In recent years,there has been increasing evidence that microcirculatory disturbance,including vasoconstriction,shunting,inad-equate perfusion,increased blood viscosity,and coagulation,is closely associated with the pathogenesis of acute pancreatitis (AP).These processes may be exacerbated by ischaemia-reperfusion injury and the generation of oxygen radicals.The anatomical features of pancreatic microcirculation,the pathophysiological mechanism of pancreatic microcirculation disturbance and related inflammatory mediators,and pro-gress in the treatment of microcirculatory disturbance in AP are reviewed.It is suggested that the pancreatic and systemic microcirculation may play a key role in the development and progression of AP.

Novel method of enantioseparation of ofloxacin by capillary electrophoresis with capactively coupled contactless conductivity detection (C~4D) using binary chiral selectors,hydroxypropyl cyclodextrin and hydroxypropyl methyl cellulose ( HP-β-CD and HPMC) ,was developed. The enantiomers of ofloxacin were baseline separated with an uncoated fused-silica capillary(45 cm×50 m i. d. ,L_(effi) = 40 cm)under the optimum separate conditions, 20 mmol/L HAc +6 mmol/L NaAc + 12 mg/L HPMC +35 mmol/L HP-β-CD,separation voltage +13 kV,electrokinetic injection 11 kV×10 s. The calibration curve of the enantiomers showed good linearity in the range from 0. 8 mg/L to 40 mg/L with LOD =0. 3 mg/L. Effects of several factors on resolutions,such as the composition of the running buffer,the pH value,separation voltage,injection method and the parameters of C~4D detector,were investigated. The efficacy of the HP-β-CD and HPMC were discussed. The proposed method has been successfully applied to monitor the enantiomer of ofloxacin contents in the commercial Ofloacin Tablets and Levofloxacin Hydrochloride Tablets,and was demonstrated simple,rapid and reproducible.

Acute pancreatitis happens rapidly and leads to patient's condition changing swiftly.Acute pancreatitis may be complicated by acute lung injury (ALI) and acute respiratory distress syndrome (ARDS),or even multiple organ dysfunction syndrome,and the mortality rate has been high.The mechanism of acute pancreatitis with complications of ALI and ARDS is intricate.It involves the uncontrolled inflammatory response,the damage and apoptosis of cell,the role of trypsin,the imbalance of coagulation and fibrinolysis,etc.These respects interrelate with each other,forming a complex network.Further study of mechanism of acute pancreatitis complicated with ALI and ARDS will supply more new target for clinical diagnosis and treatment.

Objective To study the effect of Xinji Huoliyin on the apoptosis of myocardial cell and apoptosis-related gene expression of experimental dilated cardiomyopathy rats, and explore its mechanism. Methods Sixty animals were randomly divided into 6 groups. Dilated cardiomyopathy model was made by injecting adriamycin. Experimental rats were given Xinji Huoliyin and Huangqi Shengmaiyin respectively. The genic expression of p53 and Fas was tested by S-P immunohistochemistry technique after 4 weeks. Results The apoptosis rate of myocardial cell of model group was higher than that of normal group (P

Objective To explore the perioperative nursing care of cooled radiofrequency for refractory craniofacial postherpetic neuralgia.Methods 13 refractory craniofacial postherpetic neuralgia patients were reviewed. Results Visual analogue score significantly decreasedafter the treatment (P<0.01), and severe dropsy after treatment was relieved in 2~3 weeks. Conclusion The cooled radiofrequency iseffective on refractory craniofacial postherpetic neuralgia, while the perioperative nursing care was safe, feasible, and worthy for more application.

Objective To analyze the clinical features and prognostic factors of patients with malignant tumor complicated by acute kidney injury (AKI),and provide the basis for preventing AKI and improving the prognosis.Methods Malignant tumor patients complicated by AKI were screened with the electronic medical records system from January 2001 to December 2012 at the Affiliated Hospital of Qingdao University.The clinical characteristics in the 12 years were analyzed by statistical analysis and compared.The risk factors of the hospital mortality in malignancies tumor complicated by AKI were analyzed by Logistic regression analysis.Results A total of 100 patients with malignant tumor complicated by AKI were collected,accounting for 24.94％ of AKI patients and 1.66‰ of malignant tumor patients at the same period.Malignancies were consist of hematologic malignancies (11％),non-metastatic solid tumor (47％),metastatic solid tumor (42％).The most common factor leading to AKI for malignancies was post-renal obstruction (64％),followed by nephrotoxic drugs or contrast agents (24％),hypovolemia (18％).There was no significant change of the etiologies for AKI between the first six-year and the second six-year (P ＞ 0.05).The hospital mortality of patients with malignant tumor complicated by AKI was 25％,and multivariate Logistic regression analysis showed that multiple etiologies (OR=13.356),multiple organ failure (OR=222.256),and metastatic solid tumors (OR=8.497) were the independent risk factors for hospital mortality.Conclusions AKI is a common complication in patients with malignant tumors,and the most common factor leading to AKI is postrenal obstruction.The hospital mortality in malignancies with AKI is high,which should get the attention of clinicians.

Transforming growth factor-β (TGF-β) is a multifunctional protein and regulates a wide variety of cellular bio-effects,such as proliferation,differentiation,migration and apoptosis.Studies have proven that TGF-β is one of the important cytokines that promote fibrosis,and it is confirmed to be closely related to the progression of tumor.Smad signaling is the major pathway in which TGF-β fulfills its functions.These years,it has been found that E3 ubiquitin ligases Arkadia can enhance the biological effect of TGF-β signal transduction pathway through Smad signaling pathway.Therefore,it is increasingly attracting public attention.This study will summarize the effects of Arkadia on TGF-β/Smad signal transduction pathway.

