tbuckley/cabot-search huggingface dataset:
Research in hand osteoarthritis: time for reappraisal and demand for new strategies. An opinion paper
Authors: M. Kloppenburg, T. Stamm, I. Watt, F. Kainberger, T. E Cawston, F. N Birrell, I. F Petersson, T. Saxne, T. K Kvien, B. Slatkowsky-Christensen, M. Dougados, L. Gossec, F. C Breedveld, J. S Smolen
Journal: Annals of the Rheumatic Diseases (2007)

<b>Background:</b> Osteoarthritis of the hands is a prevalent musculoskeletal disease with a considerable effect on patients' lives, but knowledge and research results in the field of hand osteoarthritis are limited. Therefore, the Disease Characteristics in Hand OA (DICHOA) initiative was founded in early 2005 with the aim of addressing key issues and facilitating research into hand osteoarthritis. <b>Objective:</b> To review and discuss current knowledge on hand osteoarthritis with regard to aetiopathogenesis, diagnostic criteria, biomarkers and clinical outcome measures. <b>Methods:</b> Recommendations were made based on a literature review. <b>Results:</b> Outcomes of hand osteoarthritis should be explored, including patient perspective on the separate components of disease activity, damage and functioning. All imaging techniques should be cross-validated for hand osteoarthritis with clinical status, including disease activity, function and performance, biomarkers and long-term outcome. New imaging modalities are available and need scoring systems and validation. The role of biomarkers in hand osteoarthritis has to be defined. <b>Conclusion:</b> Future research in hand osteoarthritis is warranted.
Osteoporosis in Older Persons: Pathophysiology and Therapeutic Approach
Authors: Neil Binkley
Journal: JAMA (2008)

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
Malignant GIST masquerading as a bleeding duodenal diverticulum
Authors: N. Gupta, B. Schirmer, R. Mishra, V. Shami
Journal: Endoscopy (2007)

A 63-year-old man was accepted in transfer with a diagnosis of gastrointestinal bleeding from a duodenal diverticulum. An apparent bleeding diverticulum was visualized on repeat endoscopy at the junction of the second and third part of the duodenum ([Figure 1]). Computed tomography scan revealed a large (15 × 10 cm) heterogeneous centrally hemorrhagic mass in the right anterior pararenal space, abutting both the pancreas and the duodenum ([Figure 2 a] and [Figure 2 b]). At laparotomy, a 15 × 12 × 10 cm mass was found in the retroperitoneum immediately posterolateral to, and intimately associated with, the second part of the duodenum ([Figure 3]). The mass was dissected with a cuff of duodenal wall, which when divided demonstrated a defect in the posterolateral wall of the duodenum, corresponding to the location of the diverticulum on endoscopy. The center of the mass had cavitated secondary to necrosis and was full of clot. This was in continuity with the lumen of the duodenum, thus giving the appearance of a bleeding diverticulum on endoscopy ([Figure 4]). Surgical pathology confirmed a spindle cell tumor consistent with high-grade gastrointestinal stromal tumor (GIST), staining positive for Vimentin and CD 117 (ckit) and negative for S100, CD56, SMA, and MSA. The patient was discharged in a stable condition, for follow-up with oncology. This constitutes the first report in the literature of a gastrointestinal stromal tumor mimicking a bleeding duodenal diverticulum.
Dreaming of a fairer world
Authors: F. Godlee
Journal: BMJ (2010)

I wrote about the paper by David Stuckler and colleagues when it went online two weeks ago ( BMJ 2010;340:c3311, doi:10.1136/bmj.c3311). Now it’s in print, and it couldn’t be more relevant to the debate in the UK and elsewhere about how much to cut from social welfare budgets and what the cuts will do to health. Much damage, is the answer from these authors. They conclude that spending on social welfare may be more important for health than spending on health care. Over the past 30 years when social spending in Europe was high mortality fell, but when it was low, mortality rose substantially.

