gebhart/patrepeval huggingface dataset:
NEVERMIND, the problem is already fixed (2010)

Traditional DSL troubleshooting solutions are reactive, relying mainly on customers to report problems, and tend to be labor-intensive, time consuming, prone to incorrect resolutions and overall can contribute to increased customer dissatisfaction. In this paper, we propose a proactive approach to facilitate troubleshooting customer edge problems and reducing customer tickets. Our system consists of: i) a ticket predictor which predicts future customer tickets; and ii) a trouble locator which helps technicians accelerate the troubleshooting process during field dispatches. Both components infer future tickets and trouble locations based on existing sparse line measurements, and the inference models are constructed automatically using supervised machine learning techniques. We propose several novel techniques to address the operational constraints in DSL networks and to enhance the accuracy of NEVERMIND. Extensive evaluations using an entire year worth of customer tickets and measurement data from a large network show that our method can predict thousands of future customer tickets per week with high accuracy and signifcantly reduce the time and effort for diagnosing these tickets. This is benefcial as it has the effect of both reducing the number of customer care calls and improving customer satisfaction.
The Newton application architecture (2002)

The application architecture of Newton, a technology for supporting personal digital assistants (PDAs), is described. It combines a dynamic, object-oriented language called NewtonScript with a hierarchical view system and a persistent object store. It also contains extensible subsystems for communications and user-input recognition. In addition to PDA devices, the portable implementation has been used to build supporting tools for desktop machines.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">&gt;</ETX>
High yields of formal CH insertion products in the reactions of polyfluorinated aromatic nitrenes (1986)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTHigh yields of formal CH insertion products in the reactions of polyfluorinated aromatic nitrenesElisa. Leyva, Mary Jennifer T. Young, and Matthew S. PlatzCite this: J. Am. Chem. Soc. 1986, 108, 26, 8307–8309Publication Date (Print):December 1, 1986Publication History Published online1 May 2002Published inissue 1 December 1986https://pubs.acs.org/doi/10.1021/ja00286a054https://doi.org/10.1021/ja00286a054research-articleACS PublicationsRequest reuse permissionsArticle Views363Altmetric-Citations50LEARN 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
Pim kinase inhibitor, SGI-1776, induces apoptosis in chronic lymphocytic leukemia cells (2009)

Pim kinases are involved in B-cell development and are overexpressed in B-cell chronic lymphocytic leukemia (CLL). We hypothesized that Pim kinase inhibition would affect B-cell survival. Identified from a screen of imidazo[1,2-b]pyridazine compounds, SGI-1776 inhibits Pim-1, Pim-2, and Pim-3. Treatment of CLL cells with SGI-1776 results in a concentration-dependent induction of apoptosis. To elucidate its mechanism of action, we evaluated the effect of SGI-1776 on Pim kinase function. Unlike in replicating cells, phosphorylation of traditional Pim-1 kinase targets, phospho-Bad (Ser112) and histone H3 (Ser10), and cell-cycle proteins were unaffected by SGI-1776, suggesting an alternative mechanism in CLL. Protein levels of total c-Myc as well as phospho-c-Myc(Ser62), a Pim-1 target site, were decreased after SGI-1776 treatment. Levels of antiapoptotic proteins Bcl-2, Bcl-X(L), XIAP, and proapoptotic Bak and Bax were unchanged; however, a significant reduction in Mcl-1 was observed that was not caused by caspase-mediated cleavage of Mcl-1 protein. The mechanism of decline in Mcl-1 was at the RNA level and was correlated with inhibition of global RNA synthesis. Consistent with a decline in new RNA synthesis, MCL-1 transcript levels were decreased after treatment with SGI-1776. These data suggest that SGI-1776 induces apoptosis in CLL and that the mechanism involves Mcl-1 reduction.
FERTILITY OF MIXED SEMEN FROM DIFFERENT RABBITS (1960)

