Wind Integrated Thermal Unit Commitment Solution Using Grey Wolf Optimizer

The augment of ecological shield and the progressive exhaustion of traditional fossil energy sources have increased the interests in integrating renewable energy sources into existing power system. Wind power is becoming worldwide a significant component of the power generation portfolio. Profuse literature have been reported for the thermal Unit Commitment (UC) solution. In this work, the UC problem has been formulated by integrating wind power generators along with thermal power system. The Wind Generator Integrated UC (WGIUC) problem is more complex in nature, that necessitates a promising optimization tool. Hence, the modern bio-inspired algorithm namely, Grey Wolf Optimization (GWO) algorithm has been chosen as the main optimization tool and real coded scheme has been incorporated to handle the operational constraints. The standard test systems are used to validate the potential of the GWO algorithm. Moreover, the ramp rate limits are also included in the mathematical WGIUC formulation. The simulation results prove that the intended algorithm has the capability of obtaining economical resolutions with good solution quality

Effect of obstructive sleep apnea on mitral valve tenting.

Obstructive apneas produce high negative intrathoracic pressure which imposes an afterload burden on the left ventricle. Such episodes might produce structural changes in the left ventricle over time. Doppler echocardiograms were obtained within 2 months of attended polysomnography. Patients were grouped according to apnea-hypopnea index (AHI): mild/no OSA (AHI \u3c 15) and mod/severe OSA (AHI ≥ 15). Mitral valve tenting height and area, left ventricular (LV) long and short axis, and LV end-diastolic volume (LVEDV), were measured along with tissue Doppler parameters. Comparisons of measurements at baseline and follow up between and within groups were obtained; correlations between absolute changes (deltas) in echocardiographic parameters were also performed. After a mean follow up of 240 days mitral valve tenting height increased significantly (1.17 ± 0.12 cm to 1.28 ± 0.17 cm, p=0.001) in mod/severe OSA as did tenting area (2.30 ± 0.41 cm2 to 2.66 ± 0.60 cm2, p=0.0002); delta tenting height correlated with delta LVEDV (rho 0.43, p=0.01) and delta tenting area (rho 0.35, p=0.04). In mild/no OSA patients there was no significant change in tenting height; there was a borderline significant increase in tenting area (2.20 ± 0.44 cm2 to 2.31 ± 0.43 cm2, p=0.05). Septal E’ decreased (8.04 ± 2.49 cm/sec to 7.10 ± 1.83 cm/sec, p=0.005) in mod/severe OSA subjects, but not in the mild/no OSA group. In conclusion, in patients with mod/severe OSA, mitral valve tenting height and tenting area increase significantly over time. This appears to be related, at least in part, to changes in LV geometry

Role of Liver Stiffness and Alcohol on HBV Infection Pathogenesis

Hepatitis B Virus (HBV) is an infection that specifically targets hepatocytes and persistence of infection leads to inflammation and liver injury. The metabolism of alcohol is also known to cause injury and inflammation in the liver. The extent of liver damage can be analyzed by determining the pressure of the tissue with an ultrasound. As you go from a healthy liver to a fibrotic liver, the pressure increases from around 2 kPa to greater than 12.5 kPa. Previous studies have found that liver stiffness affects the primary hepatocyte function and cell interaction, but the exact mechanism behind the combined role of liver stiffness and alcohol in HBV infection is still unclear. This study aimed to determine the effect of liver stiffness and alcohol metabolism on HBV infection pathogenesis. To accomplish this aim, we used a soft and stiff liver model engineered specifically to a 2 kPa (healthy liver tissue) and 25 kPa pressure (fibrotic liver tissue). HBV transfected HepG2.2.15 cells were plated on these liver model plates. To mimic alcohol metabolism, the cells were exposed to Acetaldehyde Generating System (AGS). Results showed that liver stiffness significantly increased HBV infection markers and decreased the interferon alpha signaling by up regulating USP-18. In addition, liver stiffness increased inflammasome and pro-fibrotic markers in HBV transfected cells. The combination of alcohol metabolism with liver stiffness potentiated the HBV infection. We conclude that liver stiffness impairs interferon alpha signaling thereby increasing HBV persistence, which leads to liver inflammation and fibrosis. This study of the liver environment’s role in HBV infection and alcohol metabolism paves the way to new treatment options for patients as well as introduces more accurate lab models for research.https://digitalcommons.unmc.edu/surp2021/1023/thumbnail.jp

Increased liver stiffness promotes hepatitis B progression by impairing innate immunity in CCl4-induced fibrotic HBV\u3csup\u3e+\u3c/sup\u3e transgenic mice

