Uncovering local aggregated air quality index with smartphone captured images leveraging efficient deep convolutional neural network

The prevalence and mobility of smartphones make these a widely used tool for environmental health research. However, their potential for determining aggregated air quality index (AQI) based on PM2.5 concentration in specific locations remains largely unexplored in the existing literature. In this paper, we thoroughly examine the challenges associated with predicting location-specific PM2.5 concentration using images taken with smartphone cameras. The focus of our study is on Dhaka, the capital of Bangladesh, due to its significant air pollution levels and the large population exposed to it. Our research involves the development of a Deep Convolutional Neural Network (DCNN), which we train using over a thousand outdoor images taken and annotated. These photos are captured at various locations in Dhaka, and their labels are based on PM2.5 concentration data obtained from the local US consulate, calculated using the NowCast algorithm. Through supervised learning, our model establishes a correlation index during training, enhancing its ability to function as a Picture-based Predictor of PM2.5 Concentration (PPPC). This enables the algorithm to calculate an equivalent daily averaged AQI index from a smartphone image. Unlike, popular overly parameterized models, our model shows resource efficiency since it uses fewer parameters. Furthermore, test results indicate that our model outperforms popular models like ViT and INN, as well as popular CNN-based models such as VGG19, ResNet50, and MobileNetV2, in predicting location-specific PM2.5 concentration. Our dataset is the first publicly available collection that includes atmospheric images and corresponding PM2.5 measurements from Dhaka. Our code and dataset will be made public when publishing the paper.Comment: 18 pages, 7 figures, submitted to Nature Scientific Report

Novel therapeutics against breast cancer stem cells by targeting surface markers and signaling pathways

Background: Breast cancer remains to be one of the deadliest forms of cancers, owing to the drug resistance and tumor relapse caused by breast cancer stem cells (BCSCs) despite notable advancements in radio-chemotherapies. Objectives: To find out novel therapeutics against breast cancer stem cells by aiming surface markers and signaling pathways. Methods: A systematic literature search was conducted through various electronic databases including, Pubmed, Scopus, Google scholar using the keywords "BCSCs, surface markers, signaling pathways and therapeutic options against breast cancer stem cell. Articles selected for the purpose of this review were reviewed and extensively analyzed. Results: Novel therapeutic strategies include targeting BCSCs surface markers and aberrantly activated signaling pathways or targeting their components, which play critical roles in self-renewal and defense, have been shown to be significantly effective against breast cancer. In this review, we represent a number of ways against BCSCs surface markers and hyper-activated signaling pathways to target this highly malicious entity of breast cancer more effectively in order to make a feasible and useful strategy for successful breast cancer treatment. In addition, we discuss some characteristics of BCSCs in disease progression and therapy resistance. Conclusion: BCSCs involved in cancer pathogenesis, therapy resistance and cancer recurrence. Thus, it is suggested that a multi-dimensional therapeutic approach by targeting surface markers and aberrantly activated signaling pathways of BCSCs alone or in combination with each other could really be worthwhile in the treatment of breast cancer

Electrochemical Detection of FAM134B Mutations in Oesophageal Cancer Based on DNA-Gold Affinity Interactions

nexpensive, simple and rapid DNA sensors capable of accurate and sensitive detection of cancer specific point mutations in DNA biomarkers are crucial for the routine screening of genetic mutations in cancer. Conventional approaches based on sequencing, mass spectroscopy, and fluorescence are highly effective, but they are tedious, slow and require labels and expensive equipment. Recent electrochemistry based approaches mostly rely on conventional DNA biosensing using recognition and transduction layers, and hence limited by the complicated steps of sensor fabrication associated with surface cleaning, self-assembled monolayer formation, and target hybridization. Herein we report a relatively simple and inexpensive method for detecting point mutation in cancer by using the direct adsorption of purified DNA sequences onto an unmodified gold surface. The method relies on the base dependent affinity interaction of DNA with gold. Since the affinity interaction (adsorption) trend of DNA bases follows as adenine (A) > cytosine (C) > guanine (G)> thymine (T), two DNA sequences with different DNA base compositions (i. e., amplified mutated sequences will be distinctly different than its original sequence) will have different adsorption affinity towards gold. The amount of mutation sites on a DNA sequence is quantified by monitoring the electrochemical current as a function of the relative adsorption level of DNA samples onto a bare gold electrode. This method can successfully distinguish single point mutation in DNA from oesophageal cancer. We demonstrated the clinical utility of this approach by detecting different levels of mutations in tissue samples (n=9) taken from oesophageal cancer patients. Finally, the method was validated with High Resolution Melt (HRM) curve analysis and Sanger Sequencing.Office of the Snr Dep Vice Chancellor, Institute for GlycomicsNo Full Tex

