Objective To investigate the changes of serum and urine fluorion organic fluoride poisoning by inhaling, and to probe into the clinical application value of concentrations in different degrees and at different time in patients with acute evaluating the sertm and urine fluorion concentration in acute organic fluoride poisoning by inhaling. Method A study was carried out in 23 patients, who suffered from acute organic fluoride poisoning by inhaling and were admitted Zhejiang Quhua Hospital, from December 2000 to December 2008. According to the occupational acute organic fluoride poisoning diagnostic criteria(GBZ66-2002),23 patients were divided into mild poisoning group,moderate poisoning group and severe poisoning group. Serum and urine fluorion concentration of patients at 1,2,3,4,5 d after poisoning were measured by using Ion-Selective Electrodes. Fluorion concentration of 10 staffs of Fluorine chemical company was also measured at the same period as the control group. The values of serum and urine fluorion concentration were analyzed. Differences in serum and urine fluorion concentration between groups at different time points were compared by repeated measures ANOVA and variability were deemed as statistical significance when P ＜ 0.05. Results Compared with mild poisoning group, there was no statistically significant difference ( P ＞ 0.05) in serum and urine fluorion concentration at the same time point in 1 to 5 days after poisoning in moderate poisoning group, but there was statistically significant differences ( P ＜ 0.05 or P ＜0.01) in severe poisoning group. Compared with moderate poisoning group, there was statistically significant difference ( P ＜ 0.05) in serum and urine fluorion concentration at the same time point in 1 to 5 days after poisoning in severe poisoning group. Serum fluorion concentration in 1 to 5 days after poisoning in each poisoning groupswere statistically higher than those in control group ( P ＜ 0.05), but there was statistically significant elevation ( P＜ 0.05) in urine fluorion concentration only in 1 day in mild poisoning group, in 1 to 3 days in moderate poisoning groups, in 1 to 5 days in severe poisoning group. Conclusions Serum fluorion concentration can be used as the severity index of diagnosis and determine the extent in 5 days after acute organic fluoride poisoning by inhaling,and urine fluorion concentration can also be used as diagnostic indicators of intoxication, but only in earlier stage or severe poisoning.

Animal experiment is indispensable for biomedicine research,and contributes much to the development of biomedicine.With the development of society and advance of human civilization,the welfare of experimental animals and ethical issues of animal researches are drawing extensive attention.The current study investigated the application of experimental animals in the hospital researches,explored the relationship between animal experiment and ethics of animal welfare,and analysed the status of ethics of animal welfare.Further it discussed how to strengthen ethical review of animal experiment so as to promote the ethics management of hospital researches.

AIM: To observe the effects of Salvia miltiorrhiza Bge (SMB) on left ventricular hypertrophy(LVH)in spontaneously hypertensive rats (SHR) and the expression of c-fos. METHODS: 18 SHRs in 8 weeks old were divided into three groups at random. SMB or distilled water(1 g?kg -1?d -1)was injected intraperitoneally to two groups for 10 weeks. Systolic blood pressure (SBP) and left ventricular mass index(LVMI)were measured. HE,VG and immunohistochemical staining combined with computed morphometry were used to evaluated the cardiomyocyte size and diameter, the collagen volume fraction(CVF), perivascular circumferential area (PVCA) and c-fos expression in the left ventricular tissue. RESULTS: Compared with 8-week-old rats, the SBP, LVMI, cardiomyocyte size and diameter, CVF, PCVA, c-fos expression increased markedly in the 18th week of SHRs. The LVH stopped and c-fos expression decreased whereas SBP changed slightly in animals treated with SMB. CONCLUSION: Chronic treatment with SMB can inhibit the development of LVH in SHR, which is probably related to the decease of cardiac c-fos.

