gebhart/patrepeval huggingface dataset:
Finding and preventing run-time error handling mistakes (2004)

It is difficult to write programs that behave correctly in the presence of run-time errors. Existing programming language features often provide poor support for executing clean-up code and for restoring invariants in such exceptional situations. We present a dataflow analysis for finding a certain class of error-handling mistakes: those that arise from a failure to release resources or to clean up properly along all paths. Many real-world programs violate such resource safety policies because of incorrect error handling. Our flow-sensitive analysis keeps track of outstanding obligations along program paths and does a precise modeling of control flow in the presence of exceptions. Using it, we have found over 800 error handling mistakes almost 4 million lines of Java code. The analysis is unsound and produces false positives, but a few simple filtering rules suffice to remove them in practice. The remaining mistakes were manually verified. These mistakes cause sockets, files and database handles to be leaked along some paths. We present a characterization of the most common causes of those errors and discuss the limitations of exception handling, finalizers and destructors in addressing them. Based on those errors, we propose a programming language feature that keeps track of obligations at run time and ensures that they are discharged. Finally, we present case studies to demonstrate that this feature is natural, efficient, and can improve reliability; for example, retrofitting a 34kLOC program with it resulted in a 0.5% code size decrease, a surprising 17% speed increase (from correctly deallocating resources in the presence of exceptions), and more consistent behavior.
Killing of Trypanosomatid Parasites by a Modified Bovine Host Defense Peptide, BMAP-18 (2009)

BMAP-18, a truncated form of the potent antimicrobial BMAP-27, showed low toxicity to mammalian cells, insect cells and the tsetse bacterial symbiont Sodalis glossinidius while retaining an ability to kill a variety of species and life cycle stages of pathogenic kinetoplastid parasites in vitro. BMAP-18 also inhibited secretion of TNF-alpha, an inflammatory cytokine that plays a role in the cachexia associated with African sleeping sickness. These findings support the idea that BMAP-18 should be explored as a candidate for therapy of economically important trypanosome-infected hosts, such as cattle, fish and humans, and for paratransgenic expression in Sodalis glossinidius, a bacterial symbiont in the tsetse vector, as a strategy for interference with trypanosome transmission.
Cyclic AMP induces apoptosis in multiple myeloma cells and inhibits tumor development in a mouse myeloma model (2011)

Elevation of intracellular levels of cAMP kills multiple myeloma cells in vitro and inhibits development of multiple myeloma in vivo. This strongly suggests that compounds activating the cAMP signaling pathway may be useful in the field of multiple myeloma.
INTRAVITREAL INJECTION OF VASCULAR ENDOTHELIAL GROWTH FACTOR SMALL INTERFERING RNA INHIBITS GROWTH AND LEAKAGE IN A NONHUMAN PRIMATE, LASER-INDUCED MODEL OF CHOROIDAL NEOVASCULARIZATION (2004)

Intravitreal injection of VEGF siRNA is capable of inhibiting the growth and vascular permeability of laser-induced CNV in a nonhuman primate in a dose-dependent manner. This study demonstrates preclinical proof of a principle that supports proceeding to clinical studies of VEGF siRNA in patients with exudative age-related macular degeneration.
Treatment-induced neuroplasticity following intensive naming therapy in a case of chronic Wernicke's aphasia (2010)

