tbuckley/cabot-search huggingface dataset:
Colchicine in Familial Mediterranean Fever
Authors: RIDA A. FRAYHA
Journal: Annals of Internal Medicine (1977)

Letters and Corrections1 September 1977Colchicine in Familial Mediterranean FeverRIDA A. FRAYHA, M.D.RIDA A. FRAYHA, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-87-3-382_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: The cause and pathogenesis of familial Mediterranean fever (FMF) are not clear, hence treatment, by necessity, has been empirical. Prophylactic colchicine therapy has recently been shown to be highly effective in preventing the attacks by suppressing the inflammatory reaction and its symptoms without affecting the basic biorhythm or the underlying excitatory process (1, 2). The mechanism of action of colchicine in FMF remains unclear. Colchicine is known to disrupt the intracellular microtubular structures and to interfere with cellular motility and division. Dinarello and associates (3) have recently shown that patients with FMF on colchicine have significantly fewer...References1. GOLDSTEINSCHWABE RA: Prophylactic colchicine therapy in familial Mediterranean fever. A controlled, double-blind study. Ann Intern Med 81:792-794, 1974 LinkGoogle Scholar2. ZEMERREVACHPRAS DMM: A controlled trial of colchicine in preventing attacks of familial Mediterranean fever. N Engl J Med 291:932-934, 1974 CrossrefMedlineGoogle Scholar3. DINARELLOCHUSIDFAUCI CMA: Effects of prophylactic colchicine therapy on leukocyte function in patients with familial Mediterranean fever. Arthritis Rheum 19:618-622, 1976 CrossrefMedlineGoogle Scholar4. KHACHADURIANARMENIAN AH: The management of familial paroxysmal polyserositis. Experience with low-fat diets and Clofibrate. Leb Med J 25:495-502, 1972 MedlineGoogle Scholar5. STEINSTEIN OY: Colchicine-induced inhibition of very low-density lipoprotein release by rat liver in vivo. Biochem Biophys Acta 306:142-147, 1973 CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Department of Internal Medicine American University Hospital Beirut Lebanon PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 September 1977Volume 87, Issue 3Page: 382-382KeywordsColchicineFeversPathogenesis Issue Published: 1 September 1977 PDF DownloadLoading ...
Uptake of hematoporphyrin derivative by valvular vegetations in experimental infective endocarditis.
Authors: A M Spokojny, I N Sinclair, S Schnitt, S Paulin, J R Spears
Journal: Circulation (1985)

Drugs that localize in valvular vegetations may be useful in the diagnosis and treatment of infective endocarditis. We therefore tested the hypothesis that parenterally injected hematoporphyrin derivative (HPD), which is concentrated in tumors and atherosclerotic plaques, localizes in the vegetations of experimental infective endocarditis. In 14 rabbits, various bacteria were given intra-arterially immediately after injury to the aortic valve. In 12 additional rabbits, sterile vegetations on the aortic valve were produced by the trauma caused by an indwelling catheter that had been in place over a long period. HPD, 2.5 mg/kg, was injected intravenously 1 to 2 days before the animals were killed in six rabbits with sterile vegetations and in seven rabbits with infected vegetations. In all rabbits, multiple vegetations on the aortic valve leaflets were identified. On exposure to ultraviolet light, strong porphyrin fluorescence of all vegetations, whether sterile or infected, was observed only in rabbits given HPD. In two rabbits given HPD 10 weeks after catheter implantation across the aortic valve, however, only mild fluorescence could be detected in healing endocardial vegetations. In frozen sections of HPD-laden lesions, a patchy distribution of fluorescence was observed that was similar to the pattern of HPD localization in atheromatous plaques. Since vegetations in experimental infective endocarditis selectively concentrate HPD, porphyrins could be useful in the diagnosis and treatment of infective endocarditis.
PROSPECTIVELY TRIGGERED, VOLUMETRIC CARDIAC COMPUTED TOMOGRAPHY ANGIOGRAPHY ON A 320 DETECTOR ROW PLATFORM, REDUCES LENGTH OF STAY AND RADIATION EXPOSURE COMPARED TO RADIONUCLIDE MYOCARDIAL PERFUSION IMAGING IN LOW RISK, SYMPTOMATIC PATIENTS PRESENTING TO THE EMERGENCY ROOM
Authors: Kunal Bhatt, Sarah Rinehart, Abhinav Sharma, Wassim Odeh, Zhen Qian, Jesus Gustavo Vasquez Figueroa, Benjamin Kirkland, Szilard Voros
Journal: Journal of the American College of Cardiology (2012)
Thrombomodulin's lectin-like domain reduces myocardial damage by interfering with HMGB1-mediated TLR2 signalling
Authors: Christine Herzog, Anika Lorenz, Hans-Jörg Gillmann, Arpita Chowdhury, Jan Larmann, Thomas Harendza, Frank Echtermeyer, Martin Müller, Martina Schmitz, Jörg Stypmann, Daniela G. Seidler, Martin Damm, Sebastian N. Stehr, Thea Koch, Kai C. Wollert, Edward M. Conway, Gregor Theilmeier
Journal: Cardiovascular Research (2013)

