42 research outputs found

    How students cope with part-time study

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    This study provides a qualitative test and illustration of a model of how students cope with the demands of part-time study. The model shows that students who are successful in finding the time to complete the requirements of part-time courses do so by adopting three mechanisms; sacrifice, support and the negotiation of arrangements. All three mechanisms operate in four domains, namely work, family, social lives and the self. The mechanisms and domains were related together in a three by four matrix. Data to verify and illuminate the model were gathered by the researchers through an on-line forum discussion on the topic of coping with part-time study. The researchers themselves were studying part-time in a course called Adult Education and Professional Development. Analysis of the data showed that the work domain was very important but little adaptation was possible. The family was seen as the most important domain and all three mechanisms were used. Time was commonly found for part-time study by sacrificing social lives. The self-domain was interpreted as important in establishing motivation and self-determination

    MicroRNA profiling study reveals MIR-150 in association with metastasis in nasopharyngeal carcinoma

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    © 2017 The Author(s). MicroRNAs (miRNAs) are small non-coding RNAs that play a crucial role in pathogenesis of human cancers. Several miRNAs have been shown to involve in nasopharyngeal carcinoma (NPC) pathogenesis through alteration of gene networks. A global view of the miRNA expression profile of clinical specimens would be the best way to screen out the possible miRNA candidates that may be involved in disease pathogenesis. In this study, we investigated the expression profiles of miRNA in formalin-fixed paraffin-embedded tissues from patients with undifferentiated NPC versus non-NPC controls using a miRNA real-time PCR platform, which covered a total of 95 cancer-related miRNAs. Hierarchical cluster analysis revealed that NPC and non-NPC controls were clearly segregated. Promisingly, 10 miRNA candidates were differentially expressed. Among them, 9 miRNAs were significantly up-regulated of which miR-205 and miR-196a showed the most up-regulated in NPC with the highest incidence percentage of 94.1% and 88.2%, respectively, while the unique down-regulated miR-150 was further validated in patient sera. Finally, the in vitro gain-of-function and loss-of-function assays revealed that miR-150 can modulate the epithelial-mesenchymal-transition property in NPC/HK-1 cells and led to the cell motility and invasion. miR-150 may be a potential biomarker for NPC and plays a critical role in NPC tumourigenesis.Link_to_subscribed_fulltex

    Ligand-Activated Peroxisome Proliferator-Activated Receptor-  Protects Against Ischemic Cerebral Infarction and Neuronal Apoptosis by 14-3-3  Upregulation

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    Thiazolidinediones (TZD) were reported to protect against ischemia-reperfusion (I/R) injury. Their protective actions are considered to be PPAR-γ (peroxisome proliferator-activated receptor γ)-dependent. However, it is unclear how PPAR-γ activation confers resistance to I/R

    State of E-learning in Singapore's retail industry

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    This project looks into the current state of e-learning adoption in Singapore's retail industry

    A Scale for the Management of Aggressive and Violent Behaviour (C_MAVAS): Psychometric Properties Testing in Mental Health Nurses

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    Background: This study set out to examine the psychometric properties of C_MAVAS, a newly Chinese-translated version of MAVAS, a 27-item scale assessing healthcare professionals’ attitudes to the management of patient violence. Method: The English version of the MAVAS was translated and back-translated to come up with C_MAVAS. A convenience sample of 262 qualified mental health nurses working in a local psychiatric hospital was recruited. Exploratory factor analysis tested C_MAVAS’s construct validity. Results: Content validity of the C_MAVAS was very satisfactory with validity indices of 97.4% for the overall scale and 90% to 100% for individual items. Exploratory factor analysis yielded a four-factor solution: ‘interactional perspectives on patient violence’, ‘best ways perceived for violence management’, ‘internal or biomedical perspectives on patient violence’, and ‘external perspectives on patient aggression and violence’, were important in shaping their attitudes towards managing violence and patient disruptiveness. Internal consistency of the Chinese version was barely satisfactory (Cronbach’s alpha = 0.51–0.67) for the four factors/subscales and its test-retest reliability was good (Pearson’s coefficient = 0.84). Conclusion: The findings suggest the C_MAVAS is a valid and reliable tool to measure mental health nurses’ attitudes towards patient violence/aggression in a mental hospital setting

    Targeting the Hippo Pathway in Gastric Cancer and Other Malignancies in the Digestive System: From Bench to Bedside

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    The Hippo pathway is an evolutionally conserved signaling cascade that controls organ size and tissue regeneration under physiological conditions, and its aberrations have been well studied to promote tumor initiation and progression. Dysregulation of the Hippo tumor suppressor signaling frequently occurs in gastric cancer (GC) and other solid tumors and contributes to cancer development through modulating multiple aspects, including cell proliferation, survival, metastasis, and oncotherapy resistance. In the clinic, Hippo components also possess diagnostic and prognostic values for cancer patients. Considering its crucial role in driving tumorigenesis, targeting the Hippo pathway may greatly benefit developing novel cancer therapies. This review summarizes the current research progress regarding the core components and regulation of the Hippo pathway, as well as the mechanism and functional roles of their dysregulation in gastrointestinal malignancies, especially in GC, and discusses the therapeutic potential of targeting the Hippo pathway against cancers

    Activating Transcription Factor 3 Diminishes Ischemic Cerebral Infarct and Behavioral Deficit by Downregulating Carboxyl-Terminal Modulator Protein

