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Objective:To discuss the feasibility of offering specialized courses of critical care medicine in undergraduate clinical medicine education, so as to alleviate the shortage of critical care medicine staffs and lay a foundation for improving the success rate for the treatment of critical cases.Methods:The undergraduates majoring in clinical medicine from 2008 to 2011 in Guizhou Medical University (the former Guiyang Medical College) were enrolled. After they had been enrolled in the undergraduate education for 3 years and were ready for Grade four, which meant basic medicine teaching had been completed and clinical medicine teaching was about to start, they were introduced and preached to each discipline, including critical care medicine. The undergraduates were free to choose professional direction of clinical training in Grade four. Students majoring in clinical medicine from 2012 to 2014 were free to choose their major direction when they entered the school.Results:From September 2011 to July 2019, the university had cultivated 246 undergraduates majoring in clinical critical care medicine from 2008 to 2014, and the critical care medicine professional team of affiliated hospital had undertaken 540 teaching hours. By July 2019, all students had graduated on time, with an employment rate of 100%. Forty students took postgraduate programs in our school and other schools, accounting for 16.3%.Conclusions:Professional education of critical care medicine in the undergraduate course of clinical medicine can mobilize students' interest in learning and subjective initiative, which is conducive to career selection. During the clinical training, the students can identify and timely cure critical care cases in the early stage, and partly alleviate the current shortage of critical care medical staffs.
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Objective To investigate the effects of hydrogen-rich water (HRW) on brain edema and the expression of aquaporin 4 (AQP4) in brain tissue of rats after acute traumatic brain injury (TBI) and explor the mechanism of its action. Methods Ninety male adult Sprague-Dawley (SD) rats were randomly divided into three groups: Sham group, TBI model group (TBI group) and HRW intervention group (HRW group), each group n = 30 rats. The TBI rat models were replicated by craniocerebral collision, while the Sham group rats underwent only craniotomy without collision and the cranial opening was closed by suturing and bone wax. After successful modeling, in HRW group the rats received intraperitoneal injection of HRW 5 mL/kg, and in the TBI group and Sham group, equal amount of 5 mL/kg 0.9% normal saline was given by the same method, once a day for 5 days in all the groups. The neurological severity scores (NSS) and brain water contents were detected at postoperative 6, 12, 24, 48 hours and 5 days in the three groups;the cerebral cortex expression levels of AQP4 mRNA, positive expression levels of AQP4, the cerebral cortex AQP4 protein expression, protein kinase C (PKC) activity were detected in each group. Results ① The NSS of each time point in Sham group was 0; in TBI group, the rats levels of NSS and brain water contents showed a tendency of firstly rising and then decreasing, and after postoperative 24 hours, the levels reached the peak values and then gradually decreased; in HRW group, the levels of NSS and brain water contents were reduced significantly and at postoperative 24 hours when compared with those in TBI group, the levels of decreasing amplitude in HRW group were more significant [NSS score: 5.50±1.87 vs. 10.50±2.42, brain water content: (78.78±0.65)% vs. (79.98±0.61)% , all P ＜ 0.05].② The AQP4 mRNA expression levels of sham group at all time points were 1; compared with the Sham group, the AQP4 mRNA levels of TBI group and HRW group at the time points showed a tendency of firstly decreasing and then rising and reaching the valley level at 24 hours (2-ΔΔCt: 0.33±0.06, 0.36±0.12 vs. 1, both P ＞ 0.05). ③ The immunohistochemistry detection showed that the brain AQP4 mainly expressed in astrocytes in Sham group at various time points. However, in TBI group, the positive expression of AQP4 in astrocytes in injury area at each time point was decreased, at postoperative 24 hours being the most significant; the positive expression of AQP4 in HRW group was significantly higher than that in the TBI group at each time point and since postoperative 12 hours the statistical significant difference appeared in the comparison between the two groups [Absorbance (A) value: 0.206±0.010 vs. 0.170±0.014, P ＜ 0.05]. ④ The expressions of AQP4 protein at various time points were significantly lower in TBI group compared with those of Sham group, and reached the minimum at postoperative 24 hours (gray value: 0.282±0.100 vs. 1.281±0.115, P ＜ 0.05); but in HRW group, the expressions of AQP4 protein at various time points showed significantly higher than those of TBI group, and since postoperative 12 hours the statistical significant difference occurred (gray value:0.681±0.096 vs. 0.420±0.090, P ＜ 0.05). ⑤ The activity of PKC in TBI group at each time point was significantly decreased compared with that in Sham group, but it was significantly increased in HRW group at each time point and reached the maximum at postoperative 24 hours (A value: 2.67±0.52 vs. 1.51±0.42, P ＜ 0.05). ⑥ Correlation analysis:there was an obvious negative correlation between the brain activity of PKC and brain water content (r2= 0.209, P ＜ 0.001);but there was a significant positive correlation between the activity of PKC and the expression of AQP4 protein (r2= 0.406, P ＜0.001). Conclusion HRW can improve the brain edema in rats following TBI, and the mechanism may be associated with the up-regulation of expression of AQP4 protein and PKC activity in brain tissue.