Thrombomodulin (TM), via its lectin-like domain (LLD), exhibits anti-inflammatory properties partly by sequestering the pro-inflammatory cytokine, high-mobility group box 1 (HMGB1). Since myocardial damage after ischaemia and reperfusion is mediated by inflammation, we evaluated the cardioprotective effects of the LLD of TM. Using an in vivo mouse model of transient ischaemia and in vitro models of cardiomyocyte hypoxia, we assessed the ability of the LLD to suppress HMGB1-mediated activation of the receptors, receptor for advanced glycation endproducts (RAGEs) and Toll-like receptors (TLRs) 2 and 4. Thirty-minute myocardial ischaemia was induced in isoflurane-anaesthetized mice followed by 24 h of reperfusion in wild-type (WT) mice, in mice lacking the LLD of TM (TMLeD/LeD mice), and in WT with systemic overexpression of the LLD of TM induced by hydrodynamic transfection. Infarct size, HMGB1 protein, and apoptotic cells were significantly increased in TMLeD/LeD mice when compared with WT. Neonatal rat cardiomyocytes transfected with TLR2-, TLR4-, and RAGE-siRNA were exposed to hypoxia (0.8% O2) and reoxygenation (21% O2). HMGB1 augmented hypoxia-induced apoptosis in TLR2- but not in RAGE- or TLR4-suppressed cells. Administration of HMGB1- and TLR2-blocking antibodies in TMLeD/LeD mice prior to myocardial ischaemia diminished apoptosis. Therapeutic systemic gene therapy using the LLD reduced the infarct size and HMGB1 protein levels 24 h after reperfusion. The LLD of TM suppresses HMGB1-induced and TLR2-mediated myocardial reperfusion injury and apoptosis in vitro and in vivo.
Chloride/Phosphorus in Primary Hyperparathyroidism
Authors: CHARLES Y. C. PAK
Journal: Annals of Internal Medicine (1976)

Comments1 December 1976Chloride/Phosphorus in Primary HyperparathyroidismCHARLES Y. C. PAK, M.D., JUDITH TOWNSEND, R.N.CHARLES Y. C. PAK, M.D.Search for more papers by this author, JUDITH TOWNSEND, R.N.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-85-6-830 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: In 1974 Palmer, Nelson, and Bacchus (1) reported that the ratio of serum chloride to phosphorus (Cl/P) was significantly higher in patients with primary hyperparathyroidism than in those with hypercalcemia from other causes. This observation has beenconfirmed subsequently (2, 3). The higher value of Cl/P was attributed to the stimulation of renal bicarbonate and phosphate loss by parathyroid hormone. Recently Drago and associates (3) suggested that serum Cl/P might be useful, not only in the differentiation of primary hyperparathyroidism from other causes of hypercalcemia, but also in the diagnosis of primary hyperparathyroidism itself. It was implied...References1. PALMERNELSONBACCHUS FJH: The chloride-phosphate ratio in hypercalcemia. Ann Intern Med 80:200-204, 1974 LinkGoogle Scholar2. REEVESPALMERBACHUS CFH: Differential diagnosis of hypercalcemia by the chloride/phosphate ratio. Am J Surg 130:166-171, 1975 CrossrefMedlineGoogle Scholar3. DRAGOROHNERSANFORD JTE: Diagnosis of hyperparathyroidism. Urology 7:4-6, 1976 CrossrefMedlineGoogle Scholar4. PAKOHATALAWRENCE CME: The hypercalciurias: causes, parathyroid functions, and diagnostic criteria. J Clin Invest 54:387-400, 1974 CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Southwestern Medical School University of Texas Health Science Center at Dallas Dallas, TX 75235 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited BySerum Calcium to Phosphorous (Ca/P) Ratio Is a Simple, Inexpensive, and Accurate Tool in the Diagnosis of Primary HyperparathyroidismLaboratory Diagnosis of Primary HyperparathyroidismPrimary Hyperparathyroidism and Delirium in The ElderlyValue of laboratory tests in the differential diagnosis of hypercalcemiaEffects of changes in endocrine function on water and electrolyte metabolismPrimary hyperparathyroidismPrimary Hyperparathyroidism and Other Causes of HypercalcemiaChloride/Phosphorus Ratio and HyperparathyroidismM. DÍAZ-CURIEL, M.D., J.M. CASTRILLO, M.D., A. RAPADO, M.D.Hypercalcemia: Serum Chloride and PhosphateANTTI ARO, M.D., RISTO PELKONEN, M.D., ARTO SIVULA, M.D. 1 December 1976Volume 85, Issue 6Page: 830-830KeywordsBicarbonatesChloridesHypercalcemiaHyperparathyroidismParathyroid hormonePhosphatesPhosphorus Issue Published: 1 December 1976 PDF DownloadLoading ...
CUMULATIVE EXPOSURE TO IONIZING RADIATION FROM CARDIAC IMAGING PROCEDURES
Authors: Jersey Chen, Harlan M. Krumholz, Yongfei Wang, Joseph Ross, Reza Fazel, Henry Ting, Nilay Shah, James Brink, Khurram Nasir, Andrew J. Einstein, Brahmajee K. Nallamouthu
Journal: Journal of the American College of Cardiology (2010)
Traffic-Related Air Pollution and Otitis Media
Authors: Michael Brauer, Ulrike Gehring, Bert Brunekreef, Johan de Jongste, Jorrit Gerritsen, Maroeska Rovers, Heinz-Erich Wichmann, Alet Wijga, Joachim Heinrich
Journal: Environmental Health Perspectives (2006)

