Application of combined treatment of peracetic acid and ultraviolet-C for inactivating pathogens in water and on surface of apples.

In this study, a combined treatment of peracetic acid (PAA) and 280 nm Ultraviolet-C (UVC) - Light emitting diode (LED) was applied for inactivating foodborne pathogens in water and apples. The combined treatment of PAA (50 ppm) and UVC-LED showed synergistic inactivation effects against Escherichia coli O157:H7 and Listeria monocytogenes in water. In mechanism analysis, PAA/UVC-LED treatment induced more lipid peroxidation, intracellular ROS, membrane, and DNA damage than a single treatment. Among them, membrane damage was the main synergistic inactivation mechanism of combination treatment. Cell rupture and shrink of both pathogens after PAA/UVC-LED treatment were also identified through scanning electron microscope (SEM) analysis. To examine inactivation of pathogens on the surface of apples by PAA, UVC-LED, and their combined treatment, a washing system (WS) was developed and used. Through applying the WS, PAA/UVC-LED treatment effectively inactivated two pathogens in washing solution and on the surface of apples below the detection limit (3.30 log CFU/2000 mL and 2.0 log CFU/apple) within 5 min. In addition, there was no significant difference in color or firmness of apples after PAA/UVC-LED treatment (p > 0.05).

Association between cancer genes and germ layer specificity.

Cancer signaling pathways defining cell fates are related to differentiation. During the developmental process, three germ layers (endoderm, mesoderm, and ectoderm) are formed during embryonic development that differentiate into organs via the epigenetic regulation of specific genes. To examine the relationship, the specificities of cancer gene mutations that depend on the germ layers are studied. The major organs affected by cancer were determined based on statistics from the National Cancer Information Center of Korea, and were grouped according to their germ layer origins. Then, the gene mutation frequencies were evaluated to identify any bias based on the differentiation group using the Catalogue of Somatic Mutations in Cancer (COSMIC) database. The chi-square test showed that the p-value of 152 of 166 genes was less than 0.05, and 151 genes showed p-values of less than 0.05 even after adjusting for the false discovery rate (FDR). The germ layer-specific genes were evaluated using visualization based on basic statistics, and the results matched the top ranking genes depending on organs in the COSMIC database.The current study confirmed the germ layer specificity of major cancer genes. The germ layer specificity of mutated driver genes is possibly important in cancer treatments because each mutated gene may react differently depending on the germ layer of origin. By understanding the mechanism of gene mutation in the development and progression of cancer in the context of cell-fate pathways, a more effective therapeutic strategy for cancer can be established.

The i-gel supraglottic airway device improves airway management during endobronchial ablative therapy under general anesthesia: a case report.

Endobronchial ablative therapy (EAT) in patients with preexisting obstructive airway disease can cause hypoxemia because bronchoscope insertion interferes with ventilation and a low fraction of inspired oxygen (FiO2) is essential to avoid airway fire. A man in his early 50s with moderately severe obstructive airway disease was scheduled for EAT for treatment of tracheal papillomatosis. Ventilation and oxygenation would have been difficult because of narrowing of the endotracheal tube by bronchoscopic insertion and a low FiO2; therefore, an i-gel supraglottic airway device with a larger inner diameter was inserted. All visible intratracheal papillomas were ablated by a potassium titanyl phosphate laser through the bronchoscopic port that passed through the lumen of the i-gel at an FiO2 of 0.3. During anesthesia for EAT, the i-gel supraglottic airway device provided a wider lumen for ventilation. We were thus able to provide stable ventilation at an FiO2 of 0.3 during EAT in this patient with obstructive airway disease, avoiding airway fire and hypoxemia.

Postlaryngectomy supraglottic stenosis revealed by three-dimensional computed tomography reconstruction: A case report.

RATIONALE: Supraglottic stenosis is a rare cause of airway obstruction. It can be induced by radiation, trauma, autoimmune diseases, or caustic exposure, and is often misdiagnosed as asthma. Detailed airway information is necessary to re-establish the normal functioning of the airway. PATIENT CONCERNS: A 78-year-old woman with severe dyspnea and hypercarbia was scheduled for surgery to resolve airway obstruction, previously known as supraglottic stenosis. DIAGNOSES: To determine the exact internal shape of the stenotic lesion, we reconstructed three dimensional computed tomography (CT) images depicted a tubular supraglottic stenosis. INTERVENTIONS: The patient underwent tracheotomy under monitored anesthesia care and local anesthesia, followed by general anesthesia. For long-term management of the patient, the otorhinolaryngologist excised the supraglottic stricture via micro-laryngeal surgery using a CO2 laser and applied mitomycin to prevent further obstruction. OUTCOMES: The patient recovered uneventfully after anesthesia, and symptom due to supraglottic stenosis was improved. LESSONS: During airway management of patients with postlaryngectomy supraglottic stenosis, three-dimensional reconstructed computed tomography images facilitate airway configuration in addition to endoscopy and other radiological findings.

