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Visual endotracheal intubation technique was applied in the endotracheal intubation teaching for standardized resident training as a routine teaching appliance.The residents were divided into two groups,the anesthetic speciality group and the non-anesthetic speciality group.According to the different teaching targets,teaching periods and basic abilities,the differentiated teaching Settings were built and the different teaching schemes,evaluation index and teachers were applied for the two groups respectively for fulfilling the advantages of visual laryngoscope.Until now,more than a hundred residents were educated with the endotracheal intubation,and the teaching efficiency and quality were significantly improved,which also reduced the incidence of the complications related to endotracheal intubation.
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BACKGROUND: Preliminary findings have shown that radiation can impair the mouse blood-brain barrier, which is a cause of secondary brain injury. However, there is little information concerning radiation effects on fibrinogen in plasma and fibrinogen deposition in brain tissue. OBJECTIVE: To establish the mouse model of radiation-induced brain injury, to observe the changes of fibrinogen in plasma and brain tissue, and to further understand the mechanism of radiation-induced brain injury. METHODS: Fifty Kunming mice were randomly divided into irradiation and control groups (n=25 per group). Irradiation group rats were irradiated by 60Co γ, 10 Gy, once every other day, and the total dose was 30 Gy. Learning and memory abilities were tested by Morris Water Maze before and after irradiation, the content of fibrinogen in plasma was detected, then fibrinogen in CA3 region of the hippocampus was determined by immunohistochemistry, and the ultrastructural changes of the blood-brain barrier were investigated under transmission electron microscope . RESULTS AND CONCLUSION: Compared with the control group, the swimming time and distance of the irradiated mice were reduced in the target quadrant (P＜ 0.05), while fibrinogen was increased in plasma (P＜ 0.001) and deposited in hippocampal CA3 region. The translucent zone around the basement membrane of blood-brain barrier in the irradiation group was observed under electron microscope. These results suggest that irradiation can increase fibrinogen in plasma and brain, and the fibrinogen deposited in the brain may be the cause of secondary brain injury.
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Objective To evaluate the effect of ulinastatin on the activity of Janus kinase 2/signaling transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway during focal cerebral ischemia-reperfusion (I/R) in rats.Methods Forty-eight clean-grade healthy adult male Sprague-Dawley rats,aged 6-8 weeks,weighing 230-280 g,were divided into 3 groups (n=16 each) using a random number table:sham operation group (S group),cerebral I/R group (I/R group) and ulinastatin group (U group).Focal cerebral I/R was induced by occlusion of the middle cerebral artery for 2 h followed by reperfusion.Ulinastatin 100 000 U/kg was injected via the femoral vein immediately after beginning of cerebral ischemia in group U.Neurologic deficit was evaluated and scored (NDS) at 24 h of reperfusion.The rats were then sacrificed and brains were removed for measurement of the cerebral infarct size (by TTC staining) and for determination of the expression of total JAK2,total STAT3 and phosphorylated JAK2 (p-JAK2) and phosphorylated STAT3 (p-STAT3) in the cerebral cortex.Results Compared with S group,NDS and cerebral infarct size were significantly increased,and the expression of p-STAT3 and p-JAK2 in the cerebral cortex was up-regulated in I/R group and U group (P＜0.05).Compared with I/R group,NDS and cerebral infarct size were significantly decreased,and the expression of p-STAT3 and p-JAK2 in the cerebral cortex was down-regulated in U group (P＜0.05).There was no significant difference in the expression of total JAK2 and total STAT3 in the cerebral cortex between three groups (P＞0.05).Conclusion Ulinastatin can inhibit the activity of JAK2/STAT3 signaling pathway during cerebral I/R,which may be involved in the brain protective mechanism of ulinastatin in rats.
