Objective To evaluate the diagnosis value of digestive tract clinical symptoms in multiple myeloma.Methods 21 patients with multiple myeloma with digestive tract symptoms as initial clinical manifestations were analyzed.Results In 21 patients,52% below 50 years(hepatomegaly and splenomegaly was 73%),abdominalgia and diarrhea,hematocytopenia,proteinuria were 57%,90% and 67%,respectively.Conclusion Digestive tract symptoms,especially hepatomegaly and splenomegaly,occur mostly in younger patients.Hematocytopenia and proteinuria are important clue in diagnosis of multiple myeloma.Digestive tract symptoms are the common clinical manifestations,but not chief clinical features in multiple myeloma.

Objective To investigate the effeets of ulimstatin on expression of intestinal defemin-5 mRNAin the rat model of sepsis.Method The experiment was performed in pharmaco-laboratory of medical college,Sun Yat-Sen University.sixty Sprague-Dawley rals were randomly divided into control,sepsis,pretreated andtreated groups(n=15).Semis was induced in the mts of latter three groups by cecal lifo.and puncture(CLP).The rats of pretreated group received 25 000 U/kg ulinastatin 2 hours before operation and the rats of uli-nastatin treated groups received 50 000 U/kg ulinastatin 2 hours after operation.Some pieces of ileum mucosa weretaken 12 h after CLP.Tge pathological changes were observed and the expression of RD-5 mRNA was detectedwith RT-PCR.All data were managed by SPSS 13.0 software and arIaIyzed by using One-way ANOVA and LSD-ttest.Results The expression of RD-5 mRNA in the rats of sepsis group significantly decreased compared to col-trol(P<0.05).The expression of RD-5 mRNA of pretreated and treated groups sigificantly inereased comparedto sepsis group(P<0.05);pretreated groups had more increased expression of,RD-5 mRNA compared to treatedgroups(P<0.05).Conclusions The expression of intestinal RD-5 mRNA significantly decreases in sepsis,which could be improved by the treatment of ulinadtatin leading to intestinal mucosal protection of the siqnifleant.The pretreatment may be more effective than the theTapeatic treatment in the rat model of sepsis.

ObjectiveTo investigate the unfavorable factors of intestinal mucosa repair after the intestinal epithelial injury in vivo in a mouse model of sepsis. MethodsThe method of cecal ligature and puncture (CLP) was used to induce sepsis and then the intestinal mucosa damage, epithelial cell apoptosis and the number of transformed goblet cells were observed, and the concentrations of serum TNF-αt, IL-1 and TGF-β1 and TFF3 ( trefoil factor 3) in small intestinal mucosa were determined. All above various laboratory examinations were made by different assays including H-E staining, western blot, ELISA and immunohistochemistry respectively. The experimental mice were divided into sepsis group and sham operation control group. The mice with sepsis were separately sacrificed 6 hours ( n = 7 ), 24 hours ( n = 7) and 48 hours ( n = 7) after CLP. Results In septic mice group, the injured intestinal mucosa was found 6 hours after CLP. The damage scores in mice 24 h and 48 h after CLP were higher than those 6 h after CLP, but there was no significant difference between those 24 h and 48 h after CLP. Moreover, a few goblet cells or other epithelial cells adjacent to the injured surface migrated onto the wound to cover the denuded area. The number of goblet cells was substantially decreased in mice of sepsis group 6 hours after CLP compared with sham operation control group. Compared with sham operation control group, levels of IL-1 and TNF-α significantly increased 3-4 times in mice of sepsis group at all intervals, and the phosphorylated caspase-3 increased 4 times. Although TFF3 assayed by using Western blot showed modest increase 6 h after CLP and it declined 24 h and 48 h later. A similar change was found in TGF-β1, it modestly increased 6h after CLP, but it didn't elevate 24 h and 48 h later. ConclusionsSevere sepsis keeps on the inflammatory reaction and epithelial cell apoptosis, preventing the repair of intestinal mucosa from injury.

Objective To study the establishment of rat model of asphyxia-cardiac arrest and efficacy of CPR in order to find the length of optimum time of asphyxia to cause injury.Methods One hundred and twenty-six male Sprague-Dawley rats were randomly (random number) divided into sham operation group and experimental groups.Cardiac arrest was induced by asphyxiation after intravenous injection of vecuronium bromide.The experimental groups were assigned into AP4 (four-minute asphyxia period),AP6 and AP8 subgroups in accordance with different lengths of time of asphyxia subjected to.In these groups,CPR,including pre-cordial compression and synchronized mechanical ventilation,was initiated 4,6 and 8 min after asphyxia-induced cardiac arrest,respectively.The successful ratio of resuscitation and hemodynamic variables were recorded.Brain water content,neural deficit scores (NDS),imaging changes on MR,pathological changes of brain tissue and neuronal apoptosis were evaluated at 1 d,3 d and 7 days after ROSC.All the data were analyzed by single-factor analysis of variance or Chi-square test.P ＜ 0.05 was considered statistically significant.Result The lowest NDS occurred at 1 d after ROSC,brain water content and imaging changes on MR were most obvious at 3 d after ROSC,while pathological changes of brain tissue and neuronal apoptosis increased and reached the peak at 7d after ROSC.The survival rates after 24 hours of AP4,AP6 and AP8 groups were 85％,75％ and 45％,respectively.The rate of ROSC and survival rate of AP8 group were significantly lower than those of other groups (P ＜0.01).The longer time of asphyxia the severer pathological changes of brain tissue,brain edema,neural deficit,and magnetic resonance imaging changes in all experimental groups.As compared to other groups,the brain damage index of AP8 group was most serious,while that of AP6 group was moderate.Conclusions The rat model following asphyxia-induced cardiac arrest and cardiopulmonary resuscitation was established successfully.From the evidence of survival rate and damage grade of brain tissue,asphyxia for 6 min may be the rational length of ischemic time in this model.

