tbuckley/cabot-search huggingface dataset:
Ophthalmoscopy, Retinoscopy and Refraction.
Journal: JAMA (1923)

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 Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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) 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
Further observations on luminal deformity and stenosis of nonrespiratory bronchioles in pulmonary emphysema.
Authors: A Linhartova, A E Anderson, A G Foraker
Journal: Thorax (1977)

In an endeavour to elucidate the anatomical basis for the increased resistance to airflow which characterises the most peripheral conducting air passages in pulmonary emphysema, lumina of nonrespiratory bronchioles of lungs with mainly centrilobular disease were assessed for two- and three-dimensional features by: (1) determination of percentage conformity of the lumina of individual bronchioles in histological sections to hypothetical planes through cylinders (ie, ellipses with the same areas and circumferences), and (2) comparison of luminal areas at regular intervals along bronchiolar longitudinal axes. The lumina of most nonrespiratory bronchioles from normal lungs conformed closely to their respective ellipses, thus corroborating previous observations that they are normally cylindroid. In contrast, there was a substantial excess of plane section deformities in the lumina of nonrespiratory bronchioles from the emphysematous specimens. The incidence of stenotic bronchioles (by both diameter and area determinations) was also greatly increased in emphysema. Since there was a strong positive association between such stenotic lesions and bronchiolar deformity, the latter was concluded to be a major factor in bronchiolar restriction. Furthermore, these characteristics seemed to have three-dimensional expression, for the lumina of stenotic bronchioles in emphysema were irregular in a longitudinal fashion.
Fundamentals of Biostatistics.
Journal: Annals of Internal Medicine (1969)

Bernard Rosner's FUNDAMENTALS OF BIOSTATISTICS is a practical introduction to the methods, techniques, and computation of statistics with human subjects. It prepares students for their future courses and careers by introducing the statistical methods most often used in medical literature. Rosner minimizes the amount of mathematical formulation (algebra-based) while still giving complete explanations of all the important concepts. As in previous editions, a major strength of this book is that every new concept is developed systematically through completely worked out examples from current medical research problems.
Synovitis with non-specific histological changes in synovium in chronic sarcoidosis.
Authors: D G Palmer, H R Schumacher
Journal: Annals of the Rheumatic Diseases (1984)

Polyarthritic episodes in seven patients during the course of chronic sarcoidosis involved the knees and less frequently other joints. Synovial effusions were non-inflammatory or mildly inflammatory. Needle synovial biopsies 10 days to seven weeks after the onset of joint symptoms have revealed varying patterns, including mild lining cell proliferation, occasional vascular congestion, diffuse infiltrates with lymphocytes and histiocytes, but no granulomas. These studies show distinctly less inflammation than in rheumatoid arthritis. Granulomas need not be identifiable in synovium in all chronic sarcoidosis with arthritis.
Skin Autofluorescence, a Measure of Cumulative Metabolic Stress and Advanced Glycation End Products, Predicts Mortality in Hemodialysis Patients
Authors: Robbert Meerwaldt, Jasper W.L. Hartog, Reindert Graaff, Roel J. Huisman, Thera P. Links, Nynke C. den Hollander, Susan R. Thorpe, John W. Baynes, Gerjan Navis, Rijk O.B. Gans, Andries J. Smit
Journal: Journal of the American Society of Nephrology (2005)

Tissue advanced glycation end products (AGE) are a measure of cumulative metabolic stress and trigger cytokines driven inflammatory reactions. AGE are thought to contribute to the chronic complications of diabetes and ESRD. Tissue autofluorescence is related to the accumulation of AGE. Therefore, skin autofluorescence (AF) may provide prognostic information on mortality in hemodialysis (HD) patients. Skin AF was measured noninvasively with an AF reader at baseline in 109 HD patients. Overall and cardiovascular mortality was monitored prospectively during a period of 3 yr. The AF reader was validated against AGE contents in skin biopsies from 29 dialysis patients. Forty-two of the 109 (38.5%) HD patients died. Cox regression analysis showed that AF was an independent predictor of overall and cardiovascular mortality (for overall mortality odds ratio [OR] 3.9), as were pre-existing cardiovascular disease (CVD; OR 3.1), C-reactive protein (OR 1.1), and serum albumin (OR 0.3). Multivariate analysis revealed that 65% of the variance in AF could be attributed to the independent effects of age, dialysis and renal failure duration, presence of diabetes, triglycerides levels, and C-reactive protein. AF was also independently linked to the presence of CVD at baseline (OR 8.8; P < 0.001). AF correlated with collagen-linked fluorescence (r = 0.71, P < 0.001), pentosidine (r = 0.75, P < 0.001), and carboxy(m)ethyllysine (both r = 0.45, P < 0.01). Skin AF is a strong and independent predictor of mortality in ESRD. This supports a role for AGE as a contributor to mortality and CVD and warrants interventions specifically aimed at AGE accumulation.
Electrocardiographic and Biochemical Study in Hemorrhagic Shock in Dogs Treated with Hyperbaric Oxygenation
Authors: R. ADAMS COWLEY, SAFUH ATTAR, WILLIAM G. ESMOND, EMIL BLAIR, ILSE HAWTHORNE
Journal: Circulation (1963)

