Abnormal coagulation after hepatectomy in patients with normal preoperative coagulation function.

BACKGROUND: To explore the risk factors for postoperative abnormal coagulation (PAC) and establish a predictive model for patients with normal preoperative coagulation function who underwent hepatectomy. MATERIALS AND METHODS: A total of 661 patients with normal preoperative coagulation function who underwent hepatectomy between January 2015 and December 2021 at the First Affiliated Hospital of Sun Yat-sen University were divided into two groups: the postoperative abnormal coagulation group (PAC group, n = 362) and the normal coagulation group (non-PAC group, n = 299). Univariate and multivariate logistic analyses were used to identify the risk factors for PAC. RESULTS: The incidence of PAC in 661 patients who underwent hepatectomy was 54.8% (362/661). The least absolute shrinkage and selection operator (LASSO) method was used for multivariate logistic regression analysis. The preoperative international normalized ratio (INR), intraoperative succinyl gelatin infusion and major hepatectomy were found to be independent risk factors for PAC. A nomogram for predicting the PAC after hepatectomy was constructed. The model presented a receiver operating characteristic (ROC) curve of 0.742 (95% confidence interval (CI): 0.697-0.786) in the training cohort. The validation set demonstrated a promising ROC of 0.711 (95% CI: 0.639-0.783), and the calibration curve closely approximated the true incidence. Decision curve analysis (DCA) was performed to assess the clinical usefulness of the predictive model. The risk of PAC increased when the preoperative international normalized ratio (INR) was greater than 1.025 and the volume of intraoperative succinyl gelatin infusion was greater than 1500 ml. CONCLUSION: The PAC is closely related to the preoperative INR, intraoperative succinyl gelatin infusion and major hepatectomy. A three-factor prediction model was successfully established for predicting the PAC after hepatectomy.

A nomogram for predicting acute kidney injury following hepatectomy: A propensity score matching analysis.

STUDY OBJECTIVE: The low central venous pressure (LCVP) technique is a key technique in hepatectomy, but its impact on acute kidney injury (AKI) is unclear. The purpose of this study was to explore risk factors (in particular LCVP time) for AKI following hepatectomy. DESIGN: A retrospective case-control study with propensity score matching. SETTING: Operating room. PATIENTS: A total of 1949 patients who underwent hepatectomy were studied. INTERVENTIONS: The patients were grouped with or without AKI within 7 days after surgery. Univariable and multivariable analyses were performed, including recognized intraoperative predictors. The final result is represented as a nomogram. MEASUREMENTS: Preoperative, intraoperative and postoperative data were collected. LCVP is monitored directly through a central venous catheter via the right internal jugular vein. MAIN RESULTS: AKI occurred in 148 patients (7.59%). Surgery time, minimum SBP, furosemide administration and norepinephrine were identified as independent risk factors. The area under the curve for the receiver operating characteristic curves was 0.726 (95% CI 0.668-0.783). CONCLUSION: Intraoperative parameters can be used to predict the probability of postoperative AKI. Although AKI increases the length of stay, it may not increase in-hospital mortality. LCVP time was not confirmed to be a risk factor for AKI.

CircTLK1 alleviates oxygen-glucose deprivation/reperfusion induced apoptosis in HK-2 cells through miR-136-5p/Bcl2 signal axis.

