bluuebunny/crossref_metadata_2025_split huggingface dataset:
Enhanced Predictive Power of Quantitative TWA during Routine Exercise Testing in the Finnish Cardiovascular Study
Authors: MINKKINEN MIKKO , KÄHÖNEN MIKA , VIIK JARI , NIKUS KJELL , LEHTIMÄKI TERHO , LEHTINEN RAMI , KÖÖBI TIIT , TURJANMAA VÄINÖ , KAISER WILLI , VERRIER RICHARD L. , NIEMINEN TUOMO 
Published: October 2008

Introduction: We examined whether quantification of T‐wave alternans (TWA) enhances this parameter's capacity to evaluate the risk for total and cardiovascular mortality and sudden cardiac death (SCD). Methods and Results: The Finnish Cardiovascular Study (FINCAVAS) enrolled consecutive patients (n = 2,119; 1,342 men and 777 women) with a clinically indicated exercise test with bicycle ergometer. TWA (time domain‐modified moving average method) was analyzed from precordial leads, and the results were grouped in increments of 10 μV. Hazard ratios (HR) for total and cardiovascular mortality and SCD were estimated for preexercise, routine exercise, and postexercise stages. Cox regression analysis was performed. During follow‐up of 47.1 ± 12.9 months (mean ± standard deviation [SD]), 126 patients died: 62 were cardiovascular deaths, and 33 of these deaths were sudden. During preexercise, TWA ≥ 20 μV predicted the risk for total and cardiovascular mortality (maximum HR >4.4 at 60 μV, P < 0.02 for both). During exercise, HRs of total and cardiovascular mortality were significant when TWA measured ≥50 μV, with 90 μV TWA yielding maximum HRs for total and cardiovascular death of 3.1 (P = 0.03) and 6.4 (P = 0.002), respectively. During postexercise, TWA ≥60 μV indicated risk for total and cardiovascular mortality, with maximum HR of 3.4 at 70 μV (P = 0.01) for cardiovascular mortality. SCD was strongly predicted by TWA levels ≥60 μV during exercise, with maximum HR of 4.6 at 60 μV (P = 0.002), but was not predicted during pre‐ or postexercise. Conclusion: Quantification of TWA enhances its capacity for determination of the risk for total and cardiovascular mortality and SCD in low‐risk populations. Its prognostic power is superior during exercise compared to preexercise or postexercise.
Pre‐copulation intervals, copulation frequencies, and initial progeny sex ratios in two biotypes of whitefly, Bemisia tabaci
Authors: Luan Jun‐Bo , Ruan Yong‐Ming , Zhang Li , Liu Shu‐Sheng 
Published: October 2008

AbstractThe whitefly Bemisia tabaci (Gennadius) (Homoptera: Aleyrodidae) is a species complex, and its systematic classification requires controlled crossing experiments among its genetic groups. Accurate information on pre‐copulation intervals, copulation frequencies, and initial frequency of egg fertilization of newly emerged adults is critical for designing procedures for collecting the virgin adults necessary for these experiments. In the literature, considerable variation is reported between B. tabaci populations, with respect to the length of the pre‐copulation interval and the initial frequency of egg fertilization. Here, we used a video‐recording method to observe continuously the copulation behaviour of the Mediterranean/Asia Minor/Africa (B biotype) and the Asia II (ZHJ1 biotype) groups of B. tabaci. We also recorded the initial frequency of egg fertilization, as determined by the sex of the progeny. When adults were caged in female–male pairs on leaves of cotton plants, the earliest copulation events occurred 2–6 h after emergence; at 12 h after emergence 56–84% of the females had copulated at least once, and nearly all (92–100%) had copulated at least once by 36 h after emergence. Both females and males copulated repeatedly. Approximately 80 and 20% of copulation events occurred during the photophase and scotophase, respectively. By 72 h post‐emergence, the females of the B and ZHJ1 biotypes had copulated on average 6.1 and 3.9 times, respectively. When adults were caged in groups on plants 1–13 h after emergence, 30–35% of the eggs deposited during this period were fertilized, and approximately 90% of females were fertilized by the end of the 13 h. Although timing of copulation differed in detail between the two genetic groups, the results demonstrate that B. tabaci adults can start to copulate as early as 2–6 h post‐emergence and the majority of females can become fertilized on the day that they emerge.
Combined use of entomopathogenic nematodes and Metarhizium anisopliae as a new approach for black vine weevil, Otiorhynchus sulcatus, control
Authors: Ansari M. A. , Shah F. A. , Butt T. M. 
Published: October 2008