They quote Michael Marmot: …
Recommendations of the National Heart, Lung, and Blood Institute Heart and Lung Xenotransplantation Working Group
Authors: Jeffrey Platt, Verdi DiSesa, Dorothy Gail, Judith Massicot-Fisher
Journal: Circulation (2002)

The National Heart, Lung, and Blood Institute (NHLBI) recently convened the Heart and Lung Xenotransplantation Working Group to identify hurdles to the clinical application of xenotransplantation, defined as the use of animal organs or tissue for transplantation, and to recommend possible solutions to these problems. The group consisted of experts in xenotransplantation from academia, industry, and federal agencies, and the discussions focused on those areas within the mission of the NHLBI. The areas covered included immunologic and physiological barriers to xenotransplantation, the limitations of the current animal models, the need for collaboration among groups, the high costs of studies using nonhuman primates and genetic engineering of pigs, and the unique problems of lung xenotransplantation. This report is a summary of those discussions.
REGULATION AND INHIBITION OF ARACHIDONIC ACID ω-HYDROXYLASES AND 20-HETE FORMATION
Authors: Deanna L. Kroetz, Fengyun Xu
Journal: The Annual Review of Pharmacology and Toxicology (2004)

Cytochrome P450-catalyzed metabolism of arachidonic acid is an important pathway for the formation of paracrine and autocrine mediators of numerous biological effects. The omega-hydroxylation of arachidonic acid generates significant levels of 20-hydroxyeicosatetraenoic acid (20-HETE) in numerous tissues, particularly the vasculature and kidney tubules. Members of the cytochrome P450 4A and 4F families are the major omega-hydroxylases, and the substrate selectivity and regulation of these enzymes has been the subject of numerous studies. Altered expression and function of arachidonic acid omega-hydroxylases in models of hypertension, diabetes, inflammation, and pregnancy suggest that 20-HETE may be involved in the pathogenesis of these diseases. Our understanding of the biological significance of 20-HETE has been greatly aided by the development and characterization of selective and potent inhibitors of the arachidonic acid omega-hydroxylases. This review discusses the substrate selectivity and expression of arachidonic acid omega-hydroxylases, regulation of these enzymes during disease, and the application of enzyme inhibitors to study 20-HETE function.
Demonstration of reduced mitogenic and osteoinductive activities in demineralized allogeneic bone matrix from vitamin D-deficient rats.
Authors: R T Turner, J Farley, J J Vandersteenhoven, S Epstein, N H Bell, D J Baylink
Journal: Journal of Clinical Investigation (1988)

Osteoinduction is the formation of ectopic bone that follows implantation of demineralized allogeneic bone matrix (DABM) and is believed to be secondary to the release of associated inductive factors from bone matrix. To clarify the role of vitamin D in osteoinduction, we implanted DABM from vitamin D-deficient rats (-D rats) into normal rats (+D rats). Because mitogens and osteocalcin might be involved in osteoinduction, these were measured. Mitogenic activity in extracts from mineralized allogeneic bone matrix (ABM) and DABM from both +D and -D rats was determined with an assay that utilizes monolayer cultures of embryonic chick calvarial cells. Osteocalcin in serum and DABM was measured by radioimmunoassay. DABM from -D rats did not promote osteoinduction as effectively as DABM from +D rats. Resorption of implant matrix from -D rats was diminished compared with resorption of matrix from +D rats (P less than 0.01), and the decrease was attributed to a corresponding decrease in the number of osteoclasts in the implants (P less than 0.02). Bone formation (P less than 0.01) and total implant mineralization (P less than 0.001) were significantly reduced in implants from -D rats, and the reductions corresponded with a decline in the number of osteoblasts (P less than 0.05). Mitogenic activity in DABM from +D rats was only slightly decreased as compared with activity in ABM, but DABM from -D rats contained significantly less activity (P less than 0.001). No mitogenic activity was identified in implants of DABM from either +D or -D rats 3 wk after implantation. Serum osteocalcin was significantly higher in -D as compared with +D animals. In contrast, the concentrations of osteocalcin in DABM from the two groups of animals were not significantly different from each other. These findings indicate that the diminished osteoinductive activity of DABM from -D rats results from deficiency of one or more mitogenic factors that are essential for inducing the proliferation and differentiation of bone cells at the implant site and that osteocalcin does not play a role in this regard.
Mechanisms of glucagon secretion during insulin-induced hypoglycemia in man. Role of the beta cell and arterial hyperinsulinemia.
Authors: G Bolli, P De Feo, G Perriello, S De Cosmo, P Compagnucci, F Santeusanio, P Brunetti, R H Unger
Journal: Journal of Clinical Investigation (1984)

