bluuebunny/crossref_metadata_2025_split huggingface dataset:
Mapping and Ablating Ventricular Premature Contractions That Trigger Ventricular Fibrillation: Trigger Elimination and Substrate Modification
Authors: NOGAMI AKIHIKO 
Published: September 2014

VF AblationVentricular fibrillation (VF) is a malignant arrhythmia, usually initiated by a ventricular premature contraction (VPC) during the vulnerable period of cardiac repolarization. Ablation therapy for VF has been described and increasingly reported. Targets for VF triggers are VPC preceded Purkinje potentials or the right ventricular outflow tract (RVOT) in structurally normal hearts, and VPC triggers preceded by Purkinje potentials in ischemic cardiomyopathy. The most important issue before the ablation session is the recording of the 12‐lead electrocardiogram (ECG) of the triggering event, which can prove invaluable in regionalizing the origin of the triggering VPC for more detailed mapping. In cases where the VPC is not spontaneous or inducible, ablation may be performed by pacemapping. During the session, mapping should be focused on the earliest activation and determining the earliest potential is the key to a successful ablation. However, a modification of the Purkinje network might be applied when the earliest site cannot be determined or is located close to the His‐bundle. Furthermore, the electrical isolation of the pulmonary artery (PA) can suppress RVOT type polymorphic ventricular tachycardia in some patients with rapid triggers from the PA. Suppression of VF can be achieved by not only the elimination of triggering VPCs, but also by substrate modification of possible reentry circuits in the Purkinje network, or between the PA and RVOT. Further studies are needed to evaluate the precise mechanisms of this arrhythmia.
Astaxanthin inhibits apoptosis in alveolar epithelial cells type II in vivo and in vitro through the ROS‐dependent mitochondrial signalling pathway
Authors: Song Xiaodong , Wang Bingsi , Lin Shengcui , Jing Lili , Mao Cuiping , Xu Pan , Lv Changjun , Liu Wen , Zuo Ji 
Published: September 2014

AbstractOxidative stress is an important molecular mechanism underlying lung fibrosis. The mitochondrion is a major organelle for oxidative stress in cells. Therefore, blocking the mitochondrial signalling pathway may be the best therapeutic manoeuver to ameliorate lung fibrosis. Astaxanthin (AST) is an excellent antioxidant, but no study has addressed the pathway of AST against pulmonary oxidative stress and free radicals by the mitochondrion‐mediated signalling pathway. In this study, we investigated the antioxidative effects of AST against H2O2‐ or bleomycin (BLM)‐induced mitochondrial dysfunction and reactive oxygen species (ROS) production in alveolar epithelial cells type II (AECs‐II) in vivo and in vitro. Our data show that AST blocks H2O2‐ or BLM‐induced ROS generation and dose‐dependent apoptosis in AECs‐II, as characterized by changes in cell and mitochondria morphology, translocation of apoptotic proteins, inhibition of cytochrome c (Cyt c) release, and the activation of caspase‐9, caspase‐3, Nrf‐2 and other cytoprotective genes. These data suggest that AST inhibits apoptosis in AECs‐II cells through the ROS‐dependent mitochondrial signalling pathway and may be of potential therapeutic value in lung fibrosis treatment.
Forced IDO1 expression in dendritic cells restores immunoregulatory signalling in autoimmune diabetes
Authors: Pallotta Maria Teresa , Orabona Ciriana , Bianchi Roberta , Vacca Carmine , Fallarino Francesca , Belladonna Maria Laura , Volpi Claudia , Mondanelli Giada , Gargaro Marco , Allegrucci Massimo , Talesa Vincenzo Nicola , Puccetti Paolo , Grohmann Ursula 
Published: September 2014