A modification of the standard Fine preparation for hemorrhagic shock yielding an 83 per cent mortality rate was developed. Hyperbaric oxygenation (OHP) at 3 atmospheres absolute was found to decrease the mortality rate significantly, to 26 per cent. Electrocardiographic changes induced by OHP were bradycardia and sinus arrhythmia, which were abolished by vagotomy. Tachycardia, depression of the S-T segment, with changes in the configuration of the T wave that indicated myocardial damage, was observed in shock dogs treated with OHP. All changes improved after decompression and reinfusion of shed blood. The improved survival rate is attributed to better oxygenation of the hypoxic tissues [see figure in the PDF file] by the increased physically dissolved oxygen.
Tissue factor and coronary artery disease
Authors: A Moons
Journal: Cardiovascular Research (2002)

Plaque disruption with superimposed thrombosis is the main cause of acute coronary events such as acute myocardial infarction and unstable angina. Among other factors, tissue factor seems to play an important role determining plaque thrombogenicity. Tissue factor is a potent initiator of the coagulation cascade situated within the vessel wall and is highly exposed to the blood after plaque rupture. Several mediators involved in the process of atherosclerotic plaque formation are capable of inducing tissue factor expression in cells such as monocytes, macrophages and endothelial cells, which under normal conditions do not express tissue factor or to a limited extent only. The increased expression of tissue factor is not limited to the plaque but is also found in circulating monocytes in patients with acute coronary syndromes. In addition, studies have shown an important contribution of tissue factor in the pathogenesis of thrombosis and restenosis after balloon angioplasty. Recent basic studies focus on the therapeutic inhibition of tissue factor. Specific and non-specific inhibitors of tissue factor or the tissue factor/factor VIIa complex have been developed or identified, and have been tested in experimental studies. Clinical studies are currently being initiated. In this review, we present the current knowledge on the role of tissue factor in atherosclerosis, arterial intervention and potential pharmacological approaches, with focus on acute coronary syndromes.
Apolipoprotein E Mediates the Retention of High-Density Lipoproteins by Mouse Carotid Arteries and Cultured Arterial Smooth Muscle Cell Extracellular Matrices
Authors: Katherine Olin-Lewis, Jeana L. Benton, John C. Rutledge, Denis G. Baskin, Thomas N. Wight, Alan Chait
Journal: Circulation Research (2002)

Lipoprotein retention in the vascular extracellular matrix (ECM) plays a critical role in atherogenesis. Previous studies demonstrated the presence of apo A-I and E in atherosclerotic lesions, suggesting that HDL may be trapped by the artery wall. We sought to determine mechanisms by which HDL could be bound and retained by the arterial wall, and whether apo E was a principal determinant of this binding. We evaluated in situ accumulation of fluorescently labeled DiI-human HDL±apo E in perfused carotid arteries from apo E–null mice. Apo E was important in mediating HDL binding to the vascular wall, with a 48±16% increase in accumulation of DiI-labeled apo E–containing HDL (HDL 3 +E) compared with DiI-apo E–free HDL (HDL 3 −E) ( P =0.003). To investigate possible mechanisms responsible for retention, we assessed binding of unlabeled HDL 3 −E and HDL 3 +E to ECM generated by cultured arterial smooth muscle cells. Similar to the in situ carotid artery data, HDL 3 +E bound better to the ECM than did HDL 3 −E (3-fold lower K a and 3.5-fold higher B max for HDL 3 +E versus HDL 3 −E). These differences were eliminated after either neutralization of arginine residues on apo E or digestion of matrix with chondroitin ABC lyase, suggesting that chondroitin and/or dermatan sulfate proteoglycans were responsible for apo E–mediated increased binding. These findings demonstrate that HDL can bind to both intact murine carotid arteries and smooth muscle cell–derived ECM, and that apo E is a principal determinant in mediating the ability of HDL to be trapped and retained via its interaction with ECM proteoglycans.
Bioactive compound reveals a novel function for ribosomal protein S5 in hepatic stellate cell activation and hepatic fibrosis
Authors: Wei-Heng Xu, Hong-Gang Hu, Yuan Tian, Shao-Zhan Wang, Jie Li, Jian-Zhong Li, Xing Deng, Hui Qian, Lei Qiu, Zhen-Lin Hu, Qiu-Ye Wu, Yi-Feng Chai, Cheng Guo, Wei-Fen Xie, Jun-Ping Zhang
Journal: Hepatology (2014)

