Business Groups and Corporate Social Responsibility

© 2018, Springer Science+Business Media B.V., part of Springer Nature. There is a growing literature on corporate social responsibility (CSR), but few have focused on the implications of business groups for CSR. We examine the antecedents and outcomes of CSR behaviors of group firms in Korea. We find that group affiliation is associated with higher CSR overall and for its major societal and environmental components. However, the ownership disparity between cash flow and control by controlling inside shareholders is associated with lower CSR, consistent with opportunistic rent expropriation theory. We further find that CSR initiatives can impact group firms positively in the event of bad events, consistent with insurance theory. This motive for CSR as a means of enhancing reputation capital to buffer the bad events is pronounced for group firms because of group-wide dissemination of negative reputational externality

BubR1 acetylation at prometaphase is required for modulating APC/C activity and timing of mitosis

Regulation of BubR1 is central to the control of APC/C activity. We have found that BubR1 forms a complex with PCAF and is acetylated at lysine 250. Using mass spectrometry and acetylated BubR1-specific antibodies, we have confirmed that BubR1 acetylation occurs at prometaphase. Importantly, BubR1 acetylation was required for checkpoint function, through the inhibition of ubiquitin-dependent BubR1 degradation. BubR1 degradation began before the onset of anaphase. It was noted that the pre-anaphase degradation was regulated by BubR1 acetylation. Degradation of an acetylation-mimetic form, BubR1–K250Q, was inhibited and chromosome segregation in cells expressing BubR1–K250Q was markedly delayed. By contrast, the acetylation-deficient mutant, BubR1–K250R, was unstable, and mitosis was accelerated in BubR1–K250R-expressing cells. Furthermore, we found that APC/C–Cdc20 was responsible for BubR1 degradation during mitosis. On the basis of our collective results, we propose that the acetylation status of BubR1 is a molecular switch that converts BubR1 from an inhibitor to a substrate of the APC/C complex, thus providing an efficient way to modulate APC/C activity and mitotic timing

Concurrence of Stevens-Johnson Syndrome and Bilateral Parotitis after Minocycline Therapy

Minocycline is an antibiotic of tetracycline derivatives that is commonly used in the treatment of moderate to severe acne vulgaris. It has been reported to cause rare adverse events from mild cutaneous eruption to severe forms including drug-induced lupus, serum sickness-like reaction, and hypersensitivity reactions, etc. The risks of adverse events attributed to minocycline have not been ascertained reliably and there are concerns about the safety of minocycline which could possibly result in life-threatening events such as the Stevens-Johnson syndrome. Here we demonstrate an unusual case of Stevens-Johnson syndrome in conjunction with bilateral parotitis after the intake of minocycline in a Korean boy suggesting discreet use of the drug

Comparison of on-Statin Lipid and Lipoprotein Levels for the Prediction of First Cardiovascular Event in Type 2 Diabetes Mellitus

Background A substantial cardiovascular disease risk remains even after optimal statin therapy. Comparative predictiveness of major lipid and lipoprotein parameters for cardiovascular events in patients with type 2 diabetes mellitus (T2DM) who are treated with statins is not well documented. Methods From the Korean Nationwide Cohort, 11,900 patients with T2DM (≥40 years of age) without a history of cardiovascular disease and receiving moderate- or high-intensity statins were included. The primary outcome was the first occurrence of major adverse cardiovascular events (MACE) including ischemic heart disease, ischemic stroke, and cardiovascular death. The risk of MACE was estimated according to on-statin levels of low-density lipoprotein cholesterol (LDL-C), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), and non-HDL-C. Results MACE occurred in 712 patients during a median follow-up period of 37.9 months (interquartile range, 21.7 to 54.9). Among patients achieving LDL-C levels less than 100 mg/dL, the hazard ratios for MACE per 1-standard deviation change in on-treatment values were 1.25 (95% confidence interval [CI], 1.07 to 1.47) for LDL-C, 1.31 (95% CI, 1.09 to 1.57) for non-HDL-C, 1.05 (95% CI, 0.91 to 1.21) for TG, and 1.16 (95% CI, 0.98 to 1.37) for HDL-C, after adjusting for potential confounders and lipid parameters mutually. The predictive ability of on-statin LDL-C and non-HDL-C for MACE was prominent in patients at high cardiovascular risk or those with LDL-C ≥70 mg/dL. Conclusion On-statin LDL-C and non-HDL-C levels are better predictors of the first cardiovascular event than TG or HDL-C in patients with T2DM

