Miracle-dz/UniFAR-FTUs huggingface dataset:
Outsourcing in the Persian Gulf petroleum supply chain

Purpose – The purpose of this study is to identify the challenges, the benefits, the risks and the motives of petroleum companies in the Persian Gulf toward outsourcing strategy. While the petroleum companies are faced with massive costs of operation that stem from the aging infrastructure, human capital deficit, inefficient fragmented business processes and lack of access to new technologies, outsourcing strategy toward cost savings and the overt and covert resistance of management and employees are significant barriers for creation of continuous process. Design/methodology/approach – Based on the review of existing literature, the industry ' s archives and in-depth personal interviews with senior executives of the national oil and gas companies in five Gulf countries and seven global outsourcing companies and 87 survey responses, this study develops a methodological framework which substantiates or refutes the hypotheses based on the objectives: industry challenges are the driving forces behind outsourc.
Interaction of Calcium with Native and Decarboxylated Human Factor X.

Human factor X is a two-chain, 58-kDa, vitamin K-dependent blood coagulation zymogen. The light chain of factor X consists of an NH2-terminal γ-carboxyglutamic acid (Gla) domain, followed by a few helical hydrophobic residues and the two epidermal growth factor-like domains, whereas the heavy chain contains the serine protease domain. In this study, native factor X was found to contain three classes of Ca2+-binding sites: two high affinity (K d 100 ± 30 μm), four intermediate affinity (K d 450 ± 70 μm), and five to six low affinity (K d 2 ± 0.2 mm). Decarboxylated factor X in which the Gla residues were converted to Glu retained the two high affinity sites (K d 140 ± 20 μm). In contrast, factor X lacking the Gla domain as well as a part of the helical hydrophobic residues (des-44-X) retained only one high affinity Ca2+-binding site (K d 130 ± 20 μm). Moreover, a synthetic peptide composed of residues 238–277 (58–97 in chymotrypsinogen numbering) from the protease domain of factor X bound one Ca2+ with high affinity (K d 150 ± 20 μm). From competitive inhibition assays for binding of active site-blocked factor Xa to factor Va in the prothrombinase complex, theK d for peptide-Va interaction was calculated to be ∼10 μm as compared with 30 pm for factor Xa and ∼1.5 μm for decarboxylated factor Xa. A peptide containing residues 238–262(58–82) bound Ca2+ with reduced affinity (K d ∼600 μm) and did not inhibit Xa:Va interaction. In contrast, a peptide containing residues 253–277(73–97) inhibited Xa:Va interaction (K d ∼10 μm) but did not bind Ca2+. In additional studies, Ca2+ increased the amidolytic activity of native and des-44-Xa toward a tetrapeptide substrate (benzoyl-Ile-Glu-Gly-Arg-p-nitroanilide) by approximately 1.6-fold. The half-maximal increase was observed at ∼150 μm Ca2+ and the effect was primarily on the k cat. Ca2+ also significantly protected cleavage at Arg-332-Gln-333(150–151) in the protease domain autolysis loop. Des-44-Xa in which the autolysis loop was cleaved possessed ≤5% of the amidolytic activity of the noncleaved form; however, the S1 binding site was not affected, as determined by the p-aminobenzamidine binding. Additionally, autolysis loop-cleaved, active site-blocked native factor Xa was calculated to have ∼10-fold reduced affinity for factor Va as compared with that of the noncleaved form.
Outcomes of antiretroviral treatment in programmes with and without routine viral load monitoring in southern Africa

