DEM-CFD analysis of contact electrification and electrostatic interactions during fluidization

Contact electrification and electrostatic interactions often occur in the fluidization process, which can significantly influence the dynamic behaviour of particles and the fluidization performance. In this study, a discrete element method coupled with computational fluid dynamics (DEM-CFD) is developed by implementing contact electrification and electrostatic interaction models and the combined effects of contact electrification and electrostatic interaction on fluidization are analysed. It is found that the charge of the particle system increase with the superficial gas velocity. Particles of different material properties (especially work function) can be bi-charged and form agglomerates. At low superficial gas velocities, the particle bed cannot be fully fluidized and the pressure drop tends to be stable rather than fluctuating as the gas flows through the micro-channels of agglomerates. However, at high superficial gas velocities, the agglomerates can break, inducing strong fluctuation of pressure drop. Clearly, the electrostatic phenomena and fluidization behaviour can mutually influence each other during the process

Pathogenesis and treatment of non-alcoholic steatohepatitis and its fibrosis

The initial presentation of non-alcoholic steatohepatitis (NASH) is hepatic steatosis. The dysfunction of lipid metabolism within hepatocytes caused by genetic factors, diet, and insulin resistance causes lipid accumulation. Lipotoxicity, oxidative stress, mitochondrial dysfunction, and endoplasmic reticulum stress would further contribute to hepatocyte injury and death, leading to inflammation and immune dysfunction in the liver. During the healing process, the accumulation of an excessive amount of fibrosis might occur while healing. During the development of NASH and liver fibrosis, the gut-liver axis, adipose-liver axis, and renin-angiotensin system (RAS) may be dysregulated and impaired. Translocation of bacteria or its end-products entering the liver could activate hepatocytes, Kupffer cells, and hepatic stellate cells, exacerbating hepatic steatosis, inflammation, and fibrosis. Bile acids regulate glucose and lipid metabolism through Farnesoid X receptors in the liver and intestine. Increased adipose tissue-derived non-esterified fatty acids would aggravate hepatic steatosis. Increased leptin also plays a role in hepatic fibrogenesis, and decreased adiponectin may contribute to hepatic insulin resistance. Moreover, dysregulation of peroxisome proliferator-activated receptors in the liver, adipose, and muscle tissues may impair lipid metabolism. In addition, the RAS may contribute to hepatic fatty acid metabolism, inflammation, and fibrosis. The treatment includes lifestyle modification, pharmacological therapy, and non-pharmacological therapy. Currently, weight reduction by lifestyle modification or surgery is the most effective therapy. However, vitamin E, pioglitazone, and obeticholic acid have also been suggested. In this review, we will introduce some new clinical trials and experimental therapies for the treatment of NASH and related fibrosis

Analysis of Resistance to Clarithromycin and Virulence Markers in Helicobacter pylori Clinical Isolates from Eastern Taiwan

AbstractObjectiveLittle information is available concerning the relationships between clarithromycin resistance and virulence marker genes (iceA, cagA and vacA) in Helicobacter pylori isolated in Taiwan. The aim of this study was to evaluate the possible association between clarithromycin resistance and genotypes of the virulence markers on clarithromycin-resistant H. pylori isolates obtained in eastern TaiwanMaterials and MethodsThe genotypes of the virulence marker genes (iceA, cagA and vacA) were analyzed by PCR, and the 23S rDNA region from 18 clarithromycin-resistant clinical isolates of H. pylori was amplified by PCR and sequenced.ResultsPoint mutations were found to occur in all isolates. Two isolates had A2143G, six had T2182C, one had C2227T, six had A2143G plus T2182C, and three had heterozygous alleles. The latter included a wild-type allele (A2143) plus (i) an A2143G, (ii) an A2143G plus an A2223G, and (iii) an A2143G plus a T2182C. The prevalence of the marker genes cagA, iceA1, iceA2, and both iceA1 and iceA2, in the isolates was 95.5%, 66.9%, 7.5%, and 25.6%, respectively. The vacAs1 allele was detected in all isolates, whereas the m1 and m2 alleles were found in 44.4% and 55.6% of the isolates, respectivelyConclusionThere were no significant associations between clarithromycin resistance and the presence of the cagA gene, vacA allele mosaicism, and the iceA genotypes. The most notable finding of our study was that the C2227T single mutation in 23S rDNA could also be related to the high clarithromycin minimal inhibitory concentrations in clinical isolates from eastern Taiwan

