tbuckley/cabot-search huggingface dataset:
Neuronal Gamma-Band Synchronization as a Fundamental Process in Cortical Computation
Authors: Pascal Fries
Journal: Annual Review of Neuroscience (2009)

Neuronal gamma-band synchronization is found in many cortical areas, is induced by different stimuli or tasks, and is related to several cognitive capacities. Thus, it appears as if many different gamma-band synchronization phenomena subserve many different functions. I argue that gamma-band synchronization is a fundamental process that subserves an elemental operation of cortical computation. Cortical computation unfolds in the interplay between neuronal dynamics and structural neuronal connectivity. A core motif of neuronal connectivity is convergence, which brings about both selectivity and invariance of neuronal responses. However, those core functions can be achieved simultaneously only if converging neuronal inputs are functionally segmented and if only one segment is selected at a time. This segmentation and selection can be elegantly achieved if structural connectivity interacts with neuronal synchronization. I propose that this process is at least one of the fundamental functions of gamma-band synchronization, which then subserves numerous higher cognitive functions.
STEROID THERAPY IN COLLAGEN DISEASES. *
Authors: R. L. RICHARDS
Journal: British Journal of Dermatology (1960)

Journal Article STEROID THERAPY IN COLLAGEN DISEASES. Get access R. L. RICHARDS, M.D., F.R.C.P.(Ed.). R. L. RICHARDS, M.D., F.R.C.P.(Ed.). Department of Medicine, Gardiner Institute, The University and Western Infirmary, Glasgow, W.I Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 72, Issue 1, 1 January 1960, Pages 22–30, https://doi.org/10.1111/j.1365-2133.1960.tb13810.x Published: 01 January 1960
Anaphylactic Reactions To Cetuximab In Patients With Ige Antibodies To The Xenoantigen Galactose-alpha-1,3-galactose
Authors: B MIRAKHUR, C CHUNG, T HATLEY, S SATINOVER, J HOSEN, Q ZHOU, D GOLD, D MAURO, T PLATTSMILLS
Journal: Journal of Allergy and Clinical Immunology (2008)
Circulating microRNA signature in non-alcoholic fatty liver disease: from serum non-coding RNAs to liver histology and disease pathogenesis
Authors: Carlos J Pirola, Tomas Fernández Gianotti, Gustavo O Castaño, Pablo Mallardi, Julio San Martino, María Mora Gonzalez Lopez Ledesma, Diego Flichman, Faridodin Mirshahi, Arun J Sanyal, Silvia Sookoian
Journal: Gut (2014)

<h3>Objectives</h3> We used a screening strategy of global serum microRNA (miRNA) profiling, followed by a second stage of independent replication and exploration of liver expression of selected miRNAs to study: (1) the circulating miRNA signature associated with non-alcoholic fatty liver disease (NAFLD) progression and predictive power, (2) the role of miRNAs in disease biology and (3) the association between circulating miRNAs and features of the metabolic syndrome. <h3>Methods</h3> The study used a case-control design and included patients with NAFLD proven through biopsy and healthy controls. <h3>Results</h3> Among 84 circulating miRNAs analysed, miR-122, miR-192, miR-19a and miR-19b, miR-125b, and miR-375 were upregulated &gt;2-fold (p&lt;0.05) either in simple steatosis (SS) or non-alcoholic steatohepatitis (NASH). The most dramatic and significant fold changes were observed in the serum levels of miR-122 (7.2-fold change in NASH vs controls and 3.1-fold change in NASH vs SS) and miR-192 (4.4-fold change in NASH vs controls); these results were replicated in the validation set. The majority of serum miR-122 circulate in argonaute2-free forms. Circulating miR-19a/b and miR-125b were correlated with biomarkers of atherosclerosis. Liver miR-122 expression was 10-fold (p&lt;0.03) downregulated in NASH compared with SS and was preferentially expressed at the edge of lipid-laden hepatocytes. In vitro exploration showed that overexpression of miR-122 enhances alanine aminotransferase activity. <h3>Conclusions</h3> miR-122 plays a role of physiological significance in the biology of NAFLD; circulating miRNAs mirror the histological and molecular events occurring in the liver. NAFLD has a distinguishing circulating miRNA profile associated with a global dysmetabolic disease state and cardiovascular risk.
Exon skipping and dystrophin restoration in patients with Duchenne muscular dystrophy after systemic phosphorodiamidate morpholino oligomer treatment: an open-label, phase 2, dose-escalation study
Authors: Sebahattin Cirak, Virginia Arechavala-Gomeza, Michela Guglieri, Lucy Feng, Silvia Torelli, Karen Anthony, Stephen Abbs, Maria Elena Garralda, John Bourke, Dominic J Wells, George Dickson, Matthew JA Wood, Steve D Wilton, Volker Straub, Ryszard Kole, Stephen B Shrewsbury, Caroline Sewry, Jennifer E Morgan, Kate Bushby, Francesco Muntoni
Journal: The Lancet (2011)
The Human Toll Signaling Pathway: Divergence of Nuclear Factor κB and JNK/SAPK Activation Upstream of Tumor Necrosis Factor Receptor–associated Factor 6 (TRAF6)
Authors: Marta Muzio, Gioacchino Natoli, Simona Saccani, Massimo Levrero, Alberto Mantovani
Journal: The Journal of Experimental Medicine (1998)

