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This study aimed to investigate whether the midlife cognitive activity and physical activity moderate the relationship between apolipoprotein Eε4 (APOE4) and in vivo Alzheimer’s disease (AD) pathologies. In total, 287 non-demented older adults (mean age 72 years) from the Korean Brain Aging Study for the Early diagnosis and prediction of Alzheimer’s disease cohort were included. Participants underwent a comprehensive clinical assessment including the evaluation for midlife CA and physical activity, [11C]-Pittsburgh-Compound-B-positron emission tomography (PET), [18F]-fluorodeoxyglucose PET, structural magnetic resonance imaging (MRI), and APOE genotyping. We used linear regression and regression-based mediated-moderation models for statistical analyses. Neither midlife cognitive activity nor physical activity moderated the effect of APOE4 on β-amyloid (Aβ) retention itself. Midlife cognitive activity significantly moderated the effect of APOE4 on hippocampal volume [B (SE) = − 627.580 (252.327), t = −2.488, p = 0.014]: APOE4 carriers had smaller hippocampal volume than non-carriers at relatively high cognitive activity state (p = 0.004), but not at relatively low cognitive activity condition (p = 0.937). Midlife physical activity significantly moderated the effect of Aβ retention, which was closely related to APOE4, on AD-signature region cerebral glucose metabolism [AD-CM; B (SE) = 0.004 (0.002), t = 2.030, p = 0.043]: higher Aβ accumulation was associated with lower AD-CM in relatively low physical activity condition (p < 0.001), whereas no such association was observed in relatively high physical activity state (p = 0.791). The findings suggest that high midlife cognitive activity may accelerate hippocampal atrophy induced by APOE4, whereas high midlife physical activity may delay AD-related cerebral hypometabolism by weakening the influence of APOE4-associated Aβ retention.

The language of Haggai, Zechariah, and Malachi, the three postexilic prophets, has been relatively unstudied with regard to its contribution to a diachronic understanding of Late Biblical Hebrew. Recent scholarship argues that the entire biblical corpus was written in the literary Hebrew of the Persian and Hellenistic periods with no clear-cut dichotomy between Standard Biblical Hebrew and Late Biblical Hebrew. This view posits that Early Biblical Hebrew and Late Biblical Hebrew coexisted, places the Hebrew of Haggai, Zechariah, and Malachi at the center of the controversy, and claims that these postexilic prophetic books contain primarily Early Biblical Hebrew with very few Late Biblical Hebrew elements. Through discussion of selected items in morphology, phraseology, semantics, and orthography, this study shows that, contrary to the prevailing view, Haggai, Zechariah, and Malachi make considerable use of Late Biblical Hebrew.

Enforced environmental regulations call for extending the domain of manufacturers` responsibility to the entire product life cycle. To comply with the environmental regulations, manufacturers have constructed reverse logistics networks to re-collect their leftover waste for recycling consumed resources. However, the operational activities associated with storage, loading and transportation processes within the networks inevitably impose environmental burdens. Particularly, the transportation process largely influences environmental performance due to perpetual uses of transportation vehicles. Therefore, there is a need to develop an environmentally-conscious transportation model that can efficiently manage the uses of transportation vehicles. Additionally, it is vital to analyze its significances of environmental performance to compare quantitatively it with existing models. This paper proposes a transportation model for improving environmental performance in a reverse logistics network. This paper also presents a case study to perform its comparative analysis using Life Cycle Assessment that evaluates potential environmental impacts of a product system.