AbstractIndoleamine 2,3‐dioxygenase (IDO1), a tryptophan catabolizing enzyme, is recognized as an authentic regulator of immunity in several physiopathologic conditions. We have recently demonstrated that IDO1 does not merely degrade tryptophan and produce immunoregulatory kynurenines, but it also acts as a signal‐transducing molecule, independently of its enzymic function. IDO1 signalling activity is triggered in plasmacytoid dendritic cells (pDCs) by transforming growth factor‐β (TGF‐β), an event that requires the non‐canonical NF‐κB pathway and induces long‐lasting IDO1 expression and autocrine TGF‐β production in a positive feedback loop, thus sustaining a stably regulatory phenotype in pDCs. IDO1 expression and catalytic function are defective in pDCs from non‐obese diabetic (NOD) mice, a prototypic model of autoimmune diabetes. In the present study, we found that TGF‐β failed to activate IDO1 signalling function as well as up‐regulate IDO1 expression in NOD pDCs. Moreover, TGF‐β‐treated pDCs failed to exert immunosuppressive properties in vivo. Nevertheless, transfection of NOD pDCs with Ido1 prior to TGF‐β treatment resulted in activation of the Ido1 promoter and induction of non‐canonical NF‐κB and TGF‐β, as well as decreased production of the pro‐inflammatory cytokines, interleukin 6 (IL‐6) and tumour necrosis factor‐α (TNF‐α). Overexpression of IDO1 in TGF‐β‐treated NOD pDCs also resulted in pDC ability to suppress the in vivo presentation of a pancreatic β‐cell auto‐antigen. Thus, our data suggest that a correction of IDO1 expression may restore its dual function and thus represent a proper therapeutic manoeuvre in this autoimmune setting.
Elongation factor‐2 kinase regulates TG2/β1 integrin/Src/uPAR pathway and epithelial–mesenchymal transition mediating pancreatic cancer cells invasion
Authors: Ashour Ahmed A. , Gurbuz Nilgun , Alpay Sultan Neslihan , Abdel‐Aziz Abdel‐Aziz H. , Mansour Ahmed M. , Huo Longfei , Ozpolat Bulent 
Published: September 2014

AbstractPancreatic ductal adenocarcinoma is one of the lethal cancers with extensive local tumour invasion, metastasis, early systemic dissemination and poorest prognosis. Thus, understanding the mechanisms regulating invasion/metastasis and epithelial–mesenchymal transition (EMT), is the key for developing effective therapeutic strategies for pancreatic cancer (PaCa). Eukaryotic elongation factor‐2 kinase (eEF‐2K) is an atypical kinase that we found to be highly up‐regulated in PaCa cells. However, its role in PaCa invasion/progression remains unknown. Here, we investigated the role of eEF‐2K in cellular invasion, and we found that down‐regulation of eEF‐2K, by siRNA or rottlerin, displays impairment of PaCa cells invasion/migration, with significant decreases in the expression of tissue transglutaminase (TG2), the multifunctional enzyme implicated in regulation of cell attachment, motility and survival. These events were associated with reductions in β1 integrin/uPAR/MMP‐2 expressions as well as decrease in Src activity. Furthermore, inhibition of eEF‐2K/TG2 axis suppresses the EMT, as demonstrated by the modulation of the zinc finger transcription factors, ZEB1/Snail, and the tight junction proteins, claudins. Importantly, while eEF‐2K silencing recapitulates the rottlerin‐induced inhibition of invasion and correlated events, eEF‐2K overexpression, by lentivirus‐based expression system, suppresses such rottlerin effects and potentiates PaCa cells invasion/migration capability. Collectively, our results show, for the first time, that eEF‐2K is involved in regulation of the invasive phenotype of PaCa cells through promoting a new signalling pathway, which is mediated by TG2/β1 integrin/Src/uPAR/MMP‐2, and the induction of EMT biomarkers which enhance cancer cell motility and metastatic potential. Thus, eEF‐2K could represent a novel potential therapeutic target in pancreatic cancer.
A novel functional interplay between Progesterone Receptor‐B and PTEN, via AKT, modulates autophagy in breast cancer cells
Authors: De Amicis Francesca , Guido Carmela , Santoro Marta , Lanzino Marilena , Panza Salvatore , Avena Paola , Panno Maria Luisa , Perrotta Ida , Aquila Saveria , Andò Sebastiano 
Published: September 2014

