Incidence and risk factors of venous thromboembolism in kidney transplantation patients: a prospective cohort study.

To investigate the incidence and explore the risk factors of venous thromboembolism (VTE) within 6 months after kidney transplantation. Total of 331 kidney transplant recipients were assessed by venous ultrasonography for VTE at 14 days, 1 month, 3 months, and 6 months post-transplantation. Cox forward regression were used to identify the independent risk factors of VTE. This study registration number is ChiCTR1900020567 and the date of registration was 2019/01/08. The cumulative incidence of VTE was 2.72% (9/331) within 6 months after transplant. 77.8% (7/9) of VTEs occurred in the first 3 months post-transplantation. 88.9% (1/9) of VTEs were asymptomatic, 66.7% (6/9) of VTEs were mural thromboses and in the right lower extremity. Central vena catheterization (HR = 6.94) and severe pulmonary disease (including pneumonia) (HR = 57.35) were the risk factors for VTE in kidney transplantation recipients. KT patients are the high risk population of VTE. Future interventions should be strengthen for KT patients to receive a minimum of 3-month of precautionary measures for VTE, including infection prevention, and strengthening thromboprophylaxis on the CVC or transplanted side of lower extremity.

Improving Mortality Risk Prediction with Routine Clinical Data: A Practical Machine Learning Model Based on eICU Patients.

Purpose: Mortality risk prediction helps clinicians make better decisions in patient healthcare. However, existing severity scoring systems or algorithms used in intensive care units (ICUs) often rely on laborious manual collection of complex variables and lack sufficient validation in diverse clinical environments, thus limiting their practical applicability. This study aims to evaluate the performance of machine learning models that utilize routinely collected clinical data for short-term mortality risk prediction. Patients and Methods: Using the eICU Collaborative Research Database, we identified a cohort of 12,393 ICU patients, who were randomly divided into a training group and a validation group at a ratio of 9:1. The models utilized routine variables obtained from regular medical workflows, including age, gender, physiological measurements, and usage of vasoactive medications within a 24-hour period prior to patient discharge. Four different machine learning algorithms, namely logistic regression, random forest, extreme gradient boosting (XGboost), and artificial neural network were employed to develop the mortality risk prediction model. We compared the discrimination and calibration performance of these models in assessing mortality risk within 1-week time window. Results: Among the tested models, the XGBoost algorithm demonstrated the highest performance, with an area under the receiver operating characteristic curve (AUROC) of 0.9702, an area under precision and recall curves (AUPRC) of 0.8517, and a favorable Brier score of 0.0259 for 24-hour mortality risk prediction. Although the model's performance decreased when considering larger time windows, it still achieved a comparable AUROC of 0.9184 and AUPRC of 0.5519 for 3-day mortality risk prediction. Conclusion: The findings demonstrate the feasibility of developing a highly accurate and well-calibrated model based on the XGBoost algorithm for short-term mortality risk prediction with easily accessible and interpretative data. These results enhance confidence in the application of the machine learning model to clinical practice.

[Development of mortality prediction model for critically ill patients based on multidimensional and dynamic clinical characteristics].

