Miracle-dz/UniFAR-FTUs huggingface dataset:
A Stochastic Galerkin Method for Stochastic Control Problems

In an interdisciplinary field on mathematics and physics, we examine a physical problem, fluid flow in porous media, which is represented by a stochastic partial differential equation (SPDE). We first give a priori error estimates for the solutions to an optimization problem constrained by the physical model under lower regularity assumptions than the literature. We then use the concept of Galerkin finite element methods to establish a new numerical algorithm to give approximations for our stochastic optimal physical problem. Finally, we develop original computer programs based on the algorithm and use several numerical examples of various situations to see how well our solver works by comparing its outputs to the priori error estimates. AMS subject classifications: 65M55, 65N30
SOCIAL LEARNING IN ANIMALS: CATEGORIES AND MECHANISMS

There has been relatively little research on the psychological mechanisms of social learning. This may be due, in part, to the practice of distinguishing categories of social learning in relation to ill-defined mechanisms (Davis, 1973; Galef, 1988). This practice both makes it difficult to identify empirically examples of different types of social learning, and gives the false impression that the mechanisms responsible for social learning are clearly understood. It has been proposed that social learning phenomena be subsumed within the categorization scheme currently used by investigators of asocial learning. This scheme distinguishes categories of learning according to observable conditions, namely, the type of experience that gives rise to a change in an animal (single stimulus vs. stimulus-stimulus relationship vs. response-reinforcer relationship), and the type of behaviour in which this change is detected (response evocation vs. learnability) (Rescorla, 1988). Specifically, three alignments have been proposed: (i) stimulus enhancement with single stimulus learning, (ii) observational conditioning with stimulus-stimulus learning, or Pavlovian conditioning, and (iii) observational learning with response-reinforcer learning, or instrumental conditioning. If, as the proposed alignments suggest, the conditions of social and asocial learning are the same, there is some reason to believe that the mechanisms underlying the two sets of phenomena are also the same. This is so if one makes the relatively uncontroversial assumption that phenomena which occur under similar conditions tend to be controlled by similar mechanisms. However, the proposed alignments are intended to be a set of hypotheses, rather than conclusions, about the mechanisms of social learning; as a basis for further research in which animal learning theory is applied to social learning. A concerted attempt to apply animal learning theory to social learning, to find out whether the same mechanisms are responsible for social and asocial learning, could lead both to refinements of the general theory, and to a better understanding of the mechanisms of social learning. There are precedents for these positive developments in research applying animal learning theory to food aversion learning (e.g. Domjan, 1983; Rozin & Schull, 1988) and imprinting (e.g. Bolhuis, de Vox & Kruit, 1990; Hollis, ten Cate & Bateson, 1991). Like social learning, these phenomena almost certainly play distinctive roles in the antogeny of adaptive behaviour, and they are customarily regarded as 'special kinds' of learning (Shettleworth, 1993). (ABSTRACT TRUNCATED AT 400 WORDS)
On the Discovery of Explainable and Accurate Behavioral Models for Complex Lowly-structured Business Processes

Process discovery (i.e. the automated induction of a behavioral process model from execution logs) is an important tool for business process analysts/managers, who can exploit the extracted knowledge in key process improvement and (re-)design tasks. Unfortunately, when directly applied to the logs of complex and/or lowly-structured processes, such techniques tend to produce low-quality workflow schemas, featuring both poor readability ("spaghetti-like") and low fitness (i.e. low ability to reproduce log traces). Trace clustering methods alleviate this problem, by helping detect different execution scenarios, for which simpler and more fitting workflow schemas can be eventually discovered. However, most of these methods just focus on the sequence of activities performed in each log trace, without fully exploiting all non-structural data (such as cases data and environmental variables) available in many real logs, which might well help discover more meaningful (context-related) process variants. In order to overcome these limitations, we propose a two-phase clustering-based process discovery approach, where the clusters are inherently defined through logical decision rules over context data, ensuring a satisfactory trade-off is between the readability/explainability of the discovered clusters, and the behavioral fitness of the workflow schemas eventually extracted from them. The approach has been implemented in a system prototype, which supports the discovery, evaluation and reuse of such multi-variant process models. Experimental results on a real-life log confirmed its capability to achieve compelling performances w.r. t. state-of-the-art clustering approaches, in terms of both fitness and explainability.
Central sensitization in medullary dorsal horn involves gap junctions and hemichannels