Objectives:To compare outcomes of antiretroviral therapy (ART) in South Africa, where viral load monitoring is routine, with those in Malawi and Zambia, where monitoring is based on CD4 cell counts. Methods:We included 18 706 adult patients starting ART in South Africa and 80 937 patients in Zambia or Malawi. We examined CD4 responses in models for repeated measures and the probability of switching to second-line regimens, mortality and loss to follow-up in multistate models, measuring time from 6 months. Results:In South Africa, 9.8% [95% confidence interval (CI) 9.1–10.5] had switched at 3 years, 1.3% (95% CI 0.9–1.6) remained on failing first-line regimens, 9.2% (95% CI 8.5–9.8) were lost to follow-up and 4.3% (95% CI 3.9–4.8) had died. In Malawi and Zambia, more patients were on a failing first-line regimen [3.7% (95% CI 3.6–3.9], fewer patients had switched [2.1% (95% CI 2.0–2.3)] and more patients were lost to follow-up [15.3% (95% CI 15.0–15.6)] or had died [6.3% (95% CI 6.0–6.5)]. Median CD4 cell counts were lower in South Africa at the start of ART (93 vs. 132 cells/&mgr;l; P < 0.001) but higher after 3 years (425 vs. 383 cells/&mgr;l; P < 0.001). The hazard ratio comparing South Africa with Malawi and Zambia after adjusting for age, sex, first-line regimen and CD4 cell count was 0.58 (0.50–0.66) for death and 0.53 (0.48–0.58) for loss to follow-up. Conclusion:Over 3 years of ART mortality was lower in South Africa than in Malawi or Zambia. The more favourable outcome in South Africa might be explained by viral load monitoring leading to earlier detection of treatment failure, adherence counselling and timelier switching to second-line ART.
Enlighten real-time radiosity

Using Geomerics Enlighten technology, this demo shows how dynamic real-time lighting enhances game play and visual quality in computer games. Enlighten is a cross-platform, real-time radiosity solution that can generate bounce lighting for a game level in a fraction of a frame. By combining Enlighten real-time radiosity with a fully dynamic lighting environment in Unreal Engine 3, the demo shows how lighting can add an extra dimension to the traditional first-person shooter. The demo shows the death-match level on a CUDA research platform, which provides an insight into lighting in the next generation of top-tier games. The death-match level contains 100 fighting "bots", each with a flashlight, sentry rocket turrets, and vehicles with headlights. All lights are shadow casting, and they bounce radiosity lighting. Weapon fire and explosions contribute most of the lighting to the scene. Action-filled shoot-outs light up the screen, with the radiosity lighting providing most of the fill lighting. The player can control the lighting in the immediate environment through weapon fire and see the lighting from distant fights as it illuminates the level. Dynamic changes in the time of day change the mood and atmosphere in the game, and the demo compares the appearance of the game with and without radiosity lighting.
Mesenchymal Stem Cells for Treatment of Therapy-Resistant Graft-versus-Host Disease

Background. Mesenchymal stem cells (MSC) have immunomodulatory effects. The aim was to study the effect of MSC infusion on graft-versus-host disease (GVHD). Methods. We gave MSC to eight patients with steroid-refractory grades III-IV GVHD and one who had extensive chronic GVHD. The MSC dose was median 1.0 (range 0.7 to 9)×106/kg. No acute side-effects occurred after the MSC infusions. Six patients were treated once and three patients twice. Two patients received MSC from HLA-identical siblings, six from haplo-identical family donors and four from unrelated mismatched donors. Results. Acute GVHD disappeared completely in six of eight patients. One of these developed cytomegalovirus gastroenteritis. Complete resolution was seen in gut (6), liver (1) and skin (1). Two died soon after MSC treatment with no obvious response. One of them had MSC donor DNA in the colon and a lymph node. Five patients are still alive between 2 months and 3 years after the transplantation. Their survival rate was significantly better than that of 16 patients with steroid-resistant biopsy-proven gastrointestinal GVHD, not treated with MSC during the same period (P=0.03). One patient treated for extensive chronic GVHD showed a transient response in the liver, but not in the skin and he died of Epstein-Barr virus lymphoma. Conclusion. MSC is a very promising treatment for severe steroid-resistant acute GVHD.
Nitric-oxide Synthase 2 Interacts with CD74 and Inhibits Its Cleavage by Caspase during Dendritic Cell Development*

