Objective To investigate the effects of glycine on the expression of HSP70 and TNF-α mRNA in the liver tissue of rats with traumatic shock and explore the protective mechanism of glycine a-gainst secondary liver injury after traumatic shock. Methods The traumatic shock model was established and 120 Wistar rats were divided randomly into three groups: treatment group, shock group and control group. At the beginning of resuscitation, the rats in the treatment were injected with 0.5 ml isotonic saline containing 100 mg/kg glycine, those rats in the shock group were injected only with 0.5 ml isotonic saline. The rats in three groups were killed at 3, 6, 12, 24 and 48 hours after resuscitation respectively. The ex-pression of HSP70 and TNF-α mRNA in the liver tissue were detected by RT-PCR, pathological changes were observed and serum ALT and AST were measured. Results The expressions of HSP70 and TNF-α mRNA in the liver tissue of rats in the shock group began to increase at 3 hours and both reached the peak value at 6 hours after resuscitation, but the expression of HSP70 mRNA in the treatment group reached the peak value at 12 hours after resuscitation. Compared with the control group, the expression of HSP70 mR-NA in the treatment group increased significantly and that of TNF-α mRNA decreased siganicantly, serum ALT and AST decreased and pathological damage was relieved significantly (all P < 0.05). Conclusion By enhancing the expression of HSP70 mRNA and decreasing the expression of TNF-α mRNA, glycine may play a protective role against the secondary damage of liver after traumatic shock.

Objective To investigate the dynamic changes of HSP70 mRNA expression in the liver tissue of rats with traumatic shock and the treatment effects of glycine.Methods The expression of HSP70 mRNA in the liver tissue of treatment group,shock group and control group was detected by ELISA.Pathological changes were observed,and serum ALT and AST were measured.Results The expression of HSP70 mRNA in the liver tissue of rats in the shock group and the treatment group reached peak at the 6th and 12th hour after resuscitation respectively.Serum ALT and AST increased and pathological damage aggravated with time prolonging.Compared with control group,the expression of HSPT0 mRNA in treatment group increased significantly,serum ALT and AST decreased significantly and pathologi- cal damage was significantly relieved(all P<0.05).Conclusion Glycine can increase the expression of HSPT0 mRNA and relieve the secondary damage of liver after traumatic shock.

Objective To explore the relationship between the immune function of cellin peripheral blood with the virureplication and hepatitiviru(HCV)-cAg expression in the patientwith chronihepatiti(CHC) .MethodPeripheral blood lymphocytesubpopulation ,HCV-Rnand HCV core antigen (HCV-cAg) in 63 healthy people undergoing the physical exami-nation (control group) and 85 caseof CHC(Chgroup) were analyzed by the flow cytometry ,real-time Pcand ELIS,respec-tively .ResultThe percentageof total cell,T4 cell,T8 cell,double negative cell(DN) and double positive cell(DP) in the Chgroup were (67 .37 ± 10 .43)% ,(37 .11 ± 10 .28)% ,(21 .63 ± 8 .87)% ,(7 .80 ± 4 .57)% and (0 .20 ± 0 .29)% , respectively ,the absolute contentwere in turn (0 .70 ± 0 .44) × 109/L ,(0 .37 ± 0 .22) × 109/L ,(0 .22 ± 0 .17) × 109/L ,(0 .08 ± 0.06)×109/Land(0.19±0.68)×107/L,respectively.TheratioofT4/T8was(2.18±1.26)% .Theresultsindicatedthatthe percentage of T8 cellin the Chpatientwadecreased obviously (P＜0 .01) ,which resulted in the ratio of T4/T8 raising(P＜0 .05);meanwhile ,the absolute contentof the total cell,T4 cell,T8 celland Dnwere all decreased obviously (P＜0 .05);moreove,the percentage of T4 celland Dnin the patientwith HCV-Rnpositive and HCV-cAg positive wasignificantly in-creased (P＜0 .05) .Conclusion When HCV replicating in the patientwith CHC,the T lymphocyte subpopulation haobviouab-normity .The low immune function or immune tolerance ofT cells may be the important cause of recurrence and uncurability of CHC.