Summary. (1) Mixed insemination of known numbers of spermatozoa from two rabbits produced, spermatozoon for spermatozoon, offspring in the ratio of 1 :5. This difference in spermatozoan fertility was highly significant, and consistent over four experiments. It is thought to be a consequence of, and in turn a useful measure of, differences in the viability of spermatozoa in the original ejaculates. Such differences may be of common occurrence, and their existence would not necessarily be suspected from the records of natural matings. (2) The conception rate, or percentage of inseminations yielding a litter, was shown in one experiment to increase as the number of males contributing to the inseminate increased, even though the nett total number of spermatozoa per inseminate was held constant. These observations are not fully conclusive, but are presented as a recorded experimental finding of the type expected by certain Russian workers. (3) Inseminates from one particular male alone gave no offspring, but offspring fathered by this male appeared after mixed insemination, as if the fertility of its spermatozoa had been assisted by the admixture with other semen.
Warning cigarettes may be about to become fashionable again (2011)

E-cigarettes are simple to understand. A plastic tube houses a heating element, battery, control electronics and a cartridge of liquid containing nicotine. When the user inhales at one end, a dose of liquid is vaporised and the user (or 'vaper' as many have come to be known) receives a nicotine hit.
Cytokine secretion by human aortic endothelial cells is related to degree of atherosclerosis (1992)

We have previously described a 13- to 15-kDa T-lymphocyte-specific chemotactic protein (endothelial cell-derived lymphocyte chemoattractant activity, ED-LCA) secreted by serotonin-stimulated bovine aortic endothelial cells. In the current study, we have identified a similar serotonin-induced chemotaxin secreted by human aortic endothelial cells (HAEC). Like the bovine ED-LCA, secretion of this human T-cell chemotaxin peaked at 10(-5) M serotonin, was blocked by 5-HT2-receptor antagonists, and was not induced by other vasoactive amines, such as histamine or angiotensin II. In addition, human ED-LCA had no effect on neutrophil or monocyte migration. Using HAEC and human pulmonary arterial endothelial cells (HPAEC) from the same individual, we found that serotonin-stimulated HAEC, but not HPAEC, secreted ED-LCA. Because human vascular endothelium affected by atherosclerosis is morphologically, ultrastructurally, and phenotypically distinct from unaffected areas, we evaluated the secretion of this cytokine from cultured HAEC derived from areas of aorta differentially affected by atherosclerosis. We found that the degree of atherosclerotic involvement of an individual vessel was associated with a decrease in the uptake of serotonin and a reduction in serotonin-induced ED-LCA secretion. In response to serotonin, HAEC derived from atherosclerotic plaques did not secrete ED-LCA, whereas HAEC derived from fatty streaks secreted lesser amounts of ED-LCA than HAEC derived from normal areas. These studies demonstrate that in vivo morphological heterogeneity of HAEC is maintained in vitro and is associated with alterations in function, as measured by cytokine secretion.
Laminin-332 promotes the invasion of oesophageal squamous cell carcinoma via PI3K activation (2008)

Laminin-332 is major component of epithelial basement membrane, and has an important role in cell migration and tumour invasion. Recently, the phosphatidylinositol 3-kinase (PI3K) activation induced by laminin-332 during carcinogenesis or tumour invasion has been highlighted in skin squamous cell carcinoma. The expression of laminin-332 in 126 resected oesophageal squamous cell carcinoma (ESCC) specimens was immunohistochemically examined to determine its associations with the clinicopathological characteristics, and the effect of laminin-332 on the invasiveness and the PI3K activation was assessed by in vitro experiments using ESCC cell lines (ESCCs). Sections with immunostaining signals in >30% cancer cells, which were observed in 55 of 126 cases, were judged to be positive for laminin-332. The positivity was significantly correlated with pTNM stage and poor prognosis. Inactivation of the PI3K pathway by laminin-332 blocking antibody suppressed the invasiveness of TE8 cell line, which secreted laminin-332 at high level and had high PI3K activity. The addition of the purified laminin-332 activated the PI3K pathway and increased the invasiveness of TE11 cell line, which secreted laminin-332 at lower level and had low PI3K activity. The deactivation of PI3K pathway using the PI3K inhibitor decreased the invasiveness of ESCCs and the secretion of laminin-332 in vitro. The expression of laminin-332 was one of the prognostic factors of ESCC. Laminin-332 could provide the autocrine positive-feedback loop through PI3K activation, contributing the invasive ability. Therefore, the inhibitor of PI3K pathway might be useful as the anticancer therapies for ESCC.
Caveolae-mediated Internalization of Occludin and Claudin-5 during CCL2-induced Tight Junction Remodeling in Brain Endothelial Cells (2009)

