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Musclin (MUS), an exercise-responsive myokine, has been documented to attenuate inflammation and enhance physical endurance. However, the effects of MUS on differentiation and related molecular mechanisms in adipocytes have not yet been studied. In this study, we found that treatment with MUS attenuated lipid accumulation in fully differentiated 3T3-L1 cells. Furthermore, MUS treatment enhanced lipolysis assessed by glycerol release, and caused apoptosis, whereas it reduced the expression of lipogenic proteins, such as PPARγ and processed SREBP1. Treatment with MUS augmented phosphorylated PKA expression, whereas suppressed p38 phosphorylation in 3T3-L1 adipocytes. H89, a selective PKA inhibitor reduced the effects of MUS on lipogenic lipid accumulation as well as lipolysis except for apoptosis. These results suggest that MUS promotes lipolysis and suppresses lipogenesis through a PKA/p38-dependent pathway, thereby ameliorating lipid deposition in cultured adipocytes. The current study offers the potential of MUS as a therapeutic approach for treating obesity with few side effects.

Recently, sclerostin (SCL), a circulating glycoprotein, was proposed to be a novel myokine involved in developing metabolic disorders. The association between SCL levels and insulin resistance in skeletal muscle, liver, and adipose tissue was studied in individuals with aggravated glucose tolerance. Thus, we hypothesized that elevated circulating SCL might affect skeletal muscle insulin signaling and hepatic lipid metabolism, and aimed to investigate the effects of SCL on skeletal muscle insulin resistance and hepatic steatosis in obesity using in vitro and in vivo experimental models under hyperlipidemic conditions. In the current study, we found elevated SCL messenger RNA expression levels in myocytes in obese patients. In addition to a higher blood level, SCL was expressed at an elevated level in the skeletal muscle of mice fed a high-fat diet (HFD). Higher SCL release levels and expression were also noticed in palmitate-treated C2C12 myocytes. SCL suppression by in vivo transfection improves skeletal muscle insulin resistance and hepatic steatosis in HFD-fed mice. The treatment of C2C12 myocytes with recombinant SCL aggravated insulin signaling. Furthermore, treatment with SCL augmented lipogenic lipid deposition in human primary hepatocytes. Treatment with SCL upregulated mammalian target of rapamycin (mTOR) phosphorylation and suppressed autophagy markers, thereby causing endoplasmic reticulum (ER) stress. 4-Phenylbutyric acid, a pharmacological ER stress inhibitor, abolished the effects of SCL on insulin signaling in C2C12 myocytes and lipid accumulation in primary hepatocytes. In conclusion, SCL promotes skeletal muscle insulin resistance and hepatic steatosis by upregulating ER stress via the mTOR/autophagy-mediated pathway. The present study suggests that antagonizing SCL might be a novel therapeutic strategy for simultaneously managing insulin resistance and hepatic steatosis in obesity.

The current study investigated whether netrin-1 can attenuate hepatic steatosis through PPARγ/autophagy-mediated suppression of inflammation and endoplasmic reticulum (ER) stress in experimental animal models.Hepatic steatosis was induced by a high-fat diet in experimental mice. Recombinant mouse netrin-1 was administered via the tail vein (1 μg/mouse, once every two days). Serum inflammatory cytokines and hepatic inflammatory and ER stress markers were determined in mice using ELISA and western blotting protocol.We found that netrin-1 expression was significantly increased (P 0.05) in cultured macrophages treated with supernatants of subcutaneous adipocytes in the presence of palmitate and subcutaneous fat of obese mice. Recombinant netrin-1 treatment promoted PPARγ expression and autophagy, thereby attenuating inflammation and ER stress, lipid accumulation, and the expression of lipogenic proteins in mouse primary hepatocytes. High-fat diet (HFD) treatment increased hepatic inflammation and ER stress, causing hepatic steatosis in experimental mice. However, administration of netrin-1 reversed the effects of HFD on hepatic ER stress and lipid deposition.These results suggest that subcutaneous adipose macrophage-derived netrin-1 ameliorates inflammation and ER stress in the liver, which in turn alleviates hepatic steatosis by enhancing basal PPARγ/autophagy-dependent signaling. The current study sheds light on the pathogenesis of hepatic steatosis in obesity and provides a promising therapeutic approach for treating metabolic-associated fatty liver disease (MAFLD).

