gebhart/patrepeval huggingface dataset:
Robust and Communication-Efficient Collaborative Learning (2019)

We consider a decentralized learning problem, where a set of computing nodes aim at solving a non-convex optimization problem collaboratively. It is well-known that decentralized optimization schemes face two major system bottlenecks: stragglers' delay and communication overhead. In this paper, we tackle these bottlenecks by proposing a novel decentralized and gradient-based optimization algorithm named as QuanTimed-DSGD. Our algorithm stands on two main ideas: (i) we impose a deadline on the local gradient computations of each node at each iteration of the algorithm, and (ii) the nodes exchange quantized versions of their local models. The first idea robustifies to straggling nodes and the second alleviates communication efficiency. The key technical contribution of our work is to prove that with non-vanishing noises for quantization and stochastic gradients, the proposed method exactly converges to the global optimal for convex loss functions, and finds a first-order stationary point in non-convex scenarios. Our numerical evaluations of the QuanTimed-DSGD on training benchmark datasets, MNIST and CIFAR-10, demonstrate speedups of up to 3x in run-time, compared to state-of-the-art decentralized optimization methods.
Amelioration of accelerated collagen induced arthritis by a novel calcineurin inhibitor, ISA(TX)247. (2002)

ISA(TX)247 demonstrates efficacy and safety in the treatment of established collagen induced arthritis. Together with its improved potency and nephrotoxicity profile in comparison to CSA, this agent warrants further clinical investigation in autoimmune disease. Phase II studies in rheumatoid arthritis have been initiated.
Adenosine-enhanced ischemic preconditioning: adenosine receptor involvement during ischemia and reperfusion (2001)

Adenosine-enhanced ischemic preconditioning (APC) extends the cardioprotection of ischemic preconditioning (IPC) by both significantly decreasing myocardial infarct size and significantly enhancing postischemic functional recovery. In this study, the role of adenosine receptors during ischemia-reperfusion was determined. Rabbit hearts (n = 92) were used for Langendorff perfusion. Control hearts were perfused for 180 min, global ischemia hearts received 30-min ischemia and 120-min reperfusion, and IPC hearts received 5-min ischemia and 5-min reperfusion before ischemia. APC hearts received a bolus injection of adenosine coincident with IPC. Adenosine receptor (A(1), A(2), and A(3)) antagonists were used with APC before ischemia and/or during reperfusion. GR-69019X (A(1)/A(3)) and MRS-1191/MRS-1220 (A(3)) significantly increased infarct size in APC hearts when administered before ischemia and significantly decreased functional recovery when administered during both ischemia and reperfusion (P < 0.05 vs. APC). DPCPX (A(1)) administered either before ischemia and/or during reperfusion had no effect on APC cardioprotection. APC-enhanced infarct size reduction is modulated by adenosine receptors primarily during ischemia, whereas APC-enhanced postischemic functional recovery is modulated by adenosine receptors during both ischemia and reperfusion.
LinkingPark: An Integrated Approach for Semantic Table Interpretation. (2020)

In this paper, we present LinkingPark, our system for Semantic Web Challenge on Tabular Data to Knowledge Graph Matching (SemTab 2020). LinkingPark is an integrated approach for semantic table interpretation. Our system includes a cascaded pipeline for candidate generation, an iterative coarse-to-fine entity disambiguation algorithm, a multi-pass property linking algorithm, and a type inference algorithm tackling the issue of loose ontology in Wikidata. Results on SemTab 2020 demonstrate the effectiveness of our approach.
Budesonide inhaled via Turbuhaler: a more effective treatment for asthma than beclomethasone dipropionate via Rotahaler. (1995)

As a consequence of the difference in local potency of the steroids and the fact that Turbuhaler deposits more drug particles in the lung than Rotahaler, budesonide inhaled via Turbuhaler appeared to be a more effective steroid formulation than beclomethasone dipropionate inhaled via Rotahaler.
Role of intravenous iron in the treatment of anemia in patients with gastrointestinal tract tumors undergoing chemotherapy: a single-center, observational study (2018)

FCM was well tolerated and had a positive impact in the treatment of iron-deficiency anemia in patients with gastrointestinal tract tumors undergoing chemotherapy.
Proteolytic processing of human factor VIII. Correlation of specific cleavages by thrombin, factor Xa, and activated protein C with activation and inactivation of factor VIII coagulant activity (1986)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTProteolytic processing of human factor VIII. Correlation of specific cleavages by thrombin, factor Xa, and activated protein C with activation and inactivation of factor VIII coagulant activityDan Eaton, Henry Rodriguez, and Gordon A. VeharCite this: Biochemistry 1986, 25, 2, 505–512Publication Date (Print):January 28, 1986Publication History Published online1 May 2002Published inissue 28 January 1986https://pubs.acs.org/doi/10.1021/bi00350a035https://doi.org/10.1021/bi00350a035research-articleACS PublicationsRequest reuse permissionsArticle Views936Altmetric-Citations383LEARN 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
Direct Competition between hnRNP C and U2AF65 Protects the Transcriptome from the Exonization of Alu Elements (2013)

