tbuckley/cabot-search huggingface dataset:
Lactoferrin, myeloperoxidase, lysozyme and eosinophil cationic protein in exudate in delayed type hypersensitivity
Authors: A. Lerche, H. Bisgaard, J. D. Christensen, P. Venge, R. Dahl, J. Søndergaard
Journal: Allergy (1988)

A skin window technique was used to study the morphology of leucocytes in upper dermis and exudate during nickel challenge in patients with contact allergy to nickel. Contact allergic patients and healthy volunteers tested with a skin widow without addition of nickel to the chamber medium served as controls. The morphology of the leucocytes in dermis was studied in biopsies taken 8, 24, or 48 h after skin window application, and in a parallel test the morphology of the exudate was examined by sequential collection of the chamber medium during a 48 h period. The infiltrate in dermis of contact allergic patients with nickel challenge in the chamber medium showed a time‐dependent increase of mononuclear cells, eosinophils and basophils and a concomitant decrease of polymorphonuclear granulocytes, characteristic of a combined specific and unspecific inflammation. The morphology of the exudate in contact allergic patients exposed to nickel showed a dominance of polymorphonuclear granulocytes throughout the study period, while mononuclear cells, eosinophils and basophils were detected at a much lower quantity and with a considerable delay. Further, we studied the kinetics of the leucocyte granule proteins: lactoferrin, myeloperoxidase, lysozyme and eosinophil cationic protein in exudate fluid in a parallel test. A significant higher flux was found for all during the second day of allergen exposure compared to contact allergic patients without allergen challenge as well as normal volunteers. The increased protein fluxes were not accompanied by an increased flux of polymorphonuclear granulocytes in the exudate. An unexpected difference in the kinetic profiles between the secondary granule proteins lactoferrin and lysozyme was observed in patients with and without nickel challenge as well as in controls, indicating a difference in diffusion or degradation of the two proteins before entering the chambers.
Manno-glycoconjugates of human keratinocytes in culture: effect of retinoic acid
Authors: P. W. LEDGER, A. REANO, J. Y. BONNEFOY, J. THIVOLET
Journal: British Journal of Dermatology (1984)

Journal Article Manno‐glycoconjugates of human keratinocytes in culture: effect of retinoic acid Get access P. W. LEDGER, P. W. LEDGER INSERM Unité 209, Hôpital Edouard Herriot, Pavilion R, 69374 Lyon Ccdcx 08, France Search for other works by this author on: Oxford Academic Google Scholar A. REANO, A. REANO INSERM Unité 209, Hôpital Edouard Herriot, Pavilion R, 69374 Lyon Ccdcx 08, France Search for other works by this author on: Oxford Academic Google Scholar J. Y. BONNEFOY, J. Y. BONNEFOY INSERM Unité 209, Hôpital Edouard Herriot, Pavilion R, 69374 Lyon Ccdcx 08, France Search for other works by this author on: Oxford Academic Google Scholar J. THIVOLET J. THIVOLET INSERM Unité 209, Hôpital Edouard Herriot, Pavilion R, 69374 Lyon Ccdcx 08, France Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 111, Issue s27, 1 July 1984, Pages 38–42, https://doi.org/10.1111/j.1365-2133.1984.tb15580.x Published: 01 July 1984
ABC of 1 to 7. Common rashes.
Authors: H B Valman
Journal: BMJ (1981)

ABC ofto 7H B VALMAN COMMON RASHESRashes usually occur as part of one of the com.mon infectious diseases of childhood, but these must be distinguished from dermatological causes.The characteristics of the lesions, distribution, changes with time, and accompanying features help to determine the diagnosis.A previous attack of an infectious disease makes a further attack unlikely, but a high incidence of wrong diagnoses of some rashes, particularly the misdiagnosis of rashes as being caused by rubella, detracts from the value of this history. PurpuraPurpuric lesions are caused by haemorrhages in the skin and they do not disappear on pressure.The child with purpura usually needs to be admitted immediately as he may have meningococcal septicaemia, leukaemia, or idiopathic thrombocytopenic purpura.Henoch-Schonlein purpura is more common than these conditions, however, and is distributed over the extensor surfaces of the limbs as well as the buttocks, and the purpuric lesions are usually raised.If the rash has all the characteristic features admission is not needed. Macules and papulesMacules are discrete lesions that change the colour of the skin, though they fade on pressure.They may be of any size or shape and may be pink or red.
Mitochondrial Control of Cellular Life, Stress, and Death
Authors: Lorenzo Galluzzi, Oliver Kepp, Christina Trojel-Hansen, Guido Kroemer
Journal: Circulation Research (2012)

