tbuckley/cabot-search huggingface dataset:
Toll-like receptor 2 signalling and inflammation
Authors: F Y Liew
Journal: Annals of the Rheumatic Diseases (2005)

<h3>Background and aim</h3> How patients use their nebulisers at home is vital to ensure effective treatment and optimal health outcomes for patients with chronic obstructive pulmonary disease (COPD). The aim of the study was to identify the practicalities and problems associated with nebuliser use by patients with COPD at home, which may impact on the safety and effectiveness of therapy. <h3>Design and setting</h3> A cross-sectional descriptive study in which participants were recruited from two levels of care: primary care, involving 38 GP practices in North West London, and intermediate care with a major acute hospital. <h3>Method</h3> In-depth interviews were conducted with a representative sample of 50 patients with COPD using nebulisers in their home, recruited from general practice populations and at hospital discharge. A checklist was used to record activities and patients demonstrated use of their nebuliser. Qualitative procedures were employed to identify the range of problems experienced with nebuliser use. <h3>Results</h3> A wide range of practical issues was identified at all stages: problems prior to nebulisation: setting up equipment, lack of instructions, manual dexterity and time required. Problems during medication administration: inhalation technique, duration of nebulisation and understanding how to achieve optimal efficacy. Problems post-administration: inadequate cleaning of nebuliser components, access to accessories and use of damaged parts or self-repairs. Other problems included noise, weight and non-portability of equipment. <h3>Conclusions</h3> Patients with COPD using nebulisers at home experienced problems with all aspects, many of which may be anticipated to compromise clinical outcomes. Healthcare providers should be aware of these problems to effectively support patients with COPD with the use of their nebulisers at home.
ADJUVANT-ANTIGEN RELATIONSHIPS IN THE PRODUCTION OF EXPERIMENTAL "ALLERGIC" ENCEPHALOMYELITIS IN THE GUINEA PIG
Authors: Cheng-Mei Shaw, Ellsworth C. Alvord, Willson J. Fahlberg, Marian W. Kies
Journal: The Journal of Experimental Medicine (1962)

Quantitative relationships between the amounts of encephalitogenic neural tissue and mycobacterial adjuvant are presented for the guinea pig, for comparison with similar results obtained in the mouse and presented in an accompanying paper by Lee and Schneider (27). Definite threshold amounts of both neural encephalitogenic and mycobacterial adjuvant can be defined. With the proper amounts of each component, 100 per cent of guinea pigs can be made to develop EAE, 97 per cent dying of it, and over 50 per cent becoming paralyzed by the 12th day after challenge. With moderate amounts of encephalitogen the severity and incidence of EAE can be very great, but this encephalitogenic potential can be masked if large amounts of mycobacteria are employed. The mechanism of this masking effect by excess adjuvant is not known, but speculation centers upon the possibility of competition of antigens of the mycobacteria at the expense of those of the encephalitogen.
Deadly Dermatologic Diseases: Clinicopathologic Atlas and Text
Authors: Lawrence Charles Parish
Journal: JAMA (2007)

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
A Practical Handbook of Joint Fluid Analysis
Authors: H. Currey
Journal: Annals of the Rheumatic Diseases (1985)

Amyloid arthropathy in patients with chronic renal failure 733 synovial membrane and in the carpal tunnel, but without deposition in the abdominal fat or other manifestations of generalised amyloidosis; for these reasons we think that we are probably dealing with a form of amyloidosis which is peculiar to CRF treated with periodical haemodialysis.
Vitamin D serum levels and allergic rhinitis
Authors: M. Wjst, E. Hyppönen
Journal: Allergy (2007)

In addition to its role in the regulation of calcium metabolism, vitamin D has a number of immunological effects. Several studies in children found an effect of oral supplementation on allergic sensitization but so far there are no population‐based studies of vitamin D serum levels. We therefore examined 25(OH)‐D 3 status in 18 224 adults of the Third National Health and Nutrition Examination Survey. There was no effect on sensitization to a single allergen while the prevalence of allergic rhinitis increased across quartile groups of current vitamin D serum levels. The association could be due to unrecognized confounding, however, could also point towards an altered metabolism or an increased sensitivity to vitamin D in allergic patients.
Factors contributing to relief of exertional breathlessness during hyperoxia in chronic airflow limitation.
Authors: D E O'Donnell, D J Bain, K A Webb
Journal: American Journal of Respiratory and Critical Care Medicine (1997)