Background: Renewed interest in the effects of intensity on treatment has led to development of short-term, intensive treatment protocols, such as Constraint-Induced Language Therapy (CILT), in which participants with chronic aphasia begin to show statistically significant language improvements in as little as 2 weeks. Given its relatively short treatment cycle, CILT is also a good choice of treatment methodology for studying brain/behaviour plasticity in post-stroke aphasia. Aims: This study aimed to examine differences between two short, intensive treatment protocols in a participant with chronic Wernicke's aphasia both in terms of treatment outcomes and changes in patterns of BOLD signal activation. Methods & Procedures: The participant (ACL) participated in language testing and an fMRI overt speech confrontation-naming paradigm pre and post 2 weeks of CILT, post 2 weeks of unconstrained language therapy (PACE), and 6 months post-CILT. He named 48 black/white line drawings from each of four conditions: treated (CILT or PACE), untreated, or consistently correctly named pictures. Outcomes & Results: Naming treated pictures improved, even in the scanner, while naming untreated pictures did not. About one third of PACE and three-fourths of CILT gains were maintained. Rather than a distinct pattern of activation distinguishing treated from untreated or CILT from PACE pictures, ACL recruited a frontal network during naming of all pictures that included left middle and inferior frontal cortex, SMA and pre-SMA, and that varied in spatial extent and degree of activation according to accuracy and performance expectation. In post-hoc analyses of accuracy, this frontal network was most active during incorrect trials. At 6 months post-CILT, compared to controls, incorrect naming recruited a large and significant bilateral network including right Wernicke's area homologue. Conclusions: Results suggest that short, intensive therapy can improve naming and jumpstart language recovery in chronic aphasia, whether responses are constrained to the speech modality or not. Modulation of a left frontal network was associated with accuracy in naming and may represent compensatory adaptation to improve response selection, self-monitoring, and/or inhibition.
Hypertext Transfer Protocol (HTTP) Digest Authentication Using Authentication and Key Agreement (AKA) (2002)

This memo specifies an Authentication and Key Agreement (AKA) based one-time password generation mechanism for Hypertext Transfer Protocol (HTTP) Digest access authentication. The HTTP Authentication Framework includes two authentication schemes: Basic and Digest. Both schemes employ a shared secret based mechanism for access authentication. The AKA mechanism performs user authentication and session key distribution in Universal Mobile Telecommunications System (UMTS) networks. AKA is a challenge- response based mechanism that uses symmetric cryptography.
Aging, Cellular Senescence, and Cancer (2012)

For most species, aging promotes a host of degenerative pathologies that are characterized by debilitating losses of tissue or cellular function. However, especially among vertebrates, aging also promotes hyperplastic pathologies, the most deadly of which is cancer. In contrast to the loss of function that characterizes degenerating cells and tissues, malignant (cancerous) cells must acquire new (albeit aberrant) functions that allow them to develop into a lethal tumor. This review discusses the idea that, despite seemingly opposite characteristics, the degenerative and hyperplastic pathologies of aging are at least partly linked by a common biological phenomenon: a cellular stress response known as cellular senescence. The senescence response is widely recognized as a potent tumor suppressive mechanism. However, recent evidence strengthens the idea that it also drives both degenerative and hyperplastic pathologies, most likely by promoting chronic inflammation. Thus, the senescence response may be the result of antagonistically pleiotropic gene action.
Identification of circulating neuropilin-1 and dose-dependent elevation following anti-neuropilin-1 antibody administration (2009)

Neuropilin-1 (NRP1) acts as a co-receptor for class 3 semaphorins and vascular endothelial growth factor and is an attractive angiogenesis target for cancer therapy. In addition to the transmembrane form, naturally occurring soluble NRP1 proteins containing part of the extracellular domain have been identified in tissues and a cell line. We developed ELISAs to study the existence of circulating NRP1 and to quantify it in serum. As measured by ELISAs, circulating NRP1 levels in mice, rats, monkeys and humans were 427 +/- 77, 20 +/- 3, 288 +/- 86 and 322 +/- 82 ng/ml (mean +/- standard deviation; n > or = 10), respectively. Anti-NRP1(B), a human monoclonal antibody, has been selected from a synthetic phage library. A 4-fold increase in circulating NRP1 was observed in mice receiving a single dose of 10 mg/kg anti-NRP1(B) antibody. In rats and monkeys receiving single injections of anti-NRP1(B) at different dose levels, higher doses of antibody resulted in greater and more prolonged increases in circulating NRP1. Maximum increases were 56- and 7-fold for rats and monkeys receiving 50 mg/kg anti-NRP1(B), respectively. In addition to the soluble NRP1 isoforms, for the first time, a approximately 120 kDa circulating NRP1 protein containing the complete extracellular domain was detected in serum by western blot and mass spectrometry analysis. This protein increased more than the putative soluble NRP1 bands in anti-NRP1(B) treated mouse, rat and monkey sera compared with untreated controls, suggesting that anti-NRP1(B) induced membrane NRP1 shedding.
Stimulation of Androgen-Dependent Gene Expression by the Adrenal Precursors Dehydroepiandrosterone and Androstenedione in the Rat Ventral Prostate* (1989)

