tbuckley/cabot-search huggingface dataset:
ABC of intensive care: Transport of critically ill patients
Authors: P. G M Wallace, S. A Ridley
Journal: BMJ (1999)

Intensive care patients are moved within hospital—for example, to the imaging department—or between hospitals for upgraded treatment or because of bed shortages We will concentrate on transport of adults between hospitals, but the principles are similar for transfers within hospitals. #### Principles of safe transfer Although the Intensive Care Society and the Association of Anaesthetists have recommended that retrieval teams are established in the United Kingdom, 90% of patients are accompanied by staff from the referring hospital. Over 10 000 intensive care patients are transferred annually in the United Kingdom, but most hospitals transfer fewer than 20 a year. Each hospital thus has little expertise and few people gain knowledge of transport medicine. Most patients are accompanied by on call anaesthetic trainees. Not only does this leave the base hospital with inadequate on call staff but accompanying doctors often have little experience. Specially equipped ambulances are best for transferring patients Intensive care patients have deranged physiology and require invasive monitoring and organ support. Furthermore, they tend to become unstable on movement. Transport vehicles are not conducive to active intervention and no help is available. Staff and patients are vulnerable to vehicular accidents and may be exposed to temperature and pressure changes. #### Organisational structure ##### National and regional Department of Health, purchasers, and specialist societies have responsibility for ##### Hospital or trust Consultant with overall responsibility for transfers including
Is society losing control of the medical research agenda?
Authors: Brendan Delaney
Journal: BMJ (2006)

conflicts of interest. [2]3][4][5] Clinical research is dictated by the need to promote products of industry.In this sense, academics may have indeed lost control of the clinical research agenda.Many important questions in clinical research have no connections with specific products and thus would not be supported by industry. 8Such questions may never be funded or may not be cited frequently once published.The recent increase in funding for profit may not be solely due to the need of industry to advertise.Recent cuts in government research budgets, together with the steady increase of applications for funding, provide an opening for the private sector. 9 10 Trials sponsored by industry are more likely to show favourable outcomes, 11 and be published in prestigious journals.Randomised controlled trials usually receive many citations, 12 especially if they show "positive" results.Citations strengthen the prestige of the journal, and journals may wish to publish only those papers that are likely to be cited often, thereby creating a vicious circle. The future of academic medicineOur findings are in line with the scenario of "Academic Inc," with academic medicine evolving into an efficient enterprise that is directed by profit with strong ties to other profit making corporate structures. 13 Our findings do not agree with a scenario where academic medicine disappears.Most influential research originates from the US and other wealthy countries, a situation that is dissonant with a global view of health needs.Government and the public sector still make major contributions to academic research, despite the rapid increase in industry sponsorship.Medical research should reflect public needs more closely.NAP and AAA thank A Germenis for his encouragement.This work was conducted under the
Update on allergy immunotherapy: American Academy of Allergy, Asthma &amp; Immunology/European Academy of Allergy and Clinical Immunology/PRACTALL consensus report
Authors: A. Wesley Burks, Moises A. Calderon, Thomas Casale, Linda Cox, Pascal Demoly, Marek Jutel, Harold Nelson, Cezmi A. Akdis
Journal: Journal of Allergy and Clinical Immunology (2013)
Properdin: binding to C3b and stabilization of the C3b-dependent C3 convertase.
Authors: D T Fearon, K F Austen
Journal: The Journal of Experimental Medicine (1975)

A function of P in the alternative complement pathway is to prolong the first order decay of the hemolytic sites on EAC43B in a dose-dependent manner. As the number of initial convertase sites is not changed, even when activated properdin (P) increases the t1/2 10-fold or more, P acts to stabilize rather than to uncover additional sites. P binds to EAC43 to generate EAC43P in a reaction that proceeds slightly more rapidly at 15 degrees C than at 0 degrees C, but reaches the same plateau and does not require divalent cations. The presence of P on EAC43P not only stabilizes the convertase subsequently formed on that cell, but, alternatively, permits transfer to convertase sites on other cells with the stability of the recipient intermediate being dependent on the P available for transfer. The capacity of P to bind to C3b and stabilize C3B contrasts with the inhibitory effect of the C3b inactivator on formation of this amplification convertase.
Enumeration of the frequency of Langerhans cells in epidermis
Authors: F. A.Bahmer
Journal: British Journal of Dermatology (2002)

Journal Article Enumeration of the frequency of Langerhans cells in epidermis Get access F. A.Bahmer F. A.Bahmer Department of Dermatology, Central Hospital, Sankt‐Juergen‐Strasse, 28205 Bremen, Germany fbahmer@t‐online.de Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 147, Issue 6, 1 December 2002, Pages 1277–1278, https://doi.org/10.1046/j.1365-2133.2002.05000_10.x Published: 01 December 2002
Hypophosphataemia and Hyperphosphataemia in a Hospital Population
Authors: M. G. Betro, R. W. Pain
Journal: BMJ (1972)

