OBJECTIVETo evaluate the role of p53 gene mutation in colorectal carcinoma and assess the value of peripheral blood p53 single nucleotide polymorphism (SNP) in early diagnosis of colorectal carcinoma.

METHODSNSP in axons 5-8 of p53 gene was detected using ligase detection reaction-polymerase chain reaction (LDR-PCR) in the peripheral blood of 100 patients with colorectal cancer and 100 healthy subjects.

RESULTSThe mutation rate of p53 gene was 24% (24/120) in colorectal carcinoma patients and 0% (0/120) in the healthy subjects (P<0.05).

CONCLUSIONp53 plays an important role in the carcinogenesis of colorectal carcinoma, and SNP analysis for p53 gene can be helpful in early diagnosis of colorectal carcinoma.

Adult ; Case-Control Studies ; Colorectal Neoplasms ; diagnosis ; genetics ; DNA Mutational Analysis ; DNA, Neoplasm ; genetics ; Early Detection of Cancer ; Female ; Humans ; Male ; Mutation ; Polymorphism, Single Nucleotide ; Tumor Suppressor Protein p53 ; genetics

New strategies are needed for prevention of Pseudomonas aeruginosa (P. aeruginosa) infections, a widespread disease caused by P. aeruginosa with strong drug resistance. The immunoprotective capacity of the receptor of autoinducers protein LasR/RhlR was examined in the BALB/c mice. At first, specialized expression plasmids were developed to facilitate expression of LasR/RhlR proteins in Escherichia coli (E. coli). Then, biofilms were grown from clinical isolated P. aeruginosa PA0305 to investigate the relative contributions of cell signaling for biofilm formation. Morphological characters of biofilm were quantified using Image-Pro Plus software. Fluorescence analysis demonstrated that cell signal molecule LasR/RhlR significantly (P ＜ 0.05) influenced development of P. aeruginosa biofilm. Active immunization of mice with LasR/RhlR was found to provide significant protection against homologous challenge with P. aeruginosa in mice lungs. In 10 days after lungs inoculation, the bacterial clearance rate of the immunized mice was clearly higher than that of non-immunized groups on the basis of microbiological and histological assays. The protective effects of immunization with LasR and Rh1R together were the same as the result of LasR or Rh1R immunized mice alone. These data indicate that the manner ofLasR, Rh1R or both is an important determinant of immunoprotection in mice lungs infection.

Objective To investigate the ability of invasion and migration of breast cancer MDA-MB-231 cells under serum starvation and hypoxia, and the effect of antiangiogenic drugs, rh-endostatin and bevacizumab, on the ability of invasion and migration of breast cancer cells under serum starvation and/or hypoxia, in order to explore the potential risk of antiangiogenic therapy in clinics.Mte hods The cells were randomized into 4 groups, i.e., group A:10%fetal bovine serum ( FBS) group;group B:hypoxia +10%FBS group;group C:serum starvation group;group D: hypoxia +serum starvation group; each group was further divided into three subgroups as blank control, treated with rh-endostatin and bevacizumab, respectively.Cell counting kit-8( CCK-8) was used to assess the inhibition rate of cell growth induced by endostatin and bevacizumab, in order to determine the proper working concentration and time of the two drugs.Transwell assay was conducted to detect the cell invasion and migration in vitro.The expressions of c-Met and MMP-9 were detected by Western blot.The cells treated with rh-endostatin or bevacizumab under serum starvation were tested by hybridization using Exiqon miBase 18.0 microarray.The miRNAs which exibited significant differences ( P<0.05) in miRNA hybridization were verified by real-time PCR assay. Results CCK-8 assay showed that the inhibition rates of MDA-MB-231 cells cultured with 800 mg/L rh-endostatin for 48 h and 24 h were (32.2±2.5)%and (27.0±1.3)%, respectively, showing a significant difference ( P=0.023) .The inhibition rates of MDA-MB-231 cells cultured with 80 mg/L bevacizumab for 48 h and 24 h were (30.5±1.4)%and (26.1±2.4)%, respectively , showing also a significant difference (P=0.015).The Transwell assay showed that in the starvation blank group, the number of invaded and penetrated cells were 28.8 ±2.2 and 31.4 ±1.5, respectively, significantly different from that in the rh-endostatin and bevacizumab groups (P<0.05).The relative expressions of c-Met and MMP-9 were 0.213± 0.017 and 0.542±0.048, respectively, with a significant difference from those of the groups treated with each drug ( P<0.05 for both) .The numbers of penetrated cells in the Transwell assay treated with rh-endostatin in hypoxia were 17.5±2.1 and 16.5 ±2.8, respectively, and the numbers of penetrated cells in the Transwell assay treated with bevacizumab were 16.3±3.5 and 17.5±2.4, respectively, showing no significant difference among them ( P>0.05 for both ) .The ability of migration and invasion of MDA-MB-231 cells and the expression of c-Met and MMP-9 were not impacted by hypoxia ( P>0.05) .Real-time PCR assay showed that only the levels of miR-2355 and miR375 were significantly and stably decreased in the cells which had increased ability of invasion and migration.The relative expression levels of miR375 and miR-2355 in the serum starvation blank group were 0.550±0.036 and 0.852±0.121, respectively, significantly lower than that in the groups treated with rh-endostatin or bevacizumab (P<0.05).In the serum starvation group, the expression levels of miR375 and miR-2355of cells treated with rh-endostatin were 02.95±0 .012 and 0.253±0.011, and the expression levels of cells treated with bevacizumab were 0.234±0.020 and 0.309±0.02,2 respectively, ( P>0.05 for all).Compared with the serum starvation blank group, the expression levels of miR2355 and miR375 were significantly decreased when cells were treated with rh-endostatin/bevacizumab under serum starvation, but no significant difference was found between the two drugs ( P>00.5 ).However, hypoxia did not affect the expressions of miR2355 and miR375 ( P>0.05).Conclusions The results of this study suggest that serum starvation can increase the ability of invasion and migration of breast cancer cells.Furthermore, both rh-endostatin and bevacizumab may enhance their invasion and penetration ability under serum starvation condition.

