gebhart/patrepeval huggingface dataset:
Plus de sport, plus de délinquance chez les jeunes (2005)

Le sport est idealise. Les sportifs sont les gladiateurs et les dieux des temps modernes. En France, la pratique du sport beneficie d'une image tres favorable aupres de nombre de professionnels du social, de la population ou meme des entreprises. Existe-t-il un moyen de tester la veracite de ces representations qui font de la pratique sportive un agent benefique sur la vie sociale, ses valeurs et les comportements individuels ? Deux enquetes de delinquance autodeclaree ont ete realisees en 1999 a Grenoble et Saint-Etienne et en 2003 a Grenoble ; elles portaient sur un echantillon representatif de jeunes âges de 13 ans a 19 ans dans ces agglomerations. Les questionnaires contenaient a la fois des questions sur les delits commis et sur les activites sportives pratiquees, qu'il a ete possible de rapprocher. Les resultats amenent a douter d'un effet benefique du sport sur la delinquance, puisque la pratique du sport tend a etre associee a une plus grande frequence de commission de delits.
Molecular mechanisms of proteinuria in diabetes (2008)

The epidemic of Type 2 diabetes, and the parallel rising incidence of end-stage renal disease, is progressively increasing worldwide. Kidney disease is one of the major chronic microvascular complications of diabetes, and both metabolic and haemodynamic perturbations participate in its development and progression towards end-stage renal disease. Hypertension and poor metabolic control seem to interact in causing the relentless decline in renal function seen in diabetic patients. Both high circulating glucose levels and increased glomerular capillary pressure act in conjunction in stimulating the different cellular pathways leading to kidney disease. It has been suggested that mechanical forces at the glomerular level may aggravate the metabolic insult by stimulating excessive cellular glucose uptake by up-regulating the facilitative GLUT-1 (glucose transporter-1). We propose the existence of a self-maintaining cellular mechanism whereby a haemodynamic stimulus on glomerular cells induces the up-regulation of GLUT-1, an event followed by greater glucose uptake and activation of intracellular metabolic pathways, resulting in excess TGF-beta1 (transforming growth factor-beta1) production. TGF-beta1, one of the major prosclerotic cytokines in diabetic kidney disease, maintains the up-regulation of GLUT-1, perpetuating a series of cellular events that result, as their ultimate effect, in increased extracellular matrix synthesis and altered permeability of the glomerular filtration barrier. Mechanical and metabolic coupling could represent an important mechanism of injury in the diabetic kidney.
Quantitative analysis of protein synthesis inhibition by transferrin-toxin conjugates. (1994)

A mathematical model was developed which relates the time and concentration dependence of protein synthesis inhibition of an immunotoxin to the properties of the targeting agent and the conjugated toxin. The role of the targeting agent and that of the toxin in determining the cytotoxicity were separated in this model by describing protein synthesis inhibition as a function of a cellular trafficking variable, which is calculated from the trafficking parameters of the targeting agent, and a protein synthesis inhibition constant, which is a property of the translocation and enzymatic rate constants of the toxin. Transferrin cellular trafficking parameters were determined experimentally for HeLa and SK-MEL-2 cells. Protein synthesis inhibition of transferrin-gelonin and transferrin-CRM107 conjugates in both cell lines was measured as a function of time and concentration. Analysis of the data showed that the model was a good representation of the experimental results, and correctly explained cell line differences in sensitivity to transferrin-toxin conjugates. The translocation rate constant for transferrin-CRM107 was approximately 3000 times greater than that for transferrin-gelonin. The model may be useful in understanding the factors that influence immunotoxin efficacy and in designing more lethal immunotoxins.
Segregation analysis of cryptogenic epilepsy and an empirical test of the validity of the results. (1997)

