Work-related Attitudes of Non-regular and Regular Workers in Korea: Exploring Distributive Justice as a Mediator

Raising the timely issue of the non-regular workforce in South Korea, this article examined the degree and intensity of commitment of non-regular workers (contingent and part-time workers) to their job and organization. The results showed that both contingent and parttime workers were less committed to the organization and job than regular workers. This article showed that work status affected the individual, by influencing subjective stratum and his or her perception of distributive justice, which in turn had an impact on organizational commitment and job involvement. Finally, the article stressed that nonregular workers did not constitute a homogeneous group and that, consequently, part-time workers should be treated as distinct from other types of non-regular workers. The sociological implications of the non-regular workforce were discussed

Inactivation Patterns of p16/INK4A in Oral Squamous Cell Carcinomas

The p16/INK4A is one of the major target genes in carcinogenesis and its inactivation has frequently been reported in other types of tumors. The purpose of this study is to evaluate inactivation patterns of p16/INK4A in oral squamous cell carcinoma. Six different oral cancer cell lines, SCC-4, SCC-9, SCC-15, SCC-25, KB, and SNUDH- 379 were examined for inactivation of p16/INK4A genes. In the analysis of p16/INK4A gene inactivation, PCR amplification, direct sequencing, and methylation-specific PCR methods were adopted for evaluation of homozygous deletion, point mutation, and promoter hypermethylation, respectively. Homozygous deletion was detected in SCC-25 and SCC-9. SCC-15 showed hypermethylated promoter region within p16/INK4A gene. It is suggestive in the present study that inactivation patterns of p16/INK4A were mainly homozygous deletion, promoter methylation rather than point mutation in oral squamous cancer cell lines, so treatment modalities of oral squamous cell carcinoma should be focused on these types of inactivation

Molecular mechanism underlying the apoptotic modulation by ethanol extract of Pseudolarix kaempferi in mucoepidermoid carcinoma of the salivary glands

Background Pseudolarix kaempferi is a traditional Chinese natural product that possesses the potential cytotoxic effects against cancer. However, the precise molecular mechanism underlying its cytotoxic effects has not yet been completely elucidated. Here, we clarify the mechanism via which the ethanol extract of P. kaempferi (EEPK) leads to cytotoxicity mediated by apoptosis in mucoepidermoid carcinoma (MEC) originating from the salivary glands. Methods We investigated the mechanism underlying the anticancer efficacy of EEPK in human MEC in vitro by assessing mitochondrial dysfunction, mRNA levels, and morphological changes in apoptotic cell nuclei as well as by using a cytotoxicity assay, flow cytometric analysis, and western blotting. Results EEPK inhibited the growth of two human MEC cells and stimulated the induction of caspase-mediated apoptosis that was accompanied by mitochondrial membrane depolarization. Compared with the vehicle control groups, EEPK decreased myeloid cell leukemia-1 (Mcl-1) expression in both cells whereas it significantly decreased B cell lymphoma-2 (Bcl-2) expression in MC3 cells only. The EEPK-induced altered Mcl-1 expression was caused by translational inhibition and proteasomal degradation. Additionally, EEPK significantly increased p-Bcl-2 (Ser70) expression regardless of its total forms by facilitating the activation of the c-Jun N-terminal kinase (JNK) signaling pathway, which exhibited cell context dependency. Nevertheless, JNK activation following EEPK treatment was, at least in part, required for the proapoptotic efficacy of EEPK in both cells. Conclusions This study revealed that EEPK-induced alterations of Mcl-1 inhibition and JNK/Bcl-2 phosphorylation cause apoptosis and provided basic preclinical data for future clinical trials regarding therapy for patients with MEC. Graphic abstrac

Inhibition of Akt activity induces the mesenchymal-to-epithelial reverting transition with restoring E-cadherin expression in KB and KOSCC-25B oral squamous cell carcinoma cells

