Miracle-dz/UniFAR-FTUs huggingface dataset:
Adaptive and Random Partition Software Testing

Random testing (RT) and subdomain testing are two major software testing strategies. Their simplicity makes them likely the most efficient testing strategies with respect to the time required for test case selection. However, the disadvantage of RT is its defect detection effectiveness. Adaptive testing (AT) is a feedback-based software testing strategy that has been shown to be more effective than RT and partition testing (PT). However, a major concern in the application of AT is its complexity and computational cost for test case selection. In this paper, we propose a hybrid approach that uses AT and random partition testing (RPT) in an alternating manner. The motivation for this approach is that both strategies are employed such that the underlying computational complexity of AT is reduced by introducing RPT into the testing process without affecting the defect detection effectiveness. A case study with seven real-life subject programs is presented. The experimental results demonstrate that this novel strategy considerably reduces the computational overhead of the original AT strategy but still outperforms the pure RT strategy and PT strategy in terms of the number of test cases used to detect and remove a given number of defects. In addition, a sensitivity analysis is conducted to validate the robustness of our strategy.
Nuclear Microscopy: A Novel Technique for Quantitative Imaging of Gadolinium Distribution within Tissue Sections

Abstract All clinically-approved and many novel gadolinium (Gd)-based contrast agents used to enhance signal intensity in magnetic resonance imaging (MRI) are optically silent. To verify MRI results, a “gold standard” that can map and quantify Gd down to the parts per million (ppm) levels is required. Nuclear microscopy is a relatively new technique that has this capability and is composed of a combination of three ion beam techniques: scanning transmission ion microscopy, Rutherford backscattering spectrometry, and particle induced X-ray emission used in conjunction with a high energy proton microprobe. In this proof-of-concept study, we show that in diseased aortic vessel walls obtained at 2 and 4 h after intravenous injection of the myeloperoxidase-senstitive MRI agent, bis-5-hydroxytryptamide-diethylenetriamine-pentaacetate gadolinium, there was a time-dependant Gd clearance (2 h = 18.86 ppm, 4 h = 8.65 ppm). As expected, the control animal, injected with the clinically-approved conventional agent diethylenetriamine-pentaacetate gadolinium and sacrificed 1 week after injection, revealed no significant residual Gd in the tissue. Similar to known in vivo Gd pharmacokinetics, we found that Gd concentration dropped by a factor of 2 in vessel wall tissue in 1.64 h. Further high-resolution studies revealed that Gd was relatively uniformly distributed, consistent with random agent diffusion. We conclude that nuclear microscopy is potentially very useful for validation studies involving Gd-based magnetic resonance contrast agents.
Price reversal as potential expiration day effect of stock and index futures: evidence from Warsaw Stock Exchange

This paper studies an impact of futures expiration days on the Polish equity market. From three potential expiration effects appearing in the literature (namely, the increased trading volume of underlying assets, increased volatility of their returns, and price reversal after expiration), the latest one is researched in detail for expiration days of futures on the WIG20 index, the mWIG40 index, and individual stocks. The data covers the period from January 2001 to December 2016. The phenomenon of price reversal is studied with the use of regression models, price reversal measures, and event study methodology. The results obtained for expiration days are compared with the results from non-expiration days to check whether potential price reversal can be interpreted as an effect of expiration. No price reversals after futures expirations were found in the returns of the WIG20 nor mWIG40 indexes. In the case of individual stocks, results from all of the three methods support the assumption that price reversal occurs after expiration. The reversal is immediate and is reflected in overnight returns more than in daily returns.
Leptin derived from adipocytes in injured peripheral nerves facilitates development of neuropathic pain via macrophage stimulation