OBJECTIVE: To develop a mortality prediction model for critically ill patients based on multidimensional and dynamic clinical data collected by the hospital information system (HIS) using random forest algorithm, and to compare the prediction efficiency of the model with acute physiology and chronic health evaluation II (APACHE II) model. METHODS: The clinical data of 10 925 critically ill patients aged over 14 years old admitted to the Third Xiangya Hospital of Central South University from January 2014 to June 2020 were extracted from the HIS system, and APACHE II scores of the critically ill patients were extracted. Expected mortality of patients was calculated according to the death risk calculation formula of APACHE II scoring system. A total of 689 samples with APACHE II score records were used as the test set, and the other 10 236 samples were used to establish the random forest model, of which 10% (n = 1 024) were randomly selected as the validation set and 90% (n = 9 212) were selected as the training set. According to the time series of 3 days before the end of critical illness, the clinical characteristics of patients such as general information, vital signs data, biochemical test results and intravenous drug doses were selected to develope a random forest model for predicting the mortality of critically ill patients. Using the APACHE II model as a reference, receiver operator characteristic curve (ROC curve) was drawn, and the discrimination performance of the model was evaluated through the area under the ROC curve (AUROC). According to the precision and recall, Precision-Recall curve (PR curve) was drawn, and the calibration performance of the model was evaluated through the area under the PR curve (AUPRC). Calibration curve was drawn, and the consistency between the predicted event occurrence probability of the model and the actual occurrence probability was evaluated through the calibration index Brier score. RESULTS: Among the 10 925 patients, there were 7 797 males (71.4%) and 3 128 females (28.6%). The average age was (58.9±16.3) years old. The median length of hospital stay was 12 (7, 20) days. Most patients (n = 8 538, 78.2%) were admitted to intensive care unit (ICU), and the median length of ICU stay was 66 (13, 151) hours. The hospitalized mortality was 19.0% (2 077/10 925). Compared with the survival group (n = 8 848), the patients in the death group (n = 2 077) were older (years old: 60.1±16.5 vs. 58.5±16.4, P < 0.01), the ratio of ICU admission was higher [82.8% (1 719/2 077) vs. 77.1% (6 819/8 848), P < 0.01], and the proportion of patients with hypertension, diabetes and stroke history was also higher [44.7% (928/2 077) vs. 36.3% (3 212/8 848), 20.0% (415/2 077) vs. 16.9% (1 495/8 848), 15.5% (322/2 077) vs. 10.0% (885/8 848), all P < 0.01]. In the test set data, the prediction value of random forest model for the risk of death during hospitalization of critically ill patients was greater than that of APACHE II model, which showed by that the AUROC and AUPRC of random forest model were higher than those of APACHE II model [AUROC: 0.856 (95% confidence interval was 0.812-0.896) vs. 0.783 (95% confidence interval was 0.737-0.826), AUPRC: 0.650 (95% confidence interval was 0.604-0.762) vs. 0.524 (95% confidence interval was 0.439-0.609)], and Brier score was lower than that of APACHE II model [0.104 (95% confidence interval was 0.085-0.113) vs. 0.124 (95% confidence interval was 0.107-0.141)]. CONCLUSIONS: The random forest model based on multidimensional dynamic characteristics has great application value in predicting hospital mortality risk for critically ill patients, and it is superior to the traditional APACHE II scoring system.

Human genes with relative synonymous codon usage analogous to that of polyomaviruses are involved in the mechanism of polyomavirus nephropathy.

Human polyomaviruses (HPyVs) can cause serious and deleterious infections in human. Yet, the molecular mechanism underlying these infections, particularly in polyomavirus nephropathy (PVAN), is not well-defined. In the present study, we aimed to identify human genes with codon usage bias (CUB) similar to that of HPyV genes and explore their potential involvement in the pathogenesis of PVAN. The relative synonymous codon usage (RSCU) values of genes of HPyVs and those of human genes were computed and used for Pearson correlation analysis. The involvement of the identified correlation genes in PVAN was analyzed by validating their differential expression in publicly available transcriptomics data. Functional enrichment was performed to uncover the role of sets of genes. The RSCU analysis indicated that the A- and T-ending codons are preferentially used in HPyV genes. In total, 5400 human genes were correlated to the HPyV genes. The protein-protein interaction (PPI) network indicated strong interactions between these proteins. Gene expression analysis indicated that 229 of these genes were consistently and differentially expressed between normal kidney tissues and kidney tissues from PVAN patients. Functional enrichment analysis indicated that these genes were involved in biological processes related to transcription and in pathways related to protein ubiquitination pathway, apoptosis, cellular response to stress, inflammation and immune system. The identified genes may serve as diagnostic biomarkers and potential therapeutic targets for HPyV associated diseases, especially PVAN.

Inhibition of ANXA2 regulated by SRF attenuates the development of severe acute pancreatitis by inhibiting the NF-κB signaling pathway.

