bluuebunny/crossref_metadata_2025_split huggingface dataset:
Articular Talar Injuries in Athletes
Authors: Saxena Amol , Eakin Colin 
Published: July 2007

Background The treatment options of talar osteochondral lesions are numerous. Although studies show these treatments have been used with varying success, the ability to return to activity (RTA), including sports after treatment of talar dome injuries, have not been well documented. Hypothesis A treatment plan that uses microfracture for Hepple stage 2 through 4 lesions and autogenous bone grafting for Hepple stage 5 lesions for athletes with articular lesions of the talus will produce a high rate of return to athletic activity. Study Design Case series; Level of evidence, 4. Methods Preoperative and postoperative American Orthopaedic Foot and Ankle Society (AOFAS) scores and RTA were assessed prospectively 2 to 8 years after surgery in high-demand (athletic) patients with articular injuries to the talar dome treated according to the above protocol over a 6-year period. Results There were 26 microfracture procedures and 20 bone grafts to the talus. The AOFAS scores for both microfracture (preoperative, 54.6; postoperative, 94.4) and bone graft (preoperative, 46.1; postoperative, 93.4) patients improved significantly. The RTA for the entire group was 17.0 ± 5.3 weeks; for those undergoing microfracture, RTA was 15.1 ± 4.0 weeks; and for bone grafting, it was 19.6 ± 5.9 weeks. The RTA for the bone graft group was significantly slower than that of the microfracture group. Anterolateral lesions had significantly faster RTA and higher postoperative scores compared with other lesion locations. Arthroscopically treated lesions had similar postoperative AOFAS scores to those who had arthrotomy and did not have significantly faster RTA. Forty-four (96%) “excellent/good” AOFAS scores were achieved overall for talar lesions, with the same percentage of return to sport. Conclusions Talar bone grafting required a longer time to return to activity than microfracture in high-demand patients, but both groups had similar postoperative AOFAS scores. When applied to appropriate lesions, both techniques allow athletic patients to return to sports.
Modeling Microdefects Closure Effect with Isotropic/Anisotropic Damage
Authors: Desmorat R. , Cantournet S. 
Published: July 2007

Continuum damage mechanics (CDM) for metals is often written in terms of an isotropic (scalar) damage. In this case, solutions have been proposed to represent the differences of behavior in tension and in compression also called quasi-unilateral (QU) conditions or microdefects closure effect. A recent anisotropic damage model has been developed to take into account the damage orthotropy induced by plasticity (Lemaitre, J., Demorat R. and Sauzay, M. (2000). Anisotropic Damage Law of Evolution, Eur. J. Mech. A/Solids, 19: 513—524). The purposes here are then two. First, a unified framework for isotropic and anisotropic damage is proposed. Then, it is to extend Ladevèze and Lemaitre's framework (Ladevèze, P. and Lemaitre, J. (1984). Damage Effective Stress in Quasi Unilateral Conditions, In: Proceedings of the 16th International Congress of Theoretical and Applied Mechanics, Lyngby, Denmark) for the QU conditions to anisotropic damage induced by plasticity. Yield surfaces and damage versus accumulated plastic strain curves, drawn for different loading, illustrate the effect of the QU conditions on the damage evolution.
Chemokine stromal cell-derived factor-1 induction by C/EBPβ activation is associated with all-trans-retinoic acid-induced leukemic cell differentiation
Authors: Kim KyeongJin , Kim Hyeong Hoe , Kim Joon Hong , Choi Yung Hyun , Kim Young Hee , Cheong JaeHun 
Published: July 2007

AbstractStromal cell-derived factor-1 (SDF-1/CXCL12) is one of the essential chemokines, which mediates hematopoietic differentiations. However, the mechanism by which SDF-1 expression is regulated in granulocyte differentiation is poorly understood. Here, we suggest a novel mechanism by which all-trans-retinoic acid (ATRA) induces the expression of SDF-1 during the differentiation of promyelomonocytic leukemic U937 cells. Moreover, we also demonstrate that activation of transcription factor C/EBPβ by ATRA regulates SDF-1 expression in U937 cells. In addition, we show that the cyclin-dependent kinase inhibitors p21WAF1/CIP1 and Pyk2 are up-regulated by SDF-1 and increased markedly by the costimulation of ATRA and SDF-1. Furthermore, ATRA and SDF-1α additively induce U937 cell differentiation. Indeed, silencing the expression of SDF-1 inhibits ATRA-induced granulocyte differentiation significantly. Taken together, these results indicate that SDF-1α is involved in granulocyte differentiation in response to ATRA, mediated by the activation of the transcription factor C/EBPβ.
Computational quantum mechanics: An underutilized tool in thermodynamics
Authors: Sandler Stanley I. , Castier Marcelo 
Published: July 2007

