tbuckley/cabot-search huggingface dataset:
Friend murine leukemia virus-induced leukemia is associated with the formation of mink cell focus-inducing viruses and is blocked in mice expressing endogenous mink cell focus-inducing xenotropic viral envelope genes.
Authors: S Ruscetti, L Davis, J Feild, A Oliff
Journal: The Journal of Experimental Medicine (1981)

In these studies, we have shown data that are consistent with the hypothesis that mink cell focus-inducing viruses (MCF) play an important role in the generation of an erythroproliferative disease developing after injection of certain strains of newborn mice with ecotropic Friend murine leukemia virus (F-MuLV). Resistance to this disease is correlated with the endogenous expression of an MCF/xenotropic virus-gp70-related protein that may interfere with the replication or spread of MCF viruses. These ideas are supported by the following observations: (a) after infection with F-MuLV, only 6/13 strains of mice-developed disease, and studies with crosses between susceptible and resistant strains indicated that resistance was dominant. Although F-MuLV was shown to replicate equally well in all strains tested, viruses coding for MCF-specific viral envelope proteins could be detected only in the spleens of mice from strains that were resistant to F-MuLV-induced disease and not in the spleens of mice from strains that were resistant to F-MuLV-induced disease; (b) a Friend MCF (Fr-MCF) virus isolated from the spleen of an F-MuLV-infected mouse from a susceptible strain induced the same erythroproliferative disease when injected as an appropriate pseudotype into mice from susceptible but not resistant strains of mice; and (c) resistant but not susceptible strains of mice endogenously express MCF/xenotropic virus-related envelope glycoproteins that may be responsible for resistance by blocking receptors for MCF viruses. These results not only indicate that Fr-MCF virus is a crucial intermediate in the induction of disease by F-MuLV, but also suggest that a novel gene, either an MCF/xenotropic virus-related envelope gene or a gene controlling its expression, is responsible for resistance to erythroleukemia induced by F-MuLV.
Multifactorial ERβ and NOTCH1 control of squamous differentiation and cancer
Authors: Yang Sui Brooks, Paola Ostano, Seung-Hee Jo, Jun Dai, Spiro Getsios, Piotr Dziunycz, Günther F.L. Hofbauer, Kara Cerveny, Giovanna Chiorino, Karine Lefort, G. Paolo Dotto
Journal: Journal of Clinical Investigation (2014)

Downmodulation or loss-of-function mutations of the gene encoding NOTCH1 are associated with dysfunctional squamous cell differentiation and development of squamous cell carcinoma (SCC) in skin and internal organs. While NOTCH1 receptor activation has been well characterized, little is known about how NOTCH1 gene transcription is regulated. Using bioinformatics and functional screening approaches, we identified several regulators of the NOTCH1 gene in keratinocytes, with the transcription factors DLX5 and EGR3 and estrogen receptor β (ERβ) directly controlling its expression in differentiation. DLX5 and ERG3 are required for RNA polymerase II (PolII) recruitment to the NOTCH1 locus, while ERβ controls NOTCH1 transcription through RNA PolII pause release. Expression of several identified NOTCH1 regulators, including ERβ, is frequently compromised in skin, head and neck, and lung SCCs and SCC-derived cell lines. Furthermore, a keratinocyte ERβ-dependent program of gene expression is subverted in SCCs from various body sites, and there are consistent differences in mutation and gene-expression signatures of head and neck and lung SCCs in female versus male patients. Experimentally increased ERβ expression or treatment with ERβ agonists inhibited proliferation of SCC cells and promoted NOTCH1 expression and squamous differentiation both in vitro and in mouse xenotransplants. Our data identify a link between transcriptional control of NOTCH1 expression and the estrogen response in keratinocytes, with implications for differentiation therapy of squamous cancer.
Ethylene Glycol Poisoning
Authors: R. Todd Light
Journal: JAMA (1981)

