tbuckley/cabot-search huggingface dataset:
National Health Plans: Some Economic and Financial Aspects
Authors: BERNARD S. BLOOM
Journal: Annals of Internal Medicine (1973)

The need for a national health insurance program is agreed on by most students of the problem and by many members of Congress—but its form is not. There is also little agreement on the need for changes in the organization and delivery of health care. Changes in financing are being proposed as the cure, but the problems are structural. Any government social program must meet the test of equitability in the delivery of the services and in the method of taxation used to raise revenues for program funding. All the proposed programs currently before Congress are deficient by these criteria, some more than others.
Human Bone Marrow Activates the Akt Pathway in Metastatic Prostate Cells through Transactivation of the α-Platelet–Derived Growth Factor Receptor
Authors: Nathan G. Dolloff, Mike R. Russell, Nick Loizos, Alessandro Fatatis
Journal: Cancer Research (2007)

Abstract The factors regulating the bone tropism of disseminated prostate cancer cells are still vaguely defined. We report that prostate cancer cells that metastasize to the skeleton respond to human bone marrow with a robust stimulation of the phosphatidylinositol 3-kinase/Akt pathway, whereas prostate cells that lack bone-metastatic potential respond negligibly. The majority of this Akt activation is dependent on α-platelet–derived growth factor receptor (α-PDGFR) signaling, which was shown using the small-molecule inhibitor of PDGFR signaling AG1296. Low concentrations of PDGF-AA and PDGF-BB found in bone marrow aspirates, which were detected by ELISA, do not account for the high levels of α-PDGFR signaling. Additionally, neutralizing PDGF binding using a α-PDGFR–specific antibody (IMC-3G3) failed to produce a significant inhibition of bone marrow–induced Akt activation. However, the inhibitory effect of IMC-3G3 rivaled that of AG1296 when incubation was done under conditions that stimulated α-PDGFR internalization. We conclude that α-PDGFR is activated by multiple soluble factors contained within human bone marrow, in addition to its natural ligands, and this transactivation is dependent on receptor localization to the plasma membrane. Therefore, α-PDGFR expression may provide select prostate phenotypes with a growth advantage within the bone microenvironment. [Cancer Res 2007;67(2):555–62]
Maintenance of the synthesis of large proteoglycans in anatomically intact murine articular cartilage by steroids and insulin-like growth factor I.
Authors: P.M. van der Kraan, E.L. Vitters, N.S. Postma, J Verbunt, W.B. van den Berg
Journal: Annals of the Rheumatic Diseases (1993)

OBJECTIVES--The exact regulation of the synthesis of cartilage specific molecules, such as collagen type II and aggrecan, by articular chondrocytes is unknown, but growth factors and hormones probably play an important part. The effects of glucocorticosteroids (prednisolone and triamcinolone), in combination with insulin-like growth factor I (IGF-I), on the synthesis and hydrodynamic volume of proteoglycans from murine patellar cartilage were investigated. METHODS--The in vitro effect of IGF-I and steroids on proteoglycan synthesis in murine patellar cartilage was evaluated by [35S]sulphate incorporation in combination with dissociative gel chromatography using a Sephacryl S-1000 column. The impact of in vivo prednisolone (0-5 mg/kg) on proteoglycan synthesis in murine patellar cartilage was analysed by [35S]sulphate incorporation immediately after dissection from the knee joint. RESULTS--Prednisolone stimulated proteoglycan synthesis in murine patellar cartilage from normal knees and in cartilage from knees injected with papain in vitro in the absence and presence of IGF-I. Moreover, oral administration of prednisolone for seven days to C57Bl10 mice resulted in enhanced proteoglycan synthesis in patellar cartilage. The incubation of patellar cartilage for 48 hours without serum or growth factors led to the synthesis of proteoglycans with a smaller hydrodynamic volume than those synthesised immediately after dissection of the patellae. This could either be circumvented by the addition of IGF-I or by the addition of glucocorticosteroids (prednisolone or triamcinolone) to the culture medium. CONCLUSIONS--These results show that in a dose range of 0.0003-0.3 mmol/l, glucocorticosteroids, like IGF-I, stimulate proteoglycan synthesis and maintain the synthesis of hydrodynamically large proteoglycans by chondrocytes from murine articular cartilage. This indicates that glucocorticosteroids might play a part in the preservation of matrix integrity in articular cartilage.
Lack of radiological and clinical benefit over two years of low dose prednisolone for rheumatoid arthritis: results of a randomised controlled trial
Authors: H A Capell
Journal: Annals of the Rheumatic Diseases (2004)