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Objective To evaluate the effect of dexmedetomidine on the expression of nerve growth factor (NGF) in isolated hippocampal neurons of fetal rats incubated with propofol.Methods Hippocampal neurons derived from the fetal rats of pregnant Sprague-Dawley rats at 5-13 days of gestation were primarily cultured for 7 days,and were inoculated in the culture plate at a density of 5×105 cells/ml.The neurons were randomly divided into 3 groups (n =15 each) using a random number table:control group (group C),propofol group (group P),and dexmedetomidine + propofol group (group DP).In group P,propofol with the final concentration of 100 μmol/L was added to the culture medium,and the cells were incubated for 3 h.In group DP,dexmedetomidine with the final concentration of 1 μmol/L was added to the culture medium,the cells were incubated for 30 min,and then propofol with the final concentration of 100 μmol/L was added to the culture medium,and the cells were incubated for 3 h.The viability of hippocampal neurons was assessed by CCK-8 assay.NGF mRNA expression was detected by real-time reverse transcriptase polymerase chain reaction.NGF protein expression was detected by Western blot.Results Compared with group C,the viability of hippocampal neurons was significantly decreased,and the expression of NGF protein and mRNA was down-regulated in group P (P＜0.05).Compared with group P,the viability of hippocampal neurons was significantly increased,and the expression of NGF protein and mRNA was up-regulated in group DP (P＜0.05).Conclusion Dexmedetomidine improve propofol-induced decrease in the viability of isolated hippocampal neurons of fetal rats through up-regulating the expression of NGF.
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Objective To evaluate the effect of intrathecal dexmedetomidine on the expression of G-protein-coupled inwardly rectifying K+ channel 1 (GIRK1) in dorsal root ganglia of rats with diabetic neuropathic pain (DNP).Methods A total of 144 healthy adult male SPF Sprague-Dawley rats,aged 8-10 weeks,weighing 200-220 g,were randomly divided into 4 groups (n =36 each) using a random number table:control group (group C),dexmedetomidine group (group D),group DNP,and DNP + dexmedetomidine group (group DD).DNP model was established by single intraperitoneal injection of streptozotocin (STZ) 60 mg/kg.In D and DD groups,dexmedetomidine 1.5 μg/kg was injected intrathecally at 14 days after citrate buffer or STZ injection,while the equal volume of normal saline was given in group C.The mechanical pain threshold was measured before STZ injection (T0),at 14 days after STZ injection (T1),and at 2,4 and 6 h after intrathecal injection (T:2-4).After measurement of the mechanical pain threshold at T2-4,the rats were sacrificed,and the dorsal root ganglia of the lumbar segment (L4-6) were removed for determination of the number of GIRK1 positive cells and expression of GIRK1 protein by immunofluorescence and Western blot,respectively.Results Compared with group DNP,the mechanical pain threshold was significantly increased,the number of GIRK1 positive cells in dorsal root ganglia was significantly increased,and the expression of GIRK1 was significantly up-regulated at T2-4 in group DD (P＜0.05).Compared with group D,the number of GIRK1 positive cells in dorsal root ganglia was significantly increased,and the expression of GIRK1 was significantly up-regulated at T2-4 in group DD (P＜0.05).Compared with group C,the mechanical pain threshold was significantly decreased at T1-4 in group DNP (P＜0.05).Conclusion Intrathecal dexmedetomidine attenuates DNP through up-regulating the expression of GIRK1 in dorsal root ganglia of rats.
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Objective To investigate the protection effect of dexmedetomidine against H2O2 injury in Human renal tubular epithelial cells(HK-2 cells). Methods HK-2 cells cultured in vitro were randomly divided into four groups(n = 24): control group, dexmedetomidine pretreatment group, H2O2 injury group, H2O2 injury +dexmedetomidine pretreatment group. Cell viabilities were measured by MTS assay, cell apoptosis were detected using flow cytometry, and expression of HIF-1α protein was quantified by western blot. HK-2 cells were divided into 8 groups by combining with three treatment factors such as PI3K inhibitor LY294002, dexmedetomidine and H2O2 injury. MTS assay was used to detect cell viability and western blot was used to quantify protein expression of HIF-1α,Bcl-2 and Bax after treatment in each group. Results Dexmedetomidine significantly increased the level of HIF-1α、 Bcl-2 in HK-2 cells after H2O2 injury, thus improved viabilities and reduced apotosis of cells. Moreover, effect on H2O2 injury cells of Dexmedetomidine was reversed by PI3K inhibitor LY294002. Conclusion Dexmedetomidine could protect against H2O2 injury by up-regulating HIF-1α expression through activating PI3K/Akt/mTOR signaling pathway in HK-2 cells.
