MicroRNA-377-3p exacerbates chronic obstructive pulmonary disease through suppressing ZFP36L1 expression and inducing lung fibroblast senescence.

Chronic obstructive pulmonary disease (COPD) is a leading aging related cause of global mortality. Small airway narrowing is recognized as an early and significant factor for COPD development. Senescent fibroblasts were observed to accumulate in lung of COPD patients and promote COPD progression through aberrant extracellular matrix (ECM) deposition and senescence-associated secretory phenotype (SASP). On the basis of our previous study, we further investigated the the causes for the increased levels of miR-377-3p in the blood of COPD patients, as well as its regulatory function in the pathological progression of COPD. We found that the majority of up-regulated miR-377-3p was localized in lung fibroblasts. Inhibition of miR-377-3p improved chronic smoking-induced COPD in mice. Mechanistically, miR-377-3p promoted senescence of lung fibroblasts, while knockdown of miR-377-3p attenuated bleomycin-induced senescence in lung fibroblasts. We also identified ZFP36L1 as a direct target for miR-377-3p that likely mediated its pro senescence activity in lung fibroblasts. Our data reveal that miR-377-3p is crucial for COPD pathogenesis, and may serve as a potential target for COPD therapy.

MiR-1307-5p enhances fibroblast transdifferentiation to exacerbate chronic obstructive pulmonary disease through regulating FBXL16/HIF1α axis.

Chronic obstructive pulmonary disease (COPD) is an irreversible and progressive chronic inflammatory lung disease which affects millions of people worldwide. Activated fibroblasts are observed to accumulate in lung of COPD patients and promote COPD progression through aberrant extracellular matrix (ECM) deposition. In this study, we identified that miR-1307-5p expression was significantly increased in lung fibroblasts derived from COPD patients. Mechanistically, we found that upregulation of miR-1307-5p promoted TGF-ß induced lung fibroblast activation and transdifferentiation. We also identified FBXL16 as a direct target for miR-1307-5p mediated myofibroblast activation in COPD. Knockdown of FBXL16 by siRNA prominently increased the expression of myofibroblast markers in MRC-5 fibroblasts after TGF-ß administration. Ectopic expression of FBXL16 in MRC-5 counteracted miR-1307-5p agomir-induced fibroblast transdifferentiation. Furthermore, We found that miR-1307-5p promoted pulmonary fibroblast transdifferentiation through FBXL16 regulated HIF1α degradation. In general, our findings indicate that miR-1307-5p is important for COPD pathogenesis, and may serve as a potential target for COPD treatment.

LncRNA-Fendrr protects against the ubiquitination and degradation of NLRC4 protein through HERC2 to regulate the pyroptosis of microglia.

OBJECTIVES: Targeted inhibition of inflammatory response can reduce diabetic cerebral ischemia-reperfusion (I/R) injure. Pyroptosis is characterized by caspase-1 dependence and the release of a large number of pro-inflammatory factors. LncRNA-Fendrr is associated with a variety of diseases, but Fendrr has not been studied in diabetic cerebral I/R. NLR-family CARD-containing protein 4 (NLRC4) regulate the pyroptosis of microglia cells. This study was designed to investigate whether Fendrr is involved in the effects of diabetic cerebral I/R injury. METHODS: The diabetic brain I/R model in mice was constructed. Mouse microglia cell line BV-2 cells were exposed to high glucose followed by hypoxia/reoxygenation (H/R). Fendrr and some pyroptosis-associated proteins were detected by qRT-PCR, western blot or ELISA. HE staining was used to detect pathological changes. Microglia pyroptosis was detected by TUNEL staining. RNA pull-down and RNA Immunoprecipitation were used to detect binding of Fendrr to HERC2 (E3 ubiquitin ligase), and CO-IP detected binding of HERC2 to NLRC4. The ubiquitination of NLRC4 was detected by ubiquitination experiments. RESULTS: Fendrr was significantly increased in the diabetic cerebral I/R model, and NLRC4 inflammatory complex and pyroptosis mediated inflammatory factors were increased. NLRC4 and inflammatory cytokines associated with pyroptosis were decreased in the high glucose-treated hypoxia/reoxygenation (H/R)-induced microglia after Fendrr knockdown. Fendrr bound to HERC2 protein, and HERC2 bound to NLRC4. Meanwhile, Fendrr could inhibit the ubiquitination of NLRC4, HERC2 promoted the ubiquitination of NLRC4 protein. Moreover, the effect of Fendrr overexpression in the diabetic cerebral I/R model of microglia can be reversed by HERC2 overexpression. CONCLUSION: Fendrr can protect against the ubiquitination and degradation of NLRC4 protein through E3 ubiquitin ligase HERC2, thereby accelerating the pyroptosis of microglia.

