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Background/purpose Emerging evidence suggests the significance of microRNA-155 (miR-155) in fibrogenesis and oxidative stress accumulation, but its function in oral submucous fibrosis (OSF) has not been investigated. In this study, we assessed the expression of miR-155 and its effects on the maintenance of myofibroblast activation. Methods qRT-PCR was conducted to assess the expression of miR-155 in OSF tissues and fibrotic buccal mucosal fibroblasts (fBMFs) derived from OSF samples. Collagen gel contraction, migration, and invasion capabilities were examined in fBMFs. DCFDA ROS assay was used to examine ROS generation. A luciferase reporter assay was carried out to verify the relationship between miR-155 and its potential target RPTOR. Results We showed that the expression of miR-155 was aberrantly upregulated in OSF specimens and fBMFs. Inhibition of miR-155 ameliorated various myofibroblast activities, including collagen gel contraction, migration, and invasion abilities as well as ROS production. Results from the luciferase reporter assay demonstrated that miR-155 directly interacted with its target RPTOR. Conclusion Taken together, these findings indicate that miR-155 is implicated in the pathogenesis of oxidative stress-associated OSF, possibly through the regulation of RPTOR.

Chun-Sheng Hsu,1– 4 Shin-Tsu Chang,1,5,6 Oswald Ndi Nfor,2 Kuan-Jung Lee,2 Chien-Chang Ho,7,8 Chuan-Ching Liu,1 Shiuan-Shinn Lee,2 Yung-Po Liaw2,9 1Department of Physical Medicine and Rehabilitation, Taichung Veterans General Hospital, Taichung City, 40201, Taiwan; 2Department of Public Health and Institute of Public Health, Chung Shan Medical University, Taichung City, 40201, Taiwan; 3School of Medicine, National Defense Medical Center, Taipei City, 11490, Taiwan; 4College of Medicine, National Chung Hsing University, Taichung City, 402, Taiwan; 5Department of Physical Medicine and Rehabilitation, Tri-Service General Hospital, School of Medicine, National Defense Medical Centre, Taipei City, 11490, Taiwan; 6Department of Physical Medicine and Rehabilitation, Kaohsiung Veterans General Hospital, Kaohsiung City, 813414, Taiwan; 7Department of Physical Education, Fu Jen Catholic University, New Taipei, 24205, Taiwan; 8Research and Development Center for Physical Education, Health, and Information Technology, Fu Jen Catholic University, New Taipei, 24205, Taiwan; 9Department of Medical Imaging, Chung Shan Medical University Hospital, Taichung City, 40201, TaiwanCorrespondence: Yung-Po Liaw; Shiuan-Shinn LeeDepartment of Public Health and Institute of Public Health, Chung Shan Medical University, No. 110 Sec. 1 Jianguo N. Road, Taichung City, 40201, TaiwanTel +886 424730022 ext. 11838; +886 424730022 ext.12185Fax +886 423248179Email Liawyp@csmu.edu.tw; shinn@csmu.edu.twPurpose: The Lipoprotein lipase (LPL) gene is a significant contributor to dyslipidemia. It has shown associations with several conditions including atherosclerosis, obesity, and metabolic syndrome (MetS). We assessed the interactive association between MetS and rs3779788 of the LPL gene based on aerobic exercise.Materials and Methods: Data were available for 7532 Taiwan Biobank (TWB) participants recruited between 2008 and 2016. We used multiple logistic regression to determine the odds ratios (OR) for MetS and their 95% confident intervals (C.I.). Potential variables included LPL rs3779788, aerobic exercise, sex, age, education, marital status, body mass index (BMI), smoking, alcohol consumption, midnight snacking, vegetarian diet, coffee, dietary fat, and tea drinking.Results: Aerobic exercise was protective against MetS (OR, 0.858; 95% C.I., 0.743– 0.991). Compared to CC/CT genotype, the OR for developing MetS was 0.875, (95% C.I., 0.571– 1.341) in TT individuals. The test for interaction was significant for the rs3779788 variant and aerobic exercise (p = 0.0484). In our group analyses, the OR for MetS was 0.841 (95% C.I., 0.727– 0.974) in CC/CT and 4.076 (95% C.I., 1.158– 14.346) in TT individuals who did aerobic exercise compared to those who did not.Conclusion: Our study indicated that aerobic exercise improved metabolic syndrome in Taiwanese adults with rs3779788 CC/CT genotype relative to those with TT genotype.Keywords: polymorphisms, variant, physical activity, metabolic disorders