AbstractCombined use of the entomopathogenic nematodes (EPNs), Heterorhabditis bacteriophora Poinar (Heterorhabditidae), Steinernema feltiae Bovien, and Steinernema kraussei Steiner (Steinernematidae) and the insect‐pathogenic fungus, Metarhizium anisopliae (Metsch.) Sorokin (Clavicipitaceae) was evaluated for control of third‐instar black vine weevil, Otiorhynchus sulcatus Fabricius (Coleoptera: Curculionidae). Black vine weevil larvae were exposed to various concentrations of M. anisopliae and EPNs and mortality was assessed weekly or at 3‐day intervals under laboratory and greenhouse conditions. The EPNs were added simultaneously, or 1 or 2 weeks after application of M. anisopliae. Throughout the experiments, the combined application of EPNs with M. anisopliae resulted in increased efficacy against black vine weevil. When the EPNs were applied 1 or 2 weeks after application of the fungus, 100% larval mortality was obtained, even when the biocontrol agents were used at reduced rates. The interactions observed suggest that EPN and M. anisopliae work together synergistically in potted Euonymus fortunei Blondy (Celastraceae) under greenhouse conditions and may provide a powerful and economically feasible approach for black vine weevil larval control.
Antiplatelet therapy attenuates subcellular remodelling in congestive heart failure
Authors: Sanganalmath Santosh K. , Babick Andrea P. , Barta Judit , Kumamoto Hideo , Takeda Nobuakiya , Dhalla Naranjan S. 
Published: October 2008

AbstractAntiplatelet agents, sarpogrelate (SAR), a 5‐HT2Areceptor antagonist, and cilostazol (CIL), a phosphodiesterase III (PDE‐III) inhibitor, are used for the treatment of peripheral vascular disease. We tested whether these agents affect cardiac function and subcellular remodelling in congestive heart failure (CHF) induced by myocardial infarction (MI). Three weeks after MI, rats were treated daily with 5 mg/kg SAR or CIL as well as vehicle for 5 weeks. Sham‐operated animals served as controls. At end of the treatment period, haemodynamic measurements were performed and the left ventricle was processed for the determination of sarcoplasmic reticulum (SR) Ca2+‐uptake and ‐release activities, and expression of SR Ca2+‐pump, phospholamban and ryanodine receptors, as well as myofibrillar ATPase activities, expression of α‐ and β‐myosin heavy chain (MHC) isoforms, and phosphorylation of phospholamban and cardiac troponin‐I (c Tn‐I). Marked haemodynamic changes in the MI‐induced CHF were associated with depressions in SR Ca+‐uptake and ‐release activities as well as in protein content and gene expression for SR proteins. Furthermore, myofibrillar Ca2+‐stimulated ATPase activity, as well as protein content and gene expression for α‐MHC were decreased whereas those for β‐MHC were increased in the failing heart. Also, phosphorylation levels of phospholamban and cTn‐I were reduced in failing hearts. The MI‐associated changes in cardiac function, SR and myofibillar activities, as well as SR and myofibrillar protein and gene expression were attenuated by treatment with SAR or CIL. The results suggest that SAR and CIL improve cardiac function by ameliorating subcellular remodelling in the failing heart and indicate the potential therapy of CHF with antiplatelet agents.
The somatostatin analogue octreotide inhibits angiogenesis in the earliest, but not in advanced, stages of portal hypertension in rats
Authors: Mejias Marc , Garcia‐Pras Ester , Tiani Carolina , Bosch Jaime , Fernandez Mercedes 
Published: October 2008

