bluuebunny/crossref_metadata_2025_split huggingface dataset:
Medial epicondylitis: is ultrasound guided autologous blood injection an effective treatment?
Authors: Suresh S P , Ali K E , Jones H , Connell D A 
Published: September 2006

Objective:To assess if ultrasound guided autologous blood injection is an effective treatment for medial epicondylitis.Methods:Twenty patients (13 men, 7 women) with refractory medial epicondylitis with symptom duration of 12 months underwent sonographic evaluation. Tendinosis was confirmed according to three sonographic criteria: echo texture, interstitial tears and neovascularity. The tendon was then dry needled and autologous blood was injected. Patients were reviewed at 4 weeks and at 10 months. VAS scores and modified Nirschl scores were assessed pre-procedure and post-procedure.Results:There was significant reduction in VAS pain score between pre-procedure and 10 months post-procedure when it had a median (IQR) of 1.00 (1–1.75), range 0–7. The median (IQR) Nirschl score, which at pre-procedure was 6.00 (5–7), range 4–7, had decreased at 4 weeks to 4.00 (2.25–5), range 2–7, and at 10 months to 1.00 (1–1.75), range 0–7, revealing a significant decrease (z = 3.763, p<0.001). The hypo-echoic change in the flexor tendon significantly decreased between pre-procedure, when there was a mean (SD) of 6.45 (1.47), and at 10 months, when it was 3.85 (2.37) (p<0.001). Doppler ultrasound showed that neovascularity decreased between pre-procedure, when there was a mean (SD) of 6.10 (1.62), range 4–9, and at 10 months, when it was 3.60 (2.56), range 0–9 (p<0.001).Discussion:The combined action of dry needling and autologous blood injection under ultrasound guidance appears to be an effective treatment for refractory medial epicondylitis as demonstrated by a significant decrease in VAS pain and a fall in the modified Nirschl scores.
Polymorphisms in theHBBgene relate to individual cardiorespiratory adaptation in response to endurance training
Authors: He Z , Hu Y , Feng L , Lu Y , Liu G , Xi Y , Wen L , Xu X , Xu K 
Published: September 2006

Objective:The crucial role of haemoglobin in endurance performance has been well documented. We examined whether polymorphisms in theHBBgene modified aerobic capacity.Methods:102 recruits were trained by running 5000 m three times per week for 18 weeks. Exercise intensity progressively increased from an initial heart rate corresponding to 95% of the individual baseline ventilatory threshold during the first 10 weeks to 105% during the last 8 weeks. The phenotypes measured were running economy and VO2max. Running economy was determined by measuring submaximal VO2for 5 min at a constant running speed of 12 km·h−1and VO2max was obtained during an incremental test to exhaustion. Genomic DNA was extracted from white cells of peripheral blood and the −551C/T, intron2,+16C/G and +340 A/T genotypes were examined relative to the TAA site variants by PCR-RFLP.Results:Genotype distributions were in Hardy-Weinberg equilibrium at three loci. None of the running economy and VO2max-related traits were associated with the three polymorphisms or haplotypes at baseline, while the training response of running economy was associated with −551C/T and intron2,+16C/G polymorphisms. Subjects homozygous for intron2,+16C/C or −551C/C had decreased oxygen cost of running compared to the other individuals.Discussion:It was concluded that the −551C/C or intron2,+16C/C genotype might explain part of the individual variation in the cardiorespiratory adaptation to endurance training.
ETBreceptor dependent alteration in aortic responses to ET-1 in the cardiomyopathic hamsterThis paper is one of a selection of papers published in this Special issue, entitled Second Messengers and Phosphoproteins—12th International Conference.
Authors: Al-Khoury Johny , Bkaily Ghassan , Chahine Mirna , Jacques Danielle , D'Orléans-Juste Pedro 
Published: September 2006