Abietic acid (AA), the main component of pine resin that has been traditionally used as Asian medicine, has been reported to demonstrate anti-inflammatory activities. Despite this, little is known about the effects of AA on hepatic endoplasmic reticulum (ER) stress and lipid metabolism. This study investigated the impacts of AA on ER stress and steatosis in in vitro obesity models. We found that Treatment with AA reduced lipid deposition and lipogenesis-related proteins expression in human primary hepatocytes. Augmented expression of ER stress markers (phospho-eukaryotic initiation factor-2α (eIF2α) and C/EBP homologous protein (CHOP)) in palmitate-treated hepatocytes were reversed by AA treatment. Further, AA treatment increased the expression of phospho-AMPK and oxygen-regulated protein 150 (ORP150) in hepatocytes. siRNA-associated knockdown of AMPK or ORP150 expression reduced the effects of AA on not only hepatic ER stress but also lipogenesis and apoptosis. These results denote that AA attenuates lipid accumulation in hepatocytes in the presence of palmitate through the suppression of ER stress by AMPK/ORP150 signaling. AA could be a potential candidate for treating non-alcoholic fatty liver disease.

α-ketoisocaproic acid (AKA), a metabolite of l-leucine, is one of the branched-chain amino acids (BCAAs) involved in energy metabolism. However, the effects of AKA on lipid metabolism, insulin signaling, and related mechanisms in preadipocytes have not been reported. Herein, we investigated the impacts of AKA on lipid accumulation in 3T3-L1 murine preadipocytes. Treatment with AKA for 4 days enhanced lipid accumulation and expression of lipogenic proteins, such as cleaved sterol-regulatory element-binding proteins (SREBP1) and stearoyl-CoA desaturase-1 (SCD1) in 3T3-L1 cells. Increased endoplasmic reticulum (ER) stress markers, such as phosphorylation of eukaryotic initiation factor 2 (eIF2) and CHOP, were observed in the presence of AKA. AKA treatment increased mTOR phosphorylation and reducing autophagy markers, such as LC3 conversion and degradation of p62. Treatment with rapamycin, an mTOR inhibitor, reduced the effects of AKA on ER stress and lipogenesis in 3T3-L1 preadipocytes. The present study demonstrates that AKA increases ER stress by impairing mTOR/autophagy signaling, thus promoting lipid accumulation and insulin resistance in preadipocytes. In particular, if AKA is taken together with substances that can suppress ER stress, more effective skeletal muscle gain will be possible.

Since diabetes and hypertension frequently occur together, it is thought that these conditions may have a common pathogenesis. This study was designed to evaluate the anti-diabetic function of the anti-hypertensive drug fimasartan on C2C12 mouse skeletal muscle and HepG2 human liver cells in a high glucose state.The anti-diabetic effects and mechanism of fimasartan were identified using Western blot, glucose uptake tests, oxygen consumption rate (OCR) analysis, adenosine 5'-triphosphate (ATP) enzyme-linked immunosorbent assay (ELISA), and immunofluorescence staining for diabetic biomarkers in C2C12 cells. Protein biomarkers for glycogenolysis and glycogenesis were evaluated by Western blotting and ELISA in HepG2 cells.The protein levels of phosphorylated 5' adenosine monophosphate-activated protein kinase (p-AMPK), p-AKT, insulin receptor substrate-1 (IRS-1), and glucose transporter type 4 (Glut4) were elevated in C2C12 cells treated with fimasartan. These increases were reversed by peroxisome proliferator-activated receptor delta (PPARδ) antagonist. ATP, OCR, and glucose uptake were increased in cells treated with 200 µM fimasartan. Protein levels of glycogen phosphorylase, glucose synthase, phosphorylated glycogen synthase, and glycogen synthase kinase-3 (GSK-3) were decreased in HepG2 cells treated with fimasartan. However, these effects were reversed following the addition of the PPARδ antagonist GSK0660.In conclusion, fimasartan ameliorates deteriorations in glucose metabolism as a result of a high glucose state by regulating PPARδ in skeletal muscle and liver cells.