Liver fibrosis and its endstage, cirrhosis, represent a major public health problem worldwide. Activation of hepatic stellate cells (HSCs) is a central event in hepatic fibrosis. However, the proteins that control HSC activation are incompletely understood. Here we show that (6aS, 10S, 11aR, 11bR, 11cS)-10-methylamino-dodecahydro-3a, 7a-diaza-benzo [de]anthracene-8-thione (MASM) exhibits potent inhibitory activity against liver fibrosis in vitro and in vivo associated with the reduction of Akt phosphorylation. Furthermore, ribosomal protein S5 (RPS5) was identified as a direct target of MASM, which stabilized RPS5 in cultured HSCs and in the liver of experimental animals after dimethylnitrosamine (DMN) or bile duct ligation (BDL). Functional studies revealed that RPS5 could prevent HSC activation. RPS5 overexpression in HSCs resulted in Akt dephosphorylation at both Ser473 and Thr308, and led to subsequent dephosphorylation of GSK3β or P70S6K. Progression of DMN- and BDL-induced hepatic fibrosis was aggravated by Rps5 knockdown and alleviated by RPS5 overexpression, which correlated with the modulation of Akt phosphorylation and HSC number in the fibrotic livers. Moreover, RPS5 was substantially reduced in the transdifferentiated HSCs, experimental fibrotic livers, and human cirrhosis samples. Conclusion : These results demonstrate that RPS5 is implicated in hepatic fibrogenesis and may represent a promising target for potential therapeutic intervention in liver fibrotic diseases. (Hepatology 2014;60:648–660)
Effects of propafenone and its main metabolite, 5-hydroxypropafenone, on HERG channels
Authors: C Arias
Journal: Cardiovascular Research (2003)

Objectives: Propafenone is a class Ic antiarrhythmic drug used to maintain sinus rhythm in patients with atrial fibrillation. During chronic therapy, it undergoes extensive first-pass hepatic metabolism to 5-hydroxypropafenone. In the present study we have analysed the effects of propafenone and 5-hydroxypropafenone on HERG current. Methods: The whole-cell configuration of the patch-clamp technique was used in CHO cells stably transfected with the gene encoding HERG channels. Results: Propafenone and 5-hydroxypropafenone (2 μM) inhibited HERG current by 78.7±2.3% (n=7) and 71.1±4.1% (n=7, P0.05) when measured at the end of 5-s depolarizing pulses to −10 mV. Block measured at the maximum peak of tail currents recorded at −60 mV was similar for propafenone (78.3±2.0%, n=7, P0.05) and higher for 5-hydroxypropafenone (79.3±1.5%, n=7, P<0.05). Propafenone and 5-hydroxypropafenone shifted the midpoint of the activation curve by −10.2±0.9 mV (n=7, P<0.01) and −7.4±1.1 mV (n=10, P<0.01), respectively. Both drugs accelerated the deactivation and the inactivation process of HERG current. Propafenone, but not 5-hydroxypropafenone, inhibited to a higher extent HERG current at the end of 5-s depolarizing pulses to 0 mV than after promoting the transition of HERG channels from the inactivated to the opened state. Conclusions: These results indicate that propafenone and its main active metabolite, 5-hydroxypropafenone, block HERG channels to a similar extent by binding predominantly to the open state of the channel.
Patients with antiphospholipid antibodies and venous thrombosis should receive long term anticoagulant treatment.
Authors: R H Derksen, P G de Groot, L Kater, H K Nieuwenhuis
Journal: Annals of the Rheumatic Diseases (1993)