There are ~650,000 Alu elements in transcribed regions of the human genome. These elements contain cryptic splice sites, so they are in constant danger of aberrant incorporation into mature transcripts. Despite posing a major threat to transcriptome integrity, little is known about the molecular mechanisms preventing their inclusion. Here, we present a mechanism for protecting the human transcriptome from the aberrant exonization of transposable elements. Quantitative iCLIP data show that the RNA-binding protein hnRNP C competes with the splicing factor U2AF65 at many genuine and cryptic splice sites. Loss of hnRNP C leads to formation of previously suppressed Alu exons, which severely disrupt transcript function. Minigene experiments explain disease-associated mutations in Alu elements that hamper hnRNP C binding. Thus, by preventing U2AF65 binding to Alu elements, hnRNP C plays a critical role as a genome-wide sentinel protecting the transcriptome. The findings have important implications for human evolution and disease.
MANAGING THE TRANSITION: EMPLOYMENT TO SELF‐EMPLOYMENT (1996)

This work considers women who have left jobs within organizations to set up their own businesses. The project thus explores two worlds: the world of the organization and the world of the small business owner/manager. However, it is not sufficient to limit the scope of the research to these two contexts; equally important are the spaces in‐between. An examination of the transition from employment to self‐employment is crucial in understanding the experience as a whole. Two case studies are used to illustrate how particular women managed the transition. It is then considered how this experience can be conceptualized theoretically, assessing the extent to which existing theories offer adequate frameworks for understanding. Implications for further research and the development of a more relevant conceptual model are addressed.
Epithelial cells as sentinels in mucosal immune barrier (2006)

The mucosal surface of the body is exposed to a vast array of exogenous antigens and microorganisms. Epithelial cells evoke minimal immune response to food ingredients and commensal bacteria, while they release an array of antimicrobial peptides and CXC chemokines in response to bacterial invasion or inflammatory stimuli. The mucosal antigens are transported from the gut lumen to organized lymphoid follicles by specialized epithelial M cells residing in follicle-associated epithelium (FAE). An alternative pathway of antigen uptake with neonatal Fc receptor (FcRn) is also reported. Furthermore, intestinal dendritic cells underneath epithelium directly take up luminal antigens, where epithelial fractalkine expression plays a critical role in the guidance of dendrite extrusion. Epithelial cells express polymeric Ig receptor (pIgR) that is essential for the luminal secretion of dimeric IgA produced in the lamina propria. Furthermore, soluble factors released by mucosal epithelial cells condition dendritic cells, which in turn promote Th2 response. These multiple lines of evidence clearly suggest the significant role of epithelial cells at the front line of mucosal immune defense.
Investigation of the effect of pulsed electromagnetic field on the weight of rats (2012)

Purpose: To investigate the effect of electromagnetic fields on weight at the rats.
Material and Method: 10 female Wistar Albino rats were exposed to 20 beats/s and 50 Hz frequency pulsed electromagnetic field for 4 hours daily for 60 days in experimental inverstigation laboratory. They were kept at 21±1 C° and free access to water and food. There were a control group consisting of 10 rats. Weights of the rats in both groups were measured before and after sudy. The values obtained from both groups were analyzed statistically.
Results: The mean weight of the experiment group was 242,6 gr (SD:22,4) and of the control group was 248,3 gr (SD:18,5). At the end of the 60th day the mean values of the experiment and control groups were 266,5 gr (SD:20,8) and 275,4 gr (SD:23,6) respectively. There was no statistically significant diffeence between the groups before and after study. (p>0.05)
Conclusion: 50 Hz frequency and 25 beats/s pulsed electromagnetic field did not cause any change in the weight of rats compared to control group.
Radioactive Labeling of Antibody: A Simple and Efficient Method (1983)

A simple and efficient method of covalently coupling the strong chelator diethylenetriaminepentaacetic acid to proteins was developed for radiolabeling immunoglobulin G antibodies. After being coupled and labeled with indium-111, a monoclonal antibody to carcinoembryonic antigen retained its ability to bind to its antigen in vitro and in vivo. In nude mice with a human colorectal xenograft, 41 percent of the injected radioactivity became localized in each gram of xenograft at 24 hours compared with 9 percent for control antibody and 19 percent for radioiodinated antibody to carcinoembryonic antigen.
Inducible expression of mutant alpha-synuclein decreases proteasome activity and increases sensitivity to mitochondria-dependent apoptosis (2001)

