This study examines whether a firm’s leverage can be used strategically to improve its bargaining position with an organized labor union using samples of non-financial firms listed on the Korean Stock Exchange (KSE) from 1999 to 2013. Through empirical testing, we find that the portfolio with the lowest union labor coverage has the lowest leverage, while the portfolio with the highest union labor coverage has the highest leverage. We also find that collective bargaining power positively affects leverage through the regression of leverage on the bargaining power of the labor union, regardless of the analysis methods, such as static and dynamic models. With a robustness test model that used the industry adjusted labor union concentration index (IUCI), we obtain evidence that collective bargaining power positively influences leverage, which corresponds with the regression results. In conclusion, we suggest the existence of evidence demonstrating that variables related to labor unions affect leverage levels, as suggested in previous studies.

Este trabajo analiza si una firma puede utilizar estratégicamente su apalancamiento para mejorar su posición negociadora con un sindicato. Para ello se utiliza información del mercado accionario de Corea para el periodo 1999-2013, encontrando una relación creciente entre cobertura sindical y apalancamiento. También se encuentra que el mayor poder en negociaciones colectivas afecta positivamente al apalancamiento.

We investigate the relationship between the capital structure and the economic conditions in Korean market. To find the adjustment behavior on capital structure depending on macroeconomic conditions, we use dynamic partial adjustment model to estimate adjustment speeds toward targets. As the data analyzed in the study, we use non-financial firms listed in the Korean stock exchange. Through the empirical test, we find evidence that is consistent with Hackbarth, Miao and Morellec (2006) and Cook and Tang (2010)'s arguments that firms tend to adjust faster their leverage toward target level in economic expansion. Thus, our findings support to the pecking order and market timing theories in terms of corporate finance theories on capital structure. In addition, our test results are re-confirmed with robust consistency even though we include year dummy variable in the empirical test model for controlling global financial crisis in contrast with Kim (2013).

En este trabajo investigamos la relación entre la estructura de capital y las condiciones económicas en el mercado coreano. Para conocer el comportamiento de ajuste de la estructura de capital respecto a las condiciones macroeconómicas, utilizamos un modelo de ajuste parcial dinámico que estima las velocidades de ajuste hacia los objetivos. Los datos analizados en el estudio corresponden a las empresas no financieras que cotizan en la bolsa de valores de Corea. Empíricamente encontramos evidencia que es consistente con los argumentos de Hackbarth, Miao y Morellec (2006) y Cook y Tang (2010), respecto a que las empresas tienden a ajustar más rápidamente su apalancamiento respecto al nivel objetivo durante la expansión económica. Por lo tanto, nuestros resultados apoyan las teorías de pecking order y de market timing en términos de las teorías de finanzas corporativas relativas a la estructura de capital. Además, los resultados de nuestras pruebas son consistentemente robustos a pesar de que incluimos en nuestro modelo una variable ficticia ligada al tiempo como mecanismo de control de la crisis financiera global, en contraste con Kim (2013).

AbstractBackground BmK I, a site-3-specific modulator of voltage-gated sodium channels (VGSCs), causes pain and hyperalgesia in rats, while BmK IT2, a site-4-specific modulator of VGSCs, suppresses pain-related responses. A stronger pain-related effect has been previously attributed to Buthus martensi Karsch (BmK) venom, which points out the joint pharmacological effect in the crude venom.Methods In order to detect the joint effect of BmK I and BmK IT2 on ND7-23 cells, the membrane current was measured by whole cell recording. BmK I and BmK IT2 were applied successively and jointly, and the synergistic modulations of VGSCs on ND7-23 cells were detected.Results Larger peak I Na and more negative half-activation voltage were elicited by joint application of BmK I and BmK IT2 than by application of BmK I or BmK IT2 alone. Compared to the control, co-applied BmK I and BmK IT2 also significantly prolonged the time constant of inactivation.Conclusions Our results indicated that site-4 toxin (BmK IT2) could enhance the pharmacological effect induced by site-3 toxin (BmK I), suggesting a stronger effect elicited by both toxins that alone usually exhibit opposite pharmacological effects, which is related to the allosteric interaction between receptor site 3 and site 4. Meanwhile, these results may bring a novel perspective for exploring the underlying mechanisms of scorpion sting-induced pain.

The JAK2/STAT3 signal pathway is an important component of survivor activating factor enhancement (SAFE) pathway. The objective of the present study was to determine whether the JAK2/STAT3 signaling pathway participates in hydrogen sulfide (H2S) postconditioning, protecting isolated rat hearts from ischemic-reperfusion injury. Male Sprague-Dawley rats (230-270 g) were divided into 6 groups (N = 14 per group): time-matched perfusion (Sham) group, ischemia/reperfusion (I/R) group, NaHS postconditioning group, NaHS with AG-490 group, AG-490 (5 µM) group, and dimethyl sulfoxide (DMSO; <0.2%) group. Langendorff-perfused rat hearts, with the exception of the Sham group, were subjected to 30 min of ischemia followed by 90 min of reperfusion after 20 min of equilibrium. Heart rate, left ventricular developed pressure (LVDP), left ventricular end-diastolic pressure (LVEDP), and the maximum rate of increase or decrease of left ventricular pressure (± dp/dt max) were recorded. Infarct size was determined using triphenyltetrazolium chloride (TTC) staining. Myocardial TUNEL staining was used as the in situ cell death detection method and the percentage of TUNEL-positive nuclei to all nuclei counted was used as the apoptotic index. The expression of STAT3, bcl-2 and bax was determined by Western blotting. After reperfusion, compared to the I/R group, H2S significantly improved functional recovery and decreased infarct size (23.3 ± 3.8 vs 41.2 ± 4.7%, P < 0.05) and apoptotic index (22.1 ± 3.6 vs 43.0 ± 4.8%, P < 0.05). However, H2S-mediated protection was abolished by AG-490, the JAK2 inhibitor. In conclusion, H2S postconditioning effectively protects isolated I/R rat hearts via activation of the JAK2/STAT3 signaling pathway.