Fenugreek seed powder protects mice against arsenic-induced neurobehavioral changes

The current study was designed to evaluate the protective effect of fenugreek seed powder against As-induced neurobehavioral and biochemical perturbations using a mouse model. Mice exposed to arsenic at 10 mg/kg body weight showed development of anxiety-like behavior and memory impairment compared to control mice in elevated plus maze and Morris water maze tests, respectively. A significantly decreased acetyl and butyrylcholinesterase, superoxide dismutase and glutathione reductase activities and brain-derived neurotrophic factor levels were found in the brain of arsenic-exposed mice compared to control mice. Interestingly, supplementation of fenugreek seed powder to arsenic-treated mice significantly restored the activity of cholinesterase and antioxidant enzymes (e.g. superoxide dismutase, glutathione reductase) as well as brain-derived neurotrophic factor levels in the brain tissue of arsenic-exposed mice. Consequently, reduced anxiety-like behavior, improved learning and memory were observed in fenugreek supplemented arsenic treated mice compared to only arsenic-exposed mice group. Thus, this study suggests that fenugreek seed powder reduces arsenic-induced neurotoxicity in mice

An electrochemical method for sensitive and rapid detection of FAM134B protein in colon cancer samples.

Despite the excellent diagnostic applications of the current conventional immunoassay methods such as ELISA, immunostaining and Western blot for FAM134B detection, they are laborious, expensive and required a long turnaround time. Here, we report an electrochemical approach for rapid, sensitive, and specific detection of FAM134B protein in biological (colon cancer cell extracts) and clinical (serum) samples. The approach utilises a differential pulse voltammetry (DPV) in the presence of the [Fe(CN)6]3−/4− redox system to quantify the FAM134B protein in a two-step strategy that involves (i) initial attachment of FAM134B antibody on the surface of extravidin-modified screen-printed carbon electrode, and (ii) subsequent detection of FAM134B protein present in the biological/clinical samples. The assay system was able to detect FAM134B protein at a concentration down to 10 pg μL−1 in phosphate buffered saline (pH 7.4) with a good inter-assay reproducibility (% RSD = <8.64, n = 3). We found excellent sensitivity and specificity for the analysis of FAM134B protein in a panel of colon cancer cell lines and serum samples. Finally, the assay was further validated with ELISA method. We believe that our assay could potentially lead a low-cost alternative to conventional immunological assays for target antigens analysis in point-of-care applications

Natural compounds targeting cancer stem cells: a promising resource for chemotherapy

Background: Cancer Stem Cells (CSCs) are the subpopulation of cancer cells which are directly involved in drug resistance, metastases to distant organ and cancer recurrence.Methods: A systematic literature search was conducted through various electronic databases including, Pubmed, Scopus, Google scholar using the keywords "cancer stem cells" and "natural compounds" in the present study. Articles published between 1999 and 2019 were reviewed. All the expositions concerning CSCs associated cancer pathogenesis and therapy resistance, as well as targeting these properties of CSCs by natural compounds were selected for the current study.Results: Natural compounds have always been thought as a rich source of biologically active principles, which target aberrantly activated signaling pathways and other modalities of CSCs, while tethering painful side effects commonly involved in the first-line and second-line chemo-radiotherapies. In this review, we have described the key signaling pathways activated in CSCs to maintain their survival and highlighted how natural compounds interrupt these signaling pathways to minimize therapy resistance, pathogenesis and cancer recurrence properties of CSCs, thereby providing useful strategies to treat cancer or aid in cancer therapy improvement. Like normal stem cells, CSCs rely on different signaling pathways and other properties for their maintenance. Therefore, the success of cancer treatment depends on the development of proper anti-neoplastic drugs capable of intercepting those signaling pathways as well as other properties of CSCs in order to eradicate this evasive subpopulation of cancer cells.Conclusion: Compounds of natural origin might act as an outstanding source to design novel therapies against cancer stem cells

