Hubungan di antara amalan pengurusan kualiti menyeluruh (TQM) dan inovasi produk di kalangan syarikat pemprosesan makanan industri kecil dan sederhana

Pada era globalisasi ini, keperluan pelanggan menjadi semakin sukar untuk dipenuhi telah mewujudkan persaingan sengit di kalangan organisasi menyebabkan sesuatu organisasi sangat sukar untuk bertahan. Oleh itu, pengurusan kualiti menyeluruh (TQM) menjadi falsafah pengurusan dan amalan syarikat yang membantu dalam menguruskan organisasi untuk meningkatkan keberkesanan dan prestasi keseluruhan ke arah mencapai status bertaraf dunia sejak dua dekad yang lalu (Yusof & Aspinwall, 2000). Di Malaysia, banyak organisasi mula menganggap kualiti sebagai komponen penting dalam rancangan perniagaan mereka untuk menghadapi cabaran persekitaran global yang baru. Sebilangan besar organisasi memberi tumpuan kepada Pengurusan Kualiti Menyeluruh (TQM) berbanding amalan kualiti lain (Nusrah, Ramayah & Norizan, 2006). Oleh kerana inovasi telah dikenali secara meluas sekarang, organisasi perlu menggabungkan kedua-dua aspek inovasi dan kualiti untuk mencapai prestasi yang tinggi. Oleh itu, hubungan antara TQM dan inovasi telah menjadi tumpuan dalam literatur amalan pengurusan (Feng et al., 2006)

Epigenetic regulation by RARα maintains ligand-independent transcriptional activity

Retinoic acid receptors (RARs) α, β and γ are key regulators of embryonic development. Hematopoietic differentiation is regulated by RARα, and several types of leukemia show aberrant RARα activity. Through microarray expression analysis, we identified transcripts differentially expressed between F9 wild-type (Wt) and RARα knockout cells cultured in the absence or presence of the RAR-specific ligand all trans retinoic acid (RA). We validated the decreased Mest, Tex13, Gab1, Bcl11a, Tcfap2a and HMGcs1 transcript levels, and increased Slc38a4, Stmn2, RpL39l, Ref2L, Mobp and Rlf1 transcript levels in the RARa knockout cells. The decreased Mest and Tex13 transcript levels were associated with increased promoter CpG-island methylation and increased repressive histone modifications (H3K9me3) in RARα knockout cells. Increased Slc38a4 and Stmn2 transcript levels were associated with decreased promoter CpG-island methylation and increased permissive histone modifications (H3K9/K14ac, H3K4me3) in RARα knockout cells. We demonstrated specific association of RARα and RXRα with the Mest promoter. Importantly, stable expression of a dominant negative, oncogenic PML–RARα fusion protein in F9 Wt cells recapitulated the decreased Mest transcript levels observed in RARα knockout cells. We propose that RARα plays an important role in cellular memory and imprinting by regulating the CpG methylation status of specific promoter regions

FOREIGN DOMESTIC HELPERS IN SINGAPORE

Bachelor'sBACHELOR OF SOCIAL SCIENCES (HONOURS

Co-Ordinated Regulation Of Autophagy By Mtorc1 And Protein Phosphatase 2A

Autophagy is a cellular catabolic process critical for cell viability and homeostasis. As a membrane trafficking pathway, it is closely related to endocytosis and shares many points of convergence with endocytosis. In the first part of this dissertation, I find that although the two pathways are closely related, autophagosome fusion with lysosomes is governed by a distinct molecular mechanism from endosomal fusion with lysosomes. In recent years, the discovery of autophagy-essential-genes has accelerated research into the molecular mechanisms governing autophagy. For example, inhibition of mammalian target of rapamycin (mTOR) complex-1 (mTORC1) activates autophagy by relieving its inhibitory effects on autophagy essential gene, ULK1- a mTORC1 substrate whose dephosphorylation is required for autophagy induction. Puzzlingly, I observe that amino acid starvation triggers more rapid autophagy than pharmacological inhibition of mTORC1, although they both block mTORC1 activity with similar kinetics. Here I find that in addition to mTORC1 inactivation, starvation also causes a stimulation in phosphatase activity toward ULK1. In the second part of this dissertation, I identify the starvation-stimulated phosphatase for ULK1 as the PP2A-B55? complex and attempt to elucidate the mechanism of phosphatase stimulation during starvation. I find that treatment of cells with starvation but not mTORC1 inhibitors triggers dissociation of PP2A from its inhibitor Alpha4. Furthermore, pancreatic ductal adenocarcinoma cells (PDACs), whose growth depends on high basal autophagy, possess stronger basal phosphatase activity toward ULK1 and require ULK1 for sustained anchorage-independent growth. Taken together, these results suggest that concurrent mTORC1 inactivation and PP2A-B55? stimulation fuel ULK1-dependent autophagy

The burnout syndrome among Hong Kong secondary school principals

published_or_final_versionEducationMasterMaster of Educatio

The ULK1 complex Sensing nutrient signals for autophagy activation

The Atg1/ULK1 complex plays a central role in starvation-induced autophagy, integrating signals from upstream sensors such as MTOR and AMPK and transducing them to the downstream autophagy pathway. Much progress has been made in the last few years in understanding the mechanisms by which the complex is regulated through protein-protein interactions and post-translational modifications, providing insights into how the cell modulates autophagy, particularly in response to nutrient status. However, how the ULK1 complex transduces upstream signals to the downstream central autophagy pathway is still unclear. Although the protein kinase activity of ULK1 is required for its autophagic function, its protein substrate(s) responsible for autophagy activation has not been identified. Furthermore, examples of potential ULK1-independent autophagy have emerged, indicating that under certain specific contexts, the ULK1 complex might be dispensable for autophagy activation. This raises the question of how the autophagic machinery is activated independent of the ULK1 complex and what are the biological functions of such noncanonical autophagy pathways

Innate inflammatory responses of human decidual cells to periodontopathic bacteria

OBJECTIVE: The purpose of this study was to test the hypothesis that periodontopathic bacteria exert potent proinflammatory effects in human decidua