The human homologue of Drosophila Toll (hToll) is a recently cloned receptor of the interleukin 1 receptor (IL-1R) superfamily, and has been implicated in the activation of adaptive immunity. Signaling by hToll is shown to occur through sequential recruitment of the adapter molecule MyD88 and the IL-1R–associated kinase. Tumor necrosis factor receptor–activated factor 6 (TRAF6) and the nuclear factor κB (NF-κB)–inducing kinase (NIK) are both involved in subsequent steps of NF-κB activation. Conversely, a dominant negative version of TRAF6 failed to block hToll-induced activation of stress-activated protein kinase/c-Jun NH2-terminal kinases, thus suggesting an early divergence of the two pathways.
UNICANCER-PEGASE 07 study: a randomized phase III trial evaluating postoperative docetaxel–5FU regimen after neoadjuvant dose-intense chemotherapy for treatment of inflammatory breast cancer
Authors: A. Gonçalves, J.-Y. Pierga, J.-M. Ferrero, M.-A. Mouret-Reynier, T. Bachelot, R. Delva, M. Fabbro, F. Lerebours, J.-P. Lotz, C. Linassier, N. Dohollou, J.-C. Eymard, B. Leduc, J. Lemonnier, A.-L. Martin, J.-M. Boher, P. Viens, H. Roché
Journal: Annals of Oncology (2015)
Water and Solute Movement in the Small Intestine of Patients with Sprue*
Authors: John S. Fordtran, Floyd C. Rector, T. Ward Locklear, Maynard F. Ewton
Journal: Journal of Clinical Investigation (1967)

Water and electrolyte movement in the jejunum of normal subjects and patients with sprue was measured during perfusion with isotonic electrolyte solutions. Normal subjects absorbed water, sodium, and potassium. By contrast, in patients with sprue (seven with adult celiac sprue and one with tropical sprue) who had diarrhea and steatorrhea, these substances were secreted into the intestinal lumen. This indicates that the jejunal mucosa of these patients was in a secretory state with respect to water and electrolytes.A method is presented for detecting abnormalities in the effective pore size in disease states. The method is based on the principle of restrictive diffusion and involves measuring the simultaneous diffusion rates of solutes of different molecular size. Since the method does not depend on measurement of water flow in response to osmotic pressure gradients, it can be used in disease states in which absorption and secretory processes involving water may be abnormal.The ratio of urea to tritiated water diffusion in the jejunum of normal subjects averaged 0.8, compared to 0.2 in patients with sprue. This indicates a marked decrease in the effective pore size of the jejunal mucosa in sprue. This conclusion was strengthened by the finding that erythritol and L-xylose, which are somewhat larger solutes than urea, are essentially non-absorbable in small bowel involved with sprue.
Angiotensin II–Induced Ca <sup>2+</sup> Influx in Renal Afferent and Efferent Arterioles
Authors: Kathy Loutzenhiser, Rodger Loutzenhiser
Journal: Circulation Research (2000)

