Objective The purpose of this study was to determine the relationship between microecological balance and the syndrome type of acute upper respiratory infection.Methods The nature and quantity of pharyngeal flora were assayed in 31 cases of wind-cold acute upper respiratory infection and 36 cases of wind-heat acute upper respiratory infection,with 30 healthy cases served in control group.Results There was a significant rise of concentration of pharynx flora in acute upper respiratory infection than that in control group,whereas there was a significant decrease of diversity of pharynx flora in acute upper respiratory infection than that in control.Conclusion Imbalance of pharyngeal micro-ecology is one of the major factors leading to acute upper respiratory infection,manifested as insufficiency of genuine Qi failure in guarding.

OBJECTIVETo explore the technique of temperature control on the abdomen in penetrating moxibustion through observing moxibustion time on the abdomen, abdominal skin temperature and effect after moxibustion so as to provide the safe, effective and easily applicable method for penetrating moxibustion.

METHODSThirty-two patients were selected in an observation group, 32 healthy persons in a control group. In the observation group, the penetrating moxibustion was applied to the corresponding acupoint locations according to different symptoms. In the control group, moxibustion was used on the abdomen around the umbilicus. The skin temperature was recorded once every minute. The skin temperature of known heat sensation, the time of known heat sensation, the known reduced temperature, the time of temperature reducing, the skin temperature difference, the duration of penetrating moxibustion and the reaction of moxibustion from participants were recorded.

RESULTSThe differences in the skin temperature of known heat sensation, the time of known heat sensation and the duration of penetrating moxibustion were significant statistically in comparison between the observation group and the control group (all P<0.01). The differences in the known reduced temperature, the time of temperature reducing and the skin tem- perature difference were not significant (all P>0.05). The differences were significant statistically in skin rashes and moxibustion reaction (gastrointestinal peristalsis, chills, ant climbing feeling and hunger, etc.) between the two groups (P<0.01). The differences were not significant statistically in flushing, sweating and blisters (all P>0.05).

CONCLUSION(1) The level of temperature sensitivity in the observation group is lower than that in the control group. During penetrating moxibustion, the sensations such as gastrointestinal peristalsis, chills, ant climbing feeling and hunger appear easily, suggesting the positive self-adjustment in the body. (2) During penetrating moxibustion, the warm feeling is penetrated not just from the epidermis to the abdominal cavity and lumbar region, but also up to thehead and down to the knee. (3) The flushing, sweating and skin rashes are the important indices for the effectiveness of penetrating moxibustion. (4) The temperature control is the core technique of penetrating moxibustion. The penetrating moxibustion in 28 min to 32 min and the temperature controlled in 43 degrees C to 45 degrees C can solve the moxibustion smoky impact to the environment, but also relieve pains of the patients.

Abdomen ; physiology ; Acupuncture Points ; Adult ; Case-Control Studies ; Female ; Humans ; Male ; Middle Aged ; Moxibustion ; Skin Temperature ; Thermosensing ; Young Adult

Objective To investigate the effect of propofol on the activation of c-Jun N-terminal kinase (JNK) in hippocampus following asphyxial cardiac arrest-resuscitation in rats.Methods Forty male Sprague-Dawley rats,aged 6 months,weighing 350-380 g,were randomly divided into 4 groups (n =l0 each):sham operation group (group S),asphyxial cardiac arrest-cardiopulmonary resuscitation group (group CA-CPR),propofol group (group P) and normal saline group (group NS).All the rats were tracheostomized and mechanically ventilated after anesthetization.Cardiac arrest was induced by clamping the tracheal tube at the end of exhalation until ECG activity disappeared and MAP ＜ 10 mm Hg.Resuscitation was started 3 min later.MAP ＞ 60 mm Hg and HR ＞ 250 bpm were considered to be signs of successful resuscitation.Propofol 2 mg/kg was injected intravenously at 30 min before asphyxia,followed by propofol infusion at a rate of 4 mg· kg-1 · h-1 until the start of resuscitation in group P,while the equal volume of normal saline was given in group NS.At 12 h after successful resuscitation,the animals were sacrificed and brains were harvested for determination of wet/dry brain weight (W/D) ratio in brain tissues and expression of phosphor-JNK (p-JNK) in hippocampus (by immuno-histochemistry and Western blot),and for examination of the pathological changes of hippocampus.Results Compared with group S,W/D ratio was significantly increased and the expression of p-JNK in hippocampus was up-regulated in CA-CPR,P and NS groups (P ＜ 0.05 or 0.01).Compared with group CA-CPR,W/D ratio was significantly decreased and the expression of p-JNK in hippocampus was down-regnlated in group P (P ＜ 0.05 or 0.01),and no significant change was found in the indexes mentioned above in group NS (P ＞ 0.05).The pathological changes of hippocampus were significantly attenuated in group P compared with group CA-CPR.Conclusion Propofol can inhibit the activation of JNK in hippocampus following asphyxial cardiac arrest-resuscitation in rats and thus reducing brain injury.

