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Pan-Chyr Yang

Publications and source records attributed to Pan-Chyr Yang.

At least 19 recordsLinked to original sources

Plasma signals of lung tumor promotion for molecular cancer prevention.

Predicting lung cancer risk would enhance prevention trials. Although the Canakinumab Anti-inflammatory Thrombosis Outcome Study (CANTOS) trial demonstrated reduced lung cancer incidence with interleukin (IL)-1β inhibition, the high number needed to treat (NNT) to prevent lung cancer limits its use in unselected populations. Using machine learning, we identified a 14-protein plasma signature predicting lung cancer more than 5 years before diagnosis. The signature, validated across eight cohorts, was elevated in current smokers and individuals exposed to particulate matter (PM) and linked to lung myeloid and alveolar cells. In epidermal growth factor receptor (EGFR)-driven lung adenocarcinoma, diverse epithelial lineages converged on a keratin8+/claudin4+ alveolar transitional state (KAC), whose transcriptional programs correlated with signature emergence. Components of the signature were induced by PM, oncogenic EGFR, or IL-1β, whereas IL-1β inhibition restrained PM-driven KAC expansion and early tumorigenesis. In CANTOS, the signature identified individuals who seemed to benefit more from anti-IL-1β therapy, lowering the NNT threshold and nominating circulating signals of tumor promotion for prevention.

Humans↗

A phase II study of oral vinorelbine in combination with cisplatin conducted in Taiwan in patients with unresectable localized or metastatic non-small cell lung carcinoma.

BACKGROUND: Intravenous vinorelbine plus cisplatin is widely prescribed for the treatment of NSCLC. The objective of this phase II study was to define the efficacy of an oral form of vinorelbine combined with cisplatin for first line treatment of advanced/metastatic NSCLC. PATIENTS AND METHODS: From September 2002 to December 2003, 46 chemotherapy-naive patients received 80 mg/m(2) of cisplatin on day 1 and oral vinorelbine at 60 mg/m(2) on days 1 and 8, every 3 weeks. RESULTS: After an independent panel review, the response rate was 37.5 % [95% confidence interval (CI): 22.7-54.2%] in the evaluable population and 32.6% [95% CI: 19.5-48] in the intent-to-treat population. Median progression-free survival was 5.6 months and overall survival was 11.2 months. Grades 3 and 4 neutropenia was observed in 58.7% of patients, with febrile neutropenia and neutropenic infection in 4.3 and 8.7% of patients, respectively. The main non-haematological toxicities were hypotension, fatigue (8.7% for each) and gastrointestinal disorders with rare grades 3 and 4. CONCLUSIONS: These results suggest that the combination of cisplatin at 80 mg/m(2) on day 1 with oral vinorelbine at 60 mg/m(2) on days 1 and 8, every 3 weeks, is an active regimen, associated with acceptable toxicity. Oral vinorelbine is therefore a good alternative to the i.v. formulation.

Administration, Oral↗

A five-gene signature and clinical outcome in non-small-cell lung cancer.

BACKGROUND: Current staging methods are inadequate for predicting the outcome of treatment of non-small-cell lung cancer (NSCLC). We developed a five-gene signature that is closely associated with survival of patients with NSCLC. METHODS: We used computer-generated random numbers to assign 185 frozen specimens for microarray analysis, real-time reverse-transcriptase polymerase chain reaction (RT-PCR) analysis, or both. We studied gene expression in frozen specimens of lung-cancer tissue from 125 randomly selected patients who had undergone surgical resection of NSCLC and evaluated the association between the level of expression and survival. We used risk scores and decision-tree analysis to develop a gene-expression model for the prediction of the outcome of treatment of NSCLC. For validation, we used randomly assigned specimens from 60 other patients. RESULTS: Sixteen genes that correlated with survival among patients with NSCLC were identified by analyzing microarray data and risk scores. We selected five genes (DUSP6, MMD, STAT1, ERBB3, and LCK) for RT-PCR and decision-tree analysis. The five-gene signature was an independent predictor of relapse-free and overall survival. We validated the model with data from an independent cohort of 60 patients with NSCLC and with a set of published microarray data from 86 patients with NSCLC. CONCLUSIONS: Our five-gene signature is closely associated with relapse-free and overall survival among patients with NSCLC.

