Risk factors for gingival invagination: A retrospective study.

AIM: This study aimed to identify the risk factors for gingival invagination during orthodontic treatment after premolar extraction. MATERIALS AND METHODS: The medical records of 135 patients who had undergone interdental space closure after premolar extraction were collected, and cone beam computed tomography was performed to determine the presence of gingival invagination. The risk factors were examined using mixed-effects models and generalized propensity score weighting (GPSW) to develop a predictive model. RESULTS: Univariate analysis revealed that the extraction site, buccal bone thickness 4 mm apical to the cemento-enamel junction (MB1), mid-root buccal bone thickness (MB2) and vertical skeletal relationships were related to gingival invagination (p < .05). Furthermore, a subsequent multivariable mixed-effects model analysis indicated a significantly increased risk of gingival invagination at MB1 < 1 mm (p < .001; odds ratio [ORMB1≤0.5mm] = 29.304; 95% confidence interval [CI]: 8.986-93.807; OR0.5

[Study based on the acetaldehyde dehydrogenase 2 gene polymorphism and acetaminophen-induced liver injury].

Objective: To explore the association between aldehyde dehydrogenase 2 (ALDH2) gene polymorphisms and abnormal liver function-induced by acetaminophen (APAP) drugs. Methods: An ALDH2 gene knockout mouse model was constructed using CRISPR/Cas9 gene editing technology. The obtained heterozygous mice were mated with opposite sex of heterozygotes. Genomic DNA was extracted from the tail of the offspring mouse. The polymerase chain reaction (PCR) method was used to determine the ALDH2 genotype. APAP was further used to induce acute drug-induced liver injury models in wild-type and ALDH2 knockout mice. Blood and liver tissues of mice were collected for liver function index, HE staining, F4/80 immunohistochemistry, and other detections. The intergroup mean was compared using a one-way ANOVA. The LSD- t test was used for pairwise comparison. Results: ALDH2 knockout mice were bred successfully. The genotyping of the offspring was segregated into the wild-type (ALDH2(+/+)), heterozygous mutant (ALDH2(+/-)), and homozygous mutant (ALDH2(-/-)), respectively. Biochemical and histological results after APAP modeling showed that the level of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and total bilirubin (TBil) was not significantly increased in the blank control group (P < 0.05), while the ALT, AST,ALP, and TBil were all elevated in the APAP experimental group. The levels of ALT (P  = 0.004), AST (P = 0.002), and TBil (P = 0.012) were significantly elevated among the mutant group compared to those in the wild-type group, and the expression levels of these indicators were also significantly elevated among the homozygous mutant group compared to those in the heterozygous mutant group (P = 0.003, 0 and 0.006). In addition, the ALP levels were higher in the heterozygous mutation group than those in the homozygous mutant group (P = 0.085) and wild-type group mice, but the difference was only statistically significant compared to wild-type mice (P = 0.002). HE staining results showed that mice in the APAP experimental group had hepatocyte degeneration, necrosis, and increased inflammatory cell infiltration, which was mostly evident in mutant mice. Simultaneously, the F4/80 immunohistochemical staining results showed that brown granules were visible in the liver tissue of APAP experimental group mice, and its expression levels were significantly enhanced compared to the blank control group. Conclusion: APAP-induced liver function abnormalities were associated with the ALDH2 gene polymorphism. The liver injury symptoms were increased in ALDH2 mutant mice following APAP modeling, and the ALDH2 gene defect may alleviate, to some extent, APAP-induced liver function abnormalities.

[Hemophagocytic syndrome secondary to COVID-19: a case report and literature review].

