymatic assays to examine the potential interaction between EC and p38 MAPK at the molecular level. We found that LPS caused an increase in ALI-associated lung pathology accompanied by activation of p-p38 pathway components and the transcription factor AP1. All of these effects were substantially reduced by treatment with EC. Furthermore, molecular modeling suggested that EC suppressed p38 MAPK signaling by hydrogen bonding with Glu71, Ala 111, Asp112, and Leu171 in the active site of p38α. In vitro kinase assays confirmed the ability of EC to directly inhibit purified p38 MAPK. Collectively, our data suggest that the naturally occurring compound EC could be a new therapeutic option for ALI.

Endovascular stenting of spontaneous isolated dissection of the superior mesenteric artery: A case report and literature review.

RATIONALE: Spontaneous isolated dissection of the superior mesenteric artery (SID-SMA) is a rare arterial disease that is difficult to differentiate from other diseases because of lack of specific clinical manifestation and for which there is no available optimal management strategy. PATIENT CONCERNS: A 58-year-old male patient visited our emergency room with sudden onset of moderate-severe epigastric abdominal pain of uncertain cause. DIAGNOSES: Computed tomography scanning showed a characteristic "double lumen sign" of the superior mesenteric artery, and further computed tomography angiography findings revealed a dissected segment of the superior mesenteric artery. INTERVENTIONS: Conservative management was administered for 5 days, but the abdominal pain remained. Subsequently, an endovascular stent was placed in the affected superior mesenteric artery. Postoperative antiplatelet therapy was administered for 6 months. OUTCOMES: The abdominal pain was relieved. Six months later, a follow-up of computed tomography angiography showed that the stent placed had no interval narrowing. LESSONS: Based on our review and the illustration of this case, endovascular stenting may be a preferred rescue treatment in SID-SMA patients for whom initial conservative treatment fails.

High PARP-1 expression is associated with tumor invasion and poor prognosis in gastric cancer.

Poly (adenosine diphosphate-ribose) polymerase 1 (PARP-1) was previously demonstrated to be overexpressed in numerous malignant tumors and associated with invasiveness and poor prognosis. However, the expression of the PARP-1 protein in gastric cancer and its association with clinical outcomes requires further investigation. In the present study, the expression of PARP-1 in 564 gastric cancer tissues and 335 tumor-adjacent control tissues is investigated, using tissue microarray-based immunohistochemistry. PARP-1 expression levels were demonstrated to be significantly higher in gastric cancer tissue samples, as compared with control tissue samples. In gastric cancer, high PARP-1 expression levels were significantly associated with Helicobacter pylori (H. pylori) infection (P=0.032), decreased differentiation (P<0.001), increased depth of invasion (P=0.037), presence of lymphatic invasion (P<0.001), presence of lymph node metastasis (P<0.001), and advanced tumor-node-metastasis (TNM) stage (P=0.015). High PARP-1 expression levels were associated with a significantly shorter overall survival rate (P<0.001) and disease-free survival rate (P=0.001) in patients with gastric cancer, particularly a subset of patients with H. pylori infection or an advanced TNM stage. In addition, univariate analysis indicated that PARP-1 high expression levels were significantly associated with a poor prognosis in gastric cancer. These results suggest that PARP-1 expression may be involved in the progression and prognosis of gastric cancer, particularly H. pylori-positive or advanced-stage gastric cancer.

Anti-inflammatory effect of procyanidin B1 on LPS-treated THP1 cells via interaction with the TLR4-MD-2 heterodimer and p38 MAPK and NF-κB signaling.