The aim of this study was to verify whether an alteration in the aortic endothelin-1 (ET-1) response takes place in UM-X7.1 cardiomyopathic hamsters. Our results showed that ET-1 (10−12– 10−5 mol/L) induces dose-dependent sustained increases in tension in the intact and endothelium denuded aortas from both normal and cardiomyopathic hamsters. The EC50values of ET-1 of both intact and endothelium denuded aortas of normal hamsters were similar (2.2 × 10−9 mol/L and 1.8 × 10−9 mol/L, respectively). However, in cardiomyopathic hamsters, the EC50of ET-1 in intact aortas was higher (1.5 × 10−8 mol/L) than that of the endothelium denuded preparations (2.7 × 10−9 mol/L). The EC50of ET-1 in normal and cardiomyopathic hamster denuded aortas were similar. However, the EC50of ET-1 in intact aortas of cardiomyopathic hamster was higher (1.5 × 10−8 mol/L) than that of normal hamsters (2.2 × 10−9 mol/L). Pre-treatment with the ETAreceptor antagonist ABT-627 (10−5 mol/L) of intact and endothelium denuded aortas from both normal and cardiomyopathic hamsters significantly prevented ET-1 (10−7 mol/L) from inducing an increase in tension. Pre-treatment with the ETBreceptor antagonist A-192621 (10−5 mol/L) had no effect on the ET-1-induced increase in tension in endothelium denuded aortas of both normal and cardiomyopathic hamsters, as well as in intact preparations of normal animals. However, blockade of the ETBreceptors in intact aortas of cardiomyopathic hamsters significantly (p < 0.001) potentiated the ET-1-induced increase in tension. In summary, an attenuation of the contraction response to ET-1 was found in UM-X7.1 cardiomyopathic hamsters when compared with normal age-matched hamsters. This alteration of the ET-1 effect in the aortas of cardiomyopathic hamsters seems to be dependent on the presence of the endothelium and could be due, in part, to an increase in the contribution of endothelial ETBreceptors to relaxation, which in turn acts as a physiological depressor of ET-1 vasoconstriction. Our results suggest that an increase in the endothelium ETBreceptor density may play a role in the development of hypotension in UM-X7.1 cardiomyopathic hamsters.
The Impact of Unmeasured Clinical Variables on the Accuracy of Hospital Report Cards: A Monte Carlo Study
Authors: Austin Peter C. 
Published: September 2006

Purpose. Hospital report cards are commonly produced using administrative data. The objective of this study was to determine the impact of unmeasured clinical data on the accuracy of hospitals’ report cards. Methods. Monte Carlo simulations were based on both administrative and detailed clinical data for patients hospitalized with an acute myocardial infarction in Ontario, Canada. Data were simulated such that the true performance of each hospital was known. Both clinical and administrative risk scores were randomly generated for each patient. The ability of hospital report cards to correctly identify hospitals that truly had higher than acceptable mortality was compared when both clinical and administrative data were used and when only administrative data were used. By using Monte Carlo simulations, we were able to incrementally increase the divergence between the 2 risk scores. Results. In a wide range of settings, sensitivity and specificity of hospital report cards was only negligibly greater when both administrative and clinical data were used compared to when only administrative data were used. Conclusions. Unmeasured clinical data have at most a minor impact on the accuracy of cardiac hospital report cards.
Estimation of Mortality Rates for Disease Simulation Models Using Bayesian Evidence Synthesis
Authors: McMahon Pamela M. , Zaslavsky Alan M. , Weinstein Milton C. , Kuntz Karen M. , Weeks Jane C. , Gazelle G. Scott 
Published: September 2006

Purpose. The authors propose a Bayesian approach for estimating competing risks for inputs to disease simulation models. This approach is suggested when modeling a disease that causes a large proportion of all-cause mortality, particularly when mortality from the disease of interest and other-cause mortality are both affected by the same risk factor. Methods. The authors demonstrate a Bayesian evidence synthesis by estimating other-cause mortality, stratified by smoking status, for use in a simulation model of lung cancer. National (US) survey data linked to death registries (National Health Interview Survey [NHIS]—Multiple Cause of Death files) were used to fit cause-specific hazard models for 3 causes of death (lung cancer, heart disease, and all other causes), controlling for age, sex, race, and smoking status. Synthesis of NHIS data with national vital statistics data on numbers and causes of deaths was performed in WinBUGS (version 1.4.1, MRC Biostatistics Unit, UK). Correction for inconsistencies between the NHIS and vital statistics data is described. A published cohort study was a source of prior information for smoking-related mortality. Results. Marginal posterior densities of annual mortality rates for lung cancer and other-cause death (further divided into heart disease and all other causes), stratified by 5-year age interval, race (white and black), gender, and smoking status (current, former, never), were estimated, specific to a time period (1987-1995). Overall, black current smokers experienced the highest mortality rates. Conclusions. Bayesian evidence synthesis is an effective method for estimation of cause-specific mortality rates, stratified by demographic factors.
Early acquisition of cytolytic function and transcriptional changes in a primary CD8+ T-cell response in vivo
Authors: Chiu Christopher , Heaps Adrian G. , Cerundolo Vincenzo , McMichael Andrew J. , Bangham Charles R. , Callan Margaret F. C. 
Published: September 2006