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Objective To observe the effect of hydrogen-rich water on the CD34 expression and angiogenesis in lesion boundary brain tissue of rats with traumatic brain injury (TBI).Methods A total of 54 adult male SpragueDawley (SD) rats were divided into three groups by random number table:namely sham-operated group (sham group),trauma group (TBI group),and trauma + hydrogen-rich water group (TBI+HW group),the rats in each group were subdivided into 1,3 and 7 days subgroups according to the time points after trauma,with 6 rats in each subgroup.The TBI model was reproduced by using a modified Feency method for free fall impact,and the rats in sham group were not given brain impact after craniotomy.The rats in TBI+HW group were given intraperitoneal injection of hydrogen-rich water (5 mL/kg) after TBI model reproduction,and then once a day until being sacrificed,and the rats in sham group and TBI group were given the same amount of normal saline.The neurological severity scores (NSS) for neurologic deficits were calculated at corresponding time points,and then the rats were sacrificed for brain tissue at 3 mm around lesion boundary.After hematoxylin-eosin (HE) staining,the pathological changes in lesion boundary brain tissue were observed under light microscope.The expression of CD34+ cells was observed by immunohistochemical analysis,which markers were used to count the newborn blood capillary sprouts around the traumatic brain tissue.The protein expression of CD34was determined by Western Blot.Results NSS scores at all time points in sham group were 0.NSS scores in TBI and TBI+HW groups showed a decreased tendency with time prolongation after TBI,which showed more significant in TBI+HW group,NSS scores at 3 days and 7 days were significantly lower than those of TBI group (3 day:8.67 ± 0.52 vs.11.56 ± 1.94,7 days:7.33±0.52 vs.8.17±0.98,both P ＜ 0.05).Under light microscope,the brain tissue of rats in sham group was normal.After injury,pathological changes in lesion boundary brain tissue in TBI group were characterized by obvious hemorrhagic necrosis,severe brain edema,a large number of degeneration and necrosis of nerve cells and inflammatory cell infiltration,and the pathological changes were more obvious at 3 days.The edema area in TBI+HW group was slightly smaller than that of TBI group,and the surrounding edema was slightly reduced.It was shown by immunohistochemistry that only a very small number of neoformative capillaries were found in sham group.The number of neoformative capillaries in lesion boundary brain tissue was gradually increased with time prolongation in TBI group.The number of neoformative capillaries in TBI+HW group was more significantly,which was significantly higher than that of TBI group at 3 days and 7 days after injury (cells/HP:10.59 ± 1.88 vs.8.61 ± 1.22 at 3 days,23.20 ± 3.16 vs.17.01 ± 2.64 at 7 days,both P ＜ 0.05).It was shown by Western Blot that the expression of CD34 protein at all time points in TBI group was significantly increased as compared with that of sham group.The expression of CD34 protein at 1 day and 3 days in TBI+HW group was slightly increased as compared with that of TBI group without significant difference,but it was significantly up-regulated at 7 days after injury,which was significantly higher than that of TBI group (gray value:1.36 ± 0.36 vs.0.74±0.08,P ＜ 0.05).Conclusion Hydrogen-rich water promote CD34+ cells home to the site of injured tissue in rats with TBI,is involved in angiogenesis,and improve clinical outcomes during brain functional recovery.
