With an increasing demand for stringent security systems, automated identification of individuals based on biometric methods has been a major focus of research and development over the last decade. Biometric recognition analyses unique physiological traits or behavioral characteristics, such as an iris, face, retina, voice, fingerprint, hand geometry, keystrokes or gait. The iris has a complex and unique structure that remains stable over a person’s lifetime, features that have led to its increasing interest in its use for biometric recognition. In this study, we proposed a technique incorporating Principal Component Analysis (PCA) based on Discrete Wavelet Transformation (DWT) for the extraction of the optimum features of an iris and reducing the runtime needed for iris template classification. The idea of using DWT behind PCA is to reduce the resolution of the iris template. DWT converts an iris image into four frequency sub-bands. One frequency sub-band instead of four has been used for further feature extraction by using PCA. Our experimental evaluation demonstrates the efficient performance of the proposed technique.

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Background: Welding exposes different types of fumes, gases and radiant energy that can be potentially dangerous for unsafe welder's health. Welding fumes (WFs) are a significant problem among all those exposed. WFs are a complex mixture of metallic oxides, silicates and fluorides that may result in different health effects. If a welder inhales such fumes in large quantities over a long period of time, there is a risk of various neurodegenerative diseases (NDGDs) development. Methods: We developed quantitative frameworks to identify the genetic relationship of WFs and NDGDs. We analyzed Gene Expression microarray data from WFs exposed tissues and NDGDs including Parkinson's disease (PD), Alzheimer's disease (AD), Lou Gehrig's disease (LGD), Epilepsy disease (ED), Multiple Sclerosis disease (MSD) datasets. We constructed disease-gene relationship networks and identified dysregulated pathways, ontological pathways and protein-protein interaction sub-network using multilayer network topology and neighborhood-based benchmarking. Results: We observed that WFs shares 18, 16, 13, 19 and 19 differentially expressed genes with PD, AD, LGD, ED and MSD respectively. Gene expression dysregulation along with relationship networks, pathways and ontologic analysis showed that WFs are responsible for the progression of PD, AD, LGD, ED and MSD neurodegenerative diseases. Conclusion: Our developed network-based approach to analysis and investigate the genetic effects of welding fumes on PD, AD, LGD, ED and MSD neurodegenerative diseases could be helpful to understand the causal influences of WF exposure for the progression of the NDGDs.

Welding generates and releases fumes that are hazardous to human health. Welding fumes (WFs) are a complex mix of metallic oxides, fluorides and silicates that can cause or exacerbate health problems in exposed individuals. In particular, WF inhalation over an extended period carries an increased risk of cancer, but how WFs may influence cancer behaviour or growth is unclear. To address this issue we employed a quantitative analytical framework to identify the gene expression effects of WFs that may affect the subsequent behaviour of the cancers. We examined datasets of transcript analyses made using microarray studies of WF-exposed tissues and of cancers, including datasets from colorectal cancer (CC), prostate cancer (PC), lung cancer (LC) and gastric cancer (GC). We constructed gene-disease association networks, identified signaling and ontological pathways, clustered proteinprotein interaction network using multilayer network topology, and analyzed survival function of the significant genes using Cox proportional hazards (Cox PH) model and product-limit (PL) estimator. We observed that WF exposure causes altered expression of many genes (36, 13, 25 and 17 respectively) whose expression are also altered in CC, PC, LC and GC. Gene-disease association networks, signaling and ontological pathways, protein-protein interaction network, and survival functions of the significant genes suggest ways that WFs may influence the progression of CC, PC, LC and GC. This quantitative analytical framework has identified potentially novel mechanisms by which tissue WF exposure may lead to gene expression changes in tissue gene expression that affect cancer behaviour and, thus, cancer progression, growth or establishment. Welding processes join rigid material pieces (usually metal) at their contact interface by using high temperatures to cause fusion. This process can be hazardous because it exposes the operator to extremely toxic fumes and to radiant energy 1. The International Agency for Research on Cancer (IARC) has recognized WFs and UV radiation from welding as Group 1 carcinogens 2. WFs are mainly composed of metallic oxides, silicates and fluorides, including those of magnesium, manganese, zinc, aluminum, beryllium, copper, chromium, cadmium, lead, iron, nickel and vanadium 3 .