Abstract —Angiotensin II (Ang II)–induced Ca 2+ signaling was studied in isolated rat renal arterioles using fura-2. Ang II (10 nmol/L) caused a sustained elevation in [Ca 2+ ] i , which was dependent on [Ca 2+ ] o in both vessel types. This response was blocked by nifedipine in only the afferent arteriole. Using the Mn 2+ quench technique, we found that Ang II stimulates Ca 2+ influx in both vessels. Nifedipine blocked the Ang II–induced Ca 2+ influx in afferent arterioles but not in efferent arterioles. In contrast to Ang II, KCl-induced depolarization stimulated Ca 2+ influx in only the afferent arteriole. Cyclopiazonic acid (CPA, 30 μmol/L) was used to examine the presence of store-operated Ca 2+ entry in myocytes isolated from each arteriole. In efferent myocytes, CPA induced a sustained Ca 2+ increase that was dependent on [Ca 2+ ] o and insensitive to nifedipine. This mechanism was absent in afferent myocytes. SKF 96365 inhibited Ang II–induced Ca 2+ entry in efferent arterioles and CPA-induced Ca 2+ entry in efferent myocytes over identical concentrations. Our findings thus indicate that Ang II activates differing Ca 2+ influx mechanisms in pre- and postglomerular arterioles. In the afferent arteriole, Ang II activates dihydropyridine-sensitive L-type Ca 2+ channels, presumably by membrane depolarization. In the efferent arteriole, Ang II appears to stimulate Ca 2+ entry via store-operated Ca 2+ influx.
IMMUNOHISTOCHEMICAL DEMONSTRATION OF IgG IN REED-STERNBERG AND OTHER CELLS IN HODGKIN'S DISEASE
Authors: A. J. Garvin, S. S. Spicer, R. T. Parmley, A. M. Munster
Journal: The Journal of Experimental Medicine (1974)

Spleens and lymph nodes fixed lightly for optimal immunocytochemistry or processed routinely for surgical diagnosis disclosed strong selective immunostaining for IgG in numerous immunocytes in tumor-free areas. Areas involved by Hodgkin's disease revealed, in addition, strong immunostaining for IgG but not IgM in Reed-Sternberg cells and faint to strong staining in Hodgkin cells as well. Ultrastructurally the Reed-Sternberg and Hodgkin cells displayed abundant polyribosomes and sparse granular reticulum and appeared to form unexportable IgG on unbound ribosomes.
Elevated C-Reactive Protein Is a Risk Factor for the Development of Type 2 Diabetes in Japanese Americans
Authors: Shuhei Nakanishi, Kiminori Yamane, Nozomu Kamei, Masamichi Okubo, Nobuoki Kohno
Journal: Diabetes Care (2003)

Increasing evidence from a cohort of Caucasians recently suggests that an elevated level of C-reactive protein (CRP) is associated with an increased risk of developing type 2 diabetes. However, Japanese subjects are skewed to lower CRP concentrations than westerners. Therefore, the effect of CRP on the development of type 2 diabetes among Japanese is unclear.We examined 396 male and 551 female nondiabetic Japanese Americans who underwent a 75-g oral glucose tolerance test (GTT) and were then followed for an average of 6.5 years. We investigated whether elevated serum CRP level is a risk factor in the development of type 2 diabetes among these subjects.Subjects with a high CRP level showed a significantly higher incidence of type 2 diabetes compared with subjects with a low level among both men (P = 0.028) and women (P = 0.004) in a log-rank test. In a Cox proportional hazards model dividing quartiles of CRP, the hazard ratios for diabetes development in the highest versus lowest quartile of CRP levels were 2.84 (95% CI 1.09-7.39) among men and 3.11 (1.25-7.75) among women after adjustment for age, smoking, family history of diabetes, classification of a 75-g GTT, hormone replacement therapy (among women), BMI, and homeostasis model assessment.Among Japanese Americans, CRP may be a risk factor for development of type 2 diabetes independent of either obesity or insulin resistance. Our results suggest that inflammation may be closely related to the mechanism of type 2 diabetes among Japanese Americans.
The development of a preliminary ultrasonographic scoring system for features of hand osteoarthritis
Authors: H I Keen, F Lavie, R J Wakefield, M-A D'Agostino, H B. Hammer, E Hensor, A Pendleton, D Kane, H Guerini, C Schueller-Weidekamm, M C Kortekaas, F Birrel, M Kloppenburg, T Stamm, I Watt, J S Smolen, E Maheu, M Dougados, P G Conaghan
Journal: Annals of the Rheumatic Diseases (2007)

