Association of intraoperative hypotension with acute kidney injury after liver resection surgery: an observational cohort study.

BACKGROUND: Acute kidney injury (AKI) is a major complication following liver resection. The aim of this study was to determine the risk factors for AKI after hepatic resection and whether intraoperative hypotension (IOH) was related to AKI. METHODS: Adult patients (≥ 18 years) undergoing liver resection between November 2017 and November 2019 at our hospital were retrospectively reviewed. AKI was defined as ≥50% increase in serum creatinine from baseline value within 48 h after surgery. IOH was defined as the lowest absolute mean arterial pressure (MAP) < 65 mmHg for more than 10 cumulative minutes during the surgery. Patients were divided into AKI group and non-AKI group, and were stratified by age ≥ 65 years. RESULTS: 796 patients who met our inclusion and exclusion criteria were analyzed. After multivariable regression analysis, the IOH (OR, 2.565; P = 0.009) and age ≥ 65 years (OR, 2.463; P = 0.008) were risk factors for AKI. The IOH (OR, 3.547; P = 0.012) and received red blood cell (OR, 3.032; P = 0.036) were risk factors of AKI in age ≥ 65 years patients. CONCLUSIONS: The IOH and age ≥ 65 years were risk factors for postoperative AKI, and IOH was associated with AKI in age ≥ 65 years patients following liver resection.

PU-H71 effectively induces degradation of IκB kinase ß in the presence of TNF-α.

This study is to determine if PU-H71, a heat shock protein inhibitor, induces killing of malignant breast cells together with treatment of tumor necrosis factor-α (TNF-α). The related molecular mechanisms were also studied. A primary mammary epithelial cell line HMEC2595 cells and the highly metastatic breast cell line MDA-MB-231, the HER2-positive BT-474 cells, and the ER-positive MCF7 cells were treated with PU-H71 in the presence or absence of TNF-α. The effects of PU-H71 and TNF-α treatments on cells viabilities and on intracellular signaling pathway proteins were determined using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, apoptosis assays, immunoblot assays, and luciferase assays. It was found that TNF-α enhances the toxic effects of PU-H71 on tumor cells but not normal cells. PU-H71 treatments lead to degradation of IKKß. Moreover, PU-H71 down-regulates the NF-κB transcriptional activity induced by TNF-α treatment. The experimental results indicated PU-H71 effectively induces cell killing of malignant breast cells in the presence of TNF-α, possibly through a mechanism related to degradation of IKKß. It is suggested that combination of PU-H71 and TNF-α treatments might be an effective therapeutic strategy of breast malignancies.

Comparison of anesthetic effects of dexmedetomidine and tramadol, respectively, combined with propofol in percutaneous microwave coagulation therapy for hepatocellular carcinoma.

Anesthetic effects and safety of dexmedetomidine and tramadol, respectively, combined with propofol in ultrasound-guided percutaneous microwave coagulation therapy (PMCT) for hepatocellular carcinoma (HCC) were compared. One hundred and seventy-six patients with HCC, treated by ultrasound-guided PMCT in The Affiliated Hospital of Qingdao University from January 2014 to December 2016, were retrospectively analyzed and divided into two groups: dexmedetomidine group (anesthetized with dexmedetomidine combined with propofol, n=91) and tramadol group (anesthetized with tramadol combined with propofol, n=85). Changes in heart rate (HR), mean arterial pressure (MAP), and oxygen saturation (SpO2) were recorded before oxygen inhalation (T1), intraoperationally (T2), and at 30 min postoperatively (T3), and the recovery time (recorded from the moment the use of anesthetic drugs stopped), hospital stay, visual analogue scale (VAS) score at 48 h after surgery, as well as the adverse reactions in the perioperative period were compared between the two groups. HR and SpO2 in the dexmedetomidine group at T2 and T3 were significantly lower than those in the tramadol group (P<0.05). HR and SpO2 at T2 were significantly lower than those at T1 and T3, and HR at T3 was lower than that at T1 (P<0.05). MAP in the dexmedetomidine group at T2 was significantly lower than that in the tramadol group (t=3.836, P<0.001). MAP at T2 was significantly lower than those at T1 and T3, and MAP at T3 was lower than that at T1 (P<0.05). The number of patients with shivering in the dexmedetomidine group was significantly higher than that in the tramadol group (P<0.05). Both tramadol and dexmedetomidine, respectively combined with propofol in PMCT for HCC surgery can achieve satisfactory anesthetic effects. However, tramadol combined with propofol is more effective in stabilizing the vital signs with less side-effects, and is more suitable for PMCT in patients with HCC than dexmedetomidine combined with propofol, which is worth popularizing and applying in clinic.