Dendritic cells (DC) are professional antigen-presenting cells that possess specific and efficient mechanisms to initiate immune responses. Upon encounter with pathogens, immature DC will go through a maturation process that converts them to highly immunogenic mature DC. Despite the fact that nitric oxide (NO) was produced in large amounts in maturing DC, it is still unclear whether NO is the key molecule that initiates and enhances DC maturation and T cell proliferation, respectively. Here, we report that NO donor and overexpression of either nitric-oxide synthase 2 (NOS2) or nitric-oxide synthase 3 (NOS3) alone can induce surface expression of major histocompatibility complex class II (MHC II) and both the essential co-stimulatory molecules CD80 and CD86 in immature DC. Consistently, NO donor-treated immature DC were capable of enhancing T cell proliferation in vitro in the absence of lipolysaccharide. Interestingly, NOS2 interacts with CD74 (the MHC II-associated invariant chain), and the degradation of CD74 by caspases in immature DC was inhibited upon treatment with NO donor. Because the trafficking of MHC II is CD74-dependent, the increase in cell surface localization of MHC II in maturing DC is in part due to the increase in CD74 protein expression in the presence of NOS2 and NO.
Traumatic Brain Injury Pathophysiology and Treatments: Early, Intermediate, and Late Phases Post-Injury

Traumatic Brain Injury (TBI) affects a large proportion and extensive array of individuals in the population. While precise pathological mechanisms are lacking, the growing base of knowledge concerning TBI has put increased emphasis on its understanding and treatment. Most treatments of TBI are aimed at ameliorating secondary insults arising from the injury; these insults can be characterized with respect to time post-injury, including early, intermediate, and late pathological changes. Early pathological responses are due to energy depletion and cell death secondary to excitotoxicity, the intermediate phase is characterized by neuroinflammation and the late stage by increased susceptibility to seizures and epilepsy. Current treatments of TBI have been tailored to these distinct pathological stages with some overlap. Many prophylactic, pharmacologic, and surgical treatments are used post-TBI to halt the progression of these pathologic reactions. In the present review, we discuss the mechanisms of the pathological hallmarks of TBI and both current and novel treatments which target the respective pathways.
The rpoE gene of Escherichia coli, which encodes sigma E, is essential for bacterial growth at high temperature

In vitro transcription analysis has shown that only RNA polymerase containing an alternative sigma subunit, sigma E, activates transcription from one of the rpoH promoters and the htrA promoter. The location of the rpoE gene encoding sigma E on the Escherichia coli chromosome has recently been established, but no rpoE mutant has yet become available for phenotypic testing. We cloned the rpoE gene from the lambda-ordered clones of the E. coli genome and confirmed that the reconstituted RNA polymerase containing the gene product (E sigma E) can transcribe htrA in vitro. We constructed an rpoE-defective strain by gene disruption using the cloned rpoE gene. We demonstrate that expression of htrA is completely dependent on the rpoE gene in vivo and that the rpoE gene is essential for bacterial growth at high temperature.
Neocortical neural sprouting, synaptogenesis, and behavioral recovery after neocortical infarction in rats.

BACKGROUND AND PURPOSE Neuroanatomical plasticity is well described in lesions of the hippocampus but remains a subject of some controversy in the neocortex. The purpose of the present study was to measure the neocortical distribution and density of expression of proteins known to be involved in neurite growth or synaptogenesis and to correlate the neocortical expression with behavioral recovery after a focal neocortical infarction. Focal neocortical infarction creates a circumscribed lesion in the neocortex that provides a denervation stimulus for neurite growth and synaptogenesis. METHODS Unilateral neocortical ischemia was induced in male spontaneously hypertensive Wistar rats (n = 4 per time point) by permanent occlusion of the distal middle cerebral artery and ipsilateral common carotid artery. To determine the spatial and temporal distribution of neurite growth and/or synaptogenesis, GAP-43, a growth-associated protein expressed on axonal growth cones, and synaptophysin, a calcium-binding protein found on synaptic vesicles, were examined by immunohistochemical techniques. The reaction product was measured, and the distribution was recorded. Since the resulting infarction included a portion of the forelimb neocortex, behavioral assessments of forelimb function that used the foot-fault test of Hernandez and Schallert were performed on the same rats used for immunohistochemical studies. Recovery times were 3, 7, 14, 30, and 60 days after surgery. RESULTS Both GAP-43 and synaptophysin proteins demonstrated statistically significant increases in the density of immunoreaction product as determined by optical density measurements in the neocortex of infarcted rats compared with sham controls. The GAP-43 was elevated to statistically significant levels in forelimb, hindlimb, and parietal neocortical regions medial and lateral to the infarction only at days 3, 7, and 14. In contrast, synaptophysin demonstrated no statistically significant changes in expression at 3 or 7 days but demonstrated statistically significant increases at 14, 30, and 60 days in the forelimb, hindlimb, and parietal neocortical regions medial and lateral to the infarction as well as in the contralateral parietal neocortex. Behavioral assessment of forelimb function indicated impairment of forelimb placement on the side contralateral to the infarction that trended toward control values at 14 days and was not significantly different from controls by 30 days. CONCLUSIONS These data support the occurrence of neurite growth followed by synaptogenesis in the neocortex, ipsilateral and contralateral to neocortical ischemia, in a pattern that corresponds both spatially and temporally with behavioral recovery. Thus, neuroanatomical remodeling in the neocortex provides a mechanism for recovery of function.
How not to develop a quantitative structure–activity or structure–property relationship (QSAR/QSPR)

