Objective To investigate the effect of 1-methylhydantoin (1-MH)on asthma and cough animal model, and to clarify its mechanism preliminarily.Methods 50 Wistar rats with ovalbumin-induced asthma were randomly divided into model group, 1-MH 20, 40, and 80 mg · kg-1 groups, positive control group (aminophylline, 60 mg·kg-1 ),another 10 Wistar rats served as control group.The levels of interleukin-5 (IL-5 ),eosinophil chemotactic factor (Eotaxin)and eosinophil (EOS)count in bronchoalveolar lavage fluid (BALF)were measured in various groups. 40 guinea pigs of asthma were randomly divided into model group, 1-MH 15, 30, and 60 mg·kg-1 groups, positive control group (aminophylline, 50 mg · kg-1 );the asthma incubation period of guinea pig was measured in various groups. The bronchus of 10 guinea pigs were selected and put in Krebs solution,and the antispasmodic percentages against histamine phosphate of 1-MH 0.25,0.50,and 1.00 g ·L-1 were recorded and calculated. 50 mice of cough were randomly divided into model group,1-MH 25,50,and 100 mg·kg-1 groups, positive control group (codeine, 50 mg · kg-1 );the cough incubation period and the number of cough in the mice were measured in various groups.40 guinea pigs of cough were randomly divided into model group,1-MH 15,30,and 60 mg·kg-1 groups,positive control group (codeine,20 mg·kg-1);the cough incubation period and the number of cough of the guinea pigs in various groups were measured. Results Compared with sensitized model control group,the levels of IL-5,Eotaxin and EOS count in BALF of the rats in 1-MH 40 mg·kg-1 and 80 mg·kg-1 groups were reduced (P<0.05 or P<0.01 );compared with acetylcholine-induced asthma model control group, the asthma incubation period of guinea pig in 1-MH 30 mg·kg-1 and 60 mg·kg-1 groups was prolonged(P<0.05 or P<0.01);compared with blank control group, the antispasmodic percentages against histamine phosphate in 1-MH 0.50 g · L-1 and 1.00 g · L-1 groups were increased(P<0.01);compared with mouse cough model control group,the cough incubation period of the mice was prolonged,the cough number of the mice was decreased in 50 mg·kg-1 and 100 mg·kg-1 groups(P<0.05 or P<0.01);compared with guinea pig cough model control group,the cough incubation period of the guinea pig was prolonged,the cough number of the guinea pig was decreased in 1-MH 30 mg·kg-1 and 60 mg·kg-1 groups (P<0.05 or P<0.01).Conclusion 1-MH has good antiasthmatic and antitussive effects,which may be related to inhibition of airway inflammation and relaxation of bronchial smooth muscle directly .

Objective To determine whether urinary neutrophil gelatinase-associated lipecalin (uNGAL) and urinary intedeukin-18 (uIL-18) are early markers of acute kidney injury (AKI) in critically ill patients. Methods Ninety-two critically ill patients were studied for one week after their enrollment into our hospital. During the study, 46 patients who met the RIFLE criteria were selected as AKI group and the remaining 46 patients without AKI taken as a control group. The two groups were matched for age, gender and illness severity. Urine samples were collected daily for one week. The receiver operating characteristic curve was used to evaluate the early diagnostic value of uNGAL, uIL-18 and serum creatininc (SCr). Results As compared with the levels obtained 3 days before the diagnosis of AKI, the uNGAL levels in the AKI group increased significantly (P <0. 05), while uIL-18 and SCr levels did not change 2 days prior to the diagnosis of A KI (all P > 0. 05). uNGAL and uIL-18 levels increased significantly (all P < 0. 05), while SCr levels did not change 1 day prior to the diagnosis of AKI in the AKI group (P > 0. 05). The levels of uNGAL, uIL-18 and SCr did not change significantly in the control group during the study period (all P > 0. 05). Three days before the diagnosis of AKI, concentrations of uNGAL, uIL-18 and SCr were not the predictive of AKI. Two days before the diagnosis of AKI, the area under the curve (AUC) of uNGAL was 0. 840 (95% CI 0. 672-1. 009, P < 0. 05), which indicated that uNGAL was the predictive of AKI while uIL-18 and SCr were not. One day before the diagnosis of AKI, the AUC of uNGAL and ulL-18 were 0. 830 (95 % CI 0. 711-0. 950, P < 0. 05) and 0. 818 (95 % CI 0. 697-0. 938, P < 0. 05), indicating that uNGAL and uIL-18 were the predictive of AKI while SCr was not. Conclusion uNGAL and uIL-18 may be the early predictive markers of AKI in critically ill patients.

