The Impacts of Role Overload and Role Conflict on Physicians\u27 Technology Adoption

Technology adoption is an important solution for physicians to increase work efficiency, and thus deal with role conflict among their multiple job roles. Prior studies have not investigated how multiple job roles and role conflict influence physicians’ technology adoption intentions. Based on role strain theory and role identity theory, we present a model of physicians’ technology adoption intentions to support their primary (clinical care) versus secondary (teaching or research) job roles. We test the model using surveys with 156 physicians at nine medical schools in Korea. The results of our data analysis largely support our hypotheses. Role overload in each of their job roles increases role conflict between any pair of associated roles. Furthermore, role conflict between a physician’s primary and secondary role is affected more by role overload in the secondary role than by overload in the primary role. Moreover, the impact of role conflict on technology adoption intentions is also influenced by the hierarchical relationship between two roles. This study contributes to technology adoption research by demonstrating how physicians’ job characteristics affect technology adoption

RECENT STUDIES OF TICK-BORNE INFECTIONS IN MONGOLIA

We have aimed to detect both Rickettsiae species and Babesia microti in adult ticks of Dermacentor nutalli in Tuv province; and  looked for only Rickettsiae species in Ixodes persulcatus in Selenge  province. Using the PCR and DNA sequencing techniques, we  amplified and sequenced the 16S rRNA, gltA, rOmpA genes of  Rickettsia and 18S rRNA gene of B. microti and Rickettsia species  were identified. Infection rate for Rickettsiae spp. was 82.7 %  (115/139 samples) by 16S rRNA sequencing results and among  them the highest prevalence rate was that for R. raoultii strain –  71.4 % (80/111 samples) by gltA gene sequencing and 100 %  (81/81 samples) by rOmpA gene sequencing. Canditatus Rickettsia tarasevichiae strain was detected in 27.9 % (31/11  samples) by gltA gene sequencing. Infection rate for Rickettsiae spp. in D. nutalli ticks was 84.3 % (81/96 samples) and R. raoultii  strain comprised 96.2–98.7 % among them. Adult ticks of I.  persulcatus were infected with Rickettsiae spp. with 78 % and 93.75  % of them were R. raoultii strain. Seventeen out of 97 ticks (17.5  %) were found to be infected with B. microti. Nucleotide DNA  sequencing of partial 18S rRNA and gltA genes supported the PCR  results. We have identified that the same species of ticks commonly  distributed in Mongolia have been infected with R. sibirica, R. raoultii  and B. microti. It might be the strength of our study as B.  microti have not been detected in D. nuttalli ticks yet. We are  considering to detect the tick-borne infections in humans

Expression of TLR2, TLR4, and TLR9 in dermatomyositis and polymyositis

The aim of this study was to investigate the expressions of Toll-like receptor (TLR) 2, TLR4, TLR9, and their correlations with the expression of cytokines that are associated with activation of CD4+ T cells and inflammation including interferon γ (IFNγ), interleukin 4 (IL4), interleukin 17 (IL17), and tumor necrosis factor α (TNFα) in muscle tissues of patients with dermatomyositis (DM) and polymyositis (PM). The expressions of TLR2, TLR4, TLR9, IFNγ, IL4, IL17, and TNFα were measured by real-time reverse transcription–polymerase chain reaction in muscle tissues from 14 patients with DM and PM (nine patients with DM, five patients with PM) and three controls. The expressions of TLR2, TLR4, and TLR9 were also localized with immunohistochemistry. The expression levels of TLR2, TLR4, TLR9, IFNγ, IL4, IL17, and TNFα were significantly high in patients with DM and PM compared with those in the controls, and the expression levels of TLR4 and TLR9 had significant positive correlations with the expressions of IFNγ, IL4, IL17, and TNFα. Immunohistochemistry showed that TLR2, TLR4, and TLR9 were expressed by infiltrating cells of perimysium in DM, whereas they were expressed by infiltrating cells of endomysium in PM. These results suggest that the involvement of TLR4 and TLR9 in immunopathogenesis of DM and PM might be connected with activation of CD4+ T cells

Rare Exonic Minisatellite Alleles in MUC2 Influence Susceptibility to Gastric Carcinoma