Parkinson's disease (PD) is a common progressive neurodegenerative disorder caused by the loss of dopaminergic neurons in the substantia nigra. Although mutations in alpha-synuclein have been identified in autosomal dominant PD, the mechanism by which dopaminergic neural cell death occurs remains unknown. Proteins encoded by two other genes in which mutations cause familial PD, parkin and UCH-L1, are involved in regulation of the ubiquitin-proteasome pathway, suggesting that dysregulation of the ubiquitin-proteasome pathway is involved in the mechanism by which these mutations cause PD. We established inducible PC12 cell lines in which wild-type or mutant alpha-synuclein can be de-repressed by removing doxycycline. Differentiated PC12 cell lines expressing mutant alpha-synuclein showed decreased activity of proteasomes without direct toxicity. Cells expressing mutant alpha-synuclein showed increased sensitivity to apoptotic cell death when treated with sub-toxic concentrations of an exogenous proteasome inhibitor. Apoptosis was accompanied by mitochondrial depolarization and elevation of caspase-3 and -9, and was blocked by cyclosporin A. These data suggest that expression of mutant alpha-synuclein results in sensitivity to impairment of proteasome activity, leading to mitochondrial abnormalities and neuronal cell death.
Signal quality in cardiorespiratory monitoring (2012)

and participants were provided with the grades for these 1000 ECGs. The remaining records were divided at random into Set B, a public test subset (500 ECGs available for study, with grades withheld) and Set C, a hidden test subset (500 ECGs not available for study, used only by PhysioNet for testing submitted algorithms).
Identifying quinone-like species on the surface of graphitic carbon and multi-walled carbon nanotubes using reactions with 2,4-dinitrophenylhydrazine to provide a voltammetric fingerprint (2007)

Quinone groups on the surface of edge-plane and basal-plane pyrolytic graphite electrodes, and, for the first time, “bamboo-like” multi-walled carbon nanotubes (b-MWCNTs), are labelled with a voltammetric “tag”, namely 2,4-dinitrophenylhydrazine (2,4-DNPH). The voltammetric response of these materials is studied in both aqueous and non-aqueous electrolyte solutions, and mechanisms are proposed for each media involving the voltammetrically controlled cleavage of the 2,4-DNPH adduct. Thus, these materials can be used for potentiometrically controlled chemical release, and as such may find application in, for example, drug delivery systems. In aqueous media, this cleavage results in the conversion of the surface quinonyl groups into surface arylnitroso species. This conversion is confirmed by studying the voltammetric response of the arylnitroso/arylhydroxylamine redox couple, formed after cleavage of the 2,4-DNPH adduct in the presence of L-glutathione, which has been shown in our previous work to react with arylnitroso species on the surface of graphitic carbon materials.
The Synthesis of Two New Metabolites of Catecholamines: 3,4-Dihydroxyphenylethyleneglycol and 4-Hydroxy-3-methoxyphenylethyleneglycol1 (1963)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTThe Synthesis of Two New Metabolites of Catecholamines: 3,4-Dihydroxyphenylethyleneglycol and 4-Hydroxy-3-methoxyphenylethyleneglycol1J. D. Benigni and Anthony J. VerbiscarCite this: J. Med. Chem. 1963, 6, 5, 607–608Publication Date (Print):September 1, 1963Publication History Published online1 May 2002Published inissue 1 September 1963https://pubs.acs.org/doi/10.1021/jm00341a035https://doi.org/10.1021/jm00341a035research-articleACS PublicationsRequest reuse permissionsArticle Views82Altmetric-Citations9LEARN 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
Healing of intestinal inflammation by IL-22 (2012)

An interleukin (IL)-10 family cytokine, IL-22 is characterized by several unique biological properties, including 1) the target restricted to innate cells; 2) the distinct expression pattern between large and small intestines; 3) alteration of the cellular source depending on several factors; 4) the dual abilities to serve as protective versus proinflammatory mediators in inflammatory responses; and 5) the close association with some major inflammatory bowel disease (IBD) susceptibility genes. The major functions of IL-22 in the intestine are the stimulation of epithelial cells to produce a wide variety of antibacterial proteins, the reinforcement of mucus barrier through stimulation of mucin 1 production under intestinal inflammatory conditions, and the enhancement of epithelial regeneration with goblet cell restitution. Through these beneficial functions, IL-22 contributes to the improvement of some types of experimental chronic colitis, which are mediated by T helper (Th)1 or Th2 responses. Most important, studies using both loss-of-function and gain-of-function approaches have clearly demonstrated the ability of IL-22 to promote intestinal wound healing from acute intestinal injury. These findings highlight IL-22 as an attractive and promising target for future IBD therapy. Alternatively, the enormous progress in the field of IL-22 biology has also suggested more complicated mechanisms with the IL-22 pathway than previously predicted. This review article briefly summarizes previous and current knowledge on IL-22 particularly associated with intestinal inflammation.
BDNF Overexpression in the Forebrain Rescues Huntington's Disease Phenotypes in YAC128 Mice (2010)

