BACKGROUND:Medical risks are al unsafe events or that damage to the patient during medical services. Present medical risk management is mainly qualitative experience, and lacks of regular failure analysis and risk assessment for established medical treatment.
OBJECTIVE:To construct models of medical process failure analysis and risk assessment, find possible risks during medical treatment, and propose effective measures to eliminate or decrease above risks.
METHODS:Failure mode and effects analysis during reliability engineering were used in production. That was, risk assessment was conducted in the possible technical failure modes, causes and al impacts on the product during each process. Improvement measures were made for weak link during the process. The risk could reach an acceptable level. In accordance with failure mode and effects analysis during production, the procedure of medical process failure analysis and risk assessment could be made to analyze the potential failures during medical treatment. Moreover, the improvement measures were proposed for weak link with high risks so as to prevent the occurrence of risk of significant adverse effects on patients.
RESULTS AND CONCLUSION:The methods and basic procedures of medical process failure analysis and risk assessment were established by using the experience of failure mode and effects analysis. Taking the rescue process of myocardial infarction in the emergency of a hospital as an example, the analysis of failures, reasons and impacts was performed taking“chewing 300 mg aspirin”in the rescue steps as a key. The improvement measures and suggestions were proposed for unacceptable failures and reasons. Seen from the analysis results, proposed improvement measures and suggestions can obviously decrease the risks of failures caused by this step to patients. Therefore, the application of failure mode and effects analysis in medical treatment has a strong practical value.

Huang Ti's "Nei Ching Su Wen" is the earliest classical work on medical science in ancient China. It summed up the results of observations made in long years through practice by the ancient Chinese labouring people, accumulating thereby lots of valuable knowledge and experience in different lines of medicine.Some two thousand years ago, Chinese medical scientists in the Chou and the Chin Dynasties already conceived the advanced idea of laying special emphasis on prophylactic measures, and began to adopt diet therapy as a means of medical treatment. Principles of preparing complete diet were worked out by them. And in this connection, it is mentioned in the book "Nei Ching Su Wen" that "five kinds of cereals are the means of subsistence, five kinds of cattle provide beneficial food in the form of meat, five kinds of vegetables can be used for food enrichment, and five kinds of fruits may serve as supplement." These principles point out the necessary sorts of food to constitute a complete diet and their respective positions in it. That is to say, cereals including beans and peas are the staple food and animal meat is of secondary importance, with vegetables to enrich and fruits to supplement the first two. A diet thus prepared will not only consist of all the nutritive elements needed by the human body but also represent an appropriate arrangement of the different kinds of nutrients. Such a diet is, no doubt, in accord with the dietetic theory of modern science.

Objective To study the expression of adiponectin in the peripheral blood of patients with rheumatoid arthritis (RA),and discuss its role in the pathogenesis of RA.Methods Fifty-three patients with RA and 31 healthy controls were enrolled in the study.The level of adiponectin in the peripheral blood were detected using enzyme-linked immunosorbent assay (ELISA) method and the relation with clinical and laboratory parameters were analyzed.The stastistical analysis was carried out with independent t-test,one-way ANOVA and Spearman correlation analysis.Results The level of the adiponectin in rheumatoid arthritis patients [(12±8) μg/ml] was higher than control group [(8±4) μg/ml],with statistically significant difference (t=3.694,P=0.002).The level of adiponectin of the experimental group was negatively correlated with rheumatoid factor (RF),anti-cyclic centrullinated peptides (anti-CCP) (r=-0.301,r=-0.290,P＜0.05) and positively correlated with the levels of globulin (GLO),IgA and IgM (r=0.492,r=0.431,r=0.485,P＜0.05),while no significant correlation (P＞0.05) with erythrocyte sedimentation rate (ESR),C reactive protein (CRP),disease activity score in 28 joints (DAS28),Body mass index (BMI),anti streptolysin O (ASO),IgG,liver and kidney function,triglyceride (TG) and cholesterol (TC),C3,C4 levels and prothrombin time (PT) series.The level of adiponectin of the whole experimental group was not significantly correlated with BMI (r=0.142,P＞0.05),but negatively correlated with BMI (r=0.197,P＜0.05) in patients with 10-15 years courses of disease.Conclusion Related to RF and CCP,adiponectin may be involved in the pathogenesis of chronic inflammation of RA.

Objective: To investigate the effect of dimethyl dicarboxylate biphenyl ( DDB) on the proliferation, apoptosis and PPARγ expression of hepatic stellate cells. Methods: HSC-T6 cells were cultured in 96-well plates and 6-well plates, and after the 24-hour drug treatment, the influence of DDB on the proliferation and apoptosis of HSC-T6 were detected respectively by CCK-8 kit and flow cytometry. Quantitative real-time-PCR ( Q-PCR) and Western blotting were adopted to determine the effect of DDB on the PPARγmRNA level and the protein expression in HSC-T6 cells. Results:DDB obviously inhibited the proliferation of HSC-T6 (P<0. 05) and significantly promoted the apoptosis of HSC-T6 (P<0. 05) at the experimental concentration (8-64 μmol·L-1) when compared with the control group (0 μmol·L-1). The expression of PPARγ in drug-treated HSC-T6 was notably improved. Conclusion: DDB can inhibit the proliferation and promote the apoptosis of HSC-T6 cells by up-regulating the expression of PPARγ.