To determine whether the finding of antiphospholipid antibodies in patients with venous thromboembolic episodes should influence the duration of treatment with anticoagulant drugs by mouth.A retrospective study was carried out in 19 patients with antiphospholipid antibodies and a history of venous thromboembolic episodes. The median follow up from the first venous thromboembolic episode was 93 months and the median age at this episode was 26 years. The patients had in total 34 venous thromboembolic episodes. The total follow up period comprised 32 periods with and 23 periods without anticoagulant drugs.The probability of being free of recurrent venous thromboembolic episodes, calculated by the Kaplan-Meier method, was significantly influenced by the use of anticoagulant drugs. Patients receiving oral anticoagulants had at eight years a 100% probability of survival without recurrence, whereas patients in whom anticoagulant drugs were stopped had a 50% probability of a recurrent venous thromboembolic episode at two years, and a 78% probability of recurrence at eight years.Patients with venous thromboembolic episodes and antiphospholipid antibodies have a high risk for recurrent venous thromboembolic episodes and long term treatment with anticoagulant drugs by mouth is an effective prophylaxis.
Rheumatoid factor and antibodies to cyclic citrullinated peptides are associated with severe extra-articular manifestations in rheumatoid arthritis
Authors: C Turesson, L T H Jacobsson, G Sturfelt, E L Matteson, L Mathsson, J Ronnelid
Journal: Annals of the Rheumatic Diseases (2006)

<b>Objective:</b> To study antibodies to cyclic citrullinated peptides (anti-CCP) and rheumatoid factor in patients with active, severe extra-articular rheumatoid arthritis (ExRA) compared with controls without ExRA. <b>Methods:</b> 35 consecutive patients with severe ExRA manifestations according to predefined criteria were studied. 70 patients with rheumatoid arthritis, but no ExRA manifestations, individually matched for age, sex and disease duration, served as controls. Patients were included when ExRA was diagnosed, before any new treatment was started. Anti-CCPs were detected with ELISA, rheumatoid factor was quantified using nephelometry and anti-nuclear antibodies (ANA) were investigated using indirect immune fluorescence. <b>Results:</b> Anti-CCPs were detected in 77% of patients with ExRA versus 56% of controls without ExRA (p = 0.03). Anti-CCP levels also tended to be higher in patients with ExRA (p = 0.09). Rheumatoid factor was detected in 94% <i>v</i> 71% of patients and controls, respectively (p = 0.006), and rheumatoid factor levels were higher in patients with ExRA (median interquartile range (IQR) 245 IU/ml (94–604) <i>v</i> 73 IU/ml (not detected–165); p = 0.001). Levels and occurrence of ANA did not differ between patients with ExRA and controls. Patients with ExRA had higher swollen joint counts and C reactive protein levels, but no correlations were found between anti-CCP or rheumatoid factor levels and these measures within the ExRA group. <b>Conclusion:</b> Rheumatoid factor is strongly associated with severe ExRA manifestations in patients with rheumatoid arthritis, and a similar but weaker association exists for anti-CCPs. This suggests a role for rheumatoid factor and anti-CCP in the pathogenesis of ExRA.
Exonic variants affecting pre-mRNA splicing add to genetic burden in chronic pancreatitis
Authors: Sebastian Beer, Miklós Sahin-Tóth
Journal: Gut (2013)