Objective: To improve the awareness of hemophagocytic syndrome(HPS) secondary to COVID-19 (COVID-sHPS). Methods: We reported an adult case of COVID-sHPS, including clinical presentation, laboratory examinations, histopathological findings, treatment strategy, and outcome. We also conducted literature research in PubMed database and Wanfang database using the keywords "COVID-19" and "hemophagocytic syndrome" and subsequently summarized relevant literature. Results: A 49-year-old man was admitted to our hospital after 4 weeks of recurrent fever. Prior to this hospitalization, he had received an empiric combination therapy with antibiotics and antiviral drugs against SARS-CoV-2. His vital signs were within the normal range and no abnormalities were found on physical examination on admission. After admission, throat swab nucleic acid tests were weakly positive for SARS-CoV-2, and negative for influenza and respiratory syncytial virus. Blood nucleic acid tests for cytomegalovirus and EB virus were negative, as was blood mNGS. Laboratory tests showed a series of abnormalities, including leukopenia, thrombocytopenia, low fibrinogen, elevated serum ferritin, elevated transaminase, decreased NK cell activity, and hemophagocytosis in bone marrow. According to the HPS-2004 diagnostic criteria, he was diagnosed with hemophagocytic syndrome, which was high likely to be caused by COVID-19 infection due to the lack of evidence of genetic risk factors and other clear triggers. He was initially treated with dexamethasone at a dose of 10 mg·m-2·d-1 and his condition improved rapidly. The literature search identified twenty-three articles on COVID-sHPS, 22 of which were in English. A total of 89 patients had COVID-sHPS and 55 (61.7%) were male. COVID-sHPS could occur at any age, but mainly in adults (86/89, 96%). Fever was reported in the literature with a clear description of the course of the disease. Most HPS occurred during the acute phase of COVID-19, but 3 patients developed HPS during the convalescent phase. Almost all reported cases presented with increased ferritin, elevated transaminases, elevated triglycerides, and cytopenia, mainly anemia and thrombocytopenia. In the retrieved literature, HS-score≥169 was frequently used to diagnose COVID-sHPS, and glucocorticoid in combination with immunoglobulin was the most common treatment strategy. COVID-sHPS had a poor prognosis and a high mortality rate (84.2%, 75/89). Conclusions: The prognosis of COVID-sHPS is poor, so clinicians should raise their awareness of the disease, identify high-risk suspected populations, and arrange reasonable relevant examinations for definite diagnosis and early initial treatment to improve their outcome.

[Advances in the diagnosis, treatment, and prognosis of acute decompensatory cirrhosis].

Acute decompensatory cirrhosis is a common cause of hospital admission, readmission, and death, causing a heavy burden on patients, their families, and society. This article reviews the research advancement from the perspectives of concept evolution, pathogenesis, treatment, outcome, and prognosis models, providing new ideas for preventing and treating acute decompensatory cirrhosis.

[Screening for occult cancer in patients with unprovoked venous thromboembolism].

Venous thromboembolism (VTE), which includes deep vein thrombosis and pulmonary embolism, is the third most common cardiovascular disease. Unprovoked VTE can be the initial presentation of occult cancer. Up to 10% of patients with unprovoked VTE are diagnosed with cancer within a year. Cancer screening in patients with unprovoked VTE is beneficial for early cancer diagnosis and treatment, which may theoretically reduce cancer-related morbidity and mortality. The epidemiology of occult cancer in patients with unprovoked VTE, screening strategies originated from evidence-based medicine, risk factors of cancer and different models of risk assessment are reviewed in this article.

[Study of three kinds of primary immunization schedules with poliovirus vaccine].

Objective: To compare the immunogenicity of three kinds immunization programs with poliovirus vaccine. Methods: Healthy infants aged 2 months or over were selected and divided into three groups by complete randomization method. Basic immunization with Sabin inactivated poliovirus vaccine(sIPV) and bivalent oral poliovirus vaccine(bOPV) were completed. Three kinds of basic immunization procedures were 1sIPV+2bOPV,2sIPV+1bOPV and 3sIPV, respectively.Two qualified serums that before basic immunization and 28-42 days later were collected, and measured the poliovirus neutralizing antibody with microcell neutralization method. To compare the difference by analysis of variance, rank test and χ2 test. Results: After the basic immunization, 205 subjects of the positive conversion rate of poliovirus neutralizing antibodies of types Ⅰ, Ⅱ and Ⅲwere all higher than 97.00%, and the positive rates were all higher than 98.00%, the geometric mean titer (GMT) of neutralizing antibody was significantly higher than that before basic immunization in three groups.There were significant differences in the positive rate and GMT before and after basic immunization of typeⅠ, Ⅱand Ⅲ in the three (P<0.05). The highest GMT in three groups after basic immunization were all typeⅠ, followed by type Ⅲ, and the lowest in type Ⅱ. The GMT of type Ⅱin 2sIPV+1bOPV and 3sIPV groups were both higher than that in sIPV+2bOPV group. Conclution: After three kinds of basic immunization, the poliovirus neutralizing antibodies of serum were all at high levels in three groups, which could form an effective immune barrier against poliovirus. The immunogenicity of three kinds of basic immunization programs were all well, but there were certain differences of neutralizing antibodies among three kinds basic immunization programs. The immunogenicity in 2sIPV+1bOPV and 3sIPV groups against typeⅡpoliovirus were better than that in 1sIPV+2bOPV group.

