gebhart/patrepeval huggingface dataset:
Current review on squamous intraepithelial lesions of the larynx (2008)

Squamous intraepithelial lesions (SILs) of the larynx, clinically usually defined as leukoplakia and chronic laryngitis, have remained the main controversial topic in laryngeal pathology for decades as regards classification, histological diagnosis and treatment. SILs are caused by smoking and alcohol abuse. There is also mounting evidence that gastroesophageal reflux is a potential aetiological factor. Human papillomavirus infection seems to play little if any role in laryngeal carcinogenesis. Histological classification of SILs is the central disputed aspect of these lesions. There are as yet no generally accepted criteria for histological grading of laryngeal SILs. Three currently used classifications of SILs are reviewed here: the dysplasia system, the Ljubljana classification and the binary system of squamous intraepithelial neoplasia. One of the most important issues of SILs is the risk of malignant transformation. Data in the literature are controversial because of inconsistent use of morphological criteria in different classifications. It is often difficult for clinicians to agree on the most appropriate therapeutic option for a particular grade of SIL that has been diagnosed. Transition from normal epithelium to SILs and squamous cell carcinoma is related to progressive accumulation of genetic changes leading to a clonal population of transformed epithelial cells. Despite extensive research into these genetic changes in laryngeal carcinogenesis, reliable genetic markers with diagnostic and prognostic value are still lacking.
Synthesis and screening for antideperessant activity of some aminoindanooxazolines, aminoindanooxazines, and aminoacenaphthoxazolines (1970)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTSynthesis and screening for antideperessant activity of some aminoindanooxazolines, aminoindanooxazines, and aminoacenaphthoxazolinesDonald L. Trepanier, H. Eldridge. Faith, and John N. EbleCite this: J. Med. Chem. 1970, 13, 4, 729–733Publication Date (Print):July 1, 1970Publication History Published online1 May 2002Published inissue 1 July 1970https://pubs.acs.org/doi/10.1021/jm00298a033https://doi.org/10.1021/jm00298a033research-articleACS PublicationsRequest reuse permissionsArticle Views126Altmetric-Citations3LEARN 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
Plasma Chemistry in Pulsed Electrical Discharge in Liquid (2009)

Electrical discharges in water have been studied for more than thirty years and during that time, significant progress has been made on the understanding and characterization of basic processes taking place in the water. The main molecular species formed by pulsed discharge in water are hydrogen, hydrogen peroxide and oxygen, although oxidative (hydroxyl radical) and reductive radicals (superoxide radical anion) that are produced by the discharge are responsible for the degradation of molecules. Streamer electrical discharge in water has been studied by numerous investigators and overall reactor design and pollutant degradation efficiency has been optimized. Our research group opened a new direction in plasma applications by conducting electrical discharges in relatively polar organic liquids. In that manner, we were able to produce Diamond-Like Carbon (DLC) film on the tip of a high voltage electrode by the electrical discharges in acetonitrile and dimethyl sulfoxide. We also studied electrical discharges in ionic liquids and above the ionic liquid surface, a new generation of solvents that are gaining more interest in both fundamental and applied research. The results indicated that the discharge inside the ionic liquid is destructive and leads to polymerization, whereas the discharge above the liquid surface is less destructive and could find possible applications.
Early morning akinesia in Parkinson's disease (1996)