[Progress on perioperative monitoring of cerebral blood flow autoregulation].

Cerebral blood flow autoregulation is physiologically protective mechanism to maintain the stability of cerebral blood flow. Once autoregulation is impaired, the cerebral blood flow fluctuates with blood pressure, leading to the risk of brain ischemia or cerebral hyperemia. Multiple research results indicate that cerebral blood flow can be monitored indirectly and continuously with transcranial Doppler, near infrared spectroscopy or ICP. The correlation coefficient calculated by the surrogate for cerebral blood flow and blood pressure is used to judge cerebral blood flow autoregulation. When the correlation coefficient is close to 1, cerebral blood flow will be passively fluctuated by blood pressure, indicating autoregulation is impaired. When the coefficient is less than 0, cerebral blood flow will not be changed with blood pressure, indicating autoregulaiton is intact. The status of autoregualtion is closely associated with mortality or poor neurological outcomes in patients with cardiac surgery underwent cardiopulmonary bypass, liver transplantation patients or patients with deep trendelenburg position for long time or beach chair position. Continuous monitoring of cerebral blood flow autoregulation can identify the lower or the upper limit of autoregulation, and provide information to individualize the perioperative management of blood pressure.

Propofol exerts anti-hepatocellular carcinoma by microvesicle-mediated transfer of miR-142-3p from macrophage to cancer cells.

OBJECTIVE: We previously confirmed that propofol directly inhibited the viability, proliferation, and invasiveness of hepatocellular carcinoma cells in vitro. In this study, we investigated the mechanism underlying the anti-HCC effects of propofol. METHODS: In vivo antitumor activity was investigated in tumor-bearing mice following an intraperitoneal injection of propofol, with or without clodrolip. The co-culture system was used to verify that miR-142-3p was transported from macrophages to HCC cells. A miR-142-3p inhibitor was used to down-regulate the expression of miR-142-3p. RESULTS: Propofol drastically inhibited tumor growth in tomor-bearing mice through macrophage activation, and stimulated tumor-associated macrophages (TAMs) to secrete microvesicles (MVs), which delivered miR-142-3p to HCC cells, resulting in the inhibition of HCC cell invasion. In addition, MVs collected from the plasma of the tumor-bearing mice injected with propofol suppressed tumor growth. More importantly, down-regulation of the expression miR-142-3p reversed the effect of propofol on HCC cell migration. CONCLUSIONS: This study reveals a novel role for propofol in the inhibition of HCC through MV-mediated transfer of miR-142-3p from macrophages to cancer cells in vivo.

Probenecid protects against transient focal cerebral ischemic injury by inhibiting HMGB1 release and attenuating AQP4 expression in mice.