Objective To investigate the changes of serum gastrin level in patients with colon cancer and the relationship between serum gastrin level and colon cancer occurrence and development.Methods Data of 35 patients underwent colon cancer surgery from January 2010 to January 2012 in our hospital were collected,at the same time data of 28 patients with colonic polyps and 30 cases of normal were collected as normal control.Serum gastrin levels were tested by radioimmunoassay in patients with colon cancer before surgery,1,3,7 d after surgery and they were analyzed.Results The serum gastrin level of patients with colon cancer was significantly increased compared with colon polyps and healthy controls((92.45 ± 12.98) ng/L vs (49.66 ±10.34) ng/L vs (30.12 ±6.39) ng/L;F =9.455,P ＜0.001)).Serum gastrin level in patients with obstructive colon cancer was significantly higher than that in non-obstructive cancer((129.84 ± 15.32) ng/L vs (75.34 ±11.45) ng/L,t =12.181,P ＜0.001) ;Serum gastrin levels in patients who cut off colon tumor was signifcanfly lower than before surgery((43.02 ±8.34) ng/L,(40.74 ±6.78) rig/L,(38.12 ±7.09) ng/L vs (89.45 ±12.98) ng/L;P ＜0.05).But no significant change of serum gastrin levels in patients with the colon tumor compared with the preoperative((97.34 +8.30) ng/L vs (95.82 ±7.20) ng/L vs (94.44 ±7.74) ng/L vs (100.23 ± 10.82) ng/L; P ＞ 0.05).But there was significant difference on serum gastrin levels between patients who cut off colon tumor and patients with the colon tumor(within groups:F =8.341,P =0.012 ;between groups:F =7.871,P =0.024).Conchusion Serum gastrin levels in patients with colon cancer were significantly higher than that of patients with colon polyps and normal controls.There was also a significant reduction of serum gastrin in tumor resection,and therefore gastrin may be involved in the development of colon cancer.

Objective To study the factors influenceing patients' family members to make own relative fac-tors patients' families making decision on refusal of cardiopulmonary resuscitation (CPR) to the critical patients. Method Data were registered based on Utstein Style of 522 patients aged over 15 years, who subjected to in-hos-pital cardiac arrest(CA) in Department of Emergency of The First Affiliated Hospital of Wenzhou Medical College from January 2005 to December 2008. A total of 157 patients' family made refusal decision among the 522 pa-tients, who belonged to the refusal group, and others belonged to the attempt resuscitation group. The associated factors included age, sex, marriage, household register, cause of CA, underlying diseases, capability of activity before CA, life supported with mechanical ventilation, and administration of pressor agents. The refusal decisions were evaluated by using univariate Logistical regression analysis, and then the statistical significant variables were analyzed by using muhivanate Logistical regression analysis. Results Age, household register, cause of CA(car-diac or traumatic),stroke, sudden death, cancer, capability of activity before CA, life supported with mechanical ventilation,and administration of pressor agents were the important factors of making refusal decision (P < 0.01), but sexes or marriage was insignificant related to the refusal decision (P > 0. O5). The independent risk factors re-lated to refusal decision were age (P = 0.034),cancer (P = 0.006),stroke (P = 0.003), and life supported with mechanical ventilation (P = 0.000) in multivariate Logistical regression analysis, but the protective factors were sudden death (P =0.000),cardiac CA (P =0.020) and traumatic CA(P =0.000). Conclusions Age over 60 years, cancer, stroke, and life suppoted with assisted ventilation before CA were factors associated with re-fusal decision making, yet sudden death, cardiac CA and traumatic CA were factors of accepting CPR.

Objective To investigate the changes of tissue factor(TF)and tissue factor pathway inhibitor(TFPI)at different time points after in-hospital eardiopulmonary resuscitation(CPR).and to explore the role of TF and TFPI in CPR.Method From September 2005 to September 2007,24 patients,who suffered from cardiac arrest,were selected from the of emergency medicine department,The First Affiliated Hospital,Wenzhou Medical College.The selected patients were older than 16 years old and had identified cardial :arrest time.All patients were randomly classified into two groups:those who had retum of spontaneous circulation(ROSC)(n:12)and those mthom ROSC(n=12).Ten normal healthy volunteers served as control subjects(n=10).Etiology of the car.diac arrest and clinical characteristics during eardiopulmomry resuscitation were emestered.Serial levels of"IF and TFPI at different time points of 30 min,60 min,6 h,24 h,48 h after CPR were measured by enzyme linked immunosorbent assay(ELISA)after eardarrest and CPR.Data Were expressed as mean±standard deviation twotailed t test and ANOVA and four flod table chi-square test were used for eomparisoll in SPSS 11.5 software,and chaangs were considered as statistically significant if P value was less than 0.05.Results Inpatients with ROSC.TF obviously increased at 30 min after CPR.reached peak at 6 h.1F levels in patients without ROSC wer higher compared to those of the control group and ROSC at the same time point.The levels of TPFI had no significantly differentce at 50 min after CPR,and TFPI,obviously elevated at 60 min after CPR in ROSC group compared to those ofthe control group and without-ROSC group.In comparison with control group,the ratio of TF/FPI at 30 min after CPR in without-ROSC group and ROSC group were marked elevated.The ratio of in without-ROSC group showed marked devations eompare,t to that of ROSC group.In R()sC group.the ratio of THFI peaked at 6 h after CPR and descended a after CPR.Conclusions'11le 1F and TFPI level8 after CPR in patients with in-hospital cardiac obviously increase.The levels of TF and TF/TFPI at 30 min after CPR can be used for predicting the prognosis of patients with in-hospital cardiac arrest.

