tbuckley/cabot-search huggingface dataset:
Molecular cloning of gp42, a cell-surface molecule that is selectively induced on rat natural killer cells by interleukin 2: glycolipid membrane anchoring and capacity for transmembrane signaling.
Authors: W E Seaman, E C Niemi, M R Stark, R D Goldfien, A S Pollock, J B Imboden
Journal: The Journal of Experimental Medicine (1991)

We have previously shown that in vitro culture of rat natural killer (NK) cells in high concentrations of recombinant interleukin 2 (rIL-2) leads to the expression of a surface glycoprotein with a molecular mass of approximately 42 kD. This glycoprotein, gp42, is not induced on other lymphocytes and thus provides a lineage-specific marker for rIL-2-activated NK cells. We here present the nucleotide sequence for gp42 cDNA. The open reading frame encodes 233 amino acids with three potential sites for N-linked glycosylation. The deduced amino acid sequence lacks an apparent transmembrane domain and instead contains a hydrophobic COOH terminus that is characteristic of glycosylphosphatidylinositol (GPI)-anchored surface proteins. Consistent with this, gp42 is cleaved from the NK-like cell line, RNK-16, by phosphatidylinositol-specific phospholipase C (PI-PLC), as is gp42 expressed on CHO cells that have been transformed with gp42 cDNA. On rIL-2-activated NK cells, gp42 is resistant to PI-PLC, though our studies suggest that gp42 on these cells is still expressed as a GPI-anchored molecule. Antibody to gp42 stimulates in RNK-16 cells an increase in inositol phosphates and in intracellular calciu, signals that are associated with the activation of lymphocytes, including NK cells. rIL-2-activated NK cells, however, lack this response to gp42 as well as to other stimuli. Thus, gp42, the only NK-specific activation antigen, is a GPI-anchored surface molecule with the capacity to stimulate transmembrane signaling.
Elastoderma — Disease of Elastin Accumulation within the Skin
Authors: Richard L. Kornberg, Sheldon S. Hendler, Aarne I. Oikarinen, Lois Y. Matsuoka, Jouni Uitto
Journal: New England Journal of Medicine (1985)

ELASTIC fibers, which consist of two distinct structures — elastin and the microfibrillar component — are responsible for the elasticity of tissues, such as the skin.1 2 3 4 The understanding of the normal biology of elastic fibers has been aided by the demonstration of elastin abnormalities in diseases.4 In this report we describe a disorder of elastic fibers that causes an excessive accumulation of elastin within the skin. The accumulation of elastin was documented by histopathological staining with elastic-tissue stains and by a fourfold increase in the desmosine concentration, as determined by a radioimmunoassay. However, electron microscopy of the elastic fibers revealed . . .
VALUE OF ANTROSCOPY (ENDOSCOPY OF THE ANTRUM OF HIGHMORE).Read in the Section on Laryngology and Otology, at the Forty-fifth Annual Meeting of the American Medical Association, held at San Francisco. June 5-8, 1894.
Authors: HENRY LEWIS WAGNER
Journal: JAMA (1894)

lous and suppurative forms of tonsillitis, as well as those forms of tonsillitis and pharyngitis which are symptomatic of the exanthemata, may reasonably be regarded as the most frequent causes of retro-pharyn¬ geal lymphadenitis.
The mechanism of decreased intestinal sodium and water absorption after acute volume expansion in the rat
Authors: Michael H. Humphreys, Laurence E. Earley
Journal: Journal of Clinical Investigation (1971)