The mechanisms of exertional dyspnea relief in response to supplemental oxygen (O2) in chronic airflow limitation (CAL) are not precisely known and are likely multifactorial. To explore factors contributing to the relief of dyspnea after oxygen administration, 11 patients with severe CAL (FEV1.0 = 39 +/- 3% predicted, mean +/- SEM) and mild hypoxemia (resting PaO2 = 74 +/- 2 mm Hg) breathed room air (RA) and 60% O2 during exercise at approximately 50% of their maximal incremental exercise capacity. Breathlessness ratings (Borg scale), endurance time, respiratory drive (change in mouth occlusion pressure over the first 0.1 s of inspiration, P0.1), ventilation (VE), breathing pattern, operational lung volumes, gas exchange, and metabolic parameters were compared during RA and 60% O2. PaO2 at exercise cessation during RA and 60% O2 was 65 +/- 3 mm Hg and 226 +/- 12 mm Hg, respectively (p < 0.001). With 60% O2, the mean of individual Borg/time slopes fell significantly (p < 0.05) by 23 +/- 12% and was associated with a 35 +/- 11% increase (p < 0.01) in endurance time (r = -0.64, p < 0.05). During 60% O2, slopes of P0.1 and lactate over time also fell significantly (p < 0.05), whereas delta PaCO2/time did not change significantly. At a standardized time near end-exercise, Borg, VE, and P0.1 changed during 60% O2 by -0.8 +/- 0.3 (p < 0.05), -4.1 +/- 2.0 L/min (p = 0.07), and -1.3 +/- 0.5 cm H2O/s (p < 0.05), respectively. Slopes of Borg/VE, Borg/lactate, and VE/lactate were essentially superimposable during tests on RA and O2: Borg, lactate, and VE all fell proportionally during hyperoxia. In patients with CAL and mild exercise hypoxemia, relief of exertional breathlessness during hyperoxia is explained by reduced ventilatory demand in association with reduced blood lactate levels.
Zimbabwe appeals for medical aid as it declares state of emergency over cholera epidemic
Authors: R. Truscott
Journal: BMJ (2008)

Zimbabwe has finally declared a national emergency, because of the cholera epidemic that is sweeping the country and the collapse of state hospitals, and has appealed for international help.

David Parirenyatwa, the health minister, asked for drugs, laboratory reagents, renal and laundry equipment, x ray film, boilers, food for patients, and $11m (£7m; €9m) to persuade striking doctors and nurses to resume their work.

“Our central hospitals are literally not functioning,” he said. “The emergency appeal will help us reduce the morbidity and mortality associated with the current socioeconomic environment by December 2009.”

Cholera has killed at least 575 people in …
HLA and atopic dermatitis with high serum IgE Levels
Authors: Hidehisa Saeki, Shoji Kuwata, Hidemi Nakagawa, Takafumi Etoh, Masami Yanagisawa, Mitsuko Miyamoto, Katsushi Tokunaga, Takeo Juji, Yoichi Shibata
Journal: Journal of Allergy and Clinical Immunology (1994)
Correction of Serum Sodium for Glucose Concentration in Hemodialysis Patients With Poor Glucose Control
Authors: E. Lars Penne, Stephan Thijssen, Jochen G. Raimann, Nathan W. Levin, Peter Kotanko
Journal: Diabetes Care (2010)

As a rule of thumb in clinical medicine, the serum sodium concentration decreases by 1.6 mEq/l for every 100 mg/dl increase in glucose concentration due to water shifts from the intracellular to the extracellular compartment (1). This correction factor is based on theoretical considerations and has not been well validated. An experimental study in healthy subjects found significantly greater decreases in sodium concentration than expected when using the standard correction factor, especially when glucose concentrations were above 400 mg/dl (2). It was suggested that a correction factor of 2.4 mEq/l per 100 mg/dl increase in glucose concentration might be a better overall estimate of the association between the serum sodium and glucose concentrations (2).

