tbuckley/cabot-search huggingface dataset:
P20 * VARIATIONS IN MANAGEMENT OF LOW GRADE GLIOMAS ACROSS UK NEUROSURGICAL UNITS
Authors: C. H. Zhang, S. J. Price
Journal: Neuro-Oncology (2014)

INTRODUCTION: Low grade gliomas (LGG) are slow growing tumours, with the potential of transforming into aggressive high grade gliomas. Treatment of LGG must balance risk of malignant transformation against morbidity of early aggressive treatment. We evaluated the variation in management of low grade gliomas in the UK. METHOD: A survey was sent to all adult UK neurosurgery units, addressing surgical technology, treatment choice and surveillance. 23 units participated (82% participation rate). RESULTS: All LGG patients are discussed in an MDT meeting at initial presentation. 11 units manage patients in neurosurgical oncology clinics, and 6 units had dedicated LGG clinics. Others manage patients in general neurosurgical (3), combined (2) and oncology (1) clinics. The majority of centres use intra-operative ultrasound (20) and functional MRI (19) for motor and language mapping. 11 units use intra-operative EMG. Post-operative surveillance imaging intervals range from 3 to 12 months. Most units have multimodal MRI to detect tumour transformation, but do not always use them. Only 5 units use volumetric changes and 5 use PET imaging. Two clinical scenarios were also given: for a peripheral LGG, all units would consider resection followed by surveillance. Variable responses were given for an insular LGG: 9 would manage only with active surveillance, 6 would consider resection followed by surveillance. The rest choose to biopsy, followed by surveillance (4) or radiotherapy (4). CONCLUSION: This study demonstrates variable management of LGG across the UK, particularly surveillance intervals and of tumours in eloquent areas. More research to stratify transformation risk can help guide optimal treatment.
Stop the damaging drive towards a health market, former college president demands
Authors: G. Iacobucci
Journal: BMJ (2015)

The former chair of the Royal College of General Practitioners has issued an impassioned plea to UK politicians to “stop the relentless and damaging drive towards a health market.”

Speaking at the college’s City Health conference in London, Clare Gerada, who served as chair of the college from 2010 to 2013, warned that the NHS was “withering away” as a result of the current government’s policies.

Gerada told assembled …
Hypoxia, Hypoxia-Inducible Transcription Factor, and Macrophages in Human Atherosclerotic Plaques Are Correlated With Intraplaque Angiogenesis
Authors: Judith C. Sluimer, Jean-Marie Gasc, Job L. van Wanroij, Natasja Kisters, Mathijs Groeneweg, Maarten D. Sollewijn Gelpke, Jack P. Cleutjens, Luc H. van den Akker, Pierre Corvol, Bradly G. Wouters, Mat J. Daemen, Ann-Pascale J. Bijnens
Journal: Journal of the American College of Cardiology (2008)
Eruptive vellus hair cysts presenting as bluish-grey facial discoloration masquering as naevus of Ota
Authors: K.H.N. Chan, W.Y.M. Tang, W.Y. Lam, K.K. Lo
Journal: British Journal of Dermatology (2007)

Journal Article Eruptive vellus hair cysts presenting as bluish‐grey facial discoloration masquering as naevus of Ota Get access K.H.N. Chan, K.H.N. Chan Department of Dermatology, Centre of Health Protection, Pamela Youde Nethersole Eastern Hospital, Chai Wan, Hong Kong, China *Department of Pathology, Tuen Mun Hospital, Hong Kong, China E‐mail: kingsleychanhk@yahoo.com.hk; kingsleychan@ctimail.com Search for other works by this author on: Oxford Academic Google Scholar W.Y.M. Tang, W.Y.M. Tang Department of Dermatology, Centre of Health Protection, Pamela Youde Nethersole Eastern Hospital, Chai Wan, Hong Kong, China *Department of Pathology, Tuen Mun Hospital, Hong Kong, China E‐mail: kingsleychanhk@yahoo.com.hk; kingsleychan@ctimail.com Search for other works by this author on: Oxford Academic Google Scholar W.Y. Lam, W.Y. Lam Department of Dermatology, Centre of Health Protection, Pamela Youde Nethersole Eastern Hospital, Chai Wan, Hong Kong, China *Department of Pathology, Tuen Mun Hospital, Hong Kong, China E‐mail: kingsleychanhk@yahoo.com.hk; kingsleychan@ctimail.com Search for other works by this author on: Oxford Academic Google Scholar K.K. Lo K.K. Lo Department of Dermatology, Centre of Health Protection, Pamela Youde Nethersole Eastern Hospital, Chai Wan, Hong Kong, China *Department of Pathology, Tuen Mun Hospital, Hong Kong, China E‐mail: kingsleychanhk@yahoo.com.hk; kingsleychan@ctimail.com Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 157, Issue 1, 1 July 2007, Pages 188–189, https://doi.org/10.1111/j.1365-2133.2007.07926.x Published: 01 July 2007
Heart Association Discontinues Seal of Approval
Authors: Phil Gunby
Journal: JAMA (1990)

