Cijepni soj virusa zaraznog bronhitisa patogeniji je za pileće zametke od divljeg soja 2575/98.

An avian infectious bronchitis virus (IBV) strain 2575/98 was attenuated using serial chicken embryo passage to become a vaccine in Taiwan. The aim of this study was to investigate the replication ability, pathogenicity, and tissue tropism of the wild and vaccine strains in chicken embryos. The embryos were inoculated with different titers of wild and vaccine strains. Quantification of virus in allantoic fluid was evaluated using real time RT-PCR. The results showed that the vaccine strain replicated in higher titers than the wild strain, and caused embryo death so quickly that only a few dwarfisms occurred. The embryos inoculated with wild and vaccine strains had similar lesions that were confined primarily to the chorionallantoic membrane (CAM), liver, and kidneys. The immunohistochemical data showed that IBV was present predominantly in the lungs, kidneys, and CAM. Although both strains caused hepatic damage, very few virus antigens were detected in the hepatic tissue. The pathogenicity of the vaccine becomes higher in embryos although it is lower in chickens than its wild strain. The vaccine strain could be used as a possible new vaccine candidate for IBV control.Virus zaraznog bronhitisa peradi soj 2575/98 bio je oslabljen uzastopnim pasažama u pilećim zametcima da bi poslužio kao cijepni soj u Tajvanu. Cilj je ovog rada bio istražiti mogućnost umnožavanja, patogenost i tropizam terenskog i cijepnog soja u pilećim zametcima. Zametci su bili inokulirani cijepnim sojem različitog titra. Količina virusa u alantoisnoj tekućini bila je određena RT-PCR-om u stvarnom vremenu. Rezultati su pokazali da se cijepni soj umnažao u višem titru od divljeg soja i prouzročio uginuće zametaka tako brzo da se uspjelo razviti svega nekoliko kržljavih. U inokuliranih zametaka, bez obzira na divlji ili cijepni soj, razvile su se slične promjene pretežito na korioalantoisnoj opni, jetrima i bubrezima. Imunohistokemijski je dokazano da se virus zaraznog bronhitisa prvenstveno nalazio u plućima, bubrezima i korioalantoisnoj opni. Iako su oba soja prouzročila oštećenja jetara, neznatna količina virusnog antigena bila je dokazana u jetrenom tkivu. Patogenost cijepnog soja bila je u zametcima jača, a u pilićima slabija od divljeg soja. Cijepni soj bi se mogao rabiti kao mogući kandidat za proizvodnju novog cjepiva protiv zaraznog bronhitisa

Recycling Nonmagnetic Material from De-sulferization Slag as Coarse Aggregate through Cold-Pressing Technique

Every year there was approximately 500,000 tons of de-sulferization slag generated in Taiwan, but the recycling amount was very slightly. A new approach, the cold-pressing technique that incorporates the principles of the cement chemistry and composite material was developed to recycle innocuous resources (e.g. construction residual soil, granite and lime sludge, and sediment, etc.) as recycling coarse aggregate. Even this technique also has successfully been applied to recycle stainless steel reductive slag with low volume stability. This paper aims to show that using cold-pressing technique can recycle nonmagnetic material from de-sulferization slag as coarse aggregate. Herein the cement-based composite is regarded as concrete. Particularly, the mixture proportions with a low cement amount of 100 kg/m3 and more than 70% (by weight) of nonmagnetic material from de-sulferization were designed. The test results show that the specific gravity of recycling coarse aggregate is about 1.67 in the OD state; the absorption capacity is 27.65%; the dry loose density (i.e. unit weight) is about 1,106 kg/m3; and other characteristics conform to ASTM C33. Therefore the cold-pressing technique is a new and practicable approach to recycle nonmagnetic material from de-sulferization slag in future

Poly (ADP-ribose) polymerase plays an important role in intermittent hypoxia-induced cell death in rat cerebellar granule cells

<p>Abstract</p> <p>Background</p> <p>Episodic cessation of airflow during sleep in patients with sleep apnea syndrome results in intermittent hypoxia (IH). Our aim was to investigate the effects of IH on cerebellar granule cells and to identify the mechanism of IH-induced cell death.</p> <p>Methods</p> <p>Cerebellar granule cells were freshly prepared from neonatal Sprague-Dawley rats. IH was created by culturing the cerebellar granule cells in the incubators with oscillating O₂concentration at 20% and 5% every 30 min for 1-4 days. The results of this study are based on image analysis using a confocal microscope and associated software. Cellular oxidative stress increased with increase in IH. In addition, the occurrence of cell death (apoptosis and necrosis) increased as the duration of IH increased, but decreased in the presence of an iron chelator (phenanthroline) or poly (ADP-ribose) polymerase (PARP) inhibitors [3-aminobenzamide (3-AB) and DPQ]. The fluorescence of caspase-3 remained the same regardless of the duration of IH, and Western blots did not detect activation of caspase-3. However, IH increased the ratio of apoptosis-inducing factor (AIF) translocation to the nucleus, while PARP inhibitors (3-AB) reduced this ratio.</p> <p>Results</p> <p>According to our findings, IH increased oxidative stress and subsequently leading to cell death. This effect was at least partially mediated by PARP activation, resulting in ATP depletion, calpain activation leading to AIF translocation to the nucleus.</p> <p>Conclusions</p> <p>We suggest that IH induces cell death in rat primary cerebellar granule cells by stimulating oxidative stress PARP-mediated calpain and AIF activation.</p

