gebhart/patrepeval huggingface dataset:
A novel method of inducing muscle cramps using repetitive magnetic stimulation (2000)

The lack of a practical model has hampered attempts to study the pathophysiology of muscle cramps. We investigated the feasibility, efficacy, and reproducibility of repetitive magnetic stimulation in producing experimental cramps. In 14 healthy subjects, the tibial nerve at the ankle was stimulated with a magnetic stimulator at rates beginning at 4 Hz to a maximum of 20 Hz. The frequency was gradually increased until a cramp was produced. Ten of 14 subjects demonstrated a muscle cramp. All subjects rated the discomfort of the procedure to be mild or moderate. Repeat testing yielded values that were highly reproducible. This technique holds promise for clinical studies and therapeutic trials.
Clinical presentation of heparin-induced thrombocytopenia. (1998)

Heparin-induced thrombocytopenia (HIT) is an immune-mediated adverse effect of heparin that is important because of its relatively high frequency and its strong association with paradoxic venous and arterial thrombosis. As confirmatory laboratory assays are not always immediately available, physicians usually must make initial diagnostic and treatment decisions based on the clinical presentation alone. Three characteristic features of HIT can be helpful in distinguishing it from other causes of thrombocytopenia: (1) timing of the onset of thrombocytopenia, namely, a platelet count decrease that begins between days 5 and 8 (inclusive) of beginning heparin treatment; (2) mild to moderate severity of the thrombocytopenia, with platelet counts only rarely less than 15 x 10(9)/L; and (3) the development of large-vessel venous or arterial thrombosis in association with thrombocytopenia, or any of a number of unusual characteristic sequelae of HIT (warfarin-associated venous limb gangrene, bilateral adrenal hemorrhagic infarction, heparin-induced skin lesions, or acute systemic reactions following intravenous heparin bolus). In contrast to other drug-induced immune thrombocytopenia syndromes, HIT rarely is associated with bleeding. HIT is relatively common, occurring in as many as 3% of patients who receive unfractionated (UF) heparin for 2 weeks. Between 30% and 75% of patients with HIT develop thrombosis; thus, about 1% of patients who receive a course of heparin develop HIT-associated thrombosis. The observation that HIT is less likely to occur with low-molecular-weight heparin (LMWH) suggests that HIT ultimately may be preventable.
Facile Fabrication Of Uniform Silica Films With Highly Luminescent Hydrophobic QDs Through Direct Phase Transfer (2012)

Hydrophobic CdSe/ZnS quantum dots (QDs) were embedded in a transparent functional silica film with thickness of 10-15 µm using a sol-gel method. Namely, the QDs were prepared through an organic synthesis using hexadecylamine as a capping agent. When partially hydrolyzed 3-aminopropyltrimethoxysilane (APS) sol was mixed with a toluene solution of the QDs, the ligand exchange occurred. With subsequent addition of pure H2O, the QDs were transferred into APS sol accompanied with a phase separation. The APS sol with the QDs was condensed to adjust its’ viscosity by the evaporation of solvents at room temperature. After that, functional SiO2 films with tunable QD concentrations and high photoluminescence (PL) efficiency were fabricated by a spin-coating strategy using the condensed APS sol with the QDs. The absorbance at first absorption peak of the QDs revealed a liner increase against the QD concentrations in these films. The PL peak wavelength and full width at half maximum of PL spectra of the QDs in these films remained unchange compared with their initial values in toluene. The QDs were mono-dispersed in these films according to transmission electron microscopy observation. Due to unique properties, these films are utilizable for further applications in optical and electronic devices.
Caenorhabditis elegans : modern biological analysis of an organism (1995)

Genetic and culture methods neurobiology cell biology and molecular biology genomics and informatics appendices - additional information and resources, Caenorhabditis genetics centre (laboratory designations), gene names and descriptions.
Focal adhesion kinase expression in oral cancers (1998)

Focal adhesion kinase expression appears to be increased in invasive and preinvasive oral cancers. It is speculated that enhanced expression of FAK may contribute to the aggressive phenotype of oral cancers.
Pathology reevaluation of the kociba et al. (1978) bioassay of 2,3,7,8‐TCDD: Implications for risk assessment (1991)