Objective To evaluate the role of JNK signal pathway in brain injury after resuscitation in a rat model of asphyxia cardiac arrest.Methods Forty healthy male SD rats 'weighing 300-350 g were randomly divided into 4 groups ( n =10 each):sham operation group (group SH) ; cardiac arrest group (group CA) ; group SP600125-JNK inhibitor (group SP) and dimethyl sulfexide (DMSO) group.The rats were anesthetized with intraperitoneal pentobarbital 45 mg/kg,tracheostomized and mechanically ventilated.PETCO2 was maintained at 35-45 mm Hg.Femoral artery and vein were cannulated for BP monitoring and fluid infusion.Cardiac arrest was induced by clamping tracheal tube until ECG activity disappeared and MAP ＜ 10 mm Hg.Resuscitation was started at 3 min after cardiac arrest.MAP ＞ 60 mm Hg and HR ＞ 250 bpm were considered to be signs of successful resuscitation.SP600125 20 mg/kg and DMSO 0.2 ml were injected iv as soon as chest compression was started in groups SP and DMSO respectively.The animals were sacrificed at 5 h after successful resuscitation and their brains were removed for determination of wet/dry (W/D) weight ratio and microscopic examination of hippocampus.Neuronal apoptosis was detected by TUNEL.Results Cardiac arrest significantly increased W/D ratio and the number of apoptotic cells in group CA.SP600125 iv significantly attenuated the cardiac arrest-induced increase in W/D ratio and the number of apoptotic cells but DMSO did not.Conclusion JNK signal pathway is involved in the brain injury after resuscitation in a rat model of asphyxia cardiac arrest.

Objective To evaluate the role of c-Jun N-terminal kinase (JNK) in lipopolysaccharide (LPS)-induced acute lung injury ( ALI) in rats.Methods Eighty male SD rats weighing 250-300 g were randomly divided into 4 groups ( n = 20 each) : control group (group C) ; ALI group; LPS + SP600125 (JNK inhibitor)group (group S) and LPS+ DMSO (the solvent) group (group DMSO) . ALI was induced by intravenous LPS 5mg/kg. In S and DMSO groups, SP600125 30 mg/kg and DMSO 0.2 ml were injected intravenously after LPS administration respectively. Ten animals were sacrificed by exsanguinafions at 4 h after LPS administration in each group. The broncho-alveolar lavage fluid (BALF) was colleted. The TNF-α and IL-1β concentrations in BALF were measured. The lungs were removed for microscopic examination and determination of W/D lung weight ratio. The other 10 animals in each group were observed for 48 h survival rate. Results Intravenous LPS significantly increased TNF-α and IL-1β concentrations in BALF and W/D lung weight ratio, decreased 48 h survival rate and induced histologic damage. Intravenous SP600125 30 mg/kg significantly attenuated the above-mentioned LPS-induced changes. Conclusion Activation of JNK is involved in the development of endotoxin-induced ALI in rats.

This article was aimed to explore the effect ofSan-Huang (SH) decoction on improving chemosensitivity of MCF-7 cells to epirubicin and inhibition of Aurora kinase A, in order to discuss its underlying mechanism. The inhibition of MCF-7 cells proliferation on breast cancer by SH decoction was determined by CCK-8 assay. RT-PCR and western blot were used to detect the Aurora A, p53 mRNA and protein expression level of MCF-7 cells by SH decoction. The siRNA silenced Aurora A of MCF-7 cells. CCK-8 assay was used to detect the inhibition of MCF-7 cells proliferation. CCK-8 assay and AnnexinV-FITC/PI staining were used to detect the inhibition rate and apoptosis rate of MCF-7 cells treated by the combination of SH decoction and epirubicin. Western blot analysis was used to detect the expression of apoptosis-related proteins. The results showed that SH decoction inhibited the proliferation of MCF-7 cells in a dose-dependent manner (P< 0.05). The effect of 48 h medication was better than 24 h (P < 0.05). There was no statistical difference with medication for 72 h (P > 0.05). SH decoction can regulate the Aurora A, p53 protein and mRNA expression of MCF-7 cells. siRNA silenced Aurora A, which downregulated the inhibition rate of MCF-7 cells by SH decoction for 50.0% (from 49.2% to 24.8%). The combination of SH decoction and epirubicin enhanced the effect of epirubicin on inhibiting the proliferation rate and apoptosis rate of MCF-7 cell, regulated the expression levels of apoptosis-related protein such as c-PARP, c-Caspase 3, Bcl-2, Bax, as well as the protein level of Aurora A. It was concluded that SH decoction can increase the chemosensitivity of MCF-7 cells to epirubicin, which may be related to the inhibition of Aurora Kinase A by SH decoction.

