[Objective] To observe the clinical effect of Shenfu Decoction and Compound Red Sage Injection on new infants respiratory distress syndrome.[Method] Randomly divide 42 cases into 2 groups,control group(1)take the integrated therapy:CPAP,oxgen,warming,keeping wet and anti-bacterial;the treatment group(1)take the Shenfu Decoction and Compound Red Sage Injection.Compare their cure rates after 7d.[Result] In group 1,survivable rate was 95.23%,cure rate 71.4%;and 80.95% and 47.62% respectively for other group;the clinical symptoms,signs,blood-gas analysis and X-ray result were all better in group 1 than group 2.[Conclusion] Oral taking Shenfu Decoction and Compound Red Sage Injection for vein drip can help relieve infants clinical symptoms and pass alveolus superficial active substance lack period.

To study the effect of vascular proliferation and reconstruction in chronic hepatitis B (CHB), immunohistochemical staining and in situ hybridization were used. The expression of transforming growth factor (TGF-?1) and smooth muscle actin (?-SMA) in livers of CHB were observed. The results showed that TGF-?1 and ?-SMA were related with degeneration of hepatocytes, intrahepatic vascular fibrosis and hepatic sinusoidal capillarization. The expression degree and range of TGF-?1 and ?-SMA increased with the exacerbation of liver lesion. These results suggest that vascular proliferation and reconstruction may play important roles during the process of CHB.

Objective To obtain the Cyclin D1 through cloning and prokaryotic expression of Cyclin D 1 gene.Methods The total RNA was extracted from liver cancer tissue .The Cyclin D1 cDNA was obtained by reverse transcriptase polymerase chain reaction (RT-PCR).The Cyclin D1 cDNA was sequenced, and sub-cloned to the PET32a+.The prokaryotic expressed was used to obtain the Cyclin D1.Results The 483 bp Cyclin D1 cDNA was obtained.The sequence of Cyclin D1 was corrected.The 36 KD CyclinD1 was obtained by prokaryotic expression .Conclusions The Cyclin D1 cDNA was obtained.Cyclin D1 was expressed in BL21.

Objective To study the mechanism of anti-aging effect of dimethylaminoethanol (DMAE) and compound amino acid (AA) injection by mesotheray in D-galactose-induced skin aging rat.Methods Eighty rats were randomly divided into aging treatment group (60 cases),aging control group (10 cases) and normal control group (10 cases).The skin aging models were established by subcutaneous infectim of D-galactose.From the 18th day,the aging treatment group were injected intradermally in the rats' both sides hip skin with 0.2％ DMAE+ AA,0.1％ DMAE+AA,0.2％DMAE,0.1％ DMAE,AA,and saline,once a week.After four weeks,HE,water content,superoxide dismutase (SOD) activity,hydroxyproline (HYP) and malondialdehyde (MDA) content were measured.Results Compared with the aging control group,the epidermal and the dermal thickness and the collagen area of rats skin' increased significantly in 0.2 ％ DMAE+ AA and 0.1％ DMAE+ AA treatment groups (P＜0.05).0.2％ DMAE+AA and 0.1 ％ DMAE+AA treatment groups also had higher SOD activity,HYP content and lower MDA content than other groups (P＜0.05),but no difference was noted among normal control group,0.2％ DMAE+AA and 0.1％ DMAE+AA group (P＞0.05).There were no differences in water content among groups (P＞0.05).Conclusions Intradermal injection with 0.1％ DMAE+ AA and 0.2 ％ DMAE+AA in aging rats may increase the epidermal and the dermal thickness and the collagen of rats skin' improve SOD activity,HYP content and decreased MDA content,indicating that it has ability to clear skin free radicals,enhance antioxidant capacity and skin collagen metabolism,and thus prevent skin aging.

Objective To investigate the clinical application of fecal calprotectin in inflammatory bowel disease (IBD).Methods Colonoscopy took 79 patients with IBD that were diagnosed with pathology,including 47 cases of ulcerative colitis (UC) patients,32 cases of Crohn's disease (CD).Moreover,42 cases of IBD patients without abdominal pain,diarrhea and other intestinal inflammation were used as disease control group,and 34 cases of healthy people were used as healthy control group.The level of fecal calprotectin in each group was detected by enzyme-linked immunosorbent assay (ELISA).Results The positive rate of fecal Calprotectin in IBD group,disease control group and the healthy control group was 57.0％,19.0％,and 0,respectively; each positive rate in IBD group was significantly higher than the other two groups (P ＜ 0.05).The serum concentration of fecal calprotectin in IBD group [(493.86 ±204.18) μg/g] was significantly higher than the disease control group [(71.46 ± 60.51) μg/g] and the healthy control group [(36.19 ± 13.46) μg/g] (P ＜ 0.05) ; IBD active calprotection [(1015.23 ± 324.96) μg/g] was significantly higher than resting [(52.69 ±34.71) μg/g] (P ＜0.01).Conclusions Fecal calprotectin test benefits early diagnosis of IBD,and may be taken as the diagnostic index of IBD activity.It has extensively clinical value.