Quality of Life after Epilepsy Surgery in Korea

Background and PurposeᄏTemporal changes in the quality of life (QOL) and the underlying factors after epilepsy surgery might be specific to Korea, where social stigma toward patients with epilepsy is still pronounced. MethodsᄏThe seizure characteristics, number of antiepileptic drugs (AEDs), and the presence of stigma, anxiety, and depression were assessed before and after surgery (at 6 months and around 2 years) in 32 surgery patients and 32 nonsurgery patients. The QOL was compared between these groups using the Epilepsy Surgery Inventory-55 questionnaire. The factors affecting QOL were also evaluated. ResultsᄏThe scores in the mental, physical, and role-functioning domains were significantly higher at 6 months (all p<0.01) and around 2 years (all p<0.01) than at baseline in the surgery group but not in the nonsurgery group. The factors related to QOL differed at the two followup times, with seizure freedom being important at 6 months, and AEDs and depression being important at around 2 years. ConclusionsᄏA marked increase in QOL in our population was observed after epilepsy surgery. Although the small sample limits the interpretation of the results, the QOL change in our surgery patients shows similar trends to those reported in Western countries. A full understanding of underlying factors related to QOL might aid the development of optimal strategies for improving the long-term postsurgery QOL in this population

Increased Risk of Hip Fracture in Patients with Acromegaly: A Nationwide Cohort Study in Korea

Background Acromegaly leads to various skeletal complications, and fragility fractures are emerging as a new concern in patients with acromegaly. Therefore, this study investigated the risk of fractures in Korean patients with acromegaly. Methods We used the Korean nationwide claims database from 2009 to 2019. A total of 931 patients with acromegaly who had never used an osteoporosis drug before and were treated with surgery alone were selected as study participants, and a 1:29 ratio of 26,999 age- and sex-matched osteoporosis drug-naïve controls without acromegaly were randomly selected from the database. Results The mean age was 46.2 years, and 50.0% were male. During a median follow-up of 54.1 months, there was no difference in the risks of all, vertebral, and non-vertebral fractures between the acromegaly and control groups. However, hip fracture risk was significantly higher (hazard ratio [HR], 2.73; 95% confidence interval [CI], 1.32 to 5.65), and non-hip and non-vertebral fractures risk was significantly lower (HR, 0.40; 95% CI, 0.17 to 0.98) in patients with acromegaly than in controls; these results remained robust even after adjustment for socioeconomic status and baseline comorbidities. Age, type 2 diabetes mellitus, cardio-cerebrovascular disease, fracture history, recent use of acid-suppressant medication, psychotropic medication, and opioids were risk factors for all fractures in patients with acromegaly (all P<0.05). Conclusion Compared with controls, patients surgically treated for acromegaly had a higher risk of hip fractures. The risk factors for fracture in patients with acromegaly were consistent with widely accepted risk factors in the general population

Serum fibroblast growth factor 1 and its association with pancreatic beta cell function and insulin sensitivity in adults with glucose intolerance

BackgroundBeneficial role of fibroblast growth factor 1 (FGF1) in the regulation of glucose metabolism and adipose tissue remodeling was suggested in rodents. This study aimed to investigate the association between serum FGF1 levels and metabolic parameters in adults with glucose intolerance.MethodsSerum FGF1 levels were examined using an enzyme-linked immunosorbent assay in 153 individuals with glucose intolerance. Associations between serum FGF1 levels and metabolic parameters, including body mass index (BMI), glycated hemoglobin (HbA1c), and 75 g oral glucose tolerance test-derived parameters, including insulinogenic index (IGI), Matsuda insulin sensitivity index (ISI), and disposition index (DI), were examined.ResultsSerum FGF1 was detected in 35 individuals (22.9%), possibly due to the autocrine/paracrine nature of the peptide. IGI and DI levels were significantly lower in individuals with higher FGF1 levels than in those with lower FGF1 levels or undetectable FGF1 (p=0.006 and 0.005 for IGI and DI, respectively, after adjustment for age, sex, and BMI). Univariable and multivariable analyses using the Tobit regression model also revealed a negative association between FGF1 levels and IGI and DI. The regression coefficients per 1-SD of log-transformed IGI and DI were −0.461 (p=0.013) and −0.467 (p=0.012), respectively, after adjustment for age, sex, and BMI. In contrast, serum FGF1 levels were not significantly associated with ISI, BMI, or HbA1c.ConclusionsThe serum concentration of FGF1 was significantly elevated in individuals with low insulin secretion, suggesting a possible interaction between FGF1 and beta cell function in humans