Stroke results in inflammation, brain edema, and neuronal death. However, effective neuroprotectants are not available. Recent studies have shown that high mobility group box-1 (HMGB1), a proinflammatory cytokine, contributes to ischemic brain injury. Aquaporin 4 (AQP4), a water channel protein, is considered to play a pivotal role in ischemia-induced brain edema. More recently, studies have shown that pannexin 1 channels are involved in cerebral ischemic injury and the cellular inflammatory response. Here, we examined whether the pannexin 1 channel inhibitor probenecid could reduce focal ischemic brain injury by inhibiting cerebral inflammation and edema. Transient focal ischemia was induced in C57BL/6J mice by middle cerebral artery occlusion (MCAO) for 1 h. Infarct volume, neurological score and cerebral water content were evaluated 48 h after MCAO. Immunostaining, western blot analysis and ELISA were used to assess the effects of probenecid on the cellular inflammatory response, HMGB1 release and AQP4 expression. Administration of probenecid reduced infarct size, decreased cerebral water content, inhibited neuronal death, and reduced inflammation in the brain 48 h after stroke. In addition, HMGB1 release from neurons was significantly diminished and serum HMGB1 levels were substantially reduced following probenecid treatment. Moreover, AQP4 protein expression was downregulated in the cortical penumbra following post-stroke treatment with probenecid. These results suggest that probenecid, a powerful pannexin 1 channel inhibitor, protects against ischemic brain injury by inhibiting cerebral inflammation and edema.

Inhibition of TAF1B impairs ribosome biosynthesis and suppresses cell proliferation in stomach adenocarcinoma through promoting c-MYC mRNA degradation.

Hyperactivation of ribosome biosynthesis (RiBi) is a hallmark of cancer, and targeting ribosome biogenesis has emerged as a potential therapeutic strategy. The depletion of TAF1B, a major component of selectivity factor 1 (SL1), disrupts the pre-initiation complex, preventing RNA polymerase I from binding ribosomal DNA and inhibiting the hyperactivation of RiBi. Here, we investigate the role of TAF1B, in regulating RiBi and proliferation in stomach adenocarcinoma (STAD). We disclosed that the overexpression of TAF1B correlates with poor prognosis in STAD, and found that knocking down TAF1B effectively inhibits STAD cell proliferation and survival in vitro and in vivo. TAF1B knockdown may also induce nucleolar stress, and promote c-MYC degradation in STAD cells. Furthermore, we demonstrate that TAF1B depletion impairs rRNA gene transcription and processing, leading to reduced ribosome biogenesis. Collectively, our findings suggest that TAF1B may serve as a potential therapeutic target for STAD and highlight the importance of RiBi in cancer progression.

Propofol induces apoptosis of hepatocellular carcinoma cells by upregulation of microRNA-199a expression.

Propofol is one of the extensively commonly used intravenous anaesthetic agents. The effects of Propofol on hepatocellular carcinoma (HCC) growth inhibition and apoptosis have been examined. The techniques used were the MTT assay, flow cytometry, real-time PCR to assess miR-199a expression, as also caspase-8 and caspase-9 activity in HepG2 cells treated with Propofol. Finally, we evaluated the effect of miR-199a on Propofol-induced anti-tumour activity using anti-miR-199a. Propofol efficiently inhibited the growth of HCC cells, but was less toxic to normal hepatic cells. It induced apoptosis and increased expression of miR-199a. Activation of caspase-8 and caspase-9 suggested that both extrinsic and intrinsic pathways are involved in Propofol-induced apoptosis. Anti-miR-199a reversed the effect of Propofol on apoptosis and activation of caspase-8 and caspase-9 in HepG2 cells. Propofol can effectively induce apoptosis of HCC cells and modulation of miR-199a possibly contributes to the anti-tumour action of Propofol. Hence, Propofol might be an effective drug for HCC.

Intrarenal resistance index for the assessment of acute renal injury in a rat liver transplantation model.

BACKGROUND: Acute kidney injury (AKI) is a common complication after liver transplantation (LT) and associated with a high mortality. The renal resistive index (RI) is used to assess early renal function impairment in critical care patients. However, limited data are available concerning changes of renal RI and the development of AKI early after reperfusion. We approached to investigate the changes of renal RI and AKI after reperfusion in a rat liver transplantation model. METHODS: Rats were randomly divided into sham group or LT group. Ten rats in each group were used for the hemodynamic study and twenty for Doppler measurements during the procedure. Ten rats were sacrificed 30 min or 2 h after the reperfusion. We harvested kidneys, serum and urine for further analysis of the renal function. RESULTS: The intrarenal RI increased significantly in the anhepatic stage and decreased significantly after the reperfusion in the LT group compared with sham group (P < 0.05). AKI was seen after the reperfusion in the LT group. No correlation was noted between the RI and renal function parameters 30 min after reperfusion. CONCLUSIONS: The intrarenal RI increased significantly during the anhepatic stage, and decreased significantly early after the reperfusion. Intrarenal RI was unable to assess renal function in a rat liver transplantation model.

