Objective To investigate the role of p38 MAPK on gastric ischemia/reperfusion (I/R)-induced injury in mice. Methods C57BL/6 mice were randomly divided into three groups; sham+vehicle group, I/R+vehicle group (as control), and I/R+ CNI-1493 group. The gastric I-R injury mice were prepared by occluding the celiac artery for 30 min followed by reperfusion for 1 h. Sham-operated animals underwent the same surgical procedure without clamping. Physiological saline (0.9% NaCl, 10 ml/kg) or CNI-1493(a p38 MAPK inhibitor, 10 ml/kg, 2 mg/ml) was intraperitoneally administered 1 h before ischemia. A picture of the whole stomach was obtained after fixation with formalin, and the bleeding area in the whole stomach was obtained by a digital imaging analyzer (Image J 1. 4. NIH). The levels of phospho- and total-mitogen-activated protein kinases (MAPKs including p38, JNK, and ERK), phospho-nuclear factor-κB (NF-KB) and cleaved Caspase-3 in the injured stomach tissue were determined by Western blotting analysis. Results Compared with sham+vehicle group, I/R group had markedly larger gastric bleeding area (P < 0.05), activated p38, JNK, and ERK (P <0.05), and markedly increased NF-κB p65 and cleaved Caspase-3 expression (P <0.05). Pretreatment with CNI-1493 significantly inhibited the above changes in 1/R group (P < 0. 05). Conclusion Activation of MAPK/NF-KB pathway play a very important role in I/R-induced gastric injury. Pretreatment with p38 MAPK inhibitor, CNI-1493, can inhibit MAPK/NF-κB pathway, decrease expression of apoptosis protein expression, and reduce gastric mucosal bleeding.

OBJECTIVETo investigate the incidence, pathogens, and clinical features of infection in consecutive cases from 2010 to 2012 in Peking Union Medical College Hospital.

METHODThe incidence, pathogen, treatment, and outcomes of patients with hematological diseases who had positive findings of bacterium in their samples from 2010 to 2012 were retrospectively analyzed.

RESULTSThere were 449 positive samples (5.8%) from 4 890 patients during this period, among which 388 were proved to be with pathogenic bacteria. Samples separated from patients with community-aquired infections accounted for 8.4% of all positive samples. Most community-aquired infections were caused by Gram-negative bacteria (75%), although no multidrug-resistant bacteria was observed. Samples separated from patients with nosocomial infections accounted for 91.6% of all positive samples. Respiratory tract (49.4%) and peripheral blood (32.6%) were the most common samples with positive results. Skin soft tissues (10.4%), and urine (3.7%) were less common samples. Most of the pathogenic bacteria of the nosocomial infections were Gram-negative (66.9%). The most common Gram-negative bacteria included Escherichia coli (13.8%), Pseudomonas aeruginosa (12.1%), and Klebsiella pneumonia (12.1%), while Staphylococcus aureus (10.4%), Enterococcus faecium (7.0%), and Staphylococcus epidermidis (5.1%) were the most common Gram-positive bacteria. Gram-negative bacteria consisted of most of sputum samples and peripheral blood samples. Samples from the surface of skin wound and anal swab were composed largely by Gram-positive bacteria (63.8%). The detection rates of extended-spectrum beta-lactamase-producing Klebsiella pneumonia/Klebsiella oxytoca, Escherichia coli, and Proteus mirabilis were 24.0%, 87.9% and 38.4%, respectively. The resistance to Acinetobacter baumannii was serious. Multidrug-resistant, extensive drug resistant and pan drug resistant A. baumannii acountted for 74% of all A. Baumannii infections. Stenotrophomonas maltophilia showed low resistance to sulfamethoxazole/trimethoprim, levofloxacin and minocycline. Also, 22 methicillin-resistant Staphylococcus aureus and 9 methicillin-resistant Staphylococcus Epidermidis were detected, which were only sensitive to vancomycin, teicoplanin, and linezolid. All patients were treated in the haematology wards and most of them were under agranulocytosis or immunosuppression. Finally, 22 patients reached clinical recovery through anti-infective therapy, whereas 49 patients died. Among those deaths, 42 patients attributed to severe infections and infection-associated complications. Fourteen of all the deaths might be infected with drug-resistance bacteria. There were 61 samples proved to be bacteria colonization. Nonfermenters such as Acinetobacter baumannii and Stenotrophomonas maltophilia made up for a large amount of bacteria colonization.

CONCLUSIONSThe pathogens of nosocomial infections in the hematology ward are mainly Gram-negative bacteria. The incidences and pathogens vary from different infection sites. Nosocomial infection still has a higher mortality rate. Once nonfermenters are detected positive, the pathogenic or colonial bacteria should be distinguished.

Adolescent ; Adult ; Aged ; Aged, 80 and over ; Bacteria ; isolation & purification ; Bone Marrow Transplantation ; Cross Infection ; microbiology ; Female ; Hematologic Diseases ; complications ; microbiology ; Hematology ; Hospital Departments ; statistics & numerical data ; Humans ; Male ; Middle Aged ; Retrospective Studies ; Young Adult