Objective To investigate clinical features and drug resistance of neonate septicemia caused by Streptococcus agalac-tiae in the hospital and to provide clinical guidance for treatment.Methods 42 Streptococcus agalactiae isolates in the hospital were identified and their department distribution as well as drug susceptibility was determined by using automatic VITEK-2 system and criteria released by CLSI in 2012.Results The number of cases in preterm neonatal intensive care unit,full-term neonatal intensive care unit,pediatric intensive care unit and extremely preterm neonatal intensive care unit were 3,26,7 and 6,respectively.The drug resistance rates of the isolated Streptococcus agalactiae to ampicillin,erythromycin,clindamycin,quinupristin/dalfopristin,linezolid, penicillin,tetracycline,tigecycline,vancomycin and levofloxacin were 0.0%,69.0%,71.4%,0.0%,0.0%,0.0%,74.4%,0.0%, 0.0% and 38.1%,respectively.Conclusion The antimicrobial resistance rates of Streptococcus agalactiae which caused neonatal septicemia in our hospital are relatively high.Ampicillin and penicillin are recomended in treatment for neonate septicemia caused by Streptococcus agalactiae .

A method for the determination of cinoxacin and nalidixic acid in human plasma by reverse-phase high performance liquid chromatography is introduced. The single separation system involves a RP-C18 column, a ultraviolet detector at 254 mn and CH3CN-CH3OH-0.01 mol/L HOOCOOH (30:5:65;pH 4.55). The influence of two kind of buffer (phosphate buffer and oxalate buffer) in mobile phase on the separation were studied. Oxalate buffer can improve tailing peak and decrease detection limits. Three pH values (pH 2.80,4.08,4.55) were studied, pH 4.55 can give best separation result. The detection limits of cinoxacin and nalidixic acid were 0.14 ng and 0.24 ng, respectively.

Objective To investigate the relationship between IGF2BP3 hypomethylation with colon tumor differentia?tion. Methods Tissue samples from 41 colorectal cancer were collected from March 2011 to August 2011 in our hospital, among which 19 cases were well-differentiated adenocarcinoma, 12 cases were of moderately differentiated adenocarcinoma and 10 cases were of poorly differentiated adenocarcinoma. Meanwhile biopsy samples from 12 cases of colonic colitis were collected as a control. The expression of IGF2BP3 was assessed by immunohistochemistry and Western blot. An innovate of ELISA technique was used to examine global methylation levels while IGF2BP3 methylation level was tested by methylation specific PCR technique. Results The expressions of IGFBP3 are higher in all colon cancer groups than that in colitis (P<0.05). The expression of IGFBP3 in poorly differentiated adenocarcinoma is higher than that in all the other groups, but there is no significant difference between its expressions in the well differentiated group and in the moderately differentiated adeno?carcinoma group. The global DNA level and IGFBP3 methylation level of every colon cancer group is lower than those in coli?tis (P<0.05). Also, a tendency of decreasing global DNA and IGFBP3 methylation status was observed comparing well differ?entiated towards poorly differentiated carcinomas (P<0.05). Conclusion IGF2BP3 expression in colorectal cancer is asso?ciated with differentiation of colon cancer tissue. A lower global and IGF2BP3 DNA methylation suggest a worse differentia?tion of colon cancer. DNA hypomethylation may therefore play a regulatory role in the expression of IGF2BP3 in colon cancer tissue.

OBJECTIVETo study the absorption kinetics of dehydrocavidine in rats' stomachs and intestines.

METHODThe absorption kinetics was investigated by the in situ perfusion in rats and the concentrations of drug perfusion solutions were determined by HPLC.

RESULTThe hourly absorption percentages of dehydrocavidine in stomach, small intestine were 8.88%, 2.08%, respectively. Although the absorption rate constants of dehydrocavidine in duodenum and jejunum are more than that in ileum and colon, there is no significance difference between them. The absorption rate constants kept at the same level when the concentrations of drug perfusion solution are at middle and high level. The increase of the pH of perfusion solution didnt significantly affect the absorption rate constants of the drug.

CONCLUSIONDehydrocavidine was absorbed poorly at stomach and all segments of intestine in rats, but the absorptions in stomach are better than intestine. Dehydrocavidine was absorbed mainly via passive transport mechanism between middle and high concentration levels.

Animals ; Berberine Alkaloids ; pharmacokinetics ; Colon ; metabolism ; Duodenum ; metabolism ; Hydrogen-Ion Concentration ; Ileum ; metabolism ; Intestines ; metabolism ; Jejunum ; metabolism ; Male ; Rats ; Rats, Sprague-Dawley ; Stomach ; metabolism

Up to 70% of patients with late-stage breast cancer have bone metastasis. Current treatment regimens for breast cancer bone metastasis are palliative with no therapeutic cure. Disseminated tumor cells (DTCs) colonize inside the osteogenic niches in the early stage of bone metastasis. Drug delivery into osteogenic niches to inhibit DTC colonization can prevent bone metastasis from entering its late stage and therefore cure bone metastasis. Here, we constructed a 50% DSS6 peptide conjugated nanoparticle to target the osteogenic niche. The osteogenic niche was always located at the endosteum with immature hydroxyapatite. Arsenic-manganese nanocrystals (around 14 nm) were loaded in osteogenic niche-targeted PEG-PLGA nanoparticles with an acidic environment-triggered arsenic release. Arsenic formulations greatly reduced 4T1 cell adhesion to mesenchymal stem cells (MSCs)/preosteoblasts (pre-OBs) and osteogenic differentiation of osteoblastic cells. Arsenic formulations also prevented tumor cell colonization and dormancy via altering the direct interaction between 4T1 cells and MSCs/pre-OBs. The chemotactic migration of 4T1 cells toward osteogenic cells was blocked by arsenic in mimic 3D osteogenic niche. Systemic administration of osteogenic niche-targeted arsenic nanoparticles significantly extended the survival of mice with 4T1 syngeneic bone metastasis. Our findings provide an effective approach for osteogenic niche-specific drug delivery and suggest that bone metastasis can be effectively inhibited by blockage of tumor cell colonization in the bone microenvironment.