gebhart/patrepeval huggingface dataset:
A review of the evidence for the effectiveness of sensory stimulation treatment for coma and vegetative states (1993)

Abstract This paper reviews fourteen studies that evaluate the efficacy of sensory stimulation treatment for patients in coma and vegetative states. The studies are divided according to whether they use outcome statistics, behaviour change, or physiological measures as their means of evaluation. There is also a review of the methodological considerations incumbent in research in this area. The authors conclude that sensory stimulation can alter behaviour in the unconscious patient and can reduce the duration of acute coma, and that further research is certainly warranted for economic as well as humanitarian reasons.
The collagenous domains of macrophage scavenger receptors and complement component C1q mediate their similar, but not identical, binding specificities for polyanionic ligands. (1993)

Macrophage scavenger receptors have been implicated in the development of atherosclerosis and other macrophage-associated functions, including host defense. The mechanism by which these receptors bind a wide array of polyanions, such as acetylated low density lipoprotein (Ac-LDL), with high affinity has not yet been elucidated; however, it has been proposed that the positively charged extracellular collagenous domain of scavenger receptors plays a key role in ligand binding. To test this proposal, we generated truncation mutants of the bovine and murine scavenger receptors and studied their expression in transiently transfected COS cells. These mutants contain only 8 (bovine) or 5 (murine) of the 24 Gly-X-Y tripeptide repeats found in the collagenous domains of the full-length receptors. Immunochemical analyses established that the truncation of the bovine scavenger receptor did not interfere significantly with its synthesis, trimerization, post-translational processing, intracellular transport, surface expression, or stability. However, unlike their full-length counterparts, the truncated bovine and murine receptors were unable to bind Ac-LDL. Thus, the collagenous domain was necessary for normal ligand binding. In addition, cotransfection of the expression vector for the truncated bovine scavenger receptor with that for the full-length receptor resulted in dramatically reduced activity of the full-length construct (dominant negative effect). A ligand bead-binding assay was used to show that the isolated collagenous domain from a different protein, complement component C1q, could bind a wide variety of polyanions with a specificity which was similar, but not identical, to that of scavenger receptors. These results suggest that the collagenous domain of the scavenger receptor is both necessary and sufficient to determine the broad binding specificity that characterizes this unusual receptor. Scavenger receptors and C1q, along with the mannose-binding protein, conglutinin, and lung surfactant apoprotein A, help define a set of proteins which all contain short collagenous domains and which all appear to participate in host defense. Their short collagenous domains may contribute significantly to their host-defense functions.
The Effects of Heparin Coating of Oxygenator Fibers on Platelet Adhesion and Protein Adsorption (1999)

Platelet adhesion on the cardiopulmonary bypass oxygenator membrane is associated with impaired hemostasis. We investigated the effects of heparin coating of the oxygenator membrane on protein adsorption and platelet adhesion on the surface. Noncoated and heparin-coated polypropylene membranes were incubated in whole blood with small- (1 U/mL) or large-dose (5 U/mL) heparin as an anticoagulant for 3 h at 37°C. The amount of platelets adhering on each fiber was assessed by using enzyme immunoassays using monoclonal antibodies directed against CD42b (GP Ib) and CD61 (GP IIb/IIIa). Platelet activation was assessed by measuring plasma guanosine monophosphate 140 levels. The amount and composition of the adsorbed proteins on the surface were analyzed by using a bicinchoninic acid protein assay and by using sodium dodecyl sulfate-polyacrylamide gel electrophoresis and Western blotting technique. The heparin coating of the fibers significantly reduced platelet adhesion on the surface. However, platelet activation was reduced by heparin coating only with small-dose heparinization. The adsorption of platelet adhesive proteins such as fibrinogen and von Willebrand factor was not altered, whereas that of fibronectin was increased by heparin coating. We conclude that heparin coating of the oxygenator fibers can decrease platelet adhesion without affecting adsorption of major adhesive proteins. Surface heparin coating is associated with an increased fibronectin adsorption on the fibers. Implications Heparin coating can reduce platelet adhesion and activation in the presence of small-dose heparinization, potentially reducing the inflammatory response and activation of thrombosis and fibrinolysis.
Natural killer cells and natural killer T cells (2000)