Studies were performed in rat small intestine in vivo to determine the effect of saline infusion on intestinal transport of Na(+) and H(2)O. Saline infusion decreased net Na(+) flux (J(n) (Na)) from 12.7 +/-0.8 to 6.4 +/-1.5 muEq/hr per cm in the jejunum when the intestinal perfusate contained both Na(+) and glucose. A similar fall in J(n) (Na) occurred in ileum. When mannitol was substituted for glucose in the perfusate, control absorption decreased 29% in jejunum and 18% in ileum, but saline infusion still caused a decrease in J(n) (Na) quantitatively similar to that seen when glucose was present. When choline was substituted for Na(+) in the perfusate, there was net movement of Na(+) from blood to lumen during control and this net secretion was increased further after saline infusion. These observations suggest that saline infusion has a similar effect to decrease intestinal J(n) (Na) under three widely different conditions of basal sodium transport. Permeability of intestinal mucosa to inulin was very low under basal conditions but increased fivefold after saline infusion, and the unidirectional flux of Na(+) from blood to lumen doubled. This increase in unidirectional flux of Na(+) was greater than the observed decrease in J(n) (Na).Thus, saline infusion decreased net absorption of Na(+) and H(2)O from small intestine through mechanisms which did not appear to be dependent upon the rate of Na(+) flux from lumen to blood, and in association with an increased flux of inulin and Na(+) into the intestinal lumen. The data suggest that the effect of saline infusion to decrease net absorption from the intestine could be due either to an increase in passive permeability of the epithelium which could disrupt solute gradients within the membrane or to an increase in flow of solution into the intestinal lumen.
Preventing sexual abusers of children from reoffending: systematic review of medical and psychological interventions
Authors: N. Langstrom, P. Enebrink, E.-M. Lauren, J. Lindblom, S. Werko, R. K. Hanson
Journal: BMJ (2013)

To evaluate the effectiveness of current medical and psychological interventions for individuals at risk of sexually abusing children, both in known abusers and those at risk of abusing.
Heredity, pet ownership, and confounding control in a population-based birth cohort
Authors: Catarina Almqvist, Ann-Charlotte Egmar, Marianne van Hage-Hamsten, Niklas Berglind, Göran Pershagen, S.Lennart Nordvall, Magnus Svartengren, Gunilla Hedlin, Magnus Wickman
Journal: Journal of Allergy and Clinical Immunology (2003)
Blocking the Negative Effects of Pyridoxine on Patients Receiving Levodopa
Authors: George C. Cotzias
Journal: JAMA (1971)

<h3>To the Editor.—</h3> Duvoisin et al<sup>1</sup>reported that administration of pyridoxine may cancel the therapeutic and the side effects of levodopa. This was confirmed in several centers, including our own.<sup>2</sup>Consequently, industry produced and marketed a pyridoxine-free preparation (Larobec) which covers needs for vitamins in patients receiving levodopa. While continuing our experiments with the peripheral metabolic inhibitor D, L-alpha-methyl dopahydrazine or MK 485,<sup>3</sup>we noted that diurnal variations in performance could be controlled with orally administered combinations of inhibitor and levodopa. Such combinations have also diminished the striking postprandial reemergence of symptoms otherwise experienced by some of our patients.<sup>2,3</sup>We were thus encouraged to test whether the inhibitor blocked the adverse effects of administered pyridoxine. Pyridoxine (up to 100 mg three times each day) was given orally to seven patients for at least one week while they were in a metabolic ward and were receiving combinations
Neurosurgical Treatment in Psychiatry, Pain, and Epilepsy
Authors: John E. Adams
Journal: JAMA (1977)

This volume comprises the combined proceedings of the meetings of the Fourth World Congress of Psychiatric Surgery and the Second Meeting of the European Society for Stereotactic and Functional Neurosurgery. The predominant subject of concern to the participants was "psychosurgery." As might be expected, the caliber of the presentations is varied, particularly those dealing with the purely clinical results. The initial two articles by Schneider and Valensteind cover, respectively, plasticity in the brain and the physiological mechanism by means of which the brain responds to new stimuli in the environment, termed "reinforcement." These chapters serve nicely to set the context in which to consider the effects of making lesions in the "normal" brain to modify behavior, whether the latter is psychologically aberrant or related to chronic pain or a seizure disorder. This basic work, of course, has been dealt with in greater depth in monographs oriented solely toward that subject
Autonomic modulation of ventricular arrhythmia in cesium chloride-induced long QT syndrome.
Authors: R F Hanich, J H Levine, J F Spear, E N Moore
Journal: Circulation (1988)