Aged↗

Disseminated tuberculosis: a 10-year experience in a medical center.

Disseminated tuberculosis remains a diagnostic challenge because the presentations are nonspecific. In the current retrospective study we describe the clinical characteristics and outcome of disseminated tuberculosis. From January 1995 to December 2004, patients with culture-confirmed tuberculosis who fulfilled the criteria for disseminated tuberculosis were selected and their medical records reviewed. Their clinical isolates were genotyped. Of the 3058 patients with culture-confirmed tuberculosis, 164 (5.4%) had disseminated disease; 14.0% of patients had acquired immunodeficiency syndrome. The most common radiographic finding was miliary lung lesions (47.0%); 31.1% of patients died at the end of the study. Poor prognostic factors included hypoalbuminemia, hyperbilirubinemia, renal insufficiency, and delayed antituberculosis treatment. Clinical findings suggestive of disseminated tuberculosis were miliary lung lesions, serum ferritin >1000 microg/L, infiltrative liver disease, and adjusted calcium >2.6 mmol/L. Simultaneously performing mycobacterial culture and histopathologic examination of bone marrow biopsy was more sensitive and faster than just performing mycobacterial blood culture in diagnosing disseminated tuberculosis. Of the 64 preserved Mycobacterium tuberculosis isolates, 47 (73.4%) were clustered and 27 (42.2%) were Beijing family. Since prognosis was worse in patients with delayed treatment, a high index of suspicion is required, especially in those with clinical findings suggestive of disseminated tuberculosis.

Adult↗

Sputum bacteriology in hospitalized patients with acute exacerbation of chronic obstructive pulmonary disease in Taiwan with an emphasis on Klebsiella pneumoniae and Pseudomonas aeruginosa.

BACKGROUND AND OBJECTIVE: Bacterial infection is one of the major causes of acute exacerbation of COPD (AECOPD). This study was undertaken to investigate the microbiology of AECOPD. METHODS: Medical records from 494 episodes of AECOPD in patients admitted to the National Taiwan University Hospital from January 2000 to June 2004 were reviewed. Severity of COPD was classified according to the 2003 Global Initiative for Chronic Obstructive Lung Disease guideline. RESULTS: Potential pathogenic microorganisms were isolated from patients in 328 (66.4%) episodes of AECOPD. The predominant bacteria were Klebsiella pneumoniae (19.6%), Pseudomonas aeruginosa (16.8%) and Haemophilus influenzae (7.5%), followed by Acinetobacter baumannii (6.9%), Enterobacter species (6.1%) and Staphylococcus aureus (6.1%). The incidence of Streptococcus pneumoniae was 2.4%. Spirometry results obtained within 1 year of the exacerbation were available in 186 cases. K. pneumoniae was more frequently isolated in stage I COPD (39.1%) than stage II (16.6%), III (13.8%) and IV (9.4%). No glucose non-fermentative Gram-negative bacilli were isolated in stage I patients. Multivariate logistic regression analysis revealed that P. aeruginosa (odds ratio (OR) 3.19; 95% confidence interval (CI): 1.21-8.38), intubation (OR 14.81; 95% CI: 5.08-43.12) and age (OR 1.1; 95% CI: 1.03-1.17) were independent risk factors for mortality. CONCLUSIONS: Klebsiella pneumoniae and P. aeruginosa are the most common sputum pathogens in hospitalized patients with AECOPD in Taiwan, with the former being more commonly isolated from mild COPD and the latter associated with poor clinical outcome. These results should be considered when deciding which antibiotics should initially be used to treat patients with AECOPD.

