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Sepsis is an inflammatory response syndrome caused by systemic immune disorders caused by infection.Platelets play an important role in the development of sepsis.Platelets can react with pathogenic microorganisms through adhesion, aggregation, activation, threshing, and have achieved the role of protecting in the body.At the same time, during sepsis, platelets can also interact with immune cells such as neutrophils and participate in formation of microthrombi and inflammation.Therefore, platelets have an antimicrobial effect and cooperate with other innate immune cells to form a complex intravascular immune defense system to prevent the spread of bacteria.However, if the internal immune function mediated by it is dysregulated, the host cells and tissues may be seriously collaterally damaged, resulting in sepsis-related organ dysfunction.This article reviewed the research progress of platelet immune mechanism and organ dysfunction in sepsis.
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Objective To analyse clinical features of dead children in pediatric intensive care unit(PICU) of Children's Hospital of Chongqing Medical University from 2005 to 2014.Methods Clinical data of 917 dead cases in PICU from January 2005 to December 2014 in this hospital were collected,then distribution characteristics of age,length of hospital stay,time of dead and transfer department were analysed.The death cause analysis was conducted as well.Results According to systematic classification of disease,the top 10 leading causes of death for 917 dead cases in PICU from 2005 to 2014 in this hospital were congenital deformity,infectious disease,respiratory disease,injury and poisoning,digestive system disease,tumor,symptoms,signs and abnormal clinical and laboratory findings not elsewhere classified,circulation system disease,nervous system disease,blood system disease.Compared with 2005-2014,the ratio of dead cases due to infectious diseases to the total cases was declined,while that due to non-infectious diseases was increased,there was statistically significant difference (x2 =26.29,P =0.00).Whereas,the ranks of septicopyemia and hand-foot-mouth disease in the rank order of death causes both were increased.Condusion Congenital deformity is the first cause of death in PICU of this hospital.The key to cutting children's mortality is to reduce newborn with congenital deformity.
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Objective To explore medical equipment allocation with considerations on randomly distributed and dynamic injury conditions by analyzing injury conditions transition and medical equipment stochastic service process.Methods A casualty array change model was established by injury conditions evolution analysis,Poisson process and Markov chain.Medical equipment stochastic service processes in medical facilities were probed,and the service rules were constructed.Expert investigation was carried out to acquire conditions transition indexes and to determine the vectors for conditions transition without manual intervention and their changes after treatment,then simulation tools were used to optimize medical equipment allocation.Results The emergency treatment table in some field medical station was considered as the subject,and the optimum allocation was proposed for emergency treatment table with practical data and simulation calculation.Conclusion The emergency treatment table allocation proposed was similar to the actual one in the medical station.Markov-process-based medical equipment allocation responses injury conditions changes and the fluctuation of treatment sequence,which has the result reliable and the method versatile and practical,and lays a foundation for medical equipment allocation and optimization.
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Objective To detect the expression of orphan nuclear receptor RORC gene and the level of serum interleukin-17 in acute lung injury (ALI) rats, and to explore the effects and possible regulation mechanisms of helper T lymphocyte 17 (Th17) in the ALI.Methods Twenty four SD male rats were randomly assigned to three groups, control group, model group, and pyrrolidine dithiocarbamates (PDTC) prevention group.The rats in model group and PDTC prevention group were intravenously injected LPS (6 mg/kg) for inducing ALI.The PDTC prevention group had been intraperitoneally injected PDTC (120 mg/kg) thirty minutes before LPS injection.All rats were killed twelve hours after LPS injecttion.The lung wet/dry weight ratio was measured.Lung pathologic tissue scored after hematoxylin-eosin (HE) stain.The expression of alveolar macrophages (AM) nuclear factor-KBP65 (NF-κBP65) was detected by immunohistochemistry.The level of serum IL-17 was detected by ELISA method.The expression of AM orphan nuclear receptor RORC gene was determined by SYBR Green Ⅰ real-time polymerase chain reaction.Results Compared with control group.the lung wet/dry weight ratio.lung pathologic tissue score, the expression of AM NF-κBP65.the level of serum IL-17 and the expression of AM orphan nuclear receptor RORC gene were significantly increased (P < 0.05).However, compared with model group, these changes were prevented in PDTC prevention group.Conclusions Th17 might participate in the pathological process of ALI.Activation of NF-кB might influence RORC gene expression, induce Th17 differentiation, and elevate the level of serum IL-17.