Objectives: Painful osteoarthritis (OA) of the hand is common and a validated ultrasound (US) scoring system would be valuable for epidemiological and therapeutic outcome studies. US is increasingly used to assess peripheral joints, though most of the US focus in rheumatic diseases has been on rheumatoid arthritis. We aimed to develop a preliminary US hand OA scoring system, initially focusing on relevant pathological features with potentially high reliability. Methods: A group of experts in the fields of OA, US and novel tool development agreed on domains and suggested scaling of the items to be used in US hand OA scoring systems. A multi-observer reliability exercise was then performed to evaluate the draft items. Results: Synovitis (grey scale and Power Doppler) and osteophytes (representing activity and damage domains) were included and evaluated as the initial components of the scoring system. All three features were evaluated for their presence/absence and if present were scored using a 1–3 scale. The reliability exercise demonstrated intra-reader κ values of 0.444–1.0, 0.211–1.0 and 0.087–1.0 for grey scale synovitis, power Doppler and osteophytes respectively. Inter-reader reliability κ values were 0.398, 0.327 and 0.530 grey-scale synovitis, power Doppler and osteophytes respectively. Without extensive standardisation, both intra- and inter-reader reliability were moderately good. Conclusions: The draft scoring system demonstrated substantive to almost perfect percentage exact agreement on the presence/absence of the selected OA features and moderate to substantive percentage exact agreement on semi-quantitative grading. This preliminary process provides a good basis from which to further develop an US outcome tool for hand OA that has the potential to be utilised in multicentre clinical trials.
Hepatic inflammatory pseudotumor misinterpreted as hepatocellular carcinoma
Authors: Jae Yoon Jeong, Joo Hyun Sohn, Tae Yeob Kim, Woo Kyoung Jeong, Jinoo Kim, Ju Yeon Pyo, Young Ha Oh
Journal: Clinical and Molecular Hepatology (2012)

Inflammatory pseudotumor (IPT) is a rare benign disease, but may develop in various organs. Usually, hepatic IPT can be mistaken for malignant tumor such as hepatocellular carcinoma and cholangiocarcinoma, or inflammatory lesion such as liver abscess. We report imaging features of hepatic IPT in a patient with chronic hepatitis B diagnosed by percutaneous core biopsy.
Micropuncture studies of proximal tubule albumin concentrations in normal and nephrotic rats
Authors: Donald E. Oken, Walter Flamenbaum
Journal: Journal of Clinical Investigation (1971)

The concentration of serum albumin in proximal tubule fluid of normal rats and animals with aminonucleoside nephrosis was studied using renal micropuncture techniques. Albumin was quantitated by an ultramicrodisc electrophoresis method capable of measuring 3 chi 10(-11) g of albumin, in 10 nl volumes. With this sensitivity, only small samples of tubule fluid were required for analysis. Collection times could be kept short, therefore decreasing the opportunity for sample contamination with extraneous serum albumin. The measured mean concentration of albumin in proximal tubule fluid (1 mg/100 ml in females and 0.7 mg/100 ml in males) was somewhat lower than values reported by others, but even these values are apt to have been artifactually high as a result of animal preparation and trace contamination of samples during micropuncture. Rats injected with aminonucleoside of puromycin 4 days earlier, showed a significant increase in tubule-fluid albumin concentration coincident with a fall in serum albumin concentration and a 43-fold increase in urine albumin concentration. Tubular absorption of albumin was small relative to that of water. Although albumin filtration was significantly increased over that in normal animals, the glomerular basement membrane still served as a highly efficient barrier to albumin transfer.
Angiopoietin-1 Is an Antipermeability and Anti-Inflammatory Agent In Vitro and Targets Cell Junctions
Authors: Jennifer R. Gamble, Jenny Drew, Libby Trezise, Anne Underwood, Michelle Parsons, Lisa Kasminkas, John Rudge, George Yancopoulos, Mathew A. Vadas
Journal: Circulation Research (2000)