Objectives: Leukocyte NADPH oxidase, which is active in neutrophils, is a membrane-bound enzyme that catalyzes the reduction of oxygen to O(2)(−) by using NADPH as an electron donor. Previously, we reported that casein kinase 2 (CK2), a ubiquitous and highly conserved Ser/Thr kinase, is responsible for p47(phox) phosphorylation and that phosphorylation of p47(phox) by CK2 regulates the deactivation of NADPH oxidase. Methods: Here, we report that the residue Cys(196) of p47(phox) is a target of S-nitrosylation by S-nitrosothiol and peroxynitrite and that this modification enhanced phosphorylation of p47(phox) by CK2. Results: S-Nitrosylated p47(phox) enhanced CK2 b subunit binding, presumably due to alterations in protein conformation. Discussion: Taken together, we propose that S-nitrosylation of p47(phox) regulates the deactivation of NADPH oxidase via enhancement of p47(phox) phosphorylation by CK2

The epidermis, the outermost layer of the skin, is a stratified epithelium that protects the body from the external environment. Keratinocyte stem cells (KSCs) are involved in epidermis homeostasis by maintaining epidermal integrity through a process of constant regeneration. Ultraviolet B (UVB) radiation is a major inducer of cellular damage in the epidermis. In this study, we investigated the effects of zingerone (a phenolic compound derived from spices) on UVB-induced cellular damage in KSCs. We found that zingerone significantly inhibited cellular senescence of KSCs in response to UVB irradiation. These effects were confirmed by the senescence-associated β-galactosidase and comet assays. Zingerone decreased the production of proinflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) in UVB-irradiated KSCs. Moreover, UVB-induced expression of p21, a cell cycle arrest-related gene, was reduced by zingerone treatment, whereas zingerone upregulated the expression of proliferation-related genes such as proliferating cell nuclear antigen (PCNA) and vascular endothelial growth factor (VEGF), in addition to anti-senescence-related genes including telomerase reverse transcriptase (TERT), histone deacetylase 1 (HDAC1), and DNA (cytosine-5)-methyltransferase 1 (DNMT1). The UVB-protective effects of zingerone were mediated by inhibition of p42/44 MAPK and p38 MAPK. Therefore, zingerone could potentially be used to protect the epidermis from UVB-induced damage.

BackgroundClinical significance of statin-induced high-density lipoprotein cholesterol (HDL-C) changes is not well known. We investigated the factors affecting rosuvastatin-induced HDL-C changes and their correlation with 12-month major adverse cardiovascular events (MACE) in patients with non-ST-segment elevation acute coronary syndrome (NSTE-ACS) and percutaneous coronary intervention (PCI).Materials and methodsWe analyzed 556 consecutive NSTE-ACS patients who underwent PCI and received rosuvastatin 10mg before discharge. We measured serum lipids, including total cholesterol, triglycerides (TGs), low-density lipoprotein cholesterol (LDL-C), and HDL-C at baseline and at 4 weeks. The relationship between on-treatment lipid levels, baseline lipid levels, and 12-month MACE was assessed.ResultsRosuvastatin treatment increased the mean HDL-C concentration by 1.1±9.8mg/dl (4.3±23.0%). HDL-C was increased in 312 patients (56.1%), but decreased in 244 patients (43.9%) after statin treatment. Changes in HDL-C during first month were inversely correlated with baseline HDL-C levels (r=−0.379, p

Phagocyte NADPH oxidase catalyzes the reduction of molecular oxygen to superoxide and is essential for defense against microbes. Rac2 is a low molecular weight GTP-binding protein that has been implicated in the regulation of phagocyte NADPH oxidase. Here we report that Cys(157) of Rac2 is a target of S-glutathionylation and that this modification is reversed by dithiothreitol as well as enzymatically by thioltransferase in the presence of GSH. S-glutathionylated Rac2 enhanced the binding of GTP, presumably due to structural alterations. These results elucidate the redox regulation of cysteine in Rac2 and a possible mechanism for regulating NADPH oxidase activation.

Brefeldin A (BFA), an endoplasmic reticulum (ER)-Golgi transport inhibitor, has been shown to cause accumulation of proteins in the ER, ER stress, and ultimately apoptosis. In this paper, we demonstrate that the knockdown of mitochondrial NADP(+)-dependent isocitrate dehydrogenase (IDPm), a mitochondrial NADPH-generating enzyme, by small interfering RNA (siRNA) enhanced BFA-induced apoptosis. However, attenuated IDPm activity results in the suppression of ER stress response, presumably, via the inhibition of the PI3K/Akt pathway. Collectively, our data suggest that the association of IDPm expression and ER stress confers a survival mechanism in A549 cells against BFA-induced apoptosis.