Although thousands of quantitative structure–activity and structure–property relationships (QSARs/QSPRs) have been published, as well as numerous papers on the correct procedures for QSAR/QSPR analysis, many analyses are still carried out incorrectly, or in a less than satisfactory manner. We have identified 21 types of error that continue to be perpetrated in the QSAR/QSPR literature, and each of these is discussed, with examples (including some of our own). Where appropriate, we make recommendations for avoiding errors and for improving and enhancing QSAR/QSPR analyses.
[Pathological observation and immunohistochemistry study of Type I, III, IV collagen in mitral valve and cardiac interstitium of rheumatic disease].

OBJECTIVES To examine the pathological base of mitral valve and cardiac interstitium of rheumatic disease, and to explore the relationship between Type I, and III, IV collagen in mitral and cardiac interstitium of rheumatic heart disease. METHODS HE and ABC method special staining were used to observe the mitral valve and cardiac interstitium pathology in 26 case. RESULTS Diffused collagen fibroplasia, hyaline and amyloid degeneration were noted and sometimes associated local necrosis and calcification in myocardial interstitium and in mitral valve. It was a significant pathologic characteristic of rheumatic heart disease. The localization of Type I, III and IV collagen in the valve and myocardiac tissues was studied by ABC method of immunohistochemistry. Significant fibroplasia of collagen Type I and III was found in the valve, cordae tendon and myocardial interstitium of rheumatic heart disease. The composition and secretion of collagen Type I and III were expressed not only in fibroblasts but also in myocardial cells. CONCLUSIONS The pathologic foundation of valve and myocardial fibrosis is collagen fibroplasia. The degree of fibroplasia is related to the repeated reaction of chronic rheumatic inflammation.
Effect of the phenolic compounds apigenin and carnosic acid on oral carcinogenesis in hamster induced by DMBA.

OBJECTIVE To investigate oral carcinogenesis in hamster induced by the topical application of 7,12-dimethyl benzanthracene (DMBA) to evaluate the different lesions produced and the possible preventive effects of the phenolic compounds apigenin (flavone) and carnosic acid (diterpene). MATERIALS AND METHODS Thirty-two Syrian hamsters were divided into three groups: I: 0.5% DMBA (n = 12); II: 0.5% DMBA + potassium apigenin (n = 8); III: 0.5% DMBA + carnosic acid (n = 12). All the animals were sacrificed after 11 weeks, and a macroscopic and light microscopic study was made of the lesions. RESULTS The largest number of neoplasms, showing the most aggressive biological behavior, corresponded to the control group. The group treated with potassium apigenin ranked second in tumor incidence, although the tumors were not very aggressive behavior. In the group treated with carnosic acid, only one malignancy was recorded, showing the smallest volume of all the recorded tumor lesions. CONCLUSIONS Our findings indicate that both potassium apigenin and carnosic acid have chemoprotective effects against carcinogenesis induced by DMBA in hamster.
Molecular basis of the diversity of calcium channels in cardiovascular tissues.