The effects of heat treatment conditions on the magnetic properties and microstructure of M-type strontium ferrite according to calcination temperature were analyzed. Strontium ferrite Sr0.06Ca0.52La0.52Fe11.68Co0.22O19 magnetic powder was prepared by a standard ceramic process. During experiments, the calcination temperature was varied from 1180 to 1260 °C, and sintering temperature was fixed. While the M-phase (SrFe12O19) existed with hematite (Fe2O3) in the powder calcined at below 1220 °C, the pure M-phase was observed in the powder calcined at over 1240 °C. With an increase in the calcination temperature, the magnetization of the calcined powder increases, meanwhile, the coercivity decreases. The magnetization is improved by decreasing the lattice constant c and activating the Fe3+–O–Fe3+ superexchange interaction, and the coercivity decreases by the large particle sizes due to the grain growth.

Obesity impairs wound healing with substantial alterations in skin inflammation. Patchouli alcohol (PA), extracted from patchouli, has been reported to ameliorate inflammation in various cell types. However, the effects of PA on inflammation and wound healing have not been reported to date. In the present study, we examined whether PA affects cutaneous wound healing in high fat diet (HFD)-fed mice and explored PA-mediated molecular mechanisms through in vitro experiments. We found that PA administration accelerated wound healing as well as ameliorates inflammation in skin of HFD-fed mice. PA treatment augmented AMP-activated protein kinase (AMPK) phosphorylation and TGFb1 expression. PA enhanced cell migration and suppressed inflammation in LPS-treated HaCaT cells. Further, PA increased dose-dependently AMPK phosphorylation as along with TGFb1 and cell migration markers expression. siRNA for AMPK or TGFb1 abrogated the effects of PA on cell migration and inflammation. TGFb1 siRNA mitigated PA-induced expression of cell migration markers. These results suggest that PA ameliorates wound healing via AMPK and TGFb1-mediated suppression of inflammation. In sum, PA can be used as a novel treatment strategy for wound healing in obesity or insulin resistance.

Valdecoxib (VAL) is one of the non-steroidal anti-inflammatory drugs (NSAIDs) used to treat inflammatory disorders, such as rheumatoid arthritis, osteoarthritis, and menstrual cramps. Recently, VAL ameliorates skeletal muscle insulin resistance via suppression of inflammation. However, the effects of VAL on lipid metabolism in hepatocytes have not been seen yet. This study investigated the effects of VAL on lipid accumulation and lipogenesis in human primary hepatocytes. Treatment with VAL suppressed lipid accumulation and expressions of lipogenic genes, such as processed sterol regulatory element binding proteins (SREBP1) and stearoyl-CoA desaturase-1 (SCD1) in palmitate-treated hepatocytes. Furthermore, VAL ameliorated dose-dependently palmitate-induced ER stress markers. Treatment of hepatocytes with VAL increased AMPK phosphorylation and SIRT6 expression. siRNA-mediated suppression of AMPK or SIRT6 abolished the effects of VAL on lipid accumulation, lipogenesis, and endoplasmic reticulum (ER) stress in palmitate-treated hepatocytes. Administration of VAL ameliorated hepatic lipid accumulation and lipogenic protein expression in HFD-fed mice. Moreover, in vivo AMPK siRNA transfection abolished the effects of VAL on hepatic steatosis and lipid metabolism. These results suggest that VAL suppresses ER stress through the AMPK/SIRT6 pathway, thereby attenuating hepatic steatosis under hyperlipidemic conditions. Using VAL, the current study results provide clues for developing a novel therapeutic agent for treating non-alcoholic fatty liver disease.