AbstractIn this paper, we highlight the various ways computational quantum mechanics (QM) can be used in applied thermodynamics. We start with the most rigorous procedures of calculating the interactions between molecules that can then be used in simulation and progress, in steps, to less rigorous but easily used methods, including the very successful continuum solvation models.
Bond-dissociation enthalpies in the gas phase and in organic solvents: Making ends meet
Authors: Borges dos Santos Rui M. , Costa Cabral Benedito J. , Martinho Simões José A. 
Published: July 2007

Abstract
Solvent effects are responsible for the difference between gas- and solution-phase bond-dissociation enthalpies (BDEs), and are thus crucial for understanding reactivity in solution. While solvation effects can be negligible (e.g., in reactions involving carbon-centered radicals), they may be rather significant (e.g., when oxygen-centered radicals are formed). This paper reviews a number of models which have been proposed to deal with the difference between the solvation energetics of a radical and its parent molecule. It is concluded that the radical-solvent interaction may be larger than previously anticipated.
Specific Magnetic Bead–Based Capture of Genomic DNA from Clinical Samples: Application to the Detection of Group B Streptococci in Vaginal/Anal Swabs
Authors: Parham Nicholas J , Picard François J , Peytavi Régis , Gagnon Martin , Seyrig Grégoire , Gagné Pier-Ann , Boissinot Maurice , Bergeron Michel G 
Published: July 2007

Abstract
Background: Group B streptococci (GBS) are a leading cause of sepsis and meningitis in newborns. We previously developed a rapid diagnostic system for GBS detection from vaginal/anal samples obtained from pregnant women during delivery. To facilitate the adaptation of this method for point-of-care testing, we have developed a specific and efficient GBS DNA capture method that is compatible with both PCR and nonamplification detection technologies.
Methods: Superparamagnetic beads were functionalized with oligonucleotide capture probes of different lengths and used to capture GBS genomic DNA (gDNA). A rapid extraction procedure was used to provide DNA from GBS cultures or vaginal/anal samples with added GBS. Hybridization reactions consisting of functionalized beads and target DNA in 30 μL of hybridization buffer were performed for 1 h at room temperature, followed by washing and resuspension in water. Captured DNA was then detected using quantitative PCR.
Results: A 25-mer capture probe allowed detection of 1000 genome copies of purified GBS DNA. The ability to detect GBS was improved by use of a 50-mer (100 copies) and a 70-mer capture probe (10 copies). Detection of approximately 1250 CFU/mL was achieved for diluted GBS broth culture and for vaginal/anal swab samples with added GBS.
Conclusion: Oligonucleotide-functionalized superparamagnetic microbeads efficiently capture GBS gDNA from both bacterial cultures and vaginal/anal samples with added GBS. Efficiency of gDNA capture increases with oligonucleotide length. This technology could be combined with sample preparation and detection technologies in a microfluidic system to allow point-of-care testing for GBS.
Effect of bleomycin and cisplatin on the expression profile ofSRA1, a novel member of pre-mRNA splicing factors, in HL-60 human promyelocytic leukemia cells
Authors: Katsarou Maria E. , Thomadaki Hellinida , Katsaros Nikos , Scorilas Andreas 
Published: July 2007

AbstractRecently, a new member of the human SR (Ser/Arg-rich) superfamily of pre-mRNA splicing factors, SRA1 (SR-A1), has been discovered and cloned by members of our group, the gene for which was found to be overexpessed in a series of human tumors. In the present study, we investigated the significance of alterations at the mRNA expression levels of theSRA1gene after treatment of HL-60 human promyelocytic leukemia cells with the anticancer drugs cisplatin and bleomycin. The kinetics of apoptosis and cell toxicity were investigated by DNA laddering and the MTT and trypan blue assays, respectively. Total RNA was extracted and cDNA was prepared by reverse transcription. The splicing-related genesSRA1andSC35, as well as the apoptosis-related geneBCL2(Bcl-2), were amplified by PCR using gene-specific primers. The results showed that mRNA levels ofSRA1were up-regulated upon treatment with the antibiotic bleomycin, whereas they were down-regulated by treatment of HL-60 human promyelocytic leukemia cells with cisplatin. Our results support the hypothesis that mRNA expression analysis ofSRA1may serve as a new prospective molecular marker, playing an important role in chemotherapy outcome in human leukemia.
In vivo labeling with stable isotopes as a tool for the identification of unidentified peaks in the metabolome analysis of Corynebacterium glutamicum by GC/MS
Authors: Herebian Diran , Küpper Uta , Schomburg Dietmar , Marner Franz-Josef 
Published: July 2007