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BACKGROUND: Activated by Ca2+, phospholipase A2 will aggravate the influx of Ca2+ or the release of intracellular Ca2+, and then forms a vicious circle, which results in a continuous increase in free calcium level and leads to server injury in neural cells.OBJECTIVE: To discuss the protective effects of nimodipine on acute ischemic brain injury caused by activation of phospholipase A2.DESIGN: A completely randomized controlled trial.SETTING: Intensive Care Unit (ICU) of Children's Hospital, Chongqing Medical University.MATERIALS: From January 2001 to October 2003, it was completed at the ICU of Children' s Hospital, Chongqing Medical University. Thirty male rats were selected and divided into sham operation group, ischemia group and nimodipine treated group randomly, with 10 rats in each group.METHODS: In sham operation group, the right common carotid artery was identified by blunt dissection without ligation under anesthesia in rats. In ischemia group, at 30 minutes before cerebral ischemia, 2 mL saline was injected intraperitoneally. In nimodipine treated group, at 30 minutes before cerebral ischemia, 0.2 g/L nimodipine (2 mg/kg) was injected intraperitoneally. In all the three groups, the duration between ischemia and decollation was 120 minutes. Rats were decollated under anesthesia and their brains were taken out to assess the activity of phospholipase A2, the free calcium level in brain cells, the brain water content and the changes in mRNA levels of type Ⅱ phospholipase A2 (secretive phospholipase A2) and type Ⅳ phospholipase A2 (cytoplasmic phospholipase A2) in brain tissue.pholipase A2) and type Ⅱ phospholipase A2 (cytoplasmic phospholipase A2)in brain tissue were measured in rats in all the groups.pholipsse A2 in brain tissue: In ischemia group and nimodipine treated group, the activity of phospholipase A2 were higher than that in sham operation group [(57.8 ±7.2),(42.5±6.1), (17.1±5.3)%, P＜ 0.05-0.01], and it was a litter lower in nimodipine brain cells: It was higher in nimodipine treated group and ischemia group than that in sham operation group [(775.8±105.5), (497.2±45.9), (103.8±10.3) μmol/L,P ＜ 0.05-0.01], and it was lower in nimodipine group than in ischemia group (P ＜ 0.01).that in sham operation group [(82.9±0.5), (80.0±1.1), (72.1±0.01)%, P ＜ 0.05-0.01], and it was lower in nimodipine treated group than that in ischemia group (Ppase A2 could be detected in brain tissue. And the mRNA level of type Ⅱ phospholipase A2 in brain tissue was very low. At 120 minutes after ischemia, mRNA of type Ⅱ phospholipase A2 was detectable and the expression of type Ⅱ phospholipase A2 was increased. Compared to ischemia group, the expression of type Ⅱ phospholipase A2 was not decreased in nimodipine treated group while the expression of type Ⅱ phospholipase A2 was decreased.CONCLUSION: Nimodipine is capable of decreasing the free calcium level in brain cells, the activity of phospholipase A2 in brain tissue and the brain water content after ischemia. However, it cannot significantly inhibit the expressions of type Ⅱ phospholipase A2 and type Ⅱ phospholipase A2 after cerebral ischemia.