Here we present the resistance element welding (REW) process as a novel alternative to aluminum (Al)/steel (Fe) joints for the automotive structural assembly process. Before the REW process on the SPFC980 steels and AA5052 alloys, the low-carbon steel, S20C elements were riveted to AA5052 sheets to resolve the inconsistency of properties between Al and Fe. The REW processes were conducted with the 6 input parameters from 3.5 kA to 12 kA with a welding current under 200 ms of an energization time. As a result, robust bonding was successfully achieved exceeding 9 kN of tensile-shear strengths with excellent failure energies from the welding currents in 6.5 kA–10.5 kA without any common weld defects, e.g., crack, lack of fusion, lack of penetration, undercut, etc. These results present exceptional characteristics compared with the strength of previous reported Al/Fe joining technologies. The crystallographic characteristics of the welded metals in this process were quantitatively investigated using electron backscatter diffraction (EBSD) analysis. Due to the cooling effect the phase transformation was verified by theoretical values and finite element method (FEM) computational calculation. Furthermore, the fracture behavior analysis was thoroughly performed using the in-situ digital image correlation (DIC) method. This study provides a substantial alternative to achieve robust bonding of the automotive structural Al alloy/high tensile steel through the REW process and can be extended to mass production of lightweight structural assembly applications as well.

Obesity-induced chronic low-grade inflammation and thus causes various metabolic diseases, such as insulin resistance and non-alcoholic fatty liver disease (NAFLD). Patchouli alcohol (PA), an active component extracted from patchouli, displayed anti-inflammatory effects on different cell types. However, the impact of PA on skeletal muscle insulin signaling and hepatic lipid metabolism remains unclear. This study aimed to investigate whether PA would affect insulin signaling impairment in myocytes and lipid metabolism in hepatocytes. Treatment with PA ameliorated palmitate-induced inflammation and aggravation of insulin signaling in C2C12 myocytes and lipid accumulation in HepG2 hepatocytes. Treatment of C2C12 myocytes and HepG2 cells with PA augmented AMP-activated protein kinase (AMPK) phosphorylation and Sirtuin 1 (SIRT1) expression in a dose-dependent manner. siRNA-mediated suppression of AMPK or SIRT1 mitigated the effects of PA on palmitate-induced inflammation and insulin resistance in C2C12 myocytes and lipid accumulation in HepG2 cells. Animal experiments demonstrated that PA administration increased AMPK phosphorylation and SIRT1 expression, and ameliorated inflammation, thereby attenuating skeletal muscle insulin resistance and hepatic steatosis in high-fat diet-fed mice. These results denote that PA alleviates skeletal muscle insulin resistance and hepatic steatosis through AMPK/SIRT1-dependent signaling. This study might provide a novel therapeutic approach for treating obesity-related insulin resistance and NAFLD.

In this study, we have developed the manufacturing technology for high strength gray cast irons by using the spent permanent magnet scraps. The cast specimen inoculated by using a spent magnet scraps showed the excellent tensile strength up to 306MPa. This tensile strength value is 50MPa higher than that of the specimen cast without inoculation, and is similar to that of the specimen inoculated by using the expensive misch-metal. These superior mechanical properties are attributed to complex sulfides created during solidification that promote the formation and growth of Type-A graphite. It is therefore concluded that spent magnets scrap can provide an efficient and cost-effective inoculation agent for the fabrication of high-performance gray cast iron.

Research suggests that school-aged individuals with intellectual disabilities (ID) tend to be less physically active than their typically developing peers (e.g., Shields, King, Corbett, & Imms, 2014). While these students can be successful in acquiring motor and sport-related skills during physical education, they tend not to use those skills in settings outside of school (Reid, 1993; Yang & Porretta, 1999). This can be due to difficulties with generalization. Generalization refers to the use of newly acquired skills or behaviors in non-training environments (Cooper, Heron, & Heward, 2007). Difficulties with generalization of motor skills may contribute to low levels of physical activity and sport participation by individuals with ID outside of physical education. Since the generalization of skills learned in physical education may not occur automatically, physical education teachers must plan and teach for generalized outcomes. Therefore, the purpose of this paper is to describe how physical education te...