Huntington's disease (HD) is caused by an expansion of the polyglutamine tract at the N terminus of huntingtin. This mutation reduces levels of BDNF in the striatum, likely by inhibiting cortical Bdnf gene expression and anterograde transport of BDNF from the cerebral cortex to the striatum. Substantial evidence suggests that this reduction of striatal BDNF plays a crucial role in HD pathogenesis. Here we report that overexpression of BDNF in the forebrain rescues many disease phenotypes in YAC128 mice that express a full-length human huntingtin mutant with a 128-glutamine tract. The Bdnf transgene, under the control of the promoter for α subunit of Ca(2+)/calmodulin-dependent protein kinase II, greatly increased BDNF levels in the cerebral cortex and striatum. BDNF overexpression in YAC128 mice prevented loss and atrophy of striatal neurons and motor dysfunction, normalized expression of the striatal dopamine receptor D2 and enkephalin, and improved procedural learning. Furthermore, quantitative analyses of Golgi-impregnated neurons revealed a decreased spine density and abnormal spine morphology in striatal neurons of YAC128 mice, which was also reversed by increasing BDNF levels in the striatum. These results demonstrate that reduced striatal BDNF plays a crucial role in the HD pathogenesis and suggest that attempts to restore striatal BDNF level may have therapeutic effects to the disease.
Complement Activation in the Human Brain after Traumatic Head Injury (2001)

The complement cascade has been suggested to be involved in the development of secondary brain injuries following brain contusions, based on animal experiments. The aim of the present study was to examine the possible involvement of the complement cascade following traumatic head injury in the human brain. Sixteen patients were included in this study, 12-77 years of age, treated at the neurointensive care unit for traumatic brain contusions. All of these patients were operated with frontal or temporal lobe resection due to intractable intracranial hypertension. The resected tissue was analyzed with regard to components related to complement activation. The time interval between accident and operation was 2-82 h. Brain tissue from three patients operated with hippocampectomy due to epilepsy, including temporal lobe resection, were used as controls. We found increased immunoreactivity for complement components C1q, C3b, and C3d and the membrane attack complex (MAC), C5b-9, in the immediate vicinity of neurons in the penumbra area of the contusion. These findings constitute histological evidence for activation of the complement cascade in the penumbra of cortical contusions in the human brain. Using in situ hybridization, we also found C3-mRNA in the penumbra, suggesting a local synthesis of complement. Furthermore, upregulation of the endogenous complement regulator clusterin was found in some neurons in the same area. We suggest that unknown compounds in the debris from injured neurons or myelin breakdown products trigger complement activation, including formation of C5b-9. Activated complement components may stimulate accumulation of inflammatory cells and formation of brain edema, as well as having membrane destructive effects by the end product MAC, thereby being mediators in the development of secondary brain damage.
Animation production unit (1987)

The animation workshop which I conducted at the National Conference addressed some practical aspects of animation production within primary and lower post primary year levels. It was based upon units completed during 1986 at three primary schools in Melbourne's Western Suburbs.
Dysregulated gene expressions of MEX3D, FOS and BCL2 in human induced-neuronal (iN) cells from NF1 patients: a pilot study (2017)

Direct conversion technique to produce induced-neuronal (iN) cells from human fibroblasts within 2 weeks is expected to discover unknown neuronal phenotypes of neuropsychiatric disorders. Here, we present unique gene expression profiles in iN cells from patients with neurofibromatosis type 1 (NF1), a single-gene multifaceted disorder with comparatively high co-occurrence of autism spectrum disorder (ASD). Microarray-based transcriptomic analysis on iN cells from male healthy controls and male NF1 patients (NF1-iN cells) revealed that 149 genes expressions were significantly different (110 upregulated and 39 downregulated). We validated that mRNA of MEX3D (mex-3 RNA binding family member D) was lower in NF1-iN cells by real-time PCR with 12 sex-mixed samples. In NF1-iN cells on day 14, higher expression of FOS mRNA was observed with lower expression of MEX3D mRNA. Interestingly, BCL2 mRNA was higher in NF1-iN cells on day 5 (early-period) but not on day 14. Our data suggest that aberrant molecular signals due to NF1 mutations may disturb gene expressions, a subset of which defines continuum of the neuronal phenotypes of NF1 with ASD. Further translational studies using induced pluripotent stem (iPS) cell-derived neuronal cells are needed to validate our preliminary findings especially confirming meanings of analysis using early-period iN cells.