Since the discovery that mitochondrial membrane permeabilization represents a critical step in the regulation of intrinsic apoptosis, mitochondria have been viewed as pluripotent organelles, controlling cell death as well as several aspects of cell survival. Mitochondria constitute the most prominent source of ATP and are implicated in multiple anabolic and catabolic circuitries. In addition, mitochondria coordinate cell-wide stress responses, such as autophagy, and control nonapoptotic cell death routines, such as regulated necrosis. Thus, mitochondria seem to regulate a continuum of cellular functions, spanning from physiological metabolism to stress responses and death. The involvement of mitochondria in both vital and lethal processes is crucial for both embryonic and postembryonic development, as well as for the maintenance of adult tissue homeostasis. In line with this notion, primary mitochondrial defects or alterations in the signaling pathways that converge on or emanate from mitochondria underpin a large number of human diseases, including premature aging, neurodegenerative disorders, cardiovascular disorders, and cancer. Here, we provide an overview of the molecular mechanisms that enable mitochondria to sustain cell survival, coordinate stress responses, and mediate cell death, linking these pathways--whenever relevant--to cardiovascular health and disease.
New campaign to raise awareness of oesophago-gastric cancer may lead to over-investigation, expert warns
Authors: G. Iacobucci
Journal: BMJ (2015)

Public Health England (PHE) will focus on raising awareness of the signs and symptoms of oesophago-gastric cancer in a bid to prompt people with concerns to visit their doctor as early as possible.

The latest phase of the national Be Clear on Cancer campaign will target people over 50. It will urge anyone in this age group experiencing heartburn on most days for three weeks or more to see a GP, as it could be a sign of cancer. Those in this age group who experience dysphagia will also be urged to see a doctor.

PHE said that it had launched the campaign to encourage earlier diagnosis of oesophago-gastric cancers, which are responsible for more than 10 000 deaths in England each year. It said that around 67% of people whose cancers are diagnosed at …
Sustained Platelet Glycoprotein IIb/IIIa Blockade With Oral Xemilofiban in 170 Patients After Coronary Stent Deployment
Authors: Dean J. Kereiakes, Neal Kleiman, James J. Ferguson, John Paul Runyon, Thomas M. Broderick, Nancy A. Higby, Linda H. Martin, Gary Hantsbarger, Shawn McDonald, Robert J. Anders
Journal: Circulation (1997)

Background Inhibition of platelet aggregation with parenteral glycoprotein (GP) IIb/IIIa receptor blockers can reduce the ischemic complications of angioplasty. Sustained efficacy and safety of protracted GP IIb/IIIa blockade with an orally administered agent have not previously been determined. This study is the first randomized, dose-ranging, single-blind, placebo-controlled trial of xemilofiban, an oral platelet GP IIb/IIIa receptor antagonist, administered to patients after intracoronary stent deployment. The pharmacodynamic efficacy of xemilofiban-induced platelet inhibition and clinical safety of this agent was evaluated during chronic therapy. Methods and Results After elective intracoronary stent deployment, patients were randomized to receive placebo (250 mg ticlopidine PO BID) or xemilofiban in doses of 5, 10, 15, or 20 mg PO BID. All patients received 325 mg aspirin PO QD. Inhibition of ex vivo platelet aggregation in response to 20 μmol/L ADP and 4 μg/mL collagen was measured over time after the initial dose of study drug and at 1 and 2 weeks of chronic therapy. Study drug was discontinued after 2 weeks, and all patients were followed clinically for ≥30 days. Oral xemilofiban resulted in a dose-dependent inhibition of platelet aggregation in response to both agonists that was sustained through 2 weeks of chronic therapy. Doses of xemilofiban required to achieve ≥50% inhibition of platelet aggregation were ≥10 mg, and the duration of inhibition was 8 to 10 hours. No significant hemorrhagic episodes or blood transfusions were observed in this trial. Conclusions Oral xemilofiban in doses of ≥10 mg produced ≥50% inhibition of platelet aggregation in response to ADP and collagen for 8 to 10 hours after dosing. Platelet inhibition was sustained through 2 weeks of chronic therapy. The optimal duration of oral GP IIb/IIIa blockade to effectively suppress recurrent ischemic events after coronary intervention remains to be determined.
What is the monetary value of a human life?
Authors: W I Card, G H Mooney
Journal: BMJ (1977)