We used POINTER to perform segregation analysis of cryptogenic epilepsy in 1,557 three-generation families (probands and their parents, siblings, and offspring) ascertained from voluntary organizations. Analysis of the full data set indicated that the data were most consistent with an autosomal dominant (AD) model with 61% penetrance of the susceptibility gene. However, subsequent analyses revealed that the patterns of familial aggregation differed markedly between siblings and offspring of the probands. Risks in siblings were consistent with an autosomal recessive (AR) model and inconsistent with an AD model, whereas risks in offspring were inconsistent with an AR model and more consistent with an AD model. As a further test of the validity of the AD model, we used sequential ascertainment to extend the family history information in the subset of families judged likely to carry the putative susceptibility gene because they contained at least three affected individuals. Prevalence of idiopathic/cryptogenic epilepsy was only 3.7% in newly identified relatives expected to have a 50% probability of carrying the susceptibility gene under an AD model. Approximately 30% (i.e., 50% x 61%) were expected to be affected under the AD model resulting from the segregation analysis. These results suggest that the familial distribution of cryptogenic epilepsy is inconsistent with any conventional genetic model. The differences between siblings and offspring in the patterns of familial risk are intriguing and should be investigated further.
Repair of a Critical Size Defect in the Rat Mandible Using Allogenic Type I Collagen (2001)

Mandibular fractures, resulting from either trauma or reconstructive surgery, can be challenging craniofacial problems. The morbidity of failed fracture healing is significant and may require bone grafting. Donor site morbidity and finite amounts of autogenous bone are major drawbacks of autogenous bone grafting. Similarly, the use of allografts and xenografts may be associated with an increased risk of rejection, infection, and nonunion. To circumvent the limitations of bone grafting, research efforts have focused on formulating a suitable bone substitute. The purpose of our study was to evaluate the efficacy of type I collagen implants in repairing critical sized mandibular defects in rats. Twelve male Sprague-Dawley rats (200-300g) were divided equally into control and experimental groups. Full thickness, round, four millimeter in diameter defects were created in the ramus of the right mandible of all rats using an electrical burr at low speed. The defects were irrigated of all bone chips, and either filled with a precisely fitted disk of allogenic collagen type I gel (experimental animals) or left empty (control animals). Animals were killed 6 weeks after surgery and healing of the bone defects was assessed in a blinded fashion using radiologic and histologic analysis. Radiologic analysis of the control group revealed a clear circular right mandibular defect in all animals, whereas the collagen disk implant group revealed an indistinct to nonexistent right mandibular defect in all animals. Densitometric analysis revealed a significant difference between these groups (* P = 0.01). Similarly, gross analysis of control mandibles revealed a 4mm round, soft-tissue filled defect, while implanted defects demonstrated gross bone spanning the defect. Finally, histologic analysis of all control mandibles revealed clearly demarcated bony edges at the defect border with connective tissue spanning the defect. In contrast, histological analysis of all implanted mandibles revealed indistinct bony edges at the defect border with a thin layer of osteoblasts and viable bone spanning the defects. We have demonstrated the ability of type I collagen to promote healing of a membranous bony defect that would not otherwise heal at 6 weeks. The suitability of type I collagen as a carrier matrix provides ample opportunity for tissue-engineered approaches to further facilitate bony defect healing. Promoting bone formation through tissue engineering matrices offers great promise for skeletal healing and reconstruction.
Surrogate light chain-dependent selection of Ig heavy chain V regions (1995)

Bone marrow B cell precursors frequently rearrange the Ig heavy chain variable (VH) gene segment VH81X. It is puzzling, therefore, that mature B cells in adult mice rarely express mu-heavy chains bearing this VH gene segment. We show in this work in transformed pre-B cell lines that two VH81X/mu-chains that differ in their VH-D-JH joining sequences are not assembled covalently with the B cell precursor-specific surrogate light (SL) chain and are not expressed on the cell surface. From these findings, we propose that a B cell precursor clonally expands and proceeds to the next developmental stage only if it expresses a mu-chain with a VH domain that, together with the SL chain, directs the formation of a signal-transducing mu/SL chain membrane complex. Therefore, a checkpoint exists early in B cell development, at which SL chain not only screens B cell precursors for the presence of a full-length mu-chain, but also for a VH domain that promotes the assembly of a mu/SL chain complex.
The Cataract Extraction-Refraction-Implantation Technique for IOL Power Calculation in Difficult Cases (1998)