Aged↗

Human kallikrein 8 protease confers a favorable clinical outcome in non-small cell lung cancer by suppressing tumor cell invasiveness.

The human kallikrein 8 (KLK8) gene, a member of the human tissue kallikrein gene family, encodes a serine protease. The KLK8 protein (hK8) is known to be a favorable prognostic marker in ovarian cancer, but the biological basis of this is not understood. We found that overexpressing the KLK8 gene in highly invasive lung cancer cell lines suppresses their invasiveness. This role in invasiveness was further confirmed by the fact that inhibition of endogenous KLK8 expression with a specific short hairpin RNA reduced cancer cell invasiveness. In situ degradation and cell adhesion assays showed that proteins produced from KLK8 splice variants modify the extracellular microenvironment by cleaving fibronectin. DNA microarray experiments and staining of cells for actin filaments revealed that the degradation of fibronectin by hK8 suppresses integrin signaling and retards cancer cell motility by inhibiting actin polymerization. In addition, studies in a mouse model coupled with the detection of circulating tumor cells by quantitative PCR for the human Alu sequence showed that KLK8 suppresses tumor growth and invasion in vivo. Finally, studies of clinical specimens from patients with non-small cell lung cancer showed that the time to postoperative recurrence was longer for early-stage patients (stages I and II) with high KLK8 expression (mean, 49.9 months) than for patients with low KLK8 expression (mean, 22.9 months). Collectively, these findings show that KLK8 expression confers a favorable clinical outcome in non-small cell lung cancer by suppressing tumor cell invasiveness.

Base Sequence↗

Survival outcome and predictors of gefitinib antitumor activity in East Asian chemonaive patients with advanced nonsmall cell lung cancer.

BACKGROUND: Chemonaive patients had higher response rates than chemotherapy-treated patients in previous analyses of East Asian patients with advanced nonsmall cell lung cancer. The survival outcome and the predictors for antitumor activity in chemonaive patients who received gefitinib as first-line treatment are unclear. METHODS: Clinicopathologic predictive factors, objective tumor responses, and the survival of consecutive patients with advanced, chemonaive nonsmall cell lung cancer who received gefitinib as first-line treatment were collected and analyzed. Multivariate analysis was conducted to determine independent predictive factors for gefitinib antitumor efficacy. RESULTS: One hundred ninety-six patients (112 males and 84 females) were analyzed. Ninety-six patients (49%) were never smokers. One hundred forty-four patients (73%) had adenocarcinoma or bronchioloalveolar carcinoma histology. One hundred twenty patients had an Eastern Cooperative Oncology Group performance status 0 to 2. Eighty-three patients (42%; 95% confidence interval, 36-49%) had an objective tumor response. An additional 35 patients had stable disease (disease control rate, 61%). The tumor response rate was 52% in patients who had a good performance status. Female gender, nonsmoking status, and adenocarcinoma histology all were independent predictors of response or disease control in multivariate analysis. The median survival was 11.1 months, and the 1-year survival rate of patients who had a good performance status was 47.5%. CONCLUSIONS: The response rate to gefitinib was high in East Asian chemonaive patients with advanced nonsmall cell lung cancer. Female gender, adenocarcinoma histology, and nonsmoking status all were independent predictors of gefitinib response. The survival outcome of these patients was similar to that of patients who initially received chemotherapy.

Adenocarcinoma↗

Titanium dioxide nanoparticles induce emphysema-like lung injury in mice.