AbstractThe tumour suppressor activity of the phosphatase and tensin homologue on chromosome 10 (PTEN) is subject of intense investigative efforts, although limited information on its regulation in breast cancer is available. Herein, we report that, in breast cancer cells, progesterone (OHPg), through its cognate receptor PR‐B, positively modulates PTEN expression by inducing its mRNA and protein levels, and increasing PTEN‐promoter activity. The OHPg‐dependent up‐regulation of PTEN gene activity requires binding of the PR‐B to an Sp1‐rich region within the PTEN gene promoter. Indeed, ChIP and EMSA analyses showed that OHPg treatment induced the occupancy of PTEN promoter by PR and Sp1 together with transcriptional coactivators such as SRC1 and CBP. PR‐B isoform knockdown abolished the complex formation indicating its specific involvement. The OHPg/PR‐B dependent induction of PTEN causes the down‐regulation of PI3K/AKT signal, switching on the autophagy process through an enhanced expression of UVRAG and leading to a reduced cell survival. Altogether these findings highlight a novel functional connection between OHPg/PR‐B and tumour suppressor pathways in breast cancer.
AnxA5 reduces plaque inflammation of advanced atherosclerotic lesions in apoE−/− mice
Authors: Burgmaier Mathias , Schutters Kristof , Willems Brecht , van der Vorst Emiel P.C. , Kusters Dennis , Chatrou Martijn , Norling Lucy , Biessen Erik A.L. , Cleutjens Jack , Perretti Mauro , Schurgers Leon J. , Reutelingsperger Chris P.M. 
Published: September 2014

AbstractAnnexin A5 (AnxA5) exerts anti‐inflammatory, anticoagulant and anti‐apoptotic effects through binding cell surface expressed phosphatidylserine. The actions of AnxA5 on atherosclerosis are incompletely understood. We investigated effects of exogenous AnxA5 on plaque morphology and phenotype of advanced atherosclerotic lesions in apoE−/− mice. Advanced atherosclerotic lesions were induced in 12 weeks old Western type diet fed apoE−/− mice using a collar placement around the carotid artery. After 5 weeks mice were injected either with AnxA5 (n = 8) or vehicle for another 4 weeks. AnxA5 reduced plaque macrophage content both in the intima (59% reduction, P < 0.05) and media (73% reduction, P < 0.01) of advanced atherosclerotic lesions of the carotid artery. These findings corroborated with advanced lesions of the aortic arch, where a 67% reduction in plaque macrophage content was observed with AnxA5 compared to controls (P < 0.01). AnxA5 did not change lesion extension, plaque apoptosis, collagen content, smooth muscle cell content or acellular plaque composition after 4 weeks of treatment as determined by immunohistochemistry in advanced carotid lesions. In vitro, AnxA5 exhibited anti‐inflammatory effects in macrophages and a flow chamber based assay demonstrated that AnxA5 significantly inhibited capture, rolling, adhesion as well as transmigration of peripheral blood mononuclear cells on a TNF‐α‐activated endothelial cell layer. In conclusion, short‐term treatment with AnxA5 reduces plaque inflammation of advanced lesions in apoE−/− mice likely through interfering with recruitment and activation of monocytes to the inflamed lesion site. Suppressing chronic inflammation by targeting exposed phosphatidylserine may become a viable strategy to treat patients suffering from advanced atherosclerosis.
Bacillus Cereus Contamination of UF‐Feta Cheese during Ripening and Shelf Life
Authors: Moradi‐Khatoonabadi Zhila , Ezzatpanah Hamid , Maghsoudlou Yahya , Khomeiri Morteza , Aminafshar Mehdi 
Published: September 2014