The research aimed to investigate international students' levels of motivation to work in the hospitality industry. A survey was conducted with 193 international hospitality students in Brisbane and the Gold Coast, Southeast Queensland, Australia. The research, using expectancy motivation theory, found that the level of motivation during their industry experience programs was not high. This outcome should provide valuable information for education providers and industry practitioners to help them improve motivation levels of international students who study hospitality programmes overseas. © Journal of Hospitality, Leisure, Sport and Tourism Education.

Even patients without vasospastic angina show vasoconstriction after intracoronary ergonovine administration. We evaluated the determinants of coronary artery responsiveness to ergonovine in such patients.In 165 patients with no provoked electrocardiographic changes or ischemic chest pain during an intracoronary ergonovine test, total cholesterol, triglycerides (TG), high density lipoprotein cholesterol (HDL), and low density lipoprotein cholesterol (LDL) were correlated with the arterial luminal diameters before and after ergonovine infusion and after nitroglycerin injection by quantitative coronary angiography analysis.The mean and maximal basal tone (ie, percent change between baseline luminal diameter and diameter after nitroglycerin) were 7.0 ± 9.9% and 27.9 ± 10.8%, respectively. The mean and maximal responsiveness to ergonovine (ie, percent change between minimal diameter during ergonovine infusion and diameter after nitroglycerin) were 30.3 ± 13.6% and 52.7 ± 16.0%, respectively. The TG level (r = 0.191, P = 0.016) and TG/HDL ratio (r = 0.182, P = 0.021) were positively correlated with the basal tone, whereas LDL level (r = 0.155, P = 0.048) and LDL/HDL ratio (r = 0.172, P = 0.030) were positively correlated with the responsiveness to ergonovine. By multivariate analysis, LDL level, LDL/HDL ratio, and smoking were independent predictors of more than 50% responsiveness to ergonovine.Serum lipid profile and smoking influence the basal tone and responsiveness to ergonovine of coronary artery in patients without vaospastic angina.

Purpose: The purpose of this study was to evaluate the usefulness and clinical results of arthroscopic double row repair with UU stitches for massive, full-thickness, rotator cuff tears. Materials and Methods: Between January 2007 and July 2009, we consulted on 36 massive tears in which it was possible to repair the middle area of the greater tuberosity by arthroscopy. One group consisted of 11 cases that had a double row repair with UU stitches. A second group consisted of 20 cases that had a single row repair with simple stitches. We compared the 2 groups for pain, Activities of Daily Living, UCLA score, and KSS score. We did this pre operatively, and at 6 months, 1 year and final follow-ups. Statistical analysis included Student`s t test and a paired t est. Mean age was 59 (48~70); mean follow-up was 28 (12~43) months Results: VAS scores decreased from 7.5 pre operatively to 1.5 post operatively at the last f/u in the group (p group, the score decreased from 7.6 in pre op to 1.8 post operatively at the last f/u (p0.05). Mean ADL increased from 11.5 to 25.1 at the last f/u in the group (p group the ADL score increased from 11.3 to 27.5 (p0.05). The UCLA score increased from 13.9 to 31.6 in the group (p group the score increased from 13.8 to 30.1 (p0.05). Comparing MRIs at 3 and 6 months post op, there were retears in 3 of 9 cases in the first group, and in 8 of 15 cases in the second group; there was no significant difference between the two groups (p>0.05). Conclusion: Arthroscopic double row repair with UU stitches for massive, full-thickness rotator cuff tears showed no differences in clinical results. However, it was associated with a significant difference in the incidence of retears.

This study was carried out to develop turning radius measuring method and device of using a DGPS speed sensor for agricultural tractors. The measurement system consisted of a DGPS speed sensor, a data acquisition device, a touch panel, a photo sensor, a radio modem and a notebook computer. Three methods were developed: average of turning speed-time method, integral of turning speed-time method, and speed-heading angular velocity method. Best method was average of turning speed-time method which could be used with a maximum error 2.7 cm.