Abstract —Inflammation is a basic pathological mechanism that underlies many diseases. An important component of the inflammatory response is the passage of plasma components and leukocytes from the blood vessel into the tissues. The endothelial monolayer lining blood vessels reacts to stimuli such as thrombin or vascular endothelial growth factor by changes in cell-cell junctions, an increase in permeability, and the leakage of plasma components into tissues. Other stimuli, such as tumor necrosis factor-α (TNF-α), are responsible for stimulating the transmigration of leukocytes. Here we show that angiopoietin-1, a cytokine essential in fetal angiogenesis, not only supports the localization of proteins such as platelet endothelial cell adhesion molecule-1 (PECAM-1) into junctions between endothelial cells and decreases the phosphorylation of PECAM-1 and vascular endothelial cadherin, but it also strengthens these junctions, as evidenced by a decrease in basal permeability and inhibition of permeability responses to thrombin and vascular endothelial growth factor. Furthermore, angiopoietin-1 inhibits TNF-α–stimulated leukocyte transmigration. Angiopoietin-1 may thus have a major role in maintaining the integrity of endothelial monolayers.
Physical exercise, sports, and lung function in smoking<i>versus</i>nonsmoking adolescents
Authors: T.L. Holmen, E. Barrett-Connor, J. Clausen, J. Holmen, L. Bjermer
Journal: European Respiratory Journal (2002)

Associations between adolescent smoking habits and exercise, particularly participation in sports and lung function were studied. All students aged 13–19 yrs in Nord-Trøndelag County, Norway, 1995–1997, were invited to join a cross-sectional study. Information on smoking habits and exercise was obtained by self-administered questionnaire. Spirometry was performed in accordance with American Thoracic Society standards. Of the 6,811 students (aged 13–18 yrs, without asthma), 2,993 (44%) reported never-smoking, and 1,342 (20%) reported current smoking (10% daily). Frequency of physical exercise was inversely associated with smoking, but participants in individual sports with lesser endurance, especially body-building and fighting sports, were more likely to be daily smokers than nonparticipants. Both daily (53%) and occasional smokers (43%) were more likely to have quit sports than never-smokers (26%). Never-smokers showed a positive dose-response between physical exercise and lung function (forced vital capacity and forced expiratory volume in one second, adjusted for age and height). No similar significant association was observed in daily smokers. These data suggest that smoking habits in different sports should be considered when promoting physical activity as smoking prevention, and sports organizations should include smoking prevention programmes. Adolescents with better lung function may self-select into sports; this possibility needs to be studied in a longitudinal design.
A common variant on chromosome 11q13 is associated with atopic dermatitis
Authors: Jorge Esparza-Gordillo, Stephan Weidinger, Regina Fölster-Holst, Anja Bauerfeind, Franz Ruschendorf, Giannino Patone, Klaus Rohde, Ingo Marenholz, Florian Schulz, Tamara Kerscher, Norbert Hubner, Ulrich Wahn, Stefan Schreiber, Andre Franke, Rainer Vogler, Simon Heath, Hansjörg Baurecht, Natalija Novak, Elke Rodriguez, Thomas Illig, Min-Ae Lee-Kirsch, Andrzej Ciechanowicz, Michael Kurek, Tereza Piskackova, Milan Macek, Young-Ae Lee, Andreas Ruether
Journal: Nature Genetics (2009)
Hepatitis C Virus–Associated Cancer
Authors: Ming V. Lin, Lindsay Y. King, Raymond T. Chung
Journal: Annual Review of Pathology Mechanisms of Disease (2014)