Objective To investigate the protective effects of Ulinastatin on intestinal barrier damaged after cardiopulmonary resuscitation (CPR) in rats in order to illustrate the possible mechanism.Methods Twenty-one male SD rats were divided into three groups randomly (random number) including control group (sham group, n =7), cardiopulmonary resuscitation group (CPR group, n =7) and ulinastatin group (UTI group, n =7).The rats were anesthetized with pentobarbital sodium (45-60 mg/kg) by intraperitoneal injection.The rats of sham group were only treated with endotracheal intubation.Ulinastatin (100 000 U/kg) were injected via caudal vein 2 hours prior to CPR, and cardiac arrest was made in rats and cardiopulmonary resuscitation was carried out in the UTI group, while equivalent volume of sterile saline was used instead in the CPR group.Blood and ileum samples were obtained at 48 hour after restoration of spontaneous circulation (ROSC).The levels of tumor necrosis factor alpha (TNF-α) and interleukin-1β (IL-1β) were assayed by ELISA (enzyme-linked immunosorbent assay), the protein levels of caspase-3 were determined by western blot, the intestinal mucosa were stained by terminaldeoxynucleoitidyl transferase mediated nick end labeling (TUNEL) and ileac mucosa were observed under transmission electron microscope.Data were processed with SPSS 17.0 software.Results The plasma levels of TNF-α and IL-1β were dramatically higher in CPR group than those in other two groups (CPR vs.sham, P ＜ 0.01;CPR vs.UTI, P ＜ 0.05).Moreover, the tight junctions between cells obviously broadened and loosened in the CPR group were found under electron microscope, however, this phenomenon was not obvious in the UTI group.A large number of apoptotic cells were observed by TUNEL assay in the CPR group, but a small number of apoptotic cells were observed in the UTI group.The protein levels of caspase-3 in the UTI group were higher than those in sham group, but lower than those in CPR group (both P ＜ 0.05).Conclusions Ulinastatin has protective effects on the intestinal barrier damaged after cardiopulmonary resuscitation in rats by decreasing the proinflammatory mediators in the blood, reducing the expression of caspase-3and then reducing the numbers of apoptotic intestinal cells.

Objective To investigate immunological dysfunction of intestine mucosa barrier in a rat model of sepsis. Method Sixty Sprague-Dawley rats were assigned randomly(random number) into sepsis group (n = 45)and control group (n = 15). The animals in sepsis group were subjected to cecal ligation and puncture (CLP), whereas rats of control group underwent a sham surgery. The ileac mucosa and segments were harvested 3 h, 6 h and 12 hours after CLP, and the blood samples were collected. Pathological changes, protein levels of defensin-5 (RD-5) and trefoil factor-3(TFF_3) mRNA, lymphocytes apoptosis in the intestinal mucosa were determined. In an additional experiment, the gut-origin bacterial DNA in blood was detected. Results In the septic animals, in-testinal mucosa showed marked injury with loss of ileal villi, desquamation of epithelium, detachment of the lamina propria, hemorrhage and ulceration. Compared with control, the expression of TFF_3 mRNA and level of RD-5 pro-tein were decreased and the mucosal lymphocyte apoptosis increased (P < 0.05) in sepsis group. Compared with control group, the significant differences in RD-5 and TFF_3 mRNA appeared 3 hours after CLP and those differ-ences were progressively increased in 6 hours and 12 hours after CLP in sepsis group (P < 0.05, F of RD-5 = 11. 76, F of TFF_3 = 16.86 and F of apoptosis = 122.52). In addition, the gut-origin bacterial DNA in plasma de-tected was positive in all sepsis animals. Conclusions It suggests that immunological function of intestinal mucosa is impaired in septic rats and further worsened following the course of sepsis.