<b>Background:</b> Evidence for disease modifying activity of low dose corticosteroid treatment in rheumatoid arthritis is contradictory. Studies showing radiological benefit suggest that continued treatment is required to sustain the effect. <b>Objective:</b> To evaluate the effect of low dose oral prednisolone in early rheumatoid arthritis on disease activity over two years. <b>Design:</b> Double blind placebo controlled trial. <b>Methods:</b> Patients with rheumatoid arthritis, duration &lt;3 years (n = 167), were started on a disease modifying antirheumatic drug (DMARD; sulphasalazine) and allocated by stratified randomisation to prednisolone 7 mg/day or placebo. Primary outcome measure was radiological damage, assessed by the modified Sharp method. Clinical benefit was a secondary outcome. A proactive approach to identifying and treating corticosteroid adverse events was adopted. Patients who discontinued sulphasalazine were offered an alternative DMARD. <b>Results:</b> 90 of 257 patients eligible for the study refused to participate (more women than men). Of those enrolled, 84% were seropositive for rheumatoid factor, median age 56 years, median disease duration 12 months, female to male ratio 1.8:1. Prednisolone was given to 84 patients; of these 73% continued prednisolone and 70% sulphasalazine at 2 years. Of the 83 patients on placebo, 80% continued placebo and 64% sulphasalazine at 2 years. There were no significant differences in radiological score or clinical and laboratory measures at 0 and 2 years. <b>Conclusions:</b> Low dose prednisolone conferred no radiological or clinical benefit on patients maintained on a DMARD over two years. Low dose corticosteroids have no role in the routine management of rheumatoid arthritis treated with conventional disease modifying drugs.
Requirement of the cyclic adenosine monophosphate response element-binding protein for hepatitis B virus replication
Authors: Bo Kyung Kim, Seoung Ok Lim, Yun Gyu Park
Journal: Hepatology (2008)

The cyclic adenosine monophosphate–response element (CRE)-transcription factor complex participates in the regulation of viral gene expression and pathologic processes caused by various viruses. The hepatitis B virus (HBV) enhancer I directs liver-specific transcription of viral genes and contains a CRE sequence (HBV-CRE); however, whether the HBV-CRE and CRE-binding protein (CREB) are required for the HBV life cycle remains to be determined. This study was designed to investigate the role of CREB in HBV replication and gene expression. Sequence-comparison analysis of 984 HBVs reported worldwide showed that the HBV-CRE sequence is highly conserved, indicating the possibility that it plays an important role in the HBV life cycle. The binding of CREB to the HBV-CRE site was markedly inhibited by oligonucleotides containing HBV-CRE and consensus CRE sequences in vitro and in vivo. The HBV promoter activity was demonstrated to be dependent upon the transactivation activity of CREB. Treatment with CRE decoy oligonucleotides reduced HBV promoter activity, and this was reversed by CREB overexpression. The levels of viral transcripts, DNA, and antigens were remarkably decreased in response to the overexpression of CREB mutants or treatment with the CRE decoy oligonucleotides, whereas enhancing CREB activity increased the levels of viral transcripts. In addition, introduction of a three-base mutation into the HBV-CRE led to a marked reduction in HBV messenger RNA synthesis. Conclusion: Taken together, our results demonstrate that both replication and gene expression of HBV require a functional CREB and HBV-CRE. We have also demonstrated that CRE decoy oligonucleotides and the overexpression of CREB mutants can effectively block the HBV life cycle, suggesting that interventions against CREB activity could provide a new avenue to treat HBV infection. (HEPATOLOGY 2008.)
Satire: "Food for Humans and Pets"
Authors: Leslie Iffy
Journal: JAMA (1975)

