tbuckley/cabot-search huggingface dataset:
Incidence of End-stage Renal Disease in Patients With Type 1 Diabetes
Authors: Patrik Finne
Journal: JAMA (2005)

Context End-stage renal disease (ESRD) is one of the most severe complications of type 1 diabetes.Yet, data on patients' risk of developing ESRD are sparse.Objectives To estimate the long-term risk of developing ESRD and to assess how age at diagnosis of diabetes, time period of diagnosis, and sex affect the risk.Design, Setting, and Patients A cohort of all patients younger than 30 years diagnosed as having type 1 diabetes in Finland in 1965-1999 (n=20 005) was identified from the Finnish Diabetes Register.The cohort was followed up from diagnosis of diabetes until development of ESRD (dialysis or kidney transplantation as identified from the Finnish Registry for Kidney Diseases), death, or end of follow-up on December 31, 2001.Main Outcome Measure Cumulative incidence of ESRD, accounting for death as a competing risk. ResultsThe cohort was followed up for maximally 37 years, with a median of 16.7 years.During 346 851 person-years, 632 patients developed ESRD.The cumulative incidence of ESRD was 2.2% at 20 years and 7.8% at 30 years after diagnosis.The risk of developing ESRD was lowest in patients whose diagnosis occurred at younger than 5 years.The risk of ESRD was lower for patients diagnosed as having type 1 diabetes in later years.The risk did not differ significantly between sexes.Conclusions With regard to ESRD, the prognosis of type 1 diabetes has improved during the past 4 decades.Children diagnosed as having diabetes before age 5 years have the most favorable prognosis.Overall, incidence of ESRD appears to be lower than previously estimated.
Nitric oxide mediates lipopolysaccharide-induced alteration of mitochondrial function in cultured hepatocytes and isolated perfused liver
Authors: Iwao Kurose, Shinzo Kato, Hiromasa Ishii, Dai Fukumura, Soichiro Miura, Makoto Suematsu, Masaharu Tsuchiy
Journal: Hepatology (1993)

The influence of endogenous nitric oxide, which is generated by stimulation with lipopolysaccharide, on the mitochondrial energization of rat hepatocytes was investigated in vitro and ex vivo. Using a fluorescence microscope equipped with a silicon intensifier target camera, we visualized fluorescence of rhodamine-123, a mitochondrial energization-sensitive fluorescence probe, in individual hepatocytes and measured the fluorescence intensity with a digital imaging processor. Although addition of Kupffer cells or lipopolysaccharide in a range of 0.1 to 1.0 microgram/ml caused no significant alteration in the fluorescence in hepatocytes, Kupffer cells plus 1.0 microgram/ml lipopolysaccharide reduced fluorescence intensity in the cocultured hepatocytes. The alteration of rhodamine-123 fluorescence in the hepatocytes induced by lipopolysaccharide-activated Kupffer cells was significantly inhibited by the addition of NG-monomethyl-L-arginine, a selective inhibitor of nitric oxide synthesis. The transportal infusion of lipopolysaccharide also decreased rhodamine-123 fluorescence in perfused rat liver. The decrease was significantly enhanced in the pericentral regions. Autofluorescence of NADH was elicited by continuous infusion of lipopolysaccharide; this reaction was also enhanced in the pericentral regions. We showed the main site of uptake of infused lipopolysaccharide in the hepatic lobule to be in the periportal regions with fluorescein isothiocyanate-labeled lipopolysaccharide. Our results indicate that the inhibition of mitochondrial energization occurs mainly in pericentral regions, which are distant from the lipopolysaccharide uptake site. The continuous administration of NG-monomethyl-L-arginine significantly attenuated the lipopolysaccharide-induced decrease in rhodamine-123 fluorescence and increase of the NADH contents of the hepatic lobule.(ABSTRACT TRUNCATED AT 250 WORDS)
Biomarker Profiling for Lupus Nephritis
Authors: Yajuan Li, Xiangdong Fang, Quan-Zhen Li
Journal: Genomics Proteomics & Bioinformatics (2013)

