tbuckley/cabot-search huggingface dataset:
Scientific debate on animal model in research is needed
Authors: P. Pound
Journal: BMJ (2001)

EDITOR—The editorial by Smith on animal research generated 23 responses on bmj.com, which are categorised in the table. 1 2

View this table:

Categories of electronic responses to Smith's editorial on animal research1



Five responses (and an additional letter by Botting) were published in the BMJ .3 Those selected fell into the category either of improvements to the current system, which supported the 3Rs (replacement, refinement, and reduction) approach (four letters), or of alternatives to animal research (one letter). All five letters adopted a conservative approach to the …
How patients use domiciliary oxygen.
Authors: M M Jones, J E Harvey, A E Tattersfield
Journal: BMJ (1978)

Forty-five patients in Southampton who received domiciliary oxygen were visited at home to find out how they used and coped with their oxygen. Generally, the organisation and administration of supplies presented no problems, nearly all the apparatus complied with the drug tariff, and most patients coped well with the equipment. Only two patients were taking oxygen for prescribed periods; the others were taking it when necessary for symptomatic relief. No patient received oxygen for over five hours daily. Most patients thought that they were helped by oxygen, but only four said that it allowed them to increase their level of activity, and the overall benefit seemed slight. This was partly because oxygen was usually limited to one room, so patients used oxygen after rather than during exercise. The amount of oxygen consumed differed widely, ranging from three and a half cylinders a week in three patients to less than one cylinder in six months in 17 patients. The average yearly cost of oxygen per patient ranged from 500 pounds in patients consuming one cylinder or more per week, to 15 pounds in those consuming less than one cylinder in six months. The main cost of domiciliary oxygen is determined by the number of cylinder refills, so patients who use it infrequently are a relatively small drain on resources.
Nicorandil-induced peristomal ulcers: is nicorandil also associated with gastrointestinal fistula formation?
Authors: S. Ogden, Y. Mukasa, C.C. Lyon, I.H. Coulson
Journal: British Journal of Dermatology (2007)

Journal Article Nicorandil‐induced peristomal ulcers: is nicorandil also associated with gastrointestinal fistula formation? Get access S. Ogden, S. Ogden Department of Dermatology, Burnley General Hospital, Burnley BB10 2PQ, U.K. *Department of Dermatology, York District Hospital, York YO31 8HE, U.K. E‐mail: stephanie.ogden@ntlworld.com Search for other works by this author on: Oxford Academic Google Scholar Y. Mukasa, Y. Mukasa Department of Dermatology, Burnley General Hospital, Burnley BB10 2PQ, U.K. *Department of Dermatology, York District Hospital, York YO31 8HE, U.K. E‐mail: stephanie.ogden@ntlworld.com Search for other works by this author on: Oxford Academic Google Scholar C.C. Lyon, C.C. Lyon Department of Dermatology, Burnley General Hospital, Burnley BB10 2PQ, U.K. *Department of Dermatology, York District Hospital, York YO31 8HE, U.K. E‐mail: stephanie.ogden@ntlworld.com Search for other works by this author on: Oxford Academic Google Scholar I.H. Coulson I.H. Coulson Department of Dermatology, Burnley General Hospital, Burnley BB10 2PQ, U.K. *Department of Dermatology, York District Hospital, York YO31 8HE, U.K. E‐mail: stephanie.ogden@ntlworld.com Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 156, Issue 3, 1 March 2007, Pages 608–609, https://doi.org/10.1111/j.1365-2133.2006.07698.x Published: 01 March 2007
Regulation of IL-4 Expression by Activation of Individual Alleles
Authors: Isabelle Rivière, Mary Jean Sunshine, Dan R Littman
Journal: Immunity (1998)

To study the in vivo role of IL-4-expressing cells, we developed a strategy to tag these cells, by generating mice in which one IL-4 allele was replaced with a cDNA encoding the human CD2 (huCD2) cell-surface molecule. Expression of the huCD2 reporter was, like IL-4, restricted to the appropriately polarized T helper 2 cells. However, most of the cells expressed only the IL-4 or the targeted allele. Analysis of the frequency of monoallelic versus biallelic expression suggests that the activation of each individual allele is regulated by a stochastic process whose probability can be augmented by increasing the strength of signal delivered through the TCR. Allele-specific activation may be a general feature of cytokine regulation that contributes to the functional diversity within T helper cell subpopulations.
Neo-Organoid of Marrow Mesenchymal Stromal Cells Secreting Interleukin-12 for Breast Cancer Therapy
Authors: Nicoletta Eliopoulos, Moïra Francois, Marie-Noëlle Boivin, Daniel Martineau, Jacques Galipeau
Journal: Cancer Research (2008)