<h3>To the Editor.—</h3> We read the recent case reports of massive ethylene glycol ingestion by Stokes and Aueron (1980;243:2065) and by Peterson et al.<sup>1</sup>Our own experience in a recent ethylene glycol poisoning, where the diagnosis was not evident from the patient's history and made only post mortem, caused us to review the clinical indications and available methods for ethylene glycol determination. A metabolic acidosis value with a high anion gap and a substantial discrepancy between the measured and calculated osmolality is suggestive of ethylene glycol or methyl alcohol intoxication. In either case, one must often start therapy with the infusion of ethyl alcohol, correction of the acidosis with sodium bicarbonate, and preparation for dialysis before there is laboratory confirmation. If a gas chromatograph is available for volatile toxins, a change in the usual screening conditions will include ethylene glycol among the identifiable poisons. As usually performed, volatile screens
Evaluation of a novel 308-nm monochromatic excimer light delivery system in dermatology: a pilot study in different chronic localized dermatoses
Authors: F. Aubin, M. Vigan, E. Puzenat, D. Blanc, C. Drobacheff, P. Deprez, P. Humbert, R. Laurent
Journal: British Journal of Dermatology (2005)

Journal Article Evaluation of a novel 308‐nm monochromatic excimer light delivery system in dermatology: a pilot study in different chronic localized dermatoses Get access F. Aubin, F. Aubin Photodermatology Unit, Department of Dermatology, University Hospital, 2 Place Saint‐Jacques, 25030 Besançon cedex, France François Aubin. E‐mail: francois.aubin@ufc‐chu.univ‐fcomte.fr Search for other works by this author on: Oxford Academic Google Scholar M. Vigan, M. Vigan Photodermatology Unit, Department of Dermatology, University Hospital, 2 Place Saint‐Jacques, 25030 Besançon cedex, France Search for other works by this author on: Oxford Academic Google Scholar E. Puzenat, E. Puzenat Photodermatology Unit, Department of Dermatology, University Hospital, 2 Place Saint‐Jacques, 25030 Besançon cedex, France Search for other works by this author on: Oxford Academic Google Scholar D. Blanc, D. Blanc Photodermatology Unit, Department of Dermatology, University Hospital, 2 Place Saint‐Jacques, 25030 Besançon cedex, France Search for other works by this author on: Oxford Academic Google Scholar C. Drobacheff, C. Drobacheff Photodermatology Unit, Department of Dermatology, University Hospital, 2 Place Saint‐Jacques, 25030 Besançon cedex, France Search for other works by this author on: Oxford Academic Google Scholar P. Deprez, P. Deprez Photodermatology Unit, Department of Dermatology, University Hospital, 2 Place Saint‐Jacques, 25030 Besançon cedex, France Search for other works by this author on: Oxford Academic Google Scholar P. Humbert, P. Humbert Photodermatology Unit, Department of Dermatology, University Hospital, 2 Place Saint‐Jacques, 25030 Besançon cedex, France Search for other works by this author on: Oxford Academic Google Scholar R. Laurent R. Laurent Photodermatology Unit, Department of Dermatology, University Hospital, 2 Place Saint‐Jacques, 25030 Besançon cedex, France Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 152, Issue 1, 1 January 2005, Pages 99–103, https://doi.org/10.1111/j.1365-2133.2005.06320.x Published: 01 January 2005 Article history Accepted: 12 May 2004 Published: 01 January 2005
STUDIES ON THE MECHANISM OF THE LONG CHAIN PHENOMENON OF GROUP A STREPTOCOCCI
Authors: Jerome J. Hahn, Roger M. Cole
Journal: The Journal of Experimental Medicine (1963)

The formation and destruction of long chains by growth of Group A streptococci in the presence of type-specific antibody have been studied with the fluorescent antibody technique. Long chain formation has been shown to depend on the presence of free antibody during the growth of the bacteria. Destruction of long chains has been shown to depend on the continued growth and division of the bacteria in the absence of free antibody. Univalent antibody fragments formed by proteolytic digestion of antibody globulin have been shown to have the combining properties of untreated antibody but do not result in the production of long chains. A model involving end-to-end agglutination during growth of Group A streptococci has been presented to explain the mechanism of production of long chains by growth of Group A streptococci in the presence of type-specific antibody.
Lung structure and function of infants with recurrent wheeze when asymptomatic
Authors: C. J. Llapur, T. M. Martínez, C. Coates, C. Tiller, J. L. Wiebke, X. Li, K. Applegate, H. O. Coxson, R. S. Tepper
Journal: European Respiratory Journal (2008)