Titanium dioxide nanoparticles (nanoTiO2) have been widely used as a photocatalyst in air and water cleaning. However, these nanoparticles inhalation can induce pulmonary toxicity and its mechanism is not fully understood. In this study we investigated the pulmonary toxicity of nanoTiO2 and its molecular pathogenesis. The adult male ICR mice were exposed to intratracheal single dose of 0.1 or 0.5 mg nanoTiO2 (19-21 nm) and lung tissues were collected at 3rd day, 1st wk, and 2nd wk for morphometric, microarray gene expression, and pathway analyses. NanoTiO2 can induce pulmonary emphysema, macrophages accumulation, extensive disruption of alveolar septa, type II pneumocyte hyperplasia, and epithelial cell apoptosis. NanoTiO2 induced differential expression of hundreds of genes include activation of pathways involved in cell cycle, apoptosis, chemokines, and complement cascades. In particular, nanoTiO2 up-regulates placenta growth factor (PlGF) and other chemokines (CXCL1, CXCL5, and CCL3) expressions that may cause pulmonary emphysema and alveolar epithelial cell apoptosis. Cultured human THP-1 cell-derived macrophages treated with nanoTiO2 in vitro also resulted in up-regulations of PlGF, CXCL1, CXCL5, and CCL3. These results indicated that nanoTiO2 can induce severe pulmonary emphysema, which may be caused by activation of PlGF and related inflammatory pathways.

Animals↗

Topology-based cancer classification and related pathway mining using microarray data.

Cancer classification is the critical basis for patient-tailored therapy, while pathway analysis is a promising method to discover the underlying molecular mechanisms related to cancer development by using microarray data. However, linking the molecular classification and pathway analysis with gene network approach has not been discussed yet. In this study, we developed a novel framework based on cancer class-specific gene networks for classification and pathway analysis. This framework involves a novel gene network construction, named ordering network, which exhibits the power-law node-degree distribution as seen in correlation networks. The results obtained from five public cancer datasets showed that the gene networks with ordering relationship are better than those with correlation relationship in terms of accuracy and stability of the classification performance. Furthermore, we integrated the ordering networks, classification information and pathway database to develop the topology-based pathway analysis for identifying cancer class-specific pathways, which might be essential in the biological significance of cancer. Our results suggest that the topology-based classification technology can precisely distinguish cancer subclasses and the topology-based pathway analysis can characterize the correspondent biochemical pathways even if there are subtle, but consistent, changes in gene expression, which may provide new insights into the underlying molecular mechanisms of tumorigenesis.

Gene Expression Profiling↗

Effect of connective tissue growth factor on hypoxia-inducible factor 1alpha degradation and tumor angiogenesis.

BACKGROUND: Connective tissue growth factor (CTGF) inhibits the metastatic activity of human lung cancer cells in a mouse model; however, the mechanism of this modulation is unclear. We investigated the role of angiogenesis in this process. METHODS: CL1-5 and A549 human lung adenocarcinoma cells were stably transfected with vectors containing CTGF or hypoxia-inducible factor (HIF) 1alpha or with vector controls. Transfected cells were injected into nude mice (n = 10 per group), and tumor growth, metastasis, and mouse survival were measured. Excised xenograft tumors and primary human lung adenocarcinomas (n = 24) were subjected to immunohistochemistry with antibodies to the endothelial cell marker CD31 and to CTGF. Expression of HIF-1alpha and vascular endothelial growth factor (VEGF) A was assessed in vitro by using reporter gene assays. Cells were transiently transfected with HIF-1alpha mutant and antisense arrest-defective 1 protein (ARD-1), and HIF-1alpha acetylation was assayed by immunoprecipitation. All statistical tests were two-sided. RESULTS: Xenograft tumors derived from CTGF transfectants grew more slowly than those from control-transfected cells and had reduced expression of HIF-1alpha and VEGF-A, vascularization (as assessed by CD31 expression), and metastasis (all P<.001). Xenograft tumors derived from CTGF-overexpressing cells that were transfected with HIF-1alpha had higher VEGF-A expression than CTGF-overexpressing xenografts. Mice with CTGF/HIF-1alpha xenografts had lower survival than mice carrying CTGF-overexpressing xenografts (CL1-5/Neo, mean = 69.6 days, 95% confidence interval [CI] = 53.9 to 85.3 days versus CL1-5/CTGF, mean = 102.1 days, 95% CI = 92.1 to 112.1 days; P = .001, CL1-5/CTGF, mean = 102.1 days, 95% CI = 92.1 to 112.1 days versus CL1-5/CTGF/HIF-1alpha, mean = 81.7 days, 95% CI = 66.5 to 96.9 days; P = .011, CL1-5/Neo, mean = 69.6 days, 95% CI = 53.9 to 85.3 days versus CL1-5/CTGF/HIF-1alpha, mean = 81.7 days, 95% CI = 66.5 to 96.9 days; P = .122). Tumors of patients with the same disease stage but with high CTGF protein expression had reduced microvessel density compared with tumors with low expression. Transfection with antisense-ARD1 decreased the level of acetylated HIF-1alpha and restored HIF-1alpha and VEGF-A expression in CTGF-overexpressing cells. CONCLUSION: CTGF inhibition of metastasis involves the inhibition of VEGF-A-dependent angiogenesis, possibly by promoting HIF-1alpha protein degradation.