The resources available to the health service are limited and so the amount the NHS can spend on saving human life is also limited. Rational allocation of resources requires a decision theory model, which in turn demands some monetary valuation of human life. Each of three approaches discussed--basing value on productive capacity, the NHS's implied values, or individuals' values--rests on an underlying set of non-monetary values. Choice of the underlying value will determine the method to be used in placing a monetary value on life. As the Health Service implicitly places certain values on life already, a means of making this valuation more rational and explicity can only improve the quality and quantity of health care.
Quinupristin-Dalfopristin–Resistant<i>Enterococcus faecium</i>on Chicken and in Human Stool Specimens
Authors: L. Clifford McDonald, Shannon Rossiter, Constance Mackinson, Yong Yu Wang, Susan Johnson, Maureen Sullivan, Robert Sokolow, Emilio DeBess, Laura Gilbert, James A. Benson, Bertha Hill, Frederick J. Angulo
Journal: New England Journal of Medicine (2001)

The combination of the streptogramins quinupristin and dalfopristin was approved in the United States in late 1999 for the treatment of vancomycin-resistant Enterococcus faecium infections. Since 1974, another streptogramin, virginiamycin, has been used at subtherapeutic concentrations to promote the growth of farm animals, including chickens.
Surgical validation of the accuracy of multiplane transesophageal echocardiographic planimetry in the quantification of anatomic aortic valve orifice area in patients with aortic stenosis
Authors: Ravi Kasliwal, Rajesh Rohatgi, Praveer Aggrawal, Naresh Trehan, Natesa Pandian
Journal: Journal of the American College of Cardiology (1996)
Nanoparticles against Alzheimer's disease: PEG–PACA nanoparticles are able to link the aβ-peptide and influence its aggregation kinetic
Authors: D. Brambilla, R. Verpillot, L. De Kimpe, M. Taverna, B. Le Droumaguet, J. Nicolas, M. Canovi, M. Gobbi, M. Salmona, V. Nicolas, W. Scheper, P. Couvreur, K. Andrieux
Journal: Journal of Controlled Release (2010)
Response to Letter Regarding Article, “β2-Microglobulin as a Biomarker in Peripheral Arterial Disease: Proteomic Profiling and Clinical Studies”
Authors: John P. Cooke, Eiichiro Kimura, Randall K. Harada, Nandini Nair, Balasubramanian Narasimhan, Kendall R. Beck, Andrew M. Wilson, Xiao-Ying Meng, Fujun Zhang, Eric T. Fung, Jeffrey W. Olin
Journal: Circulation (2008)
Metabolic Syndrome Is Associated With Faster Degeneration of Bioprosthetic Valves
Authors: Martin Briand, Philippe Pibarot, Jean-Pierre Després, Pierre Voisine, Jean G. Dumesnil, François Dagenais, Patrick Mathieu
Journal: Circulation (2006)

Background— Several studies have reported similarities between calcification of the native aortic valve and atherosclerosis. Recent studies also suggested that hypercholesterolemia may be a risk factor for calcific degeneration of bioprosthetic valves. The metabolic syndrome (MS) is associated with a higher risk of vascular atherosclerosis. We thus hypothesized that the atherogenic features of MS could accelerate bioprosthetic valve degeneration. Methods and Results— We included 217 patients who underwent aortic valve replacement with a bioprosthetic valve in the study. Of these patients, 71 patients (33%) had MS defined according to the modified criteria proposed by the National Cholesterol Education Program Adult Treatment Panel III. The annualized increase in mean transprosthetic gradient and the worsening of transprosthetic regurgitation measured by Doppler echocardiography were used to assess the deterioration of valve hemodynamic function. Patients with MS had higher progression of gradient (+4±5 mm Hg/year versus +2±2 mm Hg/year, P &lt;0.001), higher proportion of ≥1/3 degree worsening of regurgitation (25% versus 12%, P =0.02), and higher proportion of valve function deterioration defined as regurgitation worsening and/or ≥3 mm Hg/year increase in gradient (41% versus 25%, P =0.02) when compared with patients without MS. On multivariate analysis, MS was an independent predictor of gradient progression ( P =0.01), regurgitation worsening ( P =0.02), and valve function deterioration ( P =0.02). The other independent predictors were diabetes, renal insufficiency, and higher mean gradient at baseline. Conclusions— This is the first study to report that the MS is independently associated with faster bioprosthetic valve degeneration. This study could pave the way for the development of a new medical therapy able to significantly reduce the structural valve deterioration of bioprostheses.
Monitoring bone mineral density during antiresorptive treatment for osteoporosis
Authors: J. Compston
Journal: BMJ (2009)

