Int J Med Sci
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Background: Modern medicine recognizes that salient, inherent variations between Caucasians and Asians exist. Radical changes are occurring in the health scene with increasing emphasis centered on the recognition of inter-individual variations unique to Asians that impact on medical management and outcomes. Aim: This review analyzes distinct features or outcomes in terms of epidemiology, disease thresholds, diagnostic cutoffs and treatment responses of Asian people compared with non-Asians. ⋯ Results: An 'Asian phenotype' could be characterized across the spectrum of biomedical disciplines and underscores the major challenges clinicians must face in their daily management of a cosmopolitan population and their extrapolation of research outcomes. Conclusion: Interventions for various ailments that have traditionally ignored population differences have now entered the age of personalized, stratified or precision medicine requiring an individualized approach being adopted as a new standard of care. Factoring in Asian phenotypes is essential for the medical research community and the development of improved clinical practice guidelines across a continuum of disciplines that will ultimately translate to better human health round the world.
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Globally, morbidity and mortality due to cancer are predicted to increase in both men and women in the coming decades. Furthermore, it is estimated that two thirds of these cancer-related deaths will occur in low-and middle-income countries (LMIC). In addition to morbidity and mortality, cancer also causes an enormous economic burden, especially in developing countries. ⋯ Because of its low cost, for patients from LMIC with inoperable tumors, RT may be the only option. With the overall increase in the number of cancer patients especially in resource-starved LMIC, the need for more RT facilities further affects the economic growth of those countries. Therefore, an advanced molecular-targeted and more integrated approach involving either RT alone or with surgery and improved cancer drug access worldwide are urgent needs for cancer care.
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Randomized Controlled Trial
In vivo application of Granulocyte-Macrophage Colony-stimulating Factor enhances postoperative qualitative monocytic function.
Granulocyte macrophage colony-stimulating factor (GM-CSF) can be used as a potent stimulator for immune suppressed patients as defined by a decrease of human leukocyte antigen-D related expression on monocytes (mHLA-DR) after surgery. However, the exact role of GM-CSF on monocytic and T cell function is unclear. ⋯ Postoperative application of GM-CSF significantly enhanced qualitative monocytic function by increased mHLA-DR and TNF-α release after LPS stimulation and apparently enhanced Th17/Treg ratio. Clinical trial registered with www.controlled-trials.com (ISRCTN27114642) 05 December 2008.
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EGF-like domain 6 (EGFL6), a member of the epidermal growth factor (EGF) repeat protein superfamily, is a secreted protein that promotes endothelial cell migration and angiogenesis. The current study investigated the association between the clinicopathological characteristics and plasma level of EGFL6 in patients with oral squamous cell carcinoma (OSCC). We measured the plasma EGFL6 levels of 392 OSCC patients by using a commercial enzyme-linked immunosorbent assay. ⋯ Similar results were observed for the TCGA bioinformatics database. Moreover, plasma EGFL6 levels were significantly higher in the patients with advanced T status (p = 0.002), distant metastasis (p = 0.001), and higher TNM stage (p=0.033). In conclusion, our results suggest that plasma level of EGFL6 may be useful to assess disease progression, and especially advanced T status and higher TNM stage in patients with OSCC.
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Objectives: 4E-BP1 is a family member of eIF4E binding proteins (4E-BPs) which act as the suppressors of cap-dependent translation of RNA via competitively associating with cap-bound eIF4E. RNA translation regulation is an important manner to control the cellular responses to a series of stress conditions such as ionizing radiation (IR)-induced DNA damage response and cell cycle controlling. This study aimed to determine the mechanism of 4E-BP1 stabilization and its potential downstream target(s) in the response to IR. ⋯ Both PI3K and DNA-PKcs kinase inhibitors significantly decreased the protein level of 4E-BP1, which was associated with the accelerated degradation mediated by ubiquitination-proteasome pathway. Conclusion: PI3K kinase activity is necessary for maintaining 4E-BP1 stability. Our results also suggest 4E-BP1 a novel biological role of regulating cell cycle G2 checkpoint in responding to IR stress in association with controlling CHK2 phosphorylation.