Journal of Cataract & Refractive Surgery 24(4):p 434-435, April 1998. | DOI: 10.1016/S0886-3350(98)80277-0
Sequence determinants of protein aggregation: tools to increase protein solubility (2005)

Escherichia coli is one of the most widely used hosts for the production of recombinant proteins. However, very often the target protein accumulates into insoluble aggregates in a misfolded and biologically inactive form. Bacterial inclusion bodies are major bottlenecks in protein production and are hampering the development of top priority research areas such structural genomics. Inclusion body formation was formerly considered to occur via non-specific association of hydrophobic surfaces in folding intermediates. Increasing evidence, however, indicates that protein aggregation in bacteria resembles to the well-studied process of amyloid fibril formation. Both processes appear to rely on the formation of specific, sequence-dependent, intermolecular interactions driving the formation of structured protein aggregates. This similarity in the mechanisms of aggregation will probably allow applying anti-aggregational strategies already tested in the amyloid context to the less explored area of protein aggregation inside bacteria. Specifically, new sequence-based approaches appear as promising tools to tune protein aggregation in biotechnological processes.
Escherichia coli prlC Gene Encodes a Trypsin-Like Proteinase Regulating the Cell Cycle (1998)

Proteinase In has previously been described as displaying a trypsin-like proteinase activity that momentarily appears immediately before DNA synthesis in the cell cycle of Escherichia coli synchronized by phosphate starvation and which is closely related to the initiation of DNA replication [Kato, M., Irisawa, T., Ohtani, M., and Muramatu, M. (1992) Eur. J. Biochem. 210, 1007-1014]. We purified the proteinase In from E. coli C600 and found that the 15 amino acid residues of its amino-terminal were identical with those of oligopeptidase A (OpdA), the product of the E. coli prlC gene. The purified proteinase had a molecular mass of approximately 67 kDa, which was also the same as that of oligopeptidase A. To further elucidate the relationship between proteinase In and oligopeptidase A, we assembled an expression vector to direct the synthesis of E. coli oligopeptidase A. The protein was expressed at a high level in E. coli BL21(DE3) and was produced mostly in the soluble, active form. Both the recombinant enzyme (rPrlC) and the purified proteinase In could hydrolyze trypsin substrates for proteinase In as well as benzyloxycarbonyl Ala- Ala-Leu p-nitroanilide (Z-AALpNA), described as a synthetic substrate for oligopeptidase A. The effects of various protease inhibitors on rPrlC were also very similar to those on proteinase In. The trypsin inhibitors 4-guanidino benzoic acid 4-tert-butylphenyl ester and antipain strongly inhibited the trypsin-like proteinase activity of the recombinant enzyme, but had no effect on its Z-AALpNA hydrolyzing activity. Cobalt ion, which greatly enhanced the OpdA activity, slightly inhibited the trypsin-like activity of the recombinant enzyme. These results strongly suggest that proteinase In is encoded by the E. coli prlC gene and is a multi-functional proteinase with two separate active sites.
Monolithic color-selective ultraviolet (266–315 nm) photodetector based on a wurtzite MgxZn1−xO film (2014)

A unique ultraviolet photodetector based on a metal-semiconductor-metal structure was fabricated from a wurtzite MgxZn1−xO film with gradually changing Mg content, homoepitaxially grown on a BeO-buffered ZnO substrate. The BeO layer filtered out the substrate photoresponse. The cutoff wavelength of the photodetector under zero bias was 266 nm with a UV/visible light rejection ratio of greater than 2 orders of magnitude in the deep UV region. Applying a bias, the cutoff wavelength exhibited a prominent continuous redshift from 266 (0 V) to 315 nm (3 V), indicating the capability for multi-band UV detection on a monolithic chip. The bias-controlled wavelength-selective UV photoresponse mechanism occurred in the optically active area in a compositionally distributed MgxZn1−xO alloy that was achieved by molecular epitaxial growth.
Assembly and Protection of the Radical Enzyme, Methylmalonyl-CoA Mutase, by Its Chaperone (2006)