Abstract Lupus nephritis (LN) is one of the most severe manifestations of systemic lupus erythematosus (SLE), which is associated with significant morbidity and mortality of SLE patients. The pathogenesis of LN involves multiple factors, including genetic predisposition, epigenetic regulation and environmental interaction. Over the last decade, omics-based techniques have been extensively utilized for biomarker screening and a wide variety of variations which are associated with SLE and LN have been identified at the levels of genomics, transcriptomics and proteomics. These studies and discoveries have expanded our understanding of the molecular basis of the disease and are important for identification of potential therapeutic targets for disease prediction and early treatment. In this review, we summarize some of the recent studies targeted at the identification of LN-associated biomarkers using genomics and proteomic approaches.
Audit office says government should renegotiate PFI contracts to get better value for money
Authors: H. Mooney
Journal: BMJ (2010)

The government should do more to increase value for money and generate further efficiencies in private finance initiative (PFI) hospital contracts in a bid to save the NHS some much needed cash, the National Audit Office has concluded.

In its report on the performance and management of NHS hospital PFI contracts published today, the office found that the ability of NHS trusts to make savings from their PFI contracts is currently very limited.

The present arrangement means that trusts must pay an index linked fixed sum on a PFI contract, making it difficult for them to make savings without cutting back on services. Contractors who secure economies of scale through managing multiple PFI …
Adverse Outcomes After Hospitalization and Delirium in Persons With Alzheimer Disease
Authors: Tamara G. Fong, Richard N. Jones, Edward R. Marcantonio, Douglas Tommet, Alden L. Gross, Daniel Habtemariam, Eva Schmitt, Liang Yap, Sharon K. Inouye
Journal: Annals of Internal Medicine (2012)

Background: Hospitalization, frequently complicated by delirium, can be a life-changing event for patients with Alzheimer disease (AD). Objective: To determine risks for institutionalization, cognitive decline, or death associated with hospitalization and delirium in patients with AD. Design: Prospective cohort enrolled between 1991 and 2006 into the Massachusetts Alzheimer's Disease Research Center (MADRC) patient registry. Setting: Community-based. Participants: 771 persons aged 65 years or older with a clinical diagnosis of AD. Measurements: Hospitalization, delirium, death, and institutionalization were identified through administrative databases. Cognitive decline was defined as a decrease of 4 or more points on the Blessed Information-Memory-Concentration test score. Multivariate analysis was used to calculate adjusted relative risks (RRs). Results: Of 771 participants with AD, 367 (48%) were hospitalized and 194 (25%) developed delirium. Hospitalized patients who did not have delirium had an increased risk for death (adjusted RR, 4.7 [95% CI, 1.9 to 11.6]) and institutionalization (adjusted RR, 6.9 [CI, 4.0 to 11.7]). With delirium, risk for death (adjusted RR, 5.4 [CI, 2.3 to 12.5]) and institutionalization (adjusted RR, 9.3 [CI, 5.5 to 15.7]) increased further. With hospitalization and delirium, the adjusted RR for cognitive decline for patients with AD was 1.6 (CI, 1.2 to 2.3). Among hospitalized patients with AD, 21% of the incidences of cognitive decline, 15% of institutionalization, and 6% of deaths were associated with delirium. Limitations: Cognitive outcome was missing in 291 patients. Sensitivity analysis was performed to test the effect of missing data, and a composite outcome was used to decrease the effect of missing data. Conclusion: Approximately 1 in 8 hospitalized patients with AD who develop delirium will have at least 1 adverse outcome, including death, institutionalization, or cognitive decline, associated with delirium. Delirium prevention may represent an important strategy for reducing adverse outcomes in this population. Primary Funding Source: National Institute on Aging and the MADRC.
Protecting elderly people: flaws in ageist arguments
Authors: M. M Rivlin
Journal: BMJ (1995)

Some form of rationing is necessary in medicine, and to use age as a criterion for rationing seems initially appealing. Many of the criteria currently being used for deciding the distribution of funds depend on subjective judgments. Age, however, is objective and therefore negates the need for value judgments. Justice and fairness, it is sometimes suggested, require that finite resources should be directed at young people, who have not had a chance to live their lives, rather than at elderly people, who have already lived most of theirs. The adoption of ageist policies, however, may not result in the implied savings unless care is also withdrawn. Furthermore, ageist policies, which deny elderly people treatment on the sole grounds of their age, are both unfair and discriminatory and should therefore be resisted.
The unremitting burden on carers.
Authors: R Anderson
Journal: BMJ (1987)