Nerve injury may result in neuropathic pain, characterized by allodynia and hyperalgesia. Accumulating evidence suggests the existence of a molecular substrate for neuropathic pain produced by neurons, glia, and immune cells. Here, we show that leptin, an adipokine exclusively produced by adipocytes, is critical for the development of tactile allodynia through macrophage activation in mice with partial sciatic nerve ligation (PSL). PSL increased leptin expression in adipocytes distributed at the epineurium of the injured sciatic nerve (SCN). Leptin-deficient animals, ob/ob mice, showed an absence of PSL-induced tactile allodynia, which was reversed by the administration of leptin to the injured SCN. Perineural injection of a neutralizing antibody against leptin reproduced this attenuation. Macrophages recruited to the perineurium of the SCN expressed the leptin receptor and phosphorylated signal transducer and activator of transcription 3 (pSTAT3), a transcription factor downstream of leptin. PSL also up-regulated the accepted mediators of neuropathic pain—namely, cyclooxygenase-2, inducible nitric oxide synthase, and matrix metalloprotease-9—in the injured SCN, with transcriptional activation of their gene promoters by pSTAT3. This up-regulation was partly reproduced in a macrophage cell line treated with leptin. Administration of peritoneal macrophages treated with leptin to the injured SCN reversed the failure of ob/ob mice to develop PSL-induced tactile allodynia. We suggest that leptin induces recruited macrophages to produce pronociceptive mediators for the development of tactile allodynia. This report shows that adipocytes associated with primary afferent neurons may be involved in the development of neuropathic pain through adipokine secretion.
Urinary Excretion of Transferrin and Orosomucoid Are Increased after Acute Protein Loading in Healthy Subjects

Background/Aims: The aim of this study was to elucidate what kind of plasma proteins would change their urinary excretions when the glomerular filtration rate (GFR) was increased. Methods: We measured urinary excretions of three plasma proteins with different molecular radii (MR) and isoelectric points (pI): albumin, orosomucoid (OM) and transferrin (Tf), after acute protein loading in healthy subjects. Results: Urinary excretion of OM with more anioic charge and smaller MR than albumin, and Tf with more cationic charge and slightly larger molecular weight than albumin, significantly increased in parallel with increased creatinine clearances after acute protein loading. These renal responses returned to basal levels 9 h after protein ingestion. In contrast, increases in urinary excretion of albumin were not observed. Conclusion: Because these findings could not be explained by changes in either size or charge selectivity of shunt pores in the glomerular capillary wall, it is suggested that urinary excretion of albumin may have a special property that distinguishes it from other plasma proteins and may be a less sensitive marker to reflect changes in renal hemodynamics than the other plasma proteins.
Regulation of cell adhesion by PAI‐1

Type I plasminogen activator inhibitor (PAI‐1) is the primary inhibitor of tissue‐and urokinase‐type plasminogen activators. It circulates in plasma complexed with vitronectin (VN), the primary PAI‐1 binding protein. The somatomedin B (SMB) domain of VN contains both the high affinity PAI‐1 binding site and the specific site for urokinase plasminogen activator receptor (uPAR). PAI‐1 is able to regulate uPAR‐mediated cell adhesion by competing with uPAR for VN binding. Binding of PAI‐1 to SMD may also affect integrin‐mediated cell adhesion to VN by hindering integrin binding to the RGD sequence adjacent to the uPAR binding site.
Transcriptional Regulation of Tristetraprolin by Transforming Growth Factor-β in Human T Cells*

Transforming growth factor-β (TGF-β) is a pleiotropic cytokine that plays a critical role in modulating immune response and inflammation. We employed the Affymetrix cDNA microarray system to detect genes whose expression is regulated by TGF-β1 in a human T cell line HuT78. Tristetraprolin (TTP), a protein involved in the degradation of tumor necrosis factor-α (TNF-α) mRNA, was found to be up-regulated by TGF-β. This up-regulation was confirmed by reverse transcriptase-PCR analysis that revealed a rapid and transient induction of TTP mRNA by TGF-β1 in HuT78 cells, primary human T cells, and THP-1 macrophage-monocyte cells. In addition, de novo protein synthesis was not required for this induction, suggesting that TTP is regulated by TGF-β at the transcriptional level. To delineate the transcriptional regulation of the TTP gene, a 2.7-kb human TTP promoter region (–2682 to +56 bp relative to the transcription initiation site) was isolated. We found that this promoter was stimulated by TGF-β1 or a constitutively active TGF-β type I receptor via TGF-β-specific Smad proteins. Furthermore, a series of TTP promoter deletion constructs were used to localize the Smad-responsive region to the –583 to –263 bp portion of the promoter. In this region, the TTP promoter contained a stretch of putative Smad-binding elements that had a synergistic effect in mediating Smad activation of the promoter. These putative Smad-binding element-containing sequences were also able to bind Smad3 and Smad4 proteins purified in vitro. As TGF-β- and TTP-deficient mice exhibit overlapping phenotypes manifested by multifocal inflammation and autoimmunity, our findings that TTP transcription is under the control of TGF-β signaling would indicate a potential role of TTP in mediating the immune suppressive action of TGF-β in vivo.
Intravascular Device Infections: Epidemiology, Diagnosis, and Management