Chemotherapy has long been considered as one of useful strategies for cancer treatment. It is primarily based on the apoptosis that can selectively kill cancer cells. However, cancer cells can progressively develop an acquired resistance to apoptotic cell death, rendering refractory to chemo- and radiotherapies. Although the mechanism by which cells attained resistance to drug remains to be clarified, it might be caused by either pumping out of them or interfering with apoptotic signal cascades in response to cancer drugs. In case that cancer cells are defective in some part of apoptotic machinery by repeated exposure to anticancer drugs, alternative cell death mechanistically distinct from apoptosis could be adopted to remove cancer cells refractory to apoptosis-inducing agents. This review will mainly deal with harnessing of necrotic cell death, specifically, programmed necrosis and practical uses. Here, we begin with various defects of apoptotic death machinery in cancer cells, and then provide new perspective on programmed necrosis as an alternative anticancer approach.

The enzyme 11β-hydroxysteroid dehydrogenase 1 (11β-HSD1) is known to catalyse inactive glucocorticoids into active forms, and its dysregulation in adipose and muscle tissues has been implicated in the development of metabolic syndrome. To delineate the molecular mechanism by which active cortisol has an antagonizing effect against insulin, we optimized the metabolic production of cortisol and its biological functions in myotubes (C2C12). Myotubes supplemented with cortisone actively catalysed its conversion into cortisol, which in turn abolished phosphorylation of Akt in response to insulin treatment. This led to diminished uptake of insulin-induced glucose. This was corroborated by the application of 11β-HSD1 inhibitor glycyrrhetinic acid and a glucocorticoid receptor antagonist RU-486, which reversed completely the antagonizing effects of cortisol on insulin action. Therefore, development of specific inhibitors targeting 11β-HSD1 might be a promising way to improve impaired insulin-stimulated glucose uptake. Copyright © 2013 John Wiley & Sons, Ltd.

Upon tumour necrosis factor alpha (TNFα) stimulation, cells respond actively by way of cell survival, apoptosis or programmed necrosis. The receptor-interacting proteins 1 (RIP1) and 3 (RIP3) are responsible for TNFα-mediated programmed necrosis. To delineate the differential contributions of RIP3 and RIP1 to programmed necrosis, L929 cells were stimulated with TNFα, carbobenzoxy-valyl-alanyl-aspartyl-[O-methyl]-fluoromethylketone (zVAD) or zVAD along with TNFα following RNA interference against RIP1 and RIP3, respectively. RIP1 silencing did not protect cells from TNFα-mediated cell death, while RIP3 down-regulation made them refractory to TNFα. The heat shock protein 90 inhibitor geldanamycin (GA) down-regulated both RIP1 and RIP3 expression, which rendered cells resistant to zVAD/TNFα-mediated cell death but not to TNFα-mediated cell death alone. Therefore, the protective effect of GA on zVAD/TNFα-stimulated necrosis might be attributed to RIP3, not RIP1, down-regulation. Pretreatment of L929 cells with rapamycin mitigated zVAD-mediated cell death, while the autophagy inhibitor chloroquine did not affect necrotic cell death. Meanwhile, necrotic cell death by zVAD and TNFα was caused by reactive oxygen species generation and effectively diminished by lipid-soluble butylated hydroxyanisole. Taken together, the results indicate that RIP1 and RIP3 can independently mediate death signals being transduced by two different death stimuli, zVAD and TNFα.