BACKGROUND: Acute pancreatitis (AP) is an inflammatory process of the pancreas resulting from biliary obstruction or alcohol consumption. Approximately, 10-20% of AP can evolve into severe AP (SAP). In this study, we sought to explore the physiological roles of the transcription factor serum response factor (SRF), annexin A2 (ANXA2), and nuclear factor-kappaB (NF-κB) in SAP. METHODS: C57BL/6 mice and rat pancreatic acinar cells (AR42J) were used to establish an AP model in vivo and in vitro by cerulein with or without lipopolysaccharide (LPS). Production of pro-inflammatory cytokines (IL-1ß and TNF-α) were examined by ELISA and immunoblotting analysis. Hematoxylin and eosin (HE) staining and TUNEL staining were performed to evaluate pathological changes in the course of AP. Apoptosis was examined by flow cytometric and immunoblotting analysis. Molecular interactions were tested by dual luciferase reporter, ChIP, and Co-IP assays. RESULTS: ANXA2 was overexpressed in AP and correlated to the severity of AP. ANXA2 knockdown rescued pancreatic acinar cells against inflammation and apoptosis induced by cerulein with or without LPS. Mechanistic investigations revealed that SRF bound with the ANXA2 promoter region and repressed its expression. ANXA2 could activate the NF-κB signaling pathway by inducing the nuclear translocation of p50. SRF-mediated transcriptional repression of ANXA2-protected pancreatic acinar cells against AP-like injury through repressing the NF-κB signaling pathway. CONCLUSION: Our study highlighted a regulatory network consisting of SRF, ANXA2, and NF-κB that was involved in AP progression, possibly providing some novel targets for treating SAP.

Investigation of preoperative physical activity level in kidney transplant recipients and its impact on early postoperative recovery: A retrospective cohort study.

Objective: To retrospectively investigate the preoperative physical activity (PA) level in kidney transplant recipients (KTRs) and its impact on early postoperative recovery. Methods: A total of 113 patients who received kidney transplantation at West China Hospital of Sichuan University were enrolled in this retrospective cohort study. According to the PA level measured by the Chinese version of the International Physical Activity Questionnaire-Long Version, the patients were allocated into the low PA level group (Group L, n = 55) and medium to high PA level group (Group MH, n = 58). The kidney function recovery indicators, including estimated glomerular filtration rate (eGFR), postoperative complications, postoperative length of stay (LOS), and unscheduled readmission within three months of discharge, were evaluated and documented. A association analysis was applied to analyze and compare the association between indicators. Results: The median PA levels of the KTRs were 1701.0 MTEs * min/week. Regarding the postoperative recovery indicators, the KTRs spent a mean time of 19.63 h to achieve transfer out of bed after the operation (Group L: 19.67 h; Group MH: 19.53 h; P = 0.952) and reached a mean distance of 183.10 m as the best ambulatory training score within two days after the operation (Group L: 134.91 m; Group MH: 228.79 m; P < 0.001). The preoperative PA level showed a moderate positive association with early postoperative ambulation distance (ρ = 0.497, P < 0.001). However, no significant between-group difference in eGFR on postoperative days 1, 3, and 5 (P = 0.913, 0.335, and 0.524) or postoperative complications, including DGF (P = 0.436), infection (P = 0.479), postoperative LOS (P = 0.103), and unscheduled readmission (P = 0.698), was found. Conclusions: The preoperative PA level of KTRs is lower than that of the general population. KTRs with moderate or high preoperative PA levels showed higher ambulatory function in the early postoperative period than those with low preoperative PA levels, but no between-group differences in other early recovery indicators were observed.

Naringin improves sepsis-induced intestinal injury by modulating macrophage polarization via PPARγ/miR-21 axis.