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Objective To investigate the effect of hydrogen-rich water on cerebral edema and aquaporin 1 (AQP1) expression in rats with traumatic brain injury (TBI).Methods Ninety male Sprague-Dawley (SD) rats were randomly divided into sham operation group,TBI model group,hydrogen-rich water treatment group (H group),with 30 rats in each group.TBI model was reproduced by weight dropping method.The skulls of rats in sham operation group underwent only craniotomy without direct hit and with bone wax sealed suture.5 mL/kg of hydrogen-rich water injection was given intraperitoneally after model reproduction in H group,and equal amount of normal saline was given in sham and TBI groups,once a day for both groups for 5 days.Six rats from each group were sacrificed at 6,12,24,48 hours and 5 days after evaluating neurological severity scores (NSS).The cerebral cortex was harvested,and the pathological changes in morphology of brain tissue were observed with light microscope.The positive expression of AQP1 in cerebral cortex was observed with immunohistochemistry by light microscopy,the AQP1 mRNA expression in cerebral cortex was determined by real-time fluorescent quantization reverse transcription-polymerase chain reaction (RT-PCR),and the AQP1 protein expression in cerebral cortex was determined by Western Blot.Results ① All rats in sham operation group had a NSS of zero at each time point.NSS of TBI group was obviously raised with time prolongation,and peaked at 24 hours followed by a lower tendency,while the score in H group was significantly lower than that of TBI group,and the difference was the most obvious at 24 hours as compared with TBI group (9.83 ± 2.78 vs.13.50± 2.42,P ＜ 0.05).② It was shown by light microscope that in the TBI group there were pathological changes in cerebral cortex,including obvious irregular arrangement of nerve cells,cerebral edema,obvious bleeding,especially at 24 hours,then the cerebral edema became vanished gradually;and the positive expression of AQP1 in the pia mater at all the time points in the TBI group was significantly increased,and it was most obvious at 24 hours.Compared with TBI group,the pathological changes at time points of 12 hours to 5 days in H group was significantly lessened,and the positive expression of AQP1 in the cerebral pia mater was reduced obviously.③ Compared with sham operation group,the mRNA and protein expressions of AQP1 in cerebral cortex in TBI group were significantly elevated,peaked at 24 hours [AQP1 mRNA (2-△△Ct):7.50±0.26 vs.1,AQP1 protein (gray value):1.986±0.110 vs.0.336±0.034,both P ＜ 0.05],then they gradually declined.The mRNA and protein expressions of AQP1 in cerebral cortex were significantly decreased after hydrogen-rich water treatment [24-hour AQP1 mRNA (2-△△Ct):5.40±0.21 vs.7.50±0.26,24-hour AQP1 protein (gray value):1.246±0.137 vs.1.986±0.110,both P ＜ 0.05].Conclusions The up-regulation of AQP1 mRNA and protein in ratst cerebral cortex after TBI perhaps participates in edema formation which might be involved in the pathophysiology of cerebral edema in TBI.Early treatment with an intraperitoneally injection of hydrogen-rich water is capable of attenuating the extent of TBI-induced up-regulation of AQP1 mRNA and protein,alleviating cerebral edema,and achieving its protective effects.