AMERICAN Heart Association officials are expected to announce a revamped "Heart-Guide" nutrition-education program this summer but, in the meantime, are discontinuing HeartGuide's food package seal of approval (<i>JAMA</i>. 1988;260:1192-1193). The Heart-Guide seal was to have begun appearing about now on packages and advertising for margarines and spreads, shortenings and oils, frozen dinners and entrées, canned and frozen vegetables, and crackers. Manufacturers were to be invited to submit their products for independent testing to determine if they met the association's guidelines for total fat, saturated fat, cholesterol, and sodium content. However, some food industry groups expressed concern, the US Department of Agriculture objected to the seal's use on meat or poultry products, and the Food and Drug Administration (FDA) suggested the seal might "tend to increase consumer confusion." (Originally, there was to be an administrative fee of $40 000 per year per brand and an educational fee of $5000 to $1
A Manual of Experimental Physiology for Students of Medicine.
Authors: Winfield S. Hall, Hall Winfield Scott
Journal: JAMA (1904)

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
EPIDEMIC JAUNDICE IN NEW YORK STATE, 1921-1922
Authors: HUNTINGTON WILLIAMS
Journal: JAMA (1923)

During the winter of 1921-1922, New York State was visited over a very wide area by so-called infectious or epidemic jaundice. This disease was present at the same time in other parts of the country. Previous to the epidemic, localized outbreaks had been studied by the New York State Department of Health in the village of Philadelphia, Jefferson County, in the winter of 1915-1916; at Berkshire, Tioga County, in March, 1920, and in Chenango County during February, 1921. The disease as it appeared at Cooperstown, N. Y., during the recent state-wide epidemic, has already been described.<sup>1</sup> It may be noted that during 1896 there occurred at Albany a well-marked outbreak of epidemic jaundice. At Hudson, N. Y., a similar epidemic occurred a few years previously. Reports from practitioners indicate that at certain localities in Delaware County, Allegany County and especially in St. Lawrence County repeated outbreaks of epidemic jaundice
HOME CARE OF PATIENTS WITH ACUTE POLIOMYELITIS
Authors: Philip M. Stimson
Journal: JAMA (1952)

Until recently poliomyelitis specialists and public health authorities generally advocated prompt hospitalization not only of all patients with early poliomyelitis but also of all patients suspected of having early poliomyelitis. There were, of course, good reasons for this, perhaps the most important being that a mild early case may become a serious one later in which the ultimate outcome may vary materially according to the care received, the best care naturally being obtained only in certain hospitals. Because of the resulting demand for hospital facilities, more and more hospitals have opened their doors to poliomyelitis patients. In some communities nearly 100% of actual poliomyelitis patients are being hospitalized, including many with only trivial infections. From 10 to 30% as many additional patients are hospitalized who are found not to have poliomyelitis. Of late, the pendulum has begun to swing back to home care in selected cases. There are good reasons
Spinal Cord Injury: Progress, Promise and Priorities
Authors: M D O'Brien
Journal: Journal of the Royal Society of Medicine (2006)

The tragic accident that left Christopher Reeves quadriplegic, his considerable efforts to cope with this utilizing all possible methods, and the publicity he generated, resulted in a much greater awareness of the problems faced by patients with spinal cord injuries, and was a powerful stimulus to research in this field.

This monograph is dedicated to his memory and has been produced by an expert committee, chaired by Richard T Johnson, in collaboration with the board of Neurosciences and Behavioral Health, at the request of the New York State Spinal Cord Injuries Research Board.