Objective To investigate the renal expression of stem cell factor (SCF) in lupus nephritis (LN) and its correlation with disease activity and renal injury parameters. Methods Histochemical stain was used to examine all renal specimens (LN group n=34, chronic glomerulonephritis n=16, control group n=8). Hyhridization in situ and immunohistochemistry were used to detect the expression of SCF and infiltration of mast cells, macrophages , α-SMA (+) cells in renal tissues of the two groups. SPS software was used for tissue of the control group. However, they increased markedly in lupus nephritis and CGN (t=6.03～14.25, P< 0.01). But there was no significant difference between LN and CGN in SCF and mast cells in renal interstitium. Positive correlation was observed among the expression of SCF and α-SMA and the number of mast cells and macrophages (r=0.47～0.84, P<0.01) at their corresponding locations. The expression of SCF and ot-SMA and the number of macruphages were positively correlated with renal pathological active index, chronic index, albuminuria and the injury of renal interstitium (r=0.34～0.93, P<0.05 or 0.01); meanwhile, it was negatively correlated with Ccr(r=-0.39～0.61, P<0.01). There was significant correlation between SCF, macrophages and anti-dsDNA antibody, complement C3 level, SLE disease activity index (SLEDAI). The number of mast cells in renal interstitium was positively correlated with chronic indexes and the injury of renal interstitium (r=-0.86, r=0.93, P<0.01) and negatively correlated with Ccr (r=-0.56, P<0.01), but not correlated with active index and albuminuria (r=0.27, r=0.23, P>0.05). Conclusion The expression of SCF is widespread in kidney, and it is markedly eorrelated with various kinds of inflammatory cells, renal inherent cells, renal function, and urine protein levels. SCF may be an critical participant in the initiation and progression of renal injuries in human lupus nephritis.

Objective To investigate the relationship between interleukin (IL)-18 and podocyte injury of lupus nephritis (LN). Methods Sixty cases of biopsy proven LN patients were enrolled into the study. Thirty cases were selected as controls. The clinical and pathological data, blood and urine samples and renal tissues were collected. The Nephrin expression was detected by immunohistochemical method and IL-18 was measured by enzyme linked immunosorbent assay. The relationship between IL-18 and the Nephrin expression, clinical and pathological indicators of LN were analyzed. Results Thirty-eight cases were in active disease and 22 cases were in inactive disease in LN group according to SLE disease activity index (SLEDAI) 2000. One-way ANOVA showed that the level of plasma and urine IL-18 in the LN groups were higher than those in the control group [(200±38) ng/ml, (18±5) ng/ml] (F=110.84, 203.09, P<0.01). Plasma and urine IL-18 level in active LN group [(565 ±128) ng/ml, (200 ±47) ng/ml] was higher than that in the inactive group [(376 ±106) ng/ml, (67 ±22) ng/ml] (P<0.01), the level of IL-18 of type Ⅳ LN was significantly higher than that of typeⅢand type Ⅴ LN (P<0.01). The expression level of Nephrin in LN groups were lower than those in healthy control group (0.28±0.02)(F=136.39, P<0.01). The expression level of Nephrin in active LN group (0.13±0.03) was lower than that in the inactive group (0.18±0.02) (P<0.01), the level of typeⅣLN Nephrin was significantly 01). The Pearson correlation analysis showed that, compared with plasma IL-18, urine IL-18 level in the LN group was not only negatively correlated with the level of Nephrin and serum C3 (r=-0.780, -0.565, P<0.05), but positively correlated with 24 h UP, erythrocyte sedimentation rate (ESR), SLEDAI and GAI (r=0.546, 0.467, 0.599, 0.634, P<0.05). Serum IL-8 level was independent of albumin (ALB), C4, C reactive protein (CRP) and CI (P>0.05), and was negatively correlated with estimated glomerular filtration rate (eGFR) (r=-0.562, P<0.05). It was positively correlated with serum creatinin, blood urea nitrogen, AI, TLAI and inflammatory cell infiltration (r=0.529, 0.482, 0.665, 0.690, 0.671, P<0.05). Conclusion IL-18 has a very close relationship with podocyte injury in patients with LN, and the uIL-18 can be a potential non-invasive detection method to monitor podocyte injury in LN patients.

Objective To detect the effect and mechanism of Cyr61 on the apoptosis of renal tissue caused by early stage of ischemic acute kidney injury (AKI). Methods 30 SD rats were randomized into 5 groups, including control group, AKI group, AKI+bicarbonate group, AKI+blank virus group, and AKI+over?expression Cyr61 virus group. After animal models were created for 2h, serum and renal tissue were collected from sacrificed animals. Expression level of TNF?α was determined by ELISA. HE staining was used to observe the histologic changes of renal tissues. The levels of NF?κB p65 and TNFR1 were measured by immunohistochemical method. RT?PCR and Western blotting assay were adopted to detect the mRNA and protein expression levels of NF?κB p65, TNFR1 and Caspase3. Results Compared with control group, AKI group, AKI+bicarbonate group, AKI+blank virus group, AKI+over?expression Cyr61 virus group had obvious kidney injury. The levels of TNF?α, the mRNA and protein expression levels of NF?κB p65, TNFR1 and caspase3 were markedly up?regulated. Over?expression of Cyr61 significantly attenuated the degree of pathological injury, numbers of apoptotic renal tubular epithelial cells and increased the degree of Scr. Although compared with other groups, the level of TNF?α in kidney tissue had no difference, there was obvious decreased protein level of NF?κB p65, while the increase of TNFR1 and Caspase3 protein was moderate. Conclusions During the early stage of AKI, over expression of Cyr61 could inhibit apoptosis, which may be related to the suppression of TNFR1 transcriptional expression and interference of TNF?αpathway. Its underlying mechanism therefore deserves further research.