Disturbance of the tight junction (TJ) complexes between brain endothelial cells leads to increased paracellular permeability, allowing leukocyte entry into inflamed brain tissue and also contributing to edema formation. The current study dissects the mechanisms by which a chemokine, CCL2, induces TJ disassembly. It investigates the potential role of selective internalization of TJ transmembrane proteins (occludin and claudin-5) in increased permeability of the brain endothelial barrier in vitro. To map the internalization and intracellular fate of occludin and claudin-5, green fluorescent protein fusion proteins of these TJ proteins were generated and imaged by fluorescent microscopy with simultaneous measurement of transendothelial electrical resistance. During CCL2-induced reductions in transendothelial electrical resistance, claudin-5 and occludin became internalized via caveolae and further processed to early (EEA1+) and recycling (Rab4+) endosomes but not to late endosomes. Western blot analysis of fractions collected from a sucrose gradient showed the presence of claudin-5 and occludin in the same fractions that contained caveolin-1. For the first time, these results suggest an underlying molecular mechanism by which the pro-inflammatory chemokine CCL2 mediates brain endothelial barrier disruption during CNS inflammation.
ChemInform Abstract: Benzylic Bromination of Alkylbenzenes with Sodium Bromate‐ Bromotrimethylsilane. (1995)

Abstract ChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 100 leading journals. To access a ChemInform Abstract of an article which was published elsewhere, please select a “Full Text” option. The original article is trackable via the “References” option.
Specificity of substrate recognition by type II dehydroquinases as revealed by binding of polyanions1 (2002)

The interactions between the polyanionic ligands phosphate and sulphate and the type II dehydroquinases from Streptomyces coelicolor and Mycobacterium tuberculosis have been characterised using a combination of structural and kinetic methods. From both approaches, it is clear that interactions are more complex in the case of the latter enzyme. The data provide new insights into the differences between the two enzymes in terms of substrate recognition and catalytic efficiency and may also explain the relative potencies of rationally designed inhibitors. An improved route to the synthesis of the substrate 3-dehydroquinic acid (dehydroquinate) is described.
Protein C Nagoya, an elongated mutant of protein C, is retained within the endoplasmic reticulum and is associated with GRP78 and GRP94 (1996)

Protein C Nagoya, an elongated variant of the human protein C, is retained and degraded within the cells in which it is produced (Yamamoto et al, J Clin Invest 90:2439, 1992). To determine the subcellular localization of the protein C Nagoya, the recombinant protein C bearing this mutation was expressed in Chinese hamster ovary (CHO) cells. The mutant protein C was not secreted from the cells and remained susceptible to endo-beta-N-acetylglucosaminidase H (endo H). Immunoelectron microscopy indicated that protein C Nagoya was retained in the endoplasmic reticulum (ER), whereas wild-type protein C was observed in both the ER and the Golgi apparatus. Metabolic radiolabeling with [35S] methionine in combination with chemical cross-linking showed that the protein C Nagoya existed in the ER as a complex with 78-kD glucose-regulated protein (GRP78) and 94-kD glucose-regulated protein (GRP94). Because both GRP78 and GRP94 associate to a far lesser degree with wild-type protein C than with protein C Nagoya, our data suggest that both stress proteins function as molecular chaperones and work in concert with the folding and assembly of protein C. These findings extend our understanding the molecular pathogenesis of protein C deficiency.
Carboxypeptidase D is the only enzyme responsible for antibody C‐terminal lysine cleavage in Chinese hamster ovary (CHO) cells (2016)

