[Objective] To observe the therapeutic effect of diarrhea-predominant irritable bowel syndrome patients’ life quality with Geshanxiaoyao decoction combining acupuncture.[Methods] 300 patients were randomly divided into therapeutic group (n=150) and control 1,2,3 groups (n=50).150 cases were treated with Geshanxiaoyao decoction combined with pricking taichong,sanyinjiao,shaohai; control 1,2,3 groups were respectively treated with Li-Zhu-Chang-Le,Geshanxiaoyao decoction and acupuncture,4 weeks a course.Clinical symptoms and life quality before and after treatment were recorded and analyzed.[Results] The total effective ratio in therapeutic group(89.71%) was higher than that in control 1,2,3 groups (68.52%,74.31%,66.87%) respectively.There was significant difference between therapeutic group and control groups.[Conclusion]Geshanxiaoyao decoction combining acupuncture can effectively improve the life quality of patients with diarrhea-predominant irritable bowel syndrome.

Objective To evaluate the effect of sevoflurane postconditioning on the expression of CCAAT/enhancer-binding protein homologous protein (CHOP) in a rat model of hemorrhagic shock and resuscitation.Methods Thirty-six healthy adult male Sprague-Dawley rats,weighing 300-350 g,were divided into 3 groups (n=12 each) using a random number table:sham operation group (group S),hemorrhagic shock and resuscitation group (group HSR) and sevoflurane postconditioning group (group SP).Hemorrhagic shock was induced by withdrawing 40% of the total blood volume from the right carotid artery over an interval of 30 min,and 1 h later the removed blood was reinfused via the left jugular vein for resuscitation.Group SP inhaled 2.4% sevoflurane for 30 min starting from the onset of reinfusion.Mean arterial pressure was monitored and recorded at a 10 min interval.Before withdrawing blood (T0),immediately after the end of withdrawing blood(T1), at 1 h after the end of withdrawing blood(T2) and immediately after the end of reinfusion (T3),blood samples were collected from the common carotid artery for blood gas analysis.At 4 days after reinfusion,6 rats of each group were selected to detect spatial learning and memory ability by using Morris water maze test.The animals were then sacrificed,brains were removed for determination of neuronal apoptosis in hippocampal CA1 area using TUNEL.The rest 6 rats in each group were sacrificed at 72 h after reinfusion,and the hippocampus was isolated to detect the expression of CHOP by Western blot.Results Compared with group S,mean arterial pressure was significantly decreased,and lactic acid concentrations were increased at T1,2 in HSR and SP groups,and the escape latency was significantly prolonged,the percentage of time staying at the target quadrant was decreased,the number of apoptotic neurons in hippocampal CA1 area was increased,and the expression of CHOP was up-regulated in group HSR (P<0.05).Compared with group HSR,the escape latency was significantly shortened,the percentage of time staying at the target quadrant was increased,the number of apoptotic neurons in hippocampal CA1 area was decreased,and the expression of CHOP was down-regulated in group SP (P<0.05).Conclusion The mechanism by which sevoflurane postconditioning improves cognitive function is related to down-regulation of CHOP expression and inhibition of apoptosis in hippocampal neurons in a rat model of hemorrhagic shock and resuscitation.

Objective To investigate the antishock effect of oxygenate solution and its possible mechanism. Methods The protective effects of oxygenates hypertonic hypercolloid solution on lipid peroxidation injures in hemorrhagic shock in rabbits at 4 700 m high altitude spot was observed. Results The oxygenated solution treatment can obviously reduce the malondialdehyde(MDA) and glutathione(GSH) level in plasma and tissue ; and increase the superoxide diamutase(SOD) and glutathione peroxidase(GSH-PX) level in plasma and tissue of the hemorrhagic shock animals. Conclusions Oxygenatea solution treatment can reduce the lipid peroxidation injure, recover the equilibrium of oxidation and antioxidation with shock body in time, and promote the resuscitation of shock.

The spleen cells from the BALB/C mouse immunized with the type B toxoid were fused with aNS-1 myeloma cell line. The superatant containing the hybridoma-formed cells with growing pores wasscreened by EL1SA, in which 66.7% the pores could secrete the specific antibodies against botulin.After a Subclonizing culture by the limiting dilution technique four hybridoma cell lines(3B10, 3B11, 3G12 and 4A5) were established and could secrete the specific antibodies persistently in the culture medium. in which antibody titers came to 10-3-10-5, while they were injected into the BALB/C mice intrape ritoneally ascites rich in antibodies with a titer of 10-5-10-8 was produced. The results testing the (our monoclonal antibodies with the type A and B toxoids showed that the antibodies of 3G12and 4A5 were specific for the type B toxoid, and those of 3B10 and 3B11 had light cross reaction with the type A toxoid. Identification of 1g showed that the antibodies of 3B10 and 3G12 were of IgG1, while those of 3B11 and 4A5 of IgG2. The chromosomal assay confirmed the four cell lines to be hybridoma. The neutroligation test in mice revealed that those four monoclonal antibodies did not show any protective effects on botulin.