Naringin exhibited various pharmacological activities. However, its biological function and underlying mechanism in regulating macrophage polarization remain elusive. This study aimed to investigate the regulatory network between naringin and macrophage polarization in sepsis-induced intestinal injury. Cecal ligation and puncture (CLP) was used to establish the animal model of sepsis. Chromatin immunoprecipitation and a luciferase reporter assay were used to determine the interplay between peroxisome proliferator-activated receptor γ (PPARγ) and miR-21 promoter, as well as miR-21 and its target genes. Naringin enhanced the overall survival of septic mice and alleviated the CLP-induced inflammatory response and intestinal damage. This was accompanied by the increased expression of PPARγ in the intestines and the stimulation of ileal macrophages toward the M2 phenotype. Furthermore, in lipopolysaccharide-stimulated bone marrow-derived macrophages, naringin stimulated M2 polarization. Mechanistically, PPARγ inhibition attenuated the promotion of M2 polarization caused by naringin, and the naringin/PPARγ regulatory work was compromised by miR-21 inhibition. The present study suggested that naringin promoted M2 polarization via the PPARγ/miR-21 axis, thus relieving sepsis-induced intestinal injury. This study provides novel insights into the mechanism by which naringin alleviated sepsis-induced intestinal injury through regulation of macrophage polarization.

MiR-20b-5p modulates inflammation, apoptosis and angiogenesis in severe acute pancreatitis through autophagy by targeting AKT3.

BACKGROUND: Severe acute pancreatitis (SAP) is a common acute abdominal disease with high morbidity and mortality. However, the mechanism underlying SAP is still unclear. METHODS: Cerulean and LPS (Cer-LPS) was used to establish a rat model and an in vitro model of SAP. qRT-PCR, western blot and IHC were determined to analyse the expression of mRNA and proteins. IL-1ß, TNF-α and IL-6 levels were measured applying ELISA. H&E staining was determined to observe the pathological changes. Apoptosis was tested by AV-PI staining using flow cytometry. CCK8 assay was taken to detect cell viability. Cell migration was assessed by transwell assay. Tube formation assay was conducted to evaluate angiogenesis. Luciferase assay was used to detect relationship of miR-20b-5p and AKT3. RESULTS: MiR-20b-5p was lowly expressed in SAP models both in vivo and in vitro. Overexpression of miR-20b-5p restrained inflammation and apoptosis in Cer-LPS treated pancreatic acinar cells. Furthermore, miR-20b-5p promoted the angiogenesis of vascular endothelial cells, since the viability, migration and the capability of tube formation were increased by miR-20b-5p. Mechanically, miR-20b-5p directly targeted AKT3 to promote autophagy. Furthermore, miR-20b-5p could prevent the inflammation, apoptosis and enhance angiogenesis via enhancing autophagy, which was verified in vivo. CONCLUSION: This study demonstrated miR-20b-5p attenuates SAP through directly targeting AKT3 to regulate autophagy, subsequently inhibit inflammation and apoptosis, and promote angiogenesis. Our findings suggested a novel target of miR-20b-5p for the therapy of SAP.

Does non-invasive blood pressure measurement increase the complications and decrease indwelling time of peripheral intravenous catheters: A cohort study.

AIMS AND OBJECTIVES: To explore the efficacy of non-invasive blood pressure monitors on reducing clinical complications of peripheral intravenous catheters in renal transplant recipients. BACKGROUND: A peripheral intravenous catheter is a regular route of medication administration, but the incidence of complications such as infiltration, occlusion and phlebitis perpetuates in the clinical setting. DESIGN: This was a cohort study. METHODS: Patients were placed naturally into observation group or control group according to whether or not the two procedures (non-invasive blood pressure monitoring and peripheral intravenous catheters indwelling) were on the same arm. Univariate test and Cox regression model were used to estimate relative risk factors. The STROBE checklist was used to guide the submission. RESULTS: We identified 177 kidney recipient patients during the perioperative period with 440 peripheral intravenous catheters. There were incidences of 112 (25.5%) phlebitis, 137 (31.1%) occlusion and 150 (31.8%) infiltration. There was no significant difference between incidence of phlebitis, occlusion and infiltration between the observation group and the control group (p > .05). The observation group peripheral intravenous catheters indwelling time was 97.03 ± 6.76 hr, while it was 89.22 ± 9.55 hr for the control group. However, this difference was not significant between the two groups (p > .05). Cox risk regression showed that only a high BMI was a risk factor for peripheral intravenous catheters indwelling time. CONCLUSION: Non-invasive blood pressure monitoring did not increase complications or shorten PIVCs indwelling time among renal transplant recipients. BMI represented an independent risk factor for the peripheral intravenous catheters indwelling time. RELEVANCE TO CLINICAL PRACTICE: It is not a prohibition to take non-invasive blood pressure measurement when having a peripheral intravenous catheter, especially in some special circumstances in the clinical practice or when good prevention procedures are implemented.