Objective To investigate the ability of invasion and migration of breast cancer MDA-MB-231 cells under serum starvation and hypoxia, and the effect of antiangiogenic drugs, rh-endostatin and bevacizumab, on the ability of invasion and migration of breast cancer cells under serum starvation and/or hypoxia, in order to explore the potential risk of antiangiogenic therapy in clinics.Mte hods The cells were randomized into 4 groups, i.e., group A:10%fetal bovine serum ( FBS) group;group B:hypoxia +10%FBS group;group C:serum starvation group;group D: hypoxia +serum starvation group; each group was further divided into three subgroups as blank control, treated with rh-endostatin and bevacizumab, respectively.Cell counting kit-8( CCK-8) was used to assess the inhibition rate of cell growth induced by endostatin and bevacizumab, in order to determine the proper working concentration and time of the two drugs.Transwell assay was conducted to detect the cell invasion and migration in vitro.The expressions of c-Met and MMP-9 were detected by Western blot.The cells treated with rh-endostatin or bevacizumab under serum starvation were tested by hybridization using Exiqon miBase 18.0 microarray.The miRNAs which exibited significant differences ( P<0.05) in miRNA hybridization were verified by real-time PCR assay. Results CCK-8 assay showed that the inhibition rates of MDA-MB-231 cells cultured with 800 mg/L rh-endostatin for 48 h and 24 h were (32.2±2.5)%and (27.0±1.3)%, respectively, showing a significant difference ( P=0.023) .The inhibition rates of MDA-MB-231 cells cultured with 80 mg/L bevacizumab for 48 h and 24 h were (30.5±1.4)%and (26.1±2.4)%, respectively , showing also a significant difference (P=0.015).The Transwell assay showed that in the starvation blank group, the number of invaded and penetrated cells were 28.8 ±2.2 and 31.4 ±1.5, respectively, significantly different from that in the rh-endostatin and bevacizumab groups (P<0.05).The relative expressions of c-Met and MMP-9 were 0.213± 0.017 and 0.542±0.048, respectively, with a significant difference from those of the groups treated with each drug ( P<0.05 for both) .The numbers of penetrated cells in the Transwell assay treated with rh-endostatin in hypoxia were 17.5±2.1 and 16.5 ±2.8, respectively, and the numbers of penetrated cells in the Transwell assay treated with bevacizumab were 16.3±3.5 and 17.5±2.4, respectively, showing no significant difference among them ( P>0.05 for both ) .The ability of migration and invasion of MDA-MB-231 cells and the expression of c-Met and MMP-9 were not impacted by hypoxia ( P>0.05) .Real-time PCR assay showed that only the levels of miR-2355 and miR375 were significantly and stably decreased in the cells which had increased ability of invasion and migration.The relative expression levels of miR375 and miR-2355 in the serum starvation blank group were 0.550±0.036 and 0.852±0.121, respectively, significantly lower than that in the groups treated with rh-endostatin or bevacizumab (P<0.05).In the serum starvation group, the expression levels of miR375 and miR-2355of cells treated with rh-endostatin were 02.95±0 .012 and 0.253±0.011, and the expression levels of cells treated with bevacizumab were 0.234±0.020 and 0.309±0.02,2 respectively, ( P>0.05 for all).Compared with the serum starvation blank group, the expression levels of miR2355 and miR375 were significantly decreased when cells were treated with rh-endostatin/bevacizumab under serum starvation, but no significant difference was found between the two drugs ( P>00.5 ).However, hypoxia did not affect the expressions of miR2355 and miR375 ( P>0.05).Conclusions The results of this study suggest that serum starvation can increase the ability of invasion and migration of breast cancer cells.Furthermore, both rh-endostatin and bevacizumab may enhance their invasion and penetration ability under serum starvation condition.

Objective To investigate the change of expression pattern of microRNA in the lung with acute lung injury (ALI)/acute respiratory distress syndrome(ARDS) induced by lipopolysaccharide (LPS),and to provide an evidence that microRNAs are involved in the pathogenesis of ALI/ARDS.Methods Twenty-four C57BL mice were randomly divided into control group and LPS treated group,12 mice in each group.The rats in LPS treated group were treated with intratracheal injection of LPS at a dose of 10 mg/kg body weight into the lung.The rats in control group were treated with the same dose of saline instead.All mice were sacrificed 24 hours after operation,the left lung was excised to measure the wet-to-dry weight (W/D) ratio,and the right upper lobe was stained with hematoxylin and eosin (HE).A microRNA microarray chip was used to profile miRNA expressions in the lung of rats in both LPS treated group and control group.Online software packages were used to predict the gene targeted by microRNAs.Results Compared with the control group,the LPS treated mice had obvious respiratory symptoms,the W/D ratio was significantly increased (P ＜ 0.01),and the pathology was characterized with ALI/ARDS.The microarray chip results demonstrated that the expressions of 48 microRNAs were significantly changed in the ALI/ARDS mice.Among these miRNA,27 cases were up-regulated,21 cases were down-regulated.The target genes of these microRNAs might be involved in regulating the signal pathway of inflammation.Conclusions Some miRNAs express differently in the model of ALI/ARDS,and they may play an important role in pathophysiological process of ALI/ARDS.

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