<p>Abstract</p> <p>Background</p> <p>The Akt/PKB family of kinases is frequently activated in human cancers, including oral squamous cell carcinoma (OSCC). Akt-induced epithelial-to-mesenchymal transition (EMT) involves downregulation of E-cadherin, which appears to result from upregulation of the transcription repressor Snail. Recently, it was proposed that carcinoma cells, especially in metastatic sites, could acquire the mesenchymal-to-epithelial reverting transition (MErT) in order to adapt the microenvironments and re-expression of E-cadherin be a critical indicator of MErT. However, the precise mechanism and biologic or clinical importance of the MErT in cancers have been little known. This study aimed to investigate whether Akt inhibition would restore the expression of E-cadherin and β-catenin, reduce that of Vimentin, and induce the MErT in OSCC cells with low or negative expression of E-cadherin. We also investigate whether inhibition of Akt activity would affect the E-cadherin repressors and signaling molecules like NF-κB, ERK, and p38.</p> <p>Methods</p> <p>We screened several OSCC cell lines in order to select suitable cell line models for inducing MErT, using immunoblotting and methylation specific-PCR. We examined whether Akt inhibitor phosphatidylinositol ether lipid analogues (PIA) treatment would restore the expression of E-cadherin and β-catenin, reduce that of Vimentin, and induce the MErT in KB and KOSCC-25B cells using RT-PCR, immunoblotting, immunofluorescence analysis, and <it>in vitro </it>migration assay. We also investigated whether inhibition of Akt activity would affect the E-cadherin repressors, including Snail, Twist, and SIP-1/ZEB-2 and signaling molecules like NF-κB, ERK, JNK, and p38 using RT-PCR, immunoblotting, and immunofluorescence analysis.</p> <p>Results</p> <p>Of the 7 OSCC cell lines, KB and KOSCC-25B showed constitutively activated phosphorylated Akt and low or negative expression of E-cadherin. Inhibition of Akt activity by PIA decreased NF-κB signaling, but did not affect phosphorylation of ERK, JNK, and p38 in KB and KOSCC-25B cells. Akt inhibition led to downregulation of Snail and Twist expression. In contrast, inhibition of Akt activity by PIA did not induce any changes in SIP-1/ZEB-2 expression. PIA treatment induced the expression of E-cadherin and β-catenin, reduce that of Vimentin, restored their epithelial morphology of a polygonal shape, and reduced tumor cell migration in KB and KOSCC-25B cells, which was the corresponding feature of MErT.</p> <p>Conclusion</p> <p>All of these findings suggest that Akt inhibition could induce the MErT through decreased NF-κB signaling and downregulation of Snail and Twist in OSCC cells. A strategy involving Akt inhibition might be a useful therapeutic tool in controlling cancer dissemination and metastasis in oral cancer patients.</p

HIGH-DOSE CLOPIDOGREL LOADING IS SAFE AND EFFECTIVE IN PATIENTS WITH ST-ELEVATION MYOCARDIAL INFARCTION UNDERGOING PRIMARY PERCUTANEOUS CORONARY INTERVENTION

OBJECTIVE: The two- to fourfold higher risk of cardiovascular disease in diabetes mellitus is more strongly predicted by the postprandial than by the fasting blood glucose and lipids. We aimed to investigate the impact of postprandial changes in serum lipoprotein fractions on lipid peroxidation in type I diabetes mellitus (T1DM). DESIGN: This was a prospective observational study. SETTING: The study was performed at Antwerp University Hospital, Belgium.Subjects:Twenty-three well-controlled T1DM patients were included. INTERVENTION: Patients received a standard breakfast and lunch (&gt;50% energy as fat). Blood was sampled at fasting (F), after the post-breakfast hyperglycemic peak (BP), just before lunch (B), after the post-lunch hyperglycemic peak (LP), after the post-lunch dale (LD) and 5 h after lunch (L) for the measurement of serum lipids, lipoprotein subfraction composition, alpha-tocopherol and lipid peroxidation in vivo and in vitro. RESULTS: Serum triacylglycerols (Tgs) increased (from 1.03+/-0.40 at F to 1.60+/-0.87 mmol/l at LP, P=0.001), but cholesterol decreased by 12% in parallel with alpha-tocopherol (from 4.43+/-0.76 at F to 4.12+/-0.82 micromol/mmol total lipid at B, P=0.006). Although plasma malondialdehyde increased from 1.02+/-0.36 at F to 1.14+/-0.40 micromol/L at LP, P=0.03, copper-induced in vitro peroxidation decreased in the low-density lipoprotein and high-density lipoprotein fractions. CONCLUSIONS: In well-controlled T1DM patients moderate postprandial increases in serum Tgs are accompanied by a relative deficiency in alpha-tocopherol. Lipid peroxidation in vivo increases but cannot be ascribed to changes in the susceptibility of lipoproteins to copper-induced in vitro peroxidation</p