Objective:To investigate the anticoagulant causes, hemorrhagic susceptibility factors and clinical characteristics of patients with warfarin-related major bleeding in the emergency department of a general hospital.Methods:In a registry study from January 2017 to February 2020, 114 cases of warfarin-related major bleeding patients admitted to Department of Emergency Medicine, the First Affiliated Hospital of Wenzhou Medical University were enrolled. The descriptive methods were used to analyze anticoagulant causes, hemorrhagic susceptibility factors and clinical characteristics. Patients were divided into the international normalized ratio (INR) overrange group and the INR non-overrange group according to INR value during bleeding. The Chi-square test, Student’s t test, and Wilcoxon rank sum test were used to compare the differences between the INR overrange group and the INR non-overrange group. The Wilcoxon rank sum test and Student’s t test were used to analyze the characteristics of gastrointestinal tract bleeding and cerebral hemorrhage. Results:Warfarin-related major bleeding accounted for 0.36% (114/32 040) of first aid cases and 9.84% (114/1 158) of warfarin-taking cases, respectively. Seventy-seven cases (67.5%) of anticoagulant causes were related to atrial fibrillation (AF) and 32 cases (28.1%) were related to post-operative cardiac valve replacement. Of the bleeding susceptibility factors, HAS-BLED scored at 4.0 (3.0, 5.0), 84 cases (73.7%) had a history of drug use, 77 cases (67.5%) aged older than 65 years old, 65 cases (57.0%) had irregular INR monitoring, and 29 cases (25.4%) had recent increase in dose. Forty cases (35.1%) were gastrointestinal tract bleeding with the lowest hemoglobin (Hb) value and the highest score of HAS-BLED. Twenty-one cases (18.4%) were cerebral hemorrhage with the shortest prothrombin time (PT), the lowest INR value, the highest Hb, and the lowest score of HAS-BLED. Twelve cases (10.5%) died or gave up treatment in critical condition, including 6 cases of cerebral hemorrhage, 5 cases of gastrointestinal tract bleeding, and 1 case of hemoptysis. There were statistically significant differences in previous history of antiplatelet therapy, recent increase in dose, HAS-BLED score and bleeding site between the INR overrange group and the INR non-overrange group (all P<0.05). Conclusions:Among patients with warfarin-related major bleeding, AF and post-operative cardiac valve replacement are the main causes of warfarin anticoagulation. INR overrange is related to the previous history of antiplatelet therapy, recent increase in dose, and the high score of HAS-BLED. The gastrointestinal tract bleeding is the most common, with the lowest Hb value and the highest score of HAS-BLED. Cerebral hemorrhage is the second common, with the shortest PT, the lowest INR value, and the highest Hb. The incidence and mortality rates of warfarin-related major bleeding are relatively high.

The changes of tumor necrosis factor-alpha (TNF-alpha) and brain ultrastructure during cardiopulmonary resuscitation and the effects of ulinastation injection were observed, and the mechanism was investigated. Twenty-four adult healthy Sprague-Dawley rats were randomly divided into control group (8 rats), resuscitation group (8 rats) and ulinastatin (UTI) group (8 rats). Rats in control group underwent tracheotomy without clipping the trachea to induce circulatory and respiratory standstill. Rats in resuscitation and ulinastatin group were subjected to the procedure of establishing the model of cardiopulmonary cerebral resuscitation (CPCR). Rats in ulinastatin group were given with UTI 104 U/kg once after CPCR. In the control group, the plasma was collected immediate, 30 min, 2 h, 4 h, and 6 h after tracheotomy. In resuscitation group and UTI group, plasma was collected immediate after tracheotomy, 30 min, 2 h, 4 h and 6 h after successful resuscitation. The plasma levels of TNF-alpha were determined by radioimmunoassay (RIA). At the end of the experiment, 2 rats were randomly selected from each group and were decapitated. The cortex of the brain was taken out immediately to observe the ultrastructure changes. In control group, there were no significant differences in the level of TNF-alpha among different time points (P>0.05). In resuscitation group, the level of TNF-alpha was increased obviously after resuscitation (P<0.01) and reached its peak 2 h later after resuscitation. An increasing trend of TNF-alpha showed in UTI group. There were no differences in TNF-alpha among each sample taken after successful resuscitation and that after tracheotomy. The utrastructure of brains showed the injury in UTI group was ameliorated as compared with that in resuscitation group. In early period of CPCR, TNF-alpha was expressed rapidly and kept increasing. It indicated that TNF-alpha might take part in the tissue injury after CPCR. The administration of UTI during CACR could depress TNF-alpha and ameliorate brain injury. By regulating the expression of damaging mediator, UTI might provide a protective effect on the tissue injury after CPCR.
Brain/*ultrastructure ; *Cardiopulmonary Resuscitation ; Glycoproteins/*pharmacology ; Rats, Sprague-Dawley ; Tumor Necrosis Factor-alpha/*metabolism