Abstract Bone marrow–derived mesenchymal stromal cells (MSCs), beneficial for regenerative medicine applications due to their wide differentiation capabilities, also hold promise as cellular vehicles for the delivery of therapeutic plasma-soluble gene products due to their ease of handling, expansion, and genetic engineering. We hypothesized that MSCs, gene enhanced to express interleukin-12 (IL-12) and then embedded in a matrix, may act as an anticancer neo-organoid when delivered s.c. in autologous/syngeneic hosts. We performed such experiments in mice and noted that primary murine MSCs retrovirally engineered to secrete murine IL-12 can significantly interfere with growth of 4T1 breast cancer cells in vivo, with a more substantial anticancer action achieved when these cells are embedded in a matrix. Plasma of mice that received the IL-12 MSC-containing neo-organoids showed increased levels of IL-12 and IFN-γ. Histopathologic analysis revealed less tumor cells in implants of 4T1 cells with IL-12 MSCs, and the presence of necrotic tumor islets and necrotic capillaries, suggesting antiangiogenesis. We also showed that the anticancer effect exerted by the IL-12 MSCs is immune mediated because it is absent in immunodeficient mice, is not due to systemic IL-12 delivery, and also occurs in a B16 melanoma model. This study therefore establishes the feasibility of using gene-enhanced MSCs in a cell-based neo-organoid approach for cancer treatment. [Cancer Res 2008;68(12):4810–8]
Pathophysiology and pharmacological treatment of pulmonary hypertension in acute respiratory distress syndrome
Authors: E.D. Moloney, T.W. Evans
Journal: European Respiratory Journal (2003)

Pulmonary hypertension (PH) is a characteristic feature of the acute respiratory distress syndrome (ARDS). The magnitude of PH has been shown to correlate with the severity of lung injury in patients with ARDS independently of the severity of associated hypoxaemia and has an adverse prognostic significance. Early in the histopathological evolution of ARDS, pulmonary vasoconstriction, thromboembolism and interstitial oedema contribute to the development of PH, although pulmonary vascular remodelling probably occurs eventually. Intravenous vasodilator agents lead to an increase in intrapulmonary shunting and systemic hypotension, which can limit their therapeutic use, and have not been shown to improve survival. By contrast, rapidly metabolised vasodilators administered by inhalation induce selective pulmonary vasodilatation and decrease shunting, but again do not appear to confer a survival benefit. Research aimed at further understanding the mechanisms that underlie pulmonary hypertension, a characteristic feature of the acute respiratory distress syndrome, are expected to provide improvements in pharmacological interventions for the treatment of pulmonary hypertension in the acute respiratory distress syndrome.
Prevention of Atrial Fibrillation Following Cardiac Surgery—Reply
Authors: L. Brent Mitchell, Derek V. Exner
Journal: JAMA (2006)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Determination of HIV-1 Status of Discarded Sharps: Polymerase Chain Reaction Using Minute Quantities of Blood
Authors: Stephen Raffanti
Journal: JAMA (1990)

<h3>To the Editor.—</h3> As the number of individuals infected with human immunodeficiency virus type 1 (HIV-1) grows, the potential for accidental needle-stick injuries with contaminated blood increases. Strict adherence to infectioncontrol guidelines may limit this hazard. However, needle-stick injuries by discarded sharps present a special problem if the patient source of the needle is unknown. <h3>Report of a Case.—</h3> A nurse in an outpatient medical office had an accidental needle-stick exposure with a discarded angiocatheter. Many catheterization procedures had been performed, and the patient source was unknown. On the day of the accident, the angiocatheter was submitted to our laboratory and approximately 60 μL of serum was aspirated from the clotted blood in the hub of the needle. The sample was reactive to HIV-1 by Western immunoblot.<sup>1</sup>The needle was flushed with 300 μL of phosphate-buffered saline, and the eluant was processed for DNA extraction and polymerase
New Light on Obesity
Authors: Jules Hirsch, Rudolph L. Leibel
Journal: New England Journal of Medicine (1988)