To elucidate the mechanisms controlling the response of glucagon to hypoglycemia, a vital component of the counterregulatory hormonal response, the role of intraislet insulin was studied in seven normal subjects and five subjects with insulin-dependent diabetes mellitus (IDDM) (of less than 15-mo duration). In the normal subjects, hypoglycemia (arterial plasma glucose [PG] 53 +/- 3 mg/dl) induced by an intravenous insulin infusion (30 mU/m2 X min for 1 h, free immunoreactive insulin [FIRI] 58 +/- 2 microU/ml) elicited a 100% fall in insulin secretion and an integrated rise in glucagon of 7.5 ng/ml per 120 min. When endogenous insulin secretion was suppressed by congruent to 50 or congruent to 85% by a hyperinsulinemic-euglycemic clamp (FIRI 63 +/- 1.5 or 147 +/- 0.3 microU/ml, respectively) before hypoglycemia, the alpha cell responses to hypoglycemia were identical to those of the control study. When the endogenous insulin secretion was stimulated by congruent to 100% (hyperinsulinemic-hyperglycemic clamp, FIRI 145 +/- 1.5 microU/ml, PG 132 +/- 2 mg/dl) before hypoglycemia, the alpha cell responses to the hypoglycemia were also superimposable on those of the control study. Finally, in C-peptide negative diabetic subjects made euglycemic by a continuous overnight intravenous insulin infusion, the alpha cell responses to hypoglycemia were comparable to those of normal subjects despite absent beta cell secretion, and were not affected by antecedent hyperinsulinemia (hyperinsulinemic-euglycemic clamp for 2 h, FIRI 61 +/- 2 microU/ml). These results indicate that the glucagon response to insulin-induced hypoglycemia is independent of the level of both endogenous intraislet and exogenous arterial insulin concentration in normal man, and that this response may be normal in the absence of endogenous insulin secretion, in contrast to earlier reports. Thus, loss of beta cell function is not responsible for alpha cell failure during insulin-induced hypoglycemia in IDDM.
Accumulated Evidence on Fish Consumption and Coronary Heart Disease Mortality
Authors: Ka He, Yiqing Song, Martha L. Daviglus, Kiang Liu, Linda Van Horn, Alan R. Dyer, Philip Greenland
Journal: Circulation (2004)

Results from observational studies on fish consumption and coronary heart disease (CHD) mortality are inconsistent.A meta-analysis of cohort studies was conducted to examine the association between fish intake and CHD mortality. Studies were included if they provided a relative risk (RR) and corresponding 95% CI for CHD mortality in relation to fish consumption and the frequency of fish intake. A database was developed on the basis of 11 eligible studies and 13 cohorts, including 222 364 individuals with an average 11.8 years of follow-up. Pooled RR and 95% CI for CHD mortality were calculated by using both fixed-effect and random-effect models. A linear regression analysis of the log RR weighted by the inverse of variance was performed to assess the possible dose-response relation. Compared with those who never consumed fish or ate fish less than once per month, individuals with a higher intake of fish had lower CHD mortality. The pooled multivariate RRs for CHD mortality were 0.89 (95% CI, 0.79 to 1.01) for fish intake 1 to 3 times per month, 0.85 (95% CI, 0.76 to 0.96) for once per week, 0.77 (95% CI, 0.66 to 0.89) for 2 to 4 times per week, and 0.62 (95% CI, 0.46 to 0.82) for 5 or more times per week. Each 20-g/d increase in fish intake was related to a 7% lower risk of CHD mortality (P for trend=0.03).These results indicate that fish consumption is inversely associated with fatal CHD. Mortality from CHD may be reduced by eating fish once per week or more.
Symptomatic Paget Disease of the Hip
Authors: Lee C. Detenbeck
Journal: JAMA (1973)

