Following up with China¡¦s WTO entry, China without doubt has become the ¡¥Must-go¡¦ place for any Taiwanese enterprise which is keen to turn its operation to be international or global. However, entering Chinese market would never be a promise to lead to a subsequent successful ¡¥going-global¡¦ story without taking account of certain points as follows. How Taiwanese enterprises enter Chinese market strategically? How to efficiently as well as effectively manage the subsidiaries following their entries? How to maintain and accumulate their ownership advantage afterwards? All of these questions have become the major challenges these days faced by those Taiwanese enterprises that attempt to enter the giant China. In today¡¦s knowledge-driven economy, for the capital-, technology-, as well as knowledge- intense pharmaceutical industry, it would be even more critical to effectively link foreign subsidiaries¡¦ organizational management and coordination to the foreign investment entry modes. Consequently, Taiwanese pharmaceutical enterprises are chosen as the samples in this current research.¡@Qualitative research is conducted for this current research using case study research method. Through in-depth interviews, data are gathered from two Taiwanese pharmaceutical enterprises, representing large and small scale enterprise respectively. Finally, findings obtained of this research as the following attempts to make some contributions to Taiwanese pharmaceutical enterprises¡¦ future investment in China. 1. Enterprise¡¦s characteristics, including business scale, years of China¡¦s investment, and internationalization experience, have influence on the ownership, location, and internalization advantage. 2. Features of pharmaceutical industry in China have influence on the development of the investment advantages in China. 3. Enterprise¡¦s characteristics and China¡¦s investment advantages have influence on the subsidiary¡¦s integration and control as well as the value chain activities.

The adverse effect of the exposure to images of attractive females on women's body image and mood has been well-documented in studies conducted in various western and westernized nations. However, research designed to determine the effect of exposure to attractive female images on men has been rather neglected. Past findings indicate that after being exposed to exceptionally attractive female images, males report less satisfaction for a current relationship, rate average-looking females as less attractive, and express less affection for their significant other compared to those men exposed to control images. It is currently not known, however, whether a psychoeducational intervention might prevent the negative media exposure effect. Additionally, it is not known if the exposure effect might be moderated by dispositional characteristics of the participant. This study was designed to determine if a psychoeducational manipulation consisting of information regarding the unrealistic appearance standards currently required of women would mitigate the ratings men give of average-looking women following exposure to attractive images. Additionally, two dispositional measures were included (appearance-schematicity and female-ideal internalization) in order to evaluate whether these trait levels would moderate the effects of the exposure manipulation.the participants were 159 male undergraduate students between 18 and 30 years of age. The majority (57%) of them were Caucasian, followed by 19% who were Hispanic/Latino and 11% who were African-American. Their mean age was 19.80 (SD = 2.06) and mean BMI was 24.90 (SD = 4.20). Most of them (42%) were not seeing anyone currently, whereas 39% of them were in a committed relationship. The findings partially supported the hypotheses. The males who were exposed to the attractive female images evaluated average females less physically attractive than those exposed to a control condition (inanimate objects); however, the psychoeducation did not reduce the adverse exposure effect. Instead, the combination of neutral audio-information and control exposure condition resulted in the most favorable ratings of average females. Regarding dispositional characteristics, female-ideal internalization was associated with the loss of interest in dating average females and the overestimation of a current partner's weight after the experiment. The limitations and implications of the study findings are discussed.

The greater body mass of African American females relative to Caucasian females is a well-documented finding implicated in ethnic disparities in health outcomes. The principal aim of the current study was to evaluate a theoretical account that may explain ethnic differences in body mass index. The proposed theoretical account focused on appearance-related concerns regarding the desirability of a thin body type as motivation to engage in weight control behavior. It was hypothesized that Caucasians would evidence greater internalization of the thin ideal than African Americans, which would then be associated with greater dietary restriction and physical activity, thereby predicting lower body mass among caucasians relative to African Americans. It was expected that this model would demonstrate greater applicability to individuals who lack constitutional thinness, i.e., individuals who have struggled with weight management in the past or at present. The study's design w as cross-sectional. African American (n=113) and Caucasian (n= 633) undergraduate, unmarried, heterosexual females between the ages of 18 and 30 completed online questionnaires in which they provided information on their ethnicity,socioeconomic status, ethnic identity, thin-ideal internalization, the perceived romantic appeal of thinness, the importance of romantic need fulfillment, dietary restriction, physical activity, height, current weight, and their highest weight since attaining their current height. Structural equation modeling with LISREL 8.72 was used to evaluate the proposed model. Support for hypotheses was mixed. Among the subset of participants categorized as lacking constitutional thinness, the relationship between ethnicity and body mass was mediated by thin-ideal internalization and the perceived romantic appeal of thinness, each of which contributed independently to dietary restriction, which in turn evidenced a curvilinear relationship with body mass. Results ar e consistent with the notion that ethnic differences in body mass may be partially accounted for by differences in standards for physical appearance, which may then motivate weight control behavior to a greater extent in Caucasians than African Americans.