Objective To systematically review the clinical efficacy of transanastomotic pancreatic ductal stents placement after pancreaticoduodenectomy.Methods According to the Cochrane reviewers handbook (version 5.0 ),literatures were retrived from PubMed,Embase,Cochrane,VIP database,China Biology Medicine disc and CNKI database,and then the quality of the literatures was analyzed.Meta analysis was carried out using the RevMan software ( version 5.0.18 ).A random effects model was adopted,and the results of the meta analysis were presented with odds ratio (OR) and 95％ confidence interval (95％ CI).Results Four randomized controlled trials including 557 patients were retrieved.External stents were used in 160 patients and internal stents in 115 patients.The results of meta analysis showed no significant difference in the rate of fistula,overall postoperative morbidity and mortality between patients who did or did not receive pancreatic stents placement (OR =0.66,0.70,0.63,P ＞ 0.05 ).There were significant differences in the rate of pancreatic fistula and overall postoperative morbidity between patients who received external pancreatic stents placement and those did not receive pancreatic stents placement ( OR =0.48,0.55,P ＜ 0.05 ).There was no significant difference in the mortality rate between patients who received external pancreatic stents placement and those did not receive pancreatic stents placement (OR =0.71,P ＞ 0.05 ).There were no significant difference in the incidence of pancreatic fistula,overall postoperative morbility and mortality between patients who received internal pancreatic stents placement and those did not receive pancreatic stents placement ( x2 =0,0.75,2.11,P ＞ 0.05 ).Conclusions External pancreatic stents placement after pancreaticoduodenectomy can reduce the incidence of postoperative complications.The effects of internal pancreatic stents placement need to be proved by further highquality prospective randomized trials.

Objective To investigate the correlation of single nucleotide polymorphism of rs3731055 and rs2607775 of xeroderma pigmentosum group C (XPC) and smoking with genetic susceptibility to pancreatic cancer.Methods The clinical data of 214 patients with pancreatic cancer who were admitted to the First and Third Affiliated Hospitals of Xinjiang Medical University from January 2009 to June 2011 and 214 healthly individuals were retrospectively analyzed.The samples of venous blood of 214 patients with pancreatic cancer (case group) and 214 healthy individuals (control group) were analyzed by the Multiplex SNaPshot method.The count data were analyzed using the chi-square test.The association between the single nucleotide polymorphism of rs3731055 and rs2607775 with genetic susceptibility to pancreatic cancer was analyzed using the Logistic regression method.Results Four hundred and twenty-three samples of gene were successfully typed,including 210 in the case group and 213 in the control group.The frequency of G allele of XPC rs3731055 was 75.95％ (319/420) in the case group and 77.00％ (328/426) in the control group,with no significant difference between the 2 groups (x2 =0.12,P ＞ 0.05).The frequencies of genotypes GG,GA and AA were 58.57％ (123/210),34.76％ (73/210) and 6.67％ (14/210) in the case group,and 60.09％ (128/213),33.80％ (72/213) and 6.10％ (13/213) in the control group,with no significant difference between the 2 groups (x2=0.12,P ＞ 0.05).The frequency of C allele of XPC rs2607775 was 87.86％ (369/420) in the case group and 93.43％ (398/426) in the control group,with significant difference between the 2 groups (x2=7.75,P ＜ 0.05).The frequencies of genotypes CC,CG and GG were 77.62％ (163/210),20.48％ (43/210) and 1.90％ (4/210) in the case group,and 86.85％ (185/213),13.15％ (28/213) and 0(0/213) in the control group,with significant difference between the 2 groups (x2=8.54,P ＜ 0.05).Patients with rs2607775 GC genotype were associated with a significantly increased risk of pancreatic cancer compared with patients with rs2607775 CC genotype (adjusted OR =1.81,95％ CI:1.06-3.10,P ＜ 0.05).Patients with rs2607775 GC + GG genotype were associated with a significantly increased risk of pancreatic cancer compared with patients with rs2607775 CC (adjusted OR =1.98,95％ CI:1.16-3.36,P ＜ 0.05).The ratio of patients in the case group who smoked cigarettes ≥ 17 pack years was 25.24％ (53/210),which was significantly higher than 13.15 ％ (28/213) of the control group (x2 =11.37,P ＜ 0.05).The results of univariate analysis showed that patients who smoked cigarettes ≥ 17 pack years had higher risk of getting pancreatic cancer (adjusted OR =2.82,95％ CI:1.27-6.29,P ＜ 0.05).Patients who smoked cigarettes ≥ 17 pack years and with rs2607775 CC also had higher risk of getting pancreatic cancer (adjusted OR =2.87,95％ CI:1.18-6.99,P ＜0.05).No significant gene-environment interaction was observed between rs2607775 GC + GG and smoking ≥ 17 pack years (adjusted OR =3.65,95％ CI:0.67-20.03,P ＞ 0.05).Conclusions The polymorphisms of XPC rs2607775 may play a role in the onset of pancreatic cancer.Patients who smoke cigarettes ≥ 17 pack years are more easily to have pancreatic cancer.There is no interaction between smoking and XPC rs2607775 in influencing the progression of pancreatic cancer.