Objective To evaluate the effect of sevoflurane postconditioning on the expression of activating transcription factor 6 (ATF6) in the brain tissues in a rat model of hemorrhagic shock and resuscitation.Methods Thirty-six pathogen-free healthy adult male Sprague-Dawley rats,weighing 300-350 g,were randomized into 3 groups (n=12 each) using a random number table:sham operation group (group S);hemorrhagic shock and resuscitation group (group HSR);sevoflurane postconditioning group (group SP).Hemorrhagic shock was induced by withdrawing blood (40％ of the total blood volume) from the right common carotid artery over an interval of 30 min,and 1 h later the animals were resuscitated with infusion of the shed blood via the left jugular vein over 30 min.In group SP,2.4％ sevoflurane was inhaled for 30 min starting from the onset of infusion of the shed blood.Mean arterial pressure was recorded before withdrawing blood (T0),immediately after the end of withdrawing blood (T1),at 30 min after the end of withdrawing blood (T2),before infusion of the shed blood (T3),and immediately after infusion of the shed blood (T4).The arterial blood samples were obtained at T0,T1,T3 and T4 for blood gas analysis.At 72 h after infusion of the shed blood,6 rats were selected from each group,and cognitive function was assessed by Y-maze test.The animals were then sacrificed,and brains were removed and sliced for determination of the expression of caspase-12 in hippocampal CA1 region by immunohistochemistry.The rest 6 rats in each group were sacrificed at 72 h after infusion of the shed blood,and the hippocampus was isolated for determination of the expression of ATF6 and caspase-12 by Western blot.Results Compared with group S,mean arterial pressure was significantly decreased at T1-3 (P＜0.05),the pH value and base excess were significantly decreased at T1.3,and the blood lactic acid was significantly increased at T1,3 in HSR and SP groups,and the number of total training was significantly increased,the rate of memory retention was significantly decreased,the expression of caspase-12 in hippocampal CA 1 region was significantly up-regulated,and the expression of ATF6 and caspase-12 in hippocampal tissues was significantly up-regulated in group HSR (P＜ 0.05).Compared with group HSR,the number of total training was significantly decreased,the rate of memory retention was significantly increased,the expression of caspase-12 in hippocampal CA1 region was significantly down-regulated,and the expression of ATF6 and caspase-12 in hippocampal tissues was significantly down-regulated in group SP (P＜0.05).Conclusion The mechanism by which sevoflurane postconditioning improves cognitive function is related to down-regulation of ATF6 expression in the brain tissues in a rat model of hemorrhagic shock and resuscitation.

Objective To evaluate the effect of sevoflurane postconditioning on inositol-requiring enzyme 1 (IRE1) signaling pathway in the brain tissues in a rat model of hemorrhagic shock and resuscitation (HSR).Methods Sixty healthy adult male Sprague-Dawley rats,weighing 300-350 g,were divided into 5 groups (n =12 each) using a random number table:sham operation group (group Sham),group HSR,1.2％ sevoflurane postconditioning group (group SP1),2.4％ sevoflurane postconditioning group (group SP2) and 3.6％ sevoflurane postconditioning group (group SP3).Hemorrhagic shock was induced by withdrawing blood (40％ of the total blood volume) from the right common carotid artery over an interval of 30 min,and 1 h later the animals were resuscitated with the shed blood infused via the left jugular vein over 30 min.SP1,SP2 and SP3 groups inhaled 1.2％,2.4％ and 3.6％ sevoflurane,respectively,for 30 min starting from the beginning of infusion of the shed blood.Oxygen was inhaled for 30 min instead of sevoflurane in Sham and HSR groups.Mean arterial pressure was recorded before withdrawing blood (T0),immediately after the end of withdrawing blood (T1),at 30 min after the end of withdrawing blood (T2),before infusion of the shed blood (T3),and immediately after infusion of the shed blood (T4).Arterial blood samples were obtained at T0,T1,T3 and T4 for blood gas analysis.Morris water maze test was performed at 72 h after the end of infusion of the shed blood.The animals were then sacrificed,and brains were removed for determination of the expression of caspase-3 in hippocampal CA1 region (by immunohistochemistry) and expression of IRE1 and X-box binding protein 1 (XBP1) in hippocampal tissues (by Western blot).Results Compared with group Sham,mean arterial pressure was significantly decreased at T1-3,the pH value and base excess were decreased,lactic acid concentrations were increased,the escape latency was prolonged,the frequency of crossing the original platform was decreased,and the expression of caspase-3 in hippocampal CA1 regitn and IRE1 and X BP 1 in hippocampal tissues was up-reg ulated in group HSR (P＜0.05).Compared with group HSR,the escape latency was significantly shortened,the frequency of crossing the original platform was increased,and the expression of caspase-3 in hippocampal CA1 region and IRE1 and XBP1 in hippocampal tissues was down-regulated in SP2 and SP3 groups (P＜0.05),and no significant changes were found in the parameters mentioned above in group SP1 (P＞0.05).Conclusion The mechanism by which sevoflurane postconditioning reduces brain injury may be related to activating IRE1 signaling pathway in the brain tissues in a rat model of HSR.