One hundred cases of hypophosphataemia (</= 2.0 mg/100 ml) and 84 cases of hyperphosphataemia (>/= 5.0 mg/100 ml) occurring in a hospital population were studied in order to determine the cause of the abnormality. Examples of hyperphosphataemia due to renal failure were excluded from the study.A low serum phosphorus concentration was most frequently due to intravenous administration of carbohydrate, usually glucose, which accounted for 40% of cases. The next commonest cause was vomiting (12%). No obvious explanation could be found in 26% of cases, but in most of these factors were present which are known to affect phosphorus metabolism.No one cause of hyperphosphataemia was outstanding in frequency and in over 50% of cases no definite explanation for the abnormality could be found.
Pathologies of the West: An Anthropology of Mental Illness in Europe and America
Authors: T. Lewis
Journal: JAMA (2003)

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
Very low density lipoprotein triglyceride transport in type IV hyperlipoproteinemia and the effects of carbohydrate-rich diets
Authors: Steven H. Quarfordt, Arthur Frank, David M. Shames, Mones Berman, Daniel Steinberg
Journal: Journal of Clinical Investigation (1970)

Transport of plasma-free fatty acids (FFA) and of fatty acids in triglycerides of plasma very low density lipoproteins (VLDL-TGFA) was studied in two normal subjects, five patients with type IV hyperlipoproteinemia, and two patients with type I hyperlipoproteinemia. After intravenous pulse-labeling with albumin-bound 1-palmitate-(14)C, specific radioactivity of plasma FFA and VLDL-TGFA were determined at intervals up to 24 hr. The results were analyzed using several different multicompartmental models each compatible with the experimental data. Fractional transport of VLDL-TGFA was distinctly lower (no overlap) in the type IV patients than in the control subjects, both on a usual balanced diet (40% of calories from carbohydrate) and on a high-carbohydrate diet (80% of calories). However, net or total transport of VLDL-TGFA in the type IV patients was not clearly distinguishable from that in the control subjects, there being considerable overlap on either diet. The results suggest that in this group of type IV patients the underlying defect leading to the increased pool size of VLDL-TGFA is not overproduction but a relative defect in mechanisms for removal of VLDL-TGFA. Since some of these type IV patients had only a moderate degree of hypertriglyceridemia at the time they were studied, and since it is not established that patients with the type IV phenotype constitute a biochemically homogeneous population, the present results should not be generalized. Four studies were done (in two control subjects and two type IV patients) in which the kinetic parameters in the same individual were determined on the balanced diet and on the high-carbohydrate diet. All subjects showed an increase in VLDL-TGFA pool size. Using two of the models for analysis, all showed an increase in net transport of VLDL-TGFA; using the third model, three of the four studies showed an increase in VLDL-TGFA transport. The results are compatible with the interpretation that the carbohydrate-induced increase in VLDL-TGFA, both in controls and type IV patients, is at least in part due to an increased rate of production of VLDL-TGFA. The magnitude of the increase was approximately the same in controls and patients. Thus, metabolic adjustment to a high-carbohydrate regimen in these type IV patients may not be basically different from that in normal controls; the higher levels of VLDL-TGFA reached may simply be another reflection of a defective removal mechanism. An alternative interpretation, compatible with the data, would involve both a carbohydrate-induced increase in fractional rate of release of VLDL-TGFA from liver to plasma and a decrease in fractional removal of VLDL-TGFA from plasma without increase in net production rate. The simpler hypothesis of a single primary effect on net VLDL-TGFA production from FFA seems more likely.
A2.2 Acute Serum Amyloid A (A-SSA) Induces TIMP-1 in Dermal Fibroblasts that is Mediated Via a TLR-Dependent and Formyl Receptor-Independent Pathway
Authors: Steven O’Reilly, Rachel Cant, Marzena Ciechomska, Jacob M van Laar
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background and Objectives</h3> Systemic sclerosis (SSc) is an autoimmune connective tissue disorder characterised by inflammation and fibrosis. The fibrosis is due to an accumulation of extracellular matrix material due to enhanced deposition and/or reduced degradation. We and others have shown that abnormal production of TIMP-1 may contribute to fibrosis in SSc. Acute Serum Amyloid A (A-SAA) is an acute phase reactant and its levels correlate with ESR and CRP thus it is relevant in inflammatory conditions and has been demonstrated to be elevated in serum from SSc patients. The aim of this study was to determine the effects of A-SAA on dermal fibroblasts IL-6 and TIMP-1 secretion and its signalling mechanism downstream of ligation. <h3>Materials and Methods</h3> Human healthy dermal fibroblasts from punch biopsies were cultured at low passage and then treated with recombinant A-SAA (10 ug/ml) for 24 hours. After the set time points the cells were harvested and the supernatant removed. ELISAs were performed in triplicate for IL-6 TIMP-1, and MMP-1 levels. In some experiments cells were pretreated with 100 uM of WRW4, a specific formyl peptide receptor inhibitor with A-SAA. Also we used fibroblasts derived from a patient with a genetic non sense mutation that results in no IRAK-4 protein production and hence a halt in TLR signalling. IRAK-4 is a central downstream mediator of Toll-Like Receptor mediated signalling and is crucial for such signalling. <h3>Results</h3> Healthy human dermal fibroblasts incubated with A-SAA secreted high levels of IL-6 compared to untreated control cultures. Moreover A-SAA induced increased levels of TIMP-1 both at the mRNA levels and also the protein levels as determined by ELISA. Levels of the target of TIMP-1, MMP-1 protein levels were not altered at all. Thus the effect leads to a shift in the ratio of TIMP-1 to MMP-1 favouring ECM deposition. Pretreatment with WRW4 prior to A-SAA did not alter IL-6 or TIMP-1 expression levels, showing that the formyl peptide receptor plays no role in TIMP-1 induction mediated by addition of A-SAA. Furthermore cells derived from a gene deleted IRAK-4 patient with no IRAK-4 protein stimulated with A-SAA compared to control fibroblasts had TIMP-1, IL-6 levels compared to non-treated (media alone) dermal fibroblasts. <h3>Conclusions</h3> A-SSA induces TIMP-1, but importantly does not alter levels of TIMP-1 target MMP-1, thus shifting the TIMP-1/MMP-1 ratio. IL-6, a classic proinflammatory cytokine involved in SSc pathogenesis, is also elevated by A-SAA treatment in vitro. The signalling involved IRAK-4, a critical downstream messenger of TLR mediated signalling, but not formyl peptide receptors.
Serum leptin levels and leptin expression in growth hormone (GH)-deficient and healthy adults: Influence of GH treatment, gender, and fasting
Authors: Kurt Kristensen, Steen B. Pedersen, Sanne Fisker, Helene Nørrelund, Anne Mette Rosenfalck, J.O.L. Jørgensen, Bjørn Richelsen
Journal: Metabolism (1998)
Anesthetic Management in Electroconvulsive Therapy-Reply
Authors: John P. Callan
Journal: JAMA (1983)