An Outbreak of Coxsackievirus A16 Infection: Comparison With Other Enteroviruses in a Preschool in Taipei

Background/PurposeThe transmission rate of enteroviruses in young children remains unclear. Therefore, we carried out active surveillance in preschool children to investigate the transmission rate and clinical manifestation of enteroviruses.MethodsFrom September 2006 to December 2008, we monitored infectious diseases in children 2(–3 years of age) in a preschool in Taipei. If any child had a febrile illness or symptoms/signs of enteroviral infection [e.g. herpangina or hand-foot-and-mouth disease (HFMD)], we performed viral isolation and enterovirus polymerase chain reaction. VP1 sequencing was performed to define their serotypes. We also collected clinical data and analyzed transmission rates.ResultsThere were eight episodes of enterovirus infection during the study period. The serotypes included coxsackievirus A4 (CA4), CA2 and CA16. The transmission rates of CA4 and CA2 among children in same class were 26% and 35%, respectively. Between November 28 and December 12, 2008, 13/21 (61.9%) children contracted herpangina and/or HFMD. The average age was 2.82 (range, 2.43–3.39) years. CA16 was detected in 10/13 (76.9%) of the throat swabs by polymerase chain reaction VP1 genotyping. Compared with previous CA2 and CA4 outbreaks, CA16 had a significantly higher transmission rate (p = 0.035) and resulted in more cases of HFMD (p < 0.001). The transmission duration of coxsackie A viruses within the same class ranged from 12 to 40 days.ConclusionCompared with CA2 and CA4, CA16 infections resulted in more cases of HFMD and had significantly higher transmission rates in preschoolers

Invited; Developing low-temperature defect passivation technology with supercritical fluid technology

Current technology nodes in the process of semiconductor manufacturing have faced many bottlenecks. Therefore, a disruptive-innovative semiconductor processing technology is crucially needed to make a significant breakthrough. Our research team has developed a low temperature (RT~250°C), defect passivation technology based on the supercritical fluid (SCF) technology applied in the nano-scale device processing to overcome the key issues. The SCF technology was originally applied in the field of the extraction and the cleaning of biotechnologies. However, our research team firstly applies this technology in the optoelectronic device. Compared to current high pressure annealing (HPA) and rapid thermal annealing (RTA) methods, the SCF-based defect passivation technology features low temperature, and can be applied for various materials and devices including photoelectric device, advanced nano-device, memory device, and wide bandgap device. Currently, the prototype of the 12” supercritical fluid processing equipment has already been built, and related recipes including nitridation, oxidation, hydrogenation, and sulfurization are also implemented for various devices and applications. In this talk, we will introduce related SCF defect passivation technology and future developments for the SCF applications