To evaluate autonomic influence on arrhythmogenesis in an animal preparation of triggered activity, we gave increasing doses of cesium chloride (0.125 to 5.0 mmol/kg iv) to 24 dogs distributed equally among four protocols of autonomic intervention: control, total denervation, beta-blockade, and left stellate stimulation. All dogs underwent atrioventricular node ablation followed by ventricular pacing. A left ventricular endocardial monophasic action potential (MAP) catheter allowed for detection of "MAP early afterdepolarizations" (mEAD). mEAD amplitude was measured relative to MAP amplitude. Cesium chloride (CsCl) increased both MAP duration (132% after 0.125 mmol/kg to 188% after 1.0 mmol/kg; p less than .001) and mEAD amplitude (20% after 0.125 mmol/kg to 49% after 1.0 mmol/kg; p less than .001) in a dose-dependent fashion. All dogs exhibited ventricular ectopy at roughly equivalent doses (0.88 +/- 0.5 mmol/kg). Cesium's peak effect on MAP characteristics, sinus node automaticity, and systolic blood pressure coincided with the onset of sustained ventricular tachycardia (VT). Whereas control and denervated dogs developed VT after similar doses of CsCl (1.21 +/- 0.1 vs 1.12 +/- 0.14 mmol/kg; p = NS), none of the six beta-blocked dogs developed sustained VT. Conversely, those dogs having undergone stellate stimulation developed VT after smaller doses (0.58 +/- 0.34 mmol/kg; p less than .001) and with earlier onset (12 vs 30 sec; p less than .025). After 0.5 mmol/kg of CsCl, left stellate stimulation augmented relative mEAD amplitude compared with control (51% vs 38%; p less than .001), whereas beta-blockade had little effect (39% vs 38%; p = NS). Autonomic intervention as such can affect the arrhythmogenicity of CsCl and similarly alter MAP characteristics. Furthermore, as beta-blockade can prevent sustained arrhythmia without eliminating mEADs, autonomic tone appears to modulate the expression of mEADs as sustained VT.
CD8 Depletion–induced Late Airway Response Is Characterized by Eosinophilia, Increased Eotaxin, and Decreased IFN- γ Expression in Rats
Authors: ZOULFIA ALLAKHVERDI, BOUCHAIB LAMKHIOUED, RONALD OLIVENSTEIN, QUTAYBA HAMID, PAOLO M. RENZI
Journal: American Journal of Respiratory and Critical Care Medicine (2000)

There is an emerging body of knowledge defining the role of CD8(+) cells in the pathogenesis of allergic asthma. We have previously demonstrated in sensitized Sprague-Dawley (SD) rats that depletion of CD8(+) cells caused an increase in the late airway response (LAR) and cellular infiltration after antigen challenge. To better delineate the mechanism of CD8(+) cell involvement in the development of the LAR and airway inflammation, we investigated the pattern of chemokine and cytokine production after antigen challenge. SD rats were sensitized to ovalbumin (OA) and subsequently treated with anti-CD8 (OX-8) monoclonal antibody (mAb) for the depletion of CD8(+) cells or with control mouse anti-rat IgG(1) mAb as a control procedure. After OA challenge, CD8- depleted SD rats developed an increased LAR when compared with control rats (area under the curve: 16.65 +/- 6.6 in CD8- depleted rats versus 5.39 +/- 2.0 in control animals; p < 0.05). Compared with the control animals, the increase in the LAR was accompanied by a significantly increased eosinophilic infiltration of the airways and was associated with increased eotaxin expression (both messenger RNA [mRNA] and protein) in the CD8-depleted group. There were no differences between the groups in RANTES or monocyte chemoattractant protein-1 (MCP-1) expression. In addition, we found a significantly lower interferon gamma (IFN-gamma) mRNA expression in the CD8-depleted rats, without any effects on interleukin (IL)-4 and IL-5 mRNA expression when measured either by semiquantitative reverse transcriptase/polymerase chain reaction (RT-PCR) or by in situ hybridization for the number of cells expressing these cytokines. Taken together, these results suggest that CD8(+) cells from sensitized SD rats exhibit the functional capacity to suppress the LAR, possibly through downregulation of eotaxin expression and increased expression of IFN-gamma mRNA.
Simvastatin Preserves the Structure of Coronary Adventitial Vasa Vasorum in Experimental Hypercholesterolemia Independent of Lipid Lowering
Authors: Stephanie H. Wilson, Joerg Herrmann, Lilach O. Lerman, David R. Holmes, Claudio Napoli, Erik L. Ritman, Amir Lerman
Journal: Circulation (2002)