There seems to be no end to the contradictory statements made about human obesity. Here are a few. Obesity is the result of a metabolic defect; no, it is no more than the unfettered drive for pleasure derived from eating. Obesity is genetically determined; no, it is the consequence of an abundance of foods and a sedentary life style. Obesity can be reversed by sensible changes in life style; no, five-year treatment successes are practically nonexistent. But some facts about obesity cannot be contradicted. The laws of thermodynamics are as applicable to human obesity as to the rest of the . . .
The sebotrophic action of growth hormone (BGH) in the rat
Authors: F.J. EBLING, ERIKA EBLING, VALERIE RANDALL, J. SKINNER
Journal: British Journal of Dermatology (1975)

Sebum production of rats was assessed by measuring the levels of fat extractable by diethyl ether from samples of hair clipped immediately after shampooing with sodium lauryl sulphate and 2 days later. By the use of matched litter mates in was unequivocally demonstrated that the response of the sebaceous glands to testosterone is virtually abolished by hypophysectomy and that it can be completely restored by pure bovine growth hormone.
<scp>IL</scp>‐33 drives airway hyper‐responsiveness through <scp>IL</scp>‐13‐mediated mast cell: airway smooth muscle crosstalk
Authors: D. Kaur, E. Gomez, C. Doe, R. Berair, L. Woodman, R. Saunders, F. Hollins, F.R. Rose, Y. Amrani, R. May, J. Kearley, A. Humbles, E.S. Cohen, C.E. Brightling
Journal: Allergy (2015)

Mast cell localization within the airway smooth muscle (ASM)-bundle plays an important role in the development of airway hyper-responsiveness (AHR). Genomewide association studies implicate the 'alarmin' IL-33 in asthma, but its role in mast cell-ASM interactions is unknown.We examined the expression and functional role of IL-33 in bronchial biopsies of patients with and without asthma, ex vivo ASM, mast cells, cocultured cells and in a mouse model system.IL-33 protein expression was assessed in human bronchial tissue from 9 healthy controls, and 18 mild-to-moderate and 12 severe asthmatic patients by immunohistochemistry. IL-33 and ST2 mRNA and protein expression in human-derived ASM, epithelial and mast cells were assessed by qPCR, immunofluorescence and/or flow cytometry and ELISA. Functional assays were used to assess calcium signalling, wound repair, proliferation, apoptosis and contraction. AHR and inflammation were assessed in a mouse model.Bronchial epithelium and ASM expressed IL-33 with the latter in asthma correlating with AHR. ASM and mast cells expressed intracellular IL-33 and ST2. IL-33 stimulated mast cell IL-13 and histamine secretion independent of FcεR1 cross-linking and directly promoted ASM wound repair. Coculture of mast cells with ASM activated by IL-33 increased agonist-induced ASM contraction, and in vivo IL-33 induced AHR in a mouse cytokine installation model; both effects were IL-13 dependent.IL-33 directly promotes mast cell activation and ASM wound repair but indirectly promotes ASM contraction via upregulation of mast cell-derived IL-13. This suggests that IL-33 may present an important target to modulate mast cell-ASM crosstalk in asthma.
P680Na+/Ca2+ exchanger (NCX) function and diastolic Ca2+ leak in a model of heart failure with preserved ejection fraction
Authors: U Primessnig, A Hoell, P Wakula, BM Pieske, FR Heinzel
Journal: Cardiovascular Research (2014)