AbstractUF‐Feta cheese was analyzed among three plants for total microorganisms, aerobic spores and Bacillus cereus in three parts (core, rind and brine) during ripening and shelf life. Then, hemolysin BL, cereolysin A and cereolysin B genes as virulence factors were investigated in the B. cereus isolates. The results show that in spite of significant decrease of the total count, the variation of B. cereus spores and aerobic spores was not meaningful during shelf life. It may be due to the sporelation of B. cereus in severe condition of UF‐Feta cheese. The results also show that B. cereus is well adapted to Feta cheese condition with low pH, and can present up to the end of shelf life. Moreover, in the detection of toxin‐producing genes, 30% of isolates were found to carry three genes. In conclusion, B. cereus isolated from UF‐Feta cheese should be considered as potential enterotoxin producers. Therefore, new efforts should be undertaken to restrict these organisms during manufacturing for food safety.Practical ApplicationsBacillus cereus is a foodborne pathogen found in dairy products. However, some studies were reported that this microorganism cannot survive at low pH like UF‐Feta cheese. The results of the present study indicate that B. cereus can tolerate the acidity and storage temperature. In addition, occurrences of toxin‐producing genes which include diarrheal toxins provide useful information in risk assessment of food poisoning caused by B. cereus. Thus, the presence of it in UF‐Feta cheese may be potential risk factors for consumer health and should be considered a serious public health hazard.
Effectiveness of a home hazard modification program for reducing falls in urban community‐dwelling older adults: A randomized controlled trial
Authors: Kamei Tomoko , Kajii Fumiko , Yamamoto Yuko , Irie Yukako , Kozakai Rumi , Sugimoto Tomoko , Chigira Ayako , Niino Naoakira 
Published: September 2014

AbstractAimTo evaluate the potential improvement of fall prevention awareness and home modification behaviors and to decrease indoor falls by applying a home hazard modification program (HHMP) in community‐dwelling older adults followed up to 1 year in this randomized controlled trial.MethodsThe present authors randomly assigned 130 older adults living in theTokyo metropolitan region to either theHHMPintervention group (n = 67) or the control group (n = 63). Both groups received four, 2 h fall prevention multifactorial programs including education regarding fall risk factors, food and nutrition, foot self‐care, and exercise sessions. However, only theHHMPgroup received education and practice regarding home safety by using a model mock‐up of a typicalJapanese home.ResultsThe mean age of theHHMPgroup was 75.7 years and the control group 75.8. TheHHMPgroup showed a 10.9% reduction in overall falls, and falls indoors showed an 11.7% reduction at 52 weeks. Those aged 75 years and over showed a significant reduction in both overall falls and indoor falls at 12 weeks. Fall prevention awareness and home modifications were significantly improved in theHHMPgroup.ConclusionHHMPhas the potential to improve fall prevention awareness and home modification behaviors, and specifically decreased overall and indoor falls in 12 weeks in those aged 75 years and older in community‐dwelling older adults.
Down‐regulation of Akt by methanol extracts of Impatiens balsamina L. promotes apoptosis in human oral squamous cell carcinoma cell lines
Authors: Shin Ji‐Ae , Ryu Mi Heon , Kwon Ki‐Han , Choi BuYoung , Cho Sung‐Dae 
Published: September 2014