We examined the effects of supplemental standard carbidopa/levodopa (Std-L) on early morning akinesia in patients with Parkinson's disease (PD) who were being treated with sustained-release carbidopa/levodopa (L-CR). We compared plasma dopa levels and clinical response in 15 PD patients after a dose of Std-L and L-CR (2 hours later) and after a dose of L-CR and placebo in a double-blind, placebo-controlled, crossover study. Plasma dopa levels, total motor score, walking time, and finger tapping time were assessed every 15 minutes for the first 2 hours and then every 30 minutes for the next 3 hours. The time of onset in clinical benefit was significantly earlier with Std-L (47 minutes, range 15 to 75 minutes) as the first dose as compared with L-CR (58 minutes, range 30 to 105 minutes). Similarly, there was a significant difference in the peak plasma dopa levels (Cmax) and the time to reach peak plasma dopa levels (Tmax) with administration of Std-L (Tmax 36 minutes; Cmax 1,501 micrograms/ml) as compared with L-CR (Tmax 111 minutes, Cmax 1,260 micrograms/ml). There was no significant difference in dyskinesias between the two treatment arms. An initial morning dose of Std-L alleviates the problem of delayed-onset clinical response that commonly occurs with L-CR.
Structure and Promoter Analysis of the Gene Encoding the Mouse Helix-Loop-Helix Factor HES-5 (1995)

HES-5 is a mammalian basic helix-loop-helix factor that has a distant sequence homology to the product of the Drosophila pair-rule gene hairy. HES-5 mRNA is present exclusively in the developing nervous system, but its level decreases as neural differentiation proceeds. In this study, to characterize the molecular mechanism of the neural-specific expression of HES-5 we isolated the mouse HES-5 gene. This gene consists of three exons, and Southern blot analysis shows that it is a single copy gene. The transcription initiation site, determined by primer extension and reverse transcriptase-mediated polymerase chain reaction, is located 26 nucleotides downstream of a TATAbox. Transient transfection analysis shows that the upstream region of the HES-5 gene can direct efficient expression in neural precursor cells and moderate expression in undifferentiated NCB20 neuroblastoma-brain hybrid cells but not in glioma or fibroblast cells. The moderate level of expression in NCB20 cells decreases when differentiation into neuron-like cells is induced. Further promoter analysis shows that this undifferentiated neural-specific expression is mediated by the multiple GC stretches present in the HES-5 promoter. Gel mobility shift analysis suggests the presence of a neural precursor cell-specific protein that binds to the GC stretches. These results raise the possibility that HES-5 expression in the developing nervous system is regulated by the GC stretch-binding protein.
ChemInform Abstract: Hydrogenation of Alkanes. Part 8. Hydrogenolysis of Propane, n‐Butane and Isobutane on Rhenium/Alumina Catalysts. (1991)

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.
Use of Ubiquitin Fusions to Augment Protein Expression in Transgenic Plants1 (1999)

A major goal of plant biotechnology is the production of genetically engineered crops that express natural or foreign proteins at high levels. To enhance protein accumulation in transgenic plants, we developed a set of vectors that express proteins and peptides as C-terminal translational fusions with ubiquitin (UBQ). Studies of several proteins in tobacco (Nicotiana tabacum) showed that: (a) proteins can be readily expressed in plants as UBQ fusions; (b) by the action of endogenous UBQ-specific proteases (Ubps), these fusions are rapidly and precisely processed in vivo to release the fused protein moieties in free forms; (c) the synthesis of a protein as a UBQ fusion can significantly augment its accumulation; (d) proper processing and localization of a protein targeted to either the apoplast or the chloroplast is not affected by the N-terminal UBQ sequence; and (e) single amino acid substitutions surrounding the cleavage site can inhibit in vivo processing of the fusion by Ubps. Noncleavable UBQ fusions of beta-glucuronidase became extensively modified, with additional UBQs in planta. Because multiubiquitinated proteins are the preferred substrates of the 26S proteasome, noncleavable fusions may be useful for decreasing protein half-life. Based on their ability to augment protein accumulation and the sequence specificity of Ubps, UBQ fusions offer a versatile way to express plant proteins.
Testing of droplet-based microelectrofluidic systems (2004)