Is potentially misleading and a misuse of healthcare resources

Antiresorptive treatment for osteoporosis is usually prescribed for a minimum of five years. Although it reduces the risk of fracture, it does not relieve symptoms caused by existing fractures and may have side effects. Understandably, therefore, patients and their doctors seek reassurance that the treatment is working. The most common way to monitor response is repeated measurement of bone mineral density using dual energy x ray absorptiometry (DXA), an approach endorsed by recent guidelines.1 2 Routine monitoring is costly, however, and—if it does not reduce disease burden—may divert healthcare resources away from more deserving causes. In the linked study (doi:10.1136/bmj.b2266), Bell and colleagues assess the need to monitor the response to bisphosphonate treatment by estimating how much the effects of alendronate differ between individuals.3 

Treatment aims to reduce the rate of fractures; therefore, monitoring should detect whether treatment will reduce the risk of fracture in individual patients. The effectiveness of repeated measurement of bone mineral density to monitor treatment depends on two prerequisites. Firstly, the test used (DXA) should be able to detect a significant change in bone mineral density within a time scale …
Recent progress in the molecular genetic analysis of erythroenzymopathy
Authors: H Fujii, S Miwa
Journal: American Journal of Hematology (1990)

Abstract During the relatively recent period in which normal genes for most red cell enzymes have been isolated, the techniques of molecular biology have been applied to the studies of erythroenzymopathy. Single nucleotide substitutions have been identified in aldolase, triosephosphate isomerase, glucose 6‐phosphate dehydrogenase, and adenylate kinase variants by the cloning and nucleotide sequence of the patients' genes. Up to now, all of the enzyme‐deficient variants which have been investigated have been caused by point mutations. An exception is a hemolytic anemia secondary to increased adenosine deaminase (ADA) activity. Red cell ADA activity increases on the order of a hundred‐fold in affected individuals. The basic abnormality appears to result from overproduction of structurally normal enzyme due to abnormal transcriptional or translational efficiency.
Integrated Analysis of Myocardial Blush and ST-Segment Elevation Recovery After Successful Primary Angioplasty
Authors: Arnaldo Poli, Raffaela Fetiveau, Pietro Vandoni, Gianfranco del Rosso, Maurizio D’Urbano, Giovanni Seveso, Francesco Cafiero, Stefano De Servi
Journal: Circulation (2002)

Background — ST-segment elevation (ΣSTe) recovery and the angiographic myocardial blush (MB) grade are useful markers of microvascular reperfusion after recanalization of the infarct-related artery. We investigated the ability of a combined analysis of MB grade and ΣSTe changes to identify different patterns of myocardial reperfusion shortly after primary percutaneous coronary angioplasty (PTCA) and to predict 7-day and 6-month left ventricular (LV) functional recovery. Methods and Results — MB grade and ΣSTe recovery were evaluated shortly after successful primary PTCA (restoration of TIMI grade 3 flow) in 114 consecutive patients with ΣSTe acute myocardial infarction. LV function was assessed by 2D echocardiograms before PTCA and at 7 days and 6 months thereafter. By combining MB and ΣSTe changes, 3 main groups of patients were identified. Group 1 patients (n=60) had both significant MB (grade 2 to 3) and ΣSTe recovery (&gt;50% versus basal ΣSTe) and a high rate of 7-day (65%) and 6-month (95%) LV functional recovery. In group 2 patients (n=21), who showed MB but persistent ΣSTe, the prevalence of early LV functional recovery was low (24%) but increased up to 86% in the late phase. Group 3 patients (n=28), who had neither significant MB nor ΣSTe resolution, had poor early (18%) and late (32%) LV functional recovery. Conclusions — After successful primary PTCA, integrated analysis of MB and ΣSTe recovery allows a real-time grading of microvascular reperfusion of the infarct area and predicts the time-course and magnitude of LV functional recovery.
Successful treatment of angiokeratoma with potassium tritanyl phosphate laser
Authors: S.J. Gorse, W. James, M.S.C. Murison
Journal: British Journal of Dermatology (2004)

Journal Article Successful treatment of angiokeratoma with potassium tritanyl phosphate laser Get access S.J. Gorse, S.J. Gorse Welsh Centre for Burns and Plastic Surgery, Swansea, U.K. E‐mail: sgorse@doctors.org.uk Search for other works by this author on: Oxford Academic Google Scholar W. James, W. James Welsh Centre for Burns and Plastic Surgery, Swansea, U.K. E‐mail: sgorse@doctors.org.uk Search for other works by this author on: Oxford Academic Google Scholar M.S.C. Murison M.S.C. Murison Welsh Centre for Burns and Plastic Surgery, Swansea, U.K. E‐mail: sgorse@doctors.org.uk Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 150, Issue 3, 1 March 2004, Pages 620–622, https://doi.org/10.1111/j.1365-2133.2004.05839.x Published: 01 March 2004
Silent myocardial infarction in Wegener's granulomatosis.
Authors: T Papo, J C Piette, R Laraki, O Bletry, D L Huong, P Godeau
Journal: Annals of the Rheumatic Diseases (1995)