Acetylation↗

CRSD: a comprehensive web server for composite regulatory signature discovery.

Transcription factors (TFs) and microRNAs play important roles in the regulation of human gene expression, and the study of their combinatory regulations of gene expression is a new research field. We constructed a comprehensive web server, the composite regulatory signature database (CRSD), that can be applied in investigating complex regulatory behaviors involving gene expression signatures (GESs), microRNA regulatory signatures (MRSs) and TF regulatory signatures (TRSs). Six well-known and large-scale databases, including the human UniGene, mature microRNAs, putative promoter, TRANSFAC, pathway and Gene Ontology (GO) databases, were integrated to provide the comprehensive analysis in CRSD. Two new genome-wide databases, of MRSs and TRSs, were also constructed and further integrated into CRSD. To accomplish the microarray data analysis at one go, several methods, including microarray data pretreatment, statistical and clustering analysis, iterative enrichment analysis and motif discovery, were closely integrated in the web server, which has not been the case in previous studies. Our implementation showed that the published literature could demonstrate the results of genome-wide enrichment analysis. We conclude that CRSD is a powerful and useful bioinformatic web server and may provide new insights into gene regulation networks. CRSD and the online tutorial are publicly available at http://biochip.nchu.edu.tw/crsd1/.

3' Untranslated Regions↗

A new tumor suppressor DnaJ-like heat shock protein, HLJ1, and survival of patients with non-small-cell lung carcinoma.

BACKGROUND: We previously identified DnaJ-like heat shock protein (HLJ1) as a gene associated with tumor invasion. Here, we investigated the clinical significance of HLJ1 expression in non-small-cell lung cancer (NSCLC) patients and its role in cancer progression. METHODS: We induced HLJ1 overexpression or knockdown in human lung adenocarcinoma CL1-5 cells and analyzed cell proliferation, anchorage-independent growth, in vivo tumorigenesis, cell motility, invasion, and cell cycle progression. Expression of genes that act downstream of HLJ1 was examined by DNA microarray analysis, pathway analysis, and western blotting. We measured HLJ1 expression in tumors and adjacent normal tissues of 71 NSCLC patients by quantitative reverse transcription-polymerase chain reaction. Associations between HLJ1 expression and disease-free and overall survival were determined using the log-rank test and multivariable Cox proportional hazards regression analysis. Validation was performed in an independent cohort of 56 NSCLC patients. Loss of heterozygosity (LOH) mapping of the HLJ1 locus was analyzed in 48 paired microdissected NSCLC tumors. All statistical tests were two-sided. RESULTS: HLJ1 expression inhibited lung cancer cell proliferation, anchorage-independent growth, tumorigenesis, cell motility, and invasion, and slowed cell cycle progression through a novel STAT1/P21(WAF1) pathway that is independent of P53 and interferon. HLJ1 expression was lower in tumors than in adjacent normal tissue in 55 of 71 patients studied. NSCLC patients with high HLJI expressing tumors had reduced cancer recurrence (hazard ratio [HR] = 0.47; 95% confidence interval [CI] = 0.23 to 0.93; P = .03) and longer overall survival (HR = 0.38; 95% CI = 0.16 to 0.89; P = .03) than those with low-expressing tumors. Validation in the independent patient cohort confirmed the association between HLJ1 expression and patient outcome. LOH mapping revealed high frequencies (66.7% and 70.8%) of allelic loss and microsatellite instability (87.5% and 95.2%) of the HLJ1 locus at chromosome 1p31.1. CONCLUSIONS: HLJ1 is a novel tumor suppressor in NSCLC, and high HLJ1 expression is associated with reduced cancer recurrence and prolonged survival of NSCLC patients.