Optical biosensing strategies for DNA methylation analysis

DNA methylation is an epigenetic modification of DNA, where a methyl group is added at the fifth carbon of the cytosine base to form 5 methyl cytosine (5mC) without altering the DNA sequences. It plays important roles in regulating many cellular processes by modulating key genes expression. Alteration in DNA methylation patterns becomes particularly important in the aetiology of different diseases including cancers. Abnormal methylation pattern could contribute to the pathogenesis of cancer either by silencing key tumor suppressor genes or by activating oncogenes. Thus, DNA methylation biosensing can help in the better understanding of cancer prognosis and diagnosis and aid the development of therapies. Over the last few decades, a plethora of optical detection techniques have been developed for analyzing DNA methylation using fluorescence, Raman spectroscopy, surface plasmon resonance (SPR), electrochemiluminescence and colorimetric readouts. This paper aims to comprehensively review the optical strategies for DNA methylation detection. We also present an overview of the remaining challenges of optical strategies that still need to be focused along with the lesson learnt while working with these techniques

Roles of long noncoding RNA in triple‐negative breast cancer

Abstract Introduction Long noncoding RNAs (lncRNAs) play crucial roles in regulating various hallmarks in cancers. Triple‐negative (Estrogen receptor, ER; Human epidermal growth factor receptor 2, HER2; Progesterone receptor, PR) breast cancer (TNBC) is the most aggressive form of breast cancers with a poor prognosis and no available molecular targeted therapy. Methods We reviewed the current literature on the roles of lncRNAs in the pathogenesis, therapy resistance, and prognosis of patients with TBNC. Results LncRNAs are associated with TNBC pathogenesis, therapy resistance, and prognosis. For example, lncRNAs such as small nucleolar RNA host gene 12 (SNHG12), highly upregulated in liver cancer (HULC) HOX transcript antisense intergenic RNA (HOTAIR), lincRNA‐regulator of reprogramming (LincRNA‐ROR), etc., are aberrantly expressed in TNBC and are involved in the pathogenesis of the disease. LncRNAs act as a decoy, scaffold, or sponge to regulate the expression of genes, miRNAs, and transcription factors associated with pathogenesis and progression of TNBC. Moreover, lncRNAs such as ferritin heavy chain 1 pseudogene 3 (FTH1P3), BMP/OP‐responsive gene (BORG) contributes to the therapy resistance property of TNBC through activating ABCB1 (ATP‐binding cassette subfamily B member 1) drug efflux pumps by increasing DNA repair capacity or by inducing signaling pathway involved in therapeutic resistance. Conclusion In this review, we outline the functions of various lncRNAs along with their molecular mechanisms involved in the pathogenesis, therapeutic resistance of TBNC. Also, the prognostic implications of lncRNAs in patients with TNBC is illustrated. Moreover, potential strategies targeting lncRNAs against highly aggressive TNBC is discussed in this review

Plasticity of cancer stem cell: origin and role in disease progression and therapy resistance

In embryonic development and throughout life, there are some cells can exhibit phenotypic plasticity. Phenotypic plasticity is the ability of cells to differentiate into multiple lineages. In normal development, plasticity is highly regulated whereas cancer cells re-activate this dynamic ability for their own progression. The re-activation of these mechanisms enables cancer cells to acquire a cancer stem cell (CSC) phenotype- a subpopulation of cells with increased ability to survive in a hostile environment and resist therapeutic insults. There are several contributors fuel CSC plasticity in different stages of disease progression such as a complex network of tumour stroma, epidermal microenvironment and different sub-compartments within tumour. These factors play a key role in the transformation of tumour cells from a stable condition to a progressive state. In addition, flexibility in the metabolic state of CSCs helps in disease progression. Moreover, epigenetic changes such as chromatin, DNA methylation could stimulate the phenotypic change of CSCs. Development of resistance to therapy due to highly plastic behaviour of CSCs is a major cause of treatment failure in cancers. However, recent studies explored that plasticity can also expose the weaknesses in CSCs, thereby could be utilized for future therapeutic development. Therefore, in this review, we discuss how cancer cells acquire the plasticity, especially the role of the normal developmental process, tumour microenvironment, and epigenetic changes in the development of plasticity. We further highlight the therapeutic resistance property of CSCs attributed by plasticity. Also, outline some potential therapeutic options against plasticity of CSCs. [Figure not available: see fulltext.]