160 research outputs found
An Improved Differential Evolution Based Dynamic Economic Dispatch with Nonsmooth Fuel Cost Function
Dynamic economic dispatch (DED) is one of the major operational decisions in electric power systems. DED problem is an optimization problem with an objective to determine the optimal combination of power outputs for all generating units over a certain period of time in order to minimize the total fuel cost while satisfying dynamic operational constraints and load demand in each interval. This paper presents an improved differential evolution (IDE) method to solve the DED problem of generating units considering valve-point effects. Heuristic crossover technique and gene swap operator are introduced in the proposed approach to improve the convergence characteristic of the differential evolution (DE) algorithm. To illustrate the effectiveness of the proposed approach, two test systems consisting of five and ten generating units have been considered. The results obtained through the proposed method are compared with those reported in the literature
Common NOD2 mutations are absent in patients with Crohn's disease in India
Background: Crohn's disease is being increasingly diagnosed in the Indian subcontinent. Three apparently common mutations in the NOD2 gene are found in up to 30% of sporadic patients with Crohn's disease in western countries. We examined whether such mutations are also found in Indian patients with Crohn's disease. Methods: Venous blood was collected from 82 patients (age range: 7-65 years, 53 men) with Crohn's disease and 149 control subjects; DNA was extracted and subjected to polymerase chain reaction using specific primers. The amplified fragments of size 185, 163 and 151 bp for R702W, G908R and 1007fs, respectively, were digested with MspI, HhaI and ApaI, and the restriction pattern noted after electrophoresis. Results: Twenty-eight patients had ileocolonic disease, 26 ileal disease, 20 colonic disease and 8 had disease limited to proximal small bowel or stomach. None of the 82 patients showed any of the three NOD2 mutations. The control subjects (93 men) had a variety of chronic gastrointestinal disorders (ulcerative colitis 52, irritable bowel syndrome 30, intestinal tuberculosis 20, colon cancer 7, miscellaneous 37). None of the control subjects showed a mutation in any of the three NOD2 mutation analyses. Conclusion: The three NOD2 gene mutations described above are uncommon in Indian patients with Crohn's disease. This study complements information provided by recent studies on NOD2 mutations in Indians
Applications of Machine Learning in Chemical and Biological Oceanography
Machine learning (ML) refers to computer algorithms that predict a meaningful
output or categorize complex systems based on a large amount of data. ML is
applied in various areas including natural science, engineering, space
exploration, and even gaming development. This review focuses on the use of
machine learning in the field of chemical and biological oceanography. In the
prediction of global fixed nitrogen levels, partial carbon dioxide pressure,
and other chemical properties, the application of ML is a promising tool.
Machine learning is also utilized in the field of biological oceanography to
detect planktonic forms from various images (i.e., microscopy, FlowCAM, and
video recorders), spectrometers, and other signal processing techniques.
Moreover, ML successfully classified the mammals using their acoustics,
detecting endangered mammalian and fish species in a specific environment. Most
importantly, using environmental data, the ML proved to be an effective method
for predicting hypoxic conditions and harmful algal bloom events, an essential
measurement in terms of environmental monitoring. Furthermore, machine learning
was used to construct a number of databases for various species that will be
useful to other researchers, and the creation of new algorithms will help the
marine research community better comprehend the chemistry and biology of the
ocean.Comment: 58 Pages, 5 Figure
Synergistic Effect of Quinic Acid Derived From Syzygium cumini and Undecanoic Acid Against Candida spp. Biofilm and Virulence
In recent decades, fungal infections have incredibly increased with Candida genus as the major cause of morbidity and mortality in hospitalized and immunocompromised patients. Most of the Candida species are proficient in biofilm formation on implanted medical devices as well as human tissues. Biofilm related Candida infections are very difficult to treat using common antifungal agents owing to their increased drug resistance. To address these issues, the present study investigated the antibiofilm and antivirulent properties of Syzygium cumini derived quinic acid in combination with known antifungal compound undecanoic acid. Initially, antibiofilm potential of S. cumini leaf extract was assessed and the active principles were identified through gas chromatography and mass spectrometry analysis. Among the compounds identified, quinic acid was one of the major compounds. The interaction between quinic acid and undecanoic acid was found to be synergistic in the Fractional inhibitory concentration index (≤0.5). Results of in vitro assays and gene expression analysis suggested that the synergistic combinations of quinic acid and undecanoic acid significantly inhibited virulence traits of Candida spp. such as the biofilm formation, yeast-to-hyphal transition, extracellular polymeric substances production, filamentation, secreted hydrolases production and ergosterol biosynthesis. In addition, result of in vivo studies using Caenorhabditis elegans demonstrated the non-toxic nature of QA-UDA combination and antivirulence effect against Candida spp. For the first time, synergistic antivirulence ability of quinic acid and undecanoic acid was explored against Candida spp. Thus, results obtained from the present study suggest that combination of phytochemicals might be used an alternate therapeutic strategy for the prevention and treatment of biofilm associated Candida infection
Expressing OsiSAP8, a Zinc-Finger Associated Protein Gene, Mitigates Stress Dynamics in Existing Elite Rice Varieties of the 'Green Revolution'