The chronic bioassay of 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) reported in 1978 by Kociba et al. has been considered to be the primary evidence supporting its carcinogenicity, and is the basis for most dioxin regulations in North America and Western Europe. Because the histopathological criteria for proliferative lesions in the rat liver have changed significantly since 1978, a reevaluation of the liver slides was conducted recently by an independent panel of pathologists. Using current National Toxicology Program criteria, their study showed, in contrast to the original findings, that about two-thirds fewer tumors were present in the livers of female Sprague-Dawley rats. The no-observed-adverse-effect level (NOAEL) for hepatocellular carcinomas was 0.01 micrograms/kg/d rather than 0.001 micrograms/kg/d, which had been reported in 1978. In light of these significant findings, a quantitative dose-response assessment of 2,3,7,8-TCDD was undertaken to predict the potential carcinogenic risks to humans. Risk-specific doses (RsDs) and cancer potency factors (CPFs) were calculated by applying the linearized multistage (LMS) model to the combined incidences of hepatocellular carcinomas and adenomas, classified in accordance with the 1990 histopathological criteria. Based on the weight of evidence regarding the mechanism of action of 2,3,7,8-TCDD, body weight rather than surface area was selected as the appropriate means for scaling rodent data to predict the human response. Using the survival-adjusted data, the RsD for a 1 in 1,000,000 (10(-6)) plausible upper bound (95%) lifetime incremental cancer risk was 370 fg/kg/d based only on the incidence of hepatocellular carcinomas, and 100 fg/kg/d when hepatocellular carcinomas and adenomas were combined. The corresponding upper-bound (95%) CPFs were 2700 and 9700 (mg/kg/d)-1, respectively. These results indicate that the carcinogenic risk to humans from exposure to 2,3,7,8-TCDD is at least 16-fold lower than previous estimates derived from the Kociba et al. (1978) bioassay.
Discovery, isolation, structure elucidation, and biosynthesis of U-106305, a cholesteryl ester transfer protein inhibitor from UC 11136 (1995)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTDiscovery, isolation, structure elucidation, and biosynthesis of U-106305, a cholesteryl ester transfer protein inhibitor from UC 11136M. S. Kuo, R. J. Zielinski, J. I. Cialdella, C. K. Marschke, M. J. Dupuis, G. P. Li, D. A. Kloosterman, C. H. Spilman, and V. P. MarshallCite this: J. Am. Chem. Soc. 1995, 117, 43, 10629–10634Publication Date (Print):November 1, 1995Publication History Published online1 May 2002Published inissue 1 November 1995https://pubs.acs.org/doi/10.1021/ja00148a004https://doi.org/10.1021/ja00148a004research-articleACS PublicationsRequest reuse permissionsArticle Views498Altmetric-Citations74LEARN 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
Quantitation of Major Human Cutaneous Bacterial and Fungal Populations (2010)

Because the human skin microbiota may play roles in the causation or modification of skin diseases, we sought to provide initial quantitative analysis from different cutaneous locations. We developed quantitative PCRs to enumerate the total bacterial and fungal populations, as well as the most common bacterial and fungal genera present in six locales, in eight healthy subjects. We used a set of primers and TaqMan MGB probes based on the bacterial 16S rRNA and fungal internally transcribed spacer region, as well as bacterial genus-specific probes for Propionibacterium, Corynebacterium, Streptococcus, and Staphylococcus and a fungal genus-specific probe for Malassezia. The extent of human DNA contamination of the specimen was determined by quantitating the human housekeeping GAPDH gene. The highest level of 16S rRNA copies of bacteria was present in the axilla (4.44 ± 0.18 log(10) copies/μl [mean ± standard error of the mean]), with normalization based on GAPDH levels, but the other five locations were similar to one another (range, 2.48 to 2.89 log(10) copies/μl). There was strong symmetry between the left and right sides. The four bacterial genera accounted for 31% to 59% of total bacteria, with the highest percent composition in the axilla and the lowest in the forearm. Streptococcus was the most common genus present on the forehead and behind the ear. Corynebacterium spp. were predominant in the axilla. Fungal levels were 1 to 2 log(10) lower than for bacteria, with Malassezia spp. accounting for the majority of fungal gene copies. These results provide the first quantitation of the site and host specificities of major bacterial and fungal populations in human skin and present simple methods for their assessment in studies of disease.
IL-2 and IL-12 Alter NK Cell Responsiveness to IFN-γ-Inducible Protein 10 by Down-Regulating CXCR3 Expression (2002)