The effects of rare earth element (R.E.) and cooling rate on the eutectic reaction of flake graphite cast irons were studied by combined analysis of macro/micro-structure and cooling curve data. The correlation between eutectic reaction parameter and macro/micro-structure was systematically investigated. Two sets of chemical compositions with the different addition of R.E. were designed to cast. Three types of molds for cylindrical specimens with the different diameters were prepared to analyze cooling rate effect. The difference between undercooling temperature and cementite eutectic temperature (${\Delta}T_1

Background: Due to the increment of general interest in breast cancer and the early screening examination, the rate of early breast cancer is relatively increasing, along the rate of the successful treatment. Even at the earlier stage of breast cancer, the process of axillary lymph node metastasis is significant for treatment and prognosis of the cancer. Therefore, the aim of the study is to identify the factors that influence the lymph node metastasis among the patients with T1 breast cancer. Methods: Between January 2003 and May 2008, 204 patients diagnosed as infiltrating ductal carcinoma after the breast cancer resection at Gachon University Gil Hospital were enrolled in the study. Each patient"s age, size and location of cancer, number of tumor, tissue and nuclear grade, infiltration of lymph vessels, immunohistochemistry test result(ER, PR, p53, HER2, Ki67, etc.), and axillary lymph node status were compared. Results: 10 out of 204 patients had cancer smaller than 0.5cm(T1a), 22 patients had cancer size larger than 0.5cm and smaller than 1cm(T1b), and 172 patients had cancer size larger than 1cm(T1c). For the rate of axillary lymph node metastasis, in the group of T1a, 1/10(10%) patients showed axillary lymph node metastasis, in T1b, 2/22(9.1%) patients showed axillary lymph node metastasis and in T1c, 54/172(31.3%) patients showed axillary lymph node metastasis. The result distinguished by the size of the cancer was statistically significant(p=0.039). The number of tumor was sorted as 1, 2, and more than 3, and each integer was 179, 17, and 8 patients. The rate of axillary lymph node metastasis according to the number of tumor was 48/179(26.8%) with 1 tumor, 5/17(29.4%) with 2 tumors, and 4/8(50%) with more than 3 tumors. This result distinguished by the number of tumor was also statistically significant(p=0007). Also, Lymphovascular invasion was statistically significant(p=0001). The rate of axillary lymph node metastasis did not show the statistical significance with the age of patients, location of cancer, tissue and nuclear grade, and immunohistochemistochemical staining result. Conclusion: It Is considered that the size and the number of tumor, and lymphovascular infiltration are the significant factors influencing axillary lymph node metastasis of the T1 invasive ductal carcinoma. Furthermore, it is expected that the size and the number of tumor in preoperative ultasonography will be helpful determining the axillary lymph node dissection.

Mesenchymal stem cells(MSCs) have the potential to self-replicate, proliferate and differentiate into chondrocytes, adipocytes, osteocytes and myocytes. Recent studies indicate that vitamin K2 plays a role in bone metabolism. But the mechanism is still unclear. We evaluated effect of vitamin K2 on osteogenesis and adipogenesis of MSCs from umbilical cord blood(UCB). By exposing MSCs to osteogenic and adipogenic medium with and without vitamin K2, the effects of vitamin K2 were analyzed. The results showed that vitamin K2 inhibits adipogenesis while at the same time it stimulates osteoblastic differentiation. These data are expected to provide novel information needed for successful therapeutic development for various types of osteoporosis and similar diseases related to bone formation.

Upon tumour necrosis factor alpha (TNFα) stimulation, cells respond actively by way of cell survival, apoptosis or programmed necrosis. The receptor-interacting proteins 1 (RIP1) and 3 (RIP3) are responsible for TNFα-mediated programmed necrosis. To delineate the differential contributions of RIP3 and RIP1 to programmed necrosis, L929 cells were stimulated with TNFα, carbobenzoxy-valyl-alanyl-aspartyl-[O-methyl]-fluoromethylketone (zVAD) or zVAD along with TNFα following RNA interference against RIP1 and RIP3, respectively. RIP1 silencing did not protect cells from TNFα-mediated cell death, while RIP3 down-regulation made them refractory to TNFα. The heat shock protein 90 inhibitor geldanamycin (GA) down-regulated both RIP1 and RIP3 expression, which rendered cells resistant to zVAD/TNFα-mediated cell death but not to TNFα-mediated cell death alone. Therefore, the protective effect of GA on zVAD/TNFα-stimulated necrosis might be attributed to RIP3, not RIP1, down-regulation. Pretreatment of L929 cells with rapamycin mitigated zVAD-mediated cell death, while the autophagy inhibitor chloroquine did not affect necrotic cell death. Meanwhile, necrotic cell death by zVAD and TNFα was caused by reactive oxygen species generation and effectively diminished by lipid-soluble butylated hydroxyanisole. Taken together, the results indicate that RIP1 and RIP3 can independently mediate death signals being transduced by two different death stimuli, zVAD and TNFα.