Cadmium ions have a high affinity for thiol groups. Therefore, they may disturb many cellular functions. We recently reported that cytosolic NADP+-dependent isocitrate dehydrogenase (IDPc) functions as an antioxidant enzyme to supply NADPH, a major source of reducing equivalents to the cytosol. Cadmium decreased the activity of IDPc both as a purified enzyme and in cultured cells. In the present study, we demonstrate that the knockdown of IDPc expression in HEK293 cells greatly enhances apoptosis induced by cadmium. Transfection of HEK293 cells with an IDPc small interfering RNA significantly decreased the activity of IDPc and enhanced cellular susceptibility to cadmium-induced apoptosis as indicated by the morphological evidence of apoptosis, DNA fragmentation and condensation, cellular redox status, mitochondria redox status and function, and the modulation of apoptotic marker proteins. Taken together, our results suggest that suppressing the expression of IDPc enhances cadmium-induced apoptosis of HEK293 cells by increasing disruption of the cellular redox status.

Myeloperoxidase catalyzes the formation of hypochlorous acid (HOCI) via reaction of H2O2 with CI(-) ions. Although HOCI plays a major role in the human immune system by killing bacteria and other invading pathogens, excessive generation of this oxidant causes damage to tissues. Exposure of HeLa cells to HOCI decreased viability, inactivated antioxidant enzymes, damaged mitochondria, and modulated cellular redox status. HOCI also induced significant increases in cellular oxidative damage reflected by lipid peroxidation, protein oxidation, and DNA damage. HOCI-mediated oxidative damage to HeLa cells may perturb the cellular antioxidant defense mechanisms and subsequently lead to a pro-oxidant state.

Heat shock may increase oxidative stress due to increased production of reactive oxygen species and/or the promotion of cellular oxidation events. Sensitive to apoptosis gene (SAG) protein, a novel zinc RING finger protein that protects mammalian cells from apoptosis by redox reagents, is a metal chelator and a potential reactive oxygen species scavenger, but its antioxidant properties have not been completely defined. In this report, we demonstrate that modulation of SAG expression in U937 cells regulates heat shock-induced apoptosis. When we examined the protective role of SAG against heat shock-induced apoptosis with U937 cells transfected with the cDNA for SAG, a clear inverse relationship was observed between the amount of SAG expressed in target cells and their susceptibility to apoptosis. We also observed a significant decrease in the endogenous production of reactive oxygen species and oxidative DNA damage in SAG-overexpressed cells compared to control cells on exposure to heat shock. In addition, transfection of PC3 cells with SAG small interfering RNA markedly decreased the expression of SAG, enhancing the susceptibility of heat shock-induced apoptosis. Taken together, these results indicate that SAG may play an important role in regulating the apoptosis induced by heat shock presumably through maintaining the cellular redox status.

The current study evaluated the technical feasibility of the application of titanium dioxide () photo-catalytic air cleaners for the disinfection of bioaerosols present in indoor air. The evaluation included both laboratory and field tests and the tests of hydraulic diameter (HD) and lamp type (LT). Disinfection efficiency of photocatalytic oxidation (PCO) technique was estimated by survival ratio of bacteria or fungi calculated from the number of viable cells which form colonies on the nutrient agar plates. It was suggested that the reactor coating with did not enhance the adsorption of bioaerosols, and that the UV irradiation has certain extent of disinfection efficiency. The disinfection efficiency increased as HD decreased, most likely due to the decrease in the light intensity since the distance of the catalyst from the light source increased when increasing the HD. It was further suggested that the mass transfer effects were not as important as the light intensity effects on the PCO disinfection efficiency of bioaerosols. Germicidal lamp was superior to the black lamp for the disinfection of airborne bacteria and fungi, which is supported by the finding that the disinfection efficiencies were higher when the germicidal lamp was used compared to the black lamp in the laboratory test. These findings, combined with operational attributes such as a low pressure drop across the reactor and ambient temperature operation, can make the PCO reactor a possible tool in the effort to improve indoor bioaerosol levels.