Exact …
Research related to underlying mechanisms in atherosclerosis.
Authors: D Steinberg
Journal: Circulation (1979)

A brief resume of advances in atherosclerosis research over the past 30 years is presented, emphasizing the multidisciplinary origins of those advances. A somewhat more detailed review of progress in the lipoprotein field is presented as an example to illustrate the pace of research related to atherosclerosis. Finally, an attempt is made to identify some of the research areas that promise to yield valuable new insights in the next 30 years.
Frederick Nii Lomote Engmann
Authors: J. Baker
Journal: BMJ (2010)

Having completed his sixth form education in Ghana, Frederick Nii Lomote Engmann (“Fred”) was admitted to Emmanuel College, Cambridge. After three years he obtained a BA (Hons) in anatomy. He proceeded to St Thomas’ Hospital in London, where after another three years he qualified as an accredited doctor of medicine in June 1962. He did two house jobs and a senior house officer’s job in Britain.

He arrived back in Ghana just at the time when the first medical school in the country was being considered by senior doctors. He joined Professor Quartey (a urologist) in setting up the medical school from scratch (some people smiled at his enthusiasm, especially when he carried buckets to collect fetuses for the Anatomy Museum).

He went back to Cambridge and worked under Drs Ford …
Pressor response to saralasin (1-sar-8-ala-angiotensin II) bolus injection in hypertensive patients.
Authors: U A Waks, M H Maxwell, L Marks, E T Zawada, J J Kaufman
Journal: Circulation (1978)

A 10 mg bolus of the angiotensin blocker saralasin was injected 113 times in 68 subjects with essential or renovascular hypertension. Ninety percent of injections caused a transient increase in blood pressure, which correlated with plasma renin activity (PRA) (r = -0.54); Mean increase at 2 minutes was 21/13.4 mm Hg (P less than 0.001) and was independent of pre-injection control blood pressure, with a rapid decrease to or below control values thereafter. Thirty-seven subjects were studied on successive days before and after furosemide-induced sodium depletion (152 +/- 26 mEq [SE] sodium loss). In the low renin group, sodium depletion did not change PRA or the magnitude of the pressor response to saralasin, but significantly decreased control MAP by 13 mm Hg (P less than 0.01). In normal and high renin patients, MAP was unchanged after diuresis, but PRA increased significantly and the pressor response was attenuated. The net effect of sodium depletion was to reduce the pressor response to saralasin in all renin subgroups by 9 to 12 mm Hg. Saralasin bolus injection, unlike infusion, saturates available vascular receptors only briefly, eliminating prolonged pressor responses.
Adjuvant Chemotherapy in Colorectal Cancer: Mournful, Hopeful Perpetual Motion Machine Heads to Dim Light at End of Tunnel-Reply
Authors: Marc Buyse
Journal: JAMA (1989)

<h3>In Reply. —</h3> We could not have dreamed of clearer confirmation for the title of our article than these two letters, one claiming that randomized clinical trials of adjuvant chemotherapy in colorectal cancer are no longer needed because the benefit associated with treatment has been established clearly and the other claiming that no meaningful benefit has ever been, nor will soon be, demonstrated. We take issue with both claims and plead for a less glamorous, but more honest, acknowledgment of uncertainty. As potential patients with this disease, we find it ethically worrying that Dr Clouse would deny us the potential benefit of adjuvant therapy while Dr Bruckner would impose on us an as yet unproved therapy. We agree with the authors of the editorial<sup>1</sup>that the most rational attitude, and therefore that most consistent with ethics, is to perform further clinical trials in this disease. Such trials do not
Effect of truncal vagotomy on acid and pepsin: Response to a cholinergic drug in man
Authors: D. J. Cowley
Journal: Gut (1972)

The gastric output of acid and pepsin in response to two doses of the cholinergic drug carbachol was measured before and two months after complete truncal vagotomy and pyloroplasty in eight patients with duodenal ulcer. After vagotomy the basal output of acid and pepsin was reduced and there was no stimulation of secretion by a subthreshold dose of carbachol (0.5 units/kg) nor was there an increase in the response to a submaximal dose of carbachol (2.0 units/kg).Cannon's criteria for denervation supersensitivity of an organ were not obeyed with regard to acid or pepsin secretion.
Immunoregulation by low density lipoproteins in man. Inhibition of mitogen-induced T lymphocyte proliferation by interference with transferrin metabolism.
Authors: J A Cuthbert, P E Lipsky
Journal: Journal of Clinical Investigation (1984)