To the Editor.—  Naturally, I agree with Dr. Z. I. Sabry's suggestion, submitted at the Western Hemisphere Nutrition Congress IV (229:1858, 1974), about the necessity of birth control programs for pets. The distressing number of animals that have  be destroyed every day by the Society for the Prevention of Cruelty  Animals testifies  the validity of this suggestion.  As for Dr. Sabry's Brave New World, where zoos will be designed to allow the community rather than individuals,  have social interaction with animals, I enthusiastically endorse his plan since, indeed, this is a good way  fill our planet  capacity with the species homo sapiens . Yet, I regret  say, Dr. Sabry's plan is far from complete.  By selective breeding we should eliminate, I propose, all fat people. Thus, we could feed, perhaps, two lean individuals on the food that one overweight person customarily consumes.  Even better
Health Care Overutilization in the United States
Authors: Eduardo F. Motti
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
Effects of fibrin and α2-antiplasmin on plasminogen activation by staphylokinase
Authors: Kiyotaka Okada, Shigeru Ueshima, Tomoaki Takaishi, Haruyuki Yuasa, Hideharu Fukao, Osamu Matsuo
Journal: American Journal of Hematology (1996)

Staphylokinase obtains plasminogen activating activity by forming a complex with plasminogen. Although the enzymatic activity of staphylokinase is enhanced by fibrin, how fibrin enhances enzymatic activity has not been determined yet. The effects of fibrin, or fibrinogen fragments, on the activation of plasminogen by staphylokinase was investigated using CNBr-digested fibrinogen fragments (FCB-2 and FCB-5) and plasmin-degraded cross-linked fibrin fragments ((DD)E complex, DD fragments and E fragments). Kinetic analysis of the activity of staphylokinase revealed that its plasminogen activating activity, which was expressed as kcat/Km, was enhanced by FCB-2 (10-fold) and FCB-5 (5-fold). These fibrin fragments caused 38-, 30-, and 8.5-fold increases in activity for the DD fragment, (DD)E complex and E fragment, respectively. Although α2-antiplasmin inhibited the activation of plasminogen by staphylokinase, FCB-2 abolished its inhibitory effects, and the plasminogen activating activity of staphylokinase was restored. The inhibitory effects of a2-antiplasmin on the activation of mini-plasminogen by staphylokinase were less than for Glu-or Lys-plasminogen, and the inhibitory effect of α2-antiplasmin was not altered by fibrin or EACA. These findings indicate that the staphylokinase/plasmin-(ogen) complex reacts with fibrin even in the presence of α2-antiplasmin, and efficient plasminogen activation takes place on the surface of fibrin. © 1996 Wiley-Liss, Inc.
Risk factors for asthma among head start children: Evaluation of physical activity and allergy
Authors: V.L. Firrincieli, B. Geldmaker, N. Custis, R. Ehrensberger, E. Erwin, D. Riposo, C. Shufflebarger, L. Ferguson, T. Platts-Mills
Journal: Journal of Allergy and Clinical Immunology (2003)
Abstract P4-11-07: Quantitative Coronary Angiography Findings of Patients Who Received Previous Breast Radiotherapy
Authors: W Wang, R Wainstein, X Freixa, V Dzavik, A. Fyles
Journal: Cancer Research (2010)

Abstract Purpose: To compare the coronary angiographic findings, between patients who had previous left sided breast radiotherapy (RT) and those who had right sided RT. Methods: Between 1995 and 2009, 12696 patients who underwent curative RT for breast cancer in Princess Margaret Hospital were screened to check if they had a post-RT coronary angiogram. Two cardiologists, blinded to treatment, assessed all angiograms and measured the percentage of stenotic lesions and the mean diameter of each segment of the left anterior descending artery (LAD) and the right coronary artery (RCA) using Quantitative Coronary Angiography (QCA). Results: Ninety-one patients were included, 49 and 42 patients had left sided RT and right sided RT respectively. The median time from RT to coronary angiogram was 4.4 years (range: 22 days - 16.9 years). Nineteen patients (39%) in the left sided RT group and 17 (40%) in the right sided RT group needed coronary revascularization (percutaneous coronary intervention or by-pass surgery). The LAD territory was revascularized in 14 (29%) and 11 (26%) patients respectively. The degree of stenoses and mean vessel diameter were not significantly different between the two groups. Table 1: Quantitative The proportion of patients who developed clinically significant stenoses of coronary arteries were not statistically different between the two groups. Table 2: Patiens In 32 patient who had coronary angiograms &amp;gt;5 years after breast RT (16 left-sided and 16 right-sided), the only statistically significant finding (P&amp;lt;0.05) was marginally narrower mid RCA segments among those who had right sided RT: 2.52 mm versus 2.92 mm (P = 0.039). Conclusions: Left sided breast RT did not increase the risk of premature coronary artery disease as compared with right sided RT. However, with the limitation of short duration between radiotherapy and coronary angiogram, late development of coronary artery stenoses 10-15 years after left sided RT can not be excluded. Citation Information: Cancer Res 2010;70(24 Suppl):Abstract nr P4-11-07.
Echocardiography in the Normal Neonate
Authors: ROBERT SOLINGER, FRANCISCO ELBL, KAREEM MINHAS
Journal: Circulation (1973)