Background: Hepatitis B virus (HBV) infection develops as an acute or chronic liver disease, which progresses from steatosis, hepatitis, and fibrosis to end-stage liver diseases such as cirrhosis and hepatocellular carcinoma (HCC). An increased stromal stiffness accompanies fibrosis in chronic liver diseases and is considered a strong predictor for disease progression. The goal of this study was to establish the mechanisms by which enhanced liver stiffness regulates HBV infectivity in the fibrotic liver tissue. Methods: For in vitro studies, HBV-transfected HepG2.2.15 cells were cultured on polydimethylsiloxane gels coated by polyelectrolyte multilayer films of 2 kPa (soft) or 24 kPa (stiff) rigidity mimicking the stiffness of the healthy or fibrotic liver. For in vivo studies, hepatic fibrosis was induced in C57Bl/6 parental and HBV+ transgenic (HBVTg) mice by injecting CCl4 twice a week for 6 weeks. Results: We found higher levels of HBV markers in stiff gel-attached hepatocytes accompanied by up-regulated OPN content in cell supernatants as well as suppression of anti-viral interferon-stimulated genes (ISGs). This indicates that pre-requisite “fibrotic” stiffness increases osteopontin (OPN) content and releases and suppresses anti-viral innate immunity, causing a subsequent rise in HBV markers expression in hepatocytes. In vitro results were corroborated by data from HBVTg mice administered CCl4 (HBVTg CCl4). These mice showed higher HBV RNA, DNA, HBV core antigen (HBcAg), and HBV surface antigen (HBsAg) levels after liver fibrosis induction as judged by a rise in Col1a1, SMA, MMPs, and TIMPs mRNAs and by increased liver stiffness. Importantly, CCl4-induced the pro-fibrotic activation of liver cells, and liver stiffness was higher in HBVTg mice compared with control mice. Elevation of HBV markers and OPN levels corresponded to decreased ISG activation in HBVTg CCl4 mice vs HBVTg control mice. Conclusion: Based on our data, we conclude that liver stiffness enhances OPN levels to limit anti-viral ISG activation in hepatocytes and promote an increase in HBV infectivity, thereby contributing to end-stage liver disease progression

Microbial Production of Amylase from Cassava Waste

Bacterium mura was isolated from cassava waste, (Tamil Nadu, India) for the production of extracellular amylase. On screening for amylase producing bacteria, 5 isolates showed positive results, of which Bacterium mura showed best amylase activity. The optimal conditions for the amylase activity were found at pH 6.0 (39 U/ml) and at temperature 37°C. Amylase activity was found to be higher when lactose (31 U/ml), casein, barley (42 U/ml) and SDS (32 U/ml) were used as the carbon source, nitrogen source, agro waste source and as additives respectively. The enzyme was partially purified by dialysis and the molecular mass was found to be 65kDa by SDS-PAGE. The partially purified and crude amylase was confirmed by zymogram. The partially purified amylase was used in bread making, which improved the softening of the bread and was used as a de-sizing agent

Increased liver stiffness promotes hepatitis B progression by impairing innate immunity in CCl4-induced fibrotic HBV+ transgenic mice

BackgroundHepatitis B virus (HBV) infection develops as an acute or chronic liver disease, which progresses from steatosis, hepatitis, and fibrosis to end-stage liver diseases such as cirrhosis and hepatocellular carcinoma (HCC). An increased stromal stiffness accompanies fibrosis in chronic liver diseases and is considered a strong predictor for disease progression. The goal of this study was to establish the mechanisms by which enhanced liver stiffness regulates HBV infectivity in the fibrotic liver tissue.MethodsFor in vitro studies, HBV-transfected HepG2.2.15 cells were cultured on polydimethylsiloxane gels coated by polyelectrolyte multilayer films of 2 kPa (soft) or 24 kPa (stiff) rigidity mimicking the stiffness of the healthy or fibrotic liver. For in vivo studies, hepatic fibrosis was induced in C57Bl/6 parental and HBV+ transgenic (HBVTg) mice by injecting CCl4 twice a week for 6 weeks.ResultsWe found higher levels of HBV markers in stiff gel-attached hepatocytes accompanied by up-regulated OPN content in cell supernatants as well as suppression of anti-viral interferon-stimulated genes (ISGs). This indicates that pre-requisite “fibrotic” stiffness increases osteopontin (OPN) content and releases and suppresses anti-viral innate immunity, causing a subsequent rise in HBV markers expression in hepatocytes. In vitro results were corroborated by data from HBVTg mice administered CCl4 (HBVTg CCl4). These mice showed higher HBV RNA, DNA, HBV core antigen (HBcAg), and HBV surface antigen (HBsAg) levels after liver fibrosis induction as judged by a rise in Col1a1, SMA, MMPs, and TIMPs mRNAs and by increased liver stiffness. Importantly, CCl4-induced the pro-fibrotic activation of liver cells, and liver stiffness was higher in HBVTg mice compared with control mice. Elevation of HBV markers and OPN levels corresponded to decreased ISG activation in HBVTg CCl4 mice vs HBVTg control mice.ConclusionBased on our data, we conclude that liver stiffness enhances OPN levels to limit anti-viral ISG activation in hepatocytes and promote an increase in HBV infectivity, thereby contributing to end-stage liver disease progression