Infants with recurrent wheeze have repeated episodes of airways obstruction; however, relatively little is known about the structure and function of their lungs when not symptomatic. The current authors evaluated whether infants with recurrent wheeze have smaller airway lumens or thickened airway walls, as well as decreased airway function. High-resolution computed tomography images 1 mm thick were obtained at three anatomic locations at an elevated lung volume and at functional residual capacity. Forced expiratory flows were also measured in subjects with recurrent wheeze. Airway lumen, wall areas and lung tissue density were not significantly different for recurrent wheeze (n = 17) and control (n = 14) subjects; however, subjects with recurrent wheeze had lower forced expiratory flows than predicted. Similar findings were obtained when subjects were grouped by exposure to tobacco smoke. These findings indicate that infants with recurrent wheeze, as well as exposure to tobacco smoke, have lower airway function when not symptomatic. The lower forced expiratory flows may result from a degree of airway narrowing that could not be resolved with the methodology employed or from other mechanisms, such as more collapsible airways or decreased pulmonary elastic recoil.
Attendance vs prescription: Exercise attendance rates for people with COPD: Systematic review
Authors: Marie Williams, Lucy Lewis, Zoe McKeough, Anne Holland, Annemarie Lee, Renae McNamara, Anna Phillips, Louise Wiles, Leona Knapman, Sally Watts, Maree Milross, Tanja Effing
Journal: European Respiratory Journal (2012)

The duration, frequency, mode and intensity of exercise programs for people with COPD are recommended by international consensus statements. The question for this review was: 9How consistently are a priori criterion and attendance rates reported for people with COPD participating in exercise programs?9 A systematic search of CINAHL, Medline, Embase and CENTRAL (Cochrane), was undertaken in October 2011. Studies were eligible for inclusion if published in English, included people with COPD, assessed the effects of rehabilitation as the primary intervention (+/- adjunctive strategies) and included at least 2 weeks exercise training (+/- education). There were no limits placed on intervention site (hospital, community, home) or publication date. Data extraction processes were confirmed prospectively for consistency (>80% agreement), with pairs of reviewers extracting data independently and disagreements resolved by consensus. The search returned 752 citations (497 citations excluded from title and abstract) with 255 full text articles retrieved for review. Of the 174 articles reviewed to date, a further 21 citations have been excluded. Of the 153 studies, 100% report the prescribed frequency of training but only 54% provide information on attendance at training sessions (n = 83) and less than a third of these report a priori criteria for attendance (n = 23, 28%). These preliminary analyses suggest that reporting of attendance rates in COPD exercise trials is low, which makes it difficult to calculate dose-response relationships between exercise participation and improvements in health outcomes.
SURFACE IMMUNOGLOBULINS ON THYMUS AND THYMUS-DERIVED LYMPHOID CELLS
Authors: Arthur D. Bankhurst, Noel L. Warner, John Sprent
Journal: The Journal of Experimental Medicine (1971)

Lymphoid cells from thymus, thoracic duct lymph (TDL), and thoracic duct lymph in irradiated animals reconstituted with allogeneic thymus cells (TTDL) were labeled with radioiodinated anti-immunoglobulins using radioautographic techniques. Thymus and TTDL were labeled (14.4 and 37.0%, respectively) with anti-light chain protein after prolonged exposures (30–60 days). No labeling was observed on thymus and TTDL with anti-polyheavy chain globulin. In contrast 18.5–19.0% of TDL labeled on short exposure (6 days) with anti-polyheavy chain and anti-light chain materials. It is proposed that the difference between the labeling observed on short exposures versus long exposures can be related to the difference in surface density of immunoglobulins between nonthymus-derived (B) and thymus-derived (T) cells. The distribution of labeled cells in the thymus was preferentially among the larger cells (greater than 10 µ diameter). The TTDL population was mostly composed of a larger, blast-like population and the distribution of label was independent of size. As the thymus and TTDL preparations contain almost exclusively T cells, this represents a direct demonstration of surface immunoglobulin light chains on T lymphoid cells.
Role of Cardiac Output and the Autonomic Nervous System in the Antinatriuretic Response to Acute Constriction of the Thoracic Superior Vena Cava
Authors: Robert W. Schrier, Michael H. Humphreys, Robert C. Ufferman, Judith A. Harbottle
Journal: Circulation Research (1971)