The changes of tumor necrosis factor-alpha (TNF-alpha) and brain ultrastructure during cardiopulmonary resuscitation and the effects of ulinastation injection were observed, and the mechanism was investigated. Twenty-four adult healthy Sprague-Dawley rats were randomly divided into control group (8 rats), resuscitation group (8 rats) and ulinastatin (UTI) group (8 rats). Rats in control group underwent tracheotomy without clipping the trachea to induce circulatory and respiratory standstill. Rats in resuscitation and ulinastatin group were subjected to the procedure of establishing the model of cardiopulmonary cerebral resuscitation (CPCR). Rats in ulinastatin group were given with UTI 104 U/kg once after CPCR. In the control group, the plasma was collected immediate, 30 min, 2 h, 4 h, and 6 h after tracheotomy. In resuscitation group and UTI group, plasma was collected immediate after tracheotomy, 30 min, 2 h, 4 h and 6 h after successful resuscitation. The plasma levels of TNF-alpha were determined by radioimmunoassay (RIA). At the end of the experiment, 2 rats were randomly selected from each group and were decapitated. The cortex of the brain was taken out immediately to observe the ultrastructure changes. In control group, there were no significant differences in the level of TNF-alpha among different time points (P>0.05). In resuscitation group, the level of TNF-alpha was increased obviously after resuscitation (P<0.01) and reached its peak 2 h later after resuscitation. An increasing trend of TNF-alpha showed in UTI group. There were no differences in TNF-alpha among each sample taken after successful resuscitation and that after tracheotomy. The utrastructure of brains showed the injury in UTI group was ameliorated as compared with that in resuscitation group. In early period of CPCR, TNF-alpha was expressed rapidly and kept increasing. It indicated that TNF-alpha might take part in the tissue injury after CPCR. The administration of UTI during CACR could depress TNF-alpha and ameliorate brain injury. By regulating the expression of damaging mediator, UTI might provide a protective effect on the tissue injury after CPCR.
Animals ; Brain ; ultrastructure ; Cardiopulmonary Resuscitation ; Glycoproteins ; pharmacology ; Male ; Rats ; Rats, Sprague-Dawley ; Tumor Necrosis Factor-alpha ; metabolism

Objective To observe the changes of cell apoptosis and levels of Bcl-2 and Bax protein in myocardium after cardiopulmonary resuscitation (CPR) in rats and to study the protective effects of different doses of exogenous phosphocreatine (creatine phosphate, CP) on cell apoptosis. Methods A total of 32 male adult SD rats were randomly divided into 4 groups, namely control group ( group A), CPR group (group B), low dose CP group (group C, phosphocreatine 0. 5 g/kg given at beginning of CPR and 1.0 g/ kg 2 hour after CPR) and high dose CP group ( group D, phosphocreatine 1.0 g/kg at beginning of CPR and 2. 0 g/kg 2 hours after CPR) . Cardiac arrest was induced by asphyxiation and CPR was started 7 min after asphyxiation it groups B, C and D. Myocardium samples were taken 24 hours after CPR for detecting myocardium cell apoptosis by TUNEL method. The levels of Bcl-2 and Bax protein were measured by using immunohistochemistry. Experimental data were processed with variance analysis in SPSS package. Results Compared with group A, myocardium cell apoptosis index (AI), and the levels of Bcl-2 and Bax proteinincreased significantly in groups B, C and D (P ＜0. 01 ), and Bcl-2/Bax ratio decreased significantly (P ＜0. 01 ) . Compared with group B, myocardium cell AI and levels of Bcl-2 and Bax protein decreased significantly in groups C and D ( P ＜ 0. 01 ), and Bcl-2/Bax ratio increased significantly ( P ＜ 0. 01 ) .Compared with group C, myocardium cell AI and levels of Bcl-2 and Bax decreased significantly in group D (P ＜ 0. 05 ), and Bcl-2/Bax ratio increased significantly ( P ＜ 0. 05 ) . Conclusion Exogenous phosphocreatine, especially inlarge dose, could inhibit apoptosis of myocardium cells and alleviate myocardium injury after CPR in rats.