Composite microsystems that integrate mechanical and fluidic components are fast emerging as the next generation of system-on-chip designs. As these systems become widespread in safety-critical biomedical applications, dependability emerges as a critical performance parameter. In this paper, we present a costeffective concurrent test methodology for droplet-based microelectrofluidic systems. We present a classification of catastrophic and parametric faults in such systems and show how faults can be detected by electrostatically controlling and tracking droplet motion. We then present tolerance analysis based on Monte-Carlo simulations to characterize the impact of parameter variations on system performance. To the best of our knowledge, this constitutes the first attempt to define a fault model and to develop a test methodology for droplet-based microelectrofluidic systems. 1
Visible electroluminescence from porous silicon (1992)

It is demonstrated that photoluminescent porous Si (PS) layers exhibit definitely visible electroluminescence (EL). The PS layers were formed by anodization of single-crystal nondegenerate p-type Si wafers in an HF solution. The experimental EL cells are of the form semitransparent metal/PS layer/p-type Si/Al electrode. These cells show a rectifying junction behavior. When the forward current density reaches a certain value, stable visible (orange) light is uniformly emitted through a semitransparent electrode. A possible explanation of this is the radiative transition due to electron and hole injection into quantized states in PS.
Recombinant soluble human Fc gamma RII: production, characterization, and inhibition of the Arthus reaction. (1993)

A recombinant soluble form of human Fc gamma RII (rsFc gamma RII) was genetically engineered by the insertion of a termination codon 5' of sequences encoding the transmembrane domain of a human Fc gamma RII cDNA. Chinese hamster ovary cells were transfected with the modified cDNA and the secreted rsFc gamma RII purified from the tissue culture supernatant (to > 95%, assessed by SDS-PAGE) using heat aggregated human immunoglobulin G (IgG) immunoaffinity chromatography. The IgG-purified rsFc gamma RII was relatively homogeneous (approximately 31,000 M(r)) whereas the total unpurified rsFc gamma RII secreted into the tissue culture supernatant was heterogeneous relating to N-linked glycosylation differences. Functional in vitro activity of the rsFc gamma RII was demonstrated by: (a) ability to bind via the Fc portion of human IgG and mouse IgG (IgG2a > IgG1 > > IgG2b); (b) complete inhibition of binding of erythrocytes sensitized with rabbit IgG to membrane-bound Fc gamma RII on K562 cells; and (c) inhibition of the anti-Leu4-induced T cell proliferation assay. Blood clearance and biodistribution studies show the rsFc gamma RII was excreted predominantly through the kidney in a biphasic manner, with an alpha-phase (t1/2 approximately 25 min) and a beta-phase (t1/2 approximately 4.6 h); the kidneys were the only organs noted with tissue-specific accumulation. In vivo, the administration of rsFc gamma RII significantly inhibited the immune complex-mediated inflammatory response induced by the reversed passive Arthus reaction model in rats. There was a specific and dose-dependent relationship between the amount of rsFc gamma RII administered, and the reduction in the size and severity of the macroscopic inflammatory lesion. Histological analysis of the skin showed a diffuse neutrophil infiltrate in both control and rsFc gamma RII-treated rats, however the perivascular infiltrate and the red cell extravasation was less intense in the rsFc gamma RII-treated group. It is likely that complement activation leads to neutrophil chemotaxis, but neutrophil activation via Fc gamma RII, which results in inflammatory mediator release, is inhibited. The data indicate that rsFc gamma RII is a potential therapeutic agent for the treatment of antibody or immune complex-mediated tissue damage.
Candida glabrata, an Emerging Oral Opportunistic Pathogen (2007)