Central sensitization is a fundamental mechanism contributing to acute and chronic pain conditions. Our previous studies have documented a glutamatergic, purinergic and glial-dependent central sensitization that can be induced in rat medullary dorsal horn nociceptive neurons by mustard oil application to the tooth pulp. This study showed that carbenoxolone, a potent gap junction and hemichannel blocker, completely blocked all parameters of mustard oil-induced central sensitization tested in functionally identified medullary dorsal horn nociceptive neurons. These results represent the first evidence suggesting that gap junctions and hemichannels may have a critical role in mediating central sensitization in dorsal horn nociceptive neurons and may account for the spread as well as development of central sensitization.
Characterization of a novel Rochalimaea species, R. henselae sp. nov., isolated from blood of a febrile, human immunodeficiency virus-positive patient

Isolation of a Rochalimaea-like organism from a febrile patient infected with human immunodeficiency virus was confirmed. Analysis of 16S rRNA gene sequences, together with polymerase chain reaction and restriction endonuclease length polymorphism analysis of a portion of the citrate synthase gene, demonstrated that the agent is closely related to members of the genus Rochalimaea and that the isolate is genotypically identical to the presumptive etiologic agent of bacillary angiomatosis. However, the same genotypic analyses readily differentiated the new isolate from isolates of other recognized Rochalimaea species as well as other genera of bacteria previously suggested as putative etiologic agents of bacillary angiomatosis and related syndromes. We propose that the novel species be referred to as Rochalimaea henselae sp. now.
Cisplatin Damage: Are DNA Repair Proteins Saviors or Traitors to the Cell?

In spite of its successful use for over 30 years as an anticancer agent, there is almost no scientific article dealing with cisplatin (cis-diamminedichloroplatinum) that does not introduce its research subject with the words “. but its mechanism of action is not fully understood. ”. When we were students (some 25 years ago) and first heard of cisplatin, everything seemed so clear. Cisplatin tightly binds DNA, bends it locally at the sites of the lesions, and causes cellular demise by impeding DNA replication; at that time—we have to admit—we did not dwell very long on the question of whether it may be the steric hindrance or the structural distortion, or both, that brings about the inhibition of DNA replication. Since then, there has been much discussion in the literature of whether or not it is the progression of DNA replication that, when halted by cisplatin adducts, results in cell death. Although there is undoubtedly a strong effect on DNA replication, the latter may not be the reason but rather (one of) the consequence(s) of the lethally hit cells. Consider, for example, that cells proficient in DNA repair are able to survive despite inhibition of the DNA replication, whereas DNA-repair-deficient cells die at cisplatin concentrations that do not inhibit DNA replication. Thus, inhibition of DNA synthesis correlates with the concentration of drug but not with the different sensitivities of the cell lines. In other words, cell death does not correlate with inhibition of DNA synthesis. In fact, cisplatin lesions are not necessarily an insuperable obstacle for DNA replication, as several polymerases are capable of synthesizing past damaged DNA sites (translesion synthesis ; Figure 1).
A translocated protein tyrosine phosphatase of Pseudomonas syringae pv. tomato DC3000 modulates plant defence response to infection

Pseudomonas syringae strains translocate effector proteins into host cells via the hrp‐encoded type III protein secretion system (TTSS) to facilitate pathogenesis in susceptible plants. However, the mechanisms by which pathogenesis is favoured by these effectors are not well understood. Individual strains express multiple effectors with apparently distinct activities that are co‐ordinately regulated by the alternative sigma factor HrpL. Genes for several effectors were identified in the P. syringae pv. tomato DC3000 genome using a promoter trap assay to identify HrpL‐dependent promoters. In addition to orthologues of avrPphE and hrpW, an unusual allele of avrPphD was detected that carried an IS52 insertion. Using this avrPphD::IS52 allele as a probe, a wild‐type allele of avrPphD, hopPtoD1, and a chimeric homologue were identified in the DC3000 genome. This chimeric homologue, identified as HopPtoD2 in the annotated DC3000 genome, consisted of an amino terminal secretion domain similar to that of AvrPphD fused to a potential protein tyrosine phosphatase domain. Culture filtrates of strains expressing HopPtoD2 were able to dephosphorylate pNPP and two phosphotyrosine peptides. HopPtoD2 was shown to be translocated into Arabidopsis thaliana cells via the hrp‐encoded TTSS. A ΔhopPtoD2 mutant of DC3000 exhibited strongly reduced virulence in Arabidopsis thaliana. Ectopic expression of hopPtoD2 in P. syringae Psy61 that lacks a native hopPtoD2 orthologue delayed the development of several defence‐associated responses including programmed cell death, active oxygen production and transcription of the pathogenesis‐related gene PR1. The results indicate that HopPtoD2 is a translocated effector with protein tyrosine phosphatase activity that modulates plant defence responses.
Strategies to adapt to an uncertain climate change