Cytokine treatment of NK cells results in alterations in multiple cellular responses that include cytotoxicity, cytokine production, proliferation, and chemotaxis. To understand the molecular mechanisms underlying these responses, microarray analysis was performed and the resulting gene expression patterns were compared between unstimulated, IL-2, IL-2 plus IL-12, and IL-2 plus IL-18-stimulated NK92 cells. RNase protection assays and RT-PCR confirmed microarray predictions for changes in mRNA expression for nine genes involved in cell cycle progression, signal transduction, transcriptional activation, and chemotaxis. Multiprobe RNase protection assay also detected changes in the expression of CCR2 mRNA, a gene that was not imprinted on the microarray. We subsequently expanded our search for other chemokine receptor genes absent from the microarray and found an IL-2- and IL-12-dependent decrease in CXCR3 receptor mRNA expression in NK92 cells. A detailed analysis of CXCR3 expression in primary NK cells revealed that an IL-2 and an IL-12 together significantly decreased the CXCR3 receptor mRNA and receptor surface expression by 6 and 24 h of treatment, respectively. This decrease in receptor expression was associated with a significant reduction in chemotaxis in the presence of IFN-gamma-inducible protein-10. The decline in CXCR3 mRNA was due to transcriptional and posttranscriptional mechanisms as the addition of actinomycin D to IL-2- and IL-12-treated NK92 slightly altered the half-life of the CXCR3 mRNA. Collectively, these data suggest that IL-2 and IL-12 directly affect NK cell migratory ability by rapid and direct down-regulation of chemokine receptor mRNA expression.
Lithium transport at silicon thin film: Barrier for high-rate capability anode (2010)

The major hurdle that retards the practical application of nanostructured silicon anode in rechargeable Li-ion batteries is the capacity retention during lithiation/delithiation processes, especially at high current rate (e.g., >5 C). Since fast Li transport in the electrode is the essential of high-rate capability, the rate-limiting step exists during Li transport process and needs to be determined. We here investigate Li transport properties of Si thin film anode by first-principles calculation and find that high intrinsic energy barrier (0.88 eV) of Li surface intercalation retards fast Li transport. However, this energy barrier can be efficiently reduced by surface modification, e.g., P or Al doping. The present results should shed light on designing Si anode of Li-ion batteries with high-rate capability.
Proinflammatory activation pattern of human umbilical vein endothelial cells induced by IL‐1β, TNF‐α, and LPS (2010)

Endothelial cells play a critical role in inflammation by responding to several endogenous and exogenous proinflammatory stimuli. The three most studied factors that provide inflammatory signals to endothelial cells are lipopolysaccharide (LPS), tumor necrosis factor (TNF)-α, and interleukin (IL)-1β; however, their effects on endothelial cells were thoroughly compared at the level of gene expression only. Therefore, our aim was to assess the differences in the signaling pathways, adhesion molecules, and cytokines induced by proinflammatory factors in human umbilical vein endothelial cells (HUVEC). In this study, we demonstrated that signaling of LPS was less effective than that of IL-1β, and was significantly slower than that ofTNF-α and IL-1β, which can be partially explained by the special localization of Toll-like receptor 4 (TLR4). We showed that TLR4 is mainly localized in Golgi apparatus in HUVEC. The proinflammatory capacity of TNF-α was similar to that of IL-1β in inducing NF-κB nuclear translocation, while IL-1β was the strongest activator of MAPK pathways. Moreover, expression of E-selectin, IL-6, and IL-8 was induced most efficiently by IL-1β, while LPS and TNF-α had less effect, whereas we did not find such a difference in ICAM-1 and MCP-1 expression. Due to the higher induction of E-selectin and IL-8, IL-1β might have more important role in neutrophil recruitment than LPS and TNF-α. By above-mentioned parameters we identified a signaling and expression pattern for the three proinflammatory molecules. This pattern illustrates how complex a proinflammatory process can be, and may enable us to predict and compare the pathomechanism of various inflammatory diseases.
Camera calibration with lens distortion from low-rank textures (2011)

