Conversion of lignocellulose biomass to bioenergy through nanobiotechnology

The growing global demand for energy, particularly petroleum-based fuels, has stimulated a long-term quest for an optimal source of sustainable energy. This barrier is removed by lignocellulosic biomass, which is an economical, easily accessible, and renewable fuel source that fits sustainability standards. However, large-scale use of most of the techniques results in significant handling costs and decontamination of the inhibitors released. Taken together, these limits increase the efficacy of present solutions and create a need for the development of a novel, environmentally sustainable, productive, and cost-effective technology for lignocellulose biomass conversion. In this context, the use of nanotechnology in the treatment of lignocellulose biomass to bioenergy exchange has gained significant attention and has been extensively researched in recent years. This review discussed how nanotechnology can be used to turn biomass into energy. It gives new ideas and tools for developing new industries, which will help the economy, grow in the long run. This careful examination will also shed light on some of the minor details surrounding the different ways of biomass conversion previously explored by other experts

Identification of GSK3186899/DDD853651 as a Preclinical Development Candidate for the Treatment of Visceral Leishmaniasis

The leishmaniases are diseases that affect millions of people across the world, in particular visceral leishmaniasis (VL) which is fatal unless treated. Current standard of care for VL suffers from multiple issues and there is a limited pipeline of new candidate drugs. As such, there is a clear unmet medical need to identify new treatments. This paper describes the optimization of a phenotypic hit against Leishmania donovani, the major causative organism of VL. The key challenges were to balance solubility and metabolic stability while maintaining potency. Herein, strategies to address these shortcomings and enhance efficacy are discussed, culminating in the discovery of preclinical development candidate GSK3186899/DDD853651 (<b>1</b>) for VL

The SIB Swiss Institute of Bioinformatics' resources: focus on curated databases

The SIB Swiss Institute of Bioinformatics (www.isb-sib.ch) provides world-class bioinformatics databases, software tools, services and training to the international life science community in academia and industry. These solutions allow life scientists to turn the exponentially growing amount of data into knowledge. Here, we provide an overview of SIB's resources and competence areas, with a strong focus on curated databases and SIB's most popular and widely used resources. In particular, SIB's Bioinformatics resource portal ExPASy features over 150 resources, including UniProtKB/Swiss-Prot, ENZYME, PROSITE, neXtProt, STRING, UniCarbKB, SugarBindDB, SwissRegulon, EPD, arrayMap, Bgee, SWISS-MODEL Repository, OMA, OrthoDB and other databases, which are briefly described in this article

Graphical representation and experimental validation of the HRNH1.0 reporter.

<p>Schematic representation of the SeeSaw reporter (SSR) 1.0 (A) and SSR 2.0 (B). A GFP gene is flanked by two truncated parts of the RFP gene (RF and FP) that share 302 bp of homologous sequence. One I-SceI target site in SSR 1.0 (A), and two in opposite orientation in SSR 2.0 (B), were cloned at the 3′ end of the <i>GFP</i> gene. Expression of I-SceI generates a DSB; if the damage is resolved by NHEJ, cells will express the GFP protein, while if it is repaired using homologous sequence by HR, cells express the <i>RFP</i> gene. The PCR products used in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0077206#pone-0077206-g002" target="_blank">Figure 2F</a> are depicted as “uncut PCR fragment” and “cut and repaired PCR fragment”.</p

Cell cycle distribution after shRNA-mediated depletion of several target genes.

<p>A representative FLOW cytometry plot after downregulation of the indicated target genes with shRNA is shown.</p

Sensitivity of SSR systems to NHEJ and DNA send resection impairment.

<p>Effects of shRNA-mediated depletion of core NHEJ or DNA end resection factors for the SSR 1.0 (A) and SSR 2.0 (B). To calculate the deviation from the balance between homology-dependent versus homology-independent repair, the ratio between green versus red cells in each conditions was calculated. To facilitate comparing experiments, this ratio was normalized for each shRNA with a scrambled sequence shRNA as a control. Those shRNAs that skewed the balance towards an increase in homology-independent repair have a fold-increase of over 1 (green bars), while those with an increase in HR have a fold-decrease of less than one (red bars). Data represent a minimum of three sets of duplicated experiments.</p

DDR defects lead to an imbalance of the HR/NHEJ ratio.

<p>The HR and NHEJ balance in the SSR 1.0 (A) and SSR 2.0 (B) in cells depleted of the checkpoint factors ATM, ATR, BRCA1, RNF169, RNF8, UBC13, UBC9, PIAS1, or PIAS4, or after MG-132 inhibition of proteasome activity. The details are as given in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0077206#pone-0077206-g004" target="_blank">Figure 4</a>, except that data for the MG-132 results were normalized to cells treated with DMSO as a control.</p