The biological functions of circTLK1 in acute kidney injury (AKI), which mainly results from renal ischemia-reperfusion (IR), remain largely unknown. HK-2 cell treatment with oxygen and glucose deprivation, reoxygenation, and glucose (OGD/R) was used to simulate an AKI model that was mainly caused by renal IR. Then, the circTLK1 expression level in HK-2 cells treated with OGD/R was assessed by quantitative reverse transcription polymerase chain reaction (RT-qPCR). Functional experiments were performed with circTLK1 knockdown of HK-2 cells via Cell Counting Kit-8 (CCK8), flow cytometry (FCM), RT-qPCR, and western blotting. The circTLK1-miRNAs-mRNAs network was constructed following the ceRNA mechanism and visualized by Cytoscape software to investigate the mechanism of circTLK1 in AKI. RT-qPCR was performed to verify the relationship between circTLK1, miR-136-5p, and Bcl2. The level of miR-136-5p was knocked down to ensure its function in OGD/R-triggered apoptosis through experiments, including CCK8, FCM, RT-qPCR, and western blotting. CircTLK1 was downregulated in HK-2 cells subjected to OGD/R treatment and in mouse kidney tissues after renal IR, but the expression of miR-136-5p was the opposite. Interference with circTLK1 expression accelerated HK-2 cell apoptosis, which was overturned by miR-136-5p inhibitors. CircTLK1 targets miR-136-5p to upregulate Bcl2 expression and attenuate apoptosis in HK-2 cells. These data revealed the possible role of circTLK1 as a new biomarker for diagnosis as well as a target in AKI through the miR-136-5p/Bcl2 signaling axis.

Ischemic Preconditioning Preventing Downregulation of miR-182 Protects Intestine Against Ischemia/Reperfusion Injury by Inhibiting Apoptosis.

BACKGROUND: Intestinal ischemia/reperfusion (I/R) injury is a severe condition associated with high morbidity and mortality. Ischemic preconditioning (IPC) had been found to be the most promising strategies against I/R injury. However, the potential molecular mechanisms underlying the protective effect of IPC have not been fully disclosed. MicroRNA182 (miR-182) is closely related to apoptosis and plays an important role in I/R injury. Our recent study demonstrated that miR-182 was down-regulated in the intestinal mucosa after I/R injury. However, whether miR-182 is involved in the protective effects of IPC in the setting of intestinal I/R injury is unknown. AIMS: To investigate the role of miR-182 in the protective effect of IPC in intestine after I/R injury and potential mechanisms. METHODS: AntagomiR-182 was pretreated before IPC in mice with intestinal I/R injury. MiR-182 mimic was administered before oxygen and glucose deprivation and reperfusion (OGD/R) in mice intestinal mucosa epithelial (MIME) cells. RESULTS: IPC partially prevented the downregulation of miR-182 in mice, which was blocked by pretreatment with antagomiR-182. Compared with the IPC group, pretreatment with antagomiR-182 further increased Chiu's scores and diamine oxidase activities. Meanwhile, apoptotic cells and cleaved caspase-3 expression were increased. Compared with the OGD/R group, pretreatment with miR-182 mimic prevented the downregulation of miR-182, improved cell survival, reduced apoptosis and cleaved caspase-3 expression in MIME cells. CONCLUSIONS: The downregulation of miR-182 was partially prevented by IPC, which was involved in IPC induced intestinal protection, and the mechanisms may be associated with inhibition of apoptosis.

Effect of desmopressin administration on intraoperative blood loss and quality of the surgical field during functional endoscopic sinus surgery: a randomized, clinical trial.

BACKGROUND: Bleeding during functional endoscopic sinus surgery is a challenge for the quality of the surgical field for surgeons. This study aimed to evaluate the effect of desmopressin premedication on blood loss and the quality of the surgical field in endoscopic sinus surgery. METHODS: A total of 90 American Society of Anesthesiologists physical status I-II patients underwent endoscopic sinus surgery for chronic sinusitis. They were randomly allocated to receive either desmopressin 0.3 µg/kg or saline before the operation. Management of anesthesia was achieved with propofol and remifentanil infusions, with moderate, controlled hypotension. Blood loss and quality of the surgical field were assessed after surgery. Effects of desmopressin on anesthetic requirements and hemodynamic variables were analyzed. RESULTS: Blood loss was significantly less in the desmopressin group (mean ± SD, 42 ± 8.7 ml) than in the control group (70 ± 9.2 ml, P < 0.001). Surgeons were more satisfied with the surgical field in the desmopressin group than in the control group (median score, 4 [3-5] vs. 7 [6-9], P < 0.001). Requirements for remifentanil and esmolol were lower in the desmopressin group than in the control group. CONCLUSIONS: Premedication with desmopressin 0.3 µg/kg can effectively reduce bleeding during endoscopic sinus surgery.