Androgens play a major role in the development, growth, and function of accessory sexual organs, especially the prostate. However, the testis is not the sole source of circulating androgens in man, since the adrenal gland secretes dehydroepiandrosterone (DHEA), DHEA sulfate, and androstenedione (delta 4-dione) in large quantities. The aim of the present study was to investigate the effect of plasma concentrations of DHEA and delta 4-dione similar to those found in adult man on sensitive and specific markers of androgen action in the rat ventral prostate. In addition to ventral prostate weight, we have measured the steady state levels of the mRNAs encoding the C1 component of rat prostatic binding protein (PBP-C1) and spermine-binding protein (SBP) using 35S-labeled cDNA probes for in situ hybridization. One week after castration, ventral prostate weight fell 84%, while prostatic 5 alpha-dihydrotestosterone (DHT) and androgen-dependent mRNAs were undetectable. When administered via Silastic implants to castrated adult rats for 1 week, plasma concentrations of 1.37 +/- 0.06 ng/ml DHEA or 0.43 +/- 0.08 ng/ml delta 4-dione independently caused increases in ventral prostate weight to 33% and 65% of normal values, respectively. The same plasma levels of DHEA and delta 4-dione resulted in high intraprostatic levels of DHT to 1.19 +/- 0.34 and 3.66 +/- 0.89 ng/g tissue, respectively. Furthermore, DHEA caused an increase in the steady state levels of PBP-C1 and SBP mRNAs to 50% and 57% of the normal state, respectively, while delta 4-dione caused increases corresponding to 80% and 119% of control values, respectively. Castrated adult rats receiving testosterone at a concentration of 1.66 +/- 0.37 ng/ml plasma maintained normal ventral prostate weight and gene expression levels. The present results demonstrate that circulating levels of the adrenal steroids DHEA and delta 4-dione comparable to those found in man cause an important stimulation of androgen-dependent gene expression in the rat, probably after their conversion to DHT in the prostatic tissue itself.
Evanescent-wave gas sensing using microstructure fiber (2002)

We report the experimental demonstration of evanescent-wave gas detection with a silica-air microstructure fiber. Detection sensitivity of ~6% of that of direction absorption spectroscopy per equal length has been achieved. 0]
Interleukin-l Induces Tumor Necrosis Factor (TNF) in Human Peripheral Blood Mononuclear Cells In Vitro and a Circulating TNF-Iike Activity in Rabbits (1990)

Recombinant human interleukin-1 (IL-1), injected into rabbits, induces the synthesis of endogenous IL-1. Also, IL-1 induces its own gene expression and synthesis in human peripheral blood mononuclear cells (PBMC). In this study, tumor necrosis factor-alpha (TNF-alpha) production by PBMC of 40 individuals stimulated with IL-1 alpha or IL-1 beta was determined by specific radioimmunoassay (RIA). After 3 h of PBMC incubation with IL-1, TNF-alpha mRNA was detected. IL-1 alpha stimulated both IL-1 beta and TNF-alpha, but there was no correlation in the amount of TNF-alpha or IL-1 beta synthesized in the PBMC of 29 individuals. IL-1-stimulated adherent cells produced approximately 50% more TNF-alpha than did unfractionated PBMC. Coincubation with interferon-gamma (IFN-gamma) did not change the amount of IL-1-induced TNF-alpha, whereas in the same culture IFN-gamma inhibited (greater than 70%) IL-1-induced IL-1 production. Endogenous pyrogen and TNF-like activity were detected in the sera of rabbits 3.5 h after injection of either IL-1 alpha or -1 beta. These studies demonstrate that IL-1 induced TNF-alpha production in vivo and in vitro.
Genetic alterations of the transforming growth factor beta receptor genes in pancreatic and biliary adenocarcinomas. (1998)