Objective To establish the oxygen glucose deprivation (OGD)/reoxygenation experimental model of hippocatnpal neurons of rat in vitro, and to try to identify the length of time for producing optimum injury in this model. Method The primary hippocampal neurons of newborn Sprague-Dawley rats were cultured for 7 days and randomly (random number) divided into a control group and OGD groups. The OGD groups were assigned into 1 h, 2 h, 4 h, 6h, 8 h and 10 h subgroups in accordance with different lengths of time for oxygen glucose deprivation. The neurons of OGD groups were placed into a tri-gas incubator containing 0.5% oxygen and the culture medium was substituted with the glucose-free Earle' s balanced salt solution, simulating cerebral ischemia injury in vivo. The morphology of neurons was observed after reoxygenation for 24 hours. The MIT assay was used to determine the rate of survived cells derived from the value of optical density (OD) of cells. The lactate dehydro-genase (LDH) content in culture medium was detected to evaluate the neuron injury. The apoptotic rate of neurons was measured by using flow cytometry. Dunnett-test and Spearman correlation analysis were used to analyze the data with SPSS version 16.0 soft ware package. Results The morphological damage of neurons in OGD groups aggravated gradually, optical density and cell survival rate decreased (rs= -0.961 and rs = -0.966, P <0.01), and the amount of LDH increased (rs = 0.990, P <0.01) with longer duration of exposure to oxygen glucose deprivation, and the rate of neuron apoptosis increased obviously which was significantly statistical difference in com-parison with the control group (P < 0.05). Under the setting of oxygen glucose deprivation for 6 hours, the apop-tosis rate of neurons approximated to 50% . Conclusions The oxygen glucose deprivation/reoxygenation model of rat's hippocampal neurons in vitro was established successfully. From the findings of morphological changes and apoptosis rate of neurons, the oxygen glucose deprivation for 6 hours may be the suitable length of time for inducing neuron injury in this model.

AIM:To explore the ability of different group B streptococci ( GBS) strains on inducing platelet activation.METHODS:Six strains of GBS, separated from the septic patients with thrombocytopenia, were used as the inducers.Light transmission aggregometry was used to measure platelet aggregation.Scanning electron microscopy ( SEM) was performed to investigate the interaction of platelets with bacteria.The expression of platelet CD62P, Toll-like receptor 2 ( TLR2) and TLR4 was determined by flow cytometry and Western blotting.Furthermore, the activity of platelet TLR2 (or TLR4) was blocked by anti-TLR2 (or anti-TLR4) monoclonal antibody, and the platelet aggregation induced by GBS was detected.RESULTS:Only 3 of 6 GBS strains isolated from the septic patients induced platelet aggregation and up-regulated the expression of CD62P and TLR2 in the platelets (P<0.05), but not TLR4.Incubation with anti-TLR2 anti-body, but not anti-TLR4 antibody, significantly blocked platelet aggregation induced by GBS.CONCLUSION:Some GBS strains from the patients are able to trigger platelet activation in vitro, and platelet TLR2 may play an important role in the interaction between GBS and platelets.

[Objective] To explore the risk factors for mortality of bloodstream infections in the patients with hematologic diseases,so as to provide evidence for reasonable and effective application of treatments.[Methods] The clinical data of 242 cases of bloodstream infections who were hospitalized from Jan 2012 to Jun 2016 were analyzed retrospectively,then the analysis was performed for risk factors.The statistical analysis was processed by SPSS 19.0.[Results] A total of 266 strains of pathogens were isolated,including 99 strains of gram-positive bacteria,accounting for 37.2％,and 164 strains of gram-negative bacteria,accounting for 61.7％.Multivariate analysis showed that the significant independent risk factors for mortality were active states of hematologic diseases (P =0.007,OR =5.622,95％ CI 1.586 ～ 19.924),presentation with septic shock(P =0.007,OR =4.978,95％ CI 1.560 ～15.884),cardiac insufficiency (P =0.001,OR =11.878,95％ CI 2.760 ～ 51.120),level of albumin less than 35 g/L (P =0.036,OR =3.468,95％ CI 1.087 ～ 11.066),polymicrobial infection (P =0.010,OR =6.024,95％ CI 1.540 ～ 23.563),and Staphylococcus haemolyticus (P =0.001,OR =19.308,95％ CI 3.392 ～ 109.888)/Enterococcus (P =0.002,OR =15.266,95％ CI 2.817 ～82.728) infection.The survival curves show that the inappropriate initial antimicrobial therapy group or presentation with any one of the independent risk factors had a lower probability of survival than the control group.[Conclusions] Bloodstream infections in patients may cause high mortality rate,so it is necessary that we use antibiotic reasonably and spare no effort to reduce the mortality rate by appropriate application of antimicrobial therapy and effective intervention of the risk factors.

AIM: To investigate the protective effect of ulinastatin on rats with hemorrhagic shock. METHODS: A prospective, controlled animal study was designed. The model of hemorrhagic shock in rats was produced by Chaudry method. After 60 min, rats were resuscitated by transfusion of shed blood and normal saline, but a half of them were treated with ulinastatin. At different time points after reperfusion, the levels of tumor necrosis factor-alpha (TNF-?), interleukin-6 (IL-6), malondialdehyde (MDA) and superoxide dismutase (SOD) in serum were detected. RESULTS: The levels of TNF-?, IL-6 and MDA significantly increased and the activity of SOD decreased. In the ulinastatin-treated groups, the blood pressure and heart rate were obviously improved; the levels of TNF-?, IL-6 and MDA significantly decreased and the activity of SOD had little change after hemorrhagic shock and reperfusion. CONCLUSION: Ulinastatin has a protection effect on rats with hemorrhagic shock by suppressing the production of inflammatory factors and reducing oxidative damage.