MeaB is a recently described P-loop GTPase that plays an auxiliary role in the reaction catalyzed by the radical B12 enzyme, methylmalonyl-CoA mutase. Defects in the human homologue of MeaB result in methylmalonic aciduria, but the role of this protein in coenzyme B12 assimilation and/or utilization is not known. Methylmalonyl-CoA mutase catalyzes the isomerization of methylmalonyl-CoA to succinyl-CoA that uses reactive radical intermediates that are susceptible to oxidative inactivation. In this study, we have examined the influence of MeaB on the kinetics of the reaction catalyzed by methylmalonyl-CoA mutase and on the thermodynamics of cofactor binding. MeaB alone has a modest effect on the affinity of the mutase for the 5'-deoxyadenosylcobalamin (AdoCbl) cofactor, increasing it 2-fold from 404 +/- 71 to 210 +/- 22 nM. However, in the presence of GDP, the affinity for the cofactor decreases 5-fold to 1.89 +/- 0.33 microM, while in the presence of guanosine 5'(beta-gamma imino)triphosphate, a nonhydrolyzable analogue of GTP, the binding of AdoCbl to the mutase is not detected. Protection against oxidative inactivation of the mutase by MeaB is dependent upon the presence of nucleotides with the MeaB/GDP and MeaB/GTP complexes decelerating the rate of formation of oxidized cofactor by 3- and 15-fold, respectively. This study suggests that MeaB functions in the GTP-dependent assembly of holomethylmalonyl-CoA mutase and subsequent protection of radical intermediates during catalysis.
Drug resistance mediated by cellular stress response to the microenvironment of solid tumors. (1999)

Most solid tumors show resistance to current chemotherapy. This drug resistance can be associated with the unique physiology of solid tumors. Solid tumors generally have regions of low oxygen (hypoxia), low pH and low levels of glucose, which are not observed in normal tissues. These tumor-specific conditions commonly cause the glucose-regulated stress response of cancer cells. Accumulating evidence shows that the stress response leads to induction of resistance to multiple drugs, such as etoposide, doxorubicin, camptothecin and vincristine. This type of drug resistance is reversible and decays rapidly when stress conditions are removed. The induction of drug resistance can be partly explained by cell cycle arrest at the G1 phase in stressed cells because most anticancer drugs are primarily effective against rapidly dividing cells. Specific mechanisms, such as the decreased expression of DNA topoisomerase (topo) II alpha for the resistance to topo II poisons, are also involved in the drug resistance. Stressed cells, however, become hypersensitive to cisplatin, one of the most effective drugs against solid tumors, suggesting that preferential cytotoxicity to stressed cells may be important for the clinical efficacy against solid tumors. Further characterization of stressed cells will provide a unique target to circumvent the drug resistance of solid tumors.
Neogenin mediates the action of repulsive guidance molecule (2004)

Repulsive guidance molecule (RGM) is a recently identified protein implicated in both axonal guidance and neural tube closure. The avoidance of chick RGM in the posterior optic tectum by growing temporal, but not nasal, retinal ganglion cell axons is thought to contribute to visual map formation. In contrast to ephrins, semaphorins, netrins and slits, no receptor mechanism for RGM action has been defined. Here, an expression cloning strategy identified neogenin as a binding site for RGM, with a sub-nanomolar affinity. Consistent with selective axonal responsiveness to RGM, neogenin is expressed in a gradient across the chick retina. Neogenin is known to be one of several netrin-binding proteins but only neogenin interacts with RGM. The avoidance of RGM by temporal retinal axons is blocked by the anti-neogenin antibody and the soluble neogenin ectodomain. Dorsal root ganglion axons are unresponsive to RGM but are converted to a responsive state by neogenin expression. Thus, neogenin functions as an RGM receptor.
The Physiology of the Grid An Open Grid Services Architecture for Distributed Systems Integration (2002)