Utilizing the atrioventricular and semilunar valves as ultrasonic landmarks, a simple reproducible technic is described for the ultrasonic evaluation of the heart and its great vessels in the normal neonate. The importance of the clinical application of this method is discussed. Echocardiographic studies were performed on 240 normal newborns. Qualitative assessment was made of the interrelationships of the pulmonary, aortic, tricuspid, and mitral valves, and of interventricular septal motion. Quantitative norms were obtained for the following parameters: amplitude of motion of anterior leaflets of tricuspid and mitral valves, anteroposterior diameter of the ventricular and left atrial cavities, thickness of ventricular walls and interventricular septum, outside diameter of aortic and pulmonary roots, and interaortic and interpulmonary cusp distances.
Dietary Fish Oil Alters T Lymphocyte Cell Populations and Exacerbates Disease in a Mouse Model of Inflammatory Colitis
Authors: Hillary L. Woodworth, Sarah J. McCaskey, David M. Duriancik, Jonathan F. Clinthorne, Ingeborg M. Langohr, Elizabeth M. Gardner, Jenifer I. Fenton
Journal: Cancer Research (2010)

Inflammatory bowel diseases (IBD) increase the risk of developing colorectal cancer. Dietary components that reduce inflammation are associated with lower cancer risk. The long-chain omega-3 fatty acid docosahexaenoic acid (DHA) is present in fish oil and has potent anti-inflammatory properties. The objective of this study is to determine whether dietary fish oil enriched with DHA (DFO) could reduce experimentally induced colitis and colon cancer risk in a mouse model. When SMAD3-/- mice are exposed to Helicobacter hepaticus, mild colitis is observed 4 weeks postinfection. Mice were fed isocaloric diets modified to include corn oil, safflower oil, or DFO (doses ranging from 0.75% to 6.00%) as the fatty acid source for 8 weeks. Mice were gavaged with H. hepaticus; DFO feeding was continued; and mice were sacrificed 4 weeks after infection. The colon and cecum were collected for histopathology. Spleens and mesenteric lymph nodes were collected and analyzed for T-cell populations using flow cytometry. Contrary to expectations, DFO induced severe colitis and adenocarcinoma formation. DFO consumption was associated with decreased CD8(+) cell frequency and diminished CD69 expression on CD4(+) and CD8(+) T-cell populations. Mice consuming DFO also exhibited higher FoxP3(+) CD25(+) CD4(+) T regulatory cell frequency, FoxP3 expression, and altered L-selectin expression during infection. We concluded that DFO-fed mice may be less equipped to mount a successful response to H. hepaticus infection, increasing colon cancer risk. These results support the need to establish a tolerable upper limit for DHA intake particularly in the context of chronic inflammatory conditions such as IBD.
Heat-Related Morbidity in Brisbane, Australia: Spatial Variation and Area-Level Predictors
Authors: David M. Hondula, Adrian G. Barnett
Journal: Environmental Health Perspectives (2014)

Extreme heat is a leading weather-related cause of illness and death in many locations across the globe, including subtropical Australia. The possibility of increasingly frequent and severe heat waves warrants continued efforts to reduce this health burden, which could be accomplished by targeting intervention measures toward the most vulnerable communities.We sought to quantify spatial variability in heat-related morbidity in Brisbane, Australia, to highlight regions of the city with the greatest risk. We also aimed to find area-level social and environmental determinants of high risk within Brisbane.We used a series of hierarchical Bayesian models to examine city-wide and intracity associations between temperature and morbidity using a 2007-2011 time series of geographically referenced hospital admissions data. The models accounted for long-term time trends, seasonality, and day of week and holiday effects.On average, a 10°C increase in daily maximum temperature during the summer was associated with a 7.2% increase in hospital admissions (95% CI: 4.7, 9.8%) on the following day. Positive statistically significant relationships between admissions and temperature were found for 16 of the city's 158 areas; negative relationships were found for 5 areas. High-risk areas were associated with a lack of high income earners and higher population density.Geographically targeted public health strategies for extreme heat may be effective in Brisbane, because morbidity risk was found to be spatially variable. Emergency responders, health officials, and city planners could focus on short- and long-term intervention measures that reach communities in the city with lower incomes and higher population densities, including reduction of urban heat island effects.
Transforming growth factor beta1-induced cell death in preneoplastic foci of rat liver and sensitization by the antiestrogen tamoxifen
Authors: L Mullauer
Journal: Hepatology (1996)