Human low density lipoprotein (LDL, d = 1.020-1.050 g/ml) inhibits mitogen-stimulated T lymphocyte DNA synthesis. Because both LDL and transferrin bind to specific cell surface receptors and enter cells by the similar means of receptor-mediated endocytosis, and because transferrin is necessary for lymphocyte DNA synthesis, we investigated the possibility that LDL may inhibit mitogen-stimulated lymphocyte responses by interfering with transferrin metabolism. LDL inhibited mitogen-stimulated lymphocyte [3H]thymidine incorporation in a concentration-dependent manner. The degree of inhibition was most marked in serum-free cultures, but was also observed in serum-containing cultures. The addition of transferrin not only augmented mitogen-induced lymphocyte [3H]thymidine incorporation in serum-free medium but also completely reversed the inhibitory effect of LDL in both serum-free and serum-containing media. Similar results were obtained when lymphocyte proliferation was assayed by counting the number of cells in culture. Transferrin also reversed the inhibition of lymphocyte responses caused by very low density lipoproteins and by cholesterol. The ability of transferrin to reverse the inhibitory effect of lipoproteins was specific, in that native but not denatured transferrin was effective whereas a variety of other proteins were ineffective. These results indicate that LDL inhibits mitogen-stimulated lymphocyte responses by interfering with transferrin metabolism. LDL only inhibited lymphocyte responses after a 48-h incubation if present from the initiation of the culture. By contrast, transferrin reversed inhibition when added after 24 h of the 48-h incubation. LDL did not inhibit lymphocyte responses by nonspecifically associating with transferrin. In addition, the acquisition of specific lymphocyte transferrin receptors was not blocked by LDL. Moreover, transferrin did not prevent the binding and uptake of fluorescent-labeled LDL by activated lymphocytes. Furthermore, LDL did not prevent the binding of transferrin to its receptor. Finally, LDL inhibition did not require specific high affinity cell surface receptors for cholesterol transport by LDL because similar inhibition and reversal by transferrin were observed with lymphocytes from a patient with homozygous familial hypercholesterolemia. Thus, LDL alters lymphocyte responses in a non-LDL receptor-mediated way by interfering with transferrin metabolism after specific binding of transferrin to receptors on activated lymphocytes.
Plasma levels of C1- inhibitor complexes and cleaved C1- inhibitor in patients with hereditary angioneurotic edema.
Authors: M Cugno, J Nuijens, E Hack, A Eerenberg, D Frangi, A Agostoni, M Cicardi
Journal: Journal of Clinical Investigation (1990)

C1- inhibitor (C1(-)-Inh) catabolism in plasma of patients with hereditary angioneurotic edema (HANE) was assessed by measuring the complexes formed by C1(-)-Inh with its target proteases (C1-s, Factor XIIa, and kallikrein) and a modified (cleaved) inactive form of C1(-)-Inh (iC1(-)-Inh). This study was performed in plasma from 18 healthy subjects and 30 patients with HANE in remission: 20 with low antigen concentration (type I) and 10 (from 5 different kindreds) with dysfunctional protein (type II). Both type-I and type-II patients had increased C1(-)-C1(-)-Inh complexes (P less than 0.0001), which in type I inversely correlated with the levels of C1(-)-Inh (P less than 0.001). iC1(-)-Inh was normal in all type-I patients and in type-II patients from three families with increased C1(-)-Inh antigen, whereas iC1(-)-Inh was higher than 20 times the normal values in patients from the remaining two families with C1(-)-Inh antigen in the normal range. None of the subjects had an increase of either Factor XIIa-C1(-)-Inh or kallikrein-C1(-)-Inh complexes. This study shows that the hypercatabolism of C1(-)-Inh in HANE patients at least in part occurs via the formation of complexes with C1- and that genetically determined differences in catabolism of dysfunctional C1(-)-Inh proteins are present in type-II patients.
VEGF-A stimulates lymphangiogenesis and hemangiogenesis in inflammatory neovascularization via macrophage recruitment
Authors: Claus Cursiefen, Lu Chen, Leonardo P. Borges, David Jackson, Jingtai Cao, Czeslaw Radziejewski, Patricia A. D’Amore, M. Reza Dana, Stanley J. Wiegand, J. Wayne Streilein
Journal: Journal of Clinical Investigation (2004)