Biomarkers, Tumor↗

Design of microarray probes for virus identification and detection of emerging viruses at the genus level.

BACKGROUND: Most virus detection methods are geared towards the detection of specific single viruses or just a few known targets, and lack the capability to uncover the novel viruses that cause emerging viral infections. To address this issue, we developed a computational method that identifies the conserved viral sequences at the genus level for all viral genomes available in GenBank, and established a virus probe library. The virus probes are used not only to identify known viruses but also for discerning the genera of emerging or uncharacterized ones. RESULTS: Using the microarray approach, the identity of the virus in a test sample is determined by the signals of both genus and species-specific probes. The genera of emerging and uncharacterized viruses are determined based on hybridization of the viral sequences to the conserved probes for the existing viral genera. A detection and classification procedure to determine the identity of a virus directly from detection signals results in the rapid identification of the virus. CONCLUSION: We have demonstrated the validity and feasibility of the above strategy with a small number of viral samples. The probe design algorithm can be applied to any publicly available viral sequence database. The strategy of using separate genus and species probe sets enables the use of a straightforward virus identity calculation directly based on the hybridization signals. Our virus identification strategy has great potential in the diagnosis of viral infections. The virus genus and specific probe database and the associated summary tables are available at http://genestamp.sinica.edu.tw/virus/index.htm.

Animals↗

Knockdown of contactin-1 expression suppresses invasion and metastasis of lung adenocarcinoma.

Numerous genetic changes are associated with cancer cell metastasis and invasion. In search for key regulators of invasion and metastasis, a panel of lung cancer cell lines with different invasive ability was screened. The gene for contactin-1 was found to play an essential role in tumor invasion and metastasis. Suppression of contactin-1 expression abolished the ability of lung adenocarcinoma cells to invade Matrigel in vitro as well as the polymerization of filamentous-actin and the formation of focal adhesion structures. Furthermore, knockdown of contactin-1 resulted in extensive inhibition of tumor metastasis and in increased survival in an animal model. RhoA but not Cdc42 or Rac1 was found to serve a critical role in contactin-1-mediated invasion and metastasis. Contactin-1-specific RNA interference resulted in loss of metastatic and invasive capacity in both in vitro and in vivo models. This loss was overturned by constitutive expression of the active form of RhoA. Contactin-1 was differentially expressed in tumor tissues, and its expression correlated with tumor stage, lymph node metastasis, and patient survival. Contactin-1 is proposed to function importantly in the invasion and metastasis of lung adenocarcinoma cells via RhoA-mediated mechanisms.

Actins↗

Epidermal growth factor receptor mutations in needle biopsy/aspiration samples predict response to gefitinib therapy and survival of patients with advanced nonsmall cell lung cancer.