Symptomatic Paget disease about the hip may involve the pelvis or femur or both. Pain usually related to weight-bearing can occur and is associated with medial or concentric joint space narrowing. Surgery may be required for relief of symptoms, especially when arthrokatadysis is present. Total hip arthroplasty utilizing methylmethacrylate has been satisfactory in relieving pain and improving motion. Subtrochanteric and, less frequently, femoral neck fractures occasionally complicate Paget disease of the hip and require surgical treatment with internal fixation. Continuous pain and a mass, especially if associated with symptoms simulating those of a lumbar disk, in a patient with Paget disease about the hip should draw attention to the likelihood of malignant change.
A Physiological Approach to Aesthetic Preference
Authors: M.A. de Jong, K.R. van Mourik, H.M.C. Schellekens
Journal: Psychotherapy and Psychosomatics (1973)

Ss were presented with nine pieces of music of 1 min duration each. The pieces of music differed in tempo. There were three tempi, and three pieces of music for each tempo. During the presentations, recordings were made of heart rate (HR), respiration rate (RR) and skin conductance (SC). The scores on these measures were compared with the ratings by the Ss of the music on a rating scale that had at its extremes 'very beautiful' and 'very ugly'. Groups of Ss were recruited from three populations, each meant to represent a different approach to music. The results indicated tempo differences of HR, RR, SC, and number of galvanic skin responses (nGSR); a group difference for HR; and less pronounced musical preference differences for RR, SC, HR, and nGSR.
Lipid Research Clinics Program
Authors: David M. Gimlett
Journal: JAMA (1984)

<h3>To the Editor.—</h3> In regard to the LRC-CPPT as reported in<i>JAMA</i>,<sup>1</sup>I would like to raise one objection that I feel is important. Despite statistical manipulations, I do not find that a difference between 47 vascular deaths and 37 vascular deaths in 3,800 patients represents a significant finding. This subjective impression is reinforced by the unexplained finding that there were almost three times as many accident- and violence-related deaths in the treated patients. If the treated and placebo groups were truly comparable, then the only conclusion could be that cholestyramine caused accidents and violence. The researchers were willing to discount this possibility despite the overwhelming statistical difference and yet were not willing to discount the possibility that the much lesser statistical difference in the sought-after end point was likewise due to coincidence. Somewhere there is an error in the understanding of the statistics, control groups, or cholestyramine. What
Exorcizing the Spooks
Authors: Claude H. Organ
Journal: JAMA (1974)

<h3>To the Editor.—</h3> The comments of Dr. Lois DeBakey seemed quite sensible. Your editorial response to her implies that verbal and written literacy is, of necessity, separated from the practicing physician. This is a continuation of a philosophy operative in society today that would make physicians less literate, less knowledgeable, less responsible, and defunctionalized individuals. There is nothing inherent in our training or mission which would make this so. It is not uncommon today to witness young men with brilliant minds being unable to construct a simple complete sentence. If they have gone to less acceptable means of expression and communication, it is because of our own permissiveness as teachers and by our own poor example that we have allowed them to do so. Most assuredly, you did not intend to suggest that your publication, which has long promoted literary skill, would deliberately subvert the development of the complete individual
Effect of Intensive Glycemic Control on Levels of Markers of Inflammation in Type 1 Diabetes Mellitus in the Diabetes Control and Complications Trial
Authors: Debra A. Schaumberg, Robert J. Glynn, Alicia J. Jenkins, Timothy J. Lyons, Nader Rifai, JoAnn E. Manson, Paul M. Ridker, David M. Nathan
Journal: Circulation (2005)