Intravascular devices such as pacemakers, implantable cardioverter-defibrillators (ICDs), left ventricular assist devices (LVADs), and prosthetic vascular grafts are life-saving therapies for patients with malignant arrhythmias, heart failure, and various vascular diseases. As indications for their use have increased, so has the prevalence of infectious complications associated with these devices. We present a review of the clinical literature on the epidemiology, diagnosis, and management of infectious complications of these intravascular devices. Most intravascular device infections are thought to result from skin flora contamination during implantation. Infection of the subcutaneous portion of the device can subsequently track to deeper intravascular tissues. Infection that involves the intravascular or intracardiac portion of these devices carries a high morbidity and mortality. Despite appropriate antibiotic therapy, cure of infection is frequently possible only with device removal. Well-designed placebo-controlled, randomized studies evaluating antimicrobial therapy for treatment of intravascular device infections are lacking. In the absence of better information, authorities recommend antibiotics targeted toward cultured organisms for approximately 4 to 6 weeks and device removal.
Multiple histidine kinases regulate entry into stationary phase and sporulation in Bacillus subtilis

Protein homology studies identified five kinases potentially capable of phosphorylating the Spo0F response regulator and initiating sporulation in Bacillus subtilis. Two of these kinases, KinA and KinB, were known from previous studies to be responsible for sporulation in laboratory media. In vivo studies of the activity of four of the kinases, KinA, KinC, KinD (ykvD) and KinE (ykrQ), using abrB transcription as an indicator of Spo0A∼P level, revealed that KinC and KinD were responsible for Spo0A∼P production during the exponential phase of growth in the absence of KinA and KinB. In vitro, all four kinases dephosphorylated Spo0F∼P with the production of ATP at approximately the same rate, indicating that they possess approximately equal affinity for Spo0F. All the kinases were expressed during growth and early stationary phase, suggesting that the differential activity observed in growth and sporulation results from differential activation by signal ligands unique to each kinase.
Vitamin D Deficiency-induced Hypertension Is Associated With Vascular Oxidative Stress and Altered Heart Gene Expression

Vitamin D deficiency (VDD) is associated with an increased cardiovascular risk. We investigated the effect of VDD on the cardiovascular system of growing male rats fed with a vitamin D-deficient diet. Using isolated rat aorta, we assessed both superoxide anion and endothelial-dependent relaxations. Microarray technology was used to identify changes induced by VDD in cardiac gene expression. Compared with control, VDD increased systolic blood pressure (P < 0.05) and superoxide anion production in the aortic wall (P < 0.05) and tended to increase serum levels of angiotensin II and atrial natriuretic peptide (P < 0.15). However, VDD slightly improved maximal relaxation to acetylcholine from 75 % ± 3% to 83% ± 2% (P < 0.05). Incubation of aortic rings either with nitro-l-arginine methyl ester (l-NAME) or catalase did not eliminate the enhancement of endothelial-mediated relaxation observed in vitamin D-deficient rats. Only incubation with indometacin or calcium-activated potassium channels blockers suppressed this difference. Compared with control, the expression of 51 genes showed different expression, including several genes involved in the regulation of oxidative stress and myocardial hypertrophy. In conclusion, VDD in early life increases arterial blood pressure, promotes vascular oxidative stress, and induces changes in cardiac gene expression. However, the endothelial-mediated regulation of vasomotor tone is maintained throughout the enhancement of an NO-independent compensatory pathway.
Improving GRN re‐construction by mining hidden regulatory signals