Post-translational modification of peptidyl cis/trans prolyl isomerase Pin1 is crucial in regulation of gene stability. Pin1 phosphorylation at Ser(16) has been regarded as a marker for Pin1 isomerase activity and introduction of phosphorylation on Ser/Thr-Pro of substrate proteins is prerequisite for its binding activity with Pin1 and subsequent isomerization. Here, we found that 90 kDa ribosomal protein S6 kinase 2 (RSK2) could form a physical complex with Pin1, leading to phosphorylation of Pin1 at Ser(16) ex vivo and in vitro respectively. Intriguingly, Pin1(+/+) mouse embryonic fibroblasts (MEFs) exhibited significantly an increase in 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced RSK2 phosphorylation with a marginal Pin1 phosphorylation compared with Pin1(-/-) MEFs. Moreover, TPA-induced Ser(16) Pin1 phosphorylation as well as RSK2 phosphorylation was considerably profound in RSK(+/+) MEFs but not in RSK(-/-) MEFs. Consequently, knockdown of Pin1 using shRNA-Pin1 suppressed TPA-induced cell transformation in JB6 CI41 cells. Overall, these results indicate that Pin1 plays a critical role in TPA-induced tumorigenesis plausibly via physical interaction with RSK2 and reciprocal phosphorylation, therefore suggesting a potential therapeutic target for cancer treatment.

Cell death occurs spontaneously or in response to external stimuli, and can be largely subdivided into apoptosis and necrosis by the distinct morphological and biochemical features. Unlike apoptosis, necrosis was recognized as the passive and unwanted cell demise committed in a non-regulated and disorganized manner. However, under specific conditions such as caspase intervention, necrosis has been proposed to be regulated in a well-orchestrated way as a backup mechanism of apoptosis. The term programmed necrosis has been coined to describe such an alternative cell death. Recently, at least some regulators governing programmed necrosis have been identified and demonstrated to be interconnected via a wide network of signal pathways by further extensive studies. There is growing evidence that programmed necrosis is not only associated with pathophysiological diseases, but also provides innate immune response to viral infection. Here, we will introduce recent updates on the molecular mechanism and physiological significance of programmed necrosis.

(Gd123) powders were synthesized by the solid-state reaction method using (99.9% purity), (99.75%) and CuO (99.9%) powders. The synthesized Gd123 powder and the Gd123 powder with addition ((Gd1.5)) were used as raw powders for the fabrication of Gd123 bulk superconductors. The Gd123 and Gd1.5 bulk superconductors were fabricated by sintering or a top-seeded melt growth (TSMG) process. The superconducting transition temperature () of the sintered Gd123 was 93 K and the transition width was as large as 20 K. The of the TSMG processed Gd123 was 82 K and the transition width was also as large as 12 K. The critical current density () at 77 K and 0 T of the sintered Gd123 and TSMG processed Gd123 were as low as a few hundreds A/. The addition of 0.25 mole and 1 wt.% to Gd123 enhanced the , and magnetic flux density (H) of the TSMG processed Gd123 sample owing to the formation of the superconducting phase with high flux pinning capability. The of the TSMG processed Gd1.5 was 92 K and the transition width was 1 K. The at 77 K (0 T and 2 T) were and , respectively. The H at 77 K of the TSMG-processed Gd1.5 was 1.96 kG, which is 54% of the applied magnetic field (3.45 kG).