To extract praeruptorin A from Radix Peucedani by supercritical fluid extraction (SFE)-CO2.

Objective To investigate the feasbility of the orient differentiation from embryo hepatic Sca-1+ cell to hepatic cell or hepatic cell precursor under the induction of hepatocyte growth factor(HGF) and acor fibroblast growth factor(aFGF) in vitro. Methods Sea-1+ cells were isolated by immunomagnetic beads and their morphous were observed by contrast phase microscope. The expression of mRNA of albumin(ALB) and meta-thyroprotein were detected by RT-PCR; ALB, AFP, CK8/18 protein were detected by immunohistochemical method, and cell staining for glycogen and urea synthesis function were tested. Results The activity, purity, recovery rate of Sca-1+ cells were (94. 24±1.04) %, (85.57±1.66) %, (62. 31±1.85 ) % respectively. After the induction of HGF and aFGF, Sca1+ cells became anomalism and transformed to heptic cell in morphous,disappeared in expression of AFP protein and upregulated in expression of ALB and CK8/18 protein,upregulated in expression of ALB and transthyroprotein mRNA,cell staining of glycogen and urea synthesis function were strengthened,the cell differentiated to mature hepatic cell. Conclusion Embryo hepatic Sca-1+ cell could differentiate to hepatic cell or hepatic cell precursor under the induction of HGF and aFGF in vitro.

Objective To research the effect of mir-520c-3p targeted GPC3 to the hepatocellular carcinoma Huh-7 cell proliferation,migration,and the influence of the attack ability and find new theoretical basis for liver hepatocellular carcinoma clinical treatment.Methods The cells were divided into three groups:not transfection of mir-520c-3p group (cell group),negative control group (Nc group),and transfection of mir-520c-3p group (treat ment group).Then used fluorescence quantitative PCR and Western Blot to detect GPC3mRNA gene and protein expression quantity.Cell proliferation of change was detected by the EDU.Made use of Transwell to detect cell invasion and migration ability of the change.Results Fluorescence quantitative PCR results showed that Cell group,NC group and treatment group were 1.13 ± 0.23,1.28 ± 0.15 and 1.05 ± 0.19 (P ＞ 0.05),mir-520-3p could not reduce the GPC3mRNA; but Western Blot detection results showed that GPC3 protein expression level reduce significantly after transfection mir-520c-3p,Cell,NC and treatment group were 2.16 ± 0.08,1.99 ± 0.04 and 0.499 ± 0.05 (P ＜ 0.01).The EDU detection results showed that hepatocellular carcinoma Huh-7 cell proliferation ability obviously inhibited after transfection mir-520c-3p,Cell group,NC group and treatment group were (90.12 ± 1.93) ％,(91.02 ± 0.35) ％ and (77.73 ± 5.88) ％ (P ＜ 0.05),and Transwell test found that hepatocellular carcinoma Huh-7cell invasion abilities were restrained,Cell group,NC group and treatment group were 0.071 ±0.008,0.105 ±0.001 and 0.048 ± 0.002 (P ＜ 0.05),in the same the cells' migration abilities were reduced,Cell group,NC group and treatment group were 0.546 ± 0.010,0.328 ± 0.002 and 0.151 ± 0.002 (P ＜0.01).Conclusions Mir-520c-3p can target GPC3 so that affect hepatocellular carcinoma Huh-7 cell proliferation,invasion and migration abilities.

0.05).CONCLUSION: The high expression of GPC3 mRNA in hepatocellular carcinoma is independent to the gene mutation,and to the expression of P53 and PCNA protein.

BACKGROUND:There are many postmenopausal women taking hormone, which leads to much loss of bone mass, further inducing fragility fractures. The studies on the hormone exposure combined with ovariectomy-induced osteoporotic model are still immature, and the related molecular mechanism remains unclear. OBJECTIVE: To establish the rat osteoporotic model induced by ovariectomy combined with glucocorticoid exposure and to explore the underlying molecular mechanism. METHODS: Thirty 3-month-old female Sprague-Dawley rats were randomly divided into blank control, sham and model groups (n=10 per group). The rats in the blank control group received no intervention; rats in the sham group were clipped off a little of coeliac adipose tissue; the model rats received bilateral ovariectomy and 4-week administration of glucocorticoid. RESULTS AND CONCLUSION:At 4 weeks after modeling, compared with blank control and sham groups, the model group showed significantly lower bone mineral density of the femur, number of bone trabeculae and bone volume/total volume, and significantly wider bone trabecular spacing. Additionally, the model group revealed the damaged bone trabecular structure and thiner cortical bone. The expression level of Runx2 was downregulated whereas both collagen type 1α1 and peroxisome proliferators activated receptor γ mRNA were upregulated in the model group. These findings suggest that ovariectomized rats exposed to glucocorticoid rapidly develop femur osteoporosis, maybe by downregulating the expression of Runx2, as well as upregualting collagen type 1α1 and peroxisome proliferators activatedreceptor γ mRNA.