NK cells are important in protecting against viral infections, and they may regulate the immune response. They are activated by hematopoietic blasts and pose a barrier to bone marrow transplantation. They are also abundant in the pregnant uterine decidua, although their role there is unknown. NK cells are normally inhibited from responding to host cells by inhibitory receptors that recognize self class I MHC antigens. There is evidence that NK cells may be important in the regulation of autoimmunity, but there is even stronger evidence that NKT cells regulate autoimmunity. The mechanisms by which these cells are activated and by which they regulate other cells are now being understood at the molecular level.
Chimeric NKG2D T Cells Require Both T Cell- and Host-Derived Cytokine Secretion and Perforin Expression to Increase Tumor Antigen Presentation and Systemic Immunity (2009)

Treatment of mice bearing established ovarian tumors with T cells expressing chimeric NKG2D receptors (chNKG2D) develop protective host immune responses to tumor Ags. In this study, the mechanisms that chNKG2D T cells require to induce host immunity against ovarian tumors and which of the host immune cells are involved in tumor elimination were determined. Treatment with chNKG2D T cells led to a sustained, increased IFN-gamma production by host NK, CD4(+), and CD8(+) T cells in the spleen and at the tumor site and this continued for many weeks after T cell injection. Tumor Ag presentation was enhanced in chNKG2D T cell-treated mice, and there were greater numbers of tumor-specific T cells at the tumor site and in draining lymph nodes after treatment with chNKG2D T cells. The increase in host cell cytokine secretion and Ag presentation was dependent on chNKG2D T cell-derived perforin, IFN-gamma, and GM-CSF. Host immune mechanisms were involved in tumor elimination because inhibition of tumor growth was limited in mice that lacked perforin, IFN-gamma, NK cells, or T and B cells (Rag1(-/-)). There was no role for host-derived GM-CSF or CD1-dependent NKT cells, because mice deficient in these were able to clear tumors as well as treated wild-type B6 mice. In summary, chNKG2D T cells required both cytotoxicity and cytokine secretion as well as the participation of host immune cells for development of a host antitumor immune response and complete efficacy.
Production of human monoclonal IgG antibodies against Rhesus (D) antigen. (1984)

An Epstein-Barr virus (EBV)-transformed human B-cell line ( LB4r ) producing anti-Rhesus [Rho(D) antigen] antibody was fused with a non-immunoglobulin-producing mouse-human heteromyeloma ( SHM - D33 ) and selected in hypoxanthine/aminopterin/thymidine medium containing 0.5 microM ouabain. Surviving hybrids found to secrete specific anti-Rho(D) antibody were cloned by limiting dilution. Two clones (D4-B2 and E10-C1) producing high levels (12 and 20 micrograms/ml per 10(6) cells per 24 hr, respectively) of monospecific antibody (IgG3, lambda chain) were selected for expansion and further characterization. Compared to the parental cell line ( LB4r ), these hybridoma cell lines presented several advantages: antibody production was increased 10-fold, cloning efficiency was improved, and the EBV genome was not retained. Antibody production has been stable for greater than 8 months. These human monoclonal anti-Rho(D) antibodies have demonstrated utility in routine blood-group typing. They may also prove useful in the biochemical and genetic characterization of the Rh antigen system. Most important, they offer a source of Rh-immune globulin for the prevention of Rh immunization and alloimmune hemolytic disease of the newborn.
Irreversible enzyme inhibitors. 188. Inhibition of mammalian thymidine phosphorylase (1971)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTIrreversible enzyme inhibitors. 188. Inhibition of mammalian thymidine phosphorylaseB. R. Baker and James L. KelleyCite this: J. Med. Chem. 1971, 14, 9, 812–816Publication Date (Print):September 1, 1971Publication History Published online1 May 2002Published inissue 1 September 1971https://pubs.acs.org/doi/10.1021/jm00291a009https://doi.org/10.1021/jm00291a009research-articleACS PublicationsRequest reuse permissionsArticle Views102Altmetric-Citations16LEARN 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
Cardiac remodelling and myocardial contractility in patients with congestive heart failure treated with furosemide and enalapril. (1991)