Propofol inhibits the adhesion of hepatocellular carcinoma cells by upregulating microRNA-199a and downregulating MMP-9 expression.

BACKGROUND: Propofol is one of the extensively and commonly used intravenous anesthetics and has the ability to influence the proliferation, motility, and invasiveness of many cancer cells. In this study, the effects of propofol on hepatocellular carcinoma cells invasion ability were examined. METHODS: We assessed the invasion ability of HepG2 cells in vitro by determining enzyme activity and protein expression of MMP-9 using gelatin zymography assay and Western blot. The real-time PCR was used to evaluate the effect of propofol on microRNA-199a (miR-199a) expression, and miR-199a-2 precursor to evaluate whether over-expression of miR-199a can affect MMP-9 expression. Finally, the effect of miR-199a on propofol-induced anti-tumor activity using anti-miR-199a was assessed. RESULTS: Propofol significantly elevated the expression of miR-199a and inhibited the invasiveness of HepG2 cells. Propofol also efficiently decreased enzyme activity and protein expression of MMP-9. Moreover, the over-expression of miR-199a decreased MMP-9 protein level. Interestingly, the neutralization of miR-199a by anti-miR-199a antibody reversed the effect of propofol on alleviation of tumor invasiveness and inhibition of MMP-9 activity in HepG2 cells. CONCLUSION: Propofol decreases hepatocellular carcinoma cell invasiveness, which is partly due to the down-regulation of MMP-9 expression by miR-199a.

MicroRNA-155-5p inhibition alleviates irritable bowel syndrome by increasing claudin-1 and ZO-1 expression.

Background: Irritable bowel syndrome (IBS) is a common gastrointestinal disease. Emerging studies have demonstrated that microRNAs (miRNAs) are commonly dysregulated in patients with IBS, and aberrant miRNAs are implicated in IBS occurrence. Although miR-155-5p participates in inflammatory bowel disease (IBD) and intestinal barrier dysfunction, the role of miR-155-5p in IBS is unclear. Methods: In the present study, colon samples were obtained from IBS patients and IBS mice induced by trinitrobenzenesulfonic acid (TNBS), and the levels of miR-155-5p, claudin-1 (CLDN1), and zonula occludens-1 (ZO-1) were assessed using quantitative real-time polymerase chain reaction (qRT-PCR) and immunohistochemical analysis. The regulatory role of miR-155-5p in CLDN1 and ZO-1 expression was validated using dual luciferase reporter assay. Results: We found that miR-155-5p levels were upregulated in colon samples of IBS patients and mice compared with healthy subjects and normal mice, respectively. Meanwhile, the levels of CLDN1 and ZO-1 were decreased in colon samples of IBS patients and mice. Importantly, forced expression of miR-155-5p inhibited CLDN1 and ZO-1 expression. In IBS mice, intraperitoneal injection with miR-155-5p inhibitor increased CLDN1 and ZO-1 expression in intestinal mucosal epithelium, enhanced visceral response thresholds, and decreased myeloperoxidase (MPO) activity. Conclusions: In summary, these results suggested that miR-155-5p participated in the pathogenesis of IBS, at least in part by inhibiting CLDN1 and ZO-1 expression, indicating that miR-155-5p may be a potential therapeutic target for IBS.

Persistent postoperative hypotension caused by subclinical empty sella syndrome after a simple surgery: A case report.