BackgroundThe apoptotic activity of methanol extracts of Impatiens balsamina L. (MEIB) and related mechanisms in human oral squamous cell carcinoma (OSCC) cells have been systematically investigated.MethodsThe effects of MEIB on human OSCC cell lines were investigated using trypan blue exclusion assay, MTS assay, Western blot, 4′‐6‐diamidino‐2‐phenylindole (DAPI) staining, Live/Dead assay, Immunohistochemistry, reverse transcription–polymerase chain reaction, and promoter assay.ResultsMEIB decreased cell viability and induced apoptosis in HSC‐4 cells. Higher levels of p‐Akt expression were observed in OSCC than in normal oral mucosa (NOM), and it correlated with poor survival of the patients. MEIB dephosphorylated p‐Akt and decreased Akt expression through proteasome‐dependent degradation. LY294002 (PI3K inhibitor) decreased p‐Akt and Akt, resulting in enhancing MEIB‐induced apoptosis. MEIB down‐regulated the expression level of survivin protein at the transcriptional level and YM155 (survivin inhibitor) decreased survivin, which facilitated MEIB‐induced apoptosis. MEIB and LY294002 significantly increased Bax, thereby inducing the conformational change, mitochondrial translocation, and oligomerization. In addition, MEIB‐induced growth inhibition and apoptosis in OSC‐20, another human OSCC cells were mediated by regulating Akt and it downstream targets, survivin and Bax.ConclusionsThese results suggest that MEIB may serve as a potential drug candidate for the treatment of human OSCC.
Oral Candida carriage and prevalence of Candida species among Maras powder users and non‐users
Authors: Keten Derya , Keten Hamit S. , Goktas Mustafa T. , Ucer Huseyin , Ersoy Ozgur , Celik Mustafa 
Published: September 2014

IntroductionThe aim of this study was to investigate Candida carriage and species in Maras powder users and non‐users.Material and MethodsThis study included 100 volunteering men in 12 cafés in the city of Kahramanmaras, Turkey. A questionnaire composed of questions about socio‐demographic features and Maras powder use was filled in by the participants. Culture specimens were obtained from bilateral buccal mucosa and dorsum of the tongue with a sterile cotton‐tipped swap. The specimens were inoculated in Sabouraud Dextrose Agar (SDA).ResultsThe mean age of the participants was 48.0 ± 12.5 years (min = 20, max = 70). Fifty‐four percent of the Maras powder users and 22% of the non‐users were Candida carriers. The difference between the groups was significant (P = 0.001). The most frequently isolated species was Candida albicans at a rate of 44% in the Maras powder users and at a rate of 18% in the non‐users. Other frequent species were Candida glabrata at a rate of 6% in the Maras powder users and 2% in the control group and Candida tropicalis at a rate of 4% in the Maras powder users and 2% in the nonusers.ConclusionWe found that a significantly high rate of the Maras powder users was Candida carriers. It should be kept in mind that opportunistic infections may be caused by Candida species in Maras powder users especially with immunosuppressive conditions since Candida species are likely to lead to such infections in cases of immunosuppressive diseases.
Murmur intensity in small‐breed dogs with myxomatous mitral valve disease reflects disease severity
Authors: Ljungvall I. , Rishniw M. , Porciello F. , Ferasin L. , Ohad D. G. 
Published: September 2014

OBJECTIVESTo determine whether murmur intensity in small‐breed dogs with myxomatous mitral valve disease reflects clinical and echocardiographic disease severity.METHODSRetrospective multi‐investigator study. Records of adult dogs Ä20 kg with myxomatous mitral valve disease were examined. Murmur intensity and location were recorded and compared with echocardiographic variables and functional disease status. Murmur intensities in consecutive categories were compared for prevalences of congestive heart failure, pulmonary hypertension and cardiac remodelling.RESULTS578 dogs [107 with “soft” (30 Grade I/VI and 77 II/VI), 161 with “moderate” (Grade III/VI), 160 with “loud” (Grade IV/VI) and 150 with “thrilling” (Grade V/VI or VI/VI) murmurs] were studied. No dogs with soft murmurs had congestive heart failure, and 90% had no remodelling. However, 56% of dogs with “moderate”, 29% of dogs with “loud” and 8% of dogs with “thrilling” murmurs and subclinical myxomatous mitral valve disease also had no remodelling. Probability of a dog having congestive heart failure or pulmonary hypertension increased with increasing murmur intensity.CLINICAL SIGNIFICANCEA 4‐level murmur grading scheme separated clinically meaningful outcomes in small‐breed dogs with myxomatous mitral valve disease. Soft murmurs in small‐breed dogs are strongly indicative of subclinical heart disease. Thrilling murmurs are associated with more severe disease. Other murmurs are less informative on an individual basis.
Bacillithiol is a major buffer of the labile zinc pool in Bacillus subtilis
Authors: Ma Zhen , Chandrangsu Pete , Helmann Tyler C. , Romsang Adisak , Gaballa Ahmed , Helmann John D. 
Published: September 2014