Eleven patients with congestive heart failure class II-IV (NYHA) caused by ischemic heart disease were studied before and three months after adding enalapril to their treatment with furosemide. After an infarction the heart dilates gradually, mainly as a result of slippage of myocardial fiber bundles. It is known that the addition of an ACE-inhibitor to the medical treatment unloads the heart and gradually, within a period of 3 months, reduces heart size. Objectives of this study were to demonstrate remodelling by recording diastolic pressure-volume relations before and after treatment. The study addresses the question of whether regression of dilation, induced by the ACE-inhibitor treatment, improves the oxygen supply-demand ratio and, as a result, the contractility of the heart muscle. Treatment resulted in a reduction of vascular resistance (1479 to 1182 dyn.s.cm-5, p less than 0.05) and of the left ventricular end-diastolic (130 to 108 ml per m2 body surface area, p less than 0.05) and end-systolic (102 to 81 ml per m2 body surface area, p less than 0.01) volume index. The slope of the end-systolic pressure-volume relation, measured using vena cava occlusion and beat-to-beat recording of pressure and volume loops, remained unchanged. Indices of oxygen-supply demand ratio such as a drop of ejection fraction during exercise and parameters of active diastolic relaxation also did not change. Addition of an ACE-inhibitor induces regression of ventricular dilation, but no indications were found that it improves the condition of the cardiac muscle.
Allele-Specific Silencing of Mutant Myh6 Transcripts in Mice Suppresses Hypertrophic Cardiomyopathy (2013)

Dominant mutations in sarcomere proteins such as the myosin heavy chains (MHC) are the leading genetic causes of human hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy. We found that expression of the HCM-causing cardiac MHC gene (Myh6) R403Q mutation in mice can be selectively silenced by an RNA interference (RNAi) cassette delivered by an adeno-associated virus vector. RNAi-transduced MHC(403/+) mice developed neither hypertrophy nor myocardial fibrosis, the pathologic manifestations of HCM, for at least 6 months. Because inhibition of HCM was achieved by only a 25% reduction in the levels of the mutant transcripts, we suggest that the variable clinical phenotype in HCM patients reflects allele-specific expression and that partial silencing of mutant transcripts may have therapeutic benefit.
Marine natural products (1986)

D. J. Faulkner, Nat. Prod. Rep., 1986, 3, 1 DOI: 10.1039/NP9860300001
Wee1 Rather Than Plk1 Is Inhibited by AZD1775 at Therapeutically Relevant Concentrations (2019)

Wee1 kinase is an inhibitor of cyclin-dependent kinase (cdk)s, crucial cell cycle progression drivers. By phosphorylating cdk1 at tyrosine 15, Wee1 inhibits activation of cyclin B-cdk1 (Cdk1), preventing cells from entering mitosis with incompletely replicated or damaged DNA. Thus, inhibiting Wee1, alone or in combination with DNA damaging agents, can kill cancer cells by mitotic catastrophe, a tumor suppressive response that follows mitosis onset in the presence of under-replicated or damaged DNA. AZD1775, an orally available Wee1 inhibitor, has entered clinical trials for cancer treatment following this strategy, with promising results. Recently, however, AZD1775 has been shown to inhibit also the polo-like kinase homolog Plk1 in vitro, casting doubts on its mechanism of action. Here we asked whether, in the clinically relevant concentration range, AZD1775 inhibited Wee1 or Plk1 in transformed and non-transformed human cells. We found that in the clinically relevant, nanomolar, concentration range AZD1775 inhibited Wee1 rather than Plk1. In addition, AZD1775 treatment accelerated mitosis onset overriding the DNA replication checkpoint and hastened Plk1-dependent phosphorylation. On the contrary selective Plk1 inhibition exerted opposite effects. Thus, at therapeutic concentrations, AZD1775 inhibited Wee1 rather than Plk1. This information will help to better interpret results obtained by using AZD1775 both in the clinical and experimental settings and provide a stronger rationale for combination therapies.
Numerical study of a simple transcranial focused ultrasound system applied to blood-brain barrier opening (2010)

