Let the Avatar Brighten Your Smile: Effects of Enhancing Facial Expressions in Virtual Environments.

Previous studies demonstrated the positive effects of smiling on interpersonal outcomes. The present research examined if enhancing one's smile in a virtual environment could lead to a more positive communication experience. In the current study, participants' facial expressions were tracked and mapped on a digital avatar during a real-time dyadic conversation. The avatar's smile was rendered such that it was either a slightly enhanced version or a veridical version of the participant's actual smile. Linguistic analyses using the Linguistic Inquiry Word Count (LIWC) revealed that participants who communicated with each other via avatars that exhibited enhanced smiles used more positive words to describe their interaction experience compared to those who communicated via avatars that displayed smiling behavior reflecting the participants' actual smiles. In addition, self-report measures showed that participants in the 'enhanced smile' condition felt more positive affect after the conversation and experienced stronger social presence compared to the 'normal smile' condition. These results are particularly striking when considering the fact that most participants (>90%) were unable to detect the smiling manipulation. This is the first study to demonstrate the positive effects of transforming unacquainted individuals' actual smiling behavior during a real-time avatar-networked conversation.

Comparison of experimental mouse models of inflammatory bowel disease.

Inflammatory bowel disease (IBD) is multifactorial and involves immunological, environmental and genetic factors. Although there are no animal models that effectively mimic human IBD, experimental models allow us to analyze the mechanisms of chronic intestinal inflammation. IBD can be induced in mice by dextran sulfate sodium (DSS) or by a 2,4,6-trinitrobenzene sulfonic acid (TNBS)­ethanol enema, which evoke immune responses and colitis. In this study, in order to compare the mechanisms of inflammatory response in mice, 3 distinct models of IBD were established: 2% TNBS-induced acute colitis, 4% DSS-induced acute colitis and 2% DSS-induced chronic colitis. In addition, to evaluate the effects of TNBS on inflammasome activation, we used caspase-1 knockout (KO) mice. Changes in both body weight and survival became prominent after day 1 in the 2% TNBS­induced colitis model, and after day 5 in the 4% DSS-induced colitis model. The TNBS- and DSS-treated mice, but not the caspase-1 KO mice, showed a massive bowel edema and disruption of epithelial cells. The level of CD11b(+)Gr-1(+) myeloid-derived suppressor cells (MDSCs) was increased in all tested tissues of the TNBS- and DSS-treated groups, apart from the basal membrane (BM) in the DSS-induced colitis groups and the lamina propria (LP) in the DSS-induced chronic colitis group. We further analyzed different subsets of CD4(+) T cells in LP and found that the levels of interferon (IFN)γ­secreting (IFNγ(+)), IL-17­secreting (IL-17(+)), but not those of IL-4-secreting (IL-4(+)) T cells increased upon treatment with TNBS or DSS. In addition, discrepancies between the histopathologies of wild-type and caspase-1 KO mice indicated that the pathogenesis of IBD may be associated with the inflammasome pathway responses mediated by caspase­1 in TNBS­induced colitis.

Risk factors associated with head louse infestation in Korea.

Head louse infestation (HLI) is one of the most frequently occurring parasitic diseases in children. This study was conducted to investigate the socioeconomic and personal factors influencing HLI in the Republic of Korea. A total of 2,210 questionnaires about various factors related to HLI were obtained from children in 17 primary schools throughout the country. The rate of HLI was significantly lower in children who lived together with mother or in a family where both parents worked. In addition, HLI was lower in children whose fathers or mothers were public officers or teachers. However, HLI was higher in children who had small families and washed their hair less often. Education levels of parents and the number of children in family were not significant. Improvement of socioeconomic factors and personal hygiene will be helpful for reducing HLI.

The use of an in vitro adenosine triphosphate-based chemotherapy response assay to predict chemotherapeutic response in breast cancer.

The adenosine triphosphate-based chemotherapy response assay (ATP-CRA) has the advantages of standardization, evaluability, reproducibility, and accuracy, and can be performed on relatively small numbers of tumor cells. A total of 43 patients were enrolled in the present study, and chemosensitivity tests were successfully performed in 40 (93.0%) of these patients. Twenty of the 40 received neoadjuvant chemotherapy or chemotherapy for metastatic breast cancer. The chemotherapy regimens used were doxorubicin plus docetaxel (n=9, 45.0%) or doxorubicin plus paclitaxel (n=11, 55.0%). Mean cell death rate, as determined by ATP-CRA, was lower in non-responders than in responders to therapy (P=0.012). Sensitivity, specificity, positive predictive value, negative predictive value, and diagnostic accuracy for ATP-CRA were 78.6%, 100%, 100%, 66.7%, and 85.0%, respectively. Diagnostic accuracy achieved by immunohistochemistry using estrogen receptor or progesterone receptor was lower than that achieved using ATP-CRA. Expression of p53, erb-B2, Ki67, Bcl-2, Bcl-xL, and annexin I was not significantly associated with response to chemotherapy. Our results show that ATP-CRA has high specificity and positive predictive value for predicting response to chemotherapy.

[Gene expression profiling using oligonucleotide microarray in atrophic gastritis and intestinal metaplasia].

BACKGROUND/AIMS: The atrophic gastritis with intestinal metaplasia of gastric mucosa has been considered to be the major factor of carcinogenesis in the stomach. However, the key molecules are still poorly understood. To elucidate the molecular genetic basis, we report the results of our initial microarray data to analyze the genome pattern in patients with atrophic gastritis and intestinal metaplasia of the stomach. METHODS: We used oligonucleotide microarray technique to evaluate the gene expression profiles in atrophic gastritis with intestinal metaplasia, in comparison with those of normal mucosa. For the identification of differentially expressed genes, Significance Analysis of Microarrays (SAM) package method was used. The results were analyzed using global normalization, intensity dependent normalization, and box plot normalization. RESULTS: Eight genes including FABP, REG, OR6C1, MEP1, SLC6A1, SI, Mucin 1, and RAB23 in mucosa of atrophic gastritis and intestinal metaplasia were up-regulated by more than 10 times as compared with normal gastric mucosa. Only one gene, LOC44119 was down-regulated by more than 10 times of the expression as compared with normal gastric mucosa. In respect to the expression of known genes related to gastric carcinogenesis, 8 genes including FN1, SRMS, TP53, TP53IMP2, TP53I3, FGFR4, TGFB1, and TGFA showed up- and down-regulations more than 2 folds in expression pattern. CONCLUSIONS: We could identify a total genome pattern in patient with atrophic gastritis and intestinal metaplasia using oligonucleotide microarray. We believe that the current results will serve as a fundamental bioinformative basis for clinical applications in diagnosis and treatment of gastric cancer and precancerous lesion in the future.