Author Correction: Circular RNA circ-PRKCI promotes cell proliferation and invasion by binding to microRNA-545 in gastric cancer.

Correction to: European Review for Medical and Pharmacological Sciences 2019; 23 (21): 9418-9426-DOI: 10.26355/eurrev_201911_19435-PMID: 31773680, published online on 15 November 2019. After publication, the authors applied to change Figure 1E stating that "gastric cancer was observed from patients underlying response at Renmin Hospital of Wuhan University from March 2015 to March 2016. By the time of submission, the survival time of follow-up was only 2 years. From the 2-year follow-up data, we found that high expression of CIRC PRKCI was positively associated with a poor prognosis of GC patients". The authors claim that there is no serious change in the conclusion of the article. There are amendments to this paper. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/19435.

[Real world research on the growth pattern of preterm children with different birth weight].

Objective: To investigate the physical indices and growth status of preterm children aged 0 to 4 years with different birth weight. Methods: Following the real world research approach, the current study retrospectively collected e-chart information of 8 496 preterm children from the child health care system of the Children's Hospital of Chongqing Medical University from December 2010 to December 2017, with 203 123 full-term children followed up during the same period as controls. Premature children were divided into normal birth weight (NBW) group, low birth weight (LBW) group, and very low birth weight (VLBW) group based on their birth weights. The weight and length development within 48 months of age of preterm boys and girls in each group were measured and recorded to establish a numerical table and analyze the growth levels, growth rate, and proportionality. The t-test or chi-square test was used for between-group comparison. Results: Of the 8 496 preterm children, 4 839 were girls and 3 657 boys, including 525 in the VLBW group, with an average birth weight of (1.28±0.14) kg, 3 862 in the LBW group, with an average birth weight of (2.07±0.28) kg, and 4 109 in the NBW group, with an average birth weight of (2.86±0.35) kg. The weight at the actual age of 2-<3 months ((5.61±0.96) vs. (5.64±0.78) kg in boys, (5.11±0.67) vs. (5.18±0.71) kg in girls) and the length at the actual age of 8-<10 months ((70.3±2.4) vs. (70.6±2.4) cm in boys, (68.9±2.2) vs. (68.9±2.4) cm in girls) in the NBW group reached the average weight and length of full-term children. The difference of physical growth before 24 months of age between LBW and control group decreased as children age, with that of LBW group approaches the average of full-term children after 24 months of age, with a weight difference of 0.64-0.95 kg and height difference of 1.3-1.7 cm. The weight and height of the VLBW group were lower than those of full-term infants (2.80-2.86 kg and 3.3-4.3 cm, respectively) at 48 months of age. During 2-12 months of age, the corresponding values of the VLBW group were higher than that of the LBW and NBW groups by 0.35 kg and 0.71 kg, respectively. However, the corresponding values of the VLBW group were lower than that of the LBW and NBW groups(0.64 kg and 0.76 kg at 0-2 months of age, 1.04 kg and 1.49 kg at 12-48 months of age, respectively). The rates of delayed development, underweight, and emaciation were the highest in the VLBW group (all P<0.01), while the rates of overweight and obesity were the highest in the NBW group, with that of the VLBW group being lower than LBW group (P<0.01) at the age of 24-<36 months. Conclusions: Prior to 4 years of age, the time for preterm children to reach the average physical indices of full-term children differ by birth weights, hence warranting further examination of the corrected gestational age for preterm children. Normal birth weight preterm children present with the highest incidence of overweight and obesity and very low birth weight preterm children present with the highest incidence of growth disorders, marking both groups at high risks of malnutrition.

FOXN2 suppresses the proliferation and invasion of human hepatocellular carcinoma cells.

OBJECTIVE: The aim of this study was to explore the roles of FOXN2 (Fork head Box N2) in mediating the proliferation and invasion of hepatocellular carcinoma (HCC) cells. PATIENTS AND METHODS: Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was used to determine expression of FOXN2 in HCC tissues and cells. Transfection of plasmid containing FOXN2 was used to exogenously overexpress FOXN2 in vitro. Cell Counting Kit-8 (CCK-8) assay and transwell assay were applied to detect the proliferation and invasion of HCC cells, respectively. RESULTS: FOXN2 expression decreased significantly in both HCC tissues and cells (p<0.05). Upregulation of FOXN2 significantly inhibited the proliferation and invasion of HCC cells (p<0.05). CONCLUSIONS: FOXN2 acts as a regulator in the progression of HCC. Our findings suggest that FOXN2 may be a novel therapeutic monitoring and prognosis biomarker in HCC.