1-Nitropyrene (1-NP), one of the most abundant nitropolycyclic aromatic hydrocarbons (nitro-PAHs), is generated from the incomplete combustion of carbonaceous organic compounds. 1-NP is a specific marker of diesel exhaust and is an environmental pollutant and a probable carcinogen. Macrophages participate in immune defense against the invasive pathogens in heart, lung, and kidney infection diseases. However, no evidence has indicated that 1-NP induces apoptosis in macrophages. In the present study, 1-NP was found to induce concentration-dependent changes in various cellular functions of RAW264.7 macrophages including cell viability reduction; apoptosis generation; mitochondrial dysfunction; apoptosis-inducing factor (AIF) nuclear translocation; intracellular ROS generation; activation of the AMPK/Nrf-2/HO-1 pathway; changes in the expression of BCL-2 family proteins; and depletion of antioxidative enzymes (AOE), such as glutathione peroxidase (GPx), catalase (CAT), and superoxide dismutase (SOD) These results indicate that 1-NP induced apoptosis in macrophages through AIF nuclear translocation and ROS generation due to mitochondrial dysfunction and to the depletion of AOE from the activation of the AMPK/Nrf-2/HO-1 pathway.

Background/Purpose Oral cancer is amongst the most prevalent cancers worldwide with rising incidence. Various attempts have been made to elucidate its pathogenesis, and we sought to examine the function of a ubiquitin E3 ligase that was encoded by STUB1. Methods The mRNA expression of STUB1 in oral cancer samples and normal counterparts was determined by qRT-PCR. Numerous assays to assess the features of cancer cells, including self-renewal capacity, invasion and migration abilities were conducted following knockdown or overexpression of STUB1. Results The expression level of STUB1 was reduced in oral cancer, which was associated with a reduced relapse-free survival. Two oral cancer cell lines with low expression of STUB1 (SAS and HSC3) were chosen for the overexpression of STUB1. We showed that ectopic expression of STUB1 led to the downregulation of TGM2, a multifunctional protein that contributed to cancer progression in several cancers. Our results demonstrated that overexpression of STUB1 suppressed the cancer aggressiveness, while restoration of TGM2 reverted the effects. Last, we showed that STUB1 silencing resulted in enhanced cancer features. Conclusion The abnormal downregulation of STUB1 may lessen its suppressive effect on TGM2, which induced the onset or exacerbated the progression of oral cancer. The therapeutic approach to enhance the expression of STUB1 could be a promising direction for cancer therapy.

Bisphenol-A-glycidyldimethacrylate (BisGMA) is a resin monomer frequently used in dentin restorative treatments. The leakage of BisGMA monomer from BisGMA-based polymeric resins can lead to cytotoxicity in macrophages. Rutin has various beneficial bioeffects, including antioxidation and antiinflammation. In this study, we found that pretreatment of RAW264.7 macrophages with rutin-inhibited cytotoxicity induced by BisGMA in a concentration-dependent manner. BisGMA-induced apoptosis, which was detected by levels of phosphatidylserine from the internal to the external membrane and formation of sub-G1, and genotoxicity, which was detected by cytokinesis-blocked micronucleus and single-cell gel electrophoresis assays, were inhibited by rutin in a concentration-dependent manner. Rutin suppressed the BisGMA-induced activation of caspase-3 and -9 rather than caspase-8. Rutin inhibited the activation of the mitochondrial apoptotic pathway, including cytochrome C release and mitochondria disruption, after macrophages were treated with BisGMA. Finally, BisGMA-induced reactive oxygen species (ROS) generation and antioxidant enzyme (AOE) deactivation could be reversed by rutin. Parallel trends were observed in the elevation of AOE activation and inhibition of ROS generation, caspase-3 activity, mitochondrial apoptotic pathway activation, and genotoxicity. These results suggested that rutin suppressed BisGMA-induced cytotoxicity through genotoxicity, the mitochondrial apoptotic pathway, and relatively upstream factors, including reduction of ROS generation and induction of AOE.