Abstract
Of the hyphenated techniques used for metabolic profiling of cell and tissue extracts, GC/MS is in some ways advantageous as it allows the simultaneous fingerprinting of chemically very different metabolites, and the electron impact mass spectra recorded in many cases lead to unambiguous identification of the compounds. However, prior to chromatography, the hydrophilic substances of the cell extracts have to be converted to vaporizable derivatives, the mass spectra of which often are not known or not listed in the available spectral libraries, even if they are derived from simple biochemicals. Thus, numerous chromatographic peaks remain as yet unidentified. Attempts to identify these peaks afford the acquisition of more data on these compounds. The value of in vivo labeling of metabolites with 13C and 15N for this purpose is described.
Cleavage of the myristoylated alanine-rich C kinase substrate (MARCKS) by cysteine cathepsins in cells and tissues of stefin B-deficient mice
Authors: Kopitar-Jerala Nataša , Turk Boris 
Published: July 2007

Abstract
The myristoylated alanine-rich C kinase substrate (MARCKS) is a substrate of protein kinase C (PKC). Besides regulation at the level of gene transcription, MARCKS concentrations within the cell are also regulated by proteolytic cleavage by cathepsins and calpains, which are cysteine proteinases. Stefin B (cystatin B) is an endogenous inhibitor of lysosomal cysteine cathepsins, but not calpains. We have observed increased cleavage of MARCKS in brain and macrophages, but not in liver and kidney extracts of stefin B-deficient mice compared to wild-type mice. Processing of cathepsin B was unaltered in the brain of stefin B-deficient mice and we conclude that increased cleavage of MARCKS could be attributed to the lack of inhibitor.
Involvement of Kupffer cell-dependent signaling in T3-induced hepatocyte proliferationin vivo
Authors: Fernández Virginia , Reyes Solange , Bravo Sergio , Sepúlveda Rodrigo , Romanque Pamela , Santander Gonzalo , Castillo Iván , Varela Patricia , Tapia Gladys , Videla Luis A. 
Published: July 2007

AbstractThyroid hormone-induced calorigenesis triggers liver oxidative stress with concomitant TNF-α production by Kupffer cells and up-regulation of gene expression. Considering that cyclin-dependent kinase-2 (CDK-2) performs essential functions for cellular proliferation, our aim was to test the hypothesis thatl-3,3′,5-triiodothyronine (T3) stimulates liver cell proliferation by upstream mechanisms involving CDK-2 expression dependent on Kupffer cell signaling. T3administration induced a calorigenic response at 60–70 h after treatment, with increased TNF-α generation and hepatic oxidative stress status, as shown by enhanced protein carbonyls and decreased glutathione content compared to controls. In this time interval, liver c-jun N-terminal kinase (JNK) phosphorylation, activator protein-1 (AP-1) DNA binding, and CDK-2 expression were enhanced, with concomitantly higher levels of the proliferation markers Ki-67 and proliferating cell nuclear antigen. These changes are abolished by administration of the Kupffer cell inactivator gadolinium chloride prior to T3treatment. We conclude that T3administration triggers liver CDK-2 expression and cellular proliferation through a cascade associated with Kupffer cell-dependent TNF-α generation, JNK phosphorylation, and AP-1 activation. Since CDK-2 promotes phase S progression within the cell cycle, this response may constitute a major mechanism involved in T3-induced liver preconditioning to ischemia/reperfusion injury.
Engineering high-speed allosteric hammerhead ribozymes
Authors: Link Kristian H. , Guo Lixia , Ames Tyler D. , Yen Laising , Mulligan Richard C. , Breaker Ronald R. 
Published: July 2007

