[Summary] Hyperuricemia is a syndrome caused by increased production or reduced excretion of uric acid which is characterized by oliguria, anuria, and uremia. Recent studies found that hyperuricemia was correlated with the risk, recurrence, metastasis, and prognosis of cancer. The mechanism may be uric acid associated chronic inflammation and decrease of xanthine oxidoreductase expression in cancer cells. Current treatment of hyperuricemia is to reduce the production of uric acid by inhibition of xanthine oxidoreductase, but the side effects of systemic inhibition of xanthine oxidoreductase received more and more attention. These unwanted side effects underscore the urgent need for mechanism based preclinical studies that can identify optimal strategies for management of hyperuricemia in relevant cancer models.

This paper reviewed that high-intensity interval training (HIT) is effective on cardiorespiratory fitness and walking ability, but limited in quality of life in stroke paitents. More researches are needed to explore the differences from HIT to low and moderate intensi-ty continuous training .

Objective To find a proper way for accurate results on completing blood counts.Methods Based on the results from automatic hematology analyzer XE-2100,set up the criteria for blood cell microscopic examination.1368 blood specimen were detected and the results were analyzed according to the criteria.Statistics on the data were made to evaluate the accordance between warnings of analyzer and manual examination,likewise the reliability of the criteria.Results Comparing with microscopic examination,analyzer warning on low PLT has good accordance,Kappa value was 0.95,U value was 35.19,P

Objective To investigate the risk factors for early postoperative cognitive function in the patients with peritoneal surface malignancies after cytoreductive surgery and hyperthermic intra-peritoneal chemotherapy(CRS-HIPEC).Methods Fifty-one patients(21 men and 30 women), ranged from 25 to 65 years,42-80 kg,ASA Ⅰ-Ⅲ,undergoing CRS-HIPEC under combined intrave-nous-inhalational anesthesia,were studied.Patients were assigned into postoperative cognitive dys-function (POCD)group or non-POCD group according to their performances of visual verbal learning test,concept shifting task,letter-digit coding test and stroop color-word test 1 day before operation and 7 days after operation.Years of education,medical history,duration of operation,intraoperative blood loss,frequency of cardiovascular events,amount of fluid infused per hour and VAS scores were recorded.Venous blood samples were taken at five time points:before surgery(T0 ),30 minutes after the beginning of the procedure(T1 ),30 minutes after the beginning of HIPEC(T2 ),at the end of the surgery(T3 )and 24 hours after the surgery(T4 ),to determine the concentration of serum amyloid A (SAA).pH,PaCO 2, Hb,blood glucose were recorded at T0-T2.Then the data was statistically analyzed.Results According to the diagnostic criteria,twenty patients developed POCD 20 (39.2%). There were significant differences between POCD and non-POCD groups on age,gender, pre-operative complications and the origin of tumor(P <0.05).The concentration of SAA increased from T2 and reached the peak at T4 ,and SAA concentration for patients in POCD group was higher than that for patients in non-POCD group(P <0.05).Compared with non-POCD group,the levels of blood glucose were significantly increased in POCD group at T2 (P <0.05).Conclusion CRS-HIPEC resul-ted in exaggerated and prolonged inflammatory response.Advanced age,female,diabetes,hyperten-sion,peritoneal carcinomatosis from ovarian cancer and endometrial cancer are associated with early POCD in the patients undergoing CRS-HIPEC.