Cholinergic synaptic transmissions were altered after single sevoflurane exposure in Drosophila pupa.

PURPOSE: . Sevoflurane, one of the most used general anesthetics, is widely used in clinical practice all over the world. Previous studies indicated that sevoflurane could induce neuron apoptosis and neural deficit causing query in the safety of anesthesia using sevoflurane. The present study was designed to investigate the effects of sevoflurane on electrophysiology in Drosophila pupa whose excitatory neurotransmitter is acetylcholine early after sevoflurane exposure using whole brain recording technique. METHODS: Wide types of Drosophila (canton-s flies) were allocated to control and sevoflurane groups randomly. Sevoflurane groups (1% sevoflurane; 2% sevoflurane; 3% sevoflurane) were exposed to sevoflurane and the exposure lasted 5 hours, respectively. All flies were subjected to electrophysiology experiment using patch clamp 24 hours after exposure. RESULTS: The results showed that, 24 hours after sevoflurane exposure, frequency but not the amplitude of miniature excitatory postsynaptic currents (mEPSCs) was significantly reduced (P < 0.05). Furthermore, we explored the underlying mechanism and found that calcium currents density, which partially regulated the frequency of mEPSCs, was significantly reduced after sevoflurane exposure (P < 0.05). CONCLUSIONS: All these suggested that sevoflurane could alter the mEPSCs that are related to synaptic plasticity partially through modulating calcium channel early after sevoflurane exposure.

Effects of sevoflurane on leucine-rich repeat kinase 2-associated Drosophila model of Parkinson's disease.

Patients with Parkinson's disease (PD) often require surgery, and therefore may receive inhalation anesthesia. However, it is currently unknown whether inhalation anesthetics affect the prognosis of the disease. Leucine­rich repeat kinase 2 (LRRK2) genetic mutations are the most common cause of familial PD, contributing to ~39% of all cases in certain populations. The aim of the present study was to determine the effects of inhaled anesthetics on PD, by observing the influence of sevoflurane on a LRRK2­associated Drosophila model of PD. PD transgenic Drosophila overexpressing LRRK2 were generated by crossing flies expressing an LRRK2 upstream activation sequence, with tyrosine hydroxylase (TH)­Gal4 flies. Western blot analysis successfully verified that the transgenic Drosophila overexpressed LRRK2. Three days prior to eclosion, three genotypes of Drosophila were divided into four groups, and were exposed to air, 1, 2, or 3% sevoflurane, for 5 hours. Twenty­four hours after the exposure, the electrophysiological activities of the projection neurons (PN) in the brains of the Drosophila were recorded using a patch clamp. The locomotor activities were tested on days 5, 10, 15, 20, 25, 30, 35 and 40 following eclosion. The frequency of miniature excitatory synaptic currents (mEPSCs) obtained from the PNs of the TH­wild type LRRK2 (TH­WT) Drosophila brain, following exposure to air (1.60±0.05 Hz), was lower as compared with the wild type LRRK2 (WT) (2.51±0.07 Hz) and W1118 (2.41±0.10 Hz) Drosophila. After exposure to 1, 2 and 3% sevoflurane, the frequency of mEPSCs in the brains of the TH­WT group decreased to 0.82±0.04 Hz, 0.63±0.16 Hz and 0.55±0.04 Hz, respectively. The percentage decrease of the frequency of mEPSCs, from exposure to air to 1% sevoflurane, of the TH­WT group (48.32%±3.08%) was significantly higher, as compared with the WT (39.17%±1.42%) and W1118 (35.10%±2.66%) groups, and there was no statistical difference between the WT and W1118 groups. The transgenic TH­WT Drosophila presented an early decrease in locomotor ability, as compared with the WT and W1118 groups. Following a 5 hour exposure to sevoflurane, the percentage decrease of the climbing abilities of the TH­WT group, from exposure to air to 1% sevoflurane, were significantly lower, as compared with the WT and W1118 groups. In conclusion, sevoflurane had negative effects on the control W1118 flies, and also severely aggravated the prognosis of PD in the LRRK2­associated Drosophila model, through synaptic cholinergic deficits and impairment on locomotor abilities.