Ultraviolet (UV) radiation induces DNA damage, oxidative stress, and inflammatory processes in human keratinocytes, resulting in skin inflammation, photoaging, and photocarcinogenesis. Adequate protection of skin against the harmful effects of UV irradiation is essential. Therefore, in this study, we investigated the protective effects of afzelin, one of the flavonoids, against UV irradiation in human keratinocytes and epidermal equivalent models. Spectrophotometric measurements revealed that the afzelin extinction maxima were in the UVB and UVA range, and UV transmission below 376 nm was

Prostate cancer is one of the most commonly occurring malignancies in men, and because existing treatments are not able to manage this neoplasm adequately, novel approaches are needed. Although tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has strong antitumor activity via the induction of apoptotic cell death in a wide range of tumor cell types and has negligible toxicity to most normal cells, some prostate carcinoma cells are resistant to the apoptotic effects of TRAIL. Therefore, combinatorial approaches with TRAIL and different chemotherapeutic agents have been developed to overcome the resistance of cancer cells to TRAIL. Here, we investigated the sensitizing effects of ursolic acid (UA), a pentacyclic triterpenoid found in many plants, on TRAIL-induced prostate cancer cell apoptosis. We found TRAIL-induced prostate cancer cells apoptosis was significantly enhanced by UA, and that UA induced CHOP-dependent DR5 up-regulation. This study shows the use of UA as a sensitizer for TRAIL-induced apoptotic cell death offers a promising means of enhancing the efficacy of TRAIL-based prostate cancer treatments.

Even patients without vasospastic angina show vasoconstriction after intracoronary ergonovine administration. We evaluated the determinants of coronary artery responsiveness to ergonovine in such patients.In 165 patients with no provoked electrocardiographic changes or ischemic chest pain during an intracoronary ergonovine test, total cholesterol, triglycerides (TG), high density lipoprotein cholesterol (HDL), and low density lipoprotein cholesterol (LDL) were correlated with the arterial luminal diameters before and after ergonovine infusion and after nitroglycerin injection by quantitative coronary angiography analysis.The mean and maximal basal tone (ie, percent change between baseline luminal diameter and diameter after nitroglycerin) were 7.0 ± 9.9% and 27.9 ± 10.8%, respectively. The mean and maximal responsiveness to ergonovine (ie, percent change between minimal diameter during ergonovine infusion and diameter after nitroglycerin) were 30.3 ± 13.6% and 52.7 ± 16.0%, respectively. The TG level (r = 0.191, P = 0.016) and TG/HDL ratio (r = 0.182, P = 0.021) were positively correlated with the basal tone, whereas LDL level (r = 0.155, P = 0.048) and LDL/HDL ratio (r = 0.172, P = 0.030) were positively correlated with the responsiveness to ergonovine. By multivariate analysis, LDL level, LDL/HDL ratio, and smoking were independent predictors of more than 50% responsiveness to ergonovine.Serum lipid profile and smoking influence the basal tone and responsiveness to ergonovine of coronary artery in patients without vaospastic angina.

The phosphoinositol 3-kinase/Akt pathway plays a critical role in oncogenesis and the dysregulation of this pathway through loss of PTEN is a particularly common phenomenon in aggressive prostate cancers. Several recent studies have indicated that ursolic acid (UA), a pentacyclic triterpenoid, and its derivatives inhibit the growth of cancer cells by cell cycle arrest and the stimulation of apoptosis. In the present study, we report a novel autophagic response of UA in PTEN-deficient PC3 prostate cancer cells. As one of the major types of programmed cell death, autophagy has been observed in response to several anticancer drugs and demonstrated to be responsible for cell death. UA-induced autophagy in PC3 cells is associated with the reduced cell viability and the enhanced expression of LC3-II, an autophagosome marker in mammals, and monodansylcadaverine incorporation into autolysosomes. Furthermore, we found that UA exhibited anti-proliferative effects characterized by G1 phase arrest and autophagy at an early stage that precedes apoptosis. We also show that UA-induced autophagy in PC3 cells are mediated through the Beclin-1 and Akt/mTOR pathways. Inhibition of autophagy by either 3-methyladenine or Beclin-1/Atg5 small interfering RNA enhanced UA-induced apoptosis. Taken together, our data suggest that autophagy functions as a survival mechanism in PC3 cells against UA-induced apoptosis and a rational for the use of autophagy inhibitors in combination with UA as a novel modality of cancer therapy.