Voltage-dependent calcium (Ca2+) channels control a variety of physiological functions, such as excitation-contraction coupling in cardiac and smooth muscle. secretion of hormones and release of neurotransmitters. Studies on dissociated or cultured cells enabled us to compare their electrophysiological and pharmacological properties and their regulation in various tissues. Molecular genetics has provided a structural basis with which to observe the functional diversity of Ca2+ channels, which are composed of several subunits (alpha 1, alpha 2-delta, beta, gamma). Structure-function experiments, using expression in Xenopus oocytes, were designed to explain the molecular basis underlying this functional diversity. Six genes have been identified encoding the pore subunit (alpha 1) which determines the basic profile, i.e. the pharmacology of any Ca2+ channel. However, using a reconstitution model, the auxiliary subunits, but mainly beta subunits, for which four genes and several variants have been isolated, are able to modify the level of expression and the properties of a Ca2+ current directed by an alpha 1 subunit. Our structure-function studies are mainly designed to investigate the functional consequences of alpha 1-beta interaction on electrophysiological and pharmacological properties, especially in the case of cardiovascular Ca2+ channels. These studies should lead to a better understanding of the molecular basis underlying the differences between cardiac and vascular Ca2+ channels and also their implication in pathophysiology. Functional expression of the various combinations of subunit isoforms and identification of the precise oligomeric structure of voltage-dependent Ca2+ channels in specific cell types should help in the development of new therapeutic drugs.
Acrolein Is a Product of Lipid Peroxidation Reaction

Lipoprotein peroxidation, especially the modification of apolipoprotein B-100, has been implicated to play an important role in the pathogenesis of atherosclerosis. However, there have been few detailed insights into the chemical mechanism of derivatization of apolipoproteins during oxidation. In the present study, we provide evidence that the formation of the toxic pollutant acrolein (CH2=CH–CHO) and its conjugate with lysine residues is involved in the oxidative modification of human low density lipoprotein (LDL). Upon incubation with LDL, acrolein preferentially reacted with lysine residues. To determine the structure of acrolein-lysine adduct in protein, the reaction of acrolein with a lysine derivative was carried out. EmployingN α-acetyllysine, we detected a single product, which was identified to be a novel acrolein-lysine adduct,N α-acetyl-N ε-(3-formyl-3,4-dehydropiperidino)lysine. The acid hydrolysis of the adduct led to the derivative that was detectable with amino acid analysis. It was revealed that, uponin vitro incubation of LDL with acrolein, the lysine residues that had disappeared were partially recovered byN ε-(3-formyl-3,4-dehydropiperidino)lysine. In addition, we found that the same derivative was detected in the oxidatively modified LDL with Cu2+ and that the adduct formation was correlated with LDL peroxidation assessed by the consumption of α-tocopherol and cholesteryl ester and the concomitant formation of cholesteryl ester hydroperoxide. Enzyme-linked immunosorbent assay that measures free acrolein revealed that a considerable amount of acrolein was released from the Cu2+-oxidized LDL. Furthermore, metal-catalyzed oxidation of arachidonate was associated with the formation of acrolein, indicating that polyunsaturated fatty acids including arachidonate represent potential sources of acrolein generated during the peroxidation of LDL. These results indicate that acrolein is not just a pollutant but also a lipid peroxidation product that could be ubiquitously generated in biological systems.
Reproducibility of histomorphologic diagnoses with special reference to the kappa statistic

Systems for classification and grading used in pathology should ideally be biologically meaningful and at least be reproducible from one pathologist to another. A statistical method to evaluate reproducibility (non‐chance agreement) for several observers using nominal or ordinal categories has been developed and refined over the past few decades ‐ the kappa statistic. A high level of observed agreement among different pathologists can either signify a high level of reproducibility, if agreement by chance is low, or express a low level of reproducibility, if agreement by chance is almost as high as the observed agreement. Therefore, the observed agreement says nothing in itself, unless it is low. The kappa value, however, indicates how much better the observers are compared to a throw of the dice, and therefore gives the real credit to the agreement which was found. We have developed a user‐friendly computer program for calculating inter‐ and intra‐observer agreement of 2 or more observers. By calculating associations between different categories and different observers, the statistic furthermore obtains a function close to the parameter of accuracy. We recommend the use of the above method before a set of nominal or rank scale parameters are used for deciding prognosis and treatment of patients. By submitting a diskette the computer program will be available at no cost.