apparent direct, incre¬ mental cost to the pharmacy for com¬ puterization. Depending on the total work volume of the facilities being served by the computer system, this varies from 4 to 10 cents per prescrip¬ tion order. Using an average cost per prescription of $7.21 (civilian average cost in 1980), this adds about 1% to the cost of a prescription. However, for this added 1%, the system remains cost-beneficial, since it pro¬ vides increased personnel productivi¬ ty, decreased redundant dispensing, and prevention of therapeutic errors, thereby improving the quality of patient care and conserving re¬
Hepatic HNF4α deficiency induces periportal expression of glutamine synthetase and other pericentral enzymes
Authors: Vesna S. Stanulović, Irene Kyrmizi, Marianna Kruithof-de Julio, Maarten Hoogenkamp, Jacqueline L. M. Vermeulen, Jan M. Ruijter, Iannis Talianidis, Theodorus B. M. Hakvoort, Wouter H. Lamers
Journal: Hepatology (2007)

In liver, most genes are expressed with a porto-central gradient. The transcription factor hepatic nuclear-factor4α (HNF4α) is associated with 12% of the genes in adult liver, but its involvement in zonation of gene expression has not been investigated. A putative HNF4α-response element in the upstream enhancer of glutamine synthetase (GS), an exclusively pericentral enzyme, was protected against DNase-I and interacted with a protein that is recognized by HNF4α-specific antiserum. Chromatin-immunoprecipitation assays of HNF4α-deficient (H4LivKO) and control (H4Flox) livers with HNF4α antiserum precipitated the GS upstream enhancer DNA only from H4Flox liver. Identical results were obtained with a histone-deacetylase1 (HDAC1) antibody, but antibodies against HDAC3, SMRT and SHP did not precipitate the GS upstream enhancer. In H4Flox liver, GS, ornithine aminotransferase (OAT) and thyroid hormone-receptor β1 (TRβ1) were exclusively expressed in pericentral hepatocytes. In H4LivKO liver, this pericentral expression remained unaffected, but the genes were additionally expressed in the periportal hepatocytes, albeit at a lower level. The expression of the periportal enzyme phosphoenolpyruvate carboxykinase had declined in HNF4α-deficient hepatocytes. GS-negative cells, which were present as single, large hepatocytes or as groups of small cells near portal veins, did express HNF4α. Clusters of very small GS- and HNF4α-negative, and PCNA- and OV6-positive cells near portal veins were contiguous with streaks of brightly HNF4α-positive, OV6-, PCNA-, and PEPCK-dim cells. Conclusion: Our findings show that HNF4α suppresses the expression of pericentral proteins in periportal hepatocytes, possibly via a HDAC1-mediated mechanism. Furthermore, we show that HNF4α deficiency induces foci of regenerating hepatocytes.
Lymphogranuloma Venereum-Reply
Authors: Bruce A. McLelland
Journal: JAMA (1976)