In this paper, we investigate the focalization properties of single-element transducers at low frequencies (300 to 1000 kHz) through primate and human skulls. The study addresses the transcranial targeting involved in ultrasound- induced blood-brain barrier (BBB) opening with clinically relevant targets such as the hippocampus and the basal ganglia, which are typically affected by early Alzheimer's and Parkinson's disease, respectively. A finite-difference, timedomain simulation platform is used to solve the 3-D linear acoustic wave equation with CT-based acoustic maps of the skulls. The targeted brain structures were extracted from 3-D brain atlases registered with the skulls and used to virtually position and orient the transducers. The effect of frequency is first investigated and the targeting of the different structures is then tested. The frequency of 500 kHz provided the best tradeoff between phase aberrations and standing wave effects in the human case, whereas the frequency of 800 kHz was most suitable in the case of the primate skull. A fast periodic linear chirp method was developed and found capable of reducing the standing wave effects. Such a simple, affordable, and convenient system is concluded to be feasible for BBB opening in primates and humans and could thus allow for its broader impact and applications.
In Vitro Selection of Protein-Binding DNA Aptamers as Ligands for Biosensing Applications (2009)

Aptamers are single-stranded functional nucleic acids that possess cognate ligand recognition capability. These functional nucleic acids have been used for biosensing of a variety of ligands. Aptamers are isolated by "in vitro selection" or SELEX from random-sequence nucleic acid pools. For example, DNA aptamers that recognize a protein can be generated by applying a DNA library to an affinity column containing the protein target and retrieving the bound sequences after wash. These sequences are amplified and used for a new round of binding and amplification. The identity of enriched sequences are subsequently revealed by cloning and sequencing. The binding of individual aptamers to the protein can be confirmed by techniques such as gel mobility shift. This chapter will provide a detailed protocol for isolating protein-binding DNA aptamers.
Making brain–machine interfaces robust to future neural variability (2016)

A major hurdle to clinical translation of brain-machine interfaces (BMIs) is that current decoders, which are trained from a small quantity of recent data, become ineffective when neural recording conditions subsequently change. We tested whether a decoder could be made more robust to future neural variability by training it to handle a variety of recording conditions sampled from months of previously collected data as well as synthetic training data perturbations. We developed a new multiplicative recurrent neural network BMI decoder that successfully learned a large variety of neural-to-kinematic mappings and became more robust with larger training data sets. Here we demonstrate that when tested with a non-human primate preclinical BMI model, this decoder is robust under conditions that disabled a state-of-the-art Kalman filter-based decoder. These results validate a new BMI strategy in which accumulated data history are effectively harnessed, and may facilitate reliable BMI use by reducing decoder retraining downtime.
Novel Serine Proteases Encoded by Two Cytotoxic T Lymphocyte-Specific Genes (1986)

Genes that are expressed exclusively in cytotoxic T cells should encode proteins that are essential for target cell lysis in cell-mediated immune responses. The sequences of two cytotoxic T lymphocyte-specific complementary DNA's (cDNA's) suggest that the two genes encode serine proteases. A full-length cDNA corresponding to one of the genes was isolated and sequenced. The predicted protein resembles serine proteases in that it includes all the residues that form the catalytic triad of the active site of serine proteases. Moreover, it has sequence characteristics thought to occur only in rat mast cell protease type II. These results are in accord with the view that a protease cascade plays a key role in cytotoxic T-cell activation.
14-3-3η Autoantibodies: Diagnostic Use in Early Rheumatoid Arthritis (2015)

14-3-3η autoantibodies, alone and in combination with the 14-3-3η protein, RF, and/or ACPA identified most patients with early RA.
Functional Requirement of Plant Farnesyltransferase during Development in Arabidopsis (2000)