Protective effects of dexmedetomidine on lung in rats with one-lung ventilation.

Protective effect of dexmedetomidine (DEX) on the lungs of one-lung ventilation (OLV) rat model and its effect on inflammatory factors were investigated. Ninety-two rats were selected and divided into groups A, B, C and D (n=23) according to the principle of similar body weight. OLV rat model was established. Before modeling (15 min), rats in group C were injected with sodium chloride. Rats in group D were injected with DEX at a speed of 5 µg/kg/h. Group A rats were ventilated in both lungs for 2 h. Rats in groups B and C (0.9% sodium chloride injection + OLV) and in group D (DEX + OLV) were subjected to OLV for 2 h and bilateral ventilation for 10 min. Concentrations of interleukin (IL)-6, IL-10 and tumor necrosis factor-α (TNF-α) in lung tissue of rats were detected by ELISA. The malondialdehyde (MDA) concentration and superoxide dismutase (SOD) activity in rat lung tissue were detected by radioimmunoassay. Wet weight (W)/dry weight (D) of lung tissue was calculated and indexes of the four groups of rats were compared. Compared with group A, IL-6, TNF-α and MDA concentrations and W/D of lung tissue of rats in groups B, C and D were significantly increased (p<0.05); SOD activity and IL-10 concentration were significantly decreased (p<0.01). Compared with groups B and C, the concentrations of IL-6, TNF-α and W/D in rats of group D were significantly decreased (p<0.01), but IL-10 significantly increased (p<0.01). Compared with groups B and C, the MDA concentration in lung tissue of rats in group D was significantly decreased (p<0.01), but SOD activity significantly increased (p<0.01). DEX can inhibit the production of inflammatory factors in the development and progression of pulmonary inflammation. It can inhibit lipid peroxidation, relieve pulmonary edema, and reduce lung injury after OLV, sin order to protect the lung.

An Intron Variant of SLC2A9 Increases the Risk for Type 2 Diabetes Mellitus Complicated with Hyperuricemia in Chinese Male Population.

BACKGROUND: The aim of this study was to explore the associations of haplotypes of the glucose transporter 9 (SLC2A9) genes with type 2 diabetes mellitus (T2DM) complicated with hyperuricemia (HUA). METHODS: Overall, 608 Chinese males, enrolled from the Affiliated Hospital of Medical College of Qingdao University in 2009-2012, were genotyped. The subjects included 167 withT2DM (average age of onset (58.07±11.82 yr), 198 with HUA subjects (average age of onset (39.20±9.73) yr), 115 with T2DM complicated with HUA (average age of onset (51.24±10.09) yr), and 128 control subjects (average age (41.92±10.01) yr). Patients genotypes of the SNPs; including rs734553 was determined by PCR method. Each genotype was regressed assuming the co-dominant, dominant and the recessive models of inheritance with covariates of duration of total glucose, uric acid, urea nitrogen, triglyceride, cholesterol, and creatinine levels. RESULTS: Chi-square test revealed that rs734553polymorphism was both significantly associated with HUA as well as T2DM complicated HUA, but not with pure T2DM. After adjustment for age and gender, analysis showed that people with C allele had higher risk of HUA and T2DM complicated HUA than those without C allele. And none of the subjects had the homozygous genotype for SLC2A9 (CC). CONCLUSION: The SLC2A9 mutation increases the risk for T2DM complicated HUA in Chinese population, which suggested that intron variants between two relatively conserved exons could also be associated with diseases. In patients of T2DM complicated with HUA, the diagnosis and detection of SLC2A9 gene variants should be caused enough attention.

Effect of Epidural Dexmedetomidine Combined With Ropivacaine in Labor Analgesia: A Randomized Double-Blinded Controlled Study.