Objective:To investigate the effect of miR-154 on the apoptosis of hepatic stellate cells (HSC-T6). Methods:Hepat-ic stellate cells (HSC-T6) were transfected with miR-154 mimics and miR-154 inhibitor, and the cells were trandfected with mimics NC and inhibitor NC as the negative control. The effects of miR-154 on the proliferation of HSC-T6 were detected at different time points by CCK-8. A flow cytometry with double staining of Annexin and PI was used to detect the cell cycle and apoptosis rate of HSC-T6. Results:The proliferation ability of the cells was increased,the apoptosis rate was decreased significantly, and the proportion of cells in G0/G1 phase were decreased, and those in G2/M phase were increased significantly after transfected with miR-154 mimics. The proliferation ability of the cells was decreased,the apoptosis rate was increased significantly, and the proportion of cells in G0/G1 phase were increased, and those in G2/M phase were decreased significantly after transfected with miR-154 inhibitor. Conclusion:MiR-154 can promote the proliferation of HSC-T6 and inhibit the apoptosis of HSC-T6.

Objective:To summarize the single nucleotide polymorphisms ( SNPs) in ABCC2 and the effect on clinical drug appli-cation. Methods:According to the related articles published in domestic and abroad, the correlation between the single nucleotide pol-ymorphisms in ABCC2 and drug responses was classified and summarized. Results:ABCC2 translocator played an important role in the transmembrane transport of many physiological compounds and exogenous compounds. Numerous studies have demonstrated that the single nucleotide polymorphisms in ABCC2 possibly affected the expression or activity of ABCC2, which leading to the variation in the absorption, distribution and excretion of certain drugs and toxicants. However, the limitation and controversy were still emerged in the results. Conclusion:The influence of ABCC2 single nucleotide polymorphisms on clinical drug application shows significantly referen-tial value for the guidance of medication and the evaluation of efficacy, however, it can not be used as the only indicator yet.

Objective To research the effects of transcutaneous electrical stimulation (TES) on the expression of neurotrophin-3 (NT-3) and tumor necrosis factor-α (TNF-a) in the ventral horn of rats' spinal cords and in the injured region after spinal cord injury (SCI),and to explore the effects of TES on neuron reconstruction and functional recovery and their mechanisms. Methods Forty-eight Wistar rats were selected and divided using stochastic methods into a model group and a TES group.Using Allen's method,a complete SCI model was created at T9.Rats of the TES group were given TES treatment.Basso-Beattie-Brasnahan ( BBB ) ratings were used to evaluate locomotor function.Both groups were sampled at 1,3,5 and 7 days after the operation.Immunohistochemical techniques were used to detect the expression of NT-3 and TNF-α in the rats' spinal cords at the different time points. Results The post-operative BBB ratings of both groups showed an increasing trend.In the TES group the improvement was significantly better at 5 and 7 days than in the model group.The expression of NT-3 immuno-positive cells increased in both groups,peaking at 5 days post-operation,then declining at day 7.The expression of NT-3 positive cells at days 5 and 7 had increased significantly more in the TES group than in the model group.TNF-α immuno-positive expression increased with time in both groups,but in the TES group the expression increased substantially less than in the model group.At days 5 and 7 post-operation,the expression was significantly lower than in the model group. Conclusions TES can promote NT-3 expression in rats with SCI,inhibit the increase in TNF-α expression,and aid repair and reconstruction of neurons and related functional recovery.

ObjectiveTo investigate the value of serum procalcitonin (PCT) in diagnosing lower respiratory tract infection (LRTI) in adult.MethodsIn a retrospective study,97 patients were enrolled,who admitted into Peking University People's Hospital with suspected LRTI from July to December 2008.During analysis,the subjects are categorized into groups of LRTI with sepsis,hospital-acquired pneumonia(HAP),community-acquired pneumonia(CAP),acute exacerbation of chronic obstructive lung disease (AECOPD),other LRTI and non-infectious diseases.In these cases,the following parameters were assessed regularly,such as white blood cell count,erythrocyte sedimentation rate( ESR),C-reactive protein (CRP),PCT,bacterial culture of both sputum and blood,and Acute Physiology and Chronic Health Evaluation (APACHE)Ⅱ score.PCT levels were determined using antibody-coated tubes as a complete diagnostic-kit (LUMI test Pro-Calcitonin) in a Luminometer.ResultsMean PCT levels in groups of LRTI with sepsis, hospital-acquired pneumonia ( HAP ), community-acquired pneumonia ( CAP ), acute exacerbation of chronic obstructive lung disease( AECOPD),other LRTI,non-infectious diseases were 10.1 (0.7 -37.0),0.3(0.1 -0.8),0.2(0.1 -0.9),0.2(0.1 -0.4),0.3(0.1 -0.5),0.1 (0.1 -0.2) mg/L,respectively.There were statistical differences between these groups (H =19.898,P ＜ 0.01 ).And the PCT levels in groups of LRTI with sepsis,HAP,CAP,AECOPD,other LRTI were higher than group of non-infectious diseases ( U values were 0,18.000,81.000,20.000,all P ＜ 0.01 ).Patients with sepsis exhibited strongly higher PCT levels than patients with other lung diseases ( U values were 11.000,45.000,3.000,4.500,all P ＜ 0.01 ).Pearson correlation analysis of PCT levels with positive bacterial cultures and APACHE Ⅱ score was performed ( r =0.449).ROC analysis revealed that optimal discrimination between LRTI and non-infectious diseases could be performed at the cut-off point of 0.5 mg/L with a sensitivity of 32.6％ and specificity of 100％,while at a suggested cut-off point of 0.235 mg/L with a sensitivity of 53.9％ and specificity of 100％.Conclusions PCT is a more useful parameter for diagnosing lower respiratory tract infections( especially for those with sepsis) than other infectious markers such as CRP,ESR and white blood cell count.The sensitivity of PCT could be elevated with a reduction of the cut-off level.