ObjectiveTo investigate the protective effect of combination of triptolide and irbesartan on the podocytes in a type 2 diabetic(T2DM) rat model,and evaluate its mechanism.Methods T2DM rats were induced by fed with high-sucrose-high-fat diet combined with a low dose of streptozocin.The rats were randomly divided into 5 groups:normal control group ( NC,n =10),diabetes group ( DM,n =11),triptolide treatment group (DT,n =12),irbesartan treatment group (DI,n =12) and triptolide combined with irbesartan treatment group (DTI,n =13). Ultrastructure of podocytes was observed by electronic microscopy and urinary albumin (UAL) excretion by ELISA was determined after 8 weeks.The expression of nephrin and bone morphogenetic protein-7(BMP-7), connective tissue growth factor (CTGF),transforming growth factor (TGF)β1 mRNA and proteins were detected by immunohistochemistry,real-time PCR and Western blot. Results Increased UAL was significantly attenuated in all treatment groups.Compared to NC group,UAL in DM group was increased significantly (0.45 ± 0.09 vs 6.36 ± 0.87,P ＜ 0.01 ),while decreased in triptolide or irbesartan alone treatment group (2.48 ± 0.37 and 2.68 ±0.42,both P ＜ 0.01 ).Compared with those in control groups,kidney expression of nephrin,BMP-7 mRNA and proteins were downregulated while CTGF, TGFβ1 mRNA and proteins were significantly upregulated in T2DM rats. Triptolide or irbesartan each alone moderately ameliorated albuminuria and podocyte damage.However,their combined usage showed a dramatic therapeutic synergism,manifested by prevention of progressive albuminuria,restoration of the glomerular filtration barrier,reversal of the decline in slit diaphragm proteins,reduction expression of CTGF,TGFβ1,and upregulation of BMP-7.Conclusion Our findings show that triptolide can increase the efficacy of irbesartan,leading to a more effective prevention of kidney disease in T2DM rat model,which may through upregulation of BMP-7 and inhibition the overexpression of CTGF and TGFβ1.

Objective To investigate the role of p38MAPK in the differentiation of murine osteoblasts, and to observe the expressions of receptor activator of nuclear factor-κB ligand (RANKL) and osteoprotegerin (OPG). Methods The calvarial osteoblasts of newborn BALB/c mice were cultured in MEM medium containing 10% NCS. Raloxifene (10~(-7) mol/L) and 17β-estradiol (10~(-8) mol/L) were added respectively when cells reached 70%-80% confluence combined with or without 5 μmol/L SB202190, an inhibitor of p38MAPK. The osteoblasts alkaline phosphatase activity assays were performed 72 hours later using PNPP method, and mRNA levels of alkaliphosphatase (ALP), OPG and RANKL were determined by RT-PCR. Results 17β-estradiol and raloxifene increased ALP activity and ALP mRNA level in osteoblasts in vitro which were blocked by p38MAPK inhibitor.The mRNA levels of RANKL and OPG were up-regulated by 17β-estradiol and raloxifene while the ratio of OPG/RANKL kept constant. SB202190 (5 μmol/L) inhibited the highly expressed RANKL and OPG in osteoblasts, and obviously decreased the ratio of OPG/RANKL. Conclusions p38MAPK inhibition blocked the differentiation of osteoblasts and decreased the up-regulated OPG and RANKL expressions in osteoblasts significantly (P<0.05).

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.

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.

Objective To observe the expression of cysteine rich-protein 61 (Cyr61) on renal tubular cells,to explore its effects against hypoxic induced kidney injury and the underlying mechanisms.Methods A stably Cyr61 expressed tubular cell line Cyr61-HK2 was established based on HK2 cells and recombinant Cyr61-lentivirus.BrdU incorporation assay was used for cell proliferation.The apoptosis of cells was analyzed by flow cytometry with Annexin V and propidiumiodide staining.Western bloting was used to detect the protein expression of BAD,Akt and ERK.Results (1) Cyr61-HK2 cells displayed more proliferation ability than HK2 cells.(2) Under hypoxia condition,the apoptosis of both HK2 and Cyr61-HK2 cells increased,but the apoptosis of Cyr61-HK2 cells was lesser than HK2 cells.(3) The expression of Cyr61 led to the phosphorylation of BAD,Akt and ERK on 0 h,0.5 h,1 h (all P ＜ 0.05).Conclusion The expression of Cyr61 can promote cell proliferation and dampen cell apoptosis induced by hypoxia,which may be involved in the Akt/ERK signal pathway.