It has been considered that widowed persons have a higher risk of death. This study intended to explore whether social participation could improve this trend. A longitudinal study database was constructed to explore the trend of survival and its change with social participation in widowed persons. The Taiwan Longitudinal Study on Aging (TLSA), based on four consecutive waves of longitudinal follow-up data in 1999, 2003, 2007, and 2011 was linked with the National Death Registry from 1999 through 2012. In total, there were 1417 widowed persons and 4500 nonwidowed persons included in this study, excluding divorced and never-married people. The survival trend analysis was carried out with social participation as the main predictive factor stratified for comparative analysis. Our results showed that the widowed were older than the nonwidowed, were female-dominant, had a lower education level, were more economically stressed, and were less likely to engage in regular exercise, and thus showed generally poorer health, for example, being more vulnerable to having chronic diseases, disability with the Activities of Daily Living (ADL), cognitive impairment with the Short Portable Mental State Questionnaire (SPMSQ), and depression with The Center for Epidemiological Studies-Depression (CES-D). The death risk of the widowed was significantly higher than that of the nonwidowed, but the death trend for those with social participation was significantly lower than that of their counterparts in both the widowed and nonwidowed. After matching with gender and age for widowed persons, the widowed with social participation had a significantly lower risk of death (adjusted hazard ratio (HR), 0.83, 95% confidence interval (CI), 0.71–0.98) compared to the widowed without social participation. It was concluded that social participation can improve the death risk for the widowed, and it is worthily included in health promotion plans and social welfare services for widowed persons.

Macrophages are mainly active cells of the immune system and play a role in the defense of pathogens. However, the overactivation of macrophages by fatal pathogens can result in toxic responses. 2-hydroxyethyl methacrylate (HEMA), which is a hydrophilic monomer, is used in dental adhesive reagents and composite resins as well as biocompatible hydrogels. The mechanisms underlying the genotoxicity engendered by HEMA-induced apoptosis that leads to cytotoxicity remain unclear. Accordingly, this study was conducted to clarify such mechanisms. The results showed that HEMA induced cell toxicity in RAW264.7 macrophages depending on the concentration. A higher HEMA concentration was associated with a higher level of apoptosis and genotoxicity. Moreover, HEMA induced a concentration-dependent increase in mitochondrial dysfunction and the intrinsic caspase pathway, including the activation of caspase-3 and caspase-9. HEMA was also found to upregulate intracellular reactive oxygen species generation and to decrease the activity of antioxidant enzymes, including superoxide dismutase and catalase. Taken together, the mitochondrial-dependent intrinsic caspase pathway and intracellular reactive oxygen species accumulation were found to mediate HEMA-induced genotoxicity and apoptosis, leading to cytotoxicity in RAW264.7 macrophages.