Both Caspase and Calpain are Involved in Endoplasmic Reticulum-Targeted BNIP3-Induced Cell Death.

Bcl-2/E1B-19K-interacting protein 3 (BNIP3) is a member of the apoptotic B-cell lymphoma-2 family that regulates cell death. Although BNIP3 targeted normally to the mitochondrial outer membrane by its transmembrane domain was originally considered to be essential for its pro-apoptotic activity, accumulating evidence has shown that BNIP3 is localized to endoplasmic reticulum at physiological conditions and that forced expression of BNIP3 can initiate cell death via multiple pathways depending on the subcellular compartment it targets. Targeting BNIP3 to endoplasmic reticulum has been shown to participate in cell death during endoplasmic reticulum stress. However, the molecular events responsible for BNIP3-induced cell death in the endoplasmic reticulum remain poorly understood. In the present study, the transmembrane domain of BNIP3 was replaced with a segment of cytochrome b5 that targets BNIP3 into endoplasmic reticulum, which induced cell death as effectively as its wild-type molecule in the SW480 cell line (colon carcinoma). Furthermore, a pan-caspase inhibitor, z-VAD-fmk, and PD150606, a specific calpain inhibitor, both significantly suppressed the endoplasmic reticulum-targeted BNIP3-induced cell death. These results suggest that endoplasmic reticulum-targeted BNIP3 induced a mixed mode of cell death requiring both caspases and calpains.

MiR-769-5p inhibits cancer progression in oral squamous cell carcinoma by directly targeting JAK1/STAT3 pathway.

Oral squamous cell carcinoma (OSCC) is the most common human malignancy worldwide with a high mortality rate. MiR-769-5p has been reported to be downregulated in tissues and blood of OSCC patients. However, the exact roles and pathogenesis of miR-769-5p involved in OSCC remain unclear. The expressions of miR-769-5p and Janus kinase (JAK1) in OSCC tissues and cells were assessed by RT-qPCR and western blot assay. Expressions of apoptotic-related (Bcl-2, Bax, and cleaved-caspase 3) and EMT-associated proteins (MMP9, E-cadherin, N-cadherin, and Vimentin) were detected by western blot assay. The effect of miR-769-5p and JAK1 on proliferation, migration, invasion, and apoptosis was evaluated by CCK-8, transwell, and flow cytometry assays, respectively. The binding interaction of miR-769-5p and JAK1 were predicted by TargetScan and demonstrated by dual-luciferase reporter assays. The volume and weight of the tumor were measured in the subcutaneous transplantation experiment. MiR-769-5p was downregulated, and JAK1 was upregulated in OSCC tissues and cells. MiR-769-5p restrained Bcl-2, MMP9, N-cadherin, and Vimentin protein level and accelerated Bax, cleaved-caspase 3 and E-cadherin protein level, while JAK1 partly overturned these effects. Also, miR-769-5p suppressed proliferation, migration, invasion, and increased apoptosis of OSCC, while the reintroduction of JAK1 abolished these effects. Moreover, JAK1 was verified to be the target of miR-769-5p. In addition, miR-769-5p inhibited the development of OSCC cells in vivo. These results indicate that miR-769-5p suppressed OSCC cell development via targeting the JAK1/STAT3 pathway, providing an underlying therapeutic method for OSCC.

Circular RNA circ-PRKCI promotes cell proliferation and invasion by binding to microRNA-545 in gastric cancer.