Previous studies have shown 5- to 10-fold higher rates of apoptosis in prestages of liver cancer (putative preneoplastic cell foci [PPF]) than in unaltered liver; fasting or withdrawal of tumor promoters enhanced apoptosis even further. We studied whether transforming growth factor beta1 (TGF-beta1), an inducer of apoptosis in normal liver, might be involved in induction of apoptosis in PPF. PPF were produced in 7-week- old female Sprague-Dawley rats with a single oral dose of the genotoxic carcinogen 7,12-dimethylbenz(a)anthracene (DMBA). At 24 weeks of age, TGF-beta1 was injected into animals (40 micro g/kg intravenously) either once and they were killed 4 hours later (single-dose experiment) or eight times at 24-hour intervals and they were killed 24 hours after the last administration (multiple-dose experiment). Further subgroups received daily subcutaneous injections of tamoxifen (TAM) (8 mg/kg) for 4 consecutive weeks before TGF-beta1 treatment. In normal liver, the apoptosis incidence was low in solvent- and TAM-only-treated animals, in the single- as well as the multiple-dose experiment. TGF-beta1, increased the apoptosis incidence severalfold, and the combined administration of TGF-beta1 with TAM caused a further strong increase. The already-elevated basal apoptotic incidence in PPF was further increased by TGF-beta1, and particularly by TGF-beta1 plus TAM treatments, which resulted in a reduction of foci number and size. In summary, these results show that TGF-beta1 can induce apoptosis in PPF. This apoptosis-inducing activity is strongly enhanced by the additional treatment with the antiestrogen TAM, which by itself does not have any cell death-inducing effect in the liver or PPF. The elevated apoptotic activity of PPF in response to TGF-beta1 can lead to a selective reduction of the liver load with preneoplastic cells. (Hepatology 1996 Apr;23(4):840-7)
Results of Treatment of Thyrotoxicosis after Postoperative Relapse
Authors: D. G. McLarty, W. D. Alexander, R. McG. Harden, D. H. Clark
Journal: BMJ (1969)

Ninety patients who had a recurrence of thyrotoxicosis after thyroidectomy have been reviewed. All 10 patients who had a second operation and 18 out of 20 patients treated with a full course of antithyroid drugs relapsed. These results differ greatly from the results of treatment of the first episode of thyrotoxicosis, whether by thyroidectomy or antithyroid drugs. Radioiodine is the treatment of choice in this group of patients, despite the high incidence of hypothyroidism.
Myocardial Coefficient of Oxygen Utilization
Authors: JOHN C. SCOTT
Journal: Circulation Research (1961)

An analysis of blood oxygen values, coronary blood flow, and left ventricular oxygen consumption has been made on data obtained from 120 experiments on normal anesthetized dogs by using the N 2 O method for estimating coronary flow. The arterial oxygen content was shown to have a positive linear relationship to the myocardial arteriovenous oxygen difference (A-V,O 2 ), but a negative linear relationship to coronary flow. The coefficient of oxygen utilization showed a positive linear regression with arterial oxygen-content values above 20 volumes per cent, but an inverse relationship with arterial oxygen values below 20 volumes per cent. The significance of these relationships in the regulation of coronary flow is discussed.
Genetic Determinants of Pemetrexed Responsiveness and Nonresponsiveness in Non-small Cell Lung Cancer Cells
Authors: Ming-Fang Wu, Yi-Min Hsiao, Chuan-Fu Huang, Yu-Hsin Huang, Wan-Jung Yang, Hsiu-Wen Chan, Jinghua Tsai Chang, Jiunn-Liang Ko
Journal: Journal of Thoracic Oncology (2010)