Primary open-angle glaucoma (POAG) is the most common type of glaucoma. However, little is known about POAG in adults and exposure to air pollution. The current study aims to investigate whether exposure to particulate matter with a mass median aerodynamic diameter of ≤2.5 μm (PM2.5) is associated with POAG diagnosis. Patient data were obtained from the Longitudinal Health Insurance Database 2010 (LHID2010) of Taiwan for the 2008–2013 period. PM2.5 concentration data, collected from the Ambient Air Quality Monitoring Network established by the Environmental Protection Administration of Taiwan, were categorized into four groups according to World Health Organization (WHO) exposure standards for PM2.5. We estimated the odds ratios (ORs) and 95% CIs for risk factors for POAG with logistic regression. The OR of per WHO standard level increase was 1.193 (95% CI 1.050–1.356). Compared with the normal level, the OR of WHO 2.0 level was 1.668 (95% CI 1.045–2.663, P &lt, 0.05). After excluding confounding risk factors for POAG in this study, we determined that increased PM2.5 exposure is related to POAG risk (ORs &gt, 1, P &lt, 0.05). In this study, PM2.5 was an independent factor associated with open-angle glaucoma. Further research is required to better understand the mechanisms connecting PM2.5 and open-angle glaucoma.

Acute lung injury (ALI) is an acute and life-threatening inflammatory disease of the lung parenchyma that is associated with high mortality worldwide. No therapeutic strategies have been developed for the mitigation of the proinflammatory response that characterizes ALI. Kirenol has anti-inflammatory, antiarthritic, and immunoregulatory effects. In the present study, we investigated the protective effects of kirenol against lipopolysaccharides (LPS)-induced ALI in mice. Kirenol reduced the LPS-induced histopathology changes involving edema and thickening of the interstitial or alveolar walls, infiltration of leukocytes, formation of hyaline membrane. Pretreatment with kirenol reduced leukocytes infiltration in bronchoalveolar lavage fluid (BALF), the alveolar-capillary barrier disruption and lipid peroxidation in lung tissues induced by LPS. Kirenol significantly inhibited the secretion of cytokines, IL-1β, IL6, and TNFα, into the BALF of the mice with LPS-induced ALI through NFκB activation. Moreover, kirenol attenuated the downregulation of the antioxidant enzymes, superoxide dismutase, glutathione peroxidase, and catalase that was induced by LPS. HO-1 expression and the phosphorylation of Nrf2 and AMPK2 were also induced by kirenol. The results indicate that kirenol can be developed as a treatment strategy for ALI, and its effects are induced through the inhibition of the NF-κB proinflammatory pathway and promotion of AMPK2/Nrf2-mediated HO-1 and antioxidant enzymes (AOE) activation.

Genotoxic stress from environmental pollutants plays a critical role in cytotoxicity. The most abundant nitro-polycyclic aromatic hydrocarbon in environmental pollutants, 1-nitropyrene (1-NP), is generated during fossil fuel, diesel, and biomass combustion under sunlight. Macrophages, the key regulators of the innate immune system, provide the first line of defense against pathogens. The toxic effects of 1-NP on macrophages remain unclear. Through a lactate dehydrogenase assay, we measured the cytotoxicity induced by 1-NP. Our results revealed that 1-NP induced genotoxicity also named DNA damage, including micronucleus formation and DNA strand breaks, in a concentration-dependent manner. Furthermore, 1-NP induced p53 phosphorylation and nuclear accumulation; mitochondrial cytochrome c release; caspase-3 and -9 activation and cleavage; and poly (ADP-ribose) polymerase-1 (PARP-1) cleavage in a concentration-dependent manner. Pretreatment with the PARP inhibitor, 3-aminobenzamide, significantly reduced cytotoxicity, genotoxicity, and PARP-1 cleavage induced by 1-NP. Pretreatment with the caspase-3 inhibitor, z-DEVD-fmk, significantly reduced cytotoxicity, genotoxicity, PARP-1 cleavage, and caspase 3 activation induced by 1-NP. Pretreatment with the p53 inhibitor, pifithrin-α, significantly reduced cytotoxicity, genotoxicity, PARP-1 cleavage, caspase 3 activation, and p53 phosphorylation induced by 1-NP. We propose that cytotoxicity and genotoxicity induced by 1-NP by PARP-1 cleavage via caspase-3 and -9 activation through cytochrome c release from mitochondria and its upstream p53-dependent pathway in macrophages.