Following the widespread use of immunosuppressive therapy and broad-spectrum antimycotic prophylaxis, C. glabrata has emerged as an important opportunistic pathogen in the oral mucosa. In the past, studies on the virulence factors and host-pathogen interactions of this organism were scarce, but continued to rise in recent years. Denture-wearing, immunosuppression, antibiotic therapy, and aging are risk factors for oral colonization or infection with C. glabrata. Compared with C. albicans, C. glabrata exhibits lower oral keratinocyte-adherence capacity, but higher denture-surface-adherence ability. The role of extracellular hydrolase production in the virulence of this organism does not appear to be as important as it is in C. albicans pathogenesis. Although traditionally thought of as a non-transforming yeast organism, both phenotypic switching and pseudohyphal formation have recently been identified in C. glabrata, but their role in pathogenesis is not known. With the exception of granulocyte monocyte colony-stimulating factor, C. glabrata triggers a lower proinflammatory cytokine response in oral epithelial cells than does C. albicans, in a strain-dependent manner. C. glabrata is less susceptible to killing by human beta-defensins than is C. albicans and exhibits various degrees of resistance to the antifungal activity of salivary histatins and mucins. In addition, C. glabrata possesses both innate and acquired resistance against antifungal drugs, due to its ability to modify ergosterol biosynthesis, mitochondrial function, or antifungal efflux. This resistance allows for its relative overgrowth over other susceptible species and may contribute to the recent emergence of C. glabrata infections in chronically immunocompromised populations. Further investigations on the virulence and host-pathogen interactions of C. glabrata are needed to better define the pathogenesis of oral C. glabrata infection in susceptible hosts.
Textbook of Immunology (2019)

Building on the strengths of the first edition, the newly titled and expanded second edition remains a concise introduction to the fundamentals of immunology, with an expert synthesis of basic and clinical information., Augmented by color illustrations, and with increased emphasis on the molecular and genetic underpinnings of cellular phenomena, Textbook of Immunology covers the physiology of the immune system, disease entities related to immune system dysfunction, and the underlying pathophysiologic mechanisms of dysfunction. In response to advancing knowledge that influences the approach to presenting basic immunology, new chapters have been added on cytokines; host defense (non-specific immunity and specific immune responses); the aging immune system; and the pathophysiology, diagnosis, prevention, and therapy of AIDS., This book keeps pace with the explosion of information and data in immunology, and adeptly refines, organizes, and presents this body of knowledge to serve as a succinct introduction to modern immunologic concepts for medical students, and as an update and refresher in the basics for researchers and clinicians.
Studies of in vitro differentiation with embryonic stem cells (1994)

Embryonic stem (ES) cells were first cultured from mouse embryos little more than a decade ago, yet they are now widely used in transgenic studies which are revolutionizing mammalian genetics. Although drawing less attention, in vitro studies of mouse ES cells have also contributed widely to the understanding of mechanisms of embryonic cell differentiation and proliferation. This review focusses on the application of ES cells as in vitro models for cellular and molecular events in the early mammalian embryo. Future studies with cultured ES cells of mouse and other species should provide insights into the factors regulating the differentiation of intermediate stem cells and terminal cells for the various embryonic lineages, thus contributing profoundly to the understanding of mammalian embryogenesis as well as providing cells for therapeutic applications.
Ret Oncogene and Thyroid Carcinoma (2014)

Thyroid cancer is a malignant neoplasm that originates from follicular or parafollicular thyroid cells and is categorized as papillary (PTC), follicular (FTC), anaplastic (ATC) or medullary thyroid carcinoma (MTC). The alteration of the Rearranged during trasfection (RET) (proto-oncogene, a gene coding for a tyrosine-kinase receptor involved in the control of cell differentiation and proliferation, has been found to cause PTC and MTC. In particular, RET/PTC rearrangements and RET point mutations are related to PTC and MTC, respectively. Although RET/PTC rearrangements have been identified in both spontaneous and radiation-induced PTC, they occur more frequently in radiation-associated tumors. RET/PTC rearrangements have also been reported in follicular adenomas. Although controversial, correlations between RET/PTC rearrangements, especially RET/PTC3, and a more aggressive phenotype and a more advanced stage have been identified.
Germline point mutations in the RET proto-oncogene are associated with nearly all cases of hereditary MTC, and a strict correlation between genotype and phenotype has been demonstrated. A large spectrum of RET point mutations has been reported to date. Somatic RET mutations, almost all of which are point mutations, have been described in approximately 40-50% of sporadic MTC cases. Although RET somatic mutations have been found in different codons, the M918T mutation in exon 16 is the most frequent. Detecting germline RET point mutations is a useful tool for identifying subjects who are clinically unaffected but who will develop the disease soon or late in their life, thus allowing presymptomatic treatment. From a clinical point of view, detecting RET somatic mutations in tumoral tissue is able to predict a poor outcome of the disease. In recent years, several drugs capable of inhibiting RET activity have been demonstrated to play an important role in the treatment of radiorefractory advanced thyroid carcinomas.
Large neutral amino acids in the treatment of phenylketonuria (PKU) (2006)