The unremitting burden on carers Probably more than one and a quarter million people in Britain care for disabled or elderly people living in the community.'Most of these people could not get by without the support of their "carers."More than 10 years ago the BMJ argued that the work of carers was not sufficiently understood or supported.2Since theh their contribution has been better recognised and they have, indeed, become a cornerstone of government policy for "care in the community.""IResearch into the experience of carers has also
Morphological evidence that activated polymorphs circulate in the peripheral blood of patients with rheumatoid arthritis.
Authors: D A McCarthy, J Bernhagen, M J Taylor, A S Hamblin, I James, P W Thompson, J D Perry
Journal: Annals of the Rheumatic Diseases (1992)

Purified peripheral blood polymorphonuclear leucocytes (PMNs) from patients with rheumatoid arthritis (RA) have been found to differ from purified PMNs from normal subjects in ways that are consistent with their prior activation. However, it is currently contentious whether activated PMNs really circulate in patients with RA, or whether they are produced as an in vitro artefact of purification. Recently developed rapid leucocyte fixation and preparation technique showed that the proportion of polarised (activated) PMNs (36.9 (24.7)%, mean (SD); n = 31) was increased relative to that in control subjects (8.1 (5.6)%; n = 12). Serum cytidine deaminase levels, a biochemical marker of PMN lysis, were also increased in patients with RA (11.59 (7.26) U/ml) compared with those in controls (6.82 (3.78) U/ml), but the proportion of polarised PMNs and the levels of cytidine deaminase activity were unrelated to clinical assessments of inflammatory disease activity. Twelve patients who were not receiving drugs or who were receiving only non-steroidal anti-inflammatory drugs (NSAIDs) had more polarised PMNs than 19 patients receiving second line treatment in addition to NSAIDs (patients receiving NSAIDs, 49.6 (25.9)%; patients receiving second line treatment, 27.5 (21.1)%). Fluorescence activated cytometric analysis of CR1 and CR3 expression on PMNs from a randomly selected subgroup of patients with RA showed that the serum level of cytidine deaminase activity was correlated positively with the expression of CR1 (the C3b receptor) on the cell surface and that the proportion of polarised PMNs was positively correlated with the expression of CR3 (or CD11b/CD18), the iC3b receptor that is upregulated on activation. It is suggested that the polarised PMNs which circulate in blood samples from patients with RA represent cells which have been activated but not yet marginated, or activated cells which have marginated but subsequently returned to the circulating pool.
Surgery for Recurrent Colon Cancer
Authors: Charles M. Bagley
Journal: Annals of Internal Medicine (1999)

Letters2 February 1999Surgery for Recurrent Colon CancerCharles M. Bagley Jr., MDCharles M. Bagley Jr., MDWashington Cancer Centers; Seattle, WA 98133Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-130-3-199902020-00010 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:Goldberg and colleagues (1) have presented well-analyzed results of their attempts to resect metastatic colon cancer from various organ sites. However, the long-term disease-free survival outcome is overstated, especially in the Discussion section, where the authors state, “The 5-year disease-free survival rate of 32% seen in patients with hepatic metastasis in our study … .” However, the 32% survival rate was not seen in their entire sample of patients with hepatic metastasis but rather only in those for whom “curative intent” surgery was successfully performed. Such surgery was accomplished in only 28 of the 49 patients with ...Reference1. Goldberg RM, Fleming TR, Tangen CM, Moertel CG, Macdonald JS, Haller DG, et al . Surgery for recurrent colon cancer: strategies for identifying resectable recurrence and success rates after resection. Ann Intern Med. 1998;129:27-35. LinkGoogle Scholar Author, Article, and Disclosure InformationAffiliations: Washington Cancer Centers; Seattle, WA 98133 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetailsSee AlsoSurgery for Recurrent Colon Cancer: Strategies for Identifying Resectable Recurrence and Success Rates after Resection Richard M. Goldberg , Thomas R. Fleming , Catherine M. Tangen , Charles G. Moertel , John S. Macdonald , Daniel G. Haller , and John A. Laurie Surgery for Recurrent Colon Cancer Richard M. Goldberg , Thomas R. Fleming , and Catherine M. Tangen Surgery for Recurrent Colon Cancer Paul H. Sugarbaker Metrics 2 February 1999Volume 130, Issue 3Page: 239KeywordsColorectal cancerCurative resectionDisease free survivalLiverLung resectionLungsSurgery Issue Published: 2 February 1999 CopyrightCopyright © 1999 by American College of Physicians. All Rights Reserved.PDF DownloadLoading ...
Erratum: Corrigendum: Mutations in 15-hydroxyprostaglandin dehydrogenase cause primary hypertrophic osteoarthropathy
Authors: Sandeep Uppal, Christine P Diggle, Ian M Carr, Colin W G Fishwick, Mushtaq Ahmed, Gamal H Ibrahim, Philip S Helliwell, Anna Latos-Bieleńska, Simon E V Phillips, Alexander F Markham, Christopher P Bennett, David T Bonthron
Journal: Nature Genetics (2008)
Taxing junk food improves health outcomes, study finds
Authors: B. Roehr
Journal: BMJ (2010)