Pseudoaneurysm due to cancer is uncommon generally and is extremely rare in lung cancer. We report two cases of false aneurysms due to lung cancer that spontaneously regressed upon chemotherapy without intervention. Both patients had squamous cell carcinoma of the lung and the diagnosis of a pseudoaneurysm was made using computed tomography. There was no evidence of severe bronchial hemorrhage and the psuedoaneurysms were small and well-encased. Chemotherapy was performed and the pseudoaneurysms resolved.

Cytosolic NADP+-dependent isocitrate dehydrogenase (IDPc) is susceptible to inactivation by numerous thiol-modifying reagents. This study now reports that Cys269 of IDPc is a target for S-glutathionylation and that this modification is reversed by dithiothreitol as well as enzymatically by cytosolic glutaredoxin in the presence of GSH. Glutathionylated IDPc was significantly less susceptible than native protein to peptide fragmentation by reactive oxygen species and proteolytic digestion. Glutathionylation may play a protective role in the degradation of protein through the structural alterations of IDPc. HEK293 cells treated with diamide displayed decreased IDPc activity and accumulated glutathionylated enzyme. Using immunoprecipitation with an anti-IDPc IgG and immunoblotting with an anti-GSH IgG, we purified and positively identified glutathionylated IDPc from the kidneys of mice subjected to ischemia/reperfusion injury and from the livers of ethanol-administered rats. These results suggest that IDPc activity is modulated through enzymatic glutathionylation and deglutathionylation during oxidative stress.

Ultraviolet (UV) radiation has been shown to generate reactive oxygen species (ROS), such as singlet oxygen, superoxide radicals, hydroxyl radicals and hydrogen peroxide in a variety of cells. These ROS have the potential to damage critical cellular components such as DNA, proteins, and lipids and eventually result in physical and chemical damage to tissues that may lead to cell death. The steamed root of Rehmannia glutinosa (Saeng Jihuang, SJH) is reported to have an antioxidant activity. We investigated the effect of SJH on UV-induced apoptosis in U937 cells. Upon exposure to UV, there was a distinct difference between untreated cells and cells pre-treated with 0.5–2 mg/ml SJH for 12 hours in regard to cellular redox status and morphological change to cells. SJH pre-treated cells showed significant suppression of apoptotic features such as DNA fragmentation, damage to mitochondrial function, and modulation of apoptotic marker proteins upon exposure to UV. This study indicates that SJH may play an important role in regulating the apoptosis induced by UV presumably through scavenging of reactive oxygen species.

Myeoloperoxidase catalyses the formation of hypochlorous acid (HOCl) via reaction of H(2)O(2) with Cl(-) ion. Although HOCl is known to play a major role in the human immune system by killing bacteria and other invading pathogens, excessive generation of this oxidant is known to cause damage to tissue. Recently, it was demonstrated that the control of mitochondrial redox balance and oxidative damage is one of the primary functions of mitochondrial NADP(+)-dependent isocitrate dehydrogenase (IDPm) to supply NADPH for antioxidant systems. This study investigated whether the IDPm would be a vulnerable target of HOCl as a purified enzyme and in intact cells. Loss of enzyme activity was observed and the inactivation of IDPm was reversed by thiols. Transfection of HeLa cells with an IDPm small interfering RNA (siRNA) markedly enhanced HOCl-induced oxidative damage to cells. The HOCl-mediated damage to IDPm may result in the perturbation of the cellular antioxidant defense mechanisms and subsequently lead to a pro-oxidant condition.

Sensor node of RFID Middleware system can usually be reacted from six mouths to two years, they can be exhausted their power of storage battery only one day by communication rates and ranges. And 1:n sensor arrangement of n form command and data send-receive that is possible simulation do without interference other sensors and research to different sensor data analysis and conversion ways to convert Sensing data that accept from sensors to actuality information.