Histone deacetylase 3 associates with MeCP2 to regulate FOXO and social behavior

Mutations in MECP2 cause the neurodevelopmental disorder Rett syndrome (RTT). The RTT missense MECP2 R306C mutation prevents MeCP2 from interacting with the NCoR/histone deacetylase 3 (HDAC3) complex; however, the neuronal function of HDAC3 is incompletely understood. We found that neuronal deletion of Hdac3 in mice elicited abnormal locomotor coordination, sociability and cognition. Transcriptional and chromatin profiling revealed that HDAC3 positively regulated a subset of genes and was recruited to active gene promoters via MeCP2. HDAC3-associated promoters were enriched for the FOXO transcription factors, and FOXO acetylation was elevated in Hdac3 knockout (KO) and Mecp2 KO neurons. Human RTT-patient-derived MECP2 R306C neural progenitor cells had deficits in HDAC3 and FOXO recruitment and gene expression. Gene editing of MECP2 R306C cells to generate isogenic controls rescued HDAC3-FOXO-mediated impairments in gene expression. Our data suggest that HDAC3 interaction with MeCP2 positively regulates a subset of neuronal genes through FOXO deacetylation, and disruption of HDAC3 contributes to cognitive and social impairment.National Institutes of Health (U.S.) (Grant NS78839

TNF-α Mediates Eosinophil Cationic Protein-induced Apoptosis in BEAS-2B Cells

<p>Abstract</p> <p>Background</p> <p>Eosinophilic granulocytes are important for the human immune system. Many cationic proteins with cytotoxic activities, such as eosinophil cationic protein (ECP) and eosinophil-derived neurotoxin (EDN), are released from activated eosinophils. ECP, with low RNase activity, is widely used as a biomarker for asthma. ECP inhibits cell viability and induces apoptosis to cells. However, the specific pathway underlying the mechanisms of ECP-induced cytotoxicity remains unclear. This study investigated ECP-induced apoptosis in bronchial epithelial BEAS-2B cells and elucidated the specific pathway during apoptosis.</p> <p>Results</p> <p>To address the mechanisms involved in ECP-induced apoptosis in human BEAS-2B cells, investigation was carried out using chromatin condensation, cleavage of poly (ADP-ribose) polymerase (PARP), sub-G1 distribution in cell cycle, annexin V labeling, and general or specific caspase inhibitors. Caspase-8-dependent apoptosis was demonstrated by cleavage of caspase-8 after recombinant ECP treatment, accompanied with elevated level of tumor necrosis factor alpha (TNF-α). Moreover, ECP-induced apoptosis was effectively inhibited in the presence of neutralizing anti-TNF-α antibody.</p> <p>Conclusion</p> <p>In conclusion, our results have demonstrated that ECP increased TNF-α production in BEAS-2B cells and triggered apoptosis by caspase-8 activation through mitochondria-independent pathway.</p

A nationwide survey evaluating the environmental literacy of undergraduate students in Taiwan

The aim of this nationwide survey was to assess undergraduate students’ environmental literacy level in Taiwan. A total of 29,498 valid responses were received from a number of selected colleges and universities in Taiwan, using stratified random sampling method. A total of 70 items were used to assess the environmental literacy and the results revealed that undergraduate students had a relatively low level of environmental knowledge and behavior, while a moderate level of environmental attitudes was attained. The findings also indicated no significant correlations between knowledge and attitudes or between knowledge and behavior. However, a higher level of environmental knowledge correlated significantly with a higher degree of pro-environmental behavior, and a higher level of environmental knowledge correlated with stronger attitudes. The results also suggested that females outperformed the males in all categories. Results from this study could contribute towards further relevant policy discussion and decision-making, curriculum design and development to the improvement of environmental education in the higher education sector

Correlation of virulence genes to clinical manifestations and outcome in patients with Streptococcus dysgalactiae subspecies equisimilis bacteremia