Long Non-coding RNA FENDRR Modulates Autophagy Through Epigenetic Suppression of ATG7 via Binding PRC2 in Acute Pancreatitis.

Acute pancreatitis (AP) is an inflammatory, complicated pancreatic disease, carrying significant morbidity and mortality. However, the molecular and cellular mechanisms involved in AP pathogenesis remain to be elucidated. Here, we explore the role of FOXF1 adjacent non-coding developmental regulatory RNA (FENDRR) in AP progression. Caerulein with or without LPS- induced or taurolithocholic acid 3-sulfate (TLC-S)-induced AP mouse models and cell models were performed for the validation of FENDRR expression in vivo and in vitro, respectively. Histopathological examinations of pancreatic tissues were performed to evaluate the severity of AP. Transmission electron microscopy was utilized to visualize the autophagic vacuoles. siRNA specifically targeting FENDRR was further applied. Flow cytometry was employed to assess cell apoptosis. ELISA, immunoflureoscence, and western blotting analysis were also performed to determine the levels of inflammatory cytokines and autophagy activity. RNA immunoprecipitation (RIP) and chromatin immunoprecipitation (ChIP) assays were carried out to reveal the epigenetic regulation of FENDRR on ATG7. Additionally, silencing FENDRR was also verified in AP mouse models. Higher FENDRR and impaired autophagy were displayed in both AP mouse models and cell models. FENDRR knockdown dramatically attenuated caerulein- or TLC-S-induced AR42J cells apoptosis and autophagy suppression. Further mechanistic experiments implied that the action of FENDRR is moderately attributable to its repression of ATG7 via direct interaction with the epigenetic repressor PRC2. Moreover, the silencing of FENDRR significantly induced the promotion of ATG7, thus alleviating the development of AP in vivo. Our study highlights FENDRR as a novel target that may contribute to AP progression, suggesting a therapeutic target for AP treatment.

miR-375 Inhibits Autophagy and Further Promotes Inflammation and Apoptosis of Acinar Cells by Targeting ATG7.

OBJECTIVES: MicroRNAs have been considered to be closely related with the development of severe acute pancreatitis (SAP), and microRNA-375 (miR-375) was believed to be a marker of SAP. We aim to investigate the role of miR-375 in regulating SP. METHODS: Cerulein and lipopolysaccharide were used to establish the models of SAP. AR42J cell line was chosen for study in vitro. Flow cytometry was applied for assessing apoptosis. The contents of inflammatory factors were detected with related enzyme-linked immunosorbent assay and quantitative real-time polymerase chain reaction assays. Hematoxylin and eosin staining was applied to observe the pathological changes of pancreatic tissues. Immunohistochemistry analysis was conducted for investigating the expression of light chain 3. RESULTS: The level of miR-375 in pancreatitis tissues and cell lines was upregulated. Overexpression of miR-375 promoted inflammation and the apoptosis of acinar cells through inhibiting autophagy. The binding site between miR-375 and ATG7 was identified, and miR-375 could directly regulate the ATG7. microRNA-375 suppressed autophagy and promoted inflammation and the apoptosis of acinar cells via targeting ATG7. CONCLUSIONS: We proved that miR-375 could inhibit autophagy and promote inflammation and the apoptosis of acinar cells through regulating ATG7. This study first proves that miR-375 modulates the development of SAP through targeting ATG7.

A randomized controlled trial of the Effects of a telehealth educational intervention on medication adherence and disease activity in rheumatoid arthritis patients.