OBJECTIVE: The carcinogenic effects of circular RNA circ-PRKCI have been recognized in a variety of malignancies. However, the exact biological function of circ-PRKCI in gastric cancer has not been fully elucidated. Therefore, the aim of this study was to explore the expression of circ-PRKCI in gastric cancer (GC) and to investigate its potential regulation mechanism in the pathogenesis and progression of GC. PATIENTS AND METHODS: The expression of circ-PRKCI in 50 GC tissues and cell lines was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Statistical methods were used to analyze the relation between circ-PRKCI expression and overall survival rate of patients. The effect of circ-PRKCI on GC cell proliferation was examined by cell counting kit-8 (CCK-8) and cell colony formation assays. Meanwhile, the effect of circ-PRKCI on the invasion ability of GC cells was determined by transwell invasion assay. Flow cytometry was used to detect the apoptosis of GC cells. Bioinformatics was used to search for miRNAs that might have direct effects with circ-PRKCI. In addition, the binding of circ-PRKCI to microRNA-545 was validated using Dual-Luciferase reporter gene assay. RESULTS: Circ-PRKCI was significantly highly expressed in GC tissues, as well as cell lines. High expression of circ-PRKCI was positively associated with a poor prognosis of GC patients. Overexpression of circ-PRKCI significantly promoted the proliferation and invasion of GC cells, whereas reduced the proportion of apoptotic GC cells. Subsequent Dual-Luciferase reporter gene assay revealed that circ-PRKCI could bind to microRNA-545 and inhibit its expression in GC cells. These results indicated that circ-PRKCI might promote the development of GC by adsorbing microRNA-545 in a sponge manner. CONCLUSIONS: Circ-PRKCI can be used as a potential prognostic indicator of GC, providing a new perspective for the potential bio-molecular mechanism in GC.

Circ_0000064 adsorption of microRNA-143 promotes malignant progression of hepatocellular carcinoma.

OBJECTIVE: The aim of this study was to investigate the expression characteristics of circ_0000064 in hepatocellular carcinoma, and to further explore the underlying mechanism. PATIENTS AND METHODS: Real time quantitative-Polymerase Chain Reaction (qPCR) was used to detect the expression of circ_0000064 in 42 hepatocellular carcinoma tissues and adjacent normal tissues. Meanwhile, the relationship between circ_0000064 expression and clinical indicators, as well as the prognosis of patients with hepatocellular carcinoma, were detected. QPCR was applied to measure circ_0000064 level in hepatocellular carcinoma cell lines as well. Subsequently, the circ_0000064 knockdown model was successfully constructed using lentivirus in hepatocellular carcinoma cell lines. Cell counting kit-8 (CCK-8), colony formation assay, and flow apoptosis were performed to analyze the influence of circ_0000064 on the biological functions of hepatocellular carcinoma cells. The potential mechanism was explored using cell recovery experiments. In addition, the relationship between circ_0000064 and microRNA-143 was finally explored. RESULTS: QPCR results showed that the expression level of circ_0000064 in hepatocellular carcinoma tissues was remarkably higher than that of adjacent normal tissues, and the difference was statistically significant. Compared with patients with lower expression of circ_0000064, patients with higher expression of circ_0000064 exhibited remarkably higher pathological stage and lower overall survival rate. In vitro experiments demonstrated that the proliferation ability of the cells was remarkably reduced after the transfection of si-circ_0000064, while cell apoptosis ability significantly increased when compared with the NC group. Meanwhile, qPCR results indicated that microRNA-143 expression was negatively correlated with circ_0000064 expression in hepatocellular carcinoma. Luciferase reporter gene assay indicated that circ_0000064 could be targeted by microRNA-143 through their binding site. In addition, the cell recovery experiment confirmed that circ_0000064 and microRNA-143 could be mutually regulated, which affected the malignant progression of hepatocellular carcinoma together. CONCLUSIONS: Circ_0000064 level was remarkably upregulated in hepatocellular carcinoma and was associated with high pathological stage and poor prognosis of patients. In addition, circ_0000064 significantly promoted proliferation and inhibited apoptosis of hepatocellular carcinoma cells via modulating microRNA-143.

[Idiopathic pleuroparenehymal fibroelastosis: report of one case and review of literature].