Lymphangiogenesis, an important initial step in tumor metastasis and transplant sensitization, is mediated by the action of VEGF-C and -D on VEGFR3. In contrast, VEGF-A binds VEGFR1 and VEGFR2 and is an essential hemangiogenic factor. We re-evaluated the potential role of VEGF-A in lymphangiogenesis using a novel model in which both lymphangiogenesis and hemangiogenesis are induced in the normally avascular cornea. Administration of VEGF Trap, a receptor-based fusion protein that binds and neutralizes VEGF-A but not VEGF-C or -D, completely inhibited both hemangiogenesis and the outgrowth of LYVE-1(+) lymphatic vessels following injury. Furthermore, both lymphangiogenesis and hemangiogenesis were significantly reduced in mice transgenic for VEGF-A(164/164) or VEGF-A(188/188) (each of which expresses only one of the three principle VEGF-A isoforms). Because VEGF-A is chemotactic for macrophages and we demonstrate here that macrophages in inflamed corneas release lymphangiogenic VEGF-C/VEGF-D, we evaluated the possibility that macrophage recruitment plays a role in VEGF-A-mediated lymphangiogenesis. Either systemic depletion of all bone marrow-derived cells (by irradiation) or local depletion of macrophages in the cornea (using clodronate liposomes) prior to injury significantly inhibited both hemangiogenesis and lymphangiogenesis. We conclude that VEGF-A recruitment of monocytes/macrophages plays a crucial role in inducing inflammatory neovascularization by supplying/amplifying signals essential for pathological hemangiogenesis and lymphangiogenesis.
Why Withhold Tobacco?
Authors: J. L. Tracy
Journal: JAMA (1901)

Toledo, Sept. 25, 1901. <h3>To the Editor:</h3> —This question, whether he should be permitted to smoke or not, came up in the treatment of our late President, and possibly has in it a lesson which should be considered on account of the applicability which it may have to the treatment of surgical cases generally. Does the sudden stopping of the habitual use of tobacco make the bodily functions more resistant to the processes of disease, and more efficient in the healing of wounds? Does the nervous system, suffer and lose its balance by withholding its accustomed sedative? Are the secretory system, the excretory system, in fact all of the systems of the body, by the sudden taking from them of the load to which they have learned to adapt themselves, made stronger, or are they left stagnated because the stimulus which has been prompting them to their abnormal action has
Tryptophan Catabolism by Indoleamine 2,3-Dioxygenase 1 Alters the Balance of T <sub>H</sub> 17 to Regulatory T Cells in HIV Disease
Authors: David Favre, Jeff Mold, Peter W. Hunt, Bittoo Kanwar, P’ng Loke, Lillian Seu, Jason D. Barbour, Margaret M. Lowe, Anura Jayawardene, Francesca Aweeka, Yong Huang, Daniel C. Douek, Jason M. Brenchley, Jeffrey N. Martin, Frederick M. Hecht, Steven G. Deeks, Joseph M. McCune
Journal: Science Translational Medicine (2010)

The pathogenesis of human and simian immunodeficiency viruses is characterized by CD4(+) T cell depletion and chronic T cell activation, leading ultimately to AIDS. CD4(+) T helper (T(H)) cells provide protective immunity and immune regulation through different immune cell functional subsets, including T(H)1, T(H)2, T regulatory (T(reg)), and interleukin-17 (IL-17)-secreting T(H)17 cells. Because IL-17 can enhance host defenses against microbial agents, thus maintaining the integrity of the mucosal barrier, loss of T(H)17 cells may foster microbial translocation and sustained inflammation. Here, we study HIV-seropositive subjects and find that progressive disease is associated with the loss of T(H)17 cells and a reciprocal increase in the fraction of the immunosuppressive T(reg) cells both in peripheral blood and in rectosigmoid biopsies. The loss of T(H)17/T(reg) balance is associated with induction of indoleamine 2,3-dioxygenase 1 (IDO1) by myeloid antigen-presenting dendritic cells and with increased plasma concentration of microbial products. In vitro, the loss of T(H)17/T(reg) balance is mediated directly by the proximal tryptophan catabolite from IDO metabolism, 3-hydroxyanthranilic acid. We postulate that induction of IDO may represent a critical initiating event that results in inversion of the T(H)17/T(reg) balance and in the consequent maintenance of a chronic inflammatory state in progressive HIV disease.