BACKGROUND: Empty sella is an anatomical and radiological finding of the herniation of the subarachnoid space into the pituitary fossa leading to a flattened pituitary gland. Patients with empty sella may present with various symptoms, including headache due to intracranial hypertension and endocrine symptoms related to the specific pituitary hormones affected. Here, we report a female patient who developed persistent postoperative hypotension caused by subclinical empty sella syndrome after a simple surgery. CASE SUMMARY: A 47-year-old woman underwent vocal cord polypectomy under general anesthesia with endotracheal intubation. She denied any medical history, and her vital signs were normal before the surgery. Anesthesia and surgery were uneventful. However, she developed dizziness, headache and persistent hypotension in the ward. Thus, intravenous dopamine was started to maintain normal blood pressure, which improved her symptoms. However, she remained dependent on dopamine for over 24 h without any obvious anesthesia- and surgery-related complications. An endocrine etiology was then suspected, and further examination showed a high prolactin level, a low normal adrenocorticotropic hormone level and a low cortisol level. Magnetic resonance imaging of the brain revealed an empty sella. Therefore, she was diagnosed with empty sella syndrome and secondary adrenal insufficiency. Her symptoms disappeared one week later after daily glucocorticoid supplement. CONCLUSION: Endocrine etiologies such as pituitary and adrenal-related dysfunction should be considered in patients showing persistent postoperative hypotension when anesthesia- and surgery-related factors are excluded.

[Anesthetic management of Stanford type A aortic dissection operation].

OBJECTIVE: To explore the anesthetic management experiences of patients with Stanford A aortic dissection undergoing surgical treatment through moderate or deep hypothermia circulatory arrest (DHCA). METHODS: From June 2008 to December 2011, a total of 77 patients undergoing surgical treatment of Stanford A aortic dissection was recruited. RESULTS: Cardiopulmonary bypass (CPB) was established under general anesthesia in all patients. The procedures included moderate hypothermia (n = 51) and DHCA (n = 26). The total surgical duration was 152 - 600 (292 ± 91) min, CPB time 38 - 310 (128 ± 43) min and aortic cross-clamp time 31 - 169 (87 ± 26) min. The time of circulatory arrest under deep hypothermia was 20 - 113 (41 ± 19) min in 26 patients. Among 77 patients, there were 5 intraoperative and 7 postoperative fatalities. The remained 65 patients were discharged postoperatively and received a regular outpatient follow-up. None of them died or required reoperation. CONCLUSION: Surgical treatment is appropriate and efficient for the patients with Stanford A aortic dissection. During surgery, the keys of preventing neurological complications are blood volume monitoring and blood protection.

Prediction Model for Urinary Tract Infection in Pediatric Urological Surgery Patients.

Background: Urinary tract infection (UTI) is a common complication in pediatric urological surgery patients and is associated with long-term sequelae, including subsequent recurrent infections and renal scarring. In this study, we aimed to explore the risk factors for UTI in pediatric urological surgery patients and construct a predictive model for UTI. Materials and Methods: A total of 2,235 pediatric patients who underwent urological surgery at a tertiary hospital between February 2019 and January 2020 were included. A multivariate logistic regression model was applied to identify the predictive factors, and a predictive model was constructed using a receiver operating characteristic curve. A multifactorial predictive model was used to categorize the risk of UTI based on the weight of the evidence. Results: A total of 341 patients with UTI were identified, which corresponded to a prevalence of 15.26% in pediatric urological surgery patients. Multivariate analysis identified six significant risk factors for UTI, including age <12.0 months, upper urinary tract disease, not using an indwelling drainage tube, hospital stay ≥10 days, administration of two or more types of antibiotics, and stent implantation. A combination of the aforementioned factors produced an area under the curve value of 88.37% for preventing UTI in pediatric urological surgery patients. A multifactorial predictive model was created based on the combination of these factors. Conclusions: The constructed multifactorial model could predict UTI risk in pediatric urological surgery patients with a relatively high predictive value.

[Expression of aquaporin-4 during brain edema in rats with thioacetamide-induced acute encephalopathy].