Anti-inflammatory effects of procyanidin B1 have been documented; however, the molecular mechanisms that are involved have not been fully elucidated. Molecular docking models were applied to evaluate the binding capacity of lipopolysaccharide (LPS) and procyanidin B1 with the toll-like receptor (TLR)4/myeloid differentiation factor (MD)-2 complex. LPS-induced production of the proinflammatory cytokine tumor necrosis factor (TNF)-α in a human monocyte cell line (THP1) was measured by ELISA. mRNA expression of MD-2, TLR4, TNF receptor-associated factor (TRAF)-6, and nuclear factor (NF)-κB was measured by real-time PCR with or without an 18-h co-treatment with procyanidin B1. In addition, protein expression of phosphorylated p38 mitogen-activated protein kinase (MAPK) and NF-κB was determined by Western blotting. Structural modeling studies identified Tyr296 in TLR4 and Ser120 in MD-2 as critical sites for hydrogen bonding with procyanidin B1, similar to the sites occupied by LPS. The production of TNF-α was significantly decreased by procyanidin B1 in LPS-treated THP1 cells (p < 0.05). Procyanidin B1 also significantly suppressed levels of phosphorylated p38 MAPK and NF-κB protein, as well as mRNA levels of MD-2, TRAF-6, and NF-κB (all p < 0.05). Procyanidin B1 can compete with LPS for binding to the TLR4-MD-2 heterodimer and suppress downstream activation of p38 MAPK and NF-κB signaling pathways.

Serum S100B level may be correlated with carbon monoxide poisoning.

OBJECTIVE: To investigate the correlation between serum S100B level and carbon monoxide (CO) poisoning by meta-analysis. METHODS: By searching both English and Chinese language-based electronic databases (PubMed, EBSCO, Ovid, Springerlink, Wiley, Web of Science, Wanfang databases, China national knowledge infrastructure (CNKI), VIP database, etc.) thoroughly, we tabulated and analyzed the collected data with the use of Comprehensive Meta-analysis 2.0 (CMA 2.0). RESULTS: Totally 108 studies have been searched initially (92 studies in Chinese, 16 studies in English). Nine case-control studies (4 studies in English, 5 in Chinese) were chosen for an updated meta-analysis including 542 patients with CO poising and 236 healthy controls. Results identified that the serum S100B level were obviously higher than that in healthy controls (SMD=1.600, 95% CI=1.055-2.145, P<0.001). A subgroup based on the ethnicities revealed that the serum S100B level in Caucasian and Asian subgroups was clearly higher than serum S100B level in healthy controls (Asians: SMD=2.0624, 95% CI=1.736-3.511, P<0.001; Caucasians: SMD=0.447, 95% CI=0.197-0.697, P<0.001). CONCLUSION: Serum S100B level may be correlated with the CO poisoning and could be effective biomarker for early diagnosis and treatment monitoring in CO poisoning.

Plasma concentrations of copeptin, C-reactive protein and procalcitonin are positively correlated with APACHE II scores in patients with sepsis.

OBJECTIVE: To evaluate the correlation between Acute Physiology and Chronic Health Evaluation II (APACHE II) score and plasma concentrations of copeptin, C-reactive protein (CRP) and procalcitonin in patients with sepsis. METHODS: Patients with sepsis were prospectively enrolled. APACHE II scores were determined during the first 24 h after admission to the intensive care unit. Plasma copeptin, CRP and procalcitonin were quantified at admission, 24 h, 48 h, and 72 h. Survival at 28 days after admission was recorded. RESULTS: APACHE II score was significantly positively correlated with plasma copeptin, CRP and procalcitonin concentrations. Survivors (n = 15) had significantly lower APACHE II scores and copeptin, CRP and procalcitonin concentrations than nonsurvivors (n = 26). APACHE II score, copeptin at 72 h, CRP at 48 h and procalcitonin at 24 h were independent risk factors for death. CONCLUSION: Plasma copeptin, CRP and procalcitonin concentrations were positively correlated with APACHE II score in patients with sepsis, and reflected disease severity.

Roles of PD-1, Tim-3 and CTLA-4 in immunoregulation in regulatory T cells among patients with sepsis.