Cigarette smoking is a well-established risk factor for various diseases, such as cardiovascular diseases, neurodegeneration, and cancer. Cadmium nitrate (Cd(NO3)2) is one of the major products from the cigarette smoke. Up to now, no supporting evidence on Cd(NO3)2-induced apoptosis and its related working mechanism in neurons has been found. In present study, the mode of cell death, caspase activities, reactive oxygen species (ROS) generation, and mitochondrial dysfunction in N2a cells, which are neuron-like cells, were assessed by Annexin V-FITC and PI assays, caspase fluorometric assay, DCFH-DA fluorescence assay, and JC-1 fluorescence assay respectively. The results showed that not only Cd(NO3)2 induced apoptosis and necrosis but also the activities of caspase-3 and -9 expressed in a concentration-dependent manner. In addition, Cd(NO3)2 also induced both mitochondrial dysfunction and ROS generation in a concentration-dependent manner. All these indicated that in N2a cells parallel trends could be observed in apoptosis, caspase-3 and -9 activities, mitochondrial dysfunction, and ROS generation when induced by Cd(NO3)2. Furthermore, Cd(NO3)2-induced apoptosis, caspases activities, mitochondrial dysfunction, and ROS generation were reduced by N-acetyl-l-cysteine (NAC). These results indicated that Cd(NO3)2-induced neuronal apoptosis was reduced by NAC via intrinsic apoptotic caspase cascade activities and their up-stream factors, including mitochondrial dysfunction and ROS generation.

Acute lung injury (ALI) is a clinical syndrome with high morbidity and mortality rates mainly caused by Gram-negative bacteria. Nevertheless, an effective treatment strategy for ALI is yet to be developed. Zerumbone, a sesquiterpene isolated from Zingiber zerumbet Smith, possesses several advantageous bioeffects such as antioxidation, anti-inflammation, and antiulcer. Pretreatment of zerumbone inhibited lipopolysaccharide (LPS)-induced arterial blood gas exchange, neutrophils infiltration, and increased pulmonary vascular permeability. LPS-induced expression of intercellular adhesion molecule-1 (ICAM-1) was inhibited by zerumbone at a lower concentration than that of vascular cell adhesion molecule-1 (VCAM-1). In addition, proinflammatory cytokines, such as interleukin (IL)-1β and macrophage inflammatory protein (MIP)-2 were suppressed by zerumbone. The phosphorylation of nuclear factor (NF)-κB, a proinflammatory transcription factor, and degradation of inhibitor of κB (IκB), an inhibitor of NF-κB, were also reduced by zerumbone. Furthermore, we found the inhibitory concentration of zerumbone on phosphorylation of p38 mitogen-activated protein kinase (MAPK) and c-Jun NH2-terminal kinase (JNK) was lower than that of extracellular signal-regulated kinase (ERK). In conclusion, zerumbone could be a potential protective agent for ALI, possibly via expression of ICAM-1, IL-1β, and MIP-2. The protective mechanism of zerumbone was by reversing the activation of p38 MAPK/JNK-IκB/NF-κB pathway.

Background The let-7 family of microRNAs has been considered as tumor suppressors in various cancers; however, the role of let-7c in oral squamous cell carcinoma has not been determined yet. Methods In this study, phenotypical behaviors and the radio/chemoresistance were examined subsequent to overexpression of let-7c. In addition, the expression of let-7c in cancer stem cells (CSCs) was evaluated and the effect of let-7c on stemness characteristics was assessed. Also, luciferase activity assays were performed to test whether interleukin (IL)-8 was a putative target of let-7c. Results Our results confirmed that the expression of let-7c in CSCs was reduced, while overexpression of let-7c attenuated the oncogenicity. Moreover, ectopic expression of let-7c in CSCs downregulated the stemness hallmarks and the radio/chemoresistance. Expression and secretion of IL-8 in oral CSCs were both reduced following overexpression of let-7c. Besides, the inhibitory effect of let-7c on various stemness phenotypes was reverted by IL-8, indicating that lower expression of let-7c may confer higher cancer stemness through a failure to downregulate IL-8. Conclusion These findings revealed the significance of let-7c in the contribution of oral cancer stemness and radio/chemoresistance. Targeting let-7c and its downstream IL-8 may be beneficial to prevent cancer recurrence and metastasis of oral squamous cell carcinoma.

