Enhanced SOC estimation of lithium ion batteries with RealTime data using machine learning algorithms.

Accurately estimating Battery State of Charge (SOC) is essential for safe and optimal electric vehicle operation. This paper presents a comparative assessment of multiple machine learning regression algorithms including Support Vector Machine, Neural Network, Ensemble Method, and Gaussian Process Regression for modelling the complex relationship between real-time driving data and battery SOC. The models are trained and tested on extensive field data collected from diverse drivers across varying conditions. Statistical performance metrics evaluate the SOC prediction accuracy on the test set. Gaussian process regression demonstrates superior precision surpassing the other techniques with the lowest errors. Case studies analyse model competence in mimicking actual battery charge/discharge characteristics responding to changing drivers, temperatures, and drive cycles. The research provides a reliable data-driven framework leveraging advanced analytics for precise real-time SOC monitoring to enhance battery management.

Integrative network analysis identifies an immune-based prognostic signature as the determinant for the mesenchymal subtype in epithelial ovarian cancer.

BACKGROUND: Epithelial ovarian cancer (EOC) has been classified into four molecular subtypes, of which the mesenchymal subtype has the poorest survival. Our goal is to develop an immune-based prognostic signature by incorporating molecular subtypes for EOC patients. METHODS: The gene expression profiles of EOC samples were collected from seven public datasets as well as an internal retrospective validation cohort, containing 1192 EOC patients. Network analysis was applied to integrate the mesenchymal modalities and immune signature to establish an immune-based prognostic signature for EOC (IPSEOC). The signature was trained and validated in eight independent datasets. RESULTS: Seven immune genes were identified as key regulators of the mesenchymal subtype and were used to construct the IPSEOC. The IPSEOC significantly divided patients into high- and low-risk groups in discovery (OS: P < .0001), 6 independent public validation sets (OS: P = .04 to P = .002), and an internal retrospective validation cohort (OS: P = .025). Furthermore, pathway analysis revealed that differences between risk groups were mainly activation of mesenchymal-related signalling. Moreover, a significant correlation existed between the IPSEOC values versus clinical phenotypes including late tumor stages, drug resistance. CONCLUSION: We propose an immune-based signature, which is a promising prognostic biomarker in ovarian cancer. Prospective studies are needed to further validate its analytical accuracy and test the clinical utility.

Silencing of SENP2 in Multiple Myeloma Induces Bortezomib Resistance by Activating NF-κB Through the Modulation of IκBα Sumoylation.

The proteasome inhibitor bortezomib is the most successfully applied chemotherapeutic drug for treating multiple myeloma. However, its clinical efficacy reduced due to resistance development. The underlying molecular mechanisms of bortezomib resistance are poorly understood. In this study, by combining in silico analysis and sgRNA library based drug resistance screening assay, we identified SENP2 (Sentrin/SUMO-specific proteases-2) as a bortezomib sensitive gene and found its expression highly downregulated in bortezomib resistant multiple myeloma patient's samples. Furthermore, down regulation of SENP2 in multiple myeloma cell line RPMI8226 alleviated bortezomib induced cell proliferation inhibition and apoptosis, whereas, overexpression of SENP2 sensitized these cells to bortezomib treatment. We further demonstrate that knockdown of SENP2 in RPMI8226 cells increased SUMO2 conjugated IκBα that resulted in the activation of NF-κB. Taken together, we report that silencing of SENP2 and consequent activation of NF-κB through the modulation of IκBα sumoylation as a novel mechanism inducing bortezomib resistance in multiple myeloma.

Preparation and properties of cellulose/Thespesia lampas microfiber composite films.

The fibers from the newly identified plant Thespesia lampas (TL) were converted into microfibers in order to increase their aspect ratio. The TL microfibers (TLMFs) were used as reinforcement (1 wt. to 5 wt%) in cellulose matrix to prepare cellulose /TLMFs composite films. These composite films were characterized by polarized optical microscopy (POM), scanning electron microscopy (SEM), Fourier transform infrared (FTIR) spectroscopy, X-ray diffraction (XRD), thermogravimetric analysis (TGA) and tensile tests. The POM and SEM images indicated the uniform distribution of TLMFs but in random orientation in the composites. FTIR spectral analysis indicated the presence of minor quantity of lignin in the microfibers in spite of chemical treatment of fibers. The XRD analysis indicated higher crystallinity index for the composites than the matrix. Thermal stability of the composite films was slightly higher than the matrix. Tensile modulus and tensile strength were lower while the elongation at break of the composite films was higher than those of the cellulose matrix due to random orientation of the TLMFs in the composites. However the tensile properties and thermal stability of the cellulose/TLMFs composites were found to be higher than those of the cellulose/alkali treated TL fiber composites and hence can be considered for packaging applications.

