OBJECTIVETo study clinical characteristics and resistance of wound surface infections, so as to guide clinical diagnosis and rational administration.

METHODSThe clinical setting and laboratory results were collected by analyzing 20 strains of Bacillus cereus isolated from clinical samples in patients from our hospital from October 2011 to June 2012, including 18 males and 2 females,ranging in age from 22 to 67 years old, averaged (47.30 +/- 11.16) years old. The courses of disease ranged from 5 to 20 days. All the patients were treated with nutrition support therapy, debridement and the corresponding antibiotic therapy. The patients had anemia, low protein hyperlipidemia and wound contamination history while Bacillus cereus infected. Thirty people were selected as normal group, including 23 males and 7 females,with an average age of (45.20 +/- 15.05) years old. Infection control condition was assessed by comparing culture for pathogens and patients wound redness or exudation cases before and after treatment. Antimicrobial susceptibility test was conducted by K-B method.

RESULTSA total of 20 stains of Bacillus cereus were isolated from wound surface infections in department of orthopedics of our hospital. Among them,the infections were correlated with the wound contamination (16/20), malnutrition (20/20), and open-fracture (20/20), operation time (15 cases > 3 h). The laboratory blood test showed that the levels of TP [(49.94 +/- 8.24) g/L], ALB [(29.54 +/- 5.45 ) g/L] and Hb [(103.20 +/- 11.79) g/L] in the infection group was lower than those of control group; in the contrast, the levels of WBC [(8.35 +/- 2.31) x 10(9)/L], NEUT [(6.98 +/- 1.99) x 10(9)/L], hs-CRP [(73.60 +/- 55.14) mg/L] and CK [(900.10 +/- 1 259.12) IU/L] were higher in the infection group than those of control group, and the differences were statistically significant (P < 0.01). The diameter of inhibition zone in penicillin, cefazolin, cefuroxime, ceftazidime, cefepime, cotrimoxazole, erythromycin were less than 15 mm, and suggested that Bacillus cereus resisted to these antibiotics. However, the diameter of inhibition zone in clindamycin, vancomycin, gentamicin, ciprofloxacin, imipenem were larger than 20 mm and this data indicated that the bacteria were highly sensitive to these antibiotics.

CONCLUSIONOrthopedic patients who immunocompromised, hypoproteinemia and accompanied by open wounds and contaminated wound susceptible to infect Bacillus cereus; sensitive antimicrobial drugs should be selected on the basis of supplement albumin, symptomatic and supportive treatment.

Adult ; Aged ; Anti-Bacterial Agents ; pharmacology ; Bacillus cereus ; drug effects ; isolation & purification ; Female ; Humans ; Male ; Middle Aged ; Orthopedics ; Wound Infection ; microbiology

BACKGROUND: Arteriosclerosis obliterans (ASO) is a major cause of adult limb loss worldwide. Autophagy of vascular endothelial cell (VEC) contributes to the ASO progression. However, the molecular mechanism that controls VEC autophagy remains unclear. In this study, we aimed to explore the role of the GRB2 associated binding protein 1 (GAB1) in regulating VEC autophagy. METHODS: In vivo and in vitro studies were applied to determine the loss of adapt protein GAB1 in association with ASO progression. Histological GAB1 expression was measured in sclerotic vascular intima and normal vascular intima. Gain- and loss-of-function of GAB1 were applied in VEC to determine the effect and potential downstream signaling of GAB1. RESULTS: The autophagy repressor p62 was significantly downregulated in ASO intima as compared to that in healthy donor (0.80 vs. 0.20, t = 6.43, P < 0.05). The expression level of GAB1 mRNA (1.00 vs. 0.24, t = 7.41, P < 0.05) and protein (0.72 vs. 0.21, t = 5.97, P < 0.05) was significantly decreased in ASO group as compared with the control group. Loss of GAB1 led to a remarkable decrease in LC3II (1.19 vs. 0.68, t = 5.99, P < 0.05), whereas overexpression of GAB1 significantly led to a decrease in LC3II level (0.41 vs. 0.93, t = 7.12, P < 0.05). Phosphorylation levels of JNK and p38 were significantly associated with gain- and loss-of-function of GAB1 protein. CONCLUSION Loss of GAB1 promotes VEC autophagy which is associated with ASO. GAB1 and its downstream signaling might be potential therapeutic targets for ASO treatment.
Adaptor Proteins, Signal Transducing ; Adult ; Arteriosclerosis Obliterans/genetics* ; Autophagy ; GRB2 Adaptor Protein ; Humans ; Phosphoproteins/metabolism* ; Phosphorylation ; Protein Binding ; Signal Transduction