Objective: To analyze the clinical,imaging and pathological features of Pleuroparenehymal fibroelastosis (PPFE). Methods: The clinieal data of a patient diagnosed as PPFE admitted in department of Respiratory and Critical Care Medicine,Beijing Hospital in April 2017 were reported and the related literatures were reviewed.With "pleuroparenehymal fibroelastosis" as the search terms, and the search time before October 1st 2017 for Wanfangdata, China National Knowledge Infrastructure(CNKI), and PubMed. Results: The patient was a 46-year-old male presented with cough, shortness of breath after exercise.A CT scan of the chest revealed bilateral, irregular pleural thickening with upper lobe predominance.After 3 years of antituberculosis treatment,the disease progressed. A diagnosis of pleuroparenehymal fibroelastosis (PPFE) was confirmed by CT guided lung biopsy. A total of 132 cases were reported (including 1 case in Chinese). 88 of them were confirmed by pathology with detailed data.Clinical data of 89 reported cases with PPFE including 48 males and 41 females aged 13 to 85 years were enrolled and analyzed in the study.The common symptoms were dyspnea(62%, 55 cases),cough(58%, 52 cases),recurrent respiratory tract infection(17%, 15 cases).The main CT features are reported:pleural thickening(87%,77 cases), recurrent pneumothorax(52%,46 cases), traction bronchiectasis(30%, 27 cases),subpleural comsolidation(20%, 18 cases). All patients were proven PPFE by biopsy.34 cases received corticosteroid, 5 cases received lung transplant operation.40 cases died during the follow-up from 4 month to 84 month. Conclusions: Pleuroparenehymal fibroelastosis is a rare disease.The imaging findings were dominated by both upper lobes. Lung biopsy might be necessary. PPFE is often misdiagnosed as pulmonary tuberculosis/obsolete pulmonary tuberculosis,asbestosis,connective tissues disease and Drug-induced pneumonitis.There was no consensus on the treatment.

[Clinical characteristics and prognosis of overweight and obese patients with pulmonary thromboembolism].

Objective: To investigate the clinical characteristics and outcomes of overweight and obese patients with pulmonary embolism. Methods: This was a retrospective study of patients with pulmonary thromboembolism(PTE) in Beijing Hospital between 2009 and 2017. Data were analyzed and compared based on body mass index (BMI), and patients were classified into normal weight, overweight, and obese. Results: Among 372 patients with PTE, 159 were normal, 143 were overweight and 70 were obese. The mean age was (67.8±13.4) years, and 159(47.0%) were males. There was no significant difference in age, sex, smoking ratio, and underlying disease between the 3 groups (all P>0.05). Chest pain was less frequent in the obese group than the overweight group (P<0.05), and swollen of lower limbs was more prevalent in the obese group than the first 2 groups (all P<0.05). The levels of hemoglobin and hematocrit in the obese group were significantly higher than those in the normal group(P<0.05), while the serum uric acid levels were significantly higher than that in the normal group (P<0.05). Anticoagulation was more frequent in the overweight than the normal group(P<0.05) and Warfarin use was more frequent in the overweight and the obese than the normal group(both P<0.05). The mortality rate was higher in the normal group than those in the overweight and the obese groups (both P<0.01). Multiple logistic regression analysis after adjusting for age and sex showed that malignancy (OR=3.716, 95%CI: 1.733-7.972, P=0.001) and high risk PTE (OR=13.815, 95%CI: 4.093-46.624, P<0.001) were predictors of mortality, whereas anticoagulation (OR=0.155, 95%CI: 0.056-0.428, P<0.001), BMI≥24 (OR=0.142, 95%CI: 0.045-0.446, P=0.001) and BMI≥28 (OR=0.272, 95%CI: 0.085-0.872, P=0.029) were the predictors of survival. Conclusions: Proportion of hypertension, diabetes, coronary heart disease and hyperlipidemia were not significantly different in patients with overweight and obesity compared to patients with normal weight. Obese patients had higher levels of uric acid and hemoglobin than normal weight. Overweight and obese patients had a better survival.

[Investigation of acquired drug-resistant genes and strains relationship in Pseudomonas aeruginosa isolated from burn patients].