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Objective To investigate the effects of hydrogen rich water on the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and oxidative stress in rats with traumatic brain injury (TBI).Methods Ninety healthy male Sprague-Dawley (SD) rats were randomly divided into sham operation group, TBI group and hydrogen rich water treatment group (HW group), with 30 rats in each group.TBI model was reproduced by the modified Feeney weight dropping method.The skulls of rats in sham operation group underwent only craniotomy without direct hit.The rats in HW group received brain injury by hitting after craniotomy, followed by injection of hydrogen rich water (5 mL/kg) intraperitoneally once a day for 5 days after successful reproduction of the model.The rats in sham operation group and TBI group were given an equal amount of normal saline in same manner.Six rats from each group were sacrificed at 6, 12, 24, 48 hours and 5 days after evaluating neurological severity scores (NSS).The brain tissue in injured ipsilateral cortex was harvested.The activity of catalase (CAT), glutathione peroxidase (GSH-Px), and content of malondialdehyde (MDA) were determined by spectrophotometry.The expressions of mRNA and nucleoprotein of Nrf2 were determined by quantitative real-time polymerase chain reaction (RT-qPCR) and Western Blot.The pathological changes were observed with microscopy after hematoxylin and eosin (HE) staining.Results ① NSS score:compared with TBI group, NSS in HW group at 12, 24, 48 hours and 5 days were significantly decreased (12 hours: 9.83±2.32 vs.13.17±2.71, 24 hours: 9.83±2.79 vs.13.50±2.43, 48 hours: 7.50±2.07 vs.11.83±2.14, 5 days:5.50 ± 1.87 vs.10.50 ± 2.43, all P ＜ 0.05).② Compared with sham operation group, the activity of GSH-Px and CAT in TBI group were markedly declined after operation, while the MDA content was elevated significantly, especially at 24 hours [CAT (kU/g): 1.080±0.312 vs.3.571 ±0.758, GSH-Px (kU/g): 9.195±3.173 vs.32.385± 10.619, MDA (μmol/g): 12.282±2.896 vs.4.349± 1.511, all P ＜ 0.01].Compared with TBI group, the parameters in HW group were improved, and they were similar as sham operation group.③ RT-qPCR: no significant difference was found in the expression of Nrf2 mRNA at each time point in three groups.④ Western Blot: the expression of Nrf2 nucleoprotein (gray value) in TBI group was apparently higher than that in sham operation group, and peaked at 24 hours (0.703 ± 0.262 vs.0.238 ± 0.120, P ＜ 0.05), and the expression in HW group was obviously higher than that in TBI group, especially at 24 hours (1.110 ± 0.372 vs.0.703 ± 0.262, P ＜ 0.05).⑤ HE staining: the brain structure in sham operation group was found to be intact.However, there were different degrees of pathological changes at each time in TBI group, especially at 24 hours.The pathological damage of brain tissue in HW group was significantly milder.Conclusions Hydrogen rich water can up-regulate the expression of Nrf2, and reduce oxidative damage of traumatic brain injury in rats.Nrf2 can up-regulate the expression of its downstream antioxidant enzymes, which may be the mechanism of the upregulation expression of Nrf2 in the study.
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OBJECTIVE To investigate the vicissitudes of resistance to imipenem in Gram-negative bacilli isolated from clinical specimens.METHODS Gram-negative bacilli were isolated from various clinical specimens in our hosptial from Jan 2004 to Jan 2008.The identification and antimicrobiol susceptiblity test was determined by VITEK-AMS full automated microbiology analyzer.RESULTS A total of 6983 strains of Gram-negative bacilli were isolated,including 92 species and 2986 isolates of Enterobacteriaceae and 3961 isolates of non-fermenters,accounted for 42.8% and 56.7%,respectively.The resistant rate of Enterobacteriaceae to imipenem was lower than 1.0%.The resistant rates of Stenotrophomonas maltophilia,Burkholderia cepacia,Chryseobacterium meningosepticum,Pseudomonas aeruginosaand Acinetobacter baumannii to imipenem were 98.4%,97.0%,98.2%,70.1% and 47.5%,respectively.CONCLUSIONS Non-fermenters are predominant pathogens.Imipenem has high antimicrobial activity to Enterobacteriaceae in invro,but not to non-fermenters.The resistant rates of P.aeruginosa and A.baumannii to imipenem are increasing gradually.
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OBJECTIVE To study the distribution and antimicrobial resistance of Acinetobacter baumannii infection in our hospital.METHODS Five hundred and sixty-nine strains of A.baumannii isolated from patients with infection from Jan 2001 to Dec 2005 were collected and antimicrobial susceptibility tests were performed.RESULTS Two hundred and seventy-five strains(48.3%) of A.baumannii were from intensive care unit(ICU).Four hundred and five strains(71.2%) of A.baumannii were examined from sputum.A.baumannii had various drug resistances to 12 antibiotics,which were monitored and proved tending to strengthen.The resistance rate in the ICU was distinctly higher than the others with significant difference(P