All-polymer solar cells with bulk heterojunction nanolayers of chemically doped electron-donating and electron-accepting polymers.

We report the improved performance of all-polymer solar cells with bulk heterojunction nanolayers of an electron-donating polymer (poly(3-hexylthiophene) (P3HT)) and an electron-accepting polymer (poly(9,9-dioctylfluorene-co-benzothiadiazole) (F8BT)), which were both doped with 4-ethylbenzenesulfonic acid (EBSA). To choose the doping ratio of P3HT for all-polymer solar cells, various EBSA doping ratios (0, 1, 3, 5, 10, 20 wt%) were tested by employing optical absorption spectroscopy, photoluminescence spectroscopy, photoelectron yield spectroscopy, and space-charge-limited current (SCLC) mobility measurement. The doping reaction of P3HT with EBSA was followed by observing the colour change in solutions. The final doping ratio for P3HT was chosen as 1 wt% from the best hole mobility measured in the thickness direction, while that for F8BT was fixed as 10 wt% (F8BT-EBSA). The polymer:polymer solar cells with bulk heterojunction nanolayers of P3HT-EBSA (EBSA-doped P3HT) and F8BT-EBSA (EBSA-doped F8BT) showed greatly improved short circuit current density (J(SC)) and open circuit voltage (V(OC)), compared to the undoped solar cells. As a result, the power conversion efficiency (PCE) was enhanced by ca. 300% for the 6 : 4 (P3HT-EBSA : F8BT-EBSA) composition and ca. 400% for the 8 : 2 composition. The synchrotron-radiation grazing incidence angle X-ray diffraction (GIXD) measurement revealed that the crystallinity of the doped nanolayers significantly increased by EBSA doping owing to the formation of advanced phase segregation morphology, as supported by the surface morphology change measured by atomic force microscopy. Thus the improved PCE can be attributed to the enhanced charge transport by the formation of permanent charges and better charge percolation paths by EBSA doping.

Echocardiographic predictors of left ventricular function and clinical outcomes after successful mitral valve repair: conventional two-dimensional versus speckle-tracking parameters.

BACKGROUND: We aimed to compare conventional echocardiographic versus speckle tracking-derived parameters in predicting postoperative left ventricular (LV) dysfunction and clinical outcomes after successful mitral valve repair in patients with mitral regurgitation. METHODS: In 147 consecutive patients in sinus rhythm with severe MR, two-dimensional echocardiography and speckle-tracking imaging for global longitudinal, circumferential, and radial strains and strain rates were performed within 30 days before successful mitral valve repair. Echocardiography was repeated within 7 days in all patients, and more than 3 months after surgery in 112 patients. Clinical events were evaluated for 21±17 months. RESULTS: Multivariate linear regression analysis showed that preoperative LV systolic dimension (p=0.004) and volume (p=0.001) were independent determinants of immediate postoperative LV ejection fraction. Preoperative LV end-systolic dimension (p=0.004), LV ejection fraction (p=0.017), and circumferential strain (p=0.029) were independent predictors of late follow-up LV ejection fraction. By Cox regression analysis, preoperative end-systolic LV dimension (hazard ratio 1.26 for every 1 mm, 95% confidence interval 1.11 to 1.44, p<0.001) was the only predictor of hospital admission for heart failure. The best cutoff values of LV end-systolic dimension (≥41 mm) and volume (≥85 mL) for predicting postoperative severe LV dysfunction (ejection fraction<0.35) identified patients at high risk for event-free survival, but those of speckle-tracking parameters did not. CONCLUSIONS: Preoperative LV remodeling parameters, such as LV end-systolic dimension and volume, are superior to speckle tracking-derived deformation parameters in predicting LV dysfunction and clinical events after successful mitral valve repair in patients with severe mitral regurgitation.

Qualitative and quantitative differences in the intensity of Fas-mediated intracellular signals determine life and death in T cells.