AbstractFunctional studies show that programming of CD8+ T cells occurs early after initial antigen encounter within as little as 2 hours. To define the molecular basis of these events, we transferred TCR transgenic T cells from F5 Rag−/− mice into naive recipients and stimulated them with recombinant vaccinia expressing the immunodominant influenza epitope NP366-374. Transcription in epitope-specific cytotoxic T lymphocytes (CTLs) was analyzed using Affymetrix 430 2.0 GeneChips and quantitative polymerase chain reaction (PCR). We demonstrated an early transcriptional burst with the greatest number of genes reaching peak expression 12 hours after stimulation. Using in vivo cytotoxicity assays we demonstrated that early up-regulation of cytolytic genes was accompanied by acquisition of killing capacity within 24 hours of stimulation. However, T-cell proliferation was not observed until 48 hours. We therefore conclude that clonal expansion rather than acquisition of effector function is the rate-limiting step in the development of a primary CTL response.
MK-0457, a novel kinase inhibitor, is active in patients with chronic myeloid leukemia or acute lymphocytic leukemia with the T315I BCR-ABL mutation
Authors: Giles Francis J. , Cortes Jorge , Jones Dan , Bergstrom Donald , Kantarjian Hagop , Freedman Steven J. 
Published: September 2006

Abstract
MK-0457 (VX-680) is a small-molecule aurora kinase (AK) inhibitor with preclinical antileukemia activity. The T315I BCR-ABL mutation mediates resistance to imatinib, nilotinib, and dasatinib. MK-0457 has in vitro activity against cells expressing wild-type or mutated BCR-ABL, including the T315I BCR-ABL mutation. Three patients with T315I abl-mutated chronic myeloid leukemia (CML) or Philadelphia chromosome (Ph)–positive acute lymphocytic leukemia (ALL) have achieved clinical responses to doses of MK-04547 that are not associated with adverse events. Higher MK-0457 dose levels were associated with clinical responses and down-regulation of CrkL phosphorylation in leukemia cells. The possible role of AK inhibition in these clinical responses requires further investigation. The currently reported cases are the first observed clinical activity of a kinase inhibitor against the T315I phenotype. The observation of responses in 3 patients with T315I phenotype–refractory CML or Ph-positive ALL, at doses of MK-0457 associated with no significant extramedullary toxicity, is very encouraging.
Identification of a 2-stage platelet aggregation process mediating shear-dependent thrombus formation
Authors: Maxwell Mhairi J. , Westein Erik , Nesbitt Warwick S. , Giuliano Simon , Dopheide Sacha M. , Jackson Shaun P. 
Published: September 2006

AbstractDisturbances of blood flow at sites of atherosclerotic plaque rupture are one of the key pathogenic events promoting platelet activation and arterial thrombus formation. Shear effects of platelets have been extensively investigated in vitro; however, the mechanisms by which shear promotes platelet aggregation in vivo remain incompletely understood. By employing high-resolution imaging techniques to in vitro and in vivo thrombosis models, we demonstrate a unique mechanism initiating shear-dependent platelet aggregation involving aggregate formation between discoid platelets. These discoid platelet aggregates are initially unstable and result from the development of membrane tethers between coadhering platelets. Tether formation involves the adhesive function of GPIb/V/IX and integrin αIIbβ3, and conversion of discoid platelet aggregates into stable aggregates requires released ADP. The efficiency of this process is regulated by 3 independent variables, including the reactivity of the adhesive substrate, the level of shear flow, and the platelet density at the adhesive surface. These studies identify a new mechanism initiating platelet aggregation that is critically influenced by shear, physical proximity between translocating platelets, and membrane tether formation. Moreover, they provide a model to explain how the discoid morphology of platelets facilitates the maintenance of adhesive interactions with thrombogenic surfaces under high shear stress conditions.
Vascular endothelial growth factor-A induces plaque expansion in ApoE knock-out mice by promoting de novo leukocyte recruitment
Authors: Lucerna Markus , Zernecke Alma , de Nooijer Ramon , de Jager Saskia C. , Bot Ilze , van der Lans Christian , Kholova Ivana , Liehn Elisa A. , van Berkel Theo J. C. , Yla-Herttuala Seppo , Weber Christian , Biessen Eric A. L. 
Published: September 2006