Objective: To investigate the acquired drug-resistant genes and strains relationship in 40 strains of Pseudomonas aeruginosa isolated from burn patients. Methods: Forty strains of Pseudomonas aeruginosa isolated from burn patients hospitalized in our burn department from January 2014 to December 2015 were selected, with 20 strains from each year. Kirby-Bauer paper disk diffusion method was used to detect sensitivity of the isolated Pseudomonas aeruginosa to 9 kinds of antibiotics of cefotaxime, ceftazidime, cefepime, imipenem, meropenem, gentamicin, amikacin, ciprofloxacin, and levofloxacin. Polymerase chain reaction was applied to detect 9 kinds of acquired ß-lactamase antibiotics-resistant genes, outer membrane porin protein oprD2 genes, 12 kinds of acquired aminoglycosides antibiotics-resistant genes, and 6 kinds of acquired disinfectant-resistant genes and genetic marker genes of mobile genetic elements. Among the above genes, positive expression genes were verified by DNA sequencing and comparison. Sequences of twenty-eight acquired drug-resistant genes of the above 40 Pseudomonas aeruginosa strains were analyzed by unweighted pair-group method with arithmetic means cluster analysis. Results: Forty strains of Pseudomonas aeruginosa were resistant to the above 9 kinds of antibiotics. Two kinds of acquired ß-lactamase antibiotics-resistant genes of bla(TEM), bla(CARB), 5 kinds of acquired aminoglycosides antibiotics-resistant genes of aac(6')-Ⅰb, aac(6')-Ⅱ, ant(2″)-Ⅰ, ant(3″)-Ⅰ, and rmtB, and 3 kinds of acquired disinfectant-resistant genes and genetic marker genes of mobile genetic elements of qacE△1-sul1, merA, and intⅠ1were detected in 40 strains of Pseudomonas aeruginosa with oprD2 gene deficiency. Forty strains aggregated obviously, with a total of 7 gene modes and 3 clones. Drug-resistant gene sequences of strains of number 2 to 4, 6 to 9, 11, 14, and 17 to 39 were similar and with close relationship. Drug-resistant gene sequences of number 12 and 13 strains were similar and with close relationship. Drug-resistant sequences of number 10 and 16 strains were similar and with close relationship. Conclusions: Genes of bla(TEM), bla(CARB), aac(6')-Ⅰb, aac(6')-Ⅱ, ant(2″)-Ⅰ, rmtB, qacE△1-sul1, merA, and intⅠ1 were prevalent in these strains of Pseudomonas aeruginosa with oprD2 gene deficiency isolated from burn patients, which may play key roles in resistance of Pseudomonas aeruginosa to ß-lactamase, aminoglycoside, and quinolone antibiotics, and the drug-resistant phenotypes were in good coincidence with genotypes. Pseudomonas aeruginosa strains isolated from burn patients were with similar acquired drug-resistant genes and close relationship.

[Clinical characteristics and outcomes of patients with lung cancer, gastrointestinal cancer and urologic cancer with venous thromboembolism].

Objective: To compare the clinical characteristics and outcomes of patients with lung cancer, gastrointestinal (GI) cancer and urologic cancer with venous thromboembolism (VTE). Methods: From January 2003 to January 2013, 192 lung cancer, GI cancer and urologic cancer patients with VTE were retrospectively evaluated for the clinical characteristics and outcomes. Results: Among 192 patients, 82 cases of lung cancer, 78 cases of GI cancer, 32 cases of urologic cancer were involved. The Eastern Cooperative oncology Group Performance Status score of GI cancer group was significantly higher than those of the lung cancer and urologic cancer groups[(2.4±1.1) vs (2.0±1.4), (1.8±1.0), both P<0.05]. The proportion of smoking patients in lung cancer group was significantly higher than that in GI cancer and urologic cancer groups (79.3% vs 30.8%, 53.1%, both P<0.05), while the proportion of operation was significantly lower than that in the latter two groups (35.4% vs 53.8%, 68.8%, both P<0.05). Pathological types of cancer were mostly adenocarcinoma, and the proportion of adenocarcinoma in lung cancer and GI cancer groups was significantly higher than that in urologic cancer group (76.9%, 73.8% vs 37.9%, both P<0.001). The proportion of moderately and/or poorly differentiated histodifferentiation in the first two groups was significantly higher than that of urologic cancer group (90.0%, 95.7% vs 40.0%, both P<0.001). The proportion of patients with TNM stage Ⅲ-Ⅳ in lung cancer group was significantly higher than that of the urological cancer group (87.0% vs 64.3%, P<0.05). The incidence of VTE in lung cancer group was significantly higher than those of GI cancer and urologic cancer groups within 6 months after tumor diagnosis, chemotherapy and operation (79.3% vs 60.3%, 46.9%; 76.5% vs 48.6%, 36.4%; 92.3% vs 57.9%, 59.1%; all P<0.05). The case fatality rate within one year in lung cancer and GI cancer groups was significantly higher than that in urologic cancer group (51.2%, 52.6% vs 18.8%, both P<0.01). The median survival time of the lung cancer and GI cancer groups was significantly shorter than that of the urological cancer group (P=0.001, 0.010, respectively). Conclusions: Adenocarcinoma, advanced cancer, and poor histodifferentiation are risk factors of VTE in cancer patients. Most events of VTE occur within 6 months after a diagnosis of cancer. The prognosis of lung cancer and GI cancer complicated with VTE is worse than that of urologic cancer with VTE.