Purpose: We aimed to identify effectiveness-associated indicators and evaluate the optimal tumor reduction rate (TRR) after two cycles of neoadjuvant chemotherapy (NAC) in patients with invasive breast cancer. Methods: This retrospective case-control study included patients who underwent at least four cycles of NAC at the Department of Breast Surgery between February 2013 and February 2020. A regression nomogram model for predicting pathological responses was constructed based on potential indicators. Results: A total of 784 patients were included, of whom 170 (21.68%) reported pathological complete response (pCR) after NAC and 614 (78.32%) had residual invasive tumors. The clinical T stage, clinical N stage, molecular subtype, and TRR were identified as independent predictors of pCR. Patients with a TRR > 35% were more likely to achieve pCR (odds ratio, 5.396; 95% confidence interval [CI], 3.299–8.825). The receiver operating characteristic (ROC) curve was plotted using the probability value, and the area under the ROC curve was 0.892 (95% CI, 0.863–0.922). Conclusion TRR > 35% is predictive of pCR after two cycles of NAC, and an early evaluation model using a nomogram based on five indicators, age, clinical T stage, clinical N stage, molecular subtype, and TRR, is applicable in patients with invasive breast cancer.

Objective To analyze the independent risk factors and complications for perioperative hyperbilirubinemia in Stanford type A aortic dissection undergoing operation and investigate the management strategy of perioperative hyperbilirubi-nemia. Methods Between January 2013 and January 2018 from the department of great vessel surgery of heart centre of,290 cases of patients with Stanford type A aortic dissection undergoing operation were collected consecutively,male 210 cases,fe-male 80 cases. The related data and perioperative peak hyperbilirubinemia were recorded. According to the perioperative peak hyperbilirubinemia,patients were divided into 2 groups:≥51. 3 μmol/ L group and < 51. 3 μmol/ L group. Univariate and lo-gistic regression analysis were used to identify the independent risk factors. The perioperative complications were also recorded. Results Preoperative total bilirubin ≥ 17. 1 μmol/ L(OR = 2. 105,95％ CI: 1. 153 - 3. 125,P = 0. 016),cardiopulmonary bypass time > 3. 5 h(OR = 1. 103,95％ CI: 1. 316 - 6. 151,P = 0. 031),a large number of hemolysis(OR = 1. 503,95％CI: 1. 506 - 6. 651,P = 0. 029),the input amount of 24 h allogeneic red blood cell > 2000 ml(OR = 1. 381,95％ CI:0. 956 - 2. 552,P = 0. 036)were the independent risk factors for perioperative hyperbilirubinemia. The incidence rate of post-operative acute hepatic failure(2. 5％ vs. 0,P = 0. 021)and artificial liver therapy(2. 5％ vs. 0,P = 0. 021)in≥51. 3μmol/ L group were significantly increased. The incidence rate of postoperative acute lung injury(37. 5％ vs. 25. 2％,P =0. 039)and acute kidney injury(38. 7％ vs. 19. 5％,P = 0. 035)in 51. 3 μmol/ L group were also significantly increased. The duration of mechanical ventilation[(4. 1 ± 1. 6)days vs. (2. 8 ± 1. 3)days,P < 0. 05]and ICU stay time[(5. 1 ± 2. 3)days vs. (3. 9 ± 1. 8)days,P = 0. 035]and hospitalization time[( 19. 3 ± 3. 1)days vs. ( 17. 3 ± 2. 5)days,P = 0. 035]were sig-nificantly prolonged. Temporary nerve dysfunction(52. 5％ vs. 32. 6％,P = 0. 002)and in-hospital mortality( 17. 5％ vs. 8. 1％,P = 0. 037)were significantly increased. Conclusion Preoperative total bilirubin ≥ 17. 1 μmol/ L,cardiopulmonary bypass time > 3. 5 h,a large number of hemolysis,the input amount of 24 h allogeneic red blood cell > 2000 ml were the in-dependent risk factors for perioperative hyperbilirubinemia in Stanford type A aortic dissection. The perioperative complications in≥51. 3 μmol/ L group were significantly increased. Therefore,more attention should be paid to the independent risk factors for perioperative hyperbilirubinemia in Stanford type A aortic dissection,hyperbilirubinemia and its clearance should be moni-tored more actively and dynamically,the cause should be found more precisely,the treatment be more comprehensive to achieve to control the level of bilirubinemia and improve the prognosis.