Arabidopsis era1 was identified as an abscisic acid-hypersensitive mutant caused by disruptions or deletions of the gene for the beta subunit (AtFTB) of farnesyltransferase (FTase). The heterodimeric enzyme catalyzes the covalent attachment of the 15-carbon farnesyl diphosphate to the C terminus of regulatory proteins and is essential for growth in yeast. The first disruption of FTB in a multicellular context revealed several developmental and growth regulatory processes that require the function of FTase. The lack of FTase activity in the Arabidopsis era1-2 FTB deletion mutant resulted in enlarged meristems and organs, supernumerary organs in floral whorls, arrested development of axillary meristems, late flowering, and homeotic transformations of flowers. Complementation of era1-2 with LeFTB, the tomato gene for the beta subunit of FTase, restored a normal phenotype and confirmed that the lesion is in AtFTB alone. The effect of this lesion on control of meristem size and on developmental processes suggests the involvement of regulatory proteins that require farnesylation for their function. At least three distinct processes that require the function of FTase were identified: regulation of cellular differentiation in the meristems, meristem maintenance, and regulation of flower development. Together, these results provide a basis for future studies on the involvement of FTase in specific developmental processes and for structure-function analysis of FTase in vivo.
Detecting moving objects, ghosts, and shadows in video streams (2003)

Background subtraction methods are widely exploited for moving object detection in videos in many applications, such as traffic monitoring, human motion capture, and video surveillance. How to correctly and efficiently model and update the background model and how to deal with shadows are two of the most distinguishing and challenging aspects of such approaches. The article proposes a general-purpose method that combines statistical assumptions with the object-level knowledge of moving objects, apparent objects (ghosts), and shadows acquired in the processing of the previous frames. Pixels belonging to moving objects, ghosts, and shadows are processed differently in order to supply an object-based selective update. The proposed approach exploits color information for both background subtraction and shadow detection to improve object segmentation and background update. The approach proves fast, flexible, and precise in terms of both pixel accuracy and reactivity to background changes.
Correlation between expression and differentiation of endocan in colorectal cancer (2008)

瞄准：调查 endocan 的表示频率在渲染表面的癌症并且分析在 endocan 表示和临床的参数之间并且到学习的关系在颜色的 endocan 的角色表面的致癌作用。方法：在 72 肿瘤织物的 endocan 的表示象在 27 件正常粘膜织物样品一样颜色取样表面的癌症用原位杂交被分析，织物上的免疫组织化学微数组，西方的污点和反向抄本的聚合酶链反应(RT-PCR ) 。结果：endocan 的表示比在癌的组织样品在正常冒号和直肠组织样品是更高的(mRNA =92.6% ，蛋白质 =36%) ，并且在表面的癌症组织取样的颜色是更低的(mRNA =70.4% ，蛋白质 =36.1%) 。没有关联在染色象性别，年龄，肿瘤尺寸和 TNM 舞台那样的紧张和临床的参数之间被发现。然而， endocan 的表示断然在肤色与织物区别被相关表面的癌症。结论：endocan 的表示是下面调整的在渲染表面的癌症并且断然在肤色与织物区别被相关表面的癌症，建议 endocan 的表示与肤色的开发和区别被联系表面的癌症。
AUTOFLUORESCENCE IMAGING COLONOSCOPY IN ULCERATIVE COLITIS: COMPARISON WITH CONVENTIONAL AND NARROW‐BAND IMAGING COLONOSCOPY (2007)

Autofluorescence imaging (AFI) endoscopy is a procedure to demonstrate gastrointestinal neoplasia and inflammation as colored areas distinct from the surrounding normal tissue. In the present pilot study AFI colonoscopy findings in patients with ulcerative colitis (UC) were analyzed. Ten patients with UC were examined using conventional colonoscopy, followed by AFI colonoscopy and narrow band imaging (NBI) colonoscopy. Images under AFI colonoscopy were classified into high AF (green or white) and low AF (magenta). NBI colonoscopy determined vasculature, either into regular, irregular or obscure mucosal vascular pattern. A total of 48 colorectal segments were assessed with the three modes of colonoscopy. The AF was high in 100% of the segments with normal mucosa or with quiescent disease and in 44% of the segments with active mucosa ( P &lt; 0.001). Mucosal vascular pattern under NBI was obscure more frequently in low‐AF segments than in high‐AF segments ( P &lt; 0.001). Inflammatory infiltrate was more severe and crypt distortion was more frequent in the latter than in the former ( P &lt; 0.001). There were trends towards more frequent obscure vascular pattern and more severe inflammation in active segments with low AF than in those with high AF mucosa. These findings suggest that AF status determined by AFI colonoscopy may be a clue for subclassification of active UC.