Background/PurposeStreptococcus dysgalactiae subsp. equisimilis (SDSE) is increasingly recognized as a human pathogen responsible for invasive infection and streptococcal toxic shock syndrome (STSS). The pathogen possesses virulence genes that resemble those found in Streptococcus pyogenes (GAS). We analyzed the association between these specific toxic genes, clinical presentations, and outcome in patients with SDSE infections.MethodsPatients (older than 18 years) with community-acquired invasive bacteremia caused by SDSE bacteremia who were undergoing treatment at China Medical University Hospital from June 2007 to December 2010 were included in this study. Multiplex polymerase chain reaction was performed to identify virulence genes of the SDSE isolates. Demographic data, clinical presentations, and outcome in patients with SDSE infections were reviewed and analyzed.ResultsForty patients with 41 episodes of SDSE bacteremia were reviewed. The median age of the patients with SDSE infection was 69.7 years; 55% were female and 78% had underlying diseases. Malignancy (13, 33%) and diabetes mellitus (13, 33%) were the most common comorbidities. The 30-day mortality rate was 12%. Compared with the survivors, the non-survivors had a higher rate of diabetes mellitus (80% vs. 26%), liver cirrhosis (60% vs.11%), shock (60% vs.17%), STSS (60% vs. 8%), and a high Pittsburgh bacteremia score >4 (40% vs. 6%). Most isolates had scpA, ska, saga, and slo genes, whereas speC, speG, speH, speI, speK, smez, and ssa genes were not detected. speA gene was identified only in one patient with STSS (1/6, 17%). All isolates were susceptible to penicillin, cefotaxime, levofloxacin, moxifloxacin, vancomycin, and linezolid.ConclusionIn invasive SDSE infections, most isolates carry putative virulence genes, such as scpA, ska, saga, and slo. Clinical SDSE isolates in Taiwan remain susceptible to penicillin cefotaxime, and levofloxacin

Continuous epidermal growth factor receptor-tyrosine kinase inhibitor administration in primary lung adenocarcinoma patients harboring favorable mutations with controlled target lung tumors dose not hinder survival benefit despite small new lesions

AbstractBackgroundIn this study, we investigated the efficacy of continuous epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) administration in lung adenocarcinoma patients harboring favorable mutations regarding the progressive disease (PD) status with appearance of indolent new lesions.MethodsFrom June 2010 to October 2012, 102 patients with lung adenocarcinoma, harboring favorable EGFR mutations and treated with EGFR-TKI were analyzed. Definite new lesions were detected during EGFR-TKI therapy, even though the primary target tumors were controlled.ResultsOf the 102 patients, 57 continued and 45 discontinued EGFR-TKI therapy. The median overall survival was 529 days for the discontinuation group and 791 days for the continuation group (p = 0.0197). Median survival time after the discontinuation of EGFR-TKI was 181 days and 115 days in the discontinuation and continuation groups, respectively (p = 0.1776), whereas median survival time after the appearance of indolent new lesions was 204 days and 262 days, respectively (p = 0.0237).ConclusionContinuous EGFR-TKI administration in favorable EGFR-mutative lung adenocarcinoma patients with controlled primary tumors did not hinder the survival benefit, despite the appearance of new lesions

Adipose-Derived Mesenchymal Stem Cell Protects Kidneys against Ischemia-Reperfusion Injury through Suppressing Oxidative Stress and Inflammatory Reaction

<p>Abstract</p> <p>Background</p> <p>Reactive oxygen species are important mediators exerting toxic effects on various organs during ischemia-reperfusion (IR) injury. We hypothesized that adipose-derived mesenchymal stem cells (ADMSCs) protect the kidney against oxidative stress and inflammatory stimuli in rat during renal IR injury.</p> <p>Methods</p> <p>Adult male Sprague-Dawley (SD) rats (n = 24) were equally randomized into group 1 (sham control), group 2 (IR plus culture medium only), and group 3 (IR plus immediate intra-renal administration of 1.0 × 10⁶autologous ADMSCs, followed by intravenous ADMSCs at 6 h and 24 h after IR). The duration of ischemia was 1 h, followed by 72 hours of reperfusion before the animals were sacrificed.</p> <p>Results</p> <p>Serum creatinine and blood urea nitrogen levels and the degree of histological abnormalities were markedly lower in group 3 than in group 2 (all p < 0.03). The mRNA expressions of inflammatory, oxidative stress, and apoptotic biomarkers were lower, whereas the anti-inflammatory, anti-oxidative, and anti-apoptotic biomarkers were higher in group 3 than in group 2 (all p < 0.03). Immunofluorescent staining showed a higher number of CD31+, von Willebrand Factor+, and heme oxygenase (HO)-1+ cells in group 3 than in group 2 (all p < 0.05). Western blot showed notably higher NAD(P)H quinone oxidoreductase 1 and HO-1 activities, two indicators of anti-oxidative capacity, in group 3 than those in group 2 (all p < 0.04). Immunohistochemical staining showed higher glutathione peroxidase and glutathione reductase activities in group 3 than in group 2 (all p < 0.02)</p> <p>Conclusion</p> <p>ADMSC therapy minimized kidney damage after IR injury through suppressing oxidative stress and inflammatory response.</p