Many decisions concerning long-lived investments already need to take into account climate change. But doing so is not easy for at least two reasons. First, due to the rate of climate change, new infrastructure will have to be able to cope with a large range of changing climate conditions, which will make design more difficult and construction more expensive. Second, uncertainty in future climate makes it impossible to directly use the output of a single climate model as an input for infrastructure design, and there are good reasons to think that the needed climate informationwill not be available soon. Instead of optimizing based on the climate conditions projected by models, therefore, future infrastructure should be made more robust to possible changes in climate conditions. This aim implies that users of climate information must also change their practices and decision-making frameworks, for instance by adapting the uncertainty-management methods they currently apply to exchange rates or RD (ii) favouring reversible and flexible options; (iii) buying ‘‘safety margins’’ in new investments; (iv) promoting soft adaptation strategies, including long-term prospective; and (v) reducing decision time horizons. Moreover, it is essential to consider both negative and positive side-effects and externalities of adaptation measures. Adaptation–mitigation interactions also call for integrated design and assessment of adaptation and mitigation policies, which are often developed by distinct
Vascular stem cells-potential for clinical application.

INTRODUCTION Cell therapy is a growing area of research as an alternative to pharmaceuticals or surgery for the treatment of ischaemic disease. Studies are focusing on delivering tissue-derived cells into damaged organs to promote vascular regeneration or gain of function. SOURCES OF DATA Pubmed, clinicaltrials.gov, BHF website. AREAS OF AGREEMENT Stem cells have the potential to become a viable treatment for many diseases, as indicated by the numerous pre-clinical studies demonstrating therapeutic benefit. AREAS OF CONTROVERSY The mechanisms of action for transplanted stem cells are still open to debate. Proposed mechanism includes direct cell incorporation and paracrine action. Additionally, the secretome produced by transplanted cells remains largely unknown. GROWING POINTS Initial studies focused on delivering stem cells by injection; however, current research is utilizing biomaterials to target cell delivery to specific areas. AREAS TIMELY FOR DEVELOPING RESEARCH Whilst stem cell research in the laboratory is expanding rapidly, transition into clinical studies is hindered by the availability of equivalent clinical grade reagents.
Diphtheria toxin: mode of action and structure

INTRODUCTION. 54 OUTLINE OF THEPROBLEM. 54 INHIBITION OFPROTEIN SYNTHESIS . 56 Studies in Cell Culture . 56 Studies in Cell-Free Systems . 8 ADP-RIBOSYLATION OF EF-2 . 59 Identification of the Reaction . ADPR is Covalently Attached . 60 The Role of Toxin is Catalytic . 1 Substrate Specificity . 6 Reversibility and Thermodynamics . 62 Factors Affecting the Rate of the Forward Reaction 62 STRUCTURE-ACTIVITY RELATIONSHIPS IN THE TOXIN 63 Whole Toxin is a Proenzyme . 63 Toxicity of the Various Fragments andForms. 65 Properties of Fragment A . 65 Variations Among Toxin Preparations . 66 Nontoxic, Cross-Reacting Forms of Toxin . 7 Mechanism of the ADP-Ribosylation Reaction . 68 Pyridine Nucleotide Binding and ADP-Ribosylation Activity of Whole Toxin . 70 IS THE ADP-RIBOSYLATION REACTION RESPONSIBLE FOR TOXICITY? 71 EVENTSPRECEDING THE ADP-RIBOSYLATION REACTION IN CELLS. 72 Attachment to Specific Receptors.72 Entry and Activation Processes 3 Kinetics of Entry and Turnover 4 IMMUNOLOGY.75 Avidity Correlates with Antibody Against Fragment B.75 Immunogenicity and the Mechanism of Toxoiding. BIOLOGICAL FUNCTION AND ORIGIN OF DIPHTHERIATOXIN.77 Biological Function.7 Origin. 7 SUMMARY AND CONCLUDING REMARKS. 78 LITERATURE CITED. 80
Regulation of ABC membrane transporters in glial cells: Relevance to the pharmacotherapy of brain HIV‐1 infection