Heterogeneity of C-terminal lysine levels often observed in therapeutic monoclonal antibodies is believed to result from the proteolysis by endogenous carboxypeptidase(s) during cell culture production. Identifying the responsible carboxypeptidase(s) for C-terminal lysine cleavage in CHO cells would provide valuable insights for antibody production cell culture processes development and optimization. In this study, five carboxypeptidases, CpD, CpM, CpN, CpB, and CpE, were studied for message RNA (mRNA) expression by qRT-PCR analysis in two most commonly used blank hosts (DUXB-11 derived DHFR-deficient DP12 host and DHFR-positive CHOK1 host), used for therapeutic antibody production, as well an antibody-expressing cell line derived from each host. Our results showed that CpD had the highest mRNA expression. When CpD mRNA levels were reduced by RNAi (RNA interference) technology, C-terminal lysine levels increased, whereas there was no obvious change in C-terminal lysine levels when a different carboxypeptidase mRNA level was knocked down suggesting that carboxypeptidase D is the main contributor for C-terminal lysine processing. Most importantly, when CpD expression was knocked out by CRISPR (Clustered Regularly Interspaced Short Palindromic Repeats) technology, C-terminal lysine cleavage was completely abolished in CpD knockout cells based on mass spectrometry analysis, demonstrating that CpD is the only endogenous carboxypeptidase that cleaves antibody heavy chain C-terminal lysine in CHO cells. Hence, our work showed for the first time that the cleavage of antibody heavy chain C-terminal lysine is solely mediated by the carboxypeptidase D in CHO cells and our finding provides one solution to eliminating C-terminal lysine heterogeneity for therapeutic antibody production by knocking out CpD gene expression. Biotechnol. Bioeng. 2016;113: 2100-2106. © 2016 Wiley Periodicals, Inc.
Epithelial cells secrete the chemokine interleukin-8 in response to bacterial entry (1993)

Bacterial invasion of mucosal surfaces results in a rapid influx of polymorphonuclear leukocytes. The chemotactic stimulus responsible for this response is not known. Since epithelial cells are among the first cells entered by many enteric pathogens, we investigated the ability of epithelial cells to provide an early signal for the mucosal inflammatory response through the release of chemotactic cytokines. As shown herein, the chemokine interleukin-8 (IL-8), a potent chemoattractant and activator of polymorphonuclear leukocytes, was secreted by intestinal and cervical epithelial cells in response to bacterial entry. Moreover, a variety of different bacteria, including those that remain inside phagosomal vacuoles, e.g., Salmonella spp., and those that enter the cytoplasm, e.g., Listeria monocytogenes, stimulated this response. Increased IL-8 mRNA levels could be detected within 90 min after infection. Neither bacterial lipopolysaccharide nor noninvasive bacteria, including Escherichia coli and Enterococcus faecium, induced an IL-8 response. Moreover, tumor necrosis factor alpha, which is known to be expressed by some epithelial cells, was not detected in the culture supernatants after bacterial entry, and addition of anti-tumor necrosis factor alpha antibodies had no effect on the IL-8 response following bacterial entry. These data suggest the novel concept that epithelial cells serve as an early signaling system to host immune and inflammatory cells in the underlying mucosa following bacterial entry.
Procedure, applications, and outcomes of autologous fat grafting (2017)

To systematically review the procedure, applications, and outcomes of autologous fat grafting, a promising technique with various clinical applications. Literature review of publications concerning autologous fat grafting. Since its introduction, lipofilling has become increasingly popular; however, its results are variable and unpredictable. Several modifications have been made to the procedures of fat harvesting, processing, and injecting. Surgical excision and low negative-pressure aspiration with large-bore cannulas minimize adipocyte damage during fat harvesting. The “wet” method of fat harvesting involves fluid injection at the donor site and facilitates lipoaspiration while minimizing pain and ecchymosis. For fat processing, centrifugation at a low speed is preferable to high-speed centrifugation, gravity separation or filtration. Fat injection at the recipient site should be performed using small-gauge cannulas in a fanning out pattern over multiple sessions, rather than a single session. Fat grafts exhibit not only dermal filler properties but also regenerative potential owing to the presence of stem cells in fat tissue. Thus, the clinical applications of autologous fat grafting include correction of secondary contour defects after breast reconstruction, release of painful scar contractures, and treatment of burn scars and radiodermatitis. Lipofilling is also used in aesthetic surgery, such as facial and hand rejuvenation, augmentation rhinoplasty, and breast and gluteal augmentation. The complications of lipofilling are minimal and include bruising, swelling, pain, infection, necrosis, and calcification. Lipofilling is a low-risk procedure that can be used to correct soft-tissue defects in the face, trunk, and extremities, with minimal discomfort for patients.
Parathyroid hormone reduces acute ischemic injury of the myocardium. (1986)