[ ABSTRACT] AIM: To investigate the seroprevalence of neutralizing antibodies to human adenovirus type 5 (AdHu5) , human adenovirus type 26 (AdHu26) and chimpanzee adenovirus type 68 (AdC68) in the patients with chro-nic hepatitis B ( CHB) and the patients with primary liver cancer ( PLC) , and to provide guidance for developing safe and effective biotherapy vectors against CHB and PLC.METHODS:The blood samples from 196 patients with CHB and 193 patients with PLC were examined to assess the presence of neutralizing antibodies against AdHu5, AdHu26 and AdC68 by adenovirus neutralization assays.RESULTS:The seroprevalence rates of neutralizing antibodies to AdHu5, AdHu26 and AdC68 in the CHB patients were 84.7%, 58.2%and 39.8%, respectively.Among the patients with PLC, the prevalence rates of neutralizing antibodies were as follows:AdHu5, 75.1%;AdHu26, 66.8%;AdC68, 32.1%.CONCLUSION:The prevalence rates and titers of neutralizing antibodies against AdC68 were the lowest among the 3 adenoviruses.There-fore, AdC68 serves as more suitable biological therapy vectors for CHB and PLC than AdHu5 and AdHu26.

BACKGROUND: The establishment of amniotic fluid derived stem cells (AFS) can provide an individual reserve for cell therapy in nerve degenerative diseases.OBJECTIVE: To observe the effects of Noggin and basic fibroblast growth factor (bFGF) on AFS differentiation into neural cells.METHODS: Samples of amniotic fluid were obtained through amniocentesis by ultrasound from gestational age of 16-22 weeks for routine prenatal diagnosis. AFS were obtained from the 2~(nd) trimester amniotic fluid samples by immunomagnetic beads selection using CD117 antibody, and identified the surface antigen expression by flow cytometry after amplification. The 3~(rd) generation of AFS with good growth state were induced to differentiate into nerve cells, which were divided into the blank control,based-induced, Noggin-induced and bFGF-induced groups. The induced cell morphology was observed under inverted phase contrast microscopy, and the expression of nestin, β-Ⅲ tubulin and neurofilament in the induced cells was measured by using cell immunofluorescence detection.RESULTS AND CONCLUSION: Flow cytometry analysis indicated that most of AFS cells expressed CD44 and HLA-ABC, but negative for CD45 and HLA-DR. At 2 weeks after induction, the cell morphology exhibited significant changes with increased Nestin,β-Ⅲ tubulin and NF-positive rates in the bFGF-induced group. However, it had no significant difference in the Noggin-induced group and the based-induced group. It revealed that bFGF plays a vital role in the AFS differentiated into nerve cells.

Ischemia-reperfusion injury (IRI) is an extremely complicated pathophysiological process, which may occur during the process of myocardial infarction, stroke, organ transplantation and temporary interruption of blood flow during surgery, etc. As key molecules of immune system, macrophages play a vital role in the pathogenesis of IRI. M1 macrophages are pro-inflammatory cells and participate in the elimination of pathogens. M2 macrophages exert anti-inflammatory effect and participate in tissue repair and remodeling and extracellular matrix remodeling. The balance between macrophage phenotypes is of significance for the outcome and treatment of IRI. This article reviewed the role of macrophages in IRI, including the balance between M1/M2 macrophage phenotype, the mechanism of infiltration and recruitment into different ischemic tissues. In addition, the potential therapeutic strategies of targeting macrophages during IRI were also discussed, aiming to provide reference for alleviating IRI and promoting tissue repair.

Objective:To observe the clinical efficacy of acupuncture plus point application in managing pain after thoracoscopic radical lung cancer surgery(TRLCS). Methods:A total of 120 patients undergoing TRLCS were randomized into a treatment group and a control group,with 60 cases in each group.Both groups received patient-controlled intravenous analgesia(PCIA)to relieve postoperative wound pain.The control group did not receive any other interventions.The treatment group started acupuncture treatments 4 h after the surgery with point application between two acupuncture sessions;the acupuncture treatment was conducted 4,24,48,and 72 h after the surgery.At the above 4 time points,the visual analog scale(VAS)score and additional PCIA drug consumption were recorded.The 5-hydroxytryptamine(5-HT)content in the peripheral blood was determined 4 h and 72 h after the surgery. Results:The treatment group was superior to the control group in comparing the total effective rate(P<0.05).After the intervention,the VAS score decreased in both groups(P<0.05);the VAS score presented different decreasing patterns at each time point in the two groups,and the score dropped more significantly in the treatment group than in the control group(P<0.05).The total PICA drug consumption varied in the two groups after the surgery;the additional analgesic consumption was notably smaller in the treatment group than in the control group(P<0.05).The decrease in the 5-HT content in the peripheral blood also varied in the two groups;the peripheral blood 5-HT content was significantly lower in the treatment group than in the control group(P<0.05). Conclusion:Acupuncture plus point application can significantly relieve wound pain after TRLCS.