We welcome the comments of Schachter and Dawson. We are sure they would not choose to ignore elevated LGV-CF titers in selecting therapy for the sexual contacts of a girl who obviously had LVG. Their comments, however, might be misunderstood on the matter of therapy. It is astute that they've found positive CF titers in patients with either cervicitis or urethritis, but the sexual contacts in our study had neither problem. Our control patients also were sexually active adults, but without cervicitis, urethritis, or any prior history of venereal disease. In every instance but one, their LGV-CF titers were less than 1:8. Inasmuch as these authors agree that titers of 1:16 occur reliably in active LGV patients and in view of the serious debilitating abnormalities that can result from this disease, we believe that such patients deserved vigorous therapy. It would be an error to neglect simple treatment
EX-PRESIDENTS OF THE AMERICAN MEDICAL ASSOCIATION.
Authors: Nathan Smith Davis
Journal: JAMA (1899)

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
762-4 Importance of Microdeletions of Chromosomal Region 22q11 In the Etiology of Congenital Conotruncal Malformations: A 2 Year Prospective Study
Authors: Steven A. Webber, Eli Hatchwell, John C.K. Barber, John A. Crolla, Anthony P. Salmon, Barry R. Keeton, Nick R. Dennis, I. Karen Temple
Journal: Journal of the American College of Cardiology (1995)
Outsourcing the NHS
Authors: G. Iacobucci
Journal: BMJ (2015)

Where ideology outstrips performance

Outsourcing in the NHS in England has increased substantially over the past 15 years as both Labour and Tory led governments have pursued policies of divesting frontline care and non-medical support services to external suppliers. Department of Health figures show that the proportion of the overall NHS budget spent on private healthcare providers increased from 2.8% in 2006-07 to 6.1% in 2013-14.1 2 An independent study by Oxford Economics has calculated a growth in the private sector’s turnover from outsourced frontline healthcare services from £6.9bn (€9.3bn; $10.6bn) in 2010 to £12.2bn in 2013.3

Non-medical services such as finance, contracting, and IT have also been heavily outsourced. In 2010, the NHS Confederation estimated that the total spend on “back office” functions across the NHS in England was £2.8bn.4 It suggested that a minimum of £600m of this could be released for frontline care if it was divested from the NHS, presenting a big opportunity for the private sector.

It is difficult to quantify how much non-medical work in the NHS has been outsourced to date, but the direction of travel is clear, with the coalition government’s Health and Social Care Act 2012 set to prompt the full scale outsourcing …
Pneumatic perforation of the cecum during diagnostic sigmoidoscopy
Authors: D. Sánchez-Muñoz, C. Ortiz-Moyano, M. Ramírez-Martín del Campo, D. Núñez-Hospital, D. García-Romero, C. Delgado, P. Guerrero-Jiménez, J. Larraona-Moreno, M. Romero-Gómez
Journal: Endoscopy (2007)

An 80-year-old male patient underwent sigmoidoscopy to perform polypectomy. A complete colonoscopy 4 months before, had shown a 2 cm sessile, ulcerated polyp in the sigmoid colon, which was not resected. By this time, a stenotic mass lesion was found at the same location. Biopsies were taken and exploration finished, and the patient was referred for surgery with the diagnosis of colorectal carcinoma. Six hours after sigmoidoscopy, the patient returned to the hospital with acute abdominal pain and tenderness. X-ray showed pneumoperitoneum, undergoing emergency laparotomy. A 15 cm rupture along the cecum wall was observed. No signs of perforation were seen in the sigmoid area. Subtotal colectomy was carried out. Six months later, the patient is alive and being followed up by both surgeons and oncologists. The final diagnosis was “moderately differenced adenocarcinoma infiltrating mesenteric adipose tissue, with peritumoral and mesenteric lymph nodes extension”.