BackgroundOtitis media is one of the most common infections in young children. Although exposure to environmental tobacco smoke is a known risk factor associated with otitis media, little information is available regarding the potential association with air pollution.ObjectiveWe set out to study the relationship between exposure to traffic-related air pollution and otitis media in two birth cohorts.MethodsIndividual estimates of outdoor concentrations of traffic-related air pollutants—nitrogen dioxide, fine particles [particulate matter with aerodynamic diameters ≤ 2.5 μm (PM2.5)], and elemental carbon—were calculated for home addresses of approximately 3,700 and 650 infants from birth cohort studies in the Netherlands and Germany, respectively. Air pollution exposure was analyzed in relation to physician diagnosis of otitis media in the first 2 years of life.ResultsOdds ratios (adjusted for known major risk factors) for otitis media indicated positive associations with traffic-related air pollutants. An increase in 3 μg/m3 PM2.5, 0.5 μg/m3 elemental carbon, and 10 μg/m3 NO2 was associated with odds ratios of 1.13 (95% confidence interval, 1.00–1.27), 1.10 (1.00–1.22), and 1.14 (1.03–1.27) in the Netherlands and 1.24 (0.84–1.83), 1.10 (0.86–1.41), and 1.14 (0.87–1.49) in Germany, respectively.ConclusionsThese findings indicate an association between exposure to traffic-related air pollutants and the incidence of otitis media. Given the ubiquitous nature of air pollution exposure and the importance of otitis media to children's health, these findings have significant public health implications.
Intermittent Hypoxia Induces Early Functional Cardiovascular Remodeling in Mice
Authors: Maurice Dematteis, Cécile Julien, Christiane Guillermet, Nathalie Sturm, Sylvie Lantuejoul, Michel Mallaret, Patrick Lévy, Evelyne Gozal
Journal: American Journal of Respiratory and Critical Care Medicine (2007)

Intermittent hypoxia, a hallmark of sleep apnea, is a major factor for hypertension and impaired vasoreactivity.To examine the temporal occurrence of these two outcomes in order to provide insight into mechanisms and early cardiovascular disease identification.Functional and structural cardiovascular alterations were assessed in C57BL6 mice exposed to intermittent hypoxia (21-4% Fi(O(2)), 30-s cycle, 8 h/d) or air for up to 35 days. Blood pressure, heart rate, and urinary catecholamines were measured at Days 1 and 14. Hindquarter vasoreactivity was assessed at Days 14 and 35, including vasoconstriction to norepinephrine, endothelium-, and non-endothelium-dependent vasodilation. Aorta, heart, and hindquarter skeletal muscles were immunostained for vascular markers PECAM-1 and collagen IV.Hemodynamic alterations occurred from Day 1, characterized by blood pressure surges with bradytachyarrhythmia driven by cyclic hypoxia. At Day 14, blood pressure at normoxia was elevated, with predominant diastolic increase. With hypoxia, vasopressive catecholamines were elevated, blood pressure surged with a lower hypoxic threshold, whereas heart rate fluctuations decreased. Histologic alterations started from Day 14, with decreased endothelial PECAM-1 expression in descending aorta and left heart. Impaired peripheral vasoreactivity occurred at Day 35, including hypervasoconstriction to norepinephrine secondary to sympathetic hyperactivity, without changes in pre- and postsynaptic alpha-adrenoceptors or in endothelium- and non-endothelium-dependent vasodilation.Intermittent hypoxia induces sequential cardiovascular events suggesting increased chemoreflex and depressed baroreflex, resulting in sympathoadrenal hyperactivity, early hemodynamic alterations with proximal histologic remodeling, and delayed changes in peripheral vasoreactivity. Such early alterations before overt cardiovascular disease strengthen the need for identifying at-risk individuals for systematic treatment.
Applying to do research studies in the NHS is to be made easier
Authors: K. Chinthapalli
Journal: BMJ (2012)

