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@#In this study, a polyethylene glycol and dodecaldehyde modified bovine serum albumin (PEG-DSA) was developed, and its feasibility as a new high-efficiency micellar carrier for dasatinib (DAS) was explored.Circular dichroism, 1H NMR, elemental analysis, FT-IR and other methods were used to characterize the material structure and the single factor method was used to optimize the process of PEG-DSA/DAS micelles and non-PEGylated control micelles DSA/DAS.The results indicated that the optimal formulation was obtained with a mass ratio of 4∶1 between PEG-DSA and DAS, with average particle size of (37.21 ± 0.21) nm, polydispersion index (PDI) of (0.24 ± 0.04), Zeta potential of ? (15.68 ± 0.19) mV, drug loading (DL) capacity of (10.22 ± 0.34) %, and encapsulation efficiency (EE) of (42.73 ± 1.15) %. Compared with the currently reported nano-formulations of DAS, the drug loading of PEG-DSA/DAS micellar formulations was significantly increased with potential for further development.
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Objective To analyze the characteristics of drug resistance to quinolones and erythromycin of clinical Campylobacter jejuni (C .jejuni) strains and to further investigate its molecular mechanisms .Methods A total of 193 clinical C .jejuni strains were isolated from feces of patients with diarrhea .Drug susceptibilities to ciprofloxacin (CIP ) , gentamycin (GEN ) , azithromycin (AZI ) , erythromycin (ERY) ,chloromycetin (CHL) ,doxycycline (DOX) and tetracycline (TET) were tested using standard agar dilution method . gyrA , gyrB and parC genes were amplified by polymerase chain reaction (RCR) and analyzed for molecular mechanisms of quinolones resistance ,and 23S rRNA , rplD and rplV genes for erythromycin resistance .Chi‐square test or Fisher′s exact two‐tailed tests were used to perform the statistical analysis .Results A total of 193 clinical C . jejuni strains were isolated during 1994—2010 ,among which 43 C .jejuni strains were isolated in 1994—1999 ,80 in 2000—2005 and 70 in 2006—2010 .The drug resistance rates for CIP increased significantly from 55 .8% in 1994—1999 to 95 .0% in 2000—2005 and 94 .3% in 2005—2010 (χ2=41 .94 ,P<0 .01) .The drug resistance rates for GEN were 0 in 1994—1999 ,11 .3% in 2000—2005 and 10 .0% in 2006—2010 ,but with no statistic difference (χ2=5 .078 , P=0 .08) .The drug resistance rates for AZI were 0 in 1994—1999 ,3 .8% in 2000—2005 and 4 .3% in 2006—2010 (χ2=1 .81 ,P=0 .40) .The drug resistance rates for ERY were 0 in 1994—1999 ,1 .3% in 2000—2005 and 4 .3% in 2006—2010 (χ2 = 2 .87 , P= 0 .24 ) . T he drug resistance rates for CHL were 2 .3% in 1994—1999 ,11 .3% in 2000—2005 and 20 .0% in 2006—2010 (χ2 =7 .82 ,P=0 .02) .The drug resistance rates for DOX were 60 .5% in 1994‐1999 ,86 .3% in 2000—2005 and 82 .9% in 2006—2010 (χ2 =12 .18 ,P<0 .01) .The drug resistance rates for TET were 74 .4%in 1994—1999 ,95 .0% in 2000—2005 and 94 .3% in 2006—2010 (χ2 = 15 .46 , P< 0 .01 ) .T he drug resistance rates for CIP‐DOX‐TET were 37 .2% in 1994—1999 ,83 .8% in 2000—2005 and 80 .0% in 2006—2010 (χ2 =33 .53 ,P<0 .01) .The drug resistance rates for CHL‐CIP‐DOX‐TET were 0 in 1994—1999 ,7 .5% in 2000—2005 and 20 .0% in 2006—2010 (χ2=12 .68 ,P<0 .01) .The drug resistance rates for GEN‐CIP‐DOX‐TET were 0 in 1994—1999 ,7 .5% in 2000—2005 and 8 .6% in 2006—2010 (χ2 =3 .74 ,P=0 .15) .All 163 CIP‐resistant C .jejuni strains had C257T mutation on gyrA gene .Mutations on gyrB gene were silent .ParC gene was absent in C .jejuni .Four ERY resistant C .jejuni strains had no mutation on rplD and rplV genes , but 3 of them had A2075G mutation on 23S rRNA gene . Conclusions The antimicrobial resistance rates for C .jejuni increase remarkably over the periods .C257T mutation on gyrA gene and A2075G mutation on 23S rRNA gene are main mechanisms for quinolones resistance and erythromycin resistance ,respectively .