OBJECTIVE: To investigate the expression of aquaporin-4 (AQP4) during brain edema in rats with thioacetamide-induced acute liver failure and encephalopathy. METHODS: The rat model of acute hepatic failure and encephalopathy was induced by intraperitoneal injection of thioacetamide (TAA) at a 24-hour interval for 2 consecutive days. Thirty-two SD rats were randomly divided into the model group (n = 24) and the control group (normal saline, n = 8). And then the model group was further divided into 3 subgroups by the timepoint of decapitation: 24 h (n = 8), 48 h (n = 8) and 60 h (n = 8). Then we observed their clinical symptoms and stages of HE, indices of liver function and ammonia, liver histology and brain water content. The expression of AQP4 protein in brain tissues was measured with Western blot and the expression of AQP4mRNA with RT-PCR (reverse transcription-polymerase chain reaction). RESULTS: Typical clinical manifestations of hepatic encephalopathy occurred in all TAA-administrated rats. The model rats showed the higher indices of ALT (alanine aminotransferase), AST (aspartate aminotransferase), TBIL (total bilirubin) and ammonia than the control rats (P < 0.05). The brain water content was significantly elevated in TAA-administrated rats compared with the control (P < 0.05). The expressions of AQP4 protein and mRNA in brain tissues significantly increased in TAA-administrated rats (P < 0.05). In addition, the expressions of AQP4 protein and mRNA were positively correlated with brain water content (r = 0.536, P < 0.01; r = 0.566, P = 0.01). CONCLUSIONS: The high expression of AQP4 in rats with TAA-induced acute liver failure and encephalopathy plays a significant role during brain edema. AQP4 is one of the molecular mechanisms for the occurrence of brain edema in hepatic encephalopathy.

Anesthetic management of lung transplantation in a patient with end-stage COVID-19 pneumonia: A case report.

RATIONALE: The COVID-19 pandemic is spreading around the world and the leading cause of death is rapidly progressive respiratory failure because of lung damage and consolidation. Lung transplantation is the last line of treatment for chronic end-stage lung diseases. There were several cases of lung transplantation reported in patients with COVID-19 pneumonia. However, anesthetic management of lung transplantation in this subpopulation is rare. We report the anesthetic and perioperative management of lung transplantation in a patient with COVID-19 pneumonia. PATIENT CONCERNS: A 70-year-old man with a 7-day history of fever was diagnosed with COVID-19 pneumonia. His throat swab was positive for COVID-19, but negative for other common viruses. Chest radiography showed multiple inflammatory foci in both lungs. By day 5, he presented respiratory distress. Computed tomography (CT) scan showed progressive deterioration of both lungs. Starting on day 7, SARS-CoV-2 RNA in bronchoalveolar lavage samples were continuously negative. However, his lung condition deteriorated. By day 17, a veno-venous extracorporeal membrane oxygenation (ECMO) was initiated. After 10 days of ECMO support, the patient's lung condition did not improve. CT scan revealed bilateral parenchymal consolidation with pulmonary fibrosis and hydrothorax. DIAGNOSIS: Irreversible lung function loss induced by COVID-19 pneumonia. INTERVENTIONS: Bilateral transplantation was performed because the patient's lung condition did not improve and CT scan revealed parenchymal consolidation with pulmonary fibrosis after 10 days of ECMO support. Thirty-six hours after the surgery, ECMO was discontinued. A percutaneous transluminal coronary angioplasty and a stent implantation were performed because of acute coronary syndrome and myocardial ischemia 4 days postoperatively. OUTCOMES: The patient remained hospitalized because of requirements for intermittent assisted ventilation via tracheostomy. LESSONS: This case further supports the consideration that lung transplantation can potentially be the successful therapy for these patients who have developed irreversible lung function lose due to COVID-19 pneumonia. However, most critical patients with COVID-19 are older individuals with various comorbidities, which present new anesthetic challenges.

Effects of low central venous pressure during preanhepatic phase on blood loss and liver and renal function in liver transplantation.