Anti-ganglioside antibodies profile in Guillain-Barré syndrome: Correlation with clinical features, electrophysiological pattern, and outcome.

BACKGROUND: Guillain-Barré syndrome (GBS) and its subtypes are associated with distinct anti-ganglioside antibodies. Hence, we aimed to determine the frequency of anti-ganglioside antibodies and its correlation with clinical features, electrophysiological patterns, and outcome in patients with GBS. MATERIAL AND METHODS: The data regarding clinical features, electrophysiological patterns, and outcome at 6 months were collected and analyzed from the case records of patients diagnosed with GBS during 2008-2013 at a tertiary care hospital in south India. RESULTS: A total of 204 patients with GBS were studied, and 73 patients (mean age: 37.6 ± 17.5 years) who underwent anti-ganglioside antibody testing were analyzed. Male-to-female ratio was 2.5:1. IgG anti-ganglioside antibodies were positive in 41/73 patients. The most common IgG anti-ganglioside antibody observed in the acute demyelinating variant was anti-GT1b (n = 13; 17.8%), and, those in the acute axonal variant were anti-GM1, anti-GM2, anti-GD1b, and anti-GT1b antibodies (n = 9;12.3% each). Three patients died and 5 patients were unable to walk independently at the end of 6 months. CONCLUSIONS: The frequency of anti-ganglioside antibodies in our cohort with GBS was 56%, with IgG anti-GT1b antibody being the most common. The anti-ganglioside antibodies were significantly positive in acute motor axonal neuropathy (AMAN) subtype of GBS. The presence of anti-ganglioside antibodies was not found to be of significant use in predicting the outcome. Although it was observed that the absence, and not the presence, of anti-ganglioside antibodies was associated with antecedent infection, dysautonomia, and requirement of ventilator support, the overall disease severity was not antibody dependant.

Nucleotide biosynthetic enzyme GMP synthase is a TRIM21-controlled relay of p53 stabilization.

Nucleotide biosynthesis is fundamental to normal cell proliferation as well as to oncogenesis. Tumor suppressor p53, which prevents aberrant cell proliferation, is destabilized through ubiquitylation by MDM2. Ubiquitin-specific protease 7 (USP7) plays a dualistic role in p53 regulation and has been proposed to deubiquitylate either p53 or MDM2. Here, we show that guanosine 5'-monophosphate synthase (GMPS) is required for USP7-mediated stabilization of p53. Normally, most GMPS is sequestered in the cytoplasm, separated from nuclear USP7 and p53. In response to genotoxic stress or nucleotide deprivation, GMPS becomes nuclear and facilitates p53 stabilization by promoting its transfer from MDM2 to a GMPS-USP7 deubiquitylation complex. Intriguingly, cytoplasmic sequestration of GMPS requires ubiquitylation by TRIM21, a ubiquitin ligase associated with autoimmune disease. These results implicate a classic nucleotide biosynthetic enzyme and a ubiquitin ligase, better known for its role in autoimmune disease, in p53 control.

Remodelers organize cellular chromatin by counteracting intrinsic histone-DNA sequence preferences in a class-specific manner.

The nucleosome is the fundamental repeating unit of eukaryotic chromatin. Here, we assessed the interplay between DNA sequence and ATP-dependent chromatin-remodeling factors (remodelers) in the nucleosomal organization of a eukaryotic genome. We compared the genome-wide distribution of Drosophila NURD, (P)BAP, INO80, and ISWI, representing the four major remodeler families. Each remodeler has a unique set of genomic targets and generates distinct chromatin signatures. Remodeler loci have characteristic DNA sequence features, predicted to influence nucleosome formation. Strikingly, remodelers counteract DNA sequence-driven nucleosome distribution in two distinct ways. NURD, (P)BAP, and INO80 increase histone density at their target sequences, which intrinsically disfavor positioned nucleosome formation. In contrast, ISWI promotes open chromatin at sites that are propitious for precise nucleosome placement. Remodelers influence nucleosome organization genome-wide, reflecting their high genomic density and the propagation of nucleosome redistribution beyond remodeler binding sites. In transcriptionally silent early embryos, nucleosome organization correlates with intrinsic histone-DNA sequence preferences. Following differential expression of the genome, however, this relationship diminishes and eventually disappears. We conclude that the cellular nucleosome landscape is the result of the balance between DNA sequence-driven nucleosome placement and active nucleosome repositioning by remodelers and the transcription machinery.

Mucoadhesive patches of Salbutamol sulphate for unidirectional buccal drug delivery: development and evaluation.