AbstractVascular endothelial growth factor-A is widely used in clinical trials for the treatment of cardiac ischemia. VEGF-A was recently suggested to act in a proinflammatory manner, which could aggravate adjacent atherogenesis in VEGF-A–based therapy. To assess potential bystander effects, VEGF-A was focally overexpressed in advanced atherosclerotic plaques in ApoE−/− mice. Sheer-induced carotid artery plaques were transluminally incubated with Ad.hVEGF-A leading to neointimal overexpression of VEGF-A. Ad.hVEGF-A treatment of pre-existing lesions was seen to promote plaque expansion, with a concomitant increase in macrophage and lipid content, whereas it lowered collagen content. In general, Ad.hVEGF-A–treated plaques displayed a more vulnerable phenotype. VEGF-A overexpression was not accompanied by increased microvessel development in the neointima, suggesting that VEGF-A destabilizes atherosclerotic plaques through an angiogenesis-independent mechanism. Intravital microscopy confirmed that treatment with Ad.hVEGF-A led to an increased monocyte adhesion, which was mediated by a VCAM-1/PECAM-1–dependent pathway. VEGF-A indeed induced a differential expression of VCAM-1 and PECAM-1 in endothelial cells. Our data underline the importance of regular monitoring of stenotic vessels adjacent to the site of VEGF-A application. We propose that VCAM-1/PECAM-1–directed cotherapy may be an efficient strategy to prevent bystander effects of focal VEGF-A therapy in patients suffering from cardiovascular disease.
Safety and efficacy of risk-adapted cyclophosphamide, thalidomide, and dexamethasone in systemic AL amyloidosis
Authors: Wechalekar Ashutosh D. , Goodman Hugh J. B. , Lachmann Helen J. , Offer Mark , Hawkins Philip N. , Gillmore Julian D. 
Published: September 2006

AbstractHigh-dose melphalan with stem-cell transplantation is believed to be the most effective treatment for systemic light-chain (AL) amyloidosis, but many patients are ineligible because of the extent of their disease, and treatment-related mortality (TRM) remains substantial. We report the use of a risk-adapted oral regimen of cyclophosphamide, thalidomide, and dexamethasone (CTD) or attenuated CTD (CTDa) in 75 patients with advanced AL amyloidosis, including 44 patients with clonal relapse after prior therapy. Fifty-one (68%) patients received CTD and 24 (32%) received CTDa. A hematologic response occurred in 48 (74%) of 65 evaluable patients, including complete responses in 14 (21%) and partial responses in 34 (53%) cases. Median estimated overall survival (OS) from commencement of treatment was 41 months, and from diagnosis median was not reached with a median follow-up of 22 months. Three-year estimated OS was 100% and 82% among complete and partial hematologic responders, respectively. Toxicity necessitating cessation of therapy occurred in 8% and was at least grade 2 in 52% of patients. TRM was 4%. The clonal response rates to CTD reported here are higher than any previously reported nontransplantation regimen in AL amyloidosis, and risk adaptation allows its use in poorer risk patients. CTD merits prospective randomized study.
Dasatinib (BMS-354825) is active in Philadelphia chromosome–positive chronic myelogenous leukemia after imatinib and nilotinib (AMN107) therapy failure
Authors: Quintas-Cardama Alfonso , Kantarjian Hagop , Jones Dan , Nicaise Claude , O'Brien Susan , Giles Francis , Talpaz Moshe , Cortes Jorge 
Published: September 2006

AbstractDeveloping strategies to counteract imatinib resistance constitutes a challenge in chronic myelogenous leukemia (CML). Therapy with the tyrosine kinase inhibitors nilotinib (AMN107) and dasatinib (BMS-354825) has produced high rates of hematologic and cytogenetic response. Src kinase activation has been linked to Bcr-Abl–mediated leukemogenesis and CML progression. In addition to binding Abl kinase with less stringent conformational requirements than imatinib, dasatinib is a potent Src kinase inhibitor. In the current study, we report on 23 patients with CML (19 of them in accelerated or blastic phases) treated with dasatinib after treatment failure with both imatinib and nilotinib. More than half (13; 57%) of 23 patients responded to dasatinib: 10 (43%) had a complete hematologic response (CHR), including 7 (30%) who had a cytogenetic response (2 complete, 4 partial, and 1 minor). These results suggest that dasatinib may be active in some patients after failure with both imatinib and nilotinib.
CROPPER: a metagene creator resource for cross-platform and cross-species compendium studies
Authors: Paananen Jussi , Storvik Markus , Wong Garry 
Published: September 2006