We present a simple, accurate, and flexible method to calibrate intrinsic parameters of a camera together with (possibly significant) lens distortion. This new method can work under a wide range of practical scenarios: using multiple images of a known pattern, multiple images of an unknown pattern, single or multiple image(s) of multiple patterns, etc. Moreover, this new method does not rely on extracting any low-level features such as corners or edges. It can tolerate considerably large lens distortion, noise, error, illumination and viewpoint change, and still obtain accurate estimation of the camera parameters. The new method leverages on the recent breakthroughs in powerful high-dimensional convex optimization tools, especially those for matrix rank minimization and sparse signal recovery. We will show how the camera calibration problem can be formulated as an important extension to principal component pursuit, and solved by similar techniques. We characterize to exactly what extent the parameters can be recovered in case of ambiguity. We verify the efficacy and accuracy of the proposed algorithm with extensive experiments on real images.
GA-101, a third-generation, humanized and glyco-engineered anti-CD20 mAb for the treatment of B-cell lymphoid malignancies. (2009)

Glycart Biotechnology AG, Genentech Inc, F Hoffmann-La Roche Ltd, Biogen Idec Inc and Chugai Pharmaceutical Co Ltd are developing GA-101, a third-generation, humanized and glyco-engineered anti-CD20 IgG1 mAb, for the potential treatment of B-cell malignancies. Compared with classic type I CD20 antibodies (eg, rituximab), GA-101 binds with high affinity to the CD20 type II epitope, resulting in the induction of antibody-dependent cytotoxicity that is 5- to 100-fold greater than observed upon treatment with rituximab. GA-101 also exhibits superior direct cell killing properties than rituximab. In preclinical studies, GA-101 was significantly more potent and effective in depleting B-cells than rituximab, and induced dose-dependent antitumor activity, complete tumor regression and improved long-term survival in xenograft mouse models of B-cell malignancy. In a phase I/II clinical trial, GA-101 had a similar safety profile to rituximab, and exhibited promising efficacy in patients with relapsed/refractory CD20-positive lymphoid malignancies. At the time of publication, phase I/II trials for GA-101 were ongoing in B-cell malignancies. Based on preclinical and preliminary clinical data, GA-101 appears to be a promising therapeutic agent for CD20-positive B-cell lymphoid malignances, including non-Hodgkin lymphomas and chronic lymphocytic leukemia.
Synthesis and Characterization of 3-Arylquinazolinone and 3-Arylquinazolinethione Derivatives as Selective Estrogen Receptor Beta Modulators (2006)

On the basis of the stucture of genistein, a new series of 3-arylquinazolines was prepared and tested for their estrogen receptor (ER) alpha and beta affinities. 5,7-Dihydroxy-3-(4-hydroxyphenyl)-4(3H)-quinazolinone (1aa) acts as an agonist on both ER subtypes. It has 62-fold higher binding affinity [IC(50)(ERbeta) = 179 nM] and 38-fold higher functional potency in a transcription assay [EC(50)(ERbeta) = 76 nM] with ERbeta than with ERalpha, thus improving upon the selectivity of genistein. All of the analogues showed preferential binding affinity for ERbeta. Many are also more potent in activating transcription by ERbeta than by ERalpha. Transformation of the C=O functionality at position 4 into a C=S group provided 5,7-dihydroxy-3-(4-hydroxyphenyl)-4(3H)-quinazolinethione (1ba), which acts as an agonist on both ER subtypes but has 56-fold higher binding affinity for ERbeta over ERalpha [IC(50)(ERbeta) = 47 nM] and 215-fold higher potency in the transcription assay [EC(50)(ERbeta) = 13 nM]. These ERbeta-selective compounds may represent valuable tools in understanding the differences in structure and biological function of ERbeta and ERalpha.
Lectins as Plant Defense Proteins (1995)

tively agglutinate erythrocytes of a particular human blood group (from the Latin verb legere, which means "to select").
Complete Reconstitution of Human IκB Kinase (IKK) Complex in Yeast (2001)