Synthetic parathyroid hormone (PTH), particularly the molecular fragment containing amino acids one to 34 (1-34), has been shown to produce coronary vasodilation and systemic vasodilation without tachycardia. On this basis, we tested the hypothesis that PTH(1-34) would favorably affect oxygen balance in acutely ischemic myocardium and reduce the extent of injury after coronary occlusion. Experiments were done upon the left anterior descending coronary artery which was ligated through a thoracotomy in anesthetized dogs subjected to ligation of the left anterior descending coronary artery. After 30 minutes of ischemia, the dogs were randomly assigned to either a group which received an intracoronary infusion of 0.008 nanomoles per kilogram of body weight per minute of PTH (1-34) for ten minutes at intervals of 30 minutes or a control group which received intracoronary saline solution. PTH(1-34) increased circumflex artery blood flow 290 +/- 62 per cent (p less than 0.005) and coronary venous return from the ischemic area 190 +/- 12 per cent (p less than 0.005) while reducing mean arterial pressure 12.5 +/- 1.7 per cent (p less than 0.05) without a change in the heart rate. These hemodynamic changes resulted in a 54.3 +/- 3.7 per cent (p less than 0.005) decrease in ischemic myocardial oxygen extraction and a reduction of infarct size (25 +/- 5 per cent of myocardium at risk in treated versus 75 +/- 10 per cent in the control group). It is concluded that PTH given after coronary artery occlusion increases collateral blood flow and oxygen supply to the ischemic myocardium while reducing oxygen requirements. Thus, PTH may offer significant protection for the acutely ischemic myocardium.
UNDER-RESUSCITATION OF NEAR-LETHAL UNCONTROLLED HEMORRHAGE: EFFECTS ON MORTALITY AND END-ORGAN FUNCTION AT 72 HOURS (2001)

Laboratory studies of uncontrolled hemorrhage demonstrate that under resuscitation (UR) improves short-term survival, but at the expense of tissue perfusion. The long-term effects of UR have not been studied. The purpose of this study was to evaluate survival and the incidence of end-organ injury (EOI), 3 days following moderate and severe UR of uncontrolled hemorrhage. Thirty-four swine (14-24 kg) were assigned to 4 groups: Groups I, II, and III were hemorrhaged to a pulse pressure = 5 mmHg in the presence of a 4-mm aortic tear: Group I (control; n = 6) was not resuscitated; Group II (n = 11) was severely under resuscitated (MAP [mean arterial pressure] = 40 mmHg) for 75 min; Group III (n = 9) was moderately under resuscitated (MAP = 60 mmHg) for 75 min. After 75 min, the aortotomy was repaired, and animals were resuscitated to baseline physiologic parameters. Group IV (sham; n = 8) was instrumented, but not hemorrhaged. Seventy-two-hour mortality was 100%, 36%, 22%, and 0% for Groups I through IV (P = .001 Fisher's exact). Cardiac indices, serum bicarbonate, and systemic oxygen delivery were significantly lower in Group II as compared to Group III during the 75 min of UR (P < 0.05; repeated measures ANOVA). By 72 h, physiologic parameters in surviving animals had returned to baseline levels. Measures of kidney, liver, neurologic, and pulmonary function did not change from baseline. There was no histologic evidence of EOI. In this model, 75 min of UR did not result in EOI. There was a trend toward greater survival, and tissue perfusion was better preserved with moderate as compared to severe UR.