Fas stimulation has been reported to promote the activation and proliferation of T lymphocytes, but the intracellular signalling pathways that mediate non-apoptotic responses to Fas are poorly defined. To distinguish between the activation signalling and the death-inducing pathway downstream of Fas, we generated a novel T cell line expressing a chimeric hCD8-FasC protein and found that stimulation with the anti-CD8 antibodies induced tyrosine phosphorylation of TCR-proximal proteins, activation of Raf-1/ERK, p38 and JNK, and increased expression of CD69, Fas, and Fas ligand. Stimulation of hCD8-FasC-induced activation of an atypical NF-kappaB pathway, partial cleavage of caspases, and increased expression of TRAF1, FLIP(L) and FLIP(S), thereby protecting T cells from FasL-mediated apoptosis. The proliferative response transmitted through hCD8-FasC chimeric receptors was converted into death signals when cells were stimulated, resulting in increased expression of IL-2 and Nur77 and increased caspase cleavage. Surprisingly, both the enhanced expression of FLIP(L) and FLIP(S) and the complete inhibition of FLIP(S) expression were functionally associated with cell death induction. These findings imply that Fas is able to trigger intracellular signalling events driving both apoptosis and activation of T cells but that cell fate is determined by quantitative and qualitative differences in intracellular signalling following Fas stimulation.

Tumor necrosis factor-alpha potentiates RhoA-mediated monocyte transmigratory activity in vivo at a picomolar level.

OBJECTIVE: The serum level of tumor necrosis factor-alpha (TNF-alpha) is in the picomolar range under inflammatory conditions. We investigated whether these picomolar levels of TNF-alpha directly modulate the functional activities of circulating monocytes. METHODS AND RESULTS: In THP-1 monocytes treated with TNF-alpha (1 to 100 pmol/L/30 minutes), cytosolic RhoA small GTPase rapidly translocated to the plasma membrane via functionally active ezrin/radixin/moesin (ERM) complex, a cytoskeletal linker, and subsequent actin polymerization through NF-kappaB activation. The threonine phosphorylation of ERM was accomplished by the activation of TNF receptor type I (TNFRI) and signaling pathways involving PI3K and an atypical PKC; ie, PKCzeta. The TNF-alpha-treated monocytes (10 pmol/L) displayed more potent and prolonged generation of GTP-bound RhoA in response to secondary stimulation with RhoA-activating monocyte chemoattractant protein-1 (MCP-1). Clearly, human circulating monocytes preconditioned by 10 pmol/L TNF-alpha augmented MCP-1-mediated chemotaxis and firm adhesion on VCAM-1 and ICAM-1 in vitro and ex vivo. The elevation of serum TNF-alpha (>5 pmol/L within 16 hours), which was introduced by intraperitoneal injection of mouse-specific TNF-alpha to C57/BL6 mice, enhanced the number of CD80+ monocytes transmigrating to the JE/MCP-1-injected intraperitoneal space. CONCLUSIONS: Picomolar concentrations of TNF-alpha in the bloodstream may prime the RhoA-dependent activities of circulating monocytes to enhance recruitment to active inflammatory foci.

Proteomic profiling of cellular proteins interacting with the hepatitis C virus core protein.

Hepatitis C virus (HCV) is a causative agent of chronic hepatitis and hepatocellular carcinoma. The core protein of HCV packages the viral RNA genome to form a nucleocapsid. In addition to its function as a structural protein, core protein is involved in regulation of cellular transcription, virus-induced transformation, and pathogenesis. To gain insights into cellular functions of the core protein by identification of cellular proteins interacting with the core protein, we employed a proteomic approach. Hepatocytes soluble cytoplasmic proteins were applied to the core proteins immobilized on Ni-nitrilotriacetic resin and total bound cellular proteins were resolved by 2-DE. Analyses of interacting proteins by matrix-assisted laser desorption/ionization-time of flight mass spectrometry allowed identification of 14 cellular proteins binding to the core protein. These proteins include DEAD-box polypeptide 5, similar in function to a known protein identified previously by yeast two-hybrid screening and 13 newly identified cellular proteins. Interestingly, nine protein spots were identified as intermediate microfilament proteins, including cytokeratins (five spots for cytokeratin 8, two for cytokeratin 19, and one for cytokeratin 18) and vimentin. Cytokeratin 8 and vimentin, which were previously shown to be involved in the infection processes of other viruses, were further analyzed to confirm their in vivo interactions with the core protein by immunoblotting and immunofluorescence microscopy. We discuss the functional implications of the interactions of the core protein with newly identified cellular proteins in HCV infection and pathogenesis.