Alcohol-Induced Lysosomal Damage and Suppression of Lysosome Biogenesis Contribute to Hepatotoxicity in HIV-Exposed Liver Cells

Although the causes of hepatotoxicity among alcohol-abusing HIV patients are multifactorial, alcohol remains the least explored “second hit” for HIV-related hepatotoxicity. Here, we investigated whether metabolically derived acetaldehyde impairs lysosomes to enhance HIV-induced hepatotoxicity. We exposed Cytochrome P450 2E1 (CYP2E1)-expressing Huh 7.5 (also known as RLW) cells to an acetaldehyde-generating system (AGS) for 24 h. We then infected (or not) the cells with HIV-1ADA then exposed them again to AGS for another 48 h. Lysosome damage was assessed by galectin 3/LAMP1 co-localization and cathepsin leakage. Expression of lysosome biogenesis–transcription factor, TFEB, was measured by its protein levels and by in situ immunofluorescence. Exposure of cells to both AGS + HIV caused the greatest amount of lysosome leakage and its impaired lysosomal biogenesis, leading to intrinsic apoptosis. Furthermore, the movement of TFEB from cytosol to the nucleus via microtubules was impaired by AGS exposure. The latter impairment appeared to occur by acetylation of α-tubulin. Moreover, ZKSCAN3, a repressor of lysosome gene activation by TFEB, was amplified by AGS. Both these changes contributed to AGS-elicited disruption of lysosome biogenesis. Our findings indicate that metabolically generated acetaldehyde damages lysosomes and likely prevents their repair and restoration, thereby exacerbating HIV-induced hepatotoxicity

Acute Ethanol-Induced Liver Injury is Prevented by Betaine Administration

Binge drinking is the most common form of excessive alcohol use. Repeated episodes of binge drinking cause multiple organ injuries, including liver damage. We previously demonstrated that chronic ethanol administration causes a decline in the intrahepatic ratio of S-adenosylmethionine (SAM) to S-adenosylhomocysteine (SAH). This decline causes impairments in essential methylation reactions that result in alcohol-induced fatty liver (steatosis) and other features of alcohol-associated liver disease (ALD). Co-treatment with betaine during chronic ethanol feeding, normalizes hepatocellular SAM:SAH ratio and alleviates many features of liver damage including steatosis. Here, we sought to examine whether betaine treatment similarly protects against liver injury in an alcohol binge-drinking model. We hypothesized that ethanol binge with prior or simultaneous betaine administration would prevent or attenuate acute alcohol-induced liver damage. Male C57Bl/6 mice were gavaged twice, 12 h apart, with either 6 g ethanol/kg BW or with an equal volume/kg BW of 0.9% NaCl. Two separate groups of mice (n = 5/group) were gavaged with 4 g betaine/kg BW, either 2 h before or simultaneously with the ethanol or saline gavages. All mice were sacrificed 8 h after the last gavage and serum and liver parameters were quantified. Ethanol binges caused a 50% decrease in hepatic SAM:SAH ratio and a \u3e3-fold rise in liver triglycerides (p ≤ 0.05). These latter changes were accompanied by elevated serum AST and ALT activities and blood alcohol concentrations (BAC) that were ∼three-times higher than the legal limit of intoxication in humans. Mice that were treated with betaine 2 h before or simultaneously with the ethanol binges exhibited similar BAC as in mice given ethanol-alone. Both betaine treatments significantly elevated hepatic SAM levels thereby normalizing the SAM:SAH ratio and attenuating hepatic steatosis and other injury parameters, compared with mice given ethanol alone. Simultaneous betaine co-administration with ethanol was more effective in preventing or attenuating liver injury than betaine given before ethanol gavage. Our findings confirm the potential therapeutic value of betaine administration in preventing liver injury after binge drinking in an animal model

Aberrant post-translational protein modifications in the pathogenesis of alcohol-induced liver injury

It is likely that the majority of proteins will undergo post-translational modification, be it enzymatic or non-enzymatic. These modified protein(s) regulate activity, localization and interaction with other cellular molecules thereby maintaining cellular hemostasis. Alcohol exposure significantly alters several of these post-translational modifications leading to impairments of many essential physiological processes. Here, we present new insights into novel modifications following ethanol exposure and their role in the initiation and progression of liver injury. This critical review condenses the proceedings of a symposium at the European Society for the Biomedical Research on Alcoholism Meeting held September 12-15, 2015, in Valencia, Spain