Large neutral amino acids (LNAAs) have been used on a limited number of patients with phenylketonuria (PKU) with the purpose of decreasing the influx of phenylalanine (Phe) to the brain. In earlier studies on mice with PKU (ENU(2)/ENU(2)), LNAAs were given and a surprising decline in blood Phe concentrations was observed. The formula used in the mouse experiment (PreKUnil) lacked lysine. Therefore, a new formulation of LNAAs (NeoPhe) was developed, introducing changes in the concentration of some amino acids and adding lysine, so that such a mixture could be used in humans. The new formula was found to be effective in reducing blood Phe concentration in mice by about 50% of the elevated levels. Patients with PKU were given LNAAs and blood Phe concentrations were determined in an open-label study. Three centers--in Russia, the Ukraine and the USA--took part in the study. NeoPhe was given at 0.5 g/kg per day in three divided doses to eight subjects with PKU and at 1.0 g/kg per day to three patients, for one week. The NeoPhe resulted in decrease of elevated blood Phe by 50% in both groups. The preliminary data from this study are encouraging and a double blind placebo-controlled trial will be required to show long-term efficacy and tolerance of LNAAs in the treatment of PKU.
Urine Attenuation Ratio: A New CT Indicator of Renal Artery Stenosis (2006)

The urine CT attenuation ratio is a simple and reliable indicator with which to detect and lateralize significant RAS and is a useful adjunct to helical CTA.
Dietary arachidonic acid: harmful, harmless or helpful? (2007)

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Characterization of GSK′963: a structurally distinct, potent and selective inhibitor of RIP1 kinase (2015)

Necroptosis and signaling regulated by RIP1 kinase activity is emerging as a key driver of inflammation in a variety of disease settings. A significant amount has been learned about how RIP1 regulates necrotic cell death through the use of the RIP1 kinase inhibitor Necrostatin-1 (Nec-1). Nec-1 has been a transformational tool for exploring the function of RIP1 kinase activity; however, its utility is somewhat limited by moderate potency, off-target activity against indoleamine-2,3-dioxygenase (IDO), and poor pharmacokinetic properties. These limitations of Nec-1 have driven an effort to identify next-generation tools to study RIP1 function, and have led to the identification of 7-Cl-O-Nec-1 (Nec-1s), which has improved pharmacokinetic properties and lacks IDO inhibitory activity. Here we describe the characterization of GSK'963, a chiral small-molecule inhibitor of RIP1 kinase that is chemically distinct from both Nec-1 and Nec-1s. GSK'963 is significantly more potent than Nec-1 in both biochemical and cellular assays, inhibiting RIP1-dependent cell death with an IC50 of between 1 and 4 nM in human and murine cells. GSK'963 is >10 000-fold selective for RIP1 over 339 other kinases, lacks measurable activity against IDO and has an inactive enantiomer, GSK'962, which can be used to confirm on-target effects. The increased in vitro potency of GSK'963 also translates in vivo, where GSK'963 provides much greater protection from hypothermia at matched doses to Nec-1, in a model of TNF-induced sterile shock. Together, we believe GSK'963 represents a next-generation tool for examining the function of RIP1 in vitro and in vivo, and should help to clarify our current understanding of the role of RIP1 in contributing to disease pathogenesis.