Abstract

Background
Current genomic research methods provide researchers with enormous amounts of data. Combining data from different high-throughput research technologies commonly available in biological databases can lead to novel findings and increase research efficiency. However, combining data from different heterogeneous sources is often a very arduous task. These sources can be different microarray technology platforms, genomic databases, or experiments performed on various species. Our aim was to develop a software program that could facilitate the combining of data from heterogeneous sources, and thus allow researchers to perform genomic cross-platform/cross-species studies and to use existing experimental data for compendium studies.

Results
We have developed a web-based software resource, called CROPPER that uses the latest genomic information concerning different data identifiers and orthologous genes from the Ensembl database. CROPPER can be used to combine genomic data from different heterogeneous sources, allowing researchers to perform cross-platform/cross-species compendium studies without the need for complex computational tools or the requirement of setting up one's own in-house database. We also present an example of a simple cross-platform/cross-species compendium study based on publicly available Parkinson's disease data derived from different sources.

Conclusion
CROPPER is a user-friendly and freely available web-based software resource that can be successfully used for cross-species/cross-platform compendium studies.
An ABRE-binding factor, OSBZ8, is highly expressed in salt tolerant cultivars than in salt sensitive cultivars of indica rice
Authors: Mukherjee Kakali , Choudhury Aryadeep Roy , Gupta Bhaskar , Gupta Sudhiranjan , Sengupta Dibyendu N 
Published: September 2006

Abstract

Background
The bZIP class Abscisic acid Responsive Element (ABRE)-binding factor, OSBZ8 (38.5 kD) has been considered to regulate ABA-mediated transcription in the suspension cultured cells of japonica rice. Still, nothing is known about the expression of OSBZ8 at protein level in vegetative tissue of salt sensitive and salt tolerant rice plants. In our previous study, Electrophoretic Mobility Shift Assay (EMSA) of [32P]ABRE-DNA and nuclear extracts prepared from the lamina of Pokkali rice plants has detected the presence of an ABRE-binding factor. Northern analysis has also detected salinity stress induced accumulation of transcripts for bZIP class of factor. Therefore, OSBZ8 was considered to play an important role in the regulation of transcription in the vegetative tissue of rice. The aim of this study is to find out whether OSBZ8 has any role in regulating the NaCl-stress induced gene expression in vegetative tissue and whether the expression of OSBZ8 factor directly correlates with the stress tolerance of different varieties of indica type rice.

Results
Northern analysis of total RNA from roots and lamina of salt-sensitive M-I-48 and salt-tolerant Nonabokra, when probed with the N-terminal unique region of OSBZ8 (OSBZ8p, without the highly conserved basic region), a transcript of 1.3 kb hybridized and its level was much higher in tolerant cultivar. EMSA with Em1a, the strongest ABA Responsive Element till reported from the upstream of EmBP1, and the nuclear extracts from laminar tissue of untreated and salt-treated seedlings of three salt sensitive, one moderately sensitive and two salt tolerant indica rice cultivars showed specific binding of nuclear factor to ABRE element. Intensity of binding was low and inducible in salt sensitive rice cultivars while high and constitutive in salt tolerant cultivars. EMSA with 300 bp 5'upstream region of Rab16A gene, a well known salt stress and ABA-inducible gene of rice, showed formation of two complexes, again very weak in salt sensitive and strong in salt tolerant rice cultivar.

Conclusion
The bZIP factor OSBZ8 was found to be present in the ABRE-DNA: protein complex as shown by the supershift of the complex by the purified antiserum raised against OSBZ8p. Treatment of the seedlings with NaCl was found to enhance the complex formation, suggesting the regulation of OSBZ8 gene at both transcriptional and post-translational steps. Comparative EMSA with different varieties of rice suggests a positive correlation with the expression pattern of OSBZ8 and salt tolerance in rice cultivars.