Limited drug penetration is an obstacle that is often encountered in the treatment of CNS diseases including human immunodeficiency virus type‐1 (HIV‐1) encephalitis (HIVE). One mechanism that may contribute to this phenomenon is the expression of ATP‐binding cassette (ABC) drug efflux transporters [i.e., P‐glycoprotein (P‐gp), Multidrug Resistance‐Associated Proteins (MRP/Mrp), Breast Cancer Resistance Protein (BCRP; also known as ABCG2)] at the primary brain barrier sites (i.e., blood‐brain barrier, blood‐cerebrospinal fluid barrier). In addition, it has been recently proposed that glial cells may also contribute to the low accumulation and altered distribution of therapeutic compounds in the CNS by functioning as a “secondary barrier. ” In fact, a few studies have shown that ABC transporters are both expressed and functional in glial cells. Furthermore, commonly prescribed antiretroviral compounds (ARVs), particularly HIV‐1 protease inhibitors, are substrates for many of these same transport proteins suggesting that ABC transporters in glial cells may contribute to the overall export of these drugs from the brain. HIV‐1 infection is a chronic condition characterized by long‐term exposure of brain cellular compartments to HIV‐1 virions and soluble viral proteins. In addition, treatment of HIV‐1 infection involves long‐term administration of a multiplicity of ARVs (i.e., HAART regimens). Indeed, pathological factors associated with HIV‐1 infection and/or pharmacological factors related to treatment may alter the expression of ABC transporters and lead to changes in CNS ARV uptake and/or distribution. This review summarizes recent knowledge in this area and emphasizes the role that glial ABC transporters may play in regulating ARV transport. © 2008 Wiley‐Liss, Inc.
CD40/CD40 ligand interactions are required for T cell‐dependent production of interleukin‐12 by mouse macrophages

We have previously shown that T cell receptor‐activated mouse T helper (Th)1 clones induce the production of interleukin (IL)‐12 by splenic antigen‐presenting cells (APC). Here, we show that the expression of CD40L by activated T cells is critical for T cell‐dependent IL‐12 production by mouse macrophages. IL‐12 was produced in cultures containing alloreactive Th1 clones stimulated with allogeneic peritoneal macrophages, or in cultures of splenocytes stimulated with anti‐CD3. Anti‐CD40L monoclonal antibodies (mAb) inhibited the production of IL‐12, but not IL‐2, in these cultures by ⩾90% and had dramatic inhibitory effects on antigen‐dependent proliferation of Th1 clones. In addition, both activated T cells and a Th1 clone derived from CD40L knockout mice failed to induce IL‐12 production from splenic APC or peritoneal macrophages. Finally, macrophages cultured in the absence of T cells produced IL‐12 upon stimulation with soluble recombinant CD40L in combination with either supernatants from activated Th1 clones or with interferon‐γ and granulocyte/macrophage colony‐stimulating factor. Thus, both CD40L‐dependent and cytokine‐mediated signals from activated T cells are required to induce the production of IL‐12 by macrophages. A blockade at the level of IL‐12 production may explain, at least in part, the dramatic ability of anti‐CD40L mAb to inhibit disease in animal models that are dependent upon the generation of a cell‐mediated immune response. Moreover, a defect in T cell‐dependent induction of IL‐12 may contribute to the immune status of humans that lack functional CD40L.
Modular PID-controller design with different filtering properties

The paper presents second part of two contributions dealing with simplified modular design of filtered PD and disturbance observer (DO) based filtered PID control (DO-FPID) illustrated by example of positional servo control. This second part is devoted to the analysis of DO-FPID controller tuned for different types of nonmodelled or filter dynamics. By employing nth-order filters, openness of the new approach allows to keep nearly fixed dynamics of the transients and to change noise attenuation without necessity to repeat in the nominal case analysis of the optimal and critical tuning. Thereby, the number of tuning parameters remains minimal. Achieved performance is evaluated by newly introduced measures for deviations from monotonic, one- and two-pulse shapes of transients typical for control of plants with the dominant 2nd order dynamics.
Racial and Ethnic Differences in Predictors of Smoking Cessation