Key message: Overexpression of OsiSAP8 driven by Port Ubi2.3 from Porteresia coarctata imparts drought and salinity stress tolerance in transgenic rice. Stress associated proteins (SAPs) possess the zinc-finger domains that are wildly evolving functional and conserved regions/factors in plants to combat abiotic stresses. In this study, the promoter region of OsiSAP8, an intron-less, multiple stress inducible gene, was compared in silico with a strong constitutive promoter, Port Ubi2.3. This resulted in developing rice, resistant to drought and salinity expressing OsiSAP8 promoted by Port Ubi2.3. (Porteresia coarctata), through Agrobacterium-mediated transformation in the popular rice varieties, IR36 and IR64. Southern blot hybridization confirmed the integration of OsiSAP8, and the T0 transgenic lines of IR36 and IR64 were evaluated for their drought and salinity tolerance. The IR36-T1 progenies showed an enhanced tolerance to water withhold stress compared to wild type and IR64-T1 progenies. Physiological parameters, such as the panicle weight, number of panicles, leaf wilting, and TBARS assay, showed the transgenic IR36 to be superior. The transgenic lines performed better with higher 80-95% relative leaf water content when subjected to drought for 14 days. Gene expression analysis of OsiSAP8 in IR36 T1 showed a 1.5-fold upregulation under mannitol stress. However, IR64 T1 showed a two-fold upregulation in NaCl stress. An enhanced drought and salinity stress tolerance in the transgenic IR36 cultivar through overexpression of OsiSAP8 was observed as it had a native copy of OsiSAP8. This is perhaps the first study using a novel ubiquitin promoter (Port Ubi2.3) to generate drought and salinity stress-tolerant transgenic rice. Thus, we report the overexpression of a rice gene (OsiSAP8) by a rice promoter (Port Ubi2.3) in rice (IR36) to resist drought and salinity
Simple replication methods for producing nanoslits in thermoplastics and the transport dynamics of double-stranded DNA through these slits
Mixed-scale nano-and microfluidic networks were fabricated in thermoplastics using simple and robust methods that did not require the use of sophisticated equipment to produce the nanostructures. High-precision micromilling (HPMM) and photolithography were used to generate mixed-scale molding tools that were subsequently used for producing fluidic networks into thermoplastics such as poly(methyl methacrylate), PMMA, cyclic olefin copolymer, COC, and polycarbonate, PC. Nanoslit arrays were imprinted into the polymer using a nanoimprinting tool, which was composed of an optical mask with patterns that were 2-7 mu m in width and a depth defined by the Cr layer (100 nm), which was deposited onto glass. The device also contained a microchannel network that was hot embossed into the polymer substrate using a metal molding tool prepared via HPMM. The mixed-scale device could also be used as a master to produce a polymer stamp, which was made from polydimethylsiloxane, PDMS, and used to generate the mixed-scale fluidic network in a single step. Thermal fusion bonding of the cover plate to the substrate at a temperature below their respective T(g) was accomplished by oxygen plasma treatment of both the substrate and cover plate, which significantly reduced thermally induced structural deformation during assembly: similar to 6% for PMMA and similar to 9% for COC nanoslits. The electrokinetic transport properties of double-stranded DNA (dsDNA) through the polymeric nanoslits (PMMA and COC) were carried out. In these polymer devices, the dsDNA demonstrated a field-dependent electrophoretic mobility with intermittent transport dynamics. DNA mobilities were found to be 8.2 +/- 0.7 x 10(-4) cm(2) V(-1) s(-1) and 7.6 +/- 0.6 x 10(-4) cm(2) V(-1) s(-1) for PMMA and COC, respectively, at a field strength of 25 V cm(-1). The extension factors for lambda-DNA were 0.46 in PMMA and 0.53 in COC for the nanoslits (2-6% standard deviation).close171
<em>Enterococcus faecalis</em> Infection Causes Inflammation, Intracellular Oxphos-Independent ROS Production, and DNA Damage in Human Gastric Cancer Cells
Background: Achlorhydria caused by e.g. atrophic gastritis allows for bacterial overgrowth, which induces chronic inflammation and damage to the mucosal cells of infected individuals driving gastric malignancies and cancer. Enterococcus faecalis (E. faecalis) can colonize achlohydric stomachs and we therefore wanted to study the impact of E. faecalis infection on inflammatory response, reactive oxygen species (ROS) formation, mitochondrial respiration, and mitochondrial genetic stability in gastric mucosal cells. Methods: To separate the changes induced by bacteria from those of the inflammatory cells we established an in vitro E. faecalis infection model system using the gastric carcinoma cell line MKN74. Total ROS and superoxide was measured by fluorescence microscopy. Cellular oxygen consumption was characterized non-invasively using XF24 microplate based respirometry. Gene expression was examined by microarray, and response pathways were identified by Gene Set Analysis (GSA). Selected gene transcripts were verified by quantitative real-time polymerase chain reaction (qRT-PCR). Mitochondrial mutations were determined by sequencing. Results: Infection of MKN74 cells with E. faecalis induced intracellular ROS production through a pathway independent of oxidative phosphorylation (oxphos). Furthermore, E. faecalis infection induced mitochondrial DNA instability. Following infection, genes coding for inflammatory response proteins were transcriptionally up-regulated while DNA damage repair and cell cycle control genes were down-regulated. Cell growth slowed down when infected with viable E. faecalis and responded in a dose dependent manner to E. faecalis lysate. Conclusions: Infection by E. faecalis induced an oxphos-independent intracellular ROS response and damaged the mitochondrial genome in gastric cell culture. Finally the bacteria induced an NF-kappa B inflammatory response as well as impaired DNA damage response and cell cycle control gene expression
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