BACKGROUND: The purpose of our study is to evaluate the effect of adding dexmedetomidine to epidural ropivacaine in patients undergoing labor epidural analgesia. METHODS: Eighty healthy women were randomly assigned to 2 groups: control group (R; n=40) received epidural 0.125% ropivacaine for labor analgesia, whereas the study group (D; n=40) received epidural 0.125% ropivacaine with dexmedetomidine in addition. The blood pressure, heart rate, and the severity of pain of the parturient was assessed, the duration of the first stage and the second stage of labor time, the rate of instrumental delivery and the rate of cesarean section were recorded. The side effects (nausea and vomiting), intensity of maternal sedation, and neonatal Apgar scores were also recorded. RESULTS: The visual analog scales, systolic blood pressure, diastolic blood pressure, and heart rates of D group were significant lower than that of R group at most time intervals after epidural analgesia. The duration of the first and second stage of labor, the rate of instrumental delivery and cesarean section, neonatal 1- and 5-minute Apgar scores, umbilical artery pH, maternal motor blockade scores, intensity of maternal sedation, and the incidence of maternal complications did not show significant difference between 2 groups. CONCLUSIONS: Low concentration of epidural ropivacaine (0.125%) combined with dexmedetomidine (0.5 µg/kg) reduces the feeling of pain, and does not show the problems of motor blockage, hemodynamic instability, extension of production process, and complications such as nausea and vomiting. Our study was registered with Chinese Clinical Trial Registry (ChiCTR-IOR-15007263).

Grandinin down-regulates phosphorylation of epidermal growth factor receptor.

AIMS: Grandinin (C(46)H(34)O(30)) is a compound found in Melaleuca quinquenervia leaves and in oaks. This study is to determine effects of grandinin on malignant lung cells and the related molecular mechanisms. METHODS: Malignant cells were treated with grandinin with various concentrations. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrozolium bromide (MTT) assays and apoptosis assays were performed to determine effects of grandinin on cell viability and apoptosis. Western blotting and real time-PCR were used to determine if grandinin affects levels of phosphorylated EGFR (p-EGFR) and phosphorylated AKT (p-AKT), as well as their mRNA transcript levels. RESULTS: It was found that grandinin treatments reduce viability of malignant lung cells and induces apoptosis. When treated with grandinin (16 µM), the apoptosis of the three lung cancer cell lines MS-1, A549, and LK-2 were increased by 8-9 folds, in comparison with the cells treated with DMSO only (the control condition). Furthermore, grandinin treatments lead to down-regulation of levels of p-EGFR and p-AKT in three malignant lung cell lines. However, grandinin does not affect mRNA levels of EGFR and AKT. CONCLUSIONS: These experimental results indicated grandinin significantly reduce malignant cell viability and effectively induces apoptosis of malignant lung cells by mediating phosphorylation down-regulation of cellular signaling proteins EGFR and AKT. It is suggested that grandinin treatments might be an effective therapeutic strategy of lung malignancies upon further studies in the future.

Combined effects of 17-DMAG and TNF on cells through a mechanism related to the NF-kappaB pathway.

OBJECTIVE: The tumor necrosis factor (TNF) and the cellular NF-κB pathway protein IKKß play important roles in various cellular processes such as cell proliferation, survival, differentiation, and apoptosis. A heat shock protein 90 inhibitor, 17-DMAG, can induce apoptosis of some tumor cells. This study is to determine the combined effects of 17-DMAG and TNF on malignant cells and the related mechanisms. METHODS: We have determined effects of 17-DMAG, an Hsp90 inhibitor, and TNF treatments on the small cell lung cancer cell line (MS-1), the adenocarcinoma cell line (A549), the squamous-cell carcinoma cell line (LK-2), and the normal human bronchial epithelium cell line (NuLi-1) by using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrozolium bromide assay. To determine if 17-DMAG inhibit the expression of IKKß in the normal human NuLi-1 cells, and the malignant MS-1, A549, and LK-2 cells, immunoblotting assays and luciferase assays were performed. RESULTS: It was found that the combined treatments resulted in synergistic killing of malignant cells, which was confirmed by the apoptosis determination using a fluorescence microscopic assay following staining of the drug-treated cells with Hoescht 33258. The immunoblotting results indicated that the synergistic killing due to 17-DMAG and TNF treatments may be related to the decreases in IKKß levels in the presence of 17-DMAG. CONCLUSIONS: The results suggest that combination of 17-DMAG and TNF treatments might be useful for treating malignancies upon further study in the further. VIRTUAL SLIDES: The virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/2041198513886824.