AIMS: To examine the effects of a tailored telehealth educational intervention on medication adherence and disease activity in discharged patients with rheumatoid arthritis (RA). DESIGN: An un-blinded randomized controlled trial. METHODS: A total of 92 eligible patients were recruited from January 2015-December 2015. Participants were randomly assigned to either the intervention (N = 46) or control group (N = 46). The intervention group received four educational sessions delivered through a telephone across a 12-week intervention. The content of the education mainly included: subject's knowledge about disease; treatment goals; the importance of taking medication correctly; side effect management; remembering to take medication. The control group received only standard care including discharge instructions. Outcome measures included medication adherence and disease activity. RESULTS: The intervention group had significantly higher medication adherence compared with the control group at 12th and 24th week. There was no significant difference between two groups in disease activity at 12th and 24th week. CONCLUSIONS: The telephone-delivered tailored educational intervention effectively improved medication adherence among discharged patients with rheumatoid arthritis. However, no significant benefits of the intervention on disease activity were detected. IMPACT: Good medication adherence in rheumatoid arthritis patients contributes to controlling symptom and inflammation, preventing the progressive structural damage. This study demonstrated that the telehealth educational intervention could improve patients' medication adherence but did not have a direct impact on clinical condition in the short-term. The intervention for discharged patients with rheumatoid arthritis can be integrated into the clinical setting by the nursing staff as follow-up care. TRIAL REGISTRATION NUMBER: ChiCTR-IPR-14005722.

Downregulated microRNA-150 upregulates IRX1 to depress proliferation, migration, and invasion, but boost apoptosis of gastric cancer cells.

OBJECTIVE: Many studies have reported the correlation of microRNAs (miRNAs) with cancers, yet few have proposed the function of miR-150 in gastric cancer. This study intends to discuss the role of miR-150 in gastric cancer development by regulating IRX1. METHODS: Gastric cancer tissues and adjacent tissues were collected. MiR-150-3p, IRX1, CXCL14, and NF-κB (p65) expressions were detected. Gastric cancer cell lines SNU-1 and MKN-45 were used for subsequent cellular experiments. Cell proliferation, colony formation, migration and invasion, apoptosis, and cell cycle distribution in SNU-1 and MKN-45 cells were determined via gain-of and loss-of-function assays. The tumor growth in nude mice was also detected. RESULTS: MiR-150, CXCL14, and NF-κB (p65) were upregulated and IRX1 was downregulated in gastric cancer tissues and cells. CXCL14 and NF-κB (p65) expression was positively related to miR-150 expression and negatively to IRX1 expression. MiR-150 inhibition and IRX1 overexpression in SNU-1 cells restricted viability, colony formation, migration, and invasion abilities, but boosted apoptosis of gastric cancer cells in vitro, and also repressed tumor growth in vivo. These results could be reversed by miR-150 elevation and IRX1 silencing, and the results from in vivo and in vitro experiments were consistent. CONCLUSION: Our study reveals that miR-150 downregulation restrains proliferation, migration, and invasion, while facilitating apoptosis of gastric cancer cells by upregulating IRX1.

Effectiveness of health education by telephone follow-up on self-efficacy among discharged patients with rheumatoid arthritis: A randomised control trial.

AIMS AND OBJECTIVES: To explore the effectiveness of a health education programme by telephone follow-up on the self-efficacy of patients with rheumatoid arthritis (RA). BACKGROUND: Self-efficacy is increasingly perceived to be a cornerstone in improving the capacity of self-management. However, a paucity of research has demonstrated the effectiveness of health education by the use of a telephone follow-up for RA patients in China. DESIGN: This study was a randomised control trial. METHODS: Recruited patients were randomly divided into control and intervention groups. The intervention group accepted health education by telephone follow-up four times after the patients were discharged. The patients in the control group only accepted telephone follow-up once after they were discharged. Self-efficacy was measured by the use of the Rheumatoid Arthritis Self-Efficacy Questionnaire (RASE), and data were collected at the day before the discharge, the 12th week and the 24th week after patients were discharged. The CONSORT checklist was used to check the procedure. RESULTS: A total of 92 discharged patients with rheumatoid arthritis were enrolled. The sociodemographic indexes of the control and intervention groups had no significant differences at baseline (p > .05). The RASE score of the intervention group was higher than that of the control group (p < .05) at the 12th week and the 24th week. CONCLUSION: The HET improved the self-efficacy of the discharged patients with RA in the 12th week and the 24th week after discharge. This study demonstrated that our HET can improve the short-term and long-term effects of self-efficacy, which implies that the clinical nursing staff should increase the frequency of HET to improve the patients' knowledge and abilities of self-management. RELEVANCE TO CLINICAL PRACTICE: Patients with RA will benefit from a health education programme by telephone follow-up; thus, it is necessary for nursing managers to implement this programme.