ObjectiveTo compare the roles of Toll-like receptor-4 (TLR-4) in the acute lung injury (ALI) induced by lipopolysaccharide (LPS) and by hemorrhagic shock and resuscitation (HSR) and LPS (twohit) in mice.MethodsTwo types of mice were used in this study:free wild type mice (C3H/HeN) and TLR4 gene mutation type ( C3H/HeJ).Each type of mice was randomly divided into 2 groups ( n ＝ 18):group sham operation+ LPS (group S/LPS) and group HSR + LPS (group HSR/LPS).Hemorrhagic shock was induced by blood withdrawal until MAP was reduced to 35-45 ram Hg and maintained for 60 min (first hit).The animals were then resuscitated by infusion of shed blood and lactated Ringer' s solution.LPS 30 tμg/kg was instilled into trachea at 24 h after HSR (second hit).Arterial blood gas analysis was performed and the animals were then sacrificed by exsanguination at 0,3 and 6 h after LPS(T,,T2,T3 ).The lungs were removed.W/D lung weight ratio and MPO activity,IL-6 and 1L-10 contents in the lung tissue were determined.The changing rate of the abovementioned variables at T2,T3 based on the values at T1 were calculated.ResultsIn C3H/HeN animals the changing rate of PaO2 was significantly lower while the changing rate of W/D ratio,MPO activity and IL-6,IL-10 contents in the lung tissue were significantly higher in HSR/LPS group than in S/LPS group at T2.3.But in C3H/HeJ animals the above-mentioned variables were changed at T2.ConclusionThe role of TLR-4 in the two-hit-induced ALI is stronger than that in the LPS-induced ALI in mice.

Objective To evaluate the effect of dexmedetomidine pretreatment on lipopolysaccharide (LPS)-induced release of inflammatory mediators in primary microglias in neonatal rats.Methods Purified primary microglias were seeded in the plate and randomly divided into 3 groups with 10 holes in each group:control group (group C),LPS group (group L) and dexmedetomidine pretreatment group (group D).In group C,the cells were incubated in serum-free DMEM for 24 h.In group LPS,the cells were incubated with LPS (final concentration 1 μg/ml) for 24 h.In group D,the cells were pretreated with dexmedetomidine (final concentration 1 ng/ml) for 1 h,then LPS (final concentration 1 μg/ml) was added and the cells were incubated for 24 h.The levels of nitric oxide (NO) (by Greiss method) and prostaglandin E2 (PGE2),IL-1β and TNF-α (by ELISA) in the supernatant were measured after 24 h of incubation.The expression of inducible nitric oxide synthase (iNOS) mRNA in the cells was determined by RT-PCR.Results Compared with group C,the levels of NO,PGE2,IL-1β and TNF-α,and expression of iNOS mRNA were significantly increased in groups L and D (P ＜ 0.05).There was no significant difference in the indexes mentioned above between groups D and L (P ＞ 0.05).Conclusion Pretreatment with dexmedetomidine has no significant effect on LPS-induced release of inflammatory mediators in primary microglias in neonatal rats.

Objective To evaluate the role of p38MAPK signaling pathway in the up-regulation of heme oxygenase-1 (HO-1) expression during hemorrhagic shock and resuscitation (HSR)-induced acute lung injury (ALI) in mice. Methods Thirty-two C3H/HeN (wild-type) mice, aged 10-12 weeks, weighing 20-25 g, were randomly divided into 4 groups (n = 8 each): sham operation group (group S); group HSR; FR167653 (a p38MAPK inhibitor) group (group FR) and FR167653 + HSR group (group FR + HSR). HSR was induced according to the methods described by Ayala et al. MAP was reduced to 35-45 mm Hg and maintained for 60 min.Then the animals were resuscitated with transfusion of the shed blood and lactated Ringer's solution equivalent to the volume of shed blood. FR167653 5 mg/kg was injected intravenosly in group FR. FR167653 5 mg/kg was injected intravenously 30 min before blood-letting in group FR + HSR. The animals were sacrificed by exsanguination at 6 h after resuscitation. The lungs were immediately removed for microscopic examination. The W/D lung weight ratio was calculated and the levels of myeloperoxidase (MPO), IL-10, IL-6 and HO-1 and activated p38MAPK were determined (by ELISA).Results Compared with group S, the pathological score, W/D ratio, the levels of MPO, IL-10, IL-6 and HO-1 and the level of activated p38MAPK were significantly increased in group HSR, the pathological score, W/D ratio and the level of HO-1 were significantly increased in group HSR + FR ( P ＜ 0.01) .Compared with group HSR, the pathological score, W/D ratio, the levels of MPO, IL-10, IL-6 and HO-1 and activated p38MAPK were significantly decreased in group HSR + FR ( P ＜ 0.01 ). Conclusion p38MAPK signaling pathway mediates the up-regulation of HO-1 expression during HSR-induced ALI in mice.