AbstractBackground: Angiogenesis is an important determinant of the pathophysiology of portal hypertension contributing to the formation of portosystemic collateral vessels and the hyperdynamic splanchnic circulation associated to this syndrome. Somatostatin and its analogues, like octreotide, have been shown to be powerful inhibitors of experimental angiogenesis. Aim: To determine whether octreotide has angioinhibitory effects in portal hypertensive rats. Methods: Partial portal vein‐ligated (PPVL) rats were treated with octreotide or vehicle during 4 or 7 days. Splanchnic neovascularization and VEGF expression were determined by histological analysis and western blotting. Expression of the somatostatin receptor subtype 2 (SSTR2), which mediates the anti‐angiogenic effects of octreotide, was also analyzed. Formation of portosystemic collaterals (radioactive microspheres) and hemodynamic parameters were also measured. Results: Octreotide treatment during 4 days markedly and significantly decreased splanchnic neovascularization, VEGF expression by 63% and portal pressure by 15%, whereas portosystemic collateralization and splanchnic blood flow were not modified. After 1 week of octreotide injection, portal pressure was reduced by 20%, but inhibition of angiogenesis escaped from octreotide therapy, a phenomenon that could be related to the finding that expression of SSTR2 receptor decreased progressively (up to 78% reduction) during the evolution of portal hypertension. Conclusion: This study provides the first experimental evidence showing that octreotide may be an effective anti‐angiogenic therapy early after induction of portal hypertension, but not in advanced stages most likely due to SSTR2 down‐regulation during the progression of portal hypertension in rats. These findings shed light on new mechanisms of action of octreotide in portal hypertension.
KIBRA genetic polymorphism influences episodic memory in later life, but does not increase the risk of mild cognitive impairment
Authors: Almeida O. P. , Schwab S. G. , Lautenschlager N. T. , Morar B. , Greenop K. R. , Flicker L. , Wildenauer D. 
Published: October 2008

AbstractA common T→C polymorphism of the KIBRA gene has been recently associated with worse performance on tests of episodic memory. This should aimed to determine whether older adults with the KIBRA CC genotype (1) have worse episodic memory than T‐allele carriers and, (2) are more likely to express the phenotype of amnestic mild cognitive impairment (MCI). Our Cross‐sectional investigation of 312 adults aged 50–89 years free of dementia included genotyping of the KIBRA rs17070145 gene and the assessment of episodic memory to Establish a Registry for Alzheimer's Disease (CERAD). Participants were considered to have MCI if their memory scores were 1.5 standard deviations below the mean norm for the population. 138/312 participants carried the KIBRA CC genotype. Their immediate and delayed recall scores were significantly lower than the scores of carriers of the T allele (P < 0.05; adjusted for age, gender and pre‐morbid IQ), although the effect size of the CC genotype was weak (0.2). Amongst our volunteers, 133 had MCI, of whom 63 (47.4%) had the CC genotype. There was no association between KIBRA genotype and MCI phenotype (TT/CT versus CC; adjusted odds ratio = 1.70, 95%CI = 0.74, 3.90). We concluded that the KIBRA T→C polymorphism contributes to modulate episodic memory amongst community‐dwelling older adults free of dementia, but plays no obvious role in the phenotypic expression of MCI. Future studies should aim to clarify the long term implications of this polymorphism on cognitive function and to identify other genes involved in the modulation of memory that might confer greater risk of MCI in later life.
Mesenchymal stem cells and their use as cell replacement therapy and disease modelling tool
Authors: García‐Castro J. , Trigueros C. , Madrenas J. , Pérez‐Simón J. A. , Rodriguez R. , Menendez P. 
Published: October 2008

Introduction
Mechanisms of immunological tolerance
MSCs and cell replacement strategies
Clinical applications based on MSCs immune modulatory properties: overview of ongoing clinical trials
MSCs as a model to study cell transformation and disease
Concluding remarks
AbstractMesenchymal stem cells (MSCs) from adult somatic tissues may differentiate in vitro and in vivo into multiple mesodermal tissues including bone, cartilage, adipose tissue, tendon, ligament or even muscle. MSCs preferentially home to damaged tissues where they exert their therapeutic potential. A striking feature of the MSCs is their low inherent immunogenicity as they induce little, if any, proliferation of allogeneic lymphocytes and antigen‐presenting cells. Instead, MSCs appear to be immunosuppressive in vitro. Their multi‐lineage differentiation potential coupled to their immuno‐privileged properties is being exploited worldwide for both autologous and allo‐geneic cell replacement strategies. Here, we introduce the readers to the biology of MSCs and the mechanisms underlying immune tolerance. We then outline potential cell replacement strategies and clinical applications based on the MSCs immunological properties. Ongoing clinical trials for graft‐versus‐host‐disease, haematopoietic recovery after co‐transplantation of MSCs along with haematopoietic stem cells and tissue repair are discussed. Finally, we review the emerging area based on the use of MSCs as a target cell subset for either spontaneous or induced neoplastic transformation and, for modelling non‐haematological mesenchymal cancers such as sarcomas.
Re‐expression of alpha skeletal actin as a marker for dedifferentiation in cardiac pathologies
Authors: Driesen Ronald B. , Verheyen Fons K. , Debie Wiel , Blaauw Erik , Babiker Fawzi A. , Cornelussen Richard N.M. , Ausma Jannie , Lenders Marie‐Hélène , Borgers Marcel , Chaponnier Christine , Ramaekers Frans C. S. 
Published: October 2008