With an increasing demand for stringent security systems, automated identification of individuals based on biometric methods has been a major focus of research and development over the last decade. Biometric recognition analyses unique physiological traits or behavioral characteristics, such as an iris, face, retina, voice, fingerprint, hand geometry, keystrokes or gait. The iris has a complex and unique structure that remains stable over a person's lifetime, features that have led to its increasing interest in its use for biometric recognition. In this study, we proposed a technique incorporating Principal Component Analysis (PCA) based on Discrete Wavelet Transformation (DWT) for the extraction of the optimum features of an iris and reducing the runtime needed for iris templates classification. The idea of using DWT behind PCA is to reduce the resolution of the iris template. DWT converts an iris image into four frequency sub-bands. One frequency sub-band instead of four has been used for further feature extraction by using PCA. Our experimental evaluation demonstrates the efficient performance of the proposed technique.

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Background: Welding involves exposure to fumes, gases and radiant energy that can be hazardous to human health. Welding fumes (WFs) comprise a complex mixture of metallic oxides, silicates and fluorides that may result in different health effects. Inhalation of WFs in large quantities over a long periods may pose a risk of developing neurodegenerative diseases (NDGDs), but the nature of this risk is poorly understood. To address this we performed transcriptomic analysis to identify links between WF exposure and NDGDs. Methods: We developed quantitative frameworks to identify the gene expression relationships of WF exposure and NDGDs. We analyzed gene expression microarray data from fume-exposed tissues and NDGDs including Parkinson's disease (PD), Alzheimer's disease (AD), Lou Gehrig's disease (LGD), Epilepsy disease (ED) and multiple sclerosis disease (MSD) datasets. We constructed disease-gene relationship networks and identified dysregulated pathways, ontological pathways and protein-protein interaction sub-network using multilayer network topology and neighborhood-based benchmarking. Results: We observed that WF associated genes share 18, 16, 13, 19 and 19 differentially expressed genes with PD, AD, LGD, ED and MSD respectively. Gene expression dysregulation along with relationship networks, pathways and ontologic analysis indicate that WFs may be linked to the progression of these NDGDs. Conclusions: Our developed network-based approach to analysis and investigate the genetic effects of welding fumes on PD, AD, LGD, ED and MSD neurodegenerative diseases could be helpful to understand the causal influences of WF exposure for the progression of the NDGDs.

Background: The welding process releases potentially hazardous gases and fumes, mainly composed of metallic oxides, fluorides and silicates. Long term welding fume (WF) inhalation is a recognized health issue that carries a risk of developing chronic health problems, particularly respiratory system diseases (RSDs). Aside from general airway irritation, WFs may drive direct cellular responses in the respiratory system which increase risk of RSD, but these are not well understood. Methods: We developed a quantitative framework to identify gene expression effects of WFs that may affect RSD development. We analyzed gene expression microarray data from WF-exposed tissues and RSD-affected tissues, including chronic bronchitis (CB), asthma (AS), pulmonary edema (PE), lung cancer (LC) datasets. We built disease-gene (diseasome) association networks and identified dysregulated signaling and ontological pathways, and protein-protein interaction sub-network using neighborhood-based benchmarking and multilayer network topology. Results: We observed many genes with altered expression in WF-exposed tissues were also among differentially expressed genes (DEGs) in RSD tissues; for CB, AS, PE and LC there were 34, 27, 50 and 26 genes respectively. DEGs analysis, with disease association networks, pathways, ontological analysis and protein-protein interaction sub-network suggest significant links between WF exposure and the development of CB, AS, PE and LC. Conclusions: Our network-based analysis and investigation of the genetic links of WFs and RSDs confirm a number of genes and gene products are plausible participants in RSD development. Our results are a significant resource to identify causal influences on the development of RSDs, particularly in the context of WF exposure. † These authors hold joint first authorship of this work.