Recently, mutations in the epidermal growth factor receptor (EGFR) gene in nonsmall cell lung cancer (NSCLC) patients were reported to correlate with gefitinib response. Less than 30% of NSCLC patients are surgically resectable; however, molecular analysis has to rely on nonsurgical diagnostic tissue samples. The objective of this study is to investigate EGFR mutation analysis on needle biopsy/aspiration samples and its correlations with gefitinib response and patients' survival. EGFR mutation was assessed from DNA of 63 paraffin-embedded small needle biopsy/aspiration specimens from 62 patients with NSCLC treated with gefitinib. The peripheral blood lymphocyte DNA of the patients was sequenced to verify the EGFR mutation. EGFR mutations were found in 47% of 62 patients (60% of 20 CT-guided biopsies, 44% of 18 ultrasound-guided biopsies, 31% of 16 endoscopic biopsies and 44% of 9 effusion cell blocks). EGFR mutations were frequently present in females (p = 0.006) and never smokers (p = 0.04). Patients with EGFR mutations had a significantly better response rate compared to that of the nonmutation group (p < 0.001). Multivariate analysis showed that EGFR mutation (p < 0.001) and PS 0-1 (p = 0.02) were independently associated with a better response rate. Cox regression analysis showed that EGFR mutation was the independent prognostic factor for progression-free survival (p = 0.008) and overall survival (p = 0.03). In conclusion, EGFR mutation analysis is feasible in needle biopsy/aspiration paraffin-fixed specimens. EGFR mutation is an independent predictor of gefitinib response and survival in patients of advanced NSCLC treated by gefitinib.

Aged↗

Spontaneous bilateral bacterial empyema in a patient with nephrotic syndrome.

Spontaneous bacterial empyema (SBEM), a rare infectious complication among liver cirrhosis patients, is characterized by infection in the presence of pleural effusion without evidence of pre-existing pneumonia. The prevalence of SBEM in cirrhotic patients with hydrothorax is about 13%. However, it has previously not been reported in medical literature in patients with nephrotic syndrome. The most common microorganism identified is Escherichia coli, followed by Streptococcus species, Enterococcus species, Klebsiella pneumoniae, and Pseudomonas stutzeri. We present a patient with a history of nephrotic syndrome caused by membranous nephropathy, who received steroids and cyclophosphamide. He developed bilateral SBEM due to Aeromonas hydrophila and E. coli, which were isolated from the left- and right-side pleural fluid, respectively. The detailed clinical course, treatment, and outcome are described.

Adult↗

Pasteurization is effective against multidrug-resistant bacteria.

BACKGROUND: The emergence and rapid spread of multidrug-resistant isolates causing nosocomial infections, particularly pandrug-resistant Acinetobacter baumannii, pandrug-resistant Pseudomonas aeruginosa, methicillin-resistant Staphylococcus aureus, and extended-spectrum beta-lactamase-producing Enterobacteriaceae are of great concern worldwide. METHODS: This study investigated the efficacy of pasteurization against contamination of culture tubes and plastic bags by the above 4 important multidrug-resistant bacteria. A 5-mL bacterial suspension with approximately 10(5) and 10(9) cfu/mL of each organism was inoculated into 3 sets of plastic bags and culture tubes and subjected to pasteurization in a washer at 75 degrees C for 30 minutes. RESULTS: A nearly total eradication was found after pasteurization of these 4 drug-resistant pathogens. CONCLUSION: Pasteurization was highly effective against drug-resistant bacteria. Strict adherence to appropriate infection control management for respiratory circuits is important for reducing the spread of drug-resistant bacteria among ventilator-assisted patients.

Bacterial Infections↗

The VEGF-C/Flt-4 axis promotes invasion and metastasis of cancer cells.

Flt-4, a VEGF receptor, is activated by its specific ligand, VEGF-C. The resultant signaling pathway promotes angiogenesis and/or lymphangiogenesis. This report provides evidence that the VEGF-C/Flt-4 axis enhances cancer cell mobility and invasiveness and contributes to the promotion of cancer cell metastasis. VEGF-C/Flt-4-mediated invasion and metastasis of cancer cells were found to require upregulation of the neural cell adhesion molecule contactin-1 through activation of the Src-p38 MAPK-C/EBP-dependent pathway. Examination of tumor tissues from various types of cancers revealed high levels of Flt-4 and VEGF-C expression that correlated closely with clinical metastasis and patient survival. The VEGF-C/Flt-4 axis, through upregulation of contactin-1, may regulate the invasive capacity in different types of cancer cells.

Adenocarcinoma↗