The Department of Health has given the go ahead to plans to simplify the approval process for research studies in the NHS. The Health Research Authority (HRA), set up last year, will now consult on a proposed single assessment for new studies and trial a pilot scheme by next spring.

The authority’s chief executive, Janet Wisely, said, “The HRA welcomes the opportunity to lead this and other work, to make it easier to do good quality research in the UK. The potential for improvement by radically simplifying how we assess research is significant, and we plan to work closely and effectively with others to determine how …
Serum Lipoprotein and Cholesterol Concentrations
Authors: NEVIN S. SCRIMSHAW, MARTHA TRULSON, CARLOS TEJADA, D. MARK HEGSTED, FREDRICK J. STARE
Journal: Circulation (1957)

A previous study indicated that Guatemalan Indians, both male and female, tended to maintain low levels of serum cholesterol throughout adulthood but that beta-lipoprotein fractions increased with age, as is usually the case in populations in the United States. To investigate whether race was of importance in this unexpected dissociation between these lipid fractions, a similar study was done with a rural group in Costa Rica, which was comparable in the diet consumed and in many other environmental factors, but of pure European origin. At all ages the cholesterol values were slightly higher but the same type of dissociation was observed.
Clinical Data Release: How Soon?
Authors: Charles Marwick
Journal: JAMA (1991)

WHEN publicly funded research results have immediate effect on patient care, should the funding agency announce the findings before they are published in a scientific journal? National Institutes of Health (NIH) officials in Bethesda, Md, are pondering this question and awaiting guidelines that might help with such early release "clinical alerts." The NIH's National Cancer Institute was the first to grapple with the issue in May 1988, when it announced an adjuvant therapy for breast cancer. Then, in October 1989, that institute issued a "clinical update" on colon cancer management. This sort of decision has put the NIH at the center of discussion of whether to make early release of the information or use the traditional but usually more time-consuming route of initial publication in the scientific literature. The advice from several speakers came at a meeting called by the NIH to discuss ways in which this policy can be
Reply to Y.-T. Lan et al
Authors: Leonard L. Gunderson, J. Milburn Jessup, Frederick L. Greene
Journal: Journal of Clinical Oncology (2010)

We appreciate the thoughtful comments of Lan et al from Taiwan. We are pleased that they feel the Surveillance, Epidemiology, and End Results (SEER) outcomes data for 130,762 patients with colon cancer provide powerful evidence to support the revised staging system for colorectal cancer in the seventh edition of the American Joint Committee on Cancer (AJCC) Cancer Staging Manual. The letter by Lan et al centers on the finding that a small percentage of patients with Tis colon cancers in the SEER analysis had involved lymph nodes (114 TisN lesions in 5,935 patients with TisN0-N lesions or 1.9%). Lan et al mention the widely held concept that lymphatic vessels are not found in the mucosal layer and therefore lymph node metastases should not occur but note recent immunohistochemical data showing the presence of lymphatic channels extending to colonic mucosa in neoplastic and inflammatory conditions. In Lan’s institution, involved nodes were found in only one of 118 patients with Tis lesions who had a regional resection, and on pathologic review, the lesion was in fact T2N , not TisN , based on extension of the primary lesion into the superficial muscularis propria. Accordingly, Lan et al suggest that slides of all TisN patients in the SEER colon analysis should be re-reviewed, if possible, to be certain they were limited to the mucosa. Given the possibility of involved nodes in patients with intramucosal colorectal cancers, Lan et al also note that for patients with presumed Tis lesions, further investigation is warranted to define the high-risk group before considering local treatment options such as endoscopic mucosal or submucosal resection. Although we did not comment on patients with Tis lesions in our article, we agree with Lan et al that the finding of involved nodes in patients with intramucosal colorectal cancers (Tis) is both unexpected and uncommon (1.9% in SEER colon analysis and 2.1% in SEER rectal analysis [75 TisN lesions in 3,614 patients with TisN0-N rectal cancer). Even though it would be of interest to review the slides of all patients with TisN lesions in the SEER colon and rectal analyses, unfortunately we cannot attempt such. Many of the blocks are now unavailable for study, so a review of available material would be unavoidably biased. Given the extremely low risk of nodal involvement in patients with Tis lesions, it is reasonable to consider local treatment options in such patients, unless high-risk pathologic findings are identified when the lesion is biopsied.
Unicef seeks $900m for children and women worldwide
Authors: John Zarocostas
Journal: BMJ (2008)