Objective To investigate the effect of surgical trauma on the expression of COX-2 and PGE2in the hippocampus in aged rats. Methods Forty-five 18-month-old male SD rats weighing 500-600 g were randomly divided into 3 groups (n = 15 each): group Ⅰ control (group C); group Ⅱ anesthesia (group A) and group Ⅲ surgery + anesthesia (group S). Anesthesia was induced by intraperitoneal 1% pentobarbital sodium 50 mg/kg in group A and S. The animals underwent appendectomy and splenectomy under anesthesia in group S.Cognitive function was assessed by open field test and Y-mase test on the 1st, 3rd and 7th day after anesthesia and surgery (T1-3). The animals were sacrificed after behavior tests at T1.2.3 and the hippocampi were removed for determination of the expression of COX-2 mRNA (by RT-PCR) and PGE2 content (by ELISA). Results The time the animal spent in the central square was significantly prolonged, the number of crossing grid and standing on the back legs and the number of right response were decreased, the total reaction time was prolonged and the COX-2mRNA expression at T1 and PGE2 content in the hippocampus were increased at T1,2 in group S as compared with group C and A. There was no significant difference in the variables mentioned above between group C and A. Conclusion Surgical trauma can induce early postoperative cognitive dysfunction through up-regulation of COX-2 mRNA expression and by increasing PGE2 content in the hippocampus in aged rats.

Objective To explore whether gap junction disturbances are involved in the pathogenesis of levodopa-induced dyskinesia ( LID ). Methods The hemi-parkinsonian ( PD ) rat was treated intraperitoneally with L-dopa methylester (20 mg/kg) and benserazid (10 mg/kg) for 21 days and abnormal involuntary movement was evaluated to establish LID rat model. The experimental animals were divided into three groups: LID group, PD group and normal control group, respectively. The behavior responses of intraperitoneal injection of different doses of carbenoxolon and intracerebroventricular injection of quinine were observed to estimate the effects of gap junctional blockade on the abnormal involuntary movement ( AIM ) in the rat model of LID. Double immunofluorescence labeling was used to analyze the expression of connexin 36 ( Cx36 ) in enkephalin positive medium spiny neurons and parvalbumin ( PV ) positive interneurons in the striatum. Western blottings was used to observe the expression of Cx36 in the striatum and moter cortex. Results Behavioral characteristics indicated that high dose of carbenoxolone ( >60 mg/kg) intraperitoneal injection and intracerebroventricular injection of quinine ( 0.5, 1.0, 2.0 μmol/L, > 2.5 μmol/L ) could decrease the AIM score of LID rats. Western blotting indicated that expression of Cx36 in lesioned striatum and motor cortex of LID rat model was 219.56% ±18.12% and 226.03% ±16.33%, respectively, which induced a significant upregulation in comparison with the normal control group (104.05% ±3.82%, t=15.389, P<0.01;105.27% ±2.82%,t=8.074, P<0.01) and untreated PD group (119.31% ±8.92%, t=13.356, P<0.01; 138.20% ±17.88%, t=5.872, P<0.01). Double immunofluorescence labeling staining revealed that Cx36 expression was increased in Enk-positive striatum neurons in LID model ( 57.59% ±5.36%) compared with that in normal control group (32.67% ±4.22%) and PD group (37.24% ±0.86%, F=78.060, P<0.01). The expression of Cx36 in PV-positive interneurons was also elevated in LID group (68.49% ±11.60%) in comparison with normal control group ( 40.43% ± 2.30%) and PD group ( 31.92% ± 5.68%, F = 39.567, P < 0.01 ).Conclusions The Cx36 expression is generally increased in lesioned striatum and motor cortex of LID rat model. In the striatum, the up-regulation of Cx36 is specifically observed in Enk-positive striatum neurons and in PV-positive interneurons. The dyskinesia behavior of LID rats can be significantly reduced by treatment with gap junction blockade. All these results suggest that gap junction dysfunction may play an important role in the pathogenesis of LID.