Exploring cellular memory molecules marking competent and active transcriptions

<p>Abstract</p> <p>Background</p> <p>Development in higher eukaryotes involves programmed gene expression. Cell type-specific gene expression is established during this process and is inherited in succeeding cell cycles. Higher eukaryotes have evolved elegant mechanisms by which committed gene-expression states are transmitted through numerous cell divisions. Previous studies have shown that both DNase I-sensitive sites and the basal transcription factor TFIID remain on silenced mitotic chromosomes, suggesting that certain trans-factors might act as bookmarks, maintaining the information and transmitting it to the next generation.</p> <p>Results</p> <p>We used the mouse globin gene clusters as a model system to examine the retention of active information on M-phase chromosomes and its contribution to the persistence of transcriptional competence of these gene clusters in murine erythroleukemia cells. In cells arrested in mitosis, the erythroid-specific activator NF-E2p45 remained associated with its binding sites on the globin gene loci, while the other major erythroid factor, GATA-1, was removed from chromosome. Moreover, despite mitotic chromatin condensation, the distant regulatory regions and promoters of transcriptionally competent globin gene loci are marked by a preserved histone code consisting in active histone modifications such as H3 acetylation, H3-K4 dimethylation and K79 dimethylation. Further analysis showed that other active genes are also locally marked by the preserved active histone code throughout mitotic inactivation of transcription.</p> <p>Conclusion</p> <p>Our results imply that certain kinds of specific protein factors and active histone modifications function as cellular memory markers for both competent and active genes during mitosis, and serve as a reactivated core for the resumption of transcription when the cells exit mitosis.</p

Group A Streptococcus Subcutaneous Infection-Induced Central Nervous System Inflammation Is Attenuated by Blocking Peripheral TNF

Group A streptococcus (GAS) infection causes a strong inflammatory response associated with cytokine storms, leading to multiorgan failure, which is characterized as streptococcal toxic shock syndrome. However, little is known about GAS subcutaneous infection-mediated brain inflammation. Therefore, we used a bioluminescent GAS strain and reporter mice carrying firefly luciferase under transcriptional control of the nuclear factor-kappa B (NF-κB) promoter to concurrently monitor the host immune response and bacterial burden in a single mouse. Notably, in addition to the subcutaneous inoculation locus at the back of mice, we detected strong luminescence signals from NF-κB activation and increased inflammatory cytokine production in the brain, implying the existence of central nervous system inflammation after GAS subcutaneous infection. The inflamed brain exhibited an increased expression of glial fibrillary acidic protein and nicotinamide adenine dinucleotide phosphate oxidase components and greater microglial activation and blood–brain barrier (BBB) disruption. Furthermore, Fluoro-Jade C positive cells increased in the brain, indicating that neurons underwent degeneration. Peripheral tumor necrosis factor (TNF), which contributes to pathology in brain injury, was elevated in the circulation, and the expression of its receptor was also increased in the inflamed brain. Blockage of peripheral TNF effectively reduced brain inflammation and injury, thereby preventing BBB disruption and improving survival. Our study provides new insights into GAS-induced central nervous system inflammation, such as encephalopathy, which can be attenuated by circulating TNF blockage

Genetic population structure of the alpine species Rhododendron pseudochrysanthum sensu lato (Ericaceae) inferred from chloroplast and nuclear DNA

<p>Abstract</p> <p>Background</p> <p>A complex of incipient species with different degrees of morphological or ecological differentiation provides an ideal model for studying species divergence. We examined the phylogeography and the evolutionary history of the <it>Rhododendron pseudochrysanthum </it>s. l.</p> <p>Results</p> <p>Systematic inconsistency was detected between gene genealogies of the cpDNA and nrDNA. Rooted at <it>R. hyperythrum </it>and <it>R. formosana</it>, both trees lacked reciprocal monophyly for all members of the complex. For <it>R. pseudochrysanthum </it>s.l., the spatial distribution of the cpDNA had a noteworthy pattern showing high genetic differentiation (F_ST= 0.56-0.72) between populations in the Yushan Mountain Range and populations of the other mountain ranges.</p> <p>Conclusion</p> <p>Both incomplete lineage sorting and interspecific hybridization/introgression may have contributed to the lack of monophyly among <it>R. hyperythrum</it>, <it>R. formosana </it>and <it>R. pseudochrysanthum </it>s.l. Independent colonizations, plus low capabilities of seed dispersal in current environments, may have resulted in the genetic differentiation between populations of different mountain ranges. At the population level, the populations of Central, and Sheishan Mountains may have undergone postglacial demographic expansion, while populations of the Yushan Mountain Range are likely to have remained stable ever since the colonization. In contrast, the single population of the Alishan Mountain Range with a fixed cpDNA haplotype may have experienced bottleneck/founder's events.</p