Background— Type 1 diabetes mellitus is associated with an increased risk of cardiovascular disease (CVD) that is not fully explained by conventional risk factors. The Diabetes Control and Complications Trial (DCCT) showed that intensive diabetes therapy reduced levels of LDL cholesterol and triglycerides but increased the risk of major weight gain, which might adversely affect CVD risk. The present study examined the effect of intensive therapy on levels of several markers of inflammation that have been linked to risk of CVD. Methods and Results— We measured levels of inflammatory biomarkers in stored baseline and 3-year follow-up serum specimens from a random sample of 385 participants in the DCCT, a multicenter trial in which 1441 subjects aged 13 to 39 years with type 1 diabetes mellitus were randomized to intensive or conventional diabetes treatment. The markers included high-sensitivity C-reactive protein (hsCRP), soluble intercellular adhesion molecule type 1 (sICAM-1), soluble vascular cell adhesion molecule type 1 (sVCAM-1), and the 55-kDa soluble tumor necrosis factor-α receptor 1 (sTNF-R1). We examined the effect of intensive therapy on the change in levels of the inflammatory markers. In unadjusted analyses, levels of hsCRP and sTNF-R1 increased in both treatment groups after 3 years of follow-up, with no significant difference between groups for hsCRP ( P =0.53) but with a greater increase of sTNF-R1 in the intensive therapy group ( P =0.002). In contrast, mean levels of sICAM-1 and sVCAM-1 decreased among participants assigned to intensive therapy, whereas they did not change among those in the conventional treatment group ( P =0.03 for sICAM-1; P =0.03 for sVCAM-1). After adjustment for baseline levels and other factors, intensive therapy remained associated with a significant decrease in sICAM-1 ( P =0.02) and an increase in sTNF-R1 ( P =0.03). For hsCRP, there was a significant interaction between the top third of weight gain and treatment assignment ( P =0.03). In subgroup analyses among subjects undergoing intensive therapy, hsCRP levels increased among those who gained the most weight, whereas it decreased among those in the bottom third of weight gain ( P =0.0004). Conclusions— Intensive therapy in patients with type 1 diabetes mellitus reduced levels of sICAM-1 and increased levels of sTNF-R1 and of hsCRP among those who gained weight. These data demonstrate that the effect of intensive therapy on inflammation is complex and, to the extent that hsCRP is a risk factor, suggest that the risk of atherosclerosis among diabetic patients may be influenced by the degree of weight gain while undergoing intensive therapy.
Overexpression of Urokinase by Macrophages or Deficiency of Plasminogen Activator Inhibitor Type 1 Causes Cardiac Fibrosis in Mice
Authors: Hideaki Moriwaki, April Stempien-Otero, Michal Kremen, Aaron E. Cozen, David A. Dichek
Journal: Circulation Research (2004)

Several studies implicate elevated matrix metalloproteinase activity as a cause of cardiac fibrosis. However, it is unknown whether other proteases can also initiate cardiac fibrosis. Because absence of urokinase plasminogen activator (uPA) prevents development of cardiac fibrosis after experimental myocardial infarction in mice, we hypothesized that elevated activity of uPA or deficiency of the uPA inhibitor plasminogen activator inhibitor-1 (PAI-1) might cause cardiac fibrosis. We used mice with scavenger-receptor (SR)-directed, macrophage-targeted uPA overexpression (SR-uPA +/0 mice) and PAI-1 null mice to test these hypotheses. Our studies revealed that SR-uPA +/0 mice developed cardiac fibrosis beginning between 5 and 10 weeks of age. Fibrosis was preceded by cardiac macrophage accumulation, implicating uPA-secreting macrophages as important contributors to development of fibrosis. A key role for uPA-secreting macrophages in development of cardiac fibrosis was supported by experiments in which recipients of bone marrow transplants from SR-uPA +/0 donors but not nontransgenic donors developed cardiac macrophage accumulation and fibrosis. SR-uPA +/0 mice and recipients of SR-uPA +/0 bone marrow had neither macrophage accumulation nor fibrosis in other major organs despite the presence of higher levels of uPA in these organs than in hearts. PAI-1 null mice but not congenic, age-matched controls also developed macrophage accumulation and fibrosis in hearts but not in other organs. We conclude: (1) either elevated macrophage uPA expression or PAI-1 deficiency is sufficient to cause cardiac macrophage accumulation and fibrosis; (2) macrophages are important contributors to the development of cardiac fibrosis; and (3) the heart is particularly sensitive to the effects of excess uPA activity.