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The aim was to investigate the effects of two different ventilatory strategies: Pressure-controlled ventilation [PCV] versus volume-controlled ventilation [VCV] in elderly patients with poor pulmonary function during one-lung ventilation [OLV]. The patients were enrolled into the study having poor pulmonary function [forced expiratory volume in 1 s <1.5 L] and undergoing radical resection of pulmonary carcinoma requiring at least 2 h of OLV. Patients were respectively allocated to VCV group and PCV group. The intraoperative data, arterial, and mixed venous blood gases were obtained at baseline, 20, 40, 60, 80, 100 and 120 min after OLV and end of surgery. The postoperative data had been recorded and arterial gas measurements were performed at 6, 12 and 24 h after surgery in Intensive Care Unit. Comparison of the VCV group and PCV group, PaO[2] and P[A-a]O[2] were higher and dead space to tidal volume was lower in the PCV group [P < 0.05] after the point of OLV +60, Ppeak was higher in the VCV group [P < 0.05]. There were significant advantages in PCV groups with regard to the PaO[2] of three points in postoperation, the duration of postoperative ventilation duration, intensive care duration of stay and the days stay in hospital after surgery. The use of PCV compared with VCV during OLV in elderly patients with poor pulmonary function has significant advantages of intraoperative and postoperative oxygenation and it might be a factor, which can beneficial to postoperative recovery
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Objective To evaluate the effect of ulinastatin on the expression of aquaporin-4 (AQP4) during focal cerebral ischemia-reperfusion (I/R) in rats.Methods One hundred and thirty-five male adult SpragueDawley rats,weighing 230-280 g,were randomly divided into 3 groups (n =45 each):sham operation group (S group),I/R group and ulinastatin group (group U).The rats were anesthetized with intraperitoneal 10％ chloral hydrate 3.5 ml/kg.Focal cerebral ischemia was induced by 2 h middle cerebral artery occlusion followed by 24 repeffusion.In U group,ulinastatin 100000 U/kg was injected immediately after beginning of reperfusion,while the equal volume of normal saline was injected in S and I/R groups.The rats were sacrificed at 6,24 and 48 h of repeffusion and brains were removed for determination of infract volume (by TTC),brain water content and expression of AQP4 (by immunohistochemistry) in brain tissues.Results Compared with S group,the infarct volume and brain water content were significantly increased,and the expression of AQP4 was up-regulated at each time point in I/R and U groups (P ＜ 0.05).Compared with I/R group,the infarct volume and brain water content were significantly decreased,and the expression of AQP4 was down-regulated at each time point in U group (P ＜0.05).Conclusion The mechanism by which ulinastatin mitigates focal cerebral I/R injury is related to down-regulation of AQP4 expression in brain tissues.
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Objective To screen for new methylation association genes in HL-60 to reveal the pathogenesis of leukemia, and provide important theoretical and scientific basis for the prevention and cure of leukemia. Methods Two-dimensional fluorescence difference gel electrophoresis (F-2D-DIGE) was performed to separate the total proteins from acute myelogenous leukemia (AML) cell line HL-60 cells with or without 5-aza-2-deoxycytidine (5-aza-2-dC) treatment. Imaging software Decyder 6.5 and PDQuest were used to detect the differential expression protein spots, and matrix-assisted laser desorption/ionizaion time-of-flight mas spectrometer (MALDI-TOF MS) was adopted to identify the differential expression proteins. Results F-2D-DIGE maps of 5-aza-2-dC-untreated HL-60 and-treated HL-60 cells were established. A total of 53 differential protein spots were detected, and 35 differential proteins were successfully identified. Of the identified proteins, 32 proteins were up-regulated, and 3 proteins were down-regulated in HL-60 cells after 5-aza-2-dC treatment.Conclusion Thirty-five differential proteins may be associated with methylation in HL-60 cell line, which provides the important clues for epigenetic study of leukemia.