Antineutrophil cytoplasmic antibodies and the eosinophilia myalgia syndromeThe eosinophilia myalgia syndrome (EMS) is an inflammatory multisystem disease which emerged in epidemic form in 1989 and was linked to the ingestion of L-tryptophan.'In the acute form of the EMS, severe myalgia and pronounced blood eosinophilia are accompanied by widespread organ involve- ment with the skin, lungs, serosal mem- branes, and the peripheral nervous system being involved most frequently.2 3 The chronic form of the EMS is characterised by progressive fascial and cutaneous fibrosis, leading to a clinical picture resembling eosinophilic fasciitis, accompanied by polyneuropathy, chronic fatigue, and psychological dysfunction.3I A spectrum of vascular lesions has been described including perivascular aggregation of mononuclear cells, intimal and medial thickening and fibrosis, ultrastructural alterations of the vascular endothelium, and frank vasculitis with mural infiltration by mononuclear cells.2 5 6 The last of these was found primarily in small arteries, veins and capillaries, and by immunofluorescence microscopy no deposition of immuno- globulins or complement components was found.
Abstract 2536: Therapeutic testing of a novel PKC inhibitor GAP-107B8 on ovarian cancer cells
Authors: Fu J. Yan, Isabella Steffensen, Kenneth Garson, Barbara C. Vanderhyden
Journal: Cancer Research (2010)

Abstract Background: Ovarian cancer is the most fatal gynaecologic disease in the western world. In 2009 in North America, an estimated 23,896 women will develop ovarian cancer and an estimated 15,24050 women will die from this disease. Current treatments are limited to surgery or chemotherapy, but the disease often recurs. Thus, the development of novel cancer therapeutics remains important. The protein kinase C (PKC) family of serine/threonine kinases is involved in cellular proliferation, differentiation, apoptosis and cell polarity. One PKC isoform, PKC iota, has recently been identified as a human oncogene and has been shown to be overexpressed in serous epithelial ovarian cancers and is thus a potential therapeutic target for ovarian cancer. Objective: We have tested a novel PKC inhibitor GAP-107B8 (PharmaGap Inc., Ottawa) in vitro on a panel of nine ovarian cancer cell lines to determine its potential to inhibit cell proliferation, proliferation in soft agar, and migration. Methods: Nine ovarian cancer cell lines were treated with three different concentrations of GAP-107B8 and then screened using high throughput assays to measure the proliferation of cells in adherent and anchorage independent (soft agar) cultures. The ability of cells to migrate in the presence of GAP-107B8 was also determined. Results: We observed significant reduction in cell proliferation in 6 of 9 ovarian cancer cell lines tested, including two cell lines resistant to the standard chemotherapy. GAP-107B8 inhibited cell proliferation by 30% to 79% compared with untreated cells, with more than 50% inhibition in 4 of 7 cell lines. Treatment with GAP-107B caused a reduction in growth in soft agar in 7 of the 9 cell lines tested in vitro. GAP-107B8 inhibited growth in soft agar by 50% to 94% compared with untreated cells, with 80% or greater inhibition in 6 of 7 cell lines. Finally, 5 of 8 cell lines tested showed significant inhibition of mobility following treatment with GAP-107B8. There was 50% or greater inhibition in all 5 cell lines compared with untreated cells. Conclusion: The novel PKC inhibitor GAP-107B8 displays good efficacy in vitro in suppressing several cancer cell characteristics in a variety of ovarian cancer cell lines. Further experiments are underway to investigate the therapeutic potential of GAP-107B8 in xenograft models of ovarian cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2536.
Percutaneous Computed Tomography-Guided Coaxial Core Biopsy for Small Pulmonary Lesions with Ground-Glass Attenuation
Authors: Chia-Hung Lu, Cheng-Hsiang Hsiao, Yeun-Chung Chang, Jang-Ming Lee, Jin-Yuan Shih, Li-An Wu, Chong-Jen Yu, Hon-Man Liu, Tiffany Ting-Fang Shih, Pan-Chyr Yang
Journal: Journal of Thoracic Oncology (2011)