This study differs from previous studies of TiO2/SiO2 in that 0.5–10 μm microsized TiO2-rutile based catalysts (TR catalysts) with varying proportions of titanium and silicon were synthesized using a one-step modified hydrothermal method. At Ti/Si = 1/9, a two-dimensional channel-structured catalyst with a morphology resembling that of SBA-15 was obtained. In contrast, at Ti/Si = 3/7 or 5/5, a three-dimensional porous structure was formed, and Ti–O–Si–C bonds appeared. The structure of the TR catalyst transformed due to the decrease in C–Si bond content and the increase in C–C bond content with increasing Ti/Si ratio. The results indicated that the rutile phase was the main crystal phase of the TR catalyst. The small crystal size and large rutile phase content of the mesoporous TR catalyst contributed to the low band gap energy below 3.0 eV. Under 2 × 10 W lamp irradiation with either UVA or visible light, the three TR catalysts showed better formaldehyde (HCHO) removal efficiency than P25. Furthermore, the Taguchi method was employed to evaluate the catalytic factors by analysis of variance (ANOVA) and S/N ratio. The results revealed the contributions of each of the three factors to HCHO removal efficiency over TR catalysts to be as follows: space velocity (62%), Ti ratio (32%), and time on stream (5%). The TR catalyst with Ti/Si = 1/9 showed good HCHO removal efficiency with a high SBET (787.1 m2 g−1) and large pore volume (0.95 cm3 g−1) for a residence time of over 2.29 × 10−1 s under visible light irradiation. Microwave-assisted EG reduction was successfully applied to dope a TR catalyst with nanosized Pt particles in a short synthesis time. After Pt doping, the removal efficiency in the stream improved and stabilized. The Pt particles were Pt0 and proved effective for improving the photocatalytic removal of HCHO over the TR catalyst by prolonging the separation time of the electron–hole pairs. Overall, the Pt/TR catalyst is a potential material for pollutant removal and can be easily separated from the pollutant removal system since the catalysts are microsized.

Zerumbone, a cyclic eleven-membered sesquiterpene, is the major component of the essential oil isolated from the wild ginger, Zingiber zerumbet. There are several beneficial pharmacological activities of zerumbone including anti-inflammatory, antioxidant, and anticancer activities. Acute lung injury (ALI) is an acute pulmonary inflammatory disorder with high morbidity and mortality rate. In present study, we aimed to investigate the protective effects and mechanisms of zerumbone on endotoxin, lipopolysaccharide (LPS)-induced ALI. Mice were pretreated with zerumbone at various concentrations for 30 min followed by intratracheal administration of LPS for 6 h. Pretreatment with zerumbone not only reduced leukocytes infiltration into the alveolar space but also inhibited lung edema in LPS-induced ALI. Decreased secretion of proinflammatory cytokines such as TNFα and IL-6 caused by LPS were reversed by zerumbone. LPS-induced expressions of proinflammatory mediators, iNOS and COX-2, were inhibited by zerumbone. In addition, NFκB activation and Akt phosphorylation were inhibited by zerumbone in LPS-induced ALI. All these results suggested that the protective mechanisms of zerumbone on endotoxin-induced ALI were via inhibition of Akt-NFκB activation.