Inferring gene regulatory networks (GRNs) from gene expression data is an important but challenging issue in systems biology. Here, the authors propose a dictionary learning‐based approach that aims to infer GRNs by globally mining regulatory signals, known or latent. Gene expression is often regulated by various regulatory factors, some of which are observed and some of which are latent. The authors assume that all regulators are unknown for a target gene and the expression of the target gene can be mapped into a regulatory space spanned by all the regulators. Specifically, the authors modify the dictionary learning model, k ‐SVD, according to the sparse property of GRNs for mining the regulatory signals. The recovered regulatory signals are then used as a pool of regulatory factors to calculate a confidence score for a given transcription factor regulating a target gene. The capability of recovering hidden regulatory signals was verified on simulated data. Comparative experiments for GRN inference between the proposed algorithm (OURM) and some state‐of‐the‐art algorithms, e.g. GENIE3 and ARACNE, on real‐world data sets show the superior performance of OURM in inferring GRNs: higher area under the receiver operating characteristic curves and area under the precision–recall curves.
Nanoporous bimetallic Pt-Au alloy nanocomposites with superior catalytic activity towards electro-oxidation of methanol and formic acid.

We present a facile route to fabricate novel nanoporous bimetallic Pt-Au alloy nanocomposites by dealloying a rapidly solidified Al(75)Pt(15)Au(10) precursor under free corrosion conditions. The microstructure of the precursor and the as-dealloyed sample was characterized using X-ray diffraction, scanning electron microscopy, transmission electron microscopy, high-resolution transmission electron microscopy, and energy dispersive X-ray (EDX) analysis. The Al(75)Pt(15)Au(10) precursor is composed of a single-phase Al(2)(Au,Pt) intermetallic compound, and can be fully dealloyed in a 20 wt. % NaOH or 5 wt. % HCl aqueous solution. The dealloying leads to the formation of the nanoporous Pt(60)Au(40) nanocomposites (np-Pt(60)Au(40) NCs) with an fcc structure. The morphology, size and crystal orientation of grains in the precursor can be conserved in the resultant nanoporous alloy. The np-Pt(60)Au(40) NCs consist of two zones with distinct ligament/channel sizes and compositions. The formation mechanism of these np-Pt(60)Au(40) NCs can be rationalized based upon surface diffusion of more noble elements and spinodal decomposition during dealloying. Electrochemical measurements demonstrate that the np-Pt(60)Au(40) NCs show superior catalytic activity towards the electro-oxidation of methanol and formic acid in the acid media compared to the commercial JM-Pt/C catalyst. This material can find potential applications in catalysis related areas, such as direct methanol or formic acid fuel cells. Our findings demonstrate that dealloying is an effective and simple strategy to realize the alloying of immiscible systems under mild conditions, and to fabricate novel nanostructures with superior performance.
In vivo Evaluation of Single Dose Tetanus Toxoid Vaccine Formulation with Chitosan Microspheres

Chitosan adsorbed microspheres containing tetanus toxoid were prepared in the size range of 10 μm to 75 μm, by emulsion-cross linking technique at different speeds of agitation. The amount of tetanus toxoid incorporated into chitosan microspheres were estimated by limes flocculation test and in vivo evaluation of tetanus toxoid adsorbed chitosan microspheres were determined by toxin neutralization method using albino mice. The results of in vivo release for the batches of 10 μm and 25 μm correlates with the results of in vitro in which both the batches passes the limit of IP standard (4 Lf) where as, for the batches of 50 μm and 75 μm, the in vitro release of tetanus toxoid was 2 Lf. But our in vivo studies for the batches of 50 μm and 75 μm fail to pass the limit stated in IP. The release of tetanus toxoid from the chitosan microspheres was found to be sustained for the period of 6 months.
Impact of the Brazilian Accounting Pronouncements Committee’s New Guideline (OCPC 07) on the downsizing of companies’ Notes