There are about 11 000 spinal cord injuries a year in the USA and nearly 250 000 patients living with these injuries—mostly young men in their late twenties and early thirties. The total annual cost in the USA is about US$10 billion. This puts spinal cord injury behind multiple sclerosis—but ahead of epilepsy, Parkinson's disease, Alzheimer's disease and stroke—in terms of annual cost per patient.

The pathophysiology of spinal cord injury and, in particular, factors which determine its progression are discussed in detail. Little can be done to alter the instant effect of injury, except for prophylaxis. However, the hope is that there might be effective protocols for the immediate management which might reduce the risk of further damage and perhaps arrest the development of the lesion, and hence reduce the long-term disability. At present, management is largely that of the complications including pain, spasticity, bladder and bowel dysfunction, autonomic disturbance and pressure sores; all of which are discussed in separate sections. Prospects for neuronal repair and regeneration remain theoretical and experimental.

Among the nine appendices are the outcome of 13 published clinical trials of methylprednisolone and an analysis of 321 published clinical trials and studies from 1998 to 2003, grouped by system or clinical problem (acute care, bladder and bowel, bone density, cardiovascular, exercise and locomotion, electrical and magnetic stimulation, imaging, psychological factors, spasticity, neurological responses, outcome measures, pain, physiological responses, respiration, syringomyelia and pressure sores).

This monograph will be essential reading for all those working in the field of spinal cord injury and an invaluable reference source. It should also stimulate research granting bodies and the Government to take a greater interest in research on spinal cord injuries, which is clearly underfunded and under-resourced.
A search for retrovirus infection in systemic lupus erythematosus and rheumatoid arthritis.
Authors: B K Pelton, M North, R G Palmer, W Hylton, C Smith-Burchnell, A L Sinclair, M Malkovsky, A G Dalgleish, A M Denman
Journal: Annals of the Rheumatic Diseases (1988)

Evidence for retroviral infection in general and human immunodeficiency virus (HIV) infection in particular was sought in freshly isolated peripheral blood T cells, B cells, and monocyte-macrophages from patients with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) and also in T cell and B cell lines established from the same source. Similar cells isolated from rheumatoid synovial membrane were also examined. The strategy used for the detection of virus was cocultivation with susceptible cell lines looking for syncytia formation, reverse transcriptase production, and nucleic acid hybridisation with HIV cDNA probes. No evidence for infection was obtained.
Identification and characterization of epitopes of the receptor for hyaluronic acid–mediated motility (RHAMM/CD168) recognized by CD8+ T cells of HLA-A2–positive patients with acute myeloid leukemia
Authors: Jochen Greiner, Li Li, Mark Ringhoffer, Thomas F. E. Barth, Krzysztof Giannopoulos, Phillipe Guillaume, Gerd Ritter, Markus Wiesneth, Hartmut Döhner, Michael Schmitt
Journal: Blood (2005)
Ethics of Hematopoietic Stem Cell Transplantation in Type 1 Diabetes Mellitus—Reply
Authors: Julio C. Voltarelli, Carlos E. B. Couri, Ana B. P. L. Stracieri, Maria C. Oliveira, Daniela A. Moraes, Fabiano Pieroni, Marina Coutinho, Kelen C. R. Malmegrim, Maria C. Foss-Freitas, Belinda P. Simões, Milton C. Foss, Elizabeth Squiers, Richard K. Burt
Journal: JAMA (2007)
Habituation and Urinary Retention
Authors: Juan L. Jammes
Journal: JAMA (1975)

Four subjects with partial or episodic complete urinary retention and bladder hypotonicity with large urinary residuals underwent "habituation" treatment. Results indicated an exponential decrease in urinary residuals to 0 ml and disappearance of partial or complete urinary retention within 20 weeks. This study is presented as an example of how conditioning therapy may be applied to the treatment of certain neurological disorders.
Fibrolipoma of the mitral valve in a child. Clinical and echocardiographic features.
Authors: P Barberger-Gateau, M Paquet, D Desaulniers, J Chenard
Journal: Circulation (1978)