We read with great interest the recent paper by Rosendahl et al 1 describing the incidence of variants in CFTR , SPINK1 , CTRC and PRSS1 in a German cohort of chronic pancreatitis cases. The authors conclude that chronic pancreatitis is a complex genetic disease and the net effect of mutations in multiple susceptibility genes underlies increased disease risk. Indeed, in the studied cohort, at least one genetic risk factor was identified in 36.7% of patients. Surprisingly, however, only 6.5% of cases carried multiple risk factors, which seems to contradict the complex genetics theory of chronic pancreatitis. While it is likely that more susceptibility genes are yet to be discovered, we submit that known risk genes may have been incompletely characterised resulting in underestimation of the true genetic burden in chronic pancreatitis. Discovery studies tend to focus on exons and exon-intron boundaries and may thus miss many intronic variants. Replication studies often target previously identified variants only. Even if identified, intronic variants other than splice site mutations are often ignored due to inherent …
Response to Letter Regarding Article, “Does Sodium Nitroprusside Decrease the Incidence of Atrial Fibrillation After Myocardial Revascularization? A Pilot Study”
Authors: Raif Cavolli, Kaan Kaya, Sebnem Erturk, Oguz Mehmet, Alp Aslan, Ozan Emiroglu, Ozge Korkmaz, Refik Tasoz, Umit Ozyurda
Journal: Circulation (2009)
Minimal residual disease as biomarker for optimal biologic dosing of <scp>ARA</scp>‐<scp>C</scp> in patients with acute myeloid leukemia
Authors: Luca Maurillo, Francesco Buccisano, Alfonso Piciocchi, Maria Ilaria Del Principe, Chiara Sarlo, Ambra Di Veroli, Paola Panetta, Maria Irno‐Consalvo, Daniela Nasso, Concetta Ditto, Marco Refrigeri, Gottardo De Angelis, Raffaella Cerretti, William Arcese, Giuseppe Sconocchia, Francesco Lo‐Coco, Sergio Amadori, Adriano Venditti
Journal: American Journal of Hematology (2014)

We assessed by flow cytometry minimal residual disease (MRD) in patients with acute myeloid leukemia (AML) given standard‐dose (SDAC) and high‐dose ARA‐C (HDAC) regimens. Of 163 patients enrolled, 130 (median age, 45 years; range, 18–59 years) qualified for analysis, all achieving complete remission after treatment with SDAC ( n = 78) or HDAC ( n = 52) plus etoposide and daunorubicin. Consolidation consisted of intermediate‐dose ARA‐C and daunorubicin. MRD negativity was significantly more frequent in the SDAC vs. HDAC arm after both induction (37% vs. 15%, P = 0.007) and consolidation (44% vs. 18%, P = 0.002). Respective median residual leukemic cell counts with SDAC and HDAC use were 1.5 × 10 −3 and 4 × 10 −3 ( P = 0.033) after induction and 5.7 × 10 −4 and 2.9 × 10 −3 ( P = 0.008) after consolidation. Based on ARA‐C schedule and post‐consolidation MRD status, the four patient groups (SDAC‐MRD − , HDAC‐MRD − , SDAC‐MRD + , and HDAC‐MRD + ) displayed 5‐year overall survival rates of 60%, 33%, 24%, and 42% ( P = 0.007), respectively, with 24%, 35%, 74%, and 48% ( P &lt; 0.0001) respective cumulative incidence of relapse estimates. MRD may serve as a biomarker for optimal biologic dosing of ARA‐C, and SDAC regimen appears to yield more frequent MRD negativity. Am. J. Hematol. 90:125–131, 2015. © 2014 Wiley Periodicals, Inc.
Endothelium-dependent mechanical properties of the carotid artery in WKY and SHR. Role of angiotensin converting enzyme inhibition.
Authors: B I Levy, J Benessiano, P Poitevin, M E Safar
Journal: Circulation Research (1990)

An experimental model of in situ isolated carotid arteries has been used to evaluate the static mechanical properties of the arterial wall in 12-week-old Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR). The effects of endothelium removal and of local incubation with the converting enzyme inhibitor lisinopril (ICI Pharma 209000) on the carotid compliance (CC) were compared with the effects of total abolition of the vascular smooth muscle tone by potassium cyanide. CC measured for pressures ranging from 50 to 175 mm Hg had maximal values (0.22 +/- 0.07 microliter/mm Hg and 0.13 +/- 0.03 microliter/mm Hg, respectively, for WKY and SHR, p less than 0.001) for pressure values close to the operating pressures in both groups. Maximal values of CC were increased by 35% and 45% in WKY and SHR, respectively, after potassium cyanide poisoning (p less than 0.01). The endothelium removal induced a significant increase in CC compared with their control values (+37%, p less than 0.01, and +25%, p less than 0.01, respectively, in WKY and SHR). CC measured after endothelium removal did not significantly differ from its values measured after potassium cyanide poisoning in normotensive animals. In contrast, in hypertensive animals, CC was significantly lower after endothelium, removal than after potassium cyanide poisoning (p less than 0.01). In the presence of intact endothelium, local incubation with converting enzyme inhibitor increased CC by 23% (p less than 0.05) in WKY rats and by 14% (p less than 0.01) in SHR. In contrast, after endothelium removal, converting enzyme inhibitors did not significantly increase further CC in either strain.(ABSTRACT TRUNCATED AT 250 WORDS)