Secure authentication procedure with mobile device for ubiquitous health environments

Medical industries have brought Information Technology (IT) in their systems for both patients and medical staffs due to the numerous benefits of IT we experience at presently. Moreover, the Mobile healthcare (M-health) system has been developed as the first step of Ubiquitous Health Environment (UHE). With the mobility and multi-functions, M-health system will be able to provide more efficient and various services for both doctors and patients. Due to the invisible feature of mobile signals, hackers have easier access to hospital networks than wired network systems. This may result in several security incidents unless security protocols are well implemented. In this paper, user authentication and authorization procedures will applied as a featured component at each level of M-health systems inthe hospital environment. Accordingly, M-health system in the hospital will meet the optimal requirements as a countermeasure to its vulnerabilities

Enhanced anti-tumor effect of combination therapy with gemcitabine and apigenin in pancreatic cancer

Apigenin is a dietary flavonoid possessing therapeutic potential against cancers. This study was designed to investigate whether combination therapy with gemcitabine and apigenin enhanced anti-tumor efficacy in pancreatic cancer. In vitro, the combination treatment resulted in more growth inhibition and apoptosis through the down-regulation of NF-kappa B activity with suppression of Akt activation in pancreatic cancer cell lines (MiaPaca-2, AsPC-1). In vivo, the combination therapy augmented tumor growth inhibition through the down-regulation of NF-kappa B activity with the suppression of Akt in tumor tissue. The combination of gemcitabine and apigenin enhanced anti-tumor efficacy through Akt and NF-kappa B activity suppression and apoptosis induction

Polymorphisms of the MCP-1 and HSP70-2 genes in Korean patients with alcoholic chronic pancreatitis

Alcoholic chronic pancreatitis (ACP) develops in only a small number of alcoholics. Monocyte chemotactic protein-1 (MCP-1) and heat-shock protein 70-2 (HSP70-2) polymorphisms have been reported to be associated with the severity of acute pancreatitis. However, their role in pathogenesis of ACP has not been investigated. A genetic association study for susceptibility and severity was performed on 79 male Korean ACP patients and 82 male controls. MCP-1 and HSP70-2 genotypes were determined using a fluorescence polarization detection method. The genotypes and G allele frequencies were no different in patients and controls. However, MCP-1 G allele had an effect on the development of severe ACP, when its frequency was compared in mild to moderate and severe ACP (29.6 vs. 56.0%, P = 0.02). The MCP-1 and HSP70-2 polymorphisms do not play a major role in the development of ACP in Koreans. However, MCP-1 polymorphism may be associated with the severity of ACP

An intraspecific genetic map for watermelon constructed using an F₂ population from the cross ‘Arka Manik’ × ‘TS34’ and the location of 3 major QTLs for powdery mildew resistance (PMR), seed size (SS), and fruit shape index (FSI) identified by interval mapping (IM).

<p>Chromosomes 1 to 11 are according to [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0145665#pone.0145665.ref004" target="_blank">4</a>]. Numbers on the left side correspond to the distance in cM from the top of each chromosome. QTL positions were defined by the interval of the strongest linked markers flanking the QTL. Major QTL for PMR, SS, and FSI are represented by the blue, red, and green color, respectively.</p

Major Quantitative Trait Loci and Putative Candidate Genes for Powdery Mildew Resistance and Fruit-Related Traits Revealed by an Intraspecific Genetic Map for Watermelon (<i>Citrullus lanatus</i> var. <i>lanatus</i>)

<div><p>An intraspecific genetic map for watermelon was constructed using an F₂ population derived from ‘Arka Manik’ × ‘TS34’ and transcript sequence variants and quantitative trait loci (QTL) for resistance to powdery mildew (PMR), seed size (SS), and fruit shape (FS) were analyzed. The map consists of 14 linkage groups (LGs) defined by 174 cleaved amplified polymorphic sequences (CAPS), 2 derived-cleaved amplified polymorphic sequence markers, 20 sequence-characterized amplified regions, and 8 expressed sequence tag-simple sequence repeat markers spanning 1,404.3 cM, with a mean marker interval of 6.9 cM and an average of 14.6 markers per LG. Genetic inheritance and QTL analyses indicated that each of the PMR, SS, and FS traits is controlled by an incompletely dominant effect of major QTLs designated as <i>pmr2</i>.<i>1</i>, <i>ss2</i>.<i>1</i>, and <i>fsi3</i>.<i>1</i>, respectively. The <i>pmr2</i>.<i>1</i>, detected on chromosome 2 (Chr02), explained 80.0% of the phenotypic variation (LOD = 30.76). This QTL was flanked by two CAPS markers, wsb2-24 (4.00 cM) and wsb2-39 (13.97 cM). The <i>ss2</i>.<i>1</i>, located close to <i>pmr2</i>.<i>1</i> and CAPS marker wsb2-13 (1.00 cM) on Chr02, explained 92.3% of the phenotypic variation (LOD = 68.78). The <i>fsi3</i>.<i>1</i>, detected on Chr03, explained 79.7% of the phenotypic variation (LOD = 31.37) and was flanked by two CAPS, wsb3-24 (1.91 cM) and wsb3-9 (7.00 cM). Candidate gene-based CAPS markers were developed from the disease resistance and fruit shape gene homologs located on Chr.02 and Chr03 and were mapped on the intraspecific map. Colocalization of these markers with the major QTLs indicated that watermelon orthologs of a nucleotide-binding site-leucine-rich repeat class gene containing an RPW8 domain and a member of SUN containing the IQ67 domain are candidate genes for <i>pmr2</i>.<i>1</i> and <i>fsi3</i>.<i>1</i>, respectively. The results presented herein provide useful information for marker-assisted breeding and gene cloning for PMR and fruit-related traits.</p></div

PMR phenotypic distribution of F₂ progeny from the cross ‘Arka Manik’ × ‘TS34’.

<p>PMR phenotypic distribution of F₂ progeny from the cross ‘Arka Manik’ × ‘TS34’.</p

Pharmacogenomic landscape of patient-derived tumor cells informs precision oncology therapy.

Outcomes of anticancer therapy vary dramatically among patients due to diverse genetic and molecular backgrounds, highlighting extensive intertumoral heterogeneity. The fundamental tenet of precision oncology defines molecular characterization of tumors to guide optimal patient-tailored therapy. Towards this goal, we have established a compilation of pharmacological landscapes of 462 patient-derived tumor cells (PDCs) across 14 cancer types, together with genomic and transcriptomic profiling in 385 of these tumors. Compared with the traditional long-term cultured cancer cell line models, PDCs recapitulate the molecular properties and biology of the diseases more precisely. Here, we provide insights into dynamic pharmacogenomic associations, including molecular determinants that elicit therapeutic resistance to EGFR inhibitors, and the potential repurposing of ibrutinib (currently used in hematological malignancies) for EGFR-specific therapy in gliomas. Lastly, we present a potential implementation of PDC-derived drug sensitivities for the prediction of clinical response to targeted therapeutics using retrospective clinical studies