The association between occupational stress and psychosomatic wellbeing among Chinese nurses: A cross-sectional survey.

Occupational stress impairs nurses' psychosomatic wellbeing, which includes anxiety, depression, sleep quality, and somatic symptoms; however, few studies have focused on the associations between the subdimensions of occupational stress [workload and time pressure (WTP), professional and career issues (PC), patient care and interaction (PCI), interpersonal relationships and management problems (IRMP), resource and environment problem (REP)] and psychosomatic wellbeing among nurses in China. This study thus examined these associations using a cross-sectional survey in Sichuan, China. An online application was devised to collect data, with the scales of sociodemographic and occupational variables, Nurse Job Stressor Questionnaire, the 9- and 15-item Patient Health Questionnaires, the 7-item Generalized Anxiety Disorder scale, and the Pittsburgh Sleep Quality Index. Investigation was completed by 2889 nurses (96.7% women; mean age = 31.20 ±â€Š6.72 years). Relationships were identified by correlation and multivariate regression analyses. Most (68.3%) nurses had high levels of occupational stress. The multivariate analyses revealed that WTP was correlated with anxiety (P = .003). PC was associated with depression (P = .033) and sleep quality (P = .078). PCI was correlated with anxiety (P = .031) and somatic symptoms (P = .005). IRMP was associated with anxiety (P = .018), depression (P = .001), and somatic symptoms (P = .025). Lastly, REPs had nonsignificant relationships with depression, anxiety, sleep quality, and somatic symptoms. In sum, nurses had high levels of occupational stress; therefore, a series of strategies should be implemented to help nurses cope with the above issues, which could promote nurses' psychosomatic wellbeing, and have a buffering effect on nurses' depression, anxiety, poor sleep quality, and somatic symptoms.

Dexamethasone inhibits NF­ÐºBp65 and HMGB1 expression in the pancreas of rats with severe acute pancreatitis.

Severe acute pancreatitis (SAP) starts as a local inflammation of pancreatic tissue that induces the development of multiple extra­pancreatic organ dysfunction; however, the underlying mechanisms remain unclear. The present study was designed to evaluate the effect of dexamethasone (DXM) on pancreatic damage and to investigate the role of high­mobility group box­1 (HMGB1) and nuclear factor­κB (NF­κBp65) in the development of SAP in animal and cell models. For the in vivo experiment, 35 Sprague­Dawley rats were randomly assigned to three groups: The sham­operation control group, the SAP group and the DXM treatment group. Histological analysis revealed that, when DXM was infused into SAP rats, edema formation and structural alterations with necrosis were reduced, and the number of apoptotic cells was markedly reduced. In addition, compared with the SAP group, the expression level of HMGB1 was significantly decreased in the nucleus and the expression level of NF­κBp65 was significantly decreased in the cytoplasm from rats treated with DXM. In vitro, DXM was able to suppress the apoptosis and cell death induced by caerulein (CAE), and DXM could suppress the expression of NF­κBp65 and HMGB1 induced by CAE, as demonstrated by western blotting and immunofluorescence analysis. Therefore, these results provide an experimental basis for investigating the underlying therapeutic mechanisms of DXM treatment for SAP.

The CD40 rs1883832 Polymorphism Affects Sepsis Susceptibility and sCD40L Levels.