The IkappaB kinase (IKK) complex, composed of two catalytic subunits (IKKalpha and IKKbeta) and a regulatory subunit (IKKgamma), is the key enzyme in activation of nuclear factor kappaB (NF-kappaB). To study the mechanism and structure of the complex, we wanted to recombinantly express IKK in a model organism that lacks IKK. For this purpose, we have recombinantly reconstituted all three subunits together in yeast and have found that it is biochemically similar to IKK isolated from human cells. We show that there is one regulatory subunit per kinase subunit. Thus, the core subunit composition of IKKalpha.beta.gamma complex is alpha(1)beta(1)gamma(2), and the core subunit composition of IKKbeta.gamma is beta(2)gamma(2). The activity of the IKK complex (alpha+beta+gamma or beta+gamma) expressed in yeast (which lack NF-kappaB and IKK) is 4-5-fold higher than an equivalent amount of IKK from nonstimulated HeLa cells. In the absence of IKKgamma, IKKbeta shows a level of activity similar to that of IKK from nonstimulated HeLa cells. Thus, IKKgamma activates IKK complex in the absence of upstream stimuli. Deleting the gamma binding domain of IKKbeta or IKKalpha prevented IKKgamma induced activation of IKK complex in yeast, but it did not prevent the incorporation of IKKgamma into IKK and large complex formation. The possibility of IKK complex being under negative control in mammalian cells is discussed.
Pancreatic intraepithelial neoplasia – can we detect early pancreatic cancer? (2010)

Haugk B (2010) Histopathology 57, 503-514 Pancreatic intraepithelial neoplasia - can we detect early pancreatic cancer? Pancreatic cancer is one of the most lethal cancers, with an incidence equalling mortality. Pancreatic cancer is a heterogeneous group in which pancreatic ductal adenocarcinoma (PDAC) is the most common. It is now established that PDAC develops through stepwise progression from precursor lesions. Detection and treatment of these precursor lesions would allow curative treatment. Three precursor lesions for PDAC have been identified. Two of these - mucinous cystic neoplasms (MCNs) and intraductal papillary mucinous neoplasms (IPMNs) - are rare, radiologically detectable, cystic precursor lesions which can be cured if treated at the preinvasive stage. The third and most common precursor lesion has recently been defined as pancreatic intraepithelial neoplasia (PanIN). PanINs are microscopic lesions with no clinical correlate. They display a spectrum of cyto-architectural changes (PanIN-1, PanIN-2 and PanIN-3) mirrored in an increasing accumulation of molecular genetic changes, with PanIN-3 sharing many of the alterations with PDAC. Great advances in the understanding of pancreatic carcinogenesis have opened avenues for diagnosis and chemoprevention. However, access to the pancreas is limited, molecular tests are at the early stages and too little is known about the natural history of early PanINs to justify resection. Currently, screening focuses upon high-risk individuals only.
Some Features of Base Pair Mismatch and Heterology Repair in Escherichia coli (1987)

We have used artificially constructed heteroallelic heteroduplex molecules of bacteriophage lambda DNA to transfect Escherichia coli, and E. coli mutants deficient in various functions involved in the adenine methylation-directed mismatch repair system, MutL, MutS, MutH, and UvrD (MutU). Analysis of the allele content of single infective centers shows that this repair system often acts on several mismatches, separated by as many as 2000 bp, on one of the strands of a heteroduplex molecule. When the methyl-directed mismatch repair system is disabled by mutH or uvrD mutations, localized mismatch repair becomes prominent. This prominent localized repair that can result in separation of very closely linked markers requires the functions MutL and MutS, is independent of adenine methylation, and appears to reflect another mechanism of mismatch repair. Heterology-containing heteroduplex molecules with a deletion in one strand often escape processing. However, when the heterology includes the stem and loop structure of a transposon, Tn10, the transposon is lost.