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De, A.

Publications and source records attributed to De, A..

26 records · Page 2Linked to original sources

Computational Model for Biological Neural Network for Localisation of Sound in the Vertical Plane

We build a computational rate model for a biological neural network found in mammals that is thought to be important in the localisation of the sound in the vertical plane. We find the response of neurons in the brain stem that participate in the localisation neural circuit to pure tones, broad band noise and notched noise and compare them to experimentally obtained response of these neurons. Our model is able to reproduce the sensitivity of these neurons in the brain stem to spectral properties of sounds that are important in localisation. This is the first rate based population model that elucidates all the response properties of the neurons in the vertical localisation pathway to our knowledge.

neuroscience↗

Dynamics of the COVID -19 Related Publications

BackgroundThis study aims to analyze the dynamics of the published articles and preprints of Covid-19 related literature from different scientific databases and sharing platforms. MethodsThe PubMed, Elsevier, and Research Gate (RG) databases were under consideration in this study over a specific time. Analyses were carried out on the number of publications as (a) function of time (day), (b) journals and (c) authors. Doubling time of the number of publications was analyzed for PubMed "all articles" and Elsevier published articles. Analyzed databases were (1A) PubMed "all articles" (01/12/2019-12/06/2020) (1B) PubMed Review articles (01/12/2019-2/5/2020) and (1C) PubMed Clinical Trials (01/01/2020-30/06/2020) (2) Elsevier all publications (01/12/2019-25/05/2020) (3) RG (Article, Pre Print, Technical Report) (15/04/2020-30/4/2020). FindingsTotal publications in the observation period for PubMed, Elsevier, and RG were 23000, 5898 and 5393 respectively. The average number of publications/day for PubMed, Elsevier and RG were 70.0 {+/-}128.6, 77.6{+/-}125.3 and 255.6{+/-}205.8 respectively. PubMed shows an avalanche in the number of publication around May 10, number of publications jumped from 6.0{+/-}8.4/day to 282.5{+/-}110.3/day. The average doubling time for PubMed, Elsevier, and RG was 10.3{+/-}4 days, 20.6 days, and 2.3{+/-}2.0 days respectively. In PubMed average articles/journal was 5.2{+/-}10.3 and top 20 authors representing 935 articles are of Chinese descent. The average number of publications per author for PubMed, Elsevier, and RG was 1.2{+/-}1.4, 1.3{+/-}0.9, and 1.1{+/-}0.4 respectively. Subgroup analysis, PubMed review articles mean and median review time for each article were <0|17{+/-}17|77> and 13.9 days respectively; and reducing at a rate of-0.21 days (count)/day. InterpretationAlthough the disease has been known for around 6 months, the number of publications related to the Covid-19 until now is huge and growing very fast with time. It is essential to rationalize the publications scientifically by the researchers, authors, reviewers, and publishing houses. FundingNone

scientific communication and education↗

Dengue virus sustains viability of infected cells by counteracting apoptosis-mediated DNA breakage

NS1, a virotoxin, abundantly present in Dengue patients blood, is a major player behind disease patho-biogenesis including plasma leakage and damage to the liver. Despite the presence of NS1 in blood, Dengue is asymptomatic and self-limiting in [&ge;]80% Dengue virus (DV) infected people. We investigated this observation and found that plasmid-mediated NS1 expression and secretion in liver cells (Huh7) are sufficient to cause programmed cell death (apoptosis) and associated cellular DNA breakage. However, liver or kidney cell lines infected with DV and secreting equivalent amounts of NS1 didnt exhibit apoptotic DNA breakage. In fact, DV-infected cells showed better survival than cells in which only NS1 was transiently expressed by transfection. We also found that DV can even prevent chemical-induced apoptotic DNA damage in infected host cells. So, DV thwarts host antiviral defence i.e. apoptosis, by counteracting cellular DNA breakages and keeps the infected cells metabolically active to prolong virus replication.

microbiology↗

Spatial receptive field structure of double-opponent and simple cells in macaque primary visual cortex

The spatial processing of color is important for visual perception. Double-opponent (DO) cells likely contribute to this processing by virtue of their spatially opponent and cone-opponent receptive fields (RFs). However, the representation of visual features by DO cells in the primary visual cortex of primates is unclear because the spatial structure of their RFs has not been fully characterized. To fill this gap, we mapped the RFs of DO cells in awake macaques with colorful, dynamic white noise patterns. The spatial RF of each neuron was fitted with a Gabor function and a Difference of Gaussians (DoG) function. The Gabor function provided the more accurate description for most DO cells, a result that is incompatible with the traditionally assumed center-surround RF organization. A slightly modified (non-concentric) DoG function, in which the RFs have a circular center and a crescent-shaped surround, performed nearly as well as the Gabor model. For comparison, we also measured the RFs of simple cells. We found that the superiority of the Gabor fits over DoG fits was slightly more decisive for simple cells than for DO cells. The implications of these results on biological image processing and visual perception are discussed.

neuroscience↗

Bacterial Hyperswarming as a Protective Response to Intestinal Stress

Bacterial swarming, a collective movement on a surface, has rarely been associated with human pathophysiology. Here, we report for the first time that bacterial swarmers are associated with protection against intestinal inflammation. We show that bacterial swarmers are highly predictive of intestinal stress in mice and humans. We isolated a novel Enterobacter swarming strain, SM3, from mouse feces. SM3 and other known commensal swarmers contrast to their respective swarming-deficient, but swimming-competent isogenic strains abrogated intestinal inflammation in mice. Treatment of colitic mice with SM3, but not its mutants, enriched beneficial fecal anaerobes belonging to the family, Bacteroidales S24-7. We observed SM3 swarming associated pathways in the in vivo fecal metatranscriptomes. In vitro growth of S24-7 was enriched in presence of SM3 or its mutants conjecturing that bacterial swarming in vivo might influence SM3s access to S24-7 in the intestines. Overall, our work identifies a new paradigm in which intestinal stress allows for the emergence of swarming bacteria, which can counterintuitively heal intestinal inflammation.