Objective: To explore the influence of directed restrictive fluid management strategy (RFMS) on patients with serious burns complicated by severe inhalation injury. Methods: Sixteen patients with serious burns complicated by severe inhalation injury hospitalized in our department from December 2014 to December 2017, meeting the inclusion criteria and treated with RFMS, were enrolled in directed treatment group. Thirty-four patients with serious burns complicated by severe inhalation injury hospitalized in our department from December 2012 to December 2017, meeting the inclusion criteria and without RFMS, were enrolled in routine treatment group. Medical records of patients in 2 groups were retrospectively analyzed. Within post injury day 2, mean arterial pressure (MAP), central venous pressure (CVP), extravascular lung water index (ELWI), global end-diastolic volume index, and pulmonary vascular permeability index of patients in directed treatment group were monitored by pulse contour cardiac output monitoring technology, while MAP and CVP of patients in routine treatment group were monitored by routine method. On post injury day 3 to 7, patients in 2 groups were treated with routine fluid supplement therapy of our Department to maintain hemodynamic stability, and patients in directed treatment group were treated according to RFMS directed with goal of ELWI≤7 mL·kg^-1·m^-2. On post injury day 3 to 7, total fluid intake, total fluid output, and total fluid difference between fluid intake and output within 24 h, value of blood lactic acid, and oxygenation index of patients in 2 groups were recorded. Occurrence of acute respiratory distress syndrome (ARDS) on post injury day 3 to 7 and 8 to 28, mechanical ventilation time within post injury day 28, and occurrence of death of patients in 2 groups were counted. Data were processed with chi-square test, t test, and analysis of variance for repeated measurement. Results: The total fluid intakes within 24 h of patients in directed treatment group were close to those in routine treatment group on post injury day 3, 4, 5, 6, 7 (t=-0.835, -1.618, -2.463, -1.244, -2.552, P>0.05). The total fluid outputs and total fluid differences between fluid intake and output within 24 h of patients in 2 groups on post injury day 3 were close (t=0.931, -2.274, P>0.05). The total fluid outputs within 24 h of patients in directed treatment group were significantly higher than those in routine treatment group on post injury day 4, 5, 6, 7 (t=2.645, 2.352, 1.847, 1.152, P<0.05). The total fluid differences between fluid intake and output within 24 h of patients in directed treatment group were (2 928±768), (2 028±1 001), (2 186±815), and (2 071±963) mL, significantly lower than (4 455±960), (3 434±819), (3 233±1 022), and (3 453±829) mL in routine treatment group (t=-4.331, -3.882, -3.211, -4.024, P<0.05). The values of blood lactic acid of patients in directed treatment group and routine treatment group on post injury day 3, 4, 5, 6, 7 were close (t=0.847, 1.221, 0.994, 1.873, 1.948, P>0.05). The oxygenation indexes of patients in directed treatment group on post injury day 3 and 4 were (298±78) and (324±85) mmHg (1 mmHg=0.133 kPa ), which were close to (270±110) and (291±90) mmHg in routine treatment group (t=-1.574, 2.011, P>0.05). The oxygenation indexes of patients in directed treatment group on post injury day 5, 6, 7 were (372±88), (369±65), and (377±39) mmHg, significantly higher than (302±103), (313±89), and (336±78) mmHg in routine treatment group (t=3.657, 3.223, 2.441, P<0.05). On post injury day 3, 4, 5, 6, 7, patients with ARDS in directed treatment group were less than those in routine treatment group, but with no significantly statistical difference between the 2 groups (χ²=0.105, P>0.05). On post injury day 8 to 28, patients with ARDS in directed treatment group were significantly less than those in routine treatment group (χ²=0.827, P<0.05). The mechanical ventilation time within post injury day 28 of patients in directed treatment group was apparently shorter than that in routine treatment group (t=-2.895, P<0.05). Death of patients in directed treatment group within post injury day 28 was less than that in routine treatment group, but with no significantly statistical difference between the 2 groups (χ²=0.002, P>0.05). Conclusions Under the circumstance of hemodynamics stability, RFMS directed with goal of ELWI≤7 mL·kg^-1·m^-2 on post injury day 3 to 7 is an useful strategy, which can reduce occurrence rate of ADRS and shorten mechanical ventilation time of patients with serious burns complicated by severe inhalation injury at late stage of burns.

