Effects of propofol versus sevoflurane on cerebral oxygenation and cognitive outcome in patients with impaired cerebral oxygenation.

BACKGROUND: Postoperative neurocognitive dysfunction induced by anesthetics, particularly in elderly patients with impaired oxygenation, is a common complication of surgery and is eliciting increased interest in clinical practice. To investigate the effects of anesthetics on neurocognition, we compared the effects of propofol versus sevoflurane on cerebral oxygenation and cognitive outcome in patients with impaired cerebral oxygenation undergoing general anesthesia. METHODS: Sixty-three patients with impaired cerebral oxygenation (jugular venous bulb oxygen saturation [SjvO2] <50%) or cerebral blood flow/cerebral metabolic rate of oxygen ([CBF/CMRO2] ≤15%) undergoing elective abdominal surgery were randomly allocated into propofol group (group P) or sevoflurane group (group S). The clinical parameters and jugular venous bulb blood gas analysis were monitored throughout the surgical procedure. Cognitive function was assessed with the mini-mental state examination and Montreal Cognitive Assessment at day 1 and day 7 following surgery. S100ß protein in plasma was measured using enzyme-linked immunosorbent assay. RESULTS: The SjvO2 increased during anesthesia induction and surgery when compared to baseline but had no significant difference between group P and group S. When compared to baseline, the CBF/CMRO2 was increased only at the end of surgery and extubation in group P; however, the CBF/CMRO2 in group S was increased during anesthesia induction at 1 hour, 2 hours, end of surgery, and extubation. Furthermore, the CBF/CMRO2 in group S was significantly higher than that in group P during anesthesia induction at 1 hour, 2 hours, and end of surgery. S100ß protein did not significantly change at extubation and 1 day after surgery in both groups when compared to baseline. There was no significant difference in mini-mental state examination and Montreal Cognitive Assessment scores between group P and group S at all time points. CONCLUSION: Sevoflurane showed similar effects in postoperative neurocognitive function as propofol but could improve cerebral oxygenation in patients with impaired cerebral oxygenation.

Resveratrol affects protein kinase C activity and promotes apoptosis in human colon carcinoma cells.

BACKGROUND: Resveratrol has been reported to have potential chemopreventive and apoptosis-inducing properties in a variety of tumor cell lines. OBJECTIVE: In this study, to investigate the effects of resveratrol on protein kinase C (PKC) activity and apoptosis in human colon carcinoma cells, we used HT-29 cells and examined the PKCα and ERK1/2 signaling pathways. METHODS: To test the effects of resveratrol on the growth of HT- 29 cells, the cells were exposed to varying concentrations and assessed with the the MTT cell-viability assay. Fluorescence-activated cell sorter (FACS) analysis was applied to determine the effects of resveratrol on cell apoptosis. Western blotting was performed to determine the protein levels of PKCα and ERK1/2. In inhibition experiments, HT-29 cells were treated with Go?6976 or PD98059 for 30 min, followed by exposure to 200 µM resveratrol for 72 h. RESULTS: Resveratrol had a significant inhibitory effect on HT-29 cell growth. FACS revealed that resveratrol induced apoptosis. Western blotting showed that e phosphorylation of PKCα and ERK1/2 was significantly increased in response to resveratrol treatment. Pre-treatment with PKCα and ERK1/2 inhibitors (Go?6976 and PD98059) promoted apoptosis. CONCLUSION: Resveratrol has significant anti-proliferative effects on the colon cancer cell line HT-29. The PKC- ERK1/2 signaling pathway can partially mediate resveratrol-induced apoptosis of HT-29 cells.

Trigeminal nerve and facial nerve palsy after combined spinal-epidural anesthesia for cesarean section.

A case of emergency cesarean section due to a prolonged second stage of labor in a 29 year-old woman is presented. She had trigeminal nerve and facial nerve palsy after combined spinal-epidural anesthesia for cesarean section.

Cystatin C and serum creatinine in estimating acute kidney injury of shock patients.

BACKGROUND: Serum creatinine (SCr) is the most commonly used parameter to estimate renal function impairement, but there are some shortcomings. Many factors including age, gender, drug, diet, muscle mass and metabolic rate can influence SCr, leading to an inaccurate estimation of kidney impairment. Studies have shown that cystatin C (CysC) is not affected by factors such as muscle mass, age, gender, diet, inflammation or tumor. The present study was undertaken to compare the sensitivity of CysC and SCr in evaluating renal function impairment at early stage of shock. METHODS: Seventy-one patients aged 38.3±21.4 years, who had been treated at the Emergency Medicine Department of the First Affiliated Hospital, Sun Yat-sen University between February 2006 and June 2007, were studied. They were divided into groups A, B, C, and D according to the shock time. Serum sample was drawn from each patient at 1, 2, 3, 4 hours after shock to determine SCr and CysC. CysC and SCr were determined again at 72 hours and 7 days after shock. RESULTS: CysC increased earlier than SCr in the 71 patients, and CysC decreased slower than SCr when shock was corrected. CysC increased at 1 hour after shock. There was a negative correlationship between CysC, SCr and glomerular filtration rate (GFR), especially at early stage of shock. CONCLUSIONS: There is renal injury at early stage of shock. CysC is more sensitive than SCr in assessing renal function at the early stage of shock.

ShRNA-mediated gene silencing of beta-catenin inhibits growth of human colon cancer cells.

AIM: To observe the gene silencing mediated by the specific shRNA targeted against beta-catenin and its effect on cell proliferation and cycle distribution in the human colon cancer cell line Colo205. METHODS: Two shRNA plasmid vectors against beta-catenin were constructed and transfected into Colo205 cells with Lipofectamine2000. The down-regulations of beta-catenin, c-myc and cyclinD1 expressions were detected by RT-PCR and western blot analysis. The cell proliferation inhibitions were determined by MTT assay and soft agar colony formation assay. The effect of these two beta-catenin shRNAs on cell cycle distribution and apoptosis was examined by flow cytometry. RESULTS: These two shRNA vectors targeted against beta-catenin efficiently suppressed the expression of beta-catenin and its down stream genes, c-myc and cyclinD1. The expression inhibition rates were around 40%-50% either at the mRNA or at the protein level. The shRNA-mediated gene silencing of beta-catenin resulted in significant inhibition of cell growth both on the culture plates and in the soft agar. Moreover, the cancer cells showed significant G0/G1 arrest and increased apoptosis at 72 h post transfection due to gene silencing. CONCLUSION: These specific shRNAs targeted against beta-catenin could have a gene silencing effect and block the WNT signaling pathway. They could inhibit cell growth, increase apoptosis, and induce cell cycle arrest in Colo205 cells. ShRNA interference against beta-catenin is of potential value in gene therapy of colon cancer.