Development and Validation of a Prediction Model for Venous Thrombus Embolism (VTE) in Patients With Colorectal Cancer.

Cancer patients are at high risk of developing venous thromboembolism (VTE). The risk of VTE could be mitigated with the administration of prophylactic anticoagulants. Therefore, risk assessment models would be a useful tool in order to identify those patients who are at higher risk and will be benefited more by prophylactic anticoagulants. This study retrospectively examined 528 newly diagnosed colorectal cancer patients from January 2019 to January 2021. Specified logistic regression models were employed to screen the factors and establish prediction tools based on nomograms according to the final included variables. Discrimination, calibration, and clinical applicability were used to assess the performance of screening tools. In addition, internal verifications were conducted through 10-fold cross-verification, leave-one-out cross-validation, and Bootstrap verification. Four risk factors, closely related to the occurrence of VTE in colorectal cancer patients, were identified after univariate and multivariate logistic regression, including age, body mass index, activated partial thromboplastin time, and D-Dimer value. Besides, the risk assessment model named ABAD was built on the basis, displaying good discriminations and calibrations. The area under the curve was 0.705 (95% confidence interval [CI], 0.644 to 0.766). According to Hosmer-Lemeshow goodness-of-fit test, a good agreement between the predicted and observed VTE events in patients with newly-diagnosed gastrointestinal cancer was observed for χ2 = 6.864, P = .551. Internal validation was applied with a C-index of 0.669 in the 10-fold cross-verification, 0.658 in the leave-one-out cross verification and 0.684 in the bootstrap verification. We developed a prediction model called ABAD for newly diagnosed colorectal cancer patients, which can be used to predict the risk of VTE. After evaluation and internal verification, we believe that ABAD exhibited high predictive performance and availability and could be recommended.

Correction to: The Protective Effects of Butorphanol on Pulmonary Function of Patients with Obesity Undergoing Laparoscopic Bariatric Surgery: A Double-Blind Randomized Controlled Trial.

In the original article some of the references were ordered incorrectly.

The Protective Effects of Butorphanol on Pulmonary Function of Patients with Obesity Undergoing Laparoscopic Bariatric Surgery: a Double-Blind Randomized Controlled Trial.

BACKGROUND: Obesity is a risk factor for postoperative pulmonary complications (PPCs). Recent studies have reported the pulmonary protective role of the kappa opioid receptor (KOR). Butorphanol is a narcotic with strong KOR agonist action, and the role in pulmonary protection is uncertain. Here, we hypothesized that butorphanol exerts protective effects on pulmonary function in patients with obesity undergoing laparoscopic bariatric surgery. METHODS: Patients with a body mass index ≥ 30 kg/m2 scheduled for laparoscopic bariatric surgery were randomized to receive butorphanol or normal saline. Butorphanol was administered as an initial loading dose of 10 µg/kg at 5 min before induction followed by 5 µg/(kg h) during surgery. The primary outcome was arterial-alveolar oxygen tension ratio (a/A ratio). Secondary outcomes included other pulmonary variables, biomarkers reflecting pulmonary injury, and incidence of PPCs within 7 days after surgery. RESULTS: Patients in the butorphanol group had a significantly higher a/A ratio at 1 h after the operation began (68 ± 7 vs. 55 ± 8, P < 0.001), end of the operation (73 ± 8 vs. 59 ± 7, P < 0.001), and 1 h after extubation (83 ± 9 vs. 70 ± 5, P < 0.001) compared with those in the control group. In addition, in the butorphanol group, dead space to tidal volume ratios were significantly lower than those in the control group at the same time points (all P < 0.001). In the control group, the levels of biomarkers reflecting pulmonary injury were significantly higher than those in the butorphanol group at 3 h, 6 h, 12 h, and 24 h postoperatively (P < 0.001). The incidence of PPCs was similar in both groups. CONCLUSION: Butorphanol administration protected pulmonary function by improving oxygenation and reducing dead space ventilation in patients with obesity undergoing laparoscopic bariatric surgery. Butorphanol may therefore provide clinical benefits in patients with obesity.

Water-soluble substances of wheat: a potential preventer of aflatoxin B1-induced liver damage in broilers.

Aflatoxin B1 (AFB1) is very harmful for broiler production and public health. The water-soluble castoff in gluten production, i.e., the water-soluble substances of wheat (WSW) that contains 14% pentosan has positive effect on animal nutrient absorption, immunity, and antioxidation. Our study aims to investigate the preventive effects of WSW against AFB1-induced broiler liver injury. One day-old Arbor Acres broilers were randomly separated to 4 groups and were, respectively, fed with control diet, diet with 5 mg/kg AFB1 standard, diet with 5 mg/kg AFB1 standard and 214 ml/kg WSW, and diet with 214 ml/kg WSW continuously for 28 d. The histopathological, ultra-structural, and serological changes were tested to evaluate liver damage. The hallmarks of hepatocellular autophagy, apoptosis, and inflammation were measured by Western Blot and real-time polymerase chain reaction. The content of AFB1 in chicken liver was detected with an ultra-high performance liquid chromatography linked with the fluorescence detection method. The results showed that (i) WSW restored AFB1-induced changes in serum biochemical parameters, and ameliorated histomorphological changes in hepatocytes, (ii) WSW reduced the content of AFB1 in chicken liver, (iii) WSW alleviated AFB1-induced autophagy inhibition by up-regulating hepatic LC3, beclin-1, and down-regulating hepatic mTOR and cytoplasmic P53 expressions, (iv) WSW alleviated AFB1-induced hepatocellular apoptosis via inhibiting pro-apoptotic gene expression (nuclear P53, Caspase3, Bax), and promoting anti-apoptotic gene expression (bcl-2), (v) WSW feeding ameliorated AFB1-induced liver inflammation via impeding TLR4/NF-${{\bf \kappa }}$B and IL-1/NF-${{\bf \kappa }}$B signaling pathways, down-regulating pro-inflammatory cytokines (IL-1${{\bf \beta }}$, IL-6, and IL-8), and markedly up-regulating anti-inflammatory genes (IL-10 and HO-1). Conclusively, WSW is a potential preventer of AFB1-induced broiler liver damage by reducing the AFB1 content in liver, accelerating hepatocellular autophagy and inhibiting hepatocytes apoptosis and liver inflammation.

Nrf2 is crucial for the down-regulation of Cyp7a1 induced by arachidonic acid in Hepg2 cells.

In former research, cyp7a1 expression was decreased but Nrf2 transcription and hepatic arachidonic acid (AA) concentration were increased in high-fat diet fed mice. This study aims to investigate the influence of AA in CYP7A1 expression and the role of Nrf2 in regulating CYP7A1 in the process. HepG2 cells were administered with different concentrations of AA. Nrf2 and CYP7A1 expressions were analyzed by real-time PCR and western blot. Nrf2 silenced and over-expressed cell models were constructed by Nrf2 siRNA and eukaryotic expression vector transient transfections and were used to investigate the role of Nrf2 in regulating CYP7A1 following AA administration. The results showed that Nrf2 was increased dose-dependently but CYP7A1 was decreased dose-dependently in cells treated with increasing concentrations of AA. The expression of CYP7A1 was increased by Nrf2 silence and was decreased by Nrf2 over-expression in HepG2 cells treated with different concentrations of AA. In conclusion, Nrf2 plays a significant role in the down-regulation of CYP7A1 induced by AA in HepG2 cells.