Objective: To investigate the effects of application of citrate anticoagulation in bedside continuous blood purification (CBP) of severe burn patients with sepsis, so as to provide reference for choosing anticoagulants in CBP of these patients. Methods: Thirty severe burn patients with sepsis, conforming to the study criteria, were admitted to our burn intensive care unit from January 2014 to July 2017. Patients were divided into heparin group and citrate group according to computer randomization method, with 15 cases in each group. Patients in two groups all received bedside CBP treatment. Patients in heparin group used local heparin anticoagulation, while patients in citrate group used local citrate anticoagulation. Time of predicted single-time CBP treatment, time of single-time CBP treatment, time of accumulative CBP treatment, and rate of reaching the standard of CBP treatment time were counted. Changes of prothrombin time (PT), activated partial thromboplastin time (APTT), international normalized ratio (INR), fibrinogen, serum procalcitonin, and C-reactive protein (CRP) of patients before and after treatment were monitored. Hemorrhage in wounds, incision on trachea, and arteriovenous intubation point, and other complications during and after CBP treatment were observed. Data were processed with independent sample t test and chi-square test. Results: (1) Time of predicted single-time CBP treatment of patients in the two groups was equal. Time of single-time CBP treatment and time of accumulative CBP treatment of patients in citrate group were longer than those in heparin group. Rate of reaching the standard of CBP treatment time of patients in citrate group was significantly higher than that in heparin group (χ²=16.655, P<0.01). (2) There was no statistically significant difference in PT, APTT, INR, fibrinogen, serum procalcitonin, and CRP of patients in the two groups before CBP treatment (t=0.203, -1.006, 0.203, 0.039, -1.591, -0.824, P>0.05). PT and APTT of patients in citrate group after CBP treatment were (14.2±1.6) and (45±7) s, respectively, significantly shorter than (15.5±1.4) and (53±6) s in heparin group (t=2.395, 3.321, P<0.05 or P<0.01). INR of patients in citrate group after CBP treatment was 1.13±0.12, significantly lower than 1.24±0.12 in heparin group (t=2.395, P<0.05). Fibrinogen of patients in citrate group after CBP treatment was (3.5±0.6) g/L, significantly higher than (3.0±0.6) g/L in heparin group (t=-2.427, P<0.05). Serum procalcitonin and CRP of patients in citrate group after CBP treatment were significantly lower than those in heparin group (t=2.520, 2.710, P<0.05). Decreased degree of serum procalcitonin and CRP of patients in citrate group after CBP treatment were (1.8±0.6) ng/mL and (143±69) mg/L, respectively, significantly higher than (0.9±0.6) ng/mL and (95±50) mg/L in heparin group (t=-4.033, -2.170, P<0.05 or P<0.01). (3) During CBP treatment, patients in heparin group experienced 21 times of exacerbation of wound hemorrhage and 10 times of new hemorrhage, including 2 times of hemorrhage at incision on trachea and 8 times of hemorrhage at arteriovenous intubation point. No exacerbation of hemorrhage or new hemorrhage happened in patients of citrate group. After CBP treatment, no electrolyte disturbance happened in patients of heparin group, but 1 patient in citrate group experienced hypocalcemia. Conclusions Application of citrate anticoagulation in bedside CBP of severe burn patients with sepsis shows light impact on systematic coagulation status, and can effectively decrease inflammation reaction of burn sepsis with low rate of hemorrhage.

Berberine (BBR) is known as a classic drug for intestinal infection treatment.BBR inhibits intestinal bacteria,which is the core of its role in the treatment of intestinal infection.With the survival of local intestinal bacteria and its related metabolites on the physiological and pathological functions of the body continue to recognize the impact of it,more and more literatures have presented the effect of BBR through the impact of intestinal bacteria on the body glycol-lipid metabolism,even brain function.This allows us to re-understand the pathophysiology of BBR in inhibiting gut microbiome.In this paper,the antibacterial activity of BBR was reviewed and analyzed.The possible molecular target of BBR was analyzed according to the characteristics of prokaryotes gene expression,which was helpful to the in-depth study of BBR on intestinal bacteria.Thus,a more comprehensive understanding of the pharmacological effects of BBR is given.

OBJECTIVETo observe the clinical effects of early blood purification in the treatment of phenol burn patients complicated by acute kidney injury (AKI).