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Forty-five male mice were used and divided into three groups: i.e. experimental gastric ulcer group, saline control group and normal control group. After experimental gastric ulcer was induced, the mice of three groups received intraperitoneal injection of colchicine and were sacrificed 3h later at 3, 6, 9 and 20 days, respectively. The antral mucosa was removed and processed by Sternberger's immunocytochemical PAP method to show G cells and counterstained with hematoxylin. In normal control group, the mitotic index of the antral mucosal epithelial and glandular cells was 5.93?1.23; the percentage of G cells was 2.76?0.45; the mitotic index I of G cells (the number of the mitotic G cells per 100 G cells) was 0.85?0.18; and the mitotic index II of G cells (the number of mitotic figures of the G cells per 100 antral epithelial, glandular and G cells) was 0.02?0.01. The mitotic index of the antral mucosal epithelial and glandular cells, the percentage and the mitotic index II of G cells on 6th, 9th and 20th days in experimental gastric ulcer group was raised and showed highly significant statistical difference from that of the control group, respectively. The mitotic index I of G cells was raised on 9th day in the experimental gastric ulcer group and significant difference between experimental gastric ulcer group and the control group was found. It also revealed a significant diference in the experimental gastric ulcer group as compared with saline control group on 20th day. The percentage of G cells on 6th day was most high, but the peak of mitotic number of G cells appeared on 9th day in the experimental gastric ulcer group. The distribution of G cells was found upward in the glands near the ulcer on 3rd and 6th day than in normal control. These findings suggest that the number, origin, distribution and shape of the G cells in the pyloric glands exhibited dynamic changes with the passage of time. The results suggested that the G cells might participate in the regulation of regeneration of antral mucosa during experimental gastric ulcer.
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Objective Studies on the changes of ? EP, 5-HT, 5-HTR immunoreactive cells in pancreatic islets during experimental gastric ulcer. Methods The immunohistochemical technique was used. Results The numerical densities on area of ? EP, 5-HT, 5-HTR cells in experimental gastric ulcer group were higher than control group on the 4day,10day after operation.The peak of the numerical densities on area of ? EP and 5-HT cells appeared on the 4th day, while the peak of 5-HTR cells as on the 10th day. Part of ? EP, 5-HT,5-HTR immunoreactive material were located in A or B cells neighbourly section. Conclusion The present work proved that the ? EP, 5-HT,5-HTR cells of pancreatic islets were directly or indirectly participated in the regulation balance of endocrine during the self-healing process of the experimental gastric ulcer and here we provided morphological evidence.;
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Objective Studies on the changes of gastrin and SS immunoreactive cells in pancreatic islets during experimental gastric ulcer. Methods The immunohistochemical ABC technique was used. Results The gastrin immunoreactive cells were located in most of the pancreatic islet. The mumber of G cells in experimental gastric ulcer group were higher than that of control group on the 4th and 10th day after operation.The D cells raised on the 10th day.Conclusion The present work provides the evidence that the G and D cells of pancreatic islets might be involed in the self-healing process of the experimental gastric ulcer by endocrine or paracrine regulation.