OBJECTIVE: This study aims to elucidate the roles of PD-1, Tim-3 and CTLA-4 in sepsis. METHODS: Sepsis patients (n = 182) were selected as sepsis group and divided into three subgroups: mild sepsis group, severe sepsis group and septic shock group; 185 healthy volunteers were enrolled as control group. Flow cytometry and blood routine examination were performed for T lymphocytes and surface co-stimulatory molecules expressions. Pearson correlation test was applied for the correlation of co-stimulatory molecules expressions on T lymphocytes with critical illness in sepsis. Logistic regression analysis was conducted for risk factors in sepsis. RESULTS: Heart rate and WBC in subgroups were higher than control group (P < 0.05). The differences in APACHE II, SAP II and SOFA score among subgroups were statistically significant (P < 0.05). Compared with control group, lymphocyte ratio and percentage of CD4(+) T cells reduced in subgroups (P < 0.05). The differences in expression levels of CD4(+)PD-1(+), CD8(+)PD-1(+), and CD8(+)CTLA-4(+) showed statistical significances (P < 0.05). Apparently, expression levels of CD4(+)TIM-3(+), CD8(+)TIM-3(+), CD4(+)PD-1(+), CD8(+)PD-1(+), and CD4(+)CTLA-4(+) were positively correlated with APACHE II score (all P < 0.05). Logistic regression analysis showed that heart rate and expression level of CD4(+)PD-1(+) might be risk factors while the percentage of CD4(+) T cells might be a protective factor for sepsis (P < 0.05). CONCLUSION: PD-1 aggravates immune responses consistent with promotion of T cell exhaustion in sepsis. Expression level of CD4(+)PD-1(+) and heart rate are potential risk factors while percentage of CD4(+) T cells is a possible protective factor for sepsis.

Relationship of serum mannose-binding lectin levels with the development of sepsis: a meta-analysis.

Many studies have evaluated the association between serum levels of mannose-binding lectin (MBL) and sepsis; however, the findings are inconclusive and conflicting. For a better understanding of MBL in sepsis, we conducted a comprehensive meta-analysis. Potential relevant studies were identified covering Science Citation Index, the Cochrane Library, PubMed, Embase, CINAHL, and Current Contents Index databases. Two reviewers extracted data and assessed studies independently. Statistical analyses were conducted with the version 12.0 STATA statistical software. Ten papers were collected for meta-analysis. Results identified that sepsis patients had considerably lower MBL level than those in the controls (standardized mean difference (SMD) = 1.59, 95 % confidence interval (95%CI) = 0.86∼2.31, P < 0.001). Ethnicity-subgroup analysis showed that sepsis patients were associated with decreased serum MBL level in contrast to the healthy controls in Asians (SMD = 3.07, 95%CI = 1.27∼4.88, P = 0.001) and Caucasians (SMD = 1.00, 95%CI = 0.35∼1.65, P = 0.003). In the group-stratified subgroup analysis, subjects with lower serum MBL level did underpin susceptibility to sepsis in the infants subgroup (SMD = 2.57, 95%CI = 1.59∼3.55, P < 0.001); however, this was not the case in the adults subgroup (SMD = 0.13, 95%CI = -1.30∼1.55, P = 0.862). Our study suggests an important involvement of serum MBL level in sepsis patients considering their lower level compared to controls, especially among infants.

Artesunate Attenuates Lung Injury in Paraquat-Intoxicated Rats via Downregulation of Inflammatory Cytokines.