Echocardiographic examination, performed in a 12-year-old boy who had signs of mitral regulation, showed the presence of an abnormal mass of echoes in the left atrium and mitral orifice. These were initially interpreted as representing an atrial myxoma. Surgical exploration showed that the tumor originated from the posterior leaflet of the mitral valve, and, microscopically, the lesion was diagnosed as a fibrolipoma. The clinical and echocardiographic features of this unique type of cardiac tumor are discussed.
Homemade Nitrous Oxide: No Laughing Matter
Authors: FRANK V. MESSINA
Journal: Annals of Internal Medicine (1982)

Brief Reports1 March 1982Homemade Nitrous Oxide: No Laughing MatterFRANK V. MESSINA, M.D., JAMES W. WYNNE, M.D.FRANK V. MESSINA, M.D.Search for more papers by this author, JAMES W. WYNNE, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-96-3-333 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptNitrous oxide, a common anesthetic gas, is produced by the combustion of ammonium nitrate (NH4NO3). Extensive commercial purification removes toxic by-products such as ammonia and oxides of nitrogen, principally nitric oxide (NO) and nitrogen dioxide (NO2). Rarely does the purification fail (1). We report a patient who had acute pulmonary toxicity after inhaling homemade nitrous oxide containing high levels of nitrogen dioxide. To our knowledge, a similar case has not been reported.A 20-year-old white man with a 3-day history of dyspnea, chills, pleuritic chest pain, wheezing, and coughing mucoid sputum came to the emergency room of Shands Teaching Hospital....References1. CLUTTON-BROCK J. Two cases of poisoning by contamination of nitrous oxide with higher oxides of nitrogen during anaesthesia. Br J Anaesth. 1967;39,388-92. CrossrefMedlineGoogle Scholar2. SHEDLINWALLECHINSKYSALYER MDS eds. Laughing Gas—Nitrous Oxide. Berkeley: and/or Press; 1973:48. Google Scholar3. . Nitrogen Oxides. Washington, DC: National Academy of Sciences; 1977:268-9. Google Scholar4. DAWSONSCHENKER SM. Health effects of inhalation of ambient concentrations of nitrogen dioxide. Am Rev Respir Dis. 1979;120,281-92. Editorial. MedlineGoogle Scholar5. SPRAGUE A. Nitrous oxide as an anesthetic. Boston Med Surg J. 1864;71:169. CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: University of Florida College of Medicine and the Veterans Administration Medical Center Gainesville, Florida PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byNeurologic, psychiatric, and other medical manifestations of nitrous oxide abuse: A systematic review of the case literatureNitrous Oxide Abuse IssuesSubstances volatilesInhalantsAutoerotic accident associated with self-applied ketamineFrostbite of the face after recreational misuse of nitrous oxideFatal Nitrous Oxide AbuseAsphyxial Deaths from the Recreational Use of Nitrous OxideDrug AbuseVolatile Substances of AbuseAdulterants and SubstitutesNitrous oxide, an opioid addictive agentNitrous oxide sedation/analgesia in emergency medicine 1 March 1982Volume 96, Issue 3Page: 333-334KeywordsAcademic medicineHeartInhalationIschemiaLungsMedical servicesNitratesNitric oxideSputumToxicity Issue Published: 1 March 1982 PDF downloadLoading ...
Do House Officers Learn From Their Mistakes?
Authors: Ann Persson
Journal: JAMA (1991)

To the Editor.  —The article by Wu et al 1 raises two important issues that need further discussion. One issue is about residents taking responsibility for their mistakes and the involvement of the attending physician. The second issue concerns the possible consequences of withholding information about mistakes from the involved patients or their families.  I am encouraged that 88% of residents spoke with somebody about their mistakes. However, I find it very unsatisfactory that only 54% of residents actually discussed their mistakes with their attending physicians. We cannot expect residents to accept responsibility for their mistakes unless the attending physicians or the institution teaches them to do so. An interesting question is why the residents did not discuss their mistakes with their attending physicians. Is it because the residents thought or believed that the attending physicians would not be supportive of them?  I agree with Wu et al that residents
Evidence for the catabolism of polychlorinated biphenyl-induced cytochrome P-448 by microsomal heme oxygenase, and the inhibition of delta-aminolevulinate dehydratase by polychlorinated biphenyls.
Authors: M D Maines
Journal: The Journal of Experimental Medicine (1976)