Mucoadhesive buccal patches of Salbutamol Sulphate were prepared using five different polymers (polyvinylpyrrolidone [PVP]), polyvinyl alcohol [PVA], water soluble chitosan [CH(WS)], acid soluble chitosan [CH(AS)], hydroxypropyl methyl cellulose [HPMC])in various proportions and combinations (CH(WS)/PVP/HPMC, CH(WS)/PVA/HPMC, CH(AS)/PVP/HPMC, and CH(AS)/PVA/HPMC). A 3(2) full factorial design was used to design the experiments. A total of 72 patches were prepared. Thickness of the patches ranged between 0.3±0.003 and 0.6±0.009 mm. Mass of the patches were in the range of 68.12±4.6 to 95.02±7.2 mg. Patches showed increased mass whenever PEG -400 was used as plasticizer. The surface pH of patches were acidic to neutral (pH 4-pH 7). Patches showed satisfactory drug loading efficiency (85%to 97%). Eight formulations(C9, C18, C27, C36, D9, D18, D27, and D36)-which showed high folding endurance- were selected for further characterization. Patches with PEG -400 showed higher swelling index when compared to PG. The residence time of the patches ranged between 115 min and 120 min. Formulation C18 showed the maximum in vitro drug release of 101.4 % over a period of 120 min. Formulations D36 and C36 were best fitted to Higuchi model. The remaining formulations were best fitted to the Korsmeyer-Peppas model. Drug permeation was fast and showed the similar profile as that of the in vitro drug release. Patches were stable, during and at the end of the accelerated stability study.

Drosophila transcription factor Tramtrack69 binds MEP1 to recruit the chromatin remodeler NuRD.

ATP-dependent chromatin-remodeling complexes (remodelers) are essential regulators of chromatin structure and gene transcription. How remodelers can act in a gene-selective manner has remained enigmatic. A yeast two-hybrid screen for proteins binding the Drosophila transcription factor Tramtrack69 (TTK69) identified MEP1. Proteomic characterization revealed that MEP1 is a tightly associated subunit of the NuRD remodeler, harboring the Mi2 enzymatic core ATPase. In addition, we identified the fly homolog of human Deleted in oral cancer 1 (DOC1), also known as CDK2-associated protein 1 (CDK2AP1), as a bona fide NuRD subunit. Biochemical and genetic assays supported the functional association between MEP1, Mi2, and TTK69. Genomewide expression analysis established that TTK69, MEP1, and Mi2 cooperate closely to control transcription. The TTK69 transcriptome profile correlates poorly with remodelers other than NuRD, emphasizing the selectivity of remodeler action. On the genes examined, TTK69 is able to bind chromatin in the absence of NuRD, but targeting of NuRD is dependent on TTK69. Thus, there appears to be a hierarchical relationship in which transcription factor binding precedes remodeler recruitment.

Design, synthesis, structure-activity relationship and antibacterial activity series of novel imidazo fused quinolone carboxamides.

A series of novel 7,8 and 1,8 imidazo fused quinolone carboxamides are synthesized and evaluated against antibacterial activity. 1,8 Imidazo fused quinolones exhibit moderate antibacterial activity. Molecular modeling studies were carried out to optimize the pharmacophore.

An open-label study of tiagabine in panic disorder.

γ-aminobutyric acid (GABA) has been implicated in the pathophysiology of anxiety disorders, including panic. Tiagabine, a selective GABA reuptake inhibitor (SGRI), has been shown to reduce symptoms of anxiety. This pilot study evaluated the efficacy and safety of tiagabine in patients with panic disorder. Male and female outpatients aged 18-64 years with a DSM-IV diagnosis of severe to moderately severe panic disorder (with or without agoraphobia) received open-label tiagabine 2-20 mg/day for 10 weeks. Outcome assessments included the Sheehan Panic Disorder Scale (SPS), Panic Disorder Severity Scale (PDSS), Bandelow Panic and Agoraphobia Scale (PAS), Hamilton Rating Scale for Anxiety (HAM-A), 21-point Clinician Global Improvement Scale (CGI-21), 21-point Patient Global Improvement (PGI-21) and the Sheehan Disability Scale (SDS). Scores were recorded at baseline and weekly intervals thereafter. Adverse events were monitored throughout the study. Of the 28 patients who enrolled in the study, 23 had one post-baseline visit and were available for LOCF outcome analysis. Although statistically significant reductions from baseline were observed for all of the outcome measures, the percentage improvements on individual scales were only in the 25-32% range which is not clinically significant. Tiagabine was generally well tolerated; the most common adverse events were nausea, dizziness and headaches. Only one patient discontinued tiagabine due to adverse events. These findings suggest that administration of tiagabine may be of little benefit in patients with panic disorder.