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    Activating transcription factor 3 (ATF3) is a stress-induced transcription factor and a familiar neuronal marker for nerve injury. This factor has been shown to protect neurons from hypoxic insult in vitro by suppressing carboxyl-terminal modulator protein (CTMP) transcription, and indirectly activating the anti-apoptotic Akt/PKB cascade. Despite prior studies in vitro, whether this neuroprotective pathway also exists in the brain in vivo after ischemic insult remains to be determined. In the present study, we showed a rapid and marked induction of ATF3 mRNA throughout ischemia-reperfusion in a middle cerebral artery (MCA) occlusion model. Although the level of CTMP mRNA was quickly induced upon ischemia, its level showed only a mild increase after reperfusion. With the gain-of-function approach, both pre- and post-ischemic administration of Ad-ATF3 ameliorated brain infarct and neurological deficits. Whereas, with the loss-of-function approach, ATF3 knockout (KO) mice showed bigger infarct and worse functional outcome after ischemia. In addition, these congenital defects were rescued upon reintroducing ATF3 to the brain of KO mice. ATF3 overexpression led to a lower level of CTMP and a higher level of p-Akt(473) in the ischemic brain. On the contrary, ATF3 KO resulted in upregulation of CTMP and downregulation of p-Akt(473) instead. Furthermore, post-ischemic CTMP siRNA knockdown led to smaller infarct and better behaviors. CTMP siRNA knockdown increased the level of p-Akt(473), but did not alter the ATF3 level in the ischemic brain, upholding the ATF3→CTMP signal cascade. In summary, our proof-of-principle experiments support the existence of neuroprotective ATF3→CTMP signal cascade regulating the ischemic brain. Furthermore, these results suggest the therapeutic potential for both ATF3 overexpression and CTMP knockdown for stroke treatment

    Activating Transcription Factor 3 Diminishes Ischemic Cerebral Infarct and Behavioral Deficit by Downregulating Carboxyl-Terminal Modulator Protein

    No full text
    Activating transcription factor 3 (ATF3) is a stress-induced transcription factor and a familiar neuronal marker for nerve injury. This factor has been shown to protect neurons from hypoxic insult in vitro by suppressing carboxyl-terminal modulator protein (CTMP) transcription, and indirectly activating the anti-apoptotic Akt/PKB cascade. Despite prior studies in vitro, whether this neuroprotective pathway also exists in the brain in vivo after ischemic insult remains to be determined. In the present study, we showed a rapid and marked induction of ATF3 mRNA throughout ischemia-reperfusion in a middle cerebral artery (MCA) occlusion model. Although the level of CTMP mRNA was quickly induced upon ischemia, its level showed only a mild increase after reperfusion. With the gain-of-function approach, both pre- and post-ischemic administration of Ad-ATF3 ameliorated brain infarct and neurological deficits. Whereas, with the loss-of-function approach, ATF3 knockout (KO) mice showed bigger infarct and worse functional outcome after ischemia. In addition, these congenital defects were rescued upon reintroducing ATF3 to the brain of KO mice. ATF3 overexpression led to a lower level of CTMP and a higher level of p-Akt(473) in the ischemic brain. On the contrary, ATF3 KO resulted in upregulation of CTMP and downregulation of p-Akt(473) instead. Furthermore, post-ischemic CTMP siRNA knockdown led to smaller infarct and better behaviors. CTMP siRNA knockdown increased the level of p-Akt(473), but did not alter the ATF3 level in the ischemic brain, upholding the ATF3→CTMP signal cascade. In summary, our proof-of-principle experiments support the existence of neuroprotective ATF3→CTMP signal cascade regulating the ischemic brain. Furthermore, these results suggest the therapeutic potential for both ATF3 overexpression and CTMP knockdown for stroke treatment

    The Effectiveness of a Multidisciplinary Exercise Program in Managing Work-Related Musculoskeletal Symptoms for Low-Skilled Workers in the Low-Income Community: A Pre-Post-Follow-Up Study

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    Studies on work-related musculoskeletal symptoms (WRMSs) have been conducted mainly on different types of workforce but not many on low-skilled workers. The purpose of this study was to evaluate the effectiveness of a multidisciplinary exercise program in decreasing the number of body parts with WRMSs for low-skilled workers. This study used a repeated-measures, single-group design. One hundred and five (105) workers participated in eight weekly 90-min sessions (including 45-min workshops and 45-min exercises) in low-income community settings. The exercise program involved a 21-movement stretching exercise and a 10-movement muscle-strengthening exercise. Questionnaire and health-assessment data were collected at the baseline (N = 105) and immediately after the 8-week program (n = 86). The average age of the 105 participants was 50.5 ± 8.7 years (ranging from 31 to 67). Over 80% (n = 87) of them were female, 68.6% (n = 72) were married, and 68.6% (n = 72) had completed secondary school. They reported an average of three body parts with WRMSs at baseline (T0). By the end of the eight weeks (T1), the participants had reduced the number of WRMS-affected body parts, job stress, and incidences of working through pain, and had improved spine flexibility and handgrip strength. The factors significantly affecting the reduction in the number of body parts with WRMSs were change in the workstyle of working through pain, and self-rated health status. Our study has demonstrated that a community-based multidisciplinary program can reduce the number of body parts affected by WRMSs in low-skilled workers in low-income communities
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