Polychlorinated biphenyls (PCB) are potent inducers of hepatic microsomal CO-binding hemoprotein P-448 (P1-450) and of delta-aminolevulinate synthetase (ALAS) activity. Inorganic cobalt was able to block PCB induction of cytochrome P-448 and to modify the PCB effect on ALAS activity in a time-dependent manner. PCB were also found to decrease the activity of delta-aminolevulinic acid dehydratase (ALAD) in liver. Pretreatment of rats with cobalt (30 min) produced the following changes in PCB actions on heme metabolism in liver: (a) augmentation of the porphyrinogenic effect of PCB, as determined by the total porphyrin content and ALAS activity; (b) augmentation of PCB inhibition of ALAD activity; and (c) blockade of induction of microsomal hemoprotein (cytochrome P-448). PCB did not interfere with cobalt induction of hepatic heme oxygenase activity. The sequence of administration of the metal and the PCB was important in relation to the changes produced in hepatic ALAS activity and microsomal hemoprotein and heme contents. When cobalt was administered 24 h after PCB treatment, the magnitude of induction of ALAS by PCB was lowered, and there was a great reduction in microsomal hemoprotein and heme contents. The renal response to PCB was different than that of the liver. In the kidney, PCB blocked the induction of heme oxygenase and depletion of cellular heme produced by cobalt. Furthermore, renal microsomal heme content was increased by PCB treatment alone or in combination with cobalt. It is concluded that (a) the heme moiety of microsomal cytochrome P-448 is metabolized by the heme oxygenase system, and it is suggested that for this catabolism to take place, the hemoprotein must be first converted to the denatured form of the hemoprotein, cytochrome P-420; (b) that the synthesis of heme in the kidney and the liver are regulated through different mechanisms; and (c) that ionic cobalt controls activity of ALAS by first inhibiting synthesis of the enzyme followed by the indirect induction of the enzyme as a result of the catabolism of heme, the physiological repressor of ALAS, by the metal-induced heme oxygenase. Thus microsomal heme oxygenase may be viewed as having an overall regulatory role in relation to mictochondrial ALAS by virtue of its ability to catabolize endogenous heme.
Primary Prevention of Diabetes Mellitus
Authors: Paul Z Zimmet
Journal: Diabetes Care (1988)

Two-thirds of all deaths in developed countries are caused by the major noncommunicable diseases, e.g., cardiovascular disease, cancer, and non-insulindependent diabetes mellitus (NIDDM). There is increasing evidence that these diseases are a consequence of life-style change, and they have a number of risk factors in common. Primary prevention of both insulin-dependent diabetes mellitus (IDDM) and NIDDM has become increasingly important because of their significant morbidity and mortality and the human and economic costs associated with diabetes and its complications. Prevention of the two major forms of diabetes, IDDM and NIDDM, are quite separate issues. The former appears to be an autoimmune disorder, whereas the latter should be considered along with other life-style-related noncommunicable diseases. The primary prevention of NIDDM appears to offer the greatest promise of success. The uncertainty that still exists as to the role of obesity and other risk factors in the development of NIDDM gives support to a multiple-risk-factor intervention approach (through a healthy life-style strategy) for NIDDM prevention.
Internal Mammary Artery Implantation: Effect on Myocardial Lactate Utilization
Authors: HARVEY G. KEMP, JOEL H. MANCHESTER, EZRA A. AMSTERDAM, WARREN J. TAYLOR, RICHARD GORLIN
Journal: Circulation (1970)

Twenty-three subjects with angiographically documented coronary heart disease were studied by means of arterial and coronary sinus catheterization before and one year after internal mammary artery implantations. The pre- and postoperative patterns of lactate extraction at rest and after isoproterenol stress have been determined and correlated with clinical improvement and angiographic patency of the implant. In group I 13 subjects had implants that were angiographically seen to fill some portion of the coronary circulation. Eight of 11 who produced lactate preoperatively reverted to normal lactate extraction. Two extracted lactate at both studies. All but two had clinical improvement. No deaths occurred over a mean follow-up period of 40 months (range 20 to 64). In group II ten subjects bad implants with no visible connection to the coronary circulation. Only one subject had reversion of lactate production to extraction and two from extraction to production. Seven of ten did not improve clinically. Three deaths occurred over a mean follow-up period of 39 months (range 17 to 53). Agreement has been found between reversion to normal lactate metabolism, angiographic patency, and clinical improvement following internal mammary artery implantation.