Evaluation of new insecticide molecules for their effectiveness in the management of sugarcane early shoot borer, Chilo infuscatellus (Snellen)

An experiment was conducted at Zonal Agricultural Research Station, V.C farm, Mandya (Karnataka), India during 2015, to assess the chemical control of sugarcane early shoot borer (Chilo infuscatellus). Nine insecticides namely, Fipronil 0.3G, Chlorantraniliprole 0.4G, Chlorantraniliprole 18.5 SC, Spinosad 45SC, Flubendiamide 39.35SC, Cartap hydrochloride 4G, Phorate 10G, Carbofuran 3G, Chlorpyriphos 20EC, and compared with untreated (Check plot)using randomized block design with three replications. Significant differences were noticed among the treatments. Chlorantraniliprole 0.4G recorded lowest cumulative incidence (2.79 %) and highest per cent reduction over the control (85.78 %) which was followed by Cartap hydrochloride 4G (5.37% and 72.65%), Chlorantraniliprole 18.5 SC (5.95% and 75.62%), Flubendiamide 39.35SC (6.64% and 66.19%) and Fipronil 0.3G (6.83% and 65.22%) were found significantly superior in reducing the cumulative incidence of C. infuscatellus.In Co 86032 Cartap hydrochloride 4G was found to be the best insecticide in getting a highest cost benefit ratio (1:12.39). Other insecticides such as Fipronil 0.3G (1:8.84), Chlorantraniliprole 0.4G (1:6.96), Flubendiamide 39.35SC (1:5.42) and Spinosad 45SC (1:4.16) have also recorded better cost benefit ratio. Since Cartap hydrochloride 4G does not have crop label so we can recommend Fipronil 0.3G or Chlorantraniliprole 0.4G for the management of sugarcane early shoot borer

Combined harmonic reduction and DC voltage regulation of a single DC source five-level multilevel inverter for wind electric system

Wind power generation has increased in the past twenty years due to the development of power electronic converters. Power generation through wind has advantages over other renewable sources, such as having more efficiency, being pollution-free, and its abundant availability. Power electronic converters play a vital role in the wind energy conversion system. This paper presents a wind-electric system with a permanent magnet synchronous generator, diode rectifier, DC-DC converter (buck-Boost or Cuk converter), and a three-phase five-level inverter. The five-level inverter is a modified form of a cascaded H-bridge inverter that uses a single DC source as an input irrespective of several levels and phases. As the wind speed changes, the Permanent Magnet Synchronous Generator (PMSG) voltage and frequency changes, but for practical applications, these changes should not be allowed; hence, a voltage controller is used that maintains the output voltage of a DC converter, andthus a constant AC output is obtained. The DClink voltage is maintained at the desired voltage by a Proportional plus Integral (PI)-based voltage controller. The DC link voltage fed to the multilevel inverter (MLI) is converted to AC to feed the load. The MLI is controlled with a new Selected Harmonic Elimination (SHE), which decreases the total harmonic distortion (THD). The system is simulated with an Resistive plus Inductive (RL) load and is tested experimentally with the same load;the results prove that the Cuk converter has a better efficiency compared to the Buck-Boost converter, and the system has less THD when compared with the conventional SHE Pulse Width Modulation (PWM) technique

Corrections to “An Improved Harmonics Mitigation Scheme for a Modular Multilevel Converter” [2019 147244-147255]

In the above-named work, T. Deepa should have been listed as the second co-author of the article with the affiliation of (1): School of Electrical Engineering, Vellore Institute of Technology, Chennai 600127, India. The author's biography is also provided within this correction. Additionally, the correct zip code of affiliation (1) should be 600127, and the correct statement on financial support acknowledgement should be as follows: "This work was funded by the Renewable Energy Laboratory, Department of Communications and Networks Engineering, Prince Sultan University, Riyadh, Saudi Arabia." It is necessary to mention the nature of funding provided by Prince Sultan University and to note the correction in the spelling of the university in the same statement in the published manuscript

Chikungunya virus adaptation to Aedes albopictus mosquitoes does not correlate with acquisition of cholesterol dependence or decreased pH threshold for fusion reaction

<p>Abstract</p> <p>Background</p> <p>Chikungunya virus (CHIKV) is a mosquito transmitted alphavirus that recently caused several large scale outbreaks/epidemics of arthritic disease in tropics of Africa, Indian Ocean basin and South-East Asia. This re-emergence event was facilitated by genetic adaptation (E1-A226V substitution) of CHIKV to a newly significant mosquito vector for this virus; <it>Aedes albopictus</it>. However, the molecular mechanism explaining the positive effect of the E1-A226V mutation on CHIKV fitness in this vector remains largely unknown. Previously we demonstrated that the E1-A226V substitution is also associated with attenuated CHIKV growth in cells depleted by cholesterol.</p> <p>Methods</p> <p>In this study, using a panel of CHIKV clones that varies in sensitivity to cholesterol, we investigated the possible relationship between cholesterol dependence and <it>Ae. albopictus </it>infectivity.</p> <p>Results</p> <p>We demonstrated that there is no clear mechanistic correlation between these two phenotypes. We also showed that the E1-A226V mutation increases the pH dependence of the CHIKV fusion reaction; however, subsequent genetic analysis failed to support an association between CHIKV dependency on lower pH, and mosquito infectivity phenotypes.</p> <p>Conclusion</p> <p>the E1-A226V mutation probably acts at different steps of the CHIKV life cycle, affecting multiple functions of the virus.</p