METHODSFive phenol burn patients complicated by AKI, matched with the inclusion criteria, were hospitalized from January 2010 to July 2014. Within post injury hour 24, patients received rapid liquid support, positive wound management, and hemoperfusion (HP) combined with continuous veno-venous hemofiltration (CVVH) for 2 to 3 hours, then HP was stopped and CVVH was continued for 16 to 21 hours. HP combined with CVVH was performed for 2 to 3 times, then HP was stopped and CVVH was continued for 12 to 22 days. On post injury day (PID) 1, 3, 5, 7, 14, and 21, urea nitrogen, creatinine, ALT, AST, total bilirubin (TBIL), direct bilirubin (DBIL) in serum were determined, and the volume of liquid intake, urine, ultrafiltration, and liquid output were recorded, and the concentrations of IL-6, IL-10 and TNF-α in serum were determined by ELISA. General conditions of patients were recorded. Data were processed with one-way analysis of variance and LSD- t test.

RESULTS(1) On PID 1, the levels of urea nitrogen and creatinine were (9.0 ± 3.2) mmol/L and (115 ± 24) µmol/L respectively, which were obviously higher than normal values (with the values of 2.9-8.2 mmol/L and 45-104 µmol/L respectively). On PID 3, 5, 7 and 21, the levels of urea nitrogen were (12.5 ± 4.1), (11.2 ± 5.6), (8.7 ± 2.3) and (6.4 ± 3.9) mmol/L respectively, which were similar with the value of DID 1 (with t values 1.53, 0.76, 0.17 and 1.17 respectively, P values above 0.05). On PID 14, the level of urea nitrogen was (15.8 ± 3.3) mmol/L, which was obviously higher than the value of PID 1 (t =3 .29, P = 0.023). On PID 3, 5, 7 and 14, the levels of creatinine were (248 ± 67), (224 ± 87), (276 ± 59) and (307 ± 77) µmol/L respectively, which were obviously higher than the value of PID 1 (with t values 4.17, 2.70, 5.65 and 5.32 respectively, P values below 0.01). On PID 21, the level of creatinine was (78 ± 28) µmol/L, which was obviously lower than the value of PID 1 (t = 2.23, P = 0.041). The levels of ALT, AST, TBIL, and DBIL were higher than normal values from PID 1, and the levels were higher than normal values on PID 3, 5, 7, and 14, and they were similar with the normal values on PID 21. (2) On PID 1, 3, 5, 7, 14, and 21, the volume ratio of liquid intake to liquid output maintained from1:1 to 2:1. On PID 1, 3, 5, 7, and 14, although the volume of urine fluctuated, they were still less than 400 mL/d, and the volume for ultrafiltration showed a tendency from declining at first to a rise later. On PID 21, the volume of urine increased, and the volume for ultrafiltration decreased. (3) On PID 1, the serum concentrations of TNF-α and IL-6 increased, and the serum concentration of IL-10 decreased. On PID 3, 5, and 7, the serum concentrations of TNF-α and IL-6 decreased, and the serum concentration of IL-10 increased. On PID 14, the serum concentrations of TNF-α and IL-6 were elevated again but without a high peak value, and the serum concentration of IL-10 decreased but still higher than the value of PID 1. On PID 21, the serum concentrations of TNF-α and IL-6 obviously decreased, and the serum concentration of IL-10 obviously elevated. (4) Primary healing of the wound was achieved on PID 21 to 28. Patients were all cured and left hospital on PID 28 to 45. All the patients were followed up for 6 months to 3 years. At the last follow up, patients had no symptoms of chronic poisoning and the functions of liver and kidney were normal.

CONCLUSIONSEarly blood purification treatment is effective for phenol patients phenol burn patients complicated by AKI, and wound healing and kidney function recovery were assured.

Acute Kidney Injury ; complications ; therapy ; Biomarkers ; blood ; Burns, Chemical ; blood ; complications ; therapy ; Enzyme-Linked Immunosorbent Assay ; Hemofiltration ; Humans ; Interleukin-10 ; metabolism ; Interleukin-6 ; blood ; Phenol ; adverse effects ; Phenols ; Serum ; metabolism ; Severity of Illness Index ; Treatment Outcome ; Tumor Necrosis Factor-alpha ; blood ; Wound Healing