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The aging process of human colonic epithelium involves a slow decline in physiological vigor and an increasing susceptibility to age-related diseases, especially, colon cancer, but the molecular mechanisms of the aging and susceptibility of aged colonic epithelium to carcinogenesis is still unclear. Identification of aging related proteins in colonic epithelium will help to reveal the molecular mechanisms of colonic epithelial aging and age-related colonic diseases. Therefore, the total proteins of human normal colonic epithelial tissues from 10 young and 10 old men were separated by two-dimensional gel electrophoresis(2-DE), respectively. PDQuest software was applied to analyze 2-DE images, the differentially expressed protein spots of colonic epithelium between young and old groups were identified by matrix-assisted laser desorption/ionization time of flight mass spectrometry(MALDI-TOF-MS), and the expression levels of partial identified proteins were determined by real-time quantitative PCR and immunohistochemistry. Well-resolved, reproducible 2-DE maps of human colonic epithelial tissues from young and old men were established, 17 aging related proteins were identified by MALDI-TOF-MS, and the differential expression levels of partial identified proteins were confirmed by real-time quantitative PCR and immunohistochemistry. The results indicate that injury of mitochondrial function and decline of antioxidant capability are important reasons for the aging of human colonic epithelium, and four differential proteins (guanine nucleotide-binding protein beta subunit-like protein, stress-70 protein, 40 S ribosomal protein SA and chloride intracellular channel protein1) may be involved in susceptibility of aged colonic epithelium to carcinogenesis.
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AIM: To investigate the ocular complication after radiation therapy for nasopharyngeal carcinoma(NPC).METHODS: The authors performed a previous study on keratopathy in 213 NPC patients who received first stage radiation and had at least 10 months of follow-up. These patients were categorized into three groups depending on NPC clinic stages. Rates and proportions of keratopathy occurring in these groups were compared and analyzed with Chi-square Test and Spearman rank correlation coefficient.RESULTS: Radiation keratopathy developed in 19 patients, about 8.9% (19/213). The latency value was 3 to 30days. The effect of NPC clinic stages and radiation did on the development of keratopathy was not statistically significant (P＞0.05).CONCLUSION: The NPC clinic stages and radiation doses plays few effects on the development of keratopathy. It may play a key role that corneal nerves damage induced ocular surface diseases. It can not be excluded that individuals have different sensitivities to radiation.
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Objective To examine the changes in calcium currents in isolated dorsal root ganglion (DRG) neurons in rats with neuropathic pain.Methods The neuropathic pain model was established by modified spinal nerve ligation (SNL) 2 to 4 weeks before electrophysiologic recording. The rat DRG neurons were enzymatically dissociated. Whole -cell patch clamp technique was used to record Ca2+ current.Results In large DRG neurons the mean peak value of electric current-voltage ( Ⅰ - Ⅴ) curve was decreased significantly from ( - 105?13) pA/ pF in control group ( n = 9) to ( - 66?10) pA/pF in neuropathic pain group ( n = 11) (P 0.05) . Conclusion In neuropathic rat Ca2+ currents in large DRG neurons are decreased and the voltage dependence of the fast component of inactivation is shifted to more depolarized potentials. These changes may contribute to hyperalgesia and allodynia of neuropathic pain.
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Objective To investigate the frequency of ocular complication and the quality of patient's life after radiation therapy in nasopharyngeal carcinoma ( NPC ) . Methods 254 NPC patients who initially received radiation were followed and analysed. Visual acuity, automational visual field, slit-lamp microscopic findings, pattern visual evoked potential ( P-VEP ) and fundal findings were determined before, during and after radiation therapy. The severity of retinal impairment was assessed according to the international criteria on late tissue effects. Results The radiation dose was more than 70 Gy in 241 (94.9%)NPC patients, giving a radiation retinopathy incidence of 8. 7 % (22) patients after a mean of 46. 8 ? 14. 4 months. After being diagnosed as radiation retinopathy, 16 patients received combined-modality therapy of the modern medicine and Chinese traditional medicine. The disease condition was controlled in 56% (9) patients but progressed into optic neuropathy in 7 patients, 3 of whom developed radiation encephalopathy in 14 to 20 months after onset of retinopathy. The morbidity of radiation retinopathy was not associated with the patient' s age, but was related to the radiation dose. The retinopathy rate was as high as 13.6% in the 75-79 Gy group, which is significantly higher than 5.6% in the 70-74 Gy group ( P