Transforming growth factor beta (TGF-beta) is an extracellular ligand that binds to a heterodimeric receptor, initiating signals that regulate growth, differentiation, and apoptosis. Many cancers, including pancreatic cancer, harbor defects in TGF-beta signaling and are resistant to TGF-beta-mediated growth suppression. Genetic alterations of DPC4, which encodes a DNA binding protein that is a downstream component of the pathway, most frequently occur in pancreatic and biliary carcinomas. We searched for other targets of mutation of the TGF-beta pathway in these cancers. We report somatic alterations of the TGF-beta type I receptor gene ALK-5. Homozygous deletions of ALK-5 were identified in 1 of 97 pancreatic and 1 of 12 biliary adenocarcinomas. A germ-line variant of ALK-5, presumably a polymorphism, was identified, but no somatic intragenic mutations were identified upon sequencing of all coding regions of ALK-5. Somatic alterations of the TGF-beta type II receptor gene (TGFBR2) were identified in 4 of 97 (4.1%) pancreas cancers, including a homozygous deletion in a replication error-negative cancer and three homozygous frameshift mutations of the poly(A) tract of the TGF-beta type II receptor in replication error-positive cancers. We also studied other related type I receptors of the TGF-beta superfamily. In a panel of pancreas cancers preselected for loss of heterozygosity at the ALK-1 locus, sequencing of all coding exons of the ALK-1 gene revealed no alterations. No homozygous deletions were detected in the ALK-1, ALK-2, ALK-3, or ALK-6 genes in a panel of 86 pancreatic cancer xenografts and 11 pancreatic cancer and 22 breast cancer cell lines. The rate of genetic inactivation of TGF-beta pathway members was determined in 45 pancreatic cancers. Eighty-two % of these pancreatic cancers had genetic inactivation of the DPC4, p15, ALK-5, or TGFBR2 genes. Our results indicate that the TGF-beta type I and type II receptor genes are selective targets of genetic inactivation in pancreatic and biliary cancers.
Enhancement of Recovery from Psychiatric Illness by Methylfolate (1991)

"41 (33%) of 123 patients with acute psychiatric disorders (DSM III diagnosis of major depression or schizophrenia) had borderline or definite folate deficiency (red-cell folate below 200 micrograms/l) and took part in a double-blind, placebo-controlled trial of methylfolate, 15 mg daily, for 6 months in addition to standard psychotropic treatment. Among both depressed and schizophrenic patients methylfolate significantly improved clinical and social recovery. The differences in outcome scores between methylfolate and placebo groups became greater with time. These findings add to the evidence implicating disturbances of methylation in the nervous system in the biology of some forms of mental illness."
Niclosamide Prevents Systemic Sclerosis in a Reactive Oxygen Species–Induced Mouse Model (2016)

Systemic sclerosis (SSc) is a connective tissue disorder characterized by fibrosis of the skin and inner organs, vasculopathy, and immunological abnormalities. Recent insights on the implication of STAT3, AKT, and Wnt/β-catenin in fibrosis have prompted us to investigate, in a mouse model of ROS-induced SSc, the effects of niclosamide, an antihelmintic drug that inhibits both of these signaling pathways. SSc was induced in BALB/c mice by daily s.c. injections of hypochlorous acid (HOCl). Mice were treated or not every other day, 5 d a week, for 6 wk, by niclosamide. Skin and lung fibrosis as well as immunological features were studied. Mice exposed to HOCl developed a diffuse cutaneous SSc with pulmonary fibrosis and anti-DNA topoisomerase 1 autoantibodies. STAT3, AKT, and Wnt/β-catenin pathways were hyperactivated in the skin and the lungs of diseased mice. Niclosamide reversed fibrosis of the skin and the lungs. Beneficial immunological effects were also observed because niclosamide decreased the activation of CD4<sup>+</sup> and CD8<sup>+</sup> T cells, autoimmune B cell activation, as well as IL-4 and IL-13 production in the skin. The improvement permitted by niclosamide in the mouse model of HOCl-induced SSc as well as the well-documented safety profile of this drug provide a rationale for the evaluation of niclosamide in the management of patients affected by this disease.
Tumour oxygenation: implications for breast cancer prognosis (2013)