In both e-business and e-science, we often need to integrate services across distributed, heterogeneous, dynamic &amp;quot;virtual organizations&amp;quot; formed from the disparate resources within a single enterprise and/or from external resource sharing and service provider relationships. This integration can be technically challenging because of the need to achieve various qualities of service when running on top of different native platforms. We present an Open Grid Services Architecture that addresses these challenges. Building on concepts and technologies from the Grid and Web services communities, this architecture defines a uniform exposed service semantics (the Grid service); defines standard mechanisms for creating, naming, and discovering transient Grid service instances; provides location transparency and multiple protocol bindings for service instances; and supports integration with underlying native platform facilities. The Open Grid Services Architecture also defines, in terms of Web Services Description Language (WSDL) interfaces and associated conventions, mechanisms required for creating and composing sophisticated distributed systems, including lifetime management, change management, and notification. Service bindings can support reliable invocation, authentication, authorization, and delegation, if required. Our presentation complements an earlier foundational article, &amp;quot;The Anatomy of the Grid,&amp;quot; by describing how Grid mechanisms can implement a service-oriented architecture, explaining how Grid functionality can be incorporated into a Web services framework, and illustrating how our architecture can be applied within commercial computing as a basis for distributed system integration--within and across organizational domains.
Barnett Shale Refracture Stimulations Using a Novel Diversion Technique (2009)

Abstract Gas production from the unconventional Barnett Shale reservoir now exceeds 3 Bcf/d, which is more than 5% of total U.S. dry gas production. Typically Barnett Shale wells exhibit a rapid production decline following the initial hydraulic fracture stimulation treatment, so that, within 5 years, an operator is normally faced with a well producing below its economic threshold. To keep up with current gas demand, operators have moved to an aggressive horizontal drilling and completion program. Additionally, in an effort to increase the productivity of existing wells and book additional reserves at reduced cost, operators have restimulated their older vertical wells, with demonstrable success. This success is providing compelling opportunities to enhance refracture treatment coverage by targeting bypassed and ineffectively stimulated zones in additional vertical wells and even some horizontal wells. Because of the heterogeneous nature of this unconventional gas reservoir, the restimulation of horizontal wells is problematic, and operators have demonstrated limited success using current stimulation techniques. This paper describes a new fracture diversion technique particularly adapted for horizontal well refracture stimulation. During the treatment, a fracture diversion system (FDS) is used to create a temporary bridge within the active fracture networks. That results in differential pressure increase and causes treatment redirection to understimulated intervals along the lateral. This technique enables both fracture diversion without mechanical intervention and, when enhanced with microseismic monitoring, real-time optimization of the fracturing treatment. Refracture stimulation case studies are presented in which this novel diversion technique is successfully applied to horizontal Barnett Shale wells. This paper demonstrates how real-time hydraulic fracture monitoring has enabled operators to make informed decisions that influence fracture geometry, increase lateral coverage, and improve gas recovery. To date, more than 20 fracture diversion designs have been successfully placed. The trial wells have included both cemented and uncemented completions, with drilled azimuths selected to encourage either transverse or longitudinal fracture fairway development. With a continuing optimization of the described refracturing technique, these FDS designs and placement strategies have evolved to the point where they are consistently exhibiting fracture diversion as evidenced by movement of microseismic activity and improved lateral coverage. While this engineered fracture diversion technique is ideally suited for re-fracture stimulations, it is also applicable for stimulation of new wells where the technique enables stimulation of larger wellbore intervals when used in the same fashion as for re-fracture stimulation applications.
A region based stereo matching algorithm using cooperative optimization (2008)

This paper presents a new stereo matching algorithm based on inter-regional cooperative optimization. The proposed algorithm uses regions as matching primitives and defines the corresponding region energy functional for matching by utilizing the color Statistics of regions and the constraints on smoothness and occlusion between adjacent regions. In order to obtain a more reasonable disparity map, a cooperative optimization procedure has been employed to minimize the matching costs of all regions by introducing the cooperative and competitive mechanism between regions. Firstly, a color based segmentation method is used to segment the reference image into regions with homogeneous color. Secondly, a local window-based matching method is used to determine the initial disparity estimate of each image pixel. And then, a voting based plane fitting technique is applied to obtain the parameters of disparity plane corresponding to each image region. Finally, the disparity plane parameters of all regions are iteratively optimized by an inter-regional cooperative optimization procedure until a reasonable disparity map is obtained. The experimental Results on Middlebury test set and real stereo images indicate that the performance of our method is competitive with the best stereo matching algorithms and the disparity maps recovered are close to the ground truth data.