Heat shock may increase oxidative stress due to increased production of reactive oxygen species and/or the promotion of cellular oxidation events. Mitochondrial NADP + -dependent isocitrate dehydrogenase (IDPm) produces NADPH, an essential reducing equivalent for the antioxidant system. In this report, we demonstrate that silencing of IDPm expression in HeLa cells greatly enhances apoptosis induced by heat shock. Transfection of HeLa cells with an IDPm small interfering RNA (siRNA) markedly decreased activity of IDPm, enhancing the susceptibility of heat shock-induced apoptosis reflected by morphological evidence of apoptosis, DNA fragmentation, cellular redox status, mitochondria redox status and function, and the modulation of apoptotic marker proteins. These results indicate that IDPm may play an important role in regulating the apoptosis induced by heat shock and the sensitizing effect of IDPm siRNA on the apoptotic cell death of HeLa cells offers the possibility of developing a modifier of cancer therapy.

Ultraviolet A (UVA) irradiation is responsible for a variety of changes in cell biology. The purpose of this study was to investigate effects of aspartic acid on UVA irradiation-induced damages in the stemness properties of human adipose tissue-derived mesenchymal stem cells (hAMSCs). Furthermore, we elucidated the UVA-antagonizing mechanisms of aspartic acid. The results of this study showed that aspartic acid attenuated the UVA-induced reduction of the proliferative potential and stemness of hAMSCs, as evidenced by increased proliferative activity in the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and upregulation of stemness-related genes OCT4, NANOG, and SOX2 in response to the aspartic acid treatment. UVA-induced reduction in the mRNA level of hypoxiainducible factor (HIF)-1 alpha was also significantly recovered by aspartic acid. In addition, the antagonizing effects of aspartic acid against the UVA effects were found to be mediated by reduced production of PGE2 through the inhibition of JNK and p42/44 MAPK. Taken together, these findings show that aspartic acid improves reduced stemness of hAMSCs induced by UVA and its effects are mediated by upregulation of HIF-1 alpha via the inhibition of PGE2-cAMP signaling. In addition, aspartic acid may be used as an antagonizing agent to mitigate the effects of UVA.

Cadmium is known to exhibit high affinity for thiol groups and may therefore severely disturb many cellular functions. We have demonstrated that the control of mitochondrial redox balance and oxidative damage is one of the primary functions of mitochondrial NADP+-dependent isocitrate dehydrogenase (IDPm). When exposed to cadmium, IDPm was susceptible to loss of enzyme activity and structural alterations. Site-directed mutagenesis confirms that binding of cadmium occurs to a Cys379 of IDPm. We examined the antioxidant mechanism-mediated protective role of IDPm against cadmium-induced apoptosis with human embryonic kidney 293 cells transfected with the IDPm cDNA in sense and antisense orientations. As a result, we observed a clear inverse relationship between the amount of IDPm expressed in target cells and their susceptibility to cadmium-induced modulation of cellular redox status and apoptosis. In addition, loss of glutaredoxin (Grx, thioltransferase) activity by cadmium was more pronounced in antisense cells compared with the sense cells. When oxalomalate, a competitive inhibitor of IDPm, was administered to mice, inhibition of IDPm and Grx and enhanced susceptibility to apoptosis were observed upon their exposure to cadmium. These results suggest that IDPm plays an important protective role in cadmium-induced apoptosis by maintaining cellular redox status and by protection of Grx activity.