The sociocultural model of eating disorders suggests that awareness of a thin physical ideal directly affects internalization of that ideal, which in turn, directly affects body dissatisfaction. The current study evaluated the general accuracy of the sociocultural model and examined the potential for ethnicity to protect against eating disorder symptomatology by moderating the relationships between awareness and internalization and between internalization and body dissatisfaction. Spanish (n = 100), Mexican American (n = 100), and Euro-American (n = 100) female participants completed various questionnaires measuring sociocultural attitudes towards appearance and body dissatisfaction. Analysis of covariance with tests of homogeneity of slope and path analysis using maximum likelihood with robust standard errors tested the two relationships by ethnic group. Results supported the sociocultural model: there was strong evidence for the mediational effect of internalization on the relationship between awareness and body dissatisfaction. Furthermore, ethnicity moderated the relationships such that both relationships were significantly stronger for Euro-American women than for Mexican American or Spanish women. Within the Mexican American group level of acculturation also moderated these relationships. Taken together, the results of this study highlight how ethnicity can protect against the development of eating disorder symptoms. Denouncing the thin ideal, minimizing appearance as an indicator of female value, and emphasizing personal traits other than appearance as determinants of worth are important in protecting against the development of body dissatisfaction and more severe eating pathology.

The purpose of this program of research was to study how socialization agents can facilitate children's internalization of important but uninteresting activities. Self-determination theory (SDT; Deci & Ryan, 1980, 1985b, 1991, 2000) posits that autonomy is essential in fostering optimal (i.e. integrated) internalization. It was thus hypothesized that autonomy-support would facilitate internalization while offering rewards for compliance would thwart it. In the present thesis, two experimental studies and one longitudinal study compared the effects of autonomy-support and rewards on children's internalization and general functioning. In Study 1 and 2, we asked children to perform a tedious task in an autonomy-supportive manner or under a reward contingency. Children's affect, perception of the task's value, and free-choice engagement served as dependent measures. ANOVA results revealed positive effects associated with autonomy-support whereas no effect for rewards was found. Moreover, split-group correlational analyses showed that autonomy-support led to integrated self-regulation, whereas rewards were associated with behaviors incongruent from affect and value. / Study 3 examined the over-time impact of maternal autonomy-support on children's adjustment in school. Autonomy-support, rewards, and other parenting dimensions were measured when children were 5 years old. Regression analyses revealed that autonomy-support was positively related to teacher-rated adjustment and reading achievement when children were 8 years old whereas the use of rewards was unrelated to these outcomes. Supplemental analyses also revealed that autonomy-support was associated with children's greater integration across social and academic domains. Together, these results highlight the significance of autonomy-support in early childhood.

INTRODUCTION: Persistent Pulmonary Hypertension of the Newborn (PPHN) is defined as the failure of normal circulatory relaxation in the lungs at birth. Hypoxia is known to impede postnatal disassembly of the actin cytoskeleton in pulmonary arterial (PA) myocytes. Actin polymerization (APM), regulated by Rho GTPases, stabilizes force generation. We studied basal and thromboxane (TP)-induced APM and contraction in normoxic and hypoxic PA myocytes and rings. We also examined the downstream signaling pathways regulating hypoxia and TP-induced APM, and the role that actin plays in TP receptor internalization. METHODS: Smooth muscle myocytes from 2nd to 6th generation PAs of newborn piglets were cultured and exposed to hypoxia (10% O2) or normoxia (21% O2) for 72 hrs, then challenged with 10-6M TP-agonist U46619. APM was quantified by laser-scanning cytometry and stress fiber isolation. Downstream signaling pathways of TP receptor were studied by immunoprecipitation, Rhotekin-RBD and PAK-PBD affinity precipitation, Western blot, immunofluoresence and ELISA. Isometric force to serial concentrations of U46619 was measured in resistant PAs from PPHN and 3-day control swine. RESULTS: Hypoxia induced 2-fold APM via alpha- and gamma-actin isoforms, which contributed to increase U46619-induced contraction. Hypoxia decreased TP association with G12/13 in favor of Gαq. Basal RhoA and Cdc42 activity increased in hypoxia, while Rac activity decreased. U46619-challenge did not further alter RhoA activity in hypoxic cells, but increased Cdc42 and Rac activity. Hypoxia increased phosphorylation of LIMK and PAK, unaltered by U46619. Association of Cdc42 with N-WASp decreased in hypoxia, but increased after U46619 exposure. Jasplakinolide significantly stabilized gamma filaments, increasing force generation; cytochalasin D depolymerized all actin isoforms, which attenuated contractile force. Both actin-modifying agents prevented TP endocytosis in NM, while normalizing TP internalization in HM. CONCLUSIONS: PA myocytes exhibit marked RhoA- and Rac-dependent APM in hypoxia. The additional APM response to U46619 challenge is independent of RhoA, but requires Cdc42 signaling. Hypoxia induces APM in PA myocytes, particularly causing an increase in filamentous alpha- and gamma-actin that contributes to increased U46619-induced force generation, a characteristic of PPHN. Dynamic actin also facilitates internalization of the TP receptor. Determining the mechanism that controls TP-mediated APM maybe beneficial as a potential target for PPHN.

