A NOVEL METHOD FOR EDGE DETECTION USING BLOCK TRUNCATION CODING AND CONVOLUTION TECHNIQUE FOR MAGNETIC RESONANCE IMAGES(MRI) WITH PERFORMANCE MEASURES

In this paper, we propose a novel method to detect edges in digital images. Attention is given to magnetic resonance images (MRI) of the brain in particular.  Edge detection using block truncation coding and convolution technique are presented. The results are compared with the standard edge detection  Canny method . The results of this study are presented and discussed

Monitoring and forecasting of intensive convective precipitation with the use of the mobile meteorological radar (MMR50)

This paper is focused on current possibilities of the measurement and predictions of intense convective precipitation through the mobile meteorological radar (MMR50). This meteorological radar equipment is part of the Information, Notification and Warning system of the Zlin Region in the Czech Republic, which consists of information and communication infrastructure for dealing with extraordinary events. The first chapter describes basic principles of radar precipitation measurement, e.g. radar estimate of rainfall intensity and radar products. The second chapter presents a methodology of measuring and predicting of intense convective precipitation using the mobile meteorological radar (MMR50), including other possibilities of precipitation forecast as NWP models, aerological, satellite, station measurements, statistics of historical situations, the risk of flash floods on the degree of soils saturation and the possibility of observation of dangerous accompanying phenomena. The last chapter deals with the verification of the principles of radar measurements and forecasts in a case study on 24th July 2015. Torrential rainfall in a combination with hail and strong wind gusts caused heavy flooding in the central part of Zlin region, which caused considerable material damage. Timely and quality information about the current and future formation and development of intense convective precipitation is essential for flood prevention measures. Acquired findings and conclusions can be used for crisis management in case of a possible occurrence of flash floods.Internal Grant Agency of Tomas Bata University [IGA/ FAI/2016/023

Metabolic characterization of aggressive breast cancer cells exhibiting invasive phenotype: impact of non-cytotoxic doses of 2-DG on diminishing invasiveness

Background: Metabolic reprogramming is being recognized as a fundamental hallmark of cancer, and efforts to identify drugs that can target cancer metabolism are underway. In this study, we used human breast cancer (BC) cell lines and established their invading phenotype (INV) collected from transwell inserts to compare metabolome differences and evaluate prognostic significance of the metabolome in aggressive BC invasiveness.Methods: The invasiveness of seven human BC cell lines were compared using the transwell invasion assay. Among these, INV was collected from SUM149, which exhibited the highest invasiveness. Levels of metabolites in INV were compared with those of whole cultured SUM149 cells (WCC) using CE-TOFMS. The impact of glycolysis in INV was determined by glucose uptake assay using fluorescent derivative of glucose (2-NBDG), and significance of glycolysis, or tricarboxylic acid cycle (TCA) and electron transport chain (ETC) in the invasive process were furtherdetermined in aggressive BC cell lines, SUM149, MDA-MB-231, HCC1937, using invasion assays in the presence or absence of inhibitors of glycolysis, TCA cycle or ETC.Results: SUM149 INV sub-population exhibited a persistent hyperinvasive phenotype. INV were hyper-glycolytic with increased glucose (2-NBDG) uptake; diminished glucose-6-phosphate (G6P) levels but elevated pyruvate and lactate, along with higher expression of phosphorylated-pyruvate dehydrogenase (pPDH) compared to WCC. Notably, inhibiting of glycolysis with lower doses of 2-DG (1 mM), non-cytotoxic to MDA-MB-231 and HCC1937, was effective in diminishing invasiveness of aggressive BC cell lines. In contrast, 3-Nitropropionic acid (3-NA), an inhibitor of succinate dehydrogenase, the enzyme that oxidizes succinate to fumarate in TCA cycle, and functions as complex II of ETC, had no significant effect on their invasiveness, although levels of TCA metabolites or detection ofmitochondrial membrane potential with JC-1 staining, indicated that INV cells originally had functional TCA cycles and membrane potential.Conclusions: Hyper-glycolytic phenotype of invading cells caters to rapid energy production required for invasion while TCA cycle/ETC cater to cellular energy needs for sustenance in aggressive BC. Lower, non-cytotoxic doses of 2-DG can hamper invasion and can potentially be used as an adjuvant with other anti-cancer therapies without the usual side-effects associated with cytotoxic doses

Additional file 2: Table S1 and S2. of Selective mode of action of plumbagin through BRCA1 deficient breast cancer stem cells

Table S1.  The fold change values generated using the GeneSpring software after Microarray analysis of the HCC1937 mammospheres in comparison to the HCC1937/wt BRCA1 mammospheres and are indicative of the genes whose expression is directly or indirectly linked to BRCA1. Table S2. IC50 values of Plumbagin (PB) and Carboplatin (CP). (DOCX 11 kb

Additional file 1: Figure S1. of Selective mode of action of plumbagin through BRCA1 deficient breast cancer stem cells

Contour plot showing the distinct CD44high/24- population (indicated by black arrow) in HCC1937/wt BRCA1 cell line in support of Fig. 2a. Here, the existence of the CD44high/24-/low cell sub population possessing mesenchymal properties in HCC1937/wt BRCA1 is more evident. (B) Expression and localization of BRCA1 in HCC1937 and HCC1937/wt BRCA1 cell lines. (TIF 27522 kb

Additional file 4: Figure S3. of Selective mode of action of plumbagin through BRCA1 deficient breast cancer stem cells