Background — Previous studies have demonstrated that experimental hypercholesterolemia leads to neovascularization in the coronary artery vasa vasorum (VV). Recent evidence suggests that HMG-CoA reductase inhibitors (statins) have beneficial effects independent of lipid lowering. We aimed to determine the effect of simvastatin on coronary VV neovascularization, in the absence of cholesterol lowering. Methods and Results — Pigs were randomized to 3 groups fed a normal (N), high cholesterol (HC), or HC+simvastatin (HC+S) diet for 12 weeks. The proximal left anterior descending artery was isolated, scanned with micro-CT, and reconstructed. Quantification of the VV density in serial cross-sections along the vessel was then performed. LDL cholesterol was similarly increased in HC and HC+S compared with N. There was an increase in both VV density (4.7±0.3 versus 2.7±0.2 n/mm 2 ; P &lt;0.05) and vessel wall area (3.1±0.2 versus 1.8±0.1 mm 2 ; P &lt;0.05) in HC compared with N. The VV density in HC+S was preserved compared with HC (3.0±0.2 n/mm 2 ; P &lt;0.05), despite similar increase in vessel wall area compared with N (2.5±0.1 mm 2 ; P &lt;0.05). Coronary artery tissue expression of VEGF was increased in HC but not in HC+S compared with N. In parallel, immunoreactivity for HIF-1α, VEGF, MMP-2, and MMP-9 was accentuated in the outer media in HC but not in HC+S compared with N. Conclusions — This study demonstrates that simvastatin attenuates hypoxia in the coronary artery wall and VV neovascularization in experimental hypercholesterolemia, despite no change in plasma lipids. These data are consistent with an additional mechanism for the vascular effects of the statins, independent of cholesterol lowering.
Topical calcineurin inhibitors in treating Jessner's lymphocytic infiltration of the skin: report of a case
Authors: T-Y. Tzung, J-C. Wu
Journal: British Journal of Dermatology (2005)

British Journal of DermatologyVolume 152, Issue 2 p. 383-384 Topical calcineurin inhibitors in treating Jessner's lymphocytic infiltration of the skin: report of a case First published: 23 February 2005 https://doi.org/10.1111/j.1365-2133.2005.06349.xCitations: 11 Conflicts of interest: none declared. Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume152, Issue2February 2005Pages 383-384 RelatedInformation
Consequences of Stop Codon Reassignment on Protein Evolution in Ciliates with Alternative Genetic Codes
Authors: K. L. Ring, A. R. O. Cavalcanti
Journal: Molecular Biology and Evolution (2007)

Tetrahymena thermophila and Paramecium tetraurelia are ciliates that reassign TAA and TAG from stop codons to glutamine codons. Because of the lack of full genome sequences, few studies have concentrated on analyzing the effects of codon reassignment in protein evolution. We used the recently sequenced genome of these species to analyze the patterns of amino acid substitution in ciliates that reassign the code. We show that, as expected, the codon reassignment has a large impact on amino acid substitutions in closely related proteins; however, contrary to expectations, these effects also hold for very diverged proteins. Previous studies have used amino acid substitution data to calculate the minimization of the genetic code; our results show that because of the lasting influence of the code in the patterns of substitution, such studies are tautological. These different substitution patterns might affect alignment of ciliate proteins, as alignment programs use scoring matrices based on substitution patterns of organisms that use the standard code. We also show that glutamine is used more frequently in ciliates than in other species, as often as expected based on the presence of the 2 new reassigned codons, indicating that the frequencies of amino acids in proteomes is mostly determined by neutral processes based on their number of codons.
Clinical Performance of an Automated Stool DNA Assay for Detection of Colorectal Neoplasia
Authors: Graham P. Lidgard, Michael J. Domanico, Janelle J. Bruinsma, James Light, Zubin D. Gagrat, Rebecca L. Oldham–Haltom, Keith D. Fourrier, Hatim Allawi, Tracy C. Yab, William R. Taylor, Julie A. Simonson, Mary Devens, Russell I. Heigh, David A. Ahlquist, Barry M. Berger
Journal: Clinical Gastroenterology and Hepatology (2013)
Evidence of the Survival of Ectopically Transplanted Oral Mucosal Epithelial Stem Cells After Repeated Wounding of Cornea
Authors: Hiroaki Sugiyama, Masayuki Yamato, Kohji Nishida, Teruo Okano
Journal: Molecular Therapy (2014)