The Long-Term Effect of Cancer on Incident Stroke: A Nationwide Population-Based Cohort Study in Korea

Background and Purpose: Despite the recent growing interest in the cancer–stroke association, the long-term effect, and organ-specific association with stroke incidence in subjects with cancer have not been clearly defined.Methods: Data were obtained from the Korean National Health Insurance Service National Sample Cohort database between 2002 and 2015. To investigate the effects of cancer on stroke incidence, subjects were classified into cancer and non-cancer groups based on the period after cancer diagnosis and origin organ of cancer. To minimize the effects of selection bias, we performed a propensity score matching analysis with covariates of demographic data, vascular risk factors, antithrombotics use and statin use. Incident stroke was diagnosed based on operational definition and classified into ischemic stroke and hemorrhagic stroke.Results: Data of 20,707 subjects with cancer and 675,594 without cancer were analyzed for 7 follow-up years. The subjects with cancer had higher risk of any stroke (subdistribution hazard ratio [SHR], 1.13; 95% confidence interval [CI], 1.02–1.26; p = 0.0181) than those without cancer. Similar trend was found for ischemic stroke (SHR, 1.17; 95% CI, 1.05–1.31; p = 0.0054), but not for hemorrhagic stroke. The risk of stroke was increased in subjects with cancer in the digestive organ, respiratory and intrathoracic organ, and “others (such as breast and female and male reproductive organs)” in 3 years; however, the association disappeared thereafter except those with “others” cancer. Chemotherapy increased the risk of ischemic stroke (SHR 1.21; 95% CI, 1.03–1.41).Conclusions: Cancer increases the risk of stroke at 3 years after the diagnosis of cancer, and the effect was maintained for 7 years. The association between cancer and stroke incidence depends on the organ from which the cancer originated and chemotherapy

Cytomegalovirus induces abnormal chondrogenesis and osteogenesis during embryonic mandibular development

<p>Abstract</p> <p>Background</p> <p>Human clinical studies and mouse models clearly demonstrate that cytomegalovirus (CMV) disrupts normal organ and tissue development. Although CMV is one of the most common causes of major birth defects in humans, little is presently known about the mechanism(s) underlying CMV-induced congenital malformations. Our prior studies have demonstrated that CMV infection of first branchial arch derivatives (salivary glands and teeth) induced severely abnormal phenotypes and that CMV has a particular tropism for neural crest-derived mesenchyme (NCM). Since early embryos are barely susceptible to CMV infection, and the extant evidence suggests that the differentiation program needs to be well underway for embryonic tissues to be susceptible to viral infection and viral-induced pathology, the aim of this study was to determine if first branchial arch NCM cells are susceptible to mCMV infection prior to differentiation of NCM derivatives.</p> <p>Results</p> <p>E11 mouse mandibular processes (MANs) were infected with mouse CMV (mCMV) for up to 16 days <it>in vitr</it>o. mCMV infection of undifferentiated embryonic mouse MANs induced micrognathia consequent to decreased Meckel's cartilage chondrogenesis and mandibular osteogenesis. Specifically, mCMV infection resulted in aberrant stromal cellularity, a smaller, misshapen Meckel's cartilage, and mandibular bone and condylar dysmorphogenesis. Analysis of viral distribution indicates that mCMV primarily infects NCM cells and derivatives. Initial localization studies indicate that mCMV infection changed the cell-specific expression of FN, NF-κB2, RelA, RelB, and Shh and Smad7 proteins.</p> <p>Conclusion</p> <p>Our results indicate that mCMV dysregulation of key signaling pathways in primarily NCM cells and their derivatives severely disrupts mandibular morphogenesis and skeletogenesis. The pathogenesis appears to be centered around the canonical and noncanonical NF-κB pathways, and there is unusual juxtaposition of abnormal stromal cells and surrounding matrix. Moreover, since it is critically important that signaling molecules are expressed in appropriate cell populations during development, the aberrant localization of components of relevant signaling pathways may reveal the pathogenic mechanism underlying mandibular malformations.</p