Abstract
Full-length hammerhead ribozymes were subjected to in vitro selection to identify variants that are allosterically regulated by theophylline in the presence of a physiologically relevant concentration of Mg2+. The population of allosteric ribozymes resulting from 15 rounds of in vitro selection yielded variants with observed rate constants (k
obs) as high as 8 min-1 in the presence of theophylline and maximal k
obs increases of up to 285-fold compared to rate constants measured in the absence of effector. The selected ribozymes have kinetic characteristics that are predicted to be sufficient for cellular gene control applications, but do not exhibit any activity in reporter gene assays. The inability of the engineered RNAs to control gene expression suggests that the in vitro and in vivo folding pathways of the RNAs are different. These results provide several key pieces of information that will aid in future efforts to engineer allosteric ribozymes for gene control applications.
Analysis of programmed cell death in mouse fetal oocytes
Authors: Lobascio A M , Klinger F G , Scaldaferri M L , Farini D , De Felici M 
Published: July 2007

We report a short-term culture system that allowsto define novel characteristic of programmed cell death (PCD) in fetal oocytes and to underscore newaspects of this process. Mouse fetal oocytes culturedin conditions allowingmeiotic prophase I progression underwent apoptotic degeneration waves as revealed by TUNEL staining. TEM observations revealed recurrent atypical apoptotic morphologies characterized by the absence of chromatin margination and nuclear fragmentation; oocytes with autophagic and necrotic features were also observed. Further characterization of oocyte death evidenced DNA ladder, Annexin V binding, PARP cleavage, and usually caspase activation (namely caspase-2). In the aim to modulate the oocyte death process, we found that the addition to the culture medium of the pancaspase inhibitors Z-VAD orcaspase-2-specific inhibitor Z-VDVAD resulted in a partial and transient prevention of this process. Oocyte death was significantly reduced by the antioxidant agent NAC and partly prevented by KL and IGF-I growth factors. Finally, oocyte apoptosis was reduced by calpain inhibitor I and increased by rapamycin after prolonged culture.
These results support the notion that fetal oocytes undergo degeneration mostly by apoptosis. This process is, however, often morphologically atypical and encompasses other forms of cell death including caspase-independent apoptosis and autophagia. The observation that oocyte death occurs mainly at certain stages of meiosis and can only be attenuated by typical anti-apoptotic treatments favors the notion that it is controlled at least in part by stage-specific oocyte-autonomous meiotic checkpoints and when activated is little amenable to inhibition being the oocyte able to switch back and forth among different death pathways.
Economic Analysis of Triptan Therapy for Acute Migraine: A Medicaid Perspective
Authors: Mullins C. Daniel , Subedi Prasun R. , Healey Paul J. , Sanchez Robert J. 
Published: July 2007

Study Objective. To compare triptan therapies for migraine in terms of the cost to treat 100 migraine attacks and the cost per successfully treated patient (cost/success), by analyzing utilization and reimbursement data from state Medicaid programs.Design. Pharmacoeconomic analysis.Data Source. Clinical efficacy data were obtained from a previously published meta‐analysis for 11 triptan‐dose combinations: almotriptan 12.5 mg; eletriptan 20 and 40 mg; naratriptan 2.5 mg; rizatriptan 5 and 10 mg; sumatriptan 25, 50, and 100 mg; and zolmitriptan 2.5 and 5 mg. Triptan reimbursement data were obtained from the Medicaid Drug Rebate Program of seven geographically dispersed states (Florida, Georgia, Illinois, North Carolina, Ohio, Wisconsin, and West Virginia).Measurements and Main Results. Efficacy measures were derived based on data from the published meta‐analysis that evaluated headache pain status at 2 and 24 hours after triptan dosing. Reimbursement data for the triptans were applied to a previously developed model of migraine treatment outcomes to calculate the cost to treat 100 migraine attacks and the cost/success. Sensitivity analysis around dosing assumptions was conducted to assess robustness of estimates. Across the seven states, the two treatments associated with the lowest cost to treat 100 migraine attacks were eletriptan 20 mg (range $1549‐$1658) and eletriptan 40 mg ($1578‐$1661). Naratriptan 2.5 mg (range $1734‐$2018), sumatriptan 25 mg ($1853–1954), and zolmitriptan 5 mg ($1854‐$1960) were associated with the highest cost to treat 100 migraine attacks. Eletriptan 40 mg was associated with the lowest cost/success (range $57.03‐$60.05); naratriptan 2.5 mg ($99.39‐$115.65), sumatriptan 25 mg ($107.11‐$112.93), and rizatriptan 5 mg ($99.41‐$111.25) were associated with the highest cost/success values. Changes in dosing assumptions did not significantly change the rank ordering of triptans across either economic end point.Conclusions. Eletriptan 20‐ and 40‐mg doses were shown to be associated with the lowest cost to treat 100 migraine attacks and the lowest cost/success in both the baseline and sensitivity analyses. These findings are consistent with results of similar economic analyses that compared multiple triptan therapies.
Injectable Mesenchymal Stem Cell Therapy for Large Cartilage Defects—A Porcine Model
Authors: Lee Kevin B.L. , Hui James H.P. , Song Im Chim , Ardany Lenny , Lee Eng Hin 
Published: July 2007