Objective To evaluate the perfusion parameters in different zone of placenta using CPS,to research placental blood perfusion of different zone. Methods A total of 60 pregnant rats were divided into 3groups, 15 day,17 day and 20 day of gestation with 20 animals in each group,the placenta was divided into the central zone and marginal zone. SonoVue was injected by tail vein of rat using CPS, the time-intensity curves of the central zone and marginal zone were drawn and perfusion paramcters were calculate by software ACQ and Sonoliver. Surface area densities of different zone of placental maternal blood space was measured with histoligical method,and using immunohistochemical marked the placenta vascular. Results Arrivel time(AT) and time-to-peak(TTP) of placenta central zone was earlier than marginal zone,the peak intensity(PI) of the central zone was higher than that of the marginal zone ( P ＜ 0.05). There was significant difference between the central zone and marginal zone of surface area densities of placental maternal blood space ( P ＜0.05). PI of the central zone and marginal zone and the surface area densites of placenta was positively correlated ( P ＜0.05). The placental blood vessels was not expressed by factor Ⅷ.Laminin in the placental basement membrane expression of 20 day of gestation was not continuous or missing. Conclusions The surface area densities of central zone and marginal zone was different. CPS technique can be sensitive to detect changes of the placenta vascular bed in different zone.

AIM To investigate whether pioglitazone can protect cortical neurons from lipopolysaccharides(LPS)-induced neurotoxicity and the mechanisms responsible for this protective effect. METHODS After 7 d cultures，cultured cortical neurons were incubated with LPS 10 mg·L~(-1) for 4-24 h with or without other drugs. In co-incubation experiments, other drugs were added to the neurons 30 min or 1 h prior to incubation with LPS. The cell viability was assessed by MTT assay. The neuronal apoptosis was quantified by scoring the percentage of cells with apoptotic nuclear morphology after Hoechst 33258 staining. The cultured cells were then fixed on the 7th day and immunocytochemically stained with phosphorylated JNK1 antibody. The protein expressions of active caspase 3 and phosphorylated JNK1 were measured by Western blot. Nitric oxide (NO) generation was measured by Griess method. RESULTS The decrease of cell viability and the increase of apoptotic cells in cultured cortical neurons were observed incubated with LPS for 24 h compared with the normal controls. The cell viability of cortical neurons was decreased from (100.0±10.9)% in the normal control group to (72.3±2.1)% in the LPS-treated group and the apoptotic cell percentages were increased from (11.5±4.2)% in the normal control group to (39.5±8.2)% in the LPS group. LPS induced the increases in phospho-JNK1, active caspase 3 expression, and NO generation. Pioglitazone 0.01, 0.1 and 1 μmol·L~(-1), respectively inhibited LPS-induced decrease in cell viability and increase of apoptotic morphology, active caspase 3 expression in cultured neurons. In LPS+pioglitazone 1 μmol·L~(-1) group, cell viability was （97.8±9.7）%, the apoptotic cells percentage was (20.6±5.0)%, NO generation (6.8±1.3)μmol·L~(-1). Furthermore, pioglitazone also inhibited LPS-induced the increase in JNK1 phosphorylation and NO generation. JNK inhibitor SP600125 5 μmol·L~(-1) significantly inhibited LPS-induced neurotoxicity, cell viability was increased from (72.3±2.1)% to (109.8±11.8)%, the apoptotic cells percentage from (39.5±8.2)% decreased to (19.1±4.8)%, NO generation from （21.1±5.0）μmol·L~(-1) decreased to（4.0±1.3）μmol·L~(-1). The PPARγ antagonist GW9662 10 μmol·L~(-1) did not reverse the effects of pioglitazone. In LPS+pioglitazone 1 μmol·L~(-1)+GW9662 10 μmol·L~(-1) group, cell viability was (90.7±6.9)%, the apoptotic cells percentage was (23.4±4.1)%, and NO concentration was (5.8±0.7)μmol·L~(-1). CONCLUSION Pioglitazone protects cortical neurons against LPS insult at least via inhibiting JNK activity and NO generation, but not PPARγ activation.