AbstractDifferentiation of foetal cardiomyocytes is accompanied by sequential actin isoform expression, i.e. down‐regulation of the ‘embryonic’ alpha smooth muscle actin, followed by an up‐regulation of alpha skeletal actin (αSKA) and a final predominant expression of alpha cardiac actin (αCA). Our objective was to detect whether re‐expression of αSKA occurred during cardiomyocyte dedifferentiation, a phenomenon that has been observed in different pathologies characterized by myocardial dysfunction. Immunohistochemistry of αCA, αSKA and cardiotin was performed on left ventricle biopsies from human patients after coronary bypass surgery. Furthermore, actin isoform expression was investigated in left ventricle samples of rabbit hearts suffering from pressure‐ and volume‐overload and in adult rabbit ventricular cardiomyocytes during dedifferentiation in vitro. Atrial goat samples up to 16 weeks of sustained atrial fibrillation (AF) were studied ultrastructurally and were immunostained for αCA and αSKA. Up‐regulation of αSKA was observed in human ventricular cardiomyocytes showing down‐regulation of αCA and cardiotin. A patchy re‐expression pattern of αSKA was observed in rabbit left ventricular tissue subjected to pressure‐ and volume‐overload. Dedifferentiating cardiomyocytes in vitro revealed a degradation of the contractile apparatus and local re‐expression of αSKA. Comparable αSKA staining patterns were found in several areas of atrial goat tissue during 16 weeks of AF together with a progressive glycogen accumulation at the same time intervals. The expression of αSKA in adult dedifferentiating cardiomyocytes, in combination with PAS‐positive glycogen and decreased cardiotin expression, offers an additional tool in the evaluation of myocardial dysfunction and indicates major changes in the contractile properties of these cells.
Repression of the cardiac myosin light chain‐2 gene in skeletal muscle requires site‐specific association of antithetic regulator, Nished, and HDACs
Authors: Mathew Sumy , Galatioto Josephine , Mascareno Eduardo , Siddiqui M.A.Q. 
Published: October 2008

AbstractThe transcriptional activation mechanisms that regulate tissue‐specific expression of cardiac muscle genes have been extensively investigated, but little is known of the regulatory events involved in repression of cardiac‐specific genes in non‐cardiac cells. We have previously reported that Nished, a ubiquitous transcription factor, interacts with a positive sequence element, the Intron Regulatory Element (IRE) as well as a negatively acting element, the Cardiac‐Specific Sequence (CSS), in myosin light chain‐2 (MLC2v) gene to promote activation and repression of the gene in cardiac and skeletal muscle cells respectively. Here, we show that the negative regulation of cardiac MLC2v gene in skeletal muscle cells is mediated via the interaction of Nished with histone deacetylase (HDAC) co‐repressor. Treatment of cells with the HDAC inhibitor, Trichostatin A (TSA), alleviates the repressor activity of Nished in a dose‐dependent manner. Co‐transfection studies in primary muscle cells in culture and in Nished expressing stable skeletal muscle cell line demonstrate that Nished down‐regulates the cardiac MLC2 gene expression when its association is restricted to CSS alone. Chromatin immunoprecipitation data suggest that the CSS‐mediated repression of cardiac MLC2v gene in skeletal muscle cells excludes the participation of the positive element IRE despite the presence of an identical Nished binding site. Taken together, it appears that the negative control of MLC2v transcription is based on a dual mode of regulations, one that affords inaccessibility of IRE to Nished and second that promotes the formation of the transcription repression complex at the inhibitory CSS site to silence the cardiac gene in skeletal muscle cell.
Signal transduction of MCP‐1 expression induced by pancreatitis‐associated ascitic fluid in pancreatic acinar cells
Authors: Ramudo Laura , Yubero Sara , Manso Manuel A. , Vicente Secundino , De Dios Isabel 
Published: October 2008

