Boosting Principal Component Analysis by Genetic Algorithm

This paper presents a new method of feature extraction by combining principal component analysis and genetic algorithm. Use of multiple pre-processors in combination with principal component analysis generates alternate feature spaces for data representation. The present method works out the fusion of these multiple spaces to create higher dimensionality feature vectors. The fused feature vectors are given chromosome representation by taking feature components to be genes. Then these feature vectors are allowed to undergo genetic evolution individually. For genetic algorithm, initial population is created by calculating probability distance matrix, and by applying a probability distance metric such that all the genes which lie farther than a defined threshold are tripped to zero. The genetic evolution of fused feature vector brings out most significant feature components (genes) as survivours. A measure of significance is adapted on the basis of frequency of occurrence of the surviving genes in the current population. Finally, the feature vector is obtained by weighting the original feature components in proportion to their significance. The present algorithm is validated in combination with a neural network classifier based on error backpropagation algorithm, and by analysing a number of benchmark datasets available in the open sources.Defence Science Journal, 2010, 60(4), pp.392-398, DOI:http://dx.doi.org/10.14429/dsj.60.49

Assessment of oceanic tuna and allied fish resources of the Indian exclusive economic zone based on exploratory surveys

The present paper overview the results of survey on marine resources of the Indian EEZ including tuna and eillied fish species, their distribution, catch rates, seasonality, assessment of stocks etc. supplemented by the chartered vessels' data. The paper also presents the trends in the tuna fishing and future survey programme of the Fishery Survey of India

Analysis of Extended Threshold Wavelength Photoresponse in Nonsymmetrical p-GaAs/AlGaAs Heterostructure Photodetectors

We analyze the extended threshold wavelength photoresponse beyond the standard threshold limit (λt = 1.24/Δ, where Δ is the activation energy) in nonsymmetrical pGaAs/AlGaAs heterostructure photodetectors with a barrier energy offset. We propose that hot-cold hole carrier interactions in the p-GaAs absorber are responsible for the threshold wavelength extension. Experimental results are analyzed by considering a quasi-Fermi distribution of hot holes at a hot hole temperature (TH), which is much higher than the lattice temperature (TL). The experimental photoresponse is fitted using an escape cone model, modified with a quasi-Fermi level (EquasiF). The simulated results are found to be in good agreement with experimental data, justifying the model used

Pathological studies on Pteris cretica (L.) fern-Bovine Papilloma Virus infection in Syrian Golden Hamsters (Mesocricetus auratus)

Pteris cretica (L.) commonly known as Cretan brake is widely distributed in nature and considered as potential environmental carcinogen. However, only limited literature is available on this fern commonly taken by cattle while grazing. It is known that in cattle Bovine papilloma virus (BPV) induced benign tumours are converted into malignant with interaction of ptaquiloside (Pta) present in ferns. In the present investigation, we evaluated the pathological effects of P. cretica (PC)-BPV infection in laboratory model hamster. Though toxic principle Pta was detected in fern samples but quercetin could not be found. Tumours were successfully induced in hamsters by cutaneous wart suspension and histopathologically diagnosed as fibroma and lipofibroma. Histopathologically, hamsters showed mild to moderate vascular changes in vital organs, multiple cysts, degenerative changes, bile duct hyperplasia and necrosis in liver, haemorrhages and haemosiderosis in spleen, hypersecretory activity and prominent Peyer’s patches in ileum, degenerative changes and presence of eosinophilic casts in renal tubules. Ultrastructural study revealed apoptosis in hepatocytes, abundance of variable shaped mitochondria in renal tubular lining epithelial cells and enterocytes showed abundance of mitochondria and cytoplasmolysis in the fern fed groups. Almost all the hamsters from BPV, fern and virus infection (PC+BPV) groups developed similar type of tumorous growths. The visible growths in the hamsters of these groups were either single or double large sized except multiple tumorous growths in one hamster from PC+BPV group. However, multiple palpable subcutaneous nodules were developed at the site of scarification in all the hamsters of BPV and PC+BPV groups. Our findings suggest that the Pta containing P. cretica feeding induced hepatotoxic and nephrotoxic lesions in hamsters, but effects of P. cretica-BPV infection were found negligible

Analysis of Barrier Parameters on the Extended Threshold Wavelength of Infrared Detectors