Objective To investigate the effects of uric acid (UA) and UA under oxidative stress on cultured human umbillical vein endothelial cells (HUVEC).Methocds HUVECs were incubated with different concentration UA (0,4,8,16 mg/dL),H2O2 (500 mmol/l) and UA+H2O2 (500 mmol/l) for 24,48 and 72 hours.Then we observed the morphology of HUVECs and evaluated the proliferation of HUVECs by MTT assay.NO and ET-1 in supernatant medium was detected by ELISA.Results For the viability of HUVECs,there was no statistically significant difference between 4 mg/dL UA group and control group after incubation for 24,48 and 72 hours (P＞0.05) and between UA groups(8 mg/dL and 12 mg/dL) and control group after incubation for 24,48 and 72 hours (P＞0.05).After incubation with 12 mg/dL of UA for 48 hours or 8 mg/dL of UA for 72 hours,the viability of HUVECs decreased significantly (P ＜0.05) The viability of HUVECs in H2O2 group decreased significantly (P＜0.05).The viability of HUVECs in UA+H2O2 groups after incubation for 24 h was significantly better than H2O2 group.There was no signifiant difference in the cell viability between (8 mg/dL or 12 mg/dL) UA+H2O2 group and H2O2 group.Compared with the control group,the NO levels were decreased and the ET-1 levels were increased in the supernatants of HUVECs in 12 mg/dL UA group for 72 hours (P＜0.05).Compared with H2O2 group,the NO levels were increased and the ET-1 levels were decreased in the supematants of HUVECs in (8 mg/dL or 12 mg/dL) UA +H2O2 groups for 24 hours (P＜0.05),while for (12 mg/dL) UA +H2O2 group for 72 hours,the results were just the contary.Conclusion The effects of UA on HUVECs are related with both concentration and action rime.Acutely increased UA may protect HUVECs form injury,while long action of UA may injure HUVECs,especially under oxidative stress.

Objective To investigate the effect of hypertonic saline in the management of murine experimental severe acute pancreatitis (SAP) Methods SAP was induced in Wistar rats by intraperitoneal injection of 20% L Arginine Rats were divided into four groups ( n =12 in each group ); Healthy controls received intraperitoneal injection of distilled water of 5 ml/kg body weight initially Rats in the four groups were infused at 24 h and 48 h respectively at a dosage of 2 ml/kg body weight of distilled water in both healthy contrals, and SAP controls, of normal saline in group 3 and of hypertonic saline (7 5% sodium chloride) in group 4 Blood samples were collected at 48 h and 72 h after last injection for the measurement of plasma TNF ?、IL 6、 IL 10 All rats were sacrificed for histopathology of pancreatic and lung tissues at 72 h Results Animals that received hypertonic saline showed less pancreatic and lung damage than those resuscitated with normal saline Plasma levels of TNF ?、 IL 6 decreased significantly and plasma levels of IL 10 increased more significiently at 72 h after induction of SAP Conclusion Hypertonic saline resuscitation result in a significant attenuation of the systemic inflammatory response to severe acute pancreatitis