AbstractPancreatitis‐associated ascitic fluid (PAAF) is known to contribute to the progression of acute pancreatitis (AP). We have investigated the capability of PAAF to activate the expression of MCP‐1 in pancreatic acinar cells and the involvement of MAPK, NF‐κB and STAT3 as downstream signalling transduction pathways. The actions of dexamethasone (Dx) and N‐acetylcysteine (NAC) on the PAAF's acinar effects have also been evaluated. Acinar cells were incubated for 1 hr with PAAF collected from rats with severe AP induced by sodium taurocholate in the absence or presence of Dx (10−7 M) or NAC (30 mM). MCP‐1 mRNA expression, phospho‐p38‐MAPK, IκBα, nuclear p65 levels and nuclear translocation of STAT3 were analysed. In response to PAAF, overexpression of MCP‐1, phosphorylation of p38‐MAPK, degradation of IκBα and increases in p65 nuclear levels and STAT3 activity were found in acinar cells. PAAF‐mediated MCP‐1 up‐regulation was completely suppressed by Dx and NAC. MAPK activation was only inhibited by NAC, NF‐κB activation was repressed by Dx and NAC, and STAT3 pathway was strongly blocked by Dx and significantly reduced by NAC. In conclusion, acinar cells were activated by PAAF to produce MCP‐1, mainly via NF‐κB and STAT3 pathways. Both downstream pathways were targeted by Dx and NAC to repress the PAAF‐mediated acinar MCP‐1 up‐regulation.
MicroRNA involvement in hepatocellular carcinoma
Authors: Gramantieri Laura , Fornari Francesca , Callegari Elisa , Sabbioni Silvia , Lanza Giovanni , Croce Carlo M. , Bolondi Luigi , Negrini Massimo 
Published: October 2008

AbstractHepatocellular carcinoma (HCC) is the third cause of cancer‐related death worldwide. Curative options for HCC are limited and exclusively available for patients carrying an early stage HCC. In advanced stages, traditional chemotherapy proved to be only marginally effective or even toxic. Thus, the identification of new treatment options is needed. New targets for non‐conventional treatment will necessarily take advantage of progresses on the molecular pathogenesis of HCC. MicroRNAs (miRNAs) are a group of tiny RNAs with a fundamental role in the regulation of gene expression. Aberrant expression of several miRNAs was found to be involved in human hepatocarcinogenesis. miRNA expression signatures were correlated with bio‐pathological and clinical features of HCC. In some cases, aberrantly expressed miRNAs could be linked to cancer‐associated pathways, indicating a direct role in liver tumourigenesis. For example, up‐regulation of mir‐221 and mir‐21 could promote cell cycle progression, reduce cell death and favour angiogenesis and invasion. These findings suggest that miRNAs could become novel molecular targets for HCC treatment. The demonstration of in vivo efficacy and safety of anti‐miRNA compounds has opened the way to their use in clinical trials.
A prospective study of macrophage migration inhibitory factor as a marker of inflammatory detection
Authors: Zhang Chao , Hou Guihua , Liang Ting , Song Jing , Qu Lili , Chen Fuqiang , Xu Jia , Wang Dan , Han Jiankui 
Published: October 2008

AbstractThis study was to evaluate whether macrophage migration inhibitory factor (MIF) can be used as a better marker of inflammatory detection through the biodistribution and inflammatory imaging study with 131I‐labelled anti‐MIF McAb and control antibody in inflammatory model mice. The mRNA and protein expression of MIF in inflammatory lesions were proved by RT‐PCR and immunohistochemistry. The model mice were injected with 3.7 MBq of each agent and killed at 24, 48 and 72 hrs after injection. Whole‐body images were obtained with storage phosphor screen. The organs, blood, abscesses muscles were removed, weighed and counted with a γ counter. The percentage of uptake by organs and per gram tissues and abscess/normal tissue (%ID/g) concentration ratios were calculated. The abscesses in mice were well visualized from 24 hrs. The target‐to‐non‐target (T/NT) ratios were 6.71 ± 1.09 (24 hrs), 8.57 ± 0.81 (48 hrs) and 11.41 ± 0.37 (72 hrs) for 131I‐labelled anti‐MIF McAb group; while in control group of 131I‐IgG, T/NT ratios were 4.65 ± 0.63 (24 hrs), 6.44 ± 0.60 (48 hrs) and 8.23 ± 0.35 (72 hrs) (P < 0.05). MIF mRNA expression was threefold increased in inflammatory tissues at 24 hrs compared with normal tissues, and twofold increased at 48 hrs. MIF protein expression was stronger in the inflammatory tissues at 48 hrs after focal inflammation occurred. Our findings suggest that the 131I‐labelled anti‐MIF McAb appears to be more specific and suitable than 131I‐labelled IgG for targeting focal inflammation, which means MIF can be used as a better marker of inflammatory detection.