Background: Heart failure with preserved ejection fraction (HFPEF) is increasingly common but the established heart failure (HF) drugs are not effective. The underlying cellular mechanisms are incompletely understood. Therefore we investigated cardiomyocyte function and intracellular Ca2+ homeostasis in a model of HFPEF. Methods: Young male Wistar rats were subjected to subtotal nephrectomy (NXT) or sham operation (SOP). Serial blood/urine samples, echocardiography and pressure-volume loops at 8 and 24 weeks were performed. After sacrifice, left ventricular (LV) hypertrophy and NCX function (Caffeine induced Ca2+ transient, TAU) and protein expression (Western blot) were determined. Cardiomyocyte function (Ca2+ transients, sarcoplasmic reticulum (SR) diastolic Ca2+ leak (Ca2+ sparks) and SR Ca2+ content; Fluo4-AM) were quantified in isolated LV cardiomyocytes without and with the NCX inhibitor SEA0400 (300nM). Results: NXT rats showed stable compensated renal impairment and significantly hypertrophied LV at 8 weeks with a further increase after 24 weeks. LV systolic function (EF, dP/dt) was preserved. End diastolic pressure (EDP) volume relationship was markedly shifted left- and upwards and lung weight were significantly increased, indicating HFPEF with pulmonary congestion. LV cardiomyocytes from NXT showed no significant differences in amplitudes of Ca2+ transients. However, time for early (50%) relaxation of the Ca2+ transients at 8 weeks were significantly prolonged with a further increase after 24 weeks (RT50 17.2±2.9 and 30.8±2.7 vs. 27.6±1.8 and 41.8±2.6 ms; n≥20; p< 0.05). TAU was significantly prolonged at 8 and 24 weeks indicating reduced NCX forward mode activity, while NCX protein expression was upregulated. At 8 weeks, Ca2+ spark frequency tended to be increased (p=0.07) while SR Ca2+ content was unchanged. SEA0400 accelerated Ca2+ transient decay but did not affect Ca2+ spark frequency. At 24 weeks, Ca2+ spark frequency was increased (4.3±0.7 vs. 11.5±1.8 sparks/s/μm3; n≥20; p<0.05) and SR Ca2+ content was decreased (p<0.05). SEA0400 significantly accelerated Ca2+ transient decay and reduced Ca2+ spark frequency. Conclusion: In this model of HFPEF, relaxation of cardiomyocytes was slower and cytosolic Ca2+ decay was prolonged. Diastolic Ca2+ leak increased significantly during diseases progression. Whereas NCX forward mode activity was already reduced early despite increased NCX protein expression. Acute treatment with NCX inhibitor SEA0400 normalized cytosolic Ca2+ transients in young NXT rats suggesting a role of reverse mode NCX activity and decreased Ca2+ leak at later time points.
Increased capillary fragility at high altitude.
Authors: D J Hunter, J R Smart, L Whitton
Journal: BMJ (1986)

intravenous cefuroxime plasma creatinine concentration rose to 383 smol/l (4 3 mg/100 ml) (calculated creatinine clearance 14-5 ml/min) after three days.Ibuprofen was stopped, and within 10 days plasma creatinine concentration was 135 smol/l (1 5 mg/l00 ml).
Molecular structure and transcriptional function of the rat vascular AT1a angiotensin receptor gene.
Authors: K Takeuchi, R W Alexander, Y Nakamura, T Tsujino, T J Murphy
Journal: Circulation Research (1993)

Rat vascular angiotensin receptors (AT1a receptors) are encoded by two mRNA transcripts sharing an identical receptor coding sequence but differing in their 5' and 3' untranslated sequences. We screened male Sprague-Dawley rat genomic libraries to clone the vascular AT1a receptor gene. Two sets of overlapping clones were isolated that encode over 90 kb of genomic sequence around the AT1a receptor gene. Four overlapping clones were identified from the 5' flanking portion of the gene. These contain the promoter region and two exons, 141 bp and 89 bp in size, respectively, encoding the alternatively spliced 5' untranslated mRNA sequence. Six additional clones overlap each other but do not overlap the set of clones from the 5' flanking region of the gene. These contain a single 1977-bp exon that encodes 900 bp of the 5' and 3' untranslated sequences in addition to a 1077-bp open reading frame identical to that found in vascular smooth muscle cell AT1a receptor cDNAs. Primer extension and RNase protection studies indicate that the transcription start site for this gene begins 9 bp upstream from the most 5' sequence found within the AT1a receptor cDNAs. Our mapping studies of the cloned gene, which so far includes an uncloned gap within the second intron, indicate that the transcription start site is no less than 67 kb upstream from the receptor coding exon. Promoter-reporter assays were performed by transfection of vascular smooth muscle cells with deletions of a 3.2-kb promoter region fused to a luciferase cDNA reporter plasmid. Relatively strong basal transcriptional activity is observed from the 5'-most 2 kb of the promoter and diminishes markedly with deletions within 1 kb of the early promoter region, suggesting strong promoter elements in the more upstream regions of the gene. Deletion of a 53-bp early promoter region containing the transcription start site and a putative TATA box completely abolishes the ability of upstream elements to drive transcription of the luciferase cDNA. These results indicate that we have isolated the AT1a receptor gene and its functional promoter.
Maxisorp
Authors: L. K. Poulsen, M. F. Pedersen, H.‐J. Malling, I. Søndergaard, B. Weeke
Journal: Allergy (1989)