BACKGROUND: The present study was designed to analyze the dynamic changes in transforming growth factor beta 1 (TGF-ß1), interleukin (IL)-10, and tumor necrosis factor alpha (TNF-α) in paraquat (PQ)-intoxicated rats and to evaluate the effects of artesunate on PQ-induced lung injury. METHODS: Sixty healthy male Sprague-Dawley (SD) rats were randomly assigned to the control (n = 10), PQ (n = 25), and artesunate-treated PQ (n = 25) groups. The plasma levels of TGF-ßl, IL-10, and TNF-α were measured at 0 (control), 12, 24, 48, and 72 hours after PQ poisoning. The pathological changes in the lung tissues were also examined. RESULTS: Signs of PQ poisoning began to show at 12 hours after PQ administration; the levels of serum TGF-ß1, IL-10, and TNF-α were significantly increased (p < 0.01), compared with the control group. The effects of artesunate treatment were evident at 12 hours after PQ poisoning and became statistically significant at 48 hours, compared with the control and PQ groups, respectively (p < 0.05, p < 0.01). CONCLUSIONS: The PQ-induced lung injury was attenuated by artesunate treatment. IL-10, TNF-α, and TGF-ß1 may play an important role in PQ-induced lung injury, which can be prevented by artesunate treatment.

Quantitative determination of euphol in rat plasma by LC-MS/MS and its application to a pharmacokinetic study.

Euphol is a potential pharmacologically active ingredient isolated from Euphorbia kansui. A simple, rapid, and sensitive method to determine euphol in rat plasma was developed based on liquid chromatography-tandem mass spectrometry (LC-MS/MS) for the first time. The analyte and internal standard (IS), oleanic acid, were extracted from plasma with methanol and chromatographied on a C18 short column eluted with a mobile phase of methanol­water­formic acid (95:5:0.1, v/v/v). Detection was performed by positive ion atmospheric pressure chemical ionization in selective reaction monitoring mode. This method monitored the transitions m/z 409.0 →109.2 and m/z 439.4 → 203.2 for euphol and IS, respectively. The assay was linear over the concentration range 27­9000 ng/mL, with a limit of quantitation of 27 ng/mL. The accuracy was between ­7.04 and 4.11%, and the precision was <10.83%. This LC-MS/MS method was successfully applied to investigate the pharmacokinetic study of euphol in rats after intravenous (6 mg/kg) and oral (48 mg/kg) administration. Results showed that the absolute bioavailability of euphol was approximately 46.01%.

Effect of ß-sodium aescinate on hypoxia-inducible factor-1α expression in rat brain cortex after cardiopulmonary resuscitation.

BACKGROUND: This study was undertaken to investigate the expression of hypoxia-inducible factor-1α (HIF-1α) in rat cerebral cortex and the effects of ß-sodium aescinate (SA) administration after return of spontaneous circulation (ROSC). METHODS: SIXTY RATS WERE DIVIDED INTO THREE GROUPS: SA group, injected intraperitoneally with SA instantly after ROSC; control group, injected intraperitoneally with normal saline; and sham-operated group, without cardiac arrest or SA. The cardiac arrest model was established using asphyxiation and intravenous potassium chloride. Blood was sampled 1, 6, 12, and 24 hours after ROSC. Protein and mRNA levels of HIF-1α, VEGF and EPO were detected in the cerebral cortex by immunohistochemistry and real-time RT-PCR; serum levels of NSE and S100ß were determined by enzyme-linked immunosorbent assays. RESULTS: Serum S100ß and NSE were significantly increased in the control group versus the sham-operated group 1, 6, 12 and 24 hours after ROSC (P<0.05). Protein and mRNA levels of HIF-1α, VEGF and EPO were significantly increased in the control rats (P<0.05). Serum NSE and S100ß were significantly decreased in the SA group versus the control group 1, 6, 12 and 24 hours after ROSC (P<0.05). Protein and mRNA levels of HIF-1α, VEGF and EPO were significantly increased in the SA group (P<0.05). CONCLUSIONS: The expression of HIF-1α is increased in rat cerebral cortex after ROSC, and SA up-regulates the expression of HIF-1α. The up-regulation of HIF-1α improves the resistance of the cortex to ischemia and hypoxia and contributes to neuroprotection, possibly because of up-regulation of EPO and VEGF expression.