Graduates from some UK medical schools consistently perform better than others in postgraduate medical exams, says a study published this week.The authors say that their finding supports the introduction of a national licensing examination for doctors.The study retrospectively analysed the performance from 2003 to 2005 of 5827 doctors from 19 UK medical schools in one or more of the three examinations required for membership of the Royal College of Physicians.This is an international postgraduate assessment that is important for career progression and is attempted by about 30% of all UK medical graduates.The research group looked at performance in parts 1 and 2 of the written examination, which are multiple choice assessments, and in part 2 of the practical examination of clinical assessment skills (PACES), which uses real and simulated patients to test clinical examination and communication skills.A further analysis involved data on performance in the part 1 examination over a much longer timeframe, from 1989 to 2002.The results showed that graduates from Oxford, Cambridge, and Newcastle upon Tyne performed significantly better than average in part 1 and part 2 of the written examination (BMC Medicine 2008;6:5).Those from Liverpool, Dundee, Belfast, and Aberdeen showed significantly below average performance.Ninety one per cent of Oxford students, 76% from Cambridge, and 67% from Newcastle passed part 1 at their first attempt, whereas the figures were 32% for Liverpool, 38% for Dundee, 37% for Belfast, and 41% for Aberdeen.The overall relation between medical school and exam performance was highly significant (χ 2 =300, df=6, P<0.001).About 60% of the variance between medical schools was explained by differences in pre-admission qualifications (according to number of points gained, but not subjects taken, in A level examinations or in the Scottish highers).However, the remaining portion of the variance was still significant. Doctors from different schools vary in later postgraduate examsUK NEWS BMA advises GPs on longer opening hours, p 351 World NEWS Inquiry finds scientists collaborated with Nazis, p 353 bmj.comCharity is set up to improve adolescents' health care newS
An in vitro system for study of effects of angiotensin I on cultured endothelial cells
Authors: S. P BAGBY, W. E HOLDEN
Journal: Cardiovascular Research (1989)

Since certain non-vascular angiotensin II (AII) receptors may be activated by angiotensin I (AI), and since sustained increase in AI levels accompanies chronic treatment with converting enzyme inhibitors (CEI) which block conversion of AI to AII, the question of whether AI has significant biological effects is of clinical relevance. We therefore sought to develop an in vitro culture system in which effects of angiotensin I, independently of its conversion to AII, could be studied in cloned aortic vascular endothelial cells (VEC). This was complicated by peptide degradation during the period of observation, both by angiotensin converting enzyme (ACE) on the surface of VEC and by angiotensinases in either the serum component of culture media or associated with the cell monolayer. Accordingly, we examined the half life of AI under relevant cell culture conditions, with and without confluent fetal bovine aortic endothelial cells (FBAEC). Factors assessed included (1) fetal calf serum: commercial source, concentration in culture media, effects of converting enzyme inhibitor (CEI: MK422) and/or heat inactivation (superimposed on the commercially performed process); and (2) effect of FBAEC in monolayer culture, with and without CEI. Results showed that (1) in the absence of cells, loss of AI in culture media, when present, was solely due to the presence of fetal calf serum (FCS) and showed a dose dependent response; (2) FCS from differing sources may vary dramatically in capacity for AI breakdown; and (3) serum related AI disapperance included a heat resistant ACE like component (inhibitable by CEI) and a heat sensitive/CEI resistant component dominant at concentrations of FCS exceeding 5%. FBAEC dependent AI loss was solely due to CEI inhibitable ACE like activity, with no evidence for non-ACE angiotensin activity detectable in confluent monolayer cultures. Cloned FBAEC retained ACE like activity, which is compatible with persistence of a differentiated phenotype. Thus optimum conditions for study of effects of AI on vascular endothelial cells, with sustained AI levels over a 24 h period, can be achieved by inclusion of 10−6M MK422, provided that the culture medium is either serum free or contains FCS selected for low AI degrading activity.