Sepsis is a severe and progressive disease characterized by systemic inflammatory response syndrome (SIRS). CD40 serves as a vital link between immune response and inflammation. This study was designed to investigate the potential association between a functional single-nucleotide polymorphism (SNP) of CD40 (rs1883832) and susceptibility to sepsis. We first performed a case-control study to explore the relationship between the CD40 rs1883832 polymorphism and sepsis. CD40 mRNA expression and protein expression were determined by real-time PCR and western blotting, respectively, in peripheral blood mononuclear cells (PBMCs) from sepsis patients and healthy controls. The plasma sCD40L levels in the two groups were measured by ELISA. The results showed that the frequencies of the TT genotype and the CD40 rs1883832 T allele were significantly higher in sepsis patients than in healthy controls. Plasma sCD40L levels were also significantly increased in sepsis patients. In addition, TT genotype carriers among sepsis patients displayed the highest CD40 expression at both the mRNA and protein levels, accompanied by the highest plasma sCD40L concentrations. In conclusion, the CD40 rs1883832 T allele acts as a risk factor for increased susceptibility to sepsis and may be involved in the process of sepsis through regulation of CD40 expression and plasma sCD40L levels.

Comparison of bone marrow tissue- and adipose tissue-derived mesenchymal stem cells in the treatment of sepsis in a murine model of lipopolysaccharide-induced sepsis.

Mesenchymal stem cells (MSCs) have been reported to regulate the systemic inflammatory response and sepsis-induced immunologic injury pre-clinically. However, whether MSCs from different sources elicit identical effects remains to be elucidated. The present study compared the effect of bone marrow­derived MSCs (BMSCs) and adipose tissue-derived MSCs (ADMSCs) in a murine model of lipopolysaccharide (LPS)­induced sepsis. SPF BALB/c mice were induced with an injection of LPS (10 mg/kg; 1 mg/ml) via the tail vein. To compare the effect of MSCs on the septic mice, either saline, BMSCs or ADMSCs were injected via the tail vein 5 min following the administration of LPS. The survival rates and body temperatures of the mice were observed regularly up to 48 h. The serum levels of pro­inflammatory cytokines, including tumour necrosis factor­α, interleukin (IL)­6 and IL­8, anti­inflammatory cytokines, including IL­2, IL­4 and IL­10, and biochemical markers, including lactate, creatinine, alanine aminotransferase and aspertate aminotransferase, were analyzed at 6 h. The BMSCs and ADMSCs significantly reduced mortality rates, body­temperature fluctuations, serum levels of biochemical markers and the majority of cytokines. However, the levels of IL­8 in the BMSC and ADMSC groups were increased and decreased, respectively. These findings suggested that BMSCs and ADMSCs ameliorated sepsis-associated organ injury and mortality, and had a similar regulatory effect on pro­ and anti­inflammatory cytokines despite the different MSC sources. Therefore, BMSCs and ADMSCs may serve as novel treatment modalities for sepsis.

Decision Support System of Nursing Human Resources Allocation in General Wards Based on Hospital Information System.

AIM: To construct a Decision support system of nursing human resources allocation in general wards based on Hospital information system (HIS). METHOD: Time series prediction model and Information technical method were used based on data of HIS in West China Hospital, Sichuan University (Chengdu, P.R. China). RESULTS: This study completed the function design and system implementation of the nursing human resources allocation decision support system. DISCUSSION: The system would help nursing managers choose the optimal scheme and make scientific decisions in combination with "the actual" situation but more empirical studies are needed.

Using Hospital Information System Data to Capture Nurse Workload.

Aim Using hospital information system (HIS) data to capture nurse workload. Method Direct and indirect nursing items were included by survey and group discussion, workload of nurses is calculated by the work hour measurement of nursing item. Nursing items were matching with HIS index. An ETL (Extract, Transform, Load) tool, Microsoft SSIS, is to capture all HIS index if it happened in a day. Results The workload of a ward can be calculated automatically the day before. Discussion This study provides a new approach to achieve nursing workload. However, a confirmatory study should be implemented in the future to verify the reliability of workload.