The Influence Of Job Insecurity On Career Commitment And Attitude In Multinational Corporations

As the perception of lifelong work shifts into lifelong career in the job insecurity market, the career development of employees through professional and competitive career management has become more important than being loyal to a lifelong work. Furthermore, in the case of multinational corporations, such as differentiation from the head office policy, cultural differences in labor relations, and the liquidity of business withdrawal, such a feature has a higher possibility of job insecurity than general companies. Therefore, the purpose of this study is to verify empirically how job insecurity influences career commitment and career attitude through individual, job and career characteristics as intermediation with the members of multinational corporations as objectives. For this purpose, a total of 366 questionnaire data that targeted 27 multinational corporations were collected and analyzed. The result shows that the job insecurity of multinational corporations affects individual characteristic rather than job or career characteristic, and it is confirmed that individual characteristic has an effect on career commitment and career attitude. In the end, multinational corporations, unlike ordinary domestic companies, need active organizational career development program that corresponds to an open corporate culture as well as innovative and open systems and policies that balance both internal and external networking activities in terms of human resource management of corporations

Electrochemical detection of mismatched DNA using a MutS probe

A direct and label-free electrochemical biosensor for the detection of the protein–mismatched DNA interaction was designed using immobilized N-terminal histidine tagged Escherichia coli. MutS on a Ni-NTA coated Au electrode. General electrochemical methods, cyclic voltammetry (CV), electrochemical quartz crystal microbalance (EQCM) and impedance spectroscopy, were used to ascertain the binding affinity of mismatched DNAs to the MutS probe. The direct results of CV and impedance clearly reveal that the interaction of MutS with the CC heteroduplex was much stronger than that with AT homoduplex, which was not differentiated in previous results (GT > CT > CC ≈ AT) of a gel mobility shift assay. The EQCM technique was also able to quantitatively analyze MutS affinity to heteroduplexes

The Effect of an Intravitreal Triamcinolone Acetonide Injection for Acute Nonarteritic Anterior Ischemic Optic Neuropathy

The purpose of this case report is to evaluate the visual outcome of an intravitreal triamcinolone acetonide injection (IVTA) as a treatment for a patient with acute nonarteritic anterior ischemic optic neuropathy (NAION). A 65-year-old male patient with severe visual loss due to acute NAION was treated with 4 mg/0.1mL IVTA. Fundus examination and measurements of the patient's best-corrected visual acuity and visual field were performed before and after the injection at 2 weeks, 1 month, 3 months, and 6 months. The best-corrected visual acuity changed from 0.05 before the injection to 0.16 at 2 weeks, 0.3 at 1 month, and 0.4 at 3 months and at the final visit. Optic disc swelling had markedly decreased at 1 week postoperatively and disappeared at 2 weeks after the injection. The clinical course of this patient suggests that an IVTA may be effective in increasing visual acuity following an acute NAION. A large randomized controlled trial is needed to assess the efficacy of IVTA as a treatment for NAION

NFATc1 regulates the transcription of DNA damage-induced apoptosis suppressor

AbstractDNA damage induced apoptosis suppressor (DDIAS), or human Noxin (hNoxin), is strongly expressed in lung cancers. DDIAS knockdown induced apoptosis in non-small cell lung carcinoma A549 cells in response to DNA damage, indicating DDIAS as a potential therapeutic target in lung cancer. To understand the transcriptional regulation of DDIAS, we determined the transcription start site, promoter region, and transcription factor. We found that DDIAS transcription begins at nucleotide 212 upstream of the DDIAS translation start site. We cloned the DDIAS promoter region and identified NFAT2 as a major transcription factor (Im et al., 2016 [1]). We demonstrated that NFATc1 regulates DDIAS expression in both pancreatic cancer Panc-1 cells and lung cancer cells