There are areas of limited oxygen availability in most solid tumours, including breast cancer. Hypoxia in solid tumours is mainly a consequence of poor perfusion. Structural and functional abnormalities of newly formed tumour vessels cause spatial and temporal heterogeneity of tissue perfusion. The two principal mediators of hypoxia response, HIF-1 and HIF-2, are known to be stabilized at different oxygen levels and to have different temporal responses to hypoxia. Recently, stromal HIF-1 and HIF-2 have been suggested to have opposing roles in breast cancer progression. There is an established link between intralesional, severe hypoxia near areas of necrosis with high levels of HIF-1 and poor prognosis in breast cancer. However, the biological effects of moderate hypoxia and the hypoxic response of stromal cells are currently topics of intense investigation.
Crystal and molecular structure of bis(dithiotropolonato)nickel(II) (1971)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTCrystal and molecular structure of bis(dithiotropolonato)nickel(II)Richard Eisenberg, Gyaneshwari P. Khare, and Arthur J. SchultzCite this: J. Am. Chem. Soc. 1971, 93, 15, 3597–3602Publication Date (Print):July 1, 1971Publication History Published online1 May 2002Published inissue 1 July 1971https://pubs.acs.org/doi/10.1021/ja00744a010https://doi.org/10.1021/ja00744a010research-articleACS PublicationsRequest reuse permissionsArticle Views70Altmetric-Citations5LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InRedditEmail Other access optionsGet e-Alertsclose Get e-Alerts
Genital and Subjective Measurement of the Time Course Effects of an Acute Dose of Testosterone vs. Placebo in Postmenopausal Women (2007)

These findings in postmenopausal women combined with those of two previous investigations in premenopausal women demonstrate a probable acute-dose time delay for genital sexual effects of exogenous T with no change in self-reported sexual arousal. Further investigation is needed to determine whether acute dosing of T has a consistent and predictable impact on genital arousal that has promise for the treatment of any subgroup of women with sexual disorders.
Polysilicon overfill etch back using wet chemical spin-process technology. An alternative to traditional dry etch and CMP technigues (2003)

Wet chemical etch techniques have been used in semiconductor manufacturing since the advent of the industry. As device geometry's have shrunk, wet etching has been replaced by various dry etch and chemical mechanical polishing (CMP) techniques. In most cases it has been relegated to non-critical bulk film removal applications. Recent innovations in single wafer wet processing hardware and chemistries have given new life and applications to traditional wet etch techniques. In this study we investigated the feasibility of using a single wafer spin-processor chemically enhanced polish (CEP) system with automated endpoint capability for the removal and planarization of polysilicon over-fill in a deep trench isolation application as an alternative to dry etch and CMP techniques.
Sorafenib synergizes with metformin in NSCLC through AMPK pathway activation (2014)

The multikinase inhibitor sorafenib is under clinical investigation for the treatment of many solid tumors, but in most cases, the molecular target responsible for the clinical effect is unknown. Furthermore, enhancing the effectiveness of sorafenib using combination strategies is a major clinical challenge. Here, we identify sorafenib as an activator of AMP-activated protein kinase (AMPK), in a manner that involves either upstream LKB1 or CAMKK2. We further show in a phase II clinical trial in KRAS mutant advanced non-small cell lung cancer (NSCLC) with single agent sorafenib an improved disease control rate in patients using the antidiabetic drug metformin. Consistent with this, sorafenib and metformin act synergistically in inhibiting cellular proliferation in NSCLC in vitro and in vivo. A synergistic effect of both drugs is also seen on phosphorylation of the AMPKα activation site. Our results provide a rationale for the synergistic antiproliferative effects, given that AMPK inhibits downstream mTOR signaling. These data suggest that the combination of sorafenib with AMPK activators could have beneficial effects on tumor regression by AMPK pathway activation. The combination of metformin or other AMPK activators and sorafenib could be tested in prospective clinical trials.