Tissue engineering has become an essential tool in the development of regenerative medicine. We have developed cell sheet-based techniques for use in regenerative medicine that have already been successfully used in clinical applications. Native corneal epithelium is produced from limbal stem cells located in the transition zone between the cornea and the bulbar conjunctiva. Limbal stem cell deficiency (LSCD) is a severe defect of the limbal stem cells leading to vision loss due to conjunctival epithelial invasion and neovascularization. Rabbit LSCD models were treated with transplantable autologous oral mucosal epithelial cell (OEC) sheets fabricated on temperature-responsive cell culture surfaces, after which, the ocular surfaces were clear and smooth with no observable defects. The central part of the reconstructed ocular surface was scraped and wounded, after which proliferating epithelial cells covered the scraped area within a few days. The ocular surfaces were clear and smooth even after repeated scrapings and consisted of only OECs or heterogeneously mixed with corneal epithelial cells. This study demonstrates that transplanted cell sheets containing oral mucosal epithelial stem cells could reconstruct the ocular surface to maintain cornea homeostasis; moreover, they provide an ideal microenvironment to support the proliferation of remaining native limbal stem cells.
A poster poser--doing it in tiles
Authors: A. Shrivastava
Journal: BMJ (2008)

It was a scene familiar to many a doctor travelling to make a conference presentation. Dr Kotkar smiles as he remembers the episode at Mumbai airport: “As I boarded the aircraft I saw many anxious faces staring at me. Soon I realised that it was my long tube-like poster holder, which made me look as if I was carrying a rocket launcher. And then it would not fit inside the overhead locker even after a joint effort by me and the air hostess. I had anticipated such embarrassment but had no other option.”

Doctors and researchers often have excellent ideas for designs for illustrated posters to use in presentations at meetings and conferences. But then, to avoid situations such as Dr Kotkar’s, they ruin the effect by resorting to the conventional A4 sized landscape printout for ease of carrying, especially when long distance travel on aeroplanes is involved.

Dr Desai, who enjoys painting as a hobby and whose ideas for poster designs are appreciated by his students and colleagues, is irked by this problem. “It’s really annoying that you cannot present your best, particularly at the international level,” he said. …
Abstract 232: Protein kinase C b1 (PKCb1) inhibits the malignant phenotype of the human pancreatic tumor-derived cell line PANC1
Authors: Stéfano M. Cirigliano, Laura V. Mauro, Valeria C. Grossoni, Elisa D. Bal De Kier Joffe, Lucas L. Colombo, Lydia I. Puricelli, Alejandro J. Urtreger
Journal: Cancer Research (2012)

Abstract Pancreatic cancer is a deadly disease with a 5% overall survival after five years. Different members of the PKC family have been described as modulators of pancreatic cancer progression but, till nowadays, the relevance of each PKC isoform in this process is unclear. The aim of the present work was to study the effect of PKCb1 overexpression, on several critical determinants of tumor progression using the human pancreatic tumor-derived cell line PANC1. Cells were stably transfected with an expression vector containing the full-length PKCb1 gene (PKCb1-PANC1) or with the empty vector, as control (pMTH-PANC1). While no morphologic alterations could be detected in vitro, PKCb1 overexpression induced a significant reduction in the proliferative capacity of PANC1 cells. The reduction in this capacity could be associated with a decrease in Cyclin D1, Cyclin E and phosphorylated ERK1/2 levels, and an increase in p21 expression levels, as measured by Western blot. In addition PKCb1-PANC1 cells showed an increased resistance to cell death induced by serum starvation (% viability: 58.54±4.1 vs 39.29±4.2 in pMTH-PANC1, p&amp;lt;0.05). Using flow cytometry we could determine that serum deprivation promoted PKCb1-PANC1 arrest in the G1 phase of the cell cycle (cells in G0/G1: 86.7±1.0% vs 45.5±0.8% in pMTH-PANC1, p&amp;lt;0.05). Moreover, the overexpression of PKCb1 reduced the in vitro invasive capacity using Matrigel coated transwells (cells x 10 microscopic x400 fields: 2.22±0.9 vs 10.10±2.6 in pMTH-PANC1, p&amp;lt;0.05). This behavior could be associated with a significant inhibition of secreted proteases activity (uPA: 4.11±0.8 vs 12.32±4.1 IU/mg/24h in pMTH-PANC1, p&amp;lt;0.05 and MMP-9: 15.24±0.03 vs 24.89±2.6 AU/mg in pMTH-PANC1, p&amp;lt;0.05). When control and PANC1-PKCb1 cells were s.c. inoculated into nude mice it was observed that PKCb1 cells were almost unable to grow and form tumors while vector-transfected cells retained this ability. In sum, our results suggest that PKCb1 overexpression in human pancreatic tumor cells PANC1 induced a less malignant phenotype both in vivo and in vitro. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 232. doi:1538-7445.AM2012-232