Fine Tuning Transformer Based BERT Model for Generating the Automatic Book Summary

Major text summarization research is mainly focusing on summarizing short documents and very few works is witnessed for long document summarization. Additionally, extractive summarization is more addressed as compared with abstractive summarization. Abstractive summarization, unlike extractive summarization, does not only copy essential words from the original text but requires paraphrasing to get close to human generated summary. The machine learning, deep learning models are adapted to contemporary pre-trained models like transformers. Transformer based Language models gaining a lot of attention because of self-supervised training while fine-tuning for Natural Language Processing (NLP) downstream task like text summarization.  The proposed work is an attempt to investigate the use of transformers for abstraction. The proposed work is tested for book especially as a long document for evaluating the performance of the model

A Positive Feedback Loop of Hippo- and c-Jun-Amino-Terminal Kinase Signaling Pathways Regulates Amyloid-Beta-Mediated Neurodegeneration

Alzheimer\u27s disease (AD, OMIM: 104300) is an age-related disorder that affects millions of people. One of the underlying causes of AD is generation of hydrophobic amyloid-beta 42 (Aβ42) peptides that accumulate to form amyloid plaques. These plaques induce oxidative stress and aberrant signaling, which result in the death of neurons and other pathologies linked to neurodegeneration. We have developed a Drosophila eye model of AD by targeted misexpression of human Aβ42 in the differentiating retinal neurons, where an accumulation of Aβ42 triggers a characteristic neurodegenerative phenotype. In a forward deficiency screen to look for genetic modifiers, we identified a molecularly defined deficiency, which suppresses Aβ42-mediated neurodegeneration. This deficiency uncovers hippo (hpo) gene, a member of evolutionarily conserved Hippo signaling pathway that regulates growth. Activation of Hippo signaling causes cell death, whereas downregulation of Hippo signaling triggers cell proliferation. We found that Hippo signaling is activated in Aβ42-mediated neurodegeneration. Downregulation of Hippo signaling rescues the Aβ42-mediated neurodegeneration, whereas upregulation of Hippo signaling enhances the Aβ42-mediated neurodegeneration phenotypes. It is known that c-Jun-amino-terminal kinase (JNK) signaling pathway is upregulated in AD. We found that activation of JNK signaling enhances the Aβ42-mediated neurodegeneration, whereas downregulation of JNK signaling rescues the Aβ42-mediated neurodegeneration. We tested the nature of interactions between Hippo signaling and JNK signaling in Aβ42-mediated neurodegeneration using genetic epistasis approach. Our data suggest that Hippo signaling and JNK signaling, two independent signaling pathways, act synergistically upon accumulation of Aβ42 plaques to trigger cell death. Our studies demonstrate a novel role of Hippo signaling pathway in Aβ42-mediated neurodegeneration

Satb2 acts as a gatekeeper for major developmental transitions during early vertebrate embryogenesis

Zygotic genome activation (ZGA) initiates regionalized transcription underlying distinct cellular identities. ZGA is dependent upon dynamic chromatin architecture sculpted by conserved DNA-binding proteins. However, the direct mechanistic link between the onset of ZGA and the tissue-specific transcription remains unclear. Here, we have addressed the involvement of chromatin organizer Satb2 in orchestrating both processes during zebrafish embryogenesis. Integrative analysis of transcriptome, genome-wide occupancy and chromatin accessibility reveals contrasting molecular activities of maternally deposited and zygotically synthesized Satb2. Maternal Satb2 prevents premature transcription of zygotic genes by influencing the interplay between the pluripotency factors. By contrast, zygotic Satb2 activates transcription of the same group of genes during neural crest development and organogenesis. Thus, our comparative analysis of maternal versus zygotic function of Satb2 underscores how these antithetical activities are temporally coordinated and functionally implemented highlighting the evolutionary implications of the biphasic and bimodal regulation of landmark developmental transitions by a single determinant

Physical characterixation and in vitro biological impact of highly aggregated antibodies separated into size-enriched populations by fluorescence-activated cell sorting

An IgG2 monoclonal antibody (mAb) solution was subjected to stirring, generating high concentrations of nanometer and subvisible particles, which were then successfully size enriched into different size bins by low speed centrifugation or a combination of gravitational sedimentation and Fluorescence-Activated Cell Sorting (FACS). The size-fractionated mAb particles were assessed for their ability to elicit the release of cytokines from a population of donor-derived human peripheral blood mononuclear cells (PBMC) at two phases of the immune response. Fractions enriched in nanometer-sized particles showed a lower response than those enriched in micron-sized particles in this assay. Particles of 5–10 μm in size displayed elevated cytokine release profiles compared to other size ranges. Stir-stressed mAb particles had amorphous morphology, contained protein with partially altered secondary structure, elevated surface hydrophobicity (compared to controls), and trace levels of elemental fluorine. FACS size-enriched the mAb particle samples, yet did not notably alter the overall morphology or composition of particles as measured by Microflow imaging, Transmission Electron Microscopy, and Scanning Electron Microscopy-Energy Dispersive X-ray Spectroscopy. The utility and limitations of FACS for size separation of mAb particles and potential of in-vitro PBMC studies to rank order the immunogenic potential of various types of mAb particles is discussed