Racial/ethnic differences in the determinants of smoking cessation could have important treatment implications. The current study examined racial/ethnic differences in smoking cessation, prospective predictors of cessation, and whether the predictive ability of these factors differed by race/ethnicity. Participants were 709 employed adults recruited through the National Rural Electric Co-op Association or through natural gas pipeline corporations. Data were collected in 1990 and 1994. Although race/ethnicity was not predictive of abstinence, Hispanic, African American, and White smokers displayed differential on tobacco-, alcohol-, and work-related variables. These racial/ethnic differences highlight the specific factors that should be considered when providing smoking cessation treatment to specific populations. Limitations are noted.
Evaluating Plasmonic Light Trapping With Photoluminescence

We use photoluminescence measurements to quantify the light trapping for a range of plasmonic structures. By combining Ag nanoparticles as a scattering structure and diffuse white paint as a back surface reflector (BSR) on silicon wafers, we can achieve absorption enhancement of 62% of the Lambertian value, which is comparable with literature values for inverted pyramids of 67%. Through measurements of the effective carrier lifetime, we also establish that plasmonic Ag particles do not degrade the electrical properties of the passivation layer.
Delayed-type hypersensitivity reaction to paraphenylenediamine is mediated by 2 different pathways of antigen recognition by specific alphabeta human T-cell clones.

BACKGROUND Allergic contact dermatitis to paraphenylenediamine (PPD) is a frequent cause of morbidity and occupational disability. OBJECTIVE The aim of the study was to characterize T-cell responses to PPD and Bandrowski's base (BB), an autoxidation product of PPD, by using polyclonal and monoclonal T-lymphocyte cultures. METHODS PPD- and BB-driven proliferation of PBMCs and T-cell clones (TCCs) was assessed by means of tritiated thymidine incorporation. Surface markers were studied by means of flow cytometry, and cytokine generation was assessed with an ELISA. RESULTS TCCs, with one exception, were CD4+/CD45RO+, and T-cell receptors were alphabeta+. Three of 6 TCCs expressed Vbeta 16. TCC stimulation was HLA-DP restricted, and TCCs secreted IL-4, IL-5, and marginal levels of IFN-gamma. TCCs reacted to both PPD and BB. Presentation of BB to TCCs was dependent on viable antigen-presenting cells (APCs) pulsed for 4 hours, and fixed APCs failed to stimulate TCCs. Moreover, polyclonal responses to BB were enhanced by metabolically active enzymes, such as cytochrome P450 enzymes. BB has to be metabolized and processed. In contrast, fixation of APCs did not impair their ability to present PPD to TCC, whereas pulsing of APCs with PPD failed to stimulate TCCs. Thus PPD had to be present during the process, and polyclonal stimulation was not enhanced by cytochromes. CONCLUSION These results suggest that PPD itself can be recognized by T cells through a processing-independent pathway, whereas its autoxidation product, BB, required processing and possibly metabolism to stimulate the same TCC. Our data demonstrate that 2 distinct pathways of antigen presentation to activate specific TCCs are involved in the immune response to PPD.
What’s the Problem with the Law?: Jews, Gentiles, and Covenant Identity in Galatians 3:10–12

Galatians 3:10–12 is a passage that continues to be the subject of significant debate among Pauline scholars. Traditionally, Protestant interpreters have understood a contrast here between the “works-righteousness” system of redemption inherent to Judaism over against Paul’s “law-free” gospel of Jesus Christ. Since the advent of the New Perspective on Paul, this reading has been increasingly challenged. However, in many such readings, the Torah is still largely viewed as incompatible with the new age of the gospel. In contrast, I will argue that Paul presupposes the continuing significance of the Torah in demarcating Jewish identity, and as a basis for covenant praxis. The function of this passage is strictly to dissuade gentile Christ-followers from undergoing proselyte conversion to Judaism, which, for Paul, is irreconcilable with “in Christ” identity, as the three biblical texts cited in this section (Deut 27:26; Hab 2:4; Lev 18:5) suggest.