BACKGROUND: Although the low central venous pressure (LCVP) technique is used to decrease blood loss during liver resection, its efficacy and safety during transplant procedures are still debatable. Our study aimed to assess the effects of this technique and its clinical safety for recipients undergoing liver transplantation. METHODS: Eighty-six adult patients were randomly divided into a LCVP group and a control group. In the LCVP group, CVP was maintained below 5 mmHg or 40% lower than baseline during the preanhepatic phase by limiting infusion volume, manipulating the patient's posture, and administration of somatostatin and nitroglycerine. Recipients in the control group received standard care. Hemodynamics, blood loss, liver function, and renal function of the two groups were compared perioperatively. RESULTS: A lower CVP was maintained in the LCVP group during the preanhepatic phase, resulting in a significant decrease in blood loss (1922 +/- 1429 vs. 3111 +/- 1833 ml, P < 0.05) and transfusion volume (1200 +/- 800 vs. 2400 +/- 1200 ml, P < 0.05) intraoperatively. Compared with the control group, the LCVP group had a significantly lower mean arterial pressure at 2 h after the start of the operation (74 +/- 11 vs. 84 +/- 14 mmHg, P < 0.05), a lower lactate value at the end of the operation (5.9 +/- 3.0 vs. 7.2 +/- 3.0 mmol/l, P < 0.05), and a better preservation of liver function after the declamping of the portal vein. There were no significant differences in perioperative renal function and postoperative complications between the groups. CONCLUSIONS: The LCVP technique during the preanhepatic phase reduced intraoperative blood loss, protected liver function, and had no detrimental effects on renal function in LT.

[Development and clinical evaluation of an anesthesia information management system].

OBJECTIVE: To study the design, implementation and clinical evaluation of an anesthesia information management system. METHODS: To record, process and store peri-operative patient data automatically, all kinds of bedside monitoring equipments are connected into the system based on information integrating technology; after a statistical analysis of those patient data by data mining technology, patient status can be evaluated automatically based on risk prediction standard and decision support system, and then anesthetist could perform reasonable and safe clinical processes; with clinical processes electronically recorded, standard record tables could be generated, and clinical workflow is optimized, as well. RESULTS: With the system, kinds of patient data could be collected, stored, analyzed and archived, kinds of anesthesia documents could be generated, and patient status could be evaluated to support clinic decision. CONCLUSION: The anesthesia information management system is useful for improving anesthesia quality, decreasing risk of patient and clinician, and aiding to provide clinical proof.

[The effects of ketamine pretreated on cerebral edema and AQP4 expression after transient focal cerebral ischemia/reperfusion in rats].

OBJECTIVE: To investigate the effects of ketamine pretreatment on cerebral edema following brain ischemia reperfusion injury in rats and assess the involvement of Aquaporin 4 (AQP4) expression. METHODS: Sixty-two healthy male Sprague-Dawley rats weighing 220 -250 g were randomly divided into 3 groups: sham operation group (group Sham, n = 18); saline group (group Vehicle, n = 22); ketamine pretreatment group (group Ketamine, n = 22) . The transient focal ischemia/reperfusion was induced by introducing a silicone-coated monofilament nylon suture from the right external carotid artery into the origin of the middle cerebral artery, removing it after 90 min. In group Ketamine, the rats were exposed to ketamine (5%, 1 mg x kg(-1) x min(-1)) for 30 min before suffered from cerebral ischemia. Similarly; in group Vehicle and group Sham, the animals received saline vehicle at the same time and infusion rate. After the neurologic exams were assessed at 24 h of reperfusion, the rats were sacrificed after anesthetized, and the brains were quickly removed. To estimate cerebral edema, the wet-dry ratio was measured. Western-blot was used to detect the expression of AQP4 in the border of the infarct region. RESULTS: The neurologic function deficit was significantly serious in group Vehicle and group Ketamine compared to group Sham (P < 0.01). Ketamine pretreatment tended to improve neurologic outcome, but there was no statistical significance. The wet-dry weight ratio and AQP4 expression increased significantly in group Vehicle and group Ketamine III than those in group Sham (P < 0.01). Compared with saline vehicle, ketamine pretreatment did not decreased the wet-dry weight ratio significantly. AQP4 expression in group Ketamine was not significantly different from group Vehicle. CONCLUSION: Ketamine pretreatment did not seem to improve the neurologic deficit outcome and attenuate edema, which was involved in no change of AQP4 expression.