An Unusual Case of Unilateral Multifocal Choroiditis in a Young Male

Multifocal choroiditis is a vision‑threatening disease causing inflammation at the level of retinal pigment epithelium and outer retina. We present a unique case of unilateral multifocal choroiditis in a young nonmyopic male and its subsequent course. The patient developed visual loss due to the sub‑retinal neovascular membrane (SRNVM) in macula due to multifocal choroiditis. The SRNVM regressed with repeated intra‑vitreal injection of bevacizumab and the visual acuity improved from 6/24 at presentation to 6/12 after repeated intra‑vitreal injections of bevacizumab.Keywords: Bevacizumab, multifocal choroiditis, sub‑retinal neovascular membran

An E3 ubiquitin ligase, cullin‐4 regulates retinal differentiation in Drosophila eye

During organogenesis, cell proliferation is followed by the differentiation of specific cell types to form an organ. Any aberration in differentiation can result in developmental defects, which can result in a partial to a near‐complete loss of an organ. We employ the Drosophila eye model to understand the genetic and molecular mechanisms involved in the process of differentiation. In a forward genetic screen, we identified, cullin‐4 (cul‐4), which encodes an E3 ubiquitin ligase, to play an important role in retinal differentiation. During development, cul‐4 is known to be involved in protein degradation, regulation of genomic stability, and regulation of cell cycle. Previously, we have reported that cul‐4 regulates cell death during eye development by downregulating Wingless (Wg)/Wnt signaling pathway. We found that loss‐of‐function of cul‐4 results in a reduced eye phenotype, which can be due to onset of cell death. However, we found that loss‐of‐function of cul‐4 also affects retinal development by downregulating retinal determination (RD) gene expression. Early markers of retinal differentiation are dysregulated in cul‐4 loss of function conditions, indicating that cul‐4 is necessary for differentiation. Furthermore, loss‐of‐function of cul‐4 ectopically induces expression of negative regulators of eye development like Wg and Homothorax (Hth). During eye development, Wg is known to block the progression of a synchronous wave of differentiation referred to as Morphogenetic furrow (MF). In cul‐4 loss‐of‐function background, expression of dpp‐lacZ, a MF marker, is significantly downregulated. Our data suggest a new role of cul‐4 in retinal differentiation. These studies may have significant bearings on our understanding of early eye development

IMPACT OF SODIUM FLUORIDE AND NANO SILVER FLUORIDE-BASED VARNISHES ON REMINERALISATION OF ENAMEL CARIES: AN IN-VITRO STUDY

The provided data depicts the images obtained by Scanning electron microscope under 50x, 500x and 1000x magnification. The changes that occured on the enamel surface can be appreciated in the images. In sodium fluoride group very little deposits of minerals can be seen. However, cracks still persist. The neutral nano silver fluoride group shows polyhyderal deposits on minerals scattered all over the surface. In the acidulated nano silver fluoride group, the deposition of polyhyderal minerals has occured in abundance. The data regarding  Energy dispersive X-ray spectrophotometry  (EDS/EDX) is also presented. It provides a tabulated analysis of the elements on the examined surface. Here, the amount of calcium, phosphorus, silver and fluoride on the surface of thh enamel was analised after application of the test material.</p

Enhanced Growth of Endothelial Precursor Cells on PCG-Matrix Facilitates Accelerated, Fibrosis-Free, Wound Healing: A Diabetic Mouse Model

<div><p>Diabetes mellitus (DM)-induced endothelial progenitor cell (EPC) dysfunction causes impaired wound healing, which can be rescued by delivery of large numbers of ‘normal’ EPCs onto such wounds. The principal challenges herein are (a) the high number of EPCs required and (b) their sustained delivery onto the wounds. Most of the currently available scaffolds either serve as passive devices for cellular delivery or allow adherence and proliferation, but not both. This clearly indicates that matrices possessing both attributes are ‘the need of the day’ for efficient healing of diabetic wounds. Therefore, we developed a system that not only allows selective enrichment and expansion of EPCs, but also efficiently delivers them onto the wounds. Murine bone marrow-derived mononuclear cells (MNCs) were seeded onto a PolyCaprolactone-Gelatin (PCG) nano-fiber matrix that offers a combined advantage of strength, biocompatibility wettability; and cultured them in EGM2 to allow EPC growth. The efficacy of the PCG matrix in supporting the EPC growth and delivery was assessed by various in vitro parameters. Its efficacy in diabetic wound healing was assessed by a topical application of the PCG-EPCs onto diabetic wounds. The PCG matrix promoted a high-level attachment of EPCs and enhanced their growth, colony formation, and proliferation without compromising their viability as compared to Poly L-lactic acid (PLLA) and Vitronectin (VN), the matrix and non-matrix controls respectively. The PCG-matrix also allowed a sustained chemotactic migration of EPCs in vitro. The matrix-effected sustained delivery of EPCs onto the diabetic wounds resulted in an enhanced fibrosis-free wound healing as compared to the controls. Our data, thus, highlight the novel therapeutic potential of PCG-EPCs as a combined ‘growth and delivery system’ to achieve an accelerated fibrosis-free healing of dermal lesions, including diabetic wounds.</p></div