Studies were performed on anesthetized saline-loaded dogs to delineate the afferent and efferent mechanisms involved in the antinatriuretic response to acute constriction of the thoracic vena cava. The kidneys of the animals were denervated prior to study, and renal perfusion pressure was controlled throughout the experiment. To differentiate between the potential afferent stimuli, increased hepatic venous pressure and decreased cardiac output, the thoracic superior vena cava (TSVC) was acutely constricted to lower cardiac output without increasing hepatic venous pressure. Acute TSVC constriction caused a decrease in sodium excretion qualitatively similar to that resulting from an acute constriction of the thoracic inferior vena cava (TIVC) which generated a comparable decrease in cardiac output. This finding suggests that the afferent limb of the antinatriuretic response to acute constriction of the thoracic vena cava, either TSVC or TIVC, involves diminution in cardiac output, or some consequence thereof, rather than increased hepatic venous pressure. Additional experiments were then performed in animals with pharmacologically-induced autonomic blockade. Autonomic blockade with hexamethonium or phenoxybenzamine abolished the antinatriuretic response to constriction of either the TIVC or TSVC. This finding suggests that the efferent limb of the antinatriuretic response to thoracic vena cava constriction involves sympathetic efferent pathways, either by an intrarenal effect of circulatory catecholamines or by controlling the release of an extrarenal factor influencing sodium reabsorption.
Functional Profiling: From Microarrays via Cell-Based Assays to Novel Tumor Relevant Modulators of the Cell Cycle
Authors: Dorit Arlt, Wolfgang Huber, Urban Liebel, Christian Schmidt, Meher Majety, Mamatha Sauermann, Heiko Rosenfelder, Stephanie Bechtel, Alexander Mehrle, Detlev Bannasch, Ingo Schupp, Markus Seiler, Jeremy C. Simpson, Florian Hahne, Petra Moosmayer, Markus Ruschhaupt, Birgit Guilleaume, Ruth Wellenreuther, Rainer Pepperkok, Holger Sültmann, Annemarie Poustka, Stefan Wiemann
Journal: Cancer Research (2005)

Abstract Cancer transcription microarray studies commonly deliver long lists of “candidate” genes that are putatively associated with the respective disease. For many of these genes, no functional information, even less their relevance in pathologic conditions, is established as they were identified in large-scale genomics approaches. Strategies and tools are thus needed to distinguish genes and proteins with mere tumor association from those causally related to cancer. Here, we describe a functional profiling approach, where we analyzed 103 previously uncharacterized genes in cancer relevant assays that probed their effects on DNA replication (cell proliferation). The genes had previously been identified as differentially expressed in genome-wide microarray studies of tumors. Using an automated high-throughput assay with single-cell resolution, we discovered seven activators and nine repressors of DNA replication. These were further characterized for effects on extracellular signal-regulated kinase 1/2 (ERK1/2) signaling (G1-S transition) and anchorage-independent growth (tumorigenicity). One activator and one inhibitor protein of ERK1/2 activation and three repressors of anchorage-independent growth were identified. Data from tumor and functional profiling make these proteins novel prime candidates for further in-depth study of their roles in cancer development and progression. We have established a novel functional profiling strategy that links genomics to cell biology and showed its potential for discerning cancer relevant modulators of the cell cycle in the candidate lists from microarray studies.
INHERITED AND ACQUIRED FACTORS IN RESISTANCE TO INFECTION
Authors: Leslie T. Webster
Journal: The Journal of Experimental Medicine (1933)