SummaryIntracellular zinc levels are tightly regulated since zinc is an essential cofactor for numerous enzymes, yet can be toxic when present in excess. The majority of intracellular zinc is tightly associated with proteins and is incorporated during synthesis from a poorly defined pool of kinetically labile zinc. In Bacillus subtilis, this labile pool is sensed by equilibration with the metalloregulator Zur, as an indication of zinc sufficiency, and by CzrA, as an indication of zinc excess. Here, we demonstrate that the low‐molecular‐weight thiol bacillithiol (BSH) serves as a major buffer of the labile zinc pool. Upon shift to conditions of zinc excess, cells transiently accumulate zinc in a low‐molecular‐weight pool, and this accumulation is largely dependent on BSH. Cells lacking BSH are more sensitive to zinc stress, and they induce zinc efflux at lower external zinc concentrations. Thiol reactive agents such as diamide and cadmium induce zinc efflux by interfering with the Zn‐buffering function of BSH. Our data provide new insights into intracellular zinc buffering and may have broad relevance given the presence of BSH in pathogens and the proposed role of zinc sequestration in innate immunity.
Cleft palate in HIV‐exposed newborns of mothers on highly active antiretroviral therapy
Authors: Fasunla A.J. , Ogunbosi B.O. , Odaibo G.N. , Taiwo B. , Nwaorgu O.G.B. , Olaleye D.O. , Murphy R.L. , Adewole I.F. , Kanki P. , Akinyinka O.O. 
Published: September 2014

AbstractCleft lip/palate, though rare, is the commonest head and neck congenital malformation. Both genetic and environmental factors have been implicated in the aetiopathogenesis, but the role of in utero exposure to human immunodeficiency virus (HIV) and highly active antiretroviral therapy (HAART) is still being investigated. This short communication reports the occurrence of cleft palate in three newborns exposed in utero to HIV and HAART. This is a case series of HIV‐exposed newborns observed to have cleft palate among a larger cohort of HIV‐exposed and HIV‐unexposed newborns in a study evaluating the effect of HIV infection and HAART on newborn hearing. The Risk Ratio (RR) was calculated to detect a potential association between in utero exposure to efavirenz (EFV)‐containing antiretroviral therapy and cleft palate. Three HIV‐exposed newborns with cleft palate were identified during hearing screening performed on 126 HIV‐exposed and 121 HIV‐unexposed newborns. Two had exposure to tenofovir + lamivudine + efavirenz (TDF + 3TC + EFV), whereas the third had exposure to zidovudine + lamivudine + nevirapine (ZDV + 3TC + NVP) during the first trimester. There was no statistically significant association between presence of cleft palate and exposure to an EFV containing HAART regimen [P = 0.07, RR = 10.95 (0.94–126.84)]. This communication highlights the possible aetiologic role of HAART in cleft palate, the need for further prospective follow‐up studies and establishment of antiretroviral pregnancy, birth and neonatal registries.
Cast metal cap splint use for immobilisation of mandibular fracture
Authors: Yuffa A.D. , Bruzual L.M. , Hammond D. , Whear N.M. 
Published: September 2014

AbstractUse of cast metal cap splints in a patient with multiple fractures to sphenoid, zygoma, orbital floor and mandible unable to receive surgical treatment for reduction and fixation of fractured segments due to cervical spine fractures; technique considered in disuse by many.