The threshold wavelength (λt) of spectral photoresponse of any semiconductor photodetector is determined by the minimum energy gap (Δ=1.24/λt) of the material, or the interfacial energy gap of the heterostructure. It was shown before that the threshold limit can be extended beyond λt to obtain an extended threshold wavelength λeff(λeff≫λt) in detectors with a barrier energy offset (δEv) and a gradient. Here, in this letter, we analyze the effect of barrier parameters such as δEv and gradient on the extended threshold wavelength of infrared detectors for the temperature range up to 50 K

A transcriptomic snapshot of early molecular communication between Pasteuria penetrans and Meloidogyne incognita

© The Author(s). 2018Background: Southern root-knot nematode Meloidogyne incognita (Kofoid and White, 1919), Chitwood, 1949 is a key pest of agricultural crops. Pasteuria penetrans is a hyperparasitic bacterium capable of suppressing the nematode reproduction, and represents a typical coevolved pathogen-hyperparasite system. Attachment of Pasteuria endospores to the cuticle of second-stage nematode juveniles is the first and pivotal step in the bacterial infection. RNA-Seq was used to understand the early transcriptional response of the root-knot nematode at 8 h post Pasteuria endospore attachment. Results: A total of 52,485 transcripts were assembled from the high quality (HQ) reads, out of which 582 transcripts were found differentially expressed in the Pasteuria endospore encumbered J2 s, of which 229 were up-regulated and 353 were down-regulated. Pasteuria infection caused a suppression of the protein synthesis machinery of the nematode. Several of the differentially expressed transcripts were putatively involved in nematode innate immunity, signaling, stress responses, endospore attachment process and post-attachment behavioral modification of the juveniles. The expression profiles of fifteen selected transcripts were validated to be true by the qRT PCR. RNAi based silencing of transcripts coding for fructose bisphosphate aldolase and glucosyl transferase caused a reduction in endospore attachment as compared to the controls, whereas, silencing of aspartic protease and ubiquitin coding transcripts resulted in higher incidence of endospore attachment on the nematode cuticle. Conclusions: Here we provide evidence of an early transcriptional response by the nematode upon infection by Pasteuria prior to root invasion. We found that adhesion of Pasteuria endospores to the cuticle induced a down-regulated protein response in the nematode. In addition, we show that fructose bisphosphate aldolase, glucosyl transferase, aspartic protease and ubiquitin coding transcripts are involved in modulating the endospore attachment on the nematode cuticle. Our results add new and significant information to the existing knowledge on early molecular interaction between M. incognita and P. penetrans.Peer reviewedFinal Published versio

Structure Based Design and Synthesis of Peptide Inhibitor of Human LOX-12: In Vitro and In Vivo Analysis of a Novel Therapeutic Agent for Breast Cancer

Human breast cancer cell proliferation involves a complex interaction between growth factors, steroid hormones and peptide hormones. The interaction of growth factors, such as epidermal growth factor (EGF), with their receptors on breast cancer cells can lead to the hydrolysis of phospholipids and release of fatty acid such as arachidonic acid, which can be further metabolized by cyclooxygenase (COX) and lipoxygenase (LOX) pathways to produce prostaglandins. The high concentration of prostaglandins has been associated with chronic inflammatory diseases and several types of human cancers. This is due to the over expression COX, LOX and other inflammatory enzymes. Ten peptides were designed and synthesized by solid phase peptide synthesis and analyzed in vitro for enzyme inhibition. Out of these peptides, YWCS had shown significant inhibitory effects. The dissociation constant (KD) was determined by surface plasmon resonance (SPR) analysis and was found to be 3.39×10−8 M and 8.6×10−8 M for YWCS and baicalein (positive control), respectively. The kinetic constant Ki was 72.45×10−7 M as determined by kinetic assay. The peptide significantly reduced the cell viability of estrogen positive MCF-7 and estrogen negative MDA-MB-231 cell line with the half maximal concentration (IC50) of 75 µM and 400 µM, respectively. The peptide also induced 49.8% and 20.8% apoptosis in breast cancer cells MCF-7 and MDA-MB-231, respectively. The YWCS was also found to be least hemolytic at a concentration of 358 µM. In vivo studies had shown that the peptide significantly inhibits tumor growth in mice (p<0.017). This peptide can be used as a lead compound and complement for ongoing efforts to develop differentiation therapies for breast cancer

Pan-Cancer Analysis of lncRNA Regulation Supports Their Targeting of Cancer Genes in Each Tumor Context