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BACKGROUND: Free radicals are produced during ischemia, which can strengthen activity of lipid peroxidation; induce lesion of cell and cellular barrier, result in necrosis or apoptosis of neurons; and aggravate edema of ischemic cerebral tissue.OBJECTIVE: To observe the effects of polydatin (PD) on free radicals, lipid peroxidation, water contents and pathological morphology of brain tissue in rats with focal cerebral ischemia so as to explore its protective mechanisms.DESIGN: A randomized controlled trial.SETTING: Intensive Care Unit, Second Affiliated Hospital, Chongqing University of Medical Sciences; Pediatric Research Institute, Children's Hospital Chongqing University of Medical Sciences.MATERIALS: The experiment was carried out at the Pediatrics Medicine Institute of Chongqing Medical University from October 2001 to July 2002.Totally 48 healthy adult male Wistar rats were divided into 3 groups randomly,with 16 in each group. Group Ⅰ was sham-operated group: rats were anaesthetized, the right common carotid arteries were separated instead of being occluded. Group Ⅱ was ischemia group: to establish the right middle cerebral artery occlusion model of rats. Group Ⅲ was PD pretreatment group: polydatin (6 g/L, 12 mg/kg) were intravenously administrated 30 minutes before the onset of ischemia. Saline substituted for PD, besides, were intravenously administrated with the same way and dosage on Group Ⅰ, Group Ⅱ and Group Ⅲ.The rats were decapitated and the brains were immediately removed after cerebral ischemia 2 hours. In each group, 8 rats were chosen to be determined water contents of brain tissue, the other 8 rats were chosen to be determined levels of lipid peroxidation and free radicals in brain tissue.METHODS: According to the formula which was: wet weight-dry weight/wet weight×100%, water content of cerebral tissue was assayed. Superior liquid was taken to assay MDA with spectrophotometer thiobarbituric acid method (TBA) method, SOD activity assayed by xanthiue oxidase enzyme method, the activities of GSH-Px, CAT and NOS determined by colorimetry,the amount of protein determined by the method of Lowry. All the procedures were carried out strictly according to the instruction.malonaldehyde (MDA) and activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) and nitric oxide synthase chemia, contents of SOD, GSH-Px and CAT in cerebral tissue of PD group were obviously higher than those of ichemia model group [(226.43±8.69),(193.37±11.14) NU/mg; (244.38±12.34), (211.71±16.50) μkat/g; (59.85±9.67),water in cerebral tissue of PD group were obviously lower than those of ichemia model group [(6.38±0.54), (8.63±0.78) μmol/g; (78.72±0.43)%,tivity in ischemic tissue but the results were similar to that in ischemia model group [(12.00±1.00), (12.84±1.17) μkat/g, P ＞ 0.05] in brain tissue.ed that PD alleviated the ischemia edema of cerebral ischemia.CONCLUSION: PD can alleviate the reaction of lipid overoxidation, improve the activities of antioxidant-enxymes, reduce ischemia brain edema,protect the function of cell member, bring down the damage to ischemia neurons. It shows that PD has significant cerebral protective role on focal ischemia brain damage.
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OBJECTIVE:To investigate the protective effect of Polydatin on acute lung injury following endotoxic shock in rats.METHODS:Using a rat endotoxic shock model,animals were randomly divided into4groups∶sham operation group,en?dotoxic shock group,Polydatin treatment group and Polydatin pretreatment group.MAPs(mean artery pressures)were mea?sured at given time points.At the end of the experiment,the serum,the lung tissue,and the bronchoalveolar lavage fluid(BALF)were collected.The levels of lung coefficient,lung penetrating index(LPI),the protein concentration of BALF and the content of NOS in the lung tissue were measured.Furthermore,the histologic changes of the lung were observed under light micro?scope.RESULTS:In addition to prohibiting the dropping of MAP,Polydatin could mitigate the acute lung injury induced by endotoxin which increased the levels of lung coefficient,LPI,the protein concentration of BALF and the content of NOS in lung tissue.Enough morphological evidence could be found in pathological sections.Especially,the protective effects were more ob?vious in Polydatin pretreatment group.CONCLUSION:Polydatin has prophylactic and therapeutical effects on acute lung injury following endotoxic shock and the prophylactic effect is more marked than the therapeutic one.
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This paper analyzes the development actualities and characteristics of foreign military telemedicine equipments,and points out the developing trend of field telemedicine equipment.On the basis of the above-mentioned,the development countermeasures of Chinese army are put forward.
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Objective To develop a medical service information management system of division aid station(DAS) so as to meet the demand of medical informationization and improve the commanding capability of DAS.Methods Based on a thor-ough research on the general requirement in DAS echelon especially in its command team,Delphi 7 and modularization technology were used to design and exploit information management system.Results The system could satisfy the needs of medical service information management of DAS.Conclusion The system can be provided a powerful means for manage-ment of medical information in DAS echelon and is an indispensable part of informatization of DAS.