microbiology↗

Bite size of Caenorhabditis elegans regulates feeding, satiety and development on yeast diet

In the wild, the soil dwelling nematode Caenorhabditis elegans primarily feeds on microbes which are abundant in rotting vegetation. Recent published studies showthat several Gram-positive and Gram-negative bacterial populations predominantly constitutes the C. elegans gut microbiome but surprisingly lack any yeast species. Here, we show that C. elegans display low satiety on yeast diet of Cryptococcus neoformans, C. laurentii or S. cerevisiae. We found that average size of budding yeast cells is much larger than E. coli cells. Yeast cells also cause pharyngeal obstruction, diminished feeding, and lower level of neutral lipids in adult C. elegans. Using scanning electron microscopy, we show that the mouth size of C. elegans larvae is smaller than average yeast cell. The larvae have no detectable yeast in their alimentary canal and they undergo delayed development on yeast diet. We propose that microbial cell size or bite size could be one of the crucial factors in regulation of feeding in C. elegans.\n\nIMPORTANCEThe microbiome in C. elegans gut is composed of diverse genera of bacteria but it lacks yeast and other fungi. In this study, we provide evidence that yeast cell size is bigger than the mouth size of C. elegans larvae. We propose that \"bigger than the bite size of yeast cells is one possible reason for low satiety on yeast diet, reduced feeding, lower stored lipids and delayed development. The bite size threshold imposed by C. elegans mouth can, partly, explain absence of yeast in C. elegans native gut microbiome and \"bite size can be studied further as a determinant of microbiome diversity in other animals.

microbiology↗

Antidiabetic drugs “gliptin” affect biofilm formation by the cariogenic bacterium Streptococcus mutans through inhibition of the bacterial DPP IV-like enzyme

Streptococcus mutans, a dental caries causing odontopathogen, produces X-prolyl dipeptidyl peptidase (Sm-XPDAP, encoded by pepX), a serine protease known to have a nutritional role. Considering the potential of proteases as therapeutic targets in pathogens, this study was primarily aimed at investigating the role of Sm-XPDAP in contributing to virulence-related traits. Dipeptidyl peptidase (DPP IV), an XPDAP analogous enzyme found in mammalian tissues, is a well known therapeutic target in Type II diabetes. Based on the hypothesis that gliptins, commonly used as anti-human-DPP IV drugs, may affect bacterial growth upon inhibition of Sm-XPDAP, we have determined their ex vivo antimicrobial and anti-biofilm activity towards S. mutans. All three DPP IV drugs tested reduced biofilm formation as determined by crystal violet staining. To link the observed biofilm inhibition to the human-DPP IV analogue present in S. mutans UA159, a pepX isogenic mutant was generated. In addition to reduced biofilm formation, CLSM studies of the biofilm formed by the pepX isogenic mutant showed these were comparable to those formed in the presence of saxagliptin, suggesting a probable role of this enzyme in biofilm formation by S. mutans UA159. The effects of both pepX deletion and DPP IV drugs on the proteome were studied using LC-MS/MS. Overall, this study highlights the potential of Sm-XPDAP as a novel anti-biofilm target and suggests a template molecule to synthesize lead compounds effective against this enzyme.

microbiology↗

Soft drug-resistant ovarian cancer cells invade via two distinct mechanisms utilizing myosin IIB

The failure of chemotherapeutic drugs in treatment of various cancers is attributed to the acquisition of drug resistance. However, the invasion mechanisms of drug-resistant cancer cells remains incompletely understood. Here we address this question from a biophysical perspective by mapping the phenotypic alterations in ovarian cancer cells (OCCs) resistant to cisplatin and paclitaxel. We show that cisplatin-resistant (CisR), paclitaxel-resistant (PacR) and dual drug-resistant (i.e., resistant to both drugs) OCCs are softer and more contractile than drug-sensitive cells. Protease inhibition suppresses invasion of CisR cells but not of PacR and dual cells, suggesting protease-dependent mode of invasion in CisR cells and protease-independent mode in PacR and dual cells. Despite these differences, actomyosin contractility, mediated by the RhoA-ROCK2-Myosin IIB signaling pathway regulates both modes of invasion. Myosin IIB modulates matrix metalloproteinase-9 (MMP-9) secretion in CisR cells and nuclear squeezing in PacR and dual cells, thereby highlighting its importance as a potential therapeutic target for treatment of drug-resistant ovarian cancer cells.\n\nFinancial SupportAuthors acknowledge financial support from IIT Bombay Healthcare Initiative, CSIR andDepartment of Biotechnology (Govt. of India) (Grant # BT/PR14658/MED/31/107/2010).AK and BTwere supported by fellowships from UGC and CSIR respectively (Govt. of India).\n\nAuthors declare no competing financial interests\n\nAuthor contributions: AK, PR and SS designed the experiments. AK performed most of the experiments and analyzed the data.BT and SG developed drug resistant cell lines and did RT-PCR. MM performed western blot. AD performed AFM experiments. SD performed gelatin zymography. ABB, PM, AM and AD helped with live cell imaging experiments. AK and SS wrote the manuscript. All authors read and approved the final manuscript.\n\nSummary statement: This study identifies drug-specific differences in the modes of invasion utilized by ovarian cancer cells, and demonstrates the role of myosin IIB in regulating both modes of invasion.

biophysics↗