Trafficking of GPCRs is a dynamic process that is tightly regulated and sometimes defective in human diseases. Therefore it is important to develop new methods to allow simple and quantitative measurement of surface expression of membrane proteins. Here we describe the development and validation of a new assay for quantification of cell surface expression of GPCRs using β-lactamase as a reporter. For this assay we N-terminally fused β-lactamase (βlac) to the β2-adrenergic receptor (β2AR) and GABA b R1 (GBR1). The results obtained by the βlac assay are quantitatively and qualitatively similar to well established ELISA when measuring agonist induced internalization of β2AR. We also show that measurement of GBR1 surface expression with GBR2 co-expression is quantitatively identical between the βlac and ELISA. In conclusion, our results show that our newly developed βlac assay is quantitatively similar while being less expensive, more robust and higher throughput compared to an ELISA.

Trafficking of GPCRs is a dynamic process that is tightly regulated and sometimes defective in human diseases. Therefore it is important to develop new methods to allow simple and quantitative measurement of surface expression of membrane proteins. Here we describe the development and validation of a new assay for quantification of cell surface expression of GPCRs using β-lactamase as a reporter. For this assay we N-terminally fused β-lactamase (βlac) to the β2-adrenergic receptor (β2AR) and GABA b R1 (GBR1). The results obtained by the βlac assay are quantitatively and qualitatively similar to well established ELISA when measuring agonist induced internalization of β2AR. We also show that measurement of GBR1 surface expression with GBR2 co-expression is quantitatively identical between the βlac and ELISA. In conclusion, our results show that our newly developed βlac assay is quantitatively similar while being less expensive, more robust and higher throughput compared to an ELISA.

The muscarinic acetylcholine type 2 receptor (M2 mAChR), a member of the GPCR superfamily, is found throughout the parasympathetic nervous system where it controls pulmonary, urinary, and cardiac function, and neurotransmission. The molecular mechanisms that regulate M2 mAChR availability at the cell surface are an important component in controlling these physiological events. Since beta-arrestin proteins are known to regulate the activity of other GPCRs, we sought to identify their role in regulating M2 mAChR activity, a topic that remains contentious in the field. To achieve this goal we utilized mouse embryonic fibroblasts (MEFs) derived from beta-arrestin knockout mice lacking one or both isoforms (MEF KO1, KO2, or KO1/2 cells) in addition to exogenous expression of beta-arrestin mutants. This study demonstrates that agonist-induced internalization of M2 mAChR is beta-arrestin- and clathrin-dependent, and that the receptor stably co-localizes with beta-arrestin in early endosomal vesicles suggesting it behaves as a class B receptor. Next, we sought to identify beta-arrestin s function in regulating the post-endocytic trafficking (down-regulation) of the M2 mAChR. MEF KO1/2 cells were unable to down-regulate M2 mAChRs whereas MEF KO1 or KO2 cells retained the ability to do so. In MEFwt cells, both M2 mAChR and beta-arrestin exhibited basal ubiquitination that increased following agonist stimulation. Receptor degradation appeared to be regulated by the ubiquitination status of beta-arrestin 2, since expression of a chimeric â-arrestin 2 form fused to ubiquitin increased both constitutive and agonist-promoted down-regulation, whereas expression of a beta-arrestin 2 mutant lacking putative ubiquitination sites, beta-arrestin 2K18R, K107R, K108R, K207R, K296R, significantly blocked degradation while internalization and stable association remained intact. Upon further analysis, the beta-arrestin 2K18R, K107R, K108R, K207R, K296R mutant blocked delivery of M2 mAChR to the late endosome/lysosome, presumably where degradation occurs. Inhibition of proteasome-dependent recycling of ubiquitin blocked receptor down-regulation without affecting internalization or the ubiquitination state of the M2 mAChR while ubiquitination of beta-arrestin 2 diminished significantly. These results support a role for ubiquitinated beta-arrestin in mediating M2 mAChR sorting and degradation in the lysosome. Collectively, these studies give us new insight on the function of beta-arrestin in regulating the activity of the M2 mAChR.

Thesis (M.S.W.)--Smith College School for Social Work, 2008. / Typescript. Includes bibliographical references (leaves 72-86).