Acute lung injury (ALI) is a serious disease with high morbidity and mortality rate. Although there are effective strategies for treatment of ALI; a widely accepted specific pharmacotherapy has not yet established. Zerumbone, the major active phytochemical compound from Zingiber zerumbet Smith, exhibits various beneficial biological and pharmacological activities, such as antioxidation, anti-inflammation, immunomodulation, and anti-cancer. We aimed to study the potential protective effects and mechanisms of zerumbone in mouse model of lipopolysaccharide (LPS)-induced ALI. Pretreatment with zerumbone inhibited the histopatholgical changes such as neutrophils infiltration, increased in alveolar barrier thickness, hemorrhage, and hyaline membrane formation occurred in lungs in LPS-induced ALI. In addition, not only LPS-induced activation of myeloperoxidase (MPO) and metallopeptidase-9 (MMP-9) was suppressed by zerumbone, but also lipid peroxidation in lungs was inhibited as well. Moreover, pretreatment with zerumbone reversed the antioxidative enzymes activities, including superoxide dismutase, catalase, and glutathione peroxidase, decreased by LPS and enhanced the expression of nuclear factor erythroid 2-related factor (Nrf2) and heme oxygenase (HO-1) induced by LPS. These results from present study suggested that the protective mechanisms of zerumbone on LPS-induced ALI were via up-regulation of antioxidative enzymes and Nrf2/HO-1 pathway.

Background Mitral valve disease is the most common heart valve disease worldwide. Heart valve operation is the predominant treatment strategy for heart valve disease. This study analyzed the death risk from heart valve disease with respect to the frequency of heart valve operation and other operations in patients with mitral valve disease. Materials and methods We conducted a retrospective nationwide population-based case–control study using a claims dataset from Taiwan’s National Health Insurance Research Database. The case and control groups enrolled mitral valve disease patients from 2002 to 2013 who had either underwent an heart valve operation procedure or not, respectively. Conditional logistic regression was estimated the odds ratios (ORs) associated with various risk factors for heart valve operation-related death, including other operations and comorbidities. Results A total of 25,964 patients with mitral valve disease were recruited for the study and divided into heart valve operation (600 patients) and non-heart valve operation (25,364 patients) groups. After matching, a total of 1800 non-heart valve operation patients were selected for final analysis. Heart valve operation was associated with decreased risk of death (adjusted OR [aOR] 0.439), but operations related to other cardiovascular disease (CVD, aOR 3.691), respiratory conditions (aOR 3.210), and the urinary system (aOR 1.925) were associated with increased risk of death for patients with mitral valve disease. Patients with mitral valve disease and diabetes (aOR 1.505), chronic kidney disease (CKD, aOR 3.760), or emphysema (aOR 2.623) also had a higher risk of death. Patients who underwent more heart valve operations had a lower risk of death from mitral valve disease, but patients who underwent more other operations had a higher risk of death from mitral valve disease. Conclusions The death risk for patients with mitral valve disease patients could be lowered by more frequently performing heart valve operations. However, the risk of death is increased for patients with mitral valve disease who more frequently undergo other operations, chiefly those for other CVD system, respiratory conditions, and urinary system, or have comorbidities such as diabetes, chronic kidney disease, and emphysema.

Increased levels of high-density lipoprotein cholesterol (HDL-C) can improve endothelial function. This may help reduce cardiovascular risks and mortality. Evidence has been provided on the association between cardiometabolic traits, such as HDL-C and exercise modalities. However, there is the absence of studies investigating this association in Taiwan. We assessed the relationship between exercise type and HDL-C among Taiwanese adults. Data were collected from Taiwan Biobank (TWB), a national biomedical research database that contains the genetic information of ethnic Taiwanese residents gathered from 2008 to 2016. We enrolled 24,856 participants aged 30 to 70 years who completed a questionnaire about their recent health behaviors including smoking, drinking, and exercise. Regular exercise was categorized as non-aerobic exercise (separated as weight training, ball game, and mixed exercise) and strict aerobic exercise. Linear regression models were used to assess the effects of exercise in a questionnaire-based manner. After multivariate adjustments, HDL-C was positively associated with aerobic (&beta, = 1.33748, p &lt, 0.0001) and non-aerobic (&beta, = 2.56210, p &lt, 0.0001) exercise. Positive associations were also found for resistance training (&beta, = 4.01828, p = 0.0020), ballgame (&beta, = 2.43815, p = 0.0001), and mixed exercise (&beta, = 2.47021, p &lt, 0.0001). This study demonstrated that both aerobic and non-aerobic exercise have positive effects on HDL-C among Taiwanese adults. Among the non-aerobic exercise groups, resistance training had the greatest effect.