ABSTRACT This article aims to assess the impact of the New Guideline of the Brazilian Accounting Pronouncements Committee (Comitê de Pronunciamentos Contábeis - OCPC 07) on improving formal features (size, readability, and specificity) of Brazilian companies’ Notes. OCPC 07 is one of the world’s first guidelines issued in response to the current demand for the downsizing of companies’ Notes, which according to standard setters and market agents have become too extensive, thus characterizing a disclosure overload. This is a unique study on the subject. The results suggest the effectiveness, although limited, of the new standard in promoting a departure from the habits of secrecy and formalism rooted in centuries of legal-accounting civil law tradition, and indicate that there is still room for complementary improvement initiatives in the form of incentives for firms and increased enforcement. Three complementary methodological approaches are used: (1) an analysis of both the evolution of note size after OCPC 07 and the factors explaining that size and its variation; (2) an examination of indicators of readability, conciseness, and specificity of the note on accounting policies; and (3) a size comparison of the Notes of Brazilian and British companies, a benchmark of the common law tradition. An average reduction of 10% in Note size was found two years after the introduction of Guideline (Orientação) 07 by the (OCPC 07). This downsizing was not generalized, but instead identified only among firms in the Novo Mercado and among those audited by two of the Big Four. Even in firms that reduced their notes by at least 20%, no significant improvements in readability levels could be perceived, nor in habits of copy-pasting the auditors’ templates, which could signal a focus on firms’ real practices in the note on accounting policies. Brazilian Notes remain far from the benchmark and are still 40% longer than British ones, despite an equivalent number of pages being expected.
Measurement and characterization of micronuclei in cultured primary lung cells of mice following inhalation exposure to benzene.

The genotoxic effects of benzene in lung cells of mice exposed to single acute doses by inhalation have been estimated by cytogenetic analysis of micronuclei in primary cultures of lung fibroblasts. Mice were nose-only exposed to 1000 p.p.m. for 30 or 60 min or to 3500 p.p.m. for 30 min and sacrificed 24 h after the end of exposure. Lung fibroblasts were cultured attached to coverslips for 72 h, the last 48 h in the presence of 0.75 microgram/ml cytochalasin B. Micronuclei were scored in binucleate cells. The mechanism(s) of micronucleus induction was characterized by immunofluorescent staining of kinetochore proteins (CREST staining), which allowed micronuclei due to chromosome loss (kinetochore-positive) to be distinguished from those produced by chromosome breakage (kinetochore-negative). Three- and 4-fold statistically significant increases in total micronucleus frequencies were observed in all benzene-exposed mice with respect to unexposed controls. The effect was neither concentration nor time dependent. This is compatible with a plateau dose-effect relationship for the effects on bone marrow, which is explained by saturation of metabolism. Both chromosome loss and chromosome breakage appear to contribute to micronucleus formation, suggesting that in addition to chromosome rearrangements, aneuploidy may be a relevant early genotoxic event associated with benzene carcinogenicity. Under the same treatment conditions no micronucleus induction could be shown in spleen lymphocytes, suggesting that with very short benzene exposures cells at the first contact site with local metabolizing capacity have a higher probability of genetic alterations potentially leading to neoplasia.
Lack of Cardiotoxicity with Liposomal Doxorubicin in an Elderly Case of Ovarian Cancer

Ovarian cancer is typically a disease of elderly women, usually occurring after menopause with a peak incidence in the eighth decade of life. Elderly patients are more likely to suffer the adverse effects of chemotherapy, which may influence successive lines of treatment. We describe the case of an elderly woman with platinum-sensitive ovarian cancer treated with several lines of chemotherapy who developed acute cardiogenic pulmonary edema with her first line of therapy, which included paclitaxel, and her fourth line containing gemcitabine. However, a complete regimen of pegylated liposomal doxorubicin in association with oxaliplatin was well tolerated. Other authors have reported absence of cardiotoxicity with liposomal doxorubicin in their study populations, but no mention was made of patients with a known prior susceptibility to transient heart failure when treated with other chemotherapeutic agents. Our case provides evidence that even in these more difficult-to-treat cases, where cumulative cardiotoxicity may be relatively unpredictable, liposomal doxorubicin does not affect cardiac function.