Hepatitis C virus (HCV) is one of the major etiologic agents of liver cancer. HCV is an RNA virus that, unlike hepatitis B virus, is unable to integrate into the host genome. Through complex interactions between viral and host proteins that induce host responses and promote inflammation, fibrosis, and ultimately cirrhosis, HCV infection can result in the development of hepatocellular carcinoma (HCC). The HCV oncogenic process involves genetic and epigenetic alterations and oncogenic effects mediated by viral proteins in the activation of cellular oncogenes, inactivation of tumor-suppressor genes, and dysregulation of multiple signal-transduction pathways. Advances in genetics and gene expression profiling have enhanced our current understanding of the pathways involved in HCV-associated liver cancer development. In this review, we summarize the current understanding of mechanisms of hepatocarcinogenesis induced by HCV infection.
Antibody response of immunodeficient (xid) CBA/N mice to Escherichia coli 0113 lipopolysaccharide, a thymus-independent antigen.
Authors: J R Hiernaux, J M Jones, J A Rudbach, F Rollwagen, P J Baker
Journal: The Journal of Experimental Medicine (1983)

CBA/N mice, which possess an X-linked immunodeficiency (xid), produce a convincing antibody response to lipopolysaccharide derived from Escherichia coli 0113 (LPS 0113), a thymus-independent antigen. The antibody response produced was shown to be specific for the O-polysaccharide moiety of LPS 0113, rather than lipid A or lipid-A-associated protein. The relevance of this finding to the nature of the genetic defect of xid-mice is discussed.
Cap-Translation Inhibitor, 4EGI-1, Restores Sensitivity to ABT-737 Apoptosis through Cap-Dependent and -Independent Mechanisms in Chronic Lymphocytic Leukemia
Authors: Shaun Willimott, Daniel Beck, Matthew J. Ahearne, Victoria C. Adams, Simon D. Wagner
Journal: Clinical Cancer Research (2013)

The lymph node microenvironment promotes resistance to chemotherapy in chronic lymphocytic leukemia (CLL), partly through induction of BCL2 family prosurvival proteins. Currently available inhibitors do not target all BCL2 family prosurvival proteins and their effectiveness is also modified by proapoptotic BCL2 homology domain 3 (BH3) only protein expression. The goal of this study was to evaluate synergy between the eIF4E/eIF4G interaction inhibitor, 4EGI-1, and the BH3 mimetic, ABT-737.CLL cells were cultured in conditions to mimic the lymph node microenvironment. Protein synthesis and cap-complex formation were determined. Polysome association of mRNAs from BCL2 family survival genes was analyzed by translational profiling. The effects of 4EGI-1 and the BCL2/BCL2L1 antagonist, ABT-737, on CLL cell apoptosis were determined.Protein synthesis was increased approximately 6-fold by stromal cell/CD154 culture in a phosphoinositide 3-kinase α (PI3Kα)-specific manner and was reduced by 4EGI-1. PI3K inhibitors and 4EGI-1 also reduced cap-complex formation but only 4EGI-1 consistently reduced BCL2L1 and BCL2A1 protein levels. 4EGI-1, but not PI3K inhibitors or rapamycin, induced an endoplasmic reticulum stress response including proapoptotic NOXA and the translation inhibitor phosphorylated eIF2α. 4EGI-1 and ABT-737 synergized to cause apoptosis, independent of levels of prosurvival protein expression in individual patients.Overall protein synthesis and cap-complex formation are induced by microenvironment stimuli in CLL. Inhibition of the cap-complex was not sufficient to repress BCL2 family prosurvival expression, but 4EGI-1 inhibited BCL2A1 and BCL2L1 while inducing NOXA through cap-dependent and -independent mechanisms. 4EGI-1 and ABT-737 synergized to produce apoptosis, and these agents may be the basis for a therapeutically useful combination.