1. A colony of inbred mice has been established free from inter-current infections and from the influence of extraneous variables detrimental to a study of their resistance to natural infection. A technique of measuring the resistance of mice to natural B. enteritidis mouse typhoid infection has been developed. 2. The Rockefeller Institute albino strain showed an average 37.4 per cent mortality to B. enteritidis mouse typhoid infection. 3. By breeding from progeny of mice dying early after exposure, lines approximately 85 per cent susceptible were obtained; by breeding from unexposed progeny of mice surviving infection, lines 15 per cent susceptible were obtained. Further selection within the most susceptible and most resistant lines did not alter their reaction; selection within the less susceptible and less resistant lines increased the sought factor. These rates remained approximately the same when the susceptibles received 1/100th and the resistants ten times the standard dose. The selected mice reacted consistently when exposed to spontaneous herd infection. 4. Several strains of mice, brother to sister inbred for special factors, did not differ materially in susceptibility. White-face and selected black-and-tan strains, however, proved 89.0 and 97 per cent susceptible. 5. White-face susceptibles mated with resistant Rockefeller Institute mice gave F1 progeny, 17.7 per cent susceptible. F1 mice back-crossed to susceptibles gave progeny 61.2 per cent susceptible and back-crossed with resistants gave progeny 26.3 per cent susceptible. F2 mice mated inter se gave progeny 34.2 per cent susceptible. The results indicate that resistance factors are dominant and not sex-linked.
Immunological Responses in Women with Human Papillomavirus Type 16 (HPV-16)-Associated Anogenital Intraepithelial Neoplasia Induced by Heterologous Prime-Boost HPV-16 Oncogene Vaccination
Authors: Lucy J. C. Smyth, Mariëtte I. E. van Poelgeest, Emma J. Davidson, Kitty M. C. Kwappenberg, Debbie Burt, Peter Sehr, Michael Pawlita, Stephen Man, Julian K. Hickling, Alison N. Fiander, Amanda Tristram, Henry C. Kitchener, Rienk Offringa, Peter L. Stern, Sjoerd H. van der Burg
Journal: Clinical Cancer Research (2004)

The purpose is to study the immunogenicity of heterologous prime-boost human papillomavirus (HPV) oncogene vaccination in patients with anogenital intraepithelial neoplasia (AGIN).Twenty-nine women with high-grade AGIN received three i.m. doses of TA-CIN (HPV-16 L2/E6/E7 protein) at four weekly intervals followed by a single dermal scarification of vaccinia HPV-16/18 E6/E7 and were followed up for 12 weeks. Immunity to HPV-16 was assessed by lymphoproliferation, IFN-gamma enzyme-linked immunospot (ELISPOT), and ELISA.The patient group significantly responded to TA-CIN and not to the control antigen HPV-6 L2/E7 at all postvaccination time points when compared with baseline responses (P < or = 0.05). Ten of the patients showed at least a 3-fold increase in TA-CIN-specific proliferation at one or more time points after vaccination. Comparison of stimulation with HPV-16 E6- or E7-GST fusion proteins showed that proliferative responses were biased to HPV-16 E6. This bias was also seen by IFN-gamma ELISPOT using overlapping peptides, with HPV-16 E6- or E7-specific T cells being detected in 9 and 2 patients, respectively. In addition, vaccination resulted in the induction of antibodies against the HPV-16 oncoproteins. Of the 6 clinical responders, 2 patients showed both a proliferative TA-CIN-specific response and an E6-specific IFN-gamma response, whereas 3 other patients displayed E6-specific reactivity only. Stable disease was recorded in 19 patients, 8 of whom showed a concomitant TA-CIN-specific proliferative and/or E6-specific T-cell response. Of the 4 progressors, 2 failed to make a T-cell response and 2 responded by either proliferation or E6 ELISPOT alone.The prime-boost regimen is immunogenic in AGIN patients (humoral and cellular immunity), but there is no simple relationship between induction of systemic HPV-16-specific immunity and clinical outcome. Other factors that may play a role in the eradication of long-term established AGIN lesions need to be determined to identify the patient group that would benefit from immunotherapy with the vaccines used in this study.