Large single grain (Gd1.5) bulk superconductors were fabricated by a top-seeded melt growth (TSMG) process using an seed. The seeded Gd1.5 powder compacts with a diameter of 50 mm were subjected to the heating cycles of a TSMG process. After the TSMG process, the diameter of the single grain Gd1.5 compact was reduced to 43 mm owing to the volume contraction during the heat treatment. The superconducting transition temperature () of the top surface of the single grain Gd1.5 sample was as high as 93.5 K. The critical current densities () at 77 K and 1T and 1.5 T were in ranges of 25,200-43,900 and 10,000-23,000 , respectively. The maximum attractive force at 77 K of the sample field-cooled using an Nd-B-Fe permanent magnet (surface magnetic field of 0. 527 T) was 108.3 N; the maximum repulsive force of the zero field-cooled sample was 262 N. The magnetic flux density of the sample field-cooled at 77 K was 0.311T, which is approximately 85% of the applied magnetic field of 0.375 T. Microstructure investigation showed that many (Gd211) particles of a few in size, which are flux pinning sites of Gd123, were trapped within the (Gd123) grain; unreacted liquid and Gd211 particles were present near the edge regions of the single grain Gd1.5 bulk compact.

Purpose: Gum chewing activates chephalic-vagal reflex as in food consumption and increases the release of gastrointestinal hormones which are related with gut motility. The objective of this study was to assess whether it is effective in shortening the time of hospitalization and postoperative ileus. Methods: Twenty patients who received open abdominal surgery for colon cancer in Gachon University, Gil Hospital were collected. They were further categorized to gum-chewing group (n=10, mean age=52.0 years, range 37 to 70) and control group (n=10, mean age=59.7 years, range 35 to 75) randomly. The patients in the gum-chewing group chewed gum three times a day from the first postoperative AM until the day they began oral intake. The time of gas out was recorded in each group. Results: The mean time of gas out were 2.35 days (SD 1.2) in gum-chewing group and 2.87 days (SD 1.2) in control group (P=0.41). The mean postoperative hospital days were 10.5 days in gum-chewing group and 13.0 days in control group (P=0.23). Conclusion: There were no statistically significant results for shortnening of postoperative ileus and hospital day in this study.

Purpose: Breast cancer has been reported as the most common cancer of women in the United States, Western Europe and Korea and about 210,000 and 10,000 women in United States and Korea every year, respectively are diagnosed with it. Breast cancer is curable with an early diagnosis, and many researchers have made efforts to find a marker for this malady, heat shock protein (HSP) consists of 6 groups, it is highly preserved throughout both the prokaryotic and eukaryotic cells and it acts as a molecular chaperone that’s involved in protein folding. HSPs have been recently reported to be related with breast cancer. In this study, we investigated the changes of expression of HSP60 in tissues and cell lines of breast cancer. Methods: We obtained breast cancer tissues and normal tissues from breast cancer patients, and we purchased several cancer cell lines from American tissue culture correction. We treated the tissues and the cell lines of human breast cancer with heat shock protein. Proteins and mRNAs were isolated from the tissues and the cells and then we performed Western blotting, reverse transcriptase-Polymerase chain Reaction and fluorescence activated cell sorter analysis on them. Results: On Western blot, HSP60 was more overexpressed in the tissues and the cell lines of breast cancer than in the normal breast tissues and cell lines. The expression of HSP60 showed 2 types of molecular weight differences in the tissues and cell lines of breast cancer, and specifically, low HSP60 was over-expressed in the cancer tissues. There was no difference between the breast cancer cell lines and the normal cell lines in the expressions of HSP60 mRNA, according to the treatment with heat shock. Also, there was no relationship between phosphorylation and the structural difference of HSP60 protein, according to HSP60 protein’s molecular weight. The expression of HSP60 has been mostly reported at the mitochondria; however, in this study, it was more predominantly detected at the cytoplasm than at the mitochondria in the breast cancer cell lines. Conclusion: We conclude that HSP60 may be used as a diagnostic marker for breast cancer. Detailed investigation of the usefulness and significance of the HSP60 expression as a prognostic factor is required in further studies.