Cytotoxic effect (by MTT assay) of PB (24 h treatment) in HCC1937 (A) and HCC1937/wt BRCA1 (B) after the siRNA mediated blocking of BRCA1. HCC1937 and HCC1937/wt BRCA1 cells were treated for 48 h with full length 2.4pM siRNA for BRCA1 (Eurogentec, Liège, Belgium) (siRNA Sense (+dTdT), 19 bases in length, BRCA1 position 1857–1879, GGUCAAGUGAUGAAUAUUA) as per manufacturer’s instructions followed by treatment with PB for 24 h. (TIF 9107 kb

Role of nitric oxide in pancreatic cancer cells exhibiting the invasive phenotype

Pancreatic cancer is a highly metastatic tumor with an extremely low 5-year survival rate. Lack of efficient diagnostics and dearth of effective therapeutics that can target the cancer as well as the microenvironment niche are the reasons for limited success in treatment and management of this disease. Cell invasion through extracellular matrix (ECM) involves the complex regulation of adhesion to and detachment from ECM and its understanding is critical to metastatic potential of pancreatic cancer. To understand the characteristics of these cancer cells and their ability to metastasize, we compared human pancreatic cancer cell line, PANC-1 and its invading phenotype (INV) collected from transwell inserts. The invasive cell type, INV, exhibited higher resistance to Carbon-ion radiation compared to whole cultured (normally dish-cultured) PANC-1 (WCC), and had more efficient in vitro spheroid formation capability. Invasiveness of INV was hampered by nitric oxide synthase (NOS) inhibitors, suggesting that nitric oxide (NO) plays a cardinal role in PANC-1 invasion. In addition, in vitro studies indicated that a MEK-ERK-dependent, JAK independent mechanism through which NOS/NO modulate PANC-1 invasiveness. Suspended INV showed enhanced NO production as well as induction of several pro-metastatic, and stemness-related genes. NOS inhibitor, l-NAME, reduced the expression of these pro-metastatic or stemness-related genes, and dampened spheroid formation ability, suggesting that NO can potentially influence pancreatic cancer aggressiveness. Furthermore, xenograft studies with INV and WCC in NSG mouse model revealed a greater ability of INV compared to WCC, to metastasize to the liver and l-NAME diminished the metastatic lesions in mice injected with INV. Overall, data suggest that NO is a key player associated with resistance to radiation and metastasis of pancreatic cancer; and inhibition of NOS demonstrates therapeutic potential as observed in the animal model by specifically targeting the metastatic cells that harbor stem-like features and are potentially responsible for relapse. Keywords: Nitric oxide, Nitric oxide synthase, Pancreatic cancer, Invasion, Metastasis, Cancer stem cel

Additional file 3: Figure S2. of Selective mode of action of plumbagin through BRCA1 deficient breast cancer stem cells

Expression and localization of BRCA1 in HCC1937 and HCC1937/wt BRCA1 cell lines by immunofluorescence and western blotting. Quantitation of BRCA1 expression normalized with β-actin in western blot by densitometry analysis is also indicated. (TIF 28769 kb

Role of nitric oxide in pancreatic cancer cells exhibiting the invasive phenotype.

Pancreatic cancer is a highly metastatic tumor with an extremely low 5-year survival rate. Lack of efficient diagnostics and dearth of effective therapeutics that can target the cancer as well as the microenvironment niche are the reasons for limited success in treatment and management of this disease. Cell invasion through extracellular matrix (ECM) involves the complex regulation of adhesion to and detachment from ECM and its understanding is critical to metastatic potential of pancreatic cancer. To understand the characteristics of these cancer cells and their ability to metastasize, we compared human pancreatic cancer cell line, PANC-1 and its invading phenotype (INV) collected from transwell inserts. The invasive cell type, INV, exhibited higher resistance to Carbon-ion radiation compared to whole cultured (normally dish-cultured) PANC-1 (WCC), and had more efficient in vitro spheroid formation capability. Invasiveness of INV was hampered by nitric oxide synthase (NOS) inhibitors, suggesting that nitric oxide (NO) plays a cardinal role in PANC-1 invasion. In addition, in vitro studies indicated that a MEK-ERK-dependent, JAK independent mechanism through which NOS/NO modulate PANC-1 invasiveness. Suspended INV showed enhanced NO production as well as induction of several pro-metastatic, and stemness-related genes. NOS inhibitor, l-NAME, reduced the expression of these pro-metastatic or stemness-related genes, and dampened spheroid formation ability, suggesting that NO can potentially influence pancreatic cancer aggressiveness. Furthermore, xenograft studies with INV and WCC in NSG mouse model revealed a greater ability of INV compared to WCC, to metastasize to the liver and l-NAME diminished the metastatic lesions in mice injected with INV. Overall, data suggest that NO is a key player associated with resistance to radiation and metastasis of pancreatic cancer; and inhibition of NOS demonstrates therapeutic potential as observed in the animal model by specifically targeting the metastatic cells that harbor stem-like features and are potentially responsible for relapse

Understanding the tumour micro-environment communication network from an NOS2/COX2 perspective.

Recent findings suggest that co-expression of NOS2 and COX2 is a strong prognostic indicator in triple-negative breast cancer patients. These two key inflammation-associated enzymes are responsible for the biosynthesis of NO and PGE , respectively, and can exert their effect in both an autocrine and paracrine manner. Impairment of their physiological regulation leads to critical changes in both intra-tumoural and intercellular communication with the immune system and their adaptation to the hypoxic tumour micro-environment. Recent studies have also established a key role of NOS2-COX2 in causing metabolic shift. This review provides an extensive overview of the role of NO and PGE in shaping communication between the tumour micro-environment composed of tumour and immune cells that in turn favours tumour progression and metastasis. LINKED ARTICLES: This article is part of a themed section on Nitric Oxide 20 Years from the 1998 Nobel Prize. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v176.2/issuetoc