A DNA Sequence Directed Mutual Transcription Regulation of HSF1 and NFIX Involves Novel Heat Sensitive Protein Interactions

BACKGROUND: Though the Nuclear factor 1 family member NFIX has been strongly implicated in PDGFB-induced glioblastoma, its molecular mechanisms of action remain unknown. HSF1, a heat shock-related transcription factor is also a powerful modifier of carcinogenesis by several factors, including PDGFB. How HSF1 transcription is controlled has remained largely elusive. METHODOLOGY/PRINCIPAL FINDINGS: By combining microarray expression profiling and a yeast-two-hybrid screen, we identified that NFIX and its interactions with CGGBP1 and HMGN1 regulate expression of HSF1. We found that CGGBP1 organizes a bifunctional transcriptional complex at small CGG repeats in the HSF1 promoter. Under chronic heat shock, NFIX uses CGGBP1 and HMGN1 to get recruited to this promoter and in turn affects their binding to DNA. Results show that the interactions of NFIX with CGGBP1 and HMGN1 in the soluble fraction are heat shock sensitive due to preferential localization of CGGBP1 to heterochromatin after heat shock. HSF1 in turn was found to bind to the NFIX promoter and repress its expression in a heat shock sensitive manner. CONCLUSIONS/SIGNIFICANCE: NFIX and HSF1 exert a mutual transcriptional repressive effect on each other which requires CGG repeat in HSF1 promoter and HSF1 binding site in NFIX promoter. We unravel a unique mechanism of heat shock sensitive DNA sequence-directed reciprocal transcriptional regulation between NFIX and HSF1. Our findings provide new insights into mechanisms of transcription regulation under stress

Pericardial Patch Angioplasty Heals via an Ephrin-B2 and CD34 Positive Cell Mediated Mechanism

Pericardial patches are commonly used in vascular surgery to close arteriotomies. The mechanism of early healing after patch implantation is still not well defined. We used a rat aortic patch model to assess pericardial patch healing and examined Ephrin-B2, a marker of arterial identity, expression within the post-implantation patch. We also determined whether endothelial progenitor cells (EPC) are associated with early patch healing in the arterial environment.Wistar rats (200-250 grams) underwent infrarenal aortic arteriotomy and then closure via bovine or porcine pericardial patch angioplasty. Control groups included subcutaneously implanted patches. Patches were harvested at 0-30 days and analyzed by histology, immunohistochemistry, immunofluorescence and Western blot as well as quantitative PCR.Prior to implantation, pericardial patches are largely composed of collagen and are acellular. Following arterial implantation, increasing numbers of CD68-positive cells as well as Ephrin-B2 and CD34 dual-positive cells are found within both bovine and porcine pericardial patches, whereas the infiltrating cells are negative for vWF and α-actin. Porcine patches have a luminal monolayer of cells at day 7, compared to bovine patches that have fewer luminal cells. Subcutaneously implanted patches do not attract Ephrin-B2/CD34-positive cells. By day 30, both bovine and porcine pericardial patches develop a neointima that contains Ephrin-B2, CD34, and VEGFR2-positive cells.Both CD68-positive and Ephrin-B2 and CD34 dual-positive cells infiltrate the pericardial patch early after implantation. Arteriotomy closure via pericardial patch angioplasty shows patch adaptation to the arterial environment that may involve a foreign body response as well as localization of EPC. Arterial remodeling of pericardial patches support endothelialization and may represent a paradigm of healing of scaffolds used for tissue engineering

Dengue Virus Ensures Its Fusion in Late Endosomes Using Compartment-Specific Lipids

Many enveloped viruses invade cells via endocytosis and use different environmental factors as triggers for virus-endosome fusion that delivers viral genome into cytosol. Intriguingly, dengue virus (DEN), the most prevalent mosquito-borne virus that infects up to 100 million people each year, fuses only in late endosomes, while activation of DEN protein fusogen glycoprotein E is triggered already at pH characteristic for early endosomes. Are there any cofactors that time DEN fusion to virion entry into late endosomes? Here we show that DEN utilizes bis(monoacylglycero)phosphate, a lipid specific to late endosomes, as a co-factor for its endosomal acidification-dependent fusion machinery. Effective virus fusion to plasma- and intracellular- membranes, as well as to protein-free liposomes, requires the target membrane to contain anionic lipids such as bis(monoacylglycero)phosphate and phosphatidylserine. Anionic lipids act downstream of low-pH-dependent fusion stages and promote the advance from the earliest hemifusion intermediates to the fusion pore opening. To reach anionic lipid-enriched late endosomes, DEN travels through acidified early endosomes, but we found that low pH-dependent loss of fusogenic properties of DEN is relatively slow in the presence of anionic lipid-free target membranes. We propose that anionic lipid-dependence of DEN fusion machinery protects it against premature irreversible restructuring and inactivation and ensures viral fusion in late endosomes, where the virus encounters anionic lipids for the first time during entry. Currently there are neither vaccines nor effective therapies for DEN, and the essential role of the newly identified DEN-bis(monoacylglycero)phosphate interactions in viral genome escape from the endosome suggests a novel target for drug design