Heat shock may increase oxidative stress due to increased production of reactive oxygen species and/or the promotion of cellular oxidation events. Therefore, compounds that scavenge reactive oxygen species may regulate heat shock-induced cell death. Recently, it has been shown that the decomposition product of the spin-trapping agent alpha-phenyl-N-t-butylnitrone, N-t-butyl hydroxylamine (NtBHA), mimics alpha-phenyl-N-t-butylnitrone and is much more potent in delaying reactive oxygen species-associated senescence. We investigated the protective role of NtBHA against heat shock-induced apoptosis in U937 cells. Upon exposure to heat shock, there was a distinct difference between the untreated cells and the cells pre-treated with 0.1 mM NtBHA for 2 h in regard to apoptotic parameters, cellular redox status, and mitochondrial function. Upon exposure to heat shock, NtBHA pre-treated cells showed significant inhibition of apoptotic features such as activation of caspase-3, up-regulation of Bax, and down-regulation of Bcl-2 compared to untreated cells. This study indicates that NtBHA may play an important role in regulating the apoptosis induced by heat shock, presumably through scavenging of reactive oxygen species.

Between 1993 and 2003, we treated 21 patients with cystic meningioma (of 365 with meningioma, 5.5%). We grouped these patients according to classifications by Nauta and Rengachary and analyzed them by gender, age, tumor location, clinical manifestations, MRI features and histopathology. The mean duration of symptoms was relatively short at 1.6 months. There were five atypical and 16 benign meningiomas on histopathology. In type I and II cystic meningiomas, with intratumoral cysts, all cyst walls enhanced on MRI and had tumor cells in the cyst wall on histopathology. In type III and IV cystic meningiomas, with peritumoral cysts, the cyst wall did not enhance on MRI and only one case (type III) had tumor cells in the cyst wall on histopathology. We suggest that when the cyst wall shows contrast enhancement on imaging, the cyst wall should be completely removed at surgery. If there is no contrast enhancement, multiple biopsies of the cyst wall should be taken to assess the presence of tumor cells in the cyst wall.

Takotsubo cardiomyopathy, also called stress-induced cardiomyopathy, usually occurs in patients with severe emotional or physiologic stress. The prognosis is favorable, and the wall motion abnormlities normalize within weeks. However, stress-induced cardiomyopathy is rarely assosicated with left ventricular thrombus and thromboembolic complications. Here, we report a case of stress-induced cardiomyopathy with left ventricular thrombus that embolized to cause cerebral infarction.

Background and Objectives: Statin therapy after percutaneous coronary intervention (PCI) has been associated with re duced major adverse cardiovascular events (MACE). However, it has been less clear as to whether statin therapy before acute coronary syndrome (ACS) is beneficial. We studied the effect of previous statin therapy, initiated ≥1 month before PCI, on the outcome of patients with ACS who had undergone early invasive strategies. Subjects and Methods: We stratified 479 consecutive patients with ACS who had undergone PCI, according to preprocedural statin administration as follows: previous statin-treated patients (statin group, n=237) and statin-naive patients (control group, n=242). The incidence of periproce dural myocardial infarction (MI) and in-hospital MACE was assessed. Results: The incidence of Braunwald class III angina and MI presentation were significantly lower in the statin group than in the control group. Angiographic and procedural characteristics were similar between the two groups; however, slow/no reflow phenomenon occurred more frequently in the control group. After PCI, the incidence of periprocedural MI was higher in the control group than in the statin group (6.6% vs. 2.1%, p=0.016). Multivariate analysis revealed that no prior use of statin {odds ratio (OR)=2.8; 95% confidence interval (CI)= 1.1-7.2; p=0.038), procedural complication (OR=4.0; 95% CI=1.5-10.5; p=0.004), stent overlap (OR=4.7; 95% CI=1.3-16.4; p=0.015), and old age (OR=3.2; 95% CI=1.2-8.0; p=0.016) were independent predictors for in-hospital MACE. Conclusion: Previous statin therapy before ACS was associated with milder clinical presentation and lower incidence of in-hospital MACE after early invasive strategies. The beneficial outcome is attributable to a significant reduction in periprocedural MI after PCI. (Korean Circ J 2011;41:458-463)

Intraneural ganglion of the tibial nerve is very rare. We have experienced a case of the intraneural ganglion cyst in the tibial nerve and medial plantar nerve, which was located at the level of the ankle and foot. A 29-year-old male suffered from lumps causing numbness around the medial aspect of the sole and great toe. But there was no weakness and change of the motor function. We excised the cystic mass successfully and the neurologic symptoms disappeared.