BACKGROUND: Mucins are the major components of mucus and their genes share a common, centrally-located region of sequence that encodes tandem repeats. Mucins are well known genes with respect to their specific expression levels; however, their genomic levels are unclear because of complex genomic properties. In this study, we identified eight novel minisatellites from the entire MUC2 region and investigated how allelic variation in these minisatellites may affect susceptibility to gastrointestinal cancer. METHODOLOGY/PRINCIPLE FINDINGS: We analyzed genomic DNA from the blood of normal healthy individuals and multi-generational family groups. Six of the eight minisatellites exhibited polymorphism and were transmitted meiotically in seven families, following Mendelian inheritance. Furthermore, a case-control study was performed that compared genomic DNA from 457 cancer-free controls with DNA from individuals with gastric (455), colon (192) and rectal (271) cancers. A statistically significant association was identified between rare exonic MUC2-MS6 alleles and the occurrence of gastric cancer: odds ratio (OR), 2.56; 95% confidence interval (CI), 1.31-5.04; and p = 0.0047. We focused on an association between rare alleles and gastric cancer. Rare alleles were divided into short (40, 43 and 44) and long (47, 50 and 54), according to their TR (tandem repeats) lengths. Interestingly, short rare alleles were associated with gastric cancer (OR = 5.6, 95% CI: 1.93-16.42; p = 0.00036). Moreover, hypervariable MUC2 minisatellites were analyzed in matched blood and cancer tissue from 28 patients with gastric cancer and in 4 cases of MUC2-MS2, minisatellites were found to have undergone rearrangement. CONCLUSIONS/SIGNIFICANCE: Our observations suggest that the short rare MUC2-MS6 alleles could function as identifiers for risk of gastric cancer. Additionally, we suggest that minisatellite instability might be associated with MUC2 function in cancer cells

Cross-National Differences in Victimization : Disentangling the Impact of Composition and Context

Varying rates of criminal victimization across countries are assumed to be the outcome of countrylevel structural constraints that determine the supply ofmotivated o¡enders, as well as the differential composition within countries of suitable targets and capable guardianship. However, previous empirical tests of these ‘compositional’ and ‘contextual’ explanations of cross-national di¡erences have been performed upon macro-level crime data due to the unavailability of comparable individual-level data across countries. This limitation has had two important consequences for cross-national crime research. First, micro-/meso-level mechanisms underlying cross-national differences cannot be truly inferred from macro-level data. Secondly, the e¡ects of contextual measures (e.g. income inequality) on crime are uncontrolled for compositional heterogeneity. In this paper, these limitations are overcome by analysing individual-level victimization data across 18 countries from the International CrimeVictims Survey. Results from multi-level analyses on theft and violent victimization indicate that the national level of income inequality is positively related to risk, independent of compositional (i.e. micro- and meso-level) di¡erences. Furthermore, crossnational variation in victimization rates is not only shaped by di¡erences in national context, but also by varying composition. More speci¢cally, countries had higher crime rates the more they consisted of urban residents and regions with lowaverage social cohesion.

Disseminated Mycobacterium avium complex infection in an immunocompetent pregnant woman

BACKGROUND: Disseminated mycobacterium avium complex (MAC) occurs mainly in immunocompromised hosts, which is associated with abnormal cellular immunity. CASE PRESENTATION: A 26-year-old pregnant woman presented with fever and general weakness. Miliary lung nodules were noted on chest X-ray. Under the impression of miliary tuberculosis, anti-tuberculosis medication was administered. However, the patient was not improved. Further work-up demonstrated MAC in the sputum and placenta. The patient was treated successfully with clarithromycin-based combination regimen. CONCLUSION: This appears to be the first case of disseminated MAC in an otherwise healthy pregnant woman. Clinicians should be alert for the diagnosis of MAC infection in diverse clinical conditions

Upregulated HSP27 in human breast cancer cells reduces Herceptin susceptibility by increasing Her2 protein stability

<p>Abstract</p> <p>Background</p> <p>Elucidating the molecular mechanisms by which tumors become resistant to Herceptin is critical for the treatment of Her2-overexpressed metastatic breast cancer.</p> <p>Methods</p> <p>To further understand Herceptin resistance mechanisms at the molecular level, we used comparative proteome approaches to analyze two human breast cancer cell lines; Her2-positive SK-BR-3 cells and its Herceptin-resistant SK-BR-3 (SK-BR-3 HR) cells.</p> <p>Results</p> <p>Heat-shock protein 27 (HSP27) expression was shown to be upregulated in SK-BR-3 HR cells. Suppression of HSP27 by specific siRNA transfection increased the susceptibility of SK-BR-3 HR cells to Herceptin. In the presence of Herceptin, Her2 was downregulated in both cell lines. However, Her2 expression was reduced by a greater amount in SK-BR-3 parent cells than in SK-BR-3 HR cells. Interestingly, co-immunoprecipitation analysis showed that HSP27 can bind to Her2. In the absence of Herceptin, HSP27 expression is suppressed and Her2 expression is reduced, indicating that downregulation of Her2 by Herceptin can be obstructed by the formation of a Her2-HSP27 complex.</p> <p>Conclusion</p> <p>Our present study demonstrates that upregulated HSP27 in human breast cancer cells can reduce Herceptin susceptibility by increasing Her2 protein stability.</p