For determination of allergen‐specific IgE in cell culture supernatants and other highly diluted IgE preparations a radioallergosorbent test (RAST) based on high adsorption polystyrene test tubes has been developed (“Maxisorp RAST”). Cladosporium herbarum extract was used as a model allergen but timothy grass pollen, house dust mite and dog dander showed similar results. The test showed specificities of both allergen and immunoglobulin isotype and significant correlations ( r = 0.67–0.88) with established RAST procedures were found. Based on immunosorbent‐purified allergen‐specific IgE the estimated sensitivity was within the order of 150‐300 pg allergen‐specific IgE per ml. The within‐assay variation was 4‐9% and the inter‐assay‐variation 17–29%. The Maxisorp RAST is useful as an inhibition assay for quantitating allergenic activity down to 0.1 biological units/ml of allergen extracts.
Abstract SY09-02: Molecular mechanisms in prostate cancer in African Americans
Authors: Yirong Li, David Zhang, Qinghu Ren, Fei Ye, Garrett Daniels, Xinyu Wu, Iman Osman, Jonathan Melamed, Brian Dynlacht, Peng Lee
Journal: Cancer Research (2012)

Abstract African American men have long been known to have the highest rates of prostate cancer (PCa) in the world. In addition, age adjusted mortality rates from PCa patients are two times worse among African Americans (AA) than Caucasians (CA). The reasons for the disparity in PCa risk, incidence, clinical progression, and disease-specific death are still controversial. In addition to socioeconomic and environmental factors, such as diet, access to care, and screenings, a biologically more aggressive cancer is proposed as one important explanation for the racial disparity observed in AA men. Androgens and the androgen receptor pathway are well established key regulators of aggressive PCa behavior. Using a novel proteomic pathway analysis comparing the distinct signal pathway and network proteins different between AA and CA PCa, we identified a number of markers including stem/progenitor cell and EMT related proteins that are overexpressed in PCa among AA. Our ongoing study indicates a novel link among Notch, WNT and androgen receptor (AR) pathways. In contrast to increase in epithelial AR, our data revealed a decrease in the expression of the stromal AR in AA PCa compared to CA PCa. Androgen and its receptor inhibit proliferation of prostate stromal cells through transcriptional suppression of cyclin B1. Mechanistically, the negative regulation of cyclin B1 by AR is mediated through switching between E2F1 and E2F4 on the promoter of cyclin B1. E2F1 binds to cyclin B1 promoter and maintains its expression and subsequent cell cycle progression in AR negative stromal cells or AR positive stromal cells under androgen depleted condition. Upon stimulation with androgen in AR positive stromal cells, E2F1 is displaced from the binding site by AR and replaced with E2F4, leading to recruitment of the SMRT/HDAC3 co-repressor complex and repression of cyclin B1. Furthermore, the switch between E2F1 and E2F4 at the E2F binding site of the cyclin B1 promoter coincides with an androgen-dependent interaction between AR and E2F1 as well as cytoplasm to nucleus translocation of E2F4. In summary, our study revealed an association between distinct epithelial and stromal AR expression and PCa racial disparity as well as the molecular mechanism involved in regulating AR expression in epithelial and stromal prostate cells. 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 SY09-02. doi:1538-7445.AM2012-SY09-02
A multiparameter flow cytometry immunophenotypic algorithm for the identification of newly diagnosed symptomatic myeloma with an MGUS-like signature and long-term disease control
Authors: B Paiva, M-B Vídriales, L Rosiñol, J Martínez-López, M-V Mateos, E M Ocio, M-Á Montalbán, L Cordón, N C Gutiérrez, L Corchete, A Oriol, M-J Terol, M-A Echeveste, R De Paz, F De Arriba, L Palomera, J de la Rubia, J Díaz-Mediavilla, M Granell, A Gorosquieta, A Alegre, A Orfao, J-J Lahuerta, J Bladé, J F San Miguel
Journal: Leukemia (2013)
Correction in Abstract on Bone Lesions
Authors: Alexander E. Horwitz
Journal: JAMA (1910)

<h3>To the Editor:</h3> In the abstract of my article on bone lesions inThe Journal, July 30, page 436, the following error was made: "Syphilitic epiphyseal enlargement is bilateral." It should read: "Syphilitic epiphyseal enlargement is unilateral; rachitic epiphyseal enlargement bilateral."