Long noncoding RNAs (lncRNAs) are commonly dys-regulated in tumors, but only a handful are known toplay pathophysiological roles in cancer. We inferredlncRNAs that dysregulate cancer pathways, onco-genes, and tumor suppressors (cancer genes) bymodeling their effects on the activity of transcriptionfactors, RNA-binding proteins, and microRNAs in5,185 TCGA tumors and 1,019 ENCODE assays.Our predictions included hundreds of candidateonco- and tumor-suppressor lncRNAs (cancerlncRNAs) whose somatic alterations account for thedysregulation of dozens of cancer genes and path-ways in each of 14 tumor contexts. To demonstrateproof of concept, we showed that perturbations tar-geting OIP5-AS1 (an inferred tumor suppressor) andTUG1 and WT1-AS (inferred onco-lncRNAs) dysre-gulated cancer genes and altered proliferation ofbreast and gynecologic cancer cells. Our analysis in-dicates that, although most lncRNAs are dysregu-lated in a tumor-specific manner, some, includingOIP5-AS1, TUG1, NEAT1, MEG3, and TSIX, synergis-tically dysregulate cancer pathways in multiple tumorcontexts

Advanced material against human (Including Covid‐19) and plant viruses: nanoparticles as a feasible strategy

The SARS‐CoV‐2 virus outbreak revealed that these nano‐pathogens have the ability to rapidly change lives. Undoubtedly, SARS‐CoV‐2 as well as other viruses can cause important global impacts, affecting public health, as well as, socioeconomic development. But viruses are not only a public health concern, they are also a problem in agriculture. The current treatments are often ineffective, are prone to develop resistance, or cause considerable adverse side effects. The use of nanotechnology has played an important role to combat viral diseases. In this review three main aspects are in focus: first, the potential use of nanoparticles as carriers for drug delivery. Second, its use for treatments of some human viral diseases, and third, its application as antivirals in plants. With these three themes, the aim is to give to readers an overview of the progress in this promising area of biotechnology during the 2017–2020 period, and to provide a glance at how tangible is the effectiveness of nanotechnology against viruses. Future prospects are also discussed. It is hoped that this review can be a contribution to general knowledge for both specialized and non‐specialized readers, allowing a better knowledge of this interesting topic.REDES‐ANID. Grant Number: 180003 Universidad de La Frontera. Grant Number: DI20‐1003 FAPESP. Grant Numbers: 2018/08194‐2, 2018/02832‐7 CNPq. Grant Numbers: 404815/2018‐9, 313117/2019‐5 CONICYT/FAPESP. Grant Number: 2018/08194‐2 Coordenação de Aperfeiçoamento de Pessoal de Nível Superior. Grant Numbers: 001, ANID/FONDAP/15130015 FCT. Grant Number: PTDC/CTM‐TEX/28295/2017 FEDER POCI Portugal 2020 program COMPETE. Grant Number: UID/CTM/00264/2019 FCT/MCTE

Somatostatin Receptor 1 and 5 Double Knockout Mice Mimic Neurochemical Changes of Huntington's Disease Transgenic Mice

Selective degeneration of medium spiny neurons and preservation of medium sized aspiny interneurons in striatum has been implicated in excitotoxicity and pathophysiology of Huntington's disease (HD). However, the molecular mechanism for the selective sparing of medium sized aspiny neurons and vulnerability of projection neurons is still elusive. The pathological characteristic of HD is an extensive reduction of the striatal mass, affecting caudate putamen. Somatostatin (SST) positive neurons are selectively spared in HD and Quinolinic acid/N-methyl-D-aspartic acid induced excitotoxicity, mimic the model of HD. SST plays neuroprotective role in excitotoxicity and the biological effects of SST are mediated by five somatostatin receptor subtypes (SSTR1-5). and R6/2 mice. Conversely, the expression of somatostatin receptor subtypes, enkephalin and phosphatidylinositol 3-kinases were strain specific. SSTR1/5 appears to be important in regulating NMDARs, DARPP-32 and signaling molecules in similar fashion as seen in HD transgenic mice.This is the first comprehensive description of disease related changes upon ablation of G- protein coupled receptor gene. Our results indicate that SST and SSTRs might play an important role in regulation of neurodegeneration and targeting this pathway can provide a novel insight in understanding the pathophysiology of Huntington's disease