Background/purpose Fibroblast growth factor (FGF)-2 is known as a signaling molecule that induces tissue regeneration. Little is known about the effect of FGF-2 on cementoblasts for periodontal and periapical regeneration. The aim of this study was to investigate the effects of FGF-2 on murine immortalized cementoblast cell line (OCCM.30). Materials and methods Cell growth and proliferation was judged by using alamar blue reduction assay. Flow cytometry analysis was used to evaluate Stro-1 positive cells expression with or without FGF-2. Western blot was used to evaluate the expression of phosphorylated serine–threonine kinase Akt (p-Akt) and extracellular signal-regulated protein kinase (p-ERK) in cementoblasts. Results FGF-2 was found to increase cell growth in a dose-dependent manner (P

// Tung Yuan Wang 1, * , Chih-Yu Peng 1, 2, * , Shiuan-Shinn Lee 4 , Ming-Yung Chou 1, 2, 3 , Cheng-Chia Yu 1, 2, 3 , Yu-Chao Chang 1, 2 1 School of Dentistry, Chung Shan Medical University, Taichung, Taiwan 2 Department of Dentistry, Chung Shan Medical University Hospital, Taichung, Taiwan 3 Institute of Oral Sciences, Chung Shan Medical University, Taichung, Taiwan 4 School of Public Health, Chung Shan Medical University, Taichung, Taiwan * These authors contributed equally to this work Correspondence to: Cheng-Chia Yu, email: ccyu@csmu.edu.tw Yu-Chao Chang, email: cyc@csmu.edu.tw Keywords: arecoline, cancer stemness, oral squamous cell carcinomas Received: November 09, 2015 Accepted: August 13, 2016 Published: August 20, 2016 ABSTRACT Oral squamous cell carcinoma (OSCC), one of the most deadliest malignancies in the world, is caused primarily by areca nut chewing in Southeast Asia. The mechanisms by which areca nut participates in OSCC tumorigenesis are not well understood. In this study, we investigated the effects of low dose long-term arecoline (10 μg/mL, 90-days), a major areca nut alkaloid, on enhancement cancer stemness of human oral epithelial (OE) cells. OE cells with chronic arecoline exposure resulted in increased ALDH1 population, CD44 positivity, stemness-related transcription factors (Oct4, Nanog, and Sox2), epithelial-mesenchymal transdifferentiation (EMT) traits, chemoresistance, migration/invasiveness/anchorage independent growth and in vivo tumor growth as compared to their untreated controls. Mechanistically, ectopic miR-145 over-expression in chronic arecoline-exposed OE (AOE) cells inhibited the cancer stemness and xenografic. In AOE cells, luciferase reporter assays further revealed that miR-145 directly targets the 3′ UTR regions of Oct4 and Sox2 and overexpression of Sox2/Oct4 effectively reversed miR-145-regulated cancer stemness-associated phenomenas. Additionally, clinical results further revealed that Sox2 and Oct4 expression was inversely correlated with miR-145 in the tissues of areca quid chewing-associated OSCC patients. This study hence attempts to provide novel insight into areca nut-induced oral carcinogenesis and new intervention for the treatment of OSCC patients, especially in areca nut users.