AbstractCurrent techniques in biological resurfacing of cartilage defects require an open arthrotomy or arthroscopy and involve the direct transplantation of isolated cells and/or scaffolds or whole tissue grafts with chondrogenic potential onto the cartilage defect. Our study investigates the possibility of direct intra-articular injection of mesenchymal stem cells suspended in hyaluronic acid (HA) as an alternative to the much more invasive methods currently available. A partial-thickness (without penetration of the subchondral bone) cartilage defect was created in the medial femoral condyle of an adult minipig. Mesenchymal stem cells from the iliac crest marrow of the same pig harvested in a separate procedure and suspended in 2 milliliters of hylan G-F 20 (Synvisc) were injected intra-articularly after the creation of the defect. This was followed by two more injections of hylan G-F 20 (HA) at weekly intervals. Either saline or HA was injected into the knees of the controls. The pigs were sacrificed at 6 and 12 weeks for morphological and histological analysis. The cell-treated groups showed improved cartilage healing both histologically and morphologically at 6 and 12 weeks compared with both controls. The use of intra-articular injections of mesenchymal stem cells suspended in HA is a viable option for treating large cartilage defects. This would be further explored in clinical trials.Disclosure of potential conflicts of interest is found at the end of this article.
Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels and T-Type Calcium Channels Confer Automaticity of Embryonic Stem Cell-Derived Cardiomyocytes
Authors: Yanagi Kentoku , Takano Makoto , Narazaki Genta , Uosaki Hideki , Hoshino Takuhiro , Ishii Takahiro , Misaki Takurou , Yamashita Jun K. 
Published: July 2007

AbstractRegeneration of cardiac pacemakers is an important target of cardiac regeneration. Previously, we developed a novel embryonic stem (ES) cell differentiation system that could trace cardiovascular differentiation processes at the cellular level. In the present study, we examine expressions and functions of ion channels in ES cell-derived cardiomyocytes during their differentiation and identify ion channels that confer their automaticity. ES cell-derived Flk1+ mesoderm cells give rise to spontaneously beating cardiomyocytes on OP9 stroma cells. Spontaneously beating colonies observed at day 9.5 of Flk1+ cell culture (Flk-d9.5) were significantly decreased at Flk-d23.5. Expressions of ion channels in pacemaker cells hyperpolarization-activated cyclic nucleotide-gated (HCN)1 and -4 and voltage-gated calcium channel (Cav)3.1 and -3.2 were significantly decreased in purified cardiomyocytes at Flk-d23.5 compared with at Flk-d9.5, whereas expression of an atrial and ventricular ion channel, inward rectifier potassium channel (Kir)2.1, did not change. Blockade of HCNs and Cav ion channels significantly inhibited beating rates of cardiomyocyte colonies. Electrophysiological studies demonstrated that spontaneously beating cardiomyocytes at Flk-d9.5 showed almost similar features to those of the native mouse sinoatrial node except for relatively deep maximal diastolic potential and faster maximal upstroke velocity. Although ∼60% of myocytes at Flk-d23.5 revealed almost the same properties as those at Flk-d9.5, ∼40% of myocytes showed loss of HCN and decreased Cav3 currents and ceased spontaneous beating, with no remarkable increase of Kir2.1. Thus, HCN and Cav3 ion channels should be responsible for the maintenance of automaticity in ES cell-derived cardiomyocytes. Controlled regulation of these ion channels should be required to generate complete biological pacemakers.Disclosure of potential conflicts of interest is found at the end of this article.