The price of soda drinks and pizza affects their level of consumption and therefore has an effect on health outcomes, a 20 year US study has concluded. It suggests that imposing a tax on junk food might improve the nation’s health.

The coronary artery risk developments in young adults (CARDIA) study is notable for its scope, duration, and measurement of both physiological and economic factors. Beginning in 1985 it recruited a broadly representative sample of 5115 adults aged 18 to 30 in four cities in the United States ( Archives of Internal Medicine 2010;170:420-6).

The researchers periodically measured participants’ height, weight, insulin resistance, and other clinical factors, …
Structure of a Domain-Swapped FOXP3 Dimer on DNA and Its Function in Regulatory T Cells
Authors: Hozefa S. Bandukwala, Yongqing Wu, Markus Feuerer, Yongheng Chen, Bianca Barboza, Srimoyee Ghosh, James C. Stroud, Christophe Benoist, Diane Mathis, Anjana Rao, Lin Chen
Journal: Immunity (2011)
Early atopic disease and early childhood immunization – is there a link?
Authors: C. Grüber, J. Warner, D. Hill, V. Bauchau
Journal: Allergy (2008)

Background: There are frequent concerns about early immunizations among the parents of children at heightened risk for atopy. The study assessed the effect of vaccine immunization before the first birthday on eczema severity and allergic sensitization in the second year of life. Methods: A total of 2184 infants, aged 1–2 years, with established atopic dermatitis and a family history of allergy, from 97 study centres in 10 European countries, South Africa and Australia were included. Exposure to vaccines (diphtheria, tetanus, pertussis, polio, Haemophilus influenzae Type B, hepatitis B, mumps, measles, rubella, varicella, BCG, meningococci and pneumococci) and immunization dates were recorded from immunization cards. Immunoglobulin E (IgE) was determined by RAST and eczema severity was assessed by scoring atopic dermatitis (SCORAD). Results: Immunization against any target was not associated with an increased risk of allergic sensitization to food or inhalant allergens. Varicella immunization (only 0.7% immunized) was inversely associated with total IgE &gt; 30 kU/l (OR 0.27; 95% CI 0.08–0.87) and eczema severity (OR 0.34; 95% CI 0.12–0.93). Pertussis immunization (only 1.7% nonimmunized) was inversely associated with eczema severity (OR 0.30; 95% CI 0.10–0.89). Cumulative received vaccine doses were inversely associated with eczema severity ( P = 0.0107). The immunization coverage of infants before and after the onset of atopic dermatitis was similar. Conclusion: In children at heightened risk for atopy, common childhood immunization in the first year is not associated with an increased risk of more severe eczema or allergic sensitization. Parents of atopic children should be encouraged to fully immunize their children.
Influence of Digoxin Immune Fab Therapy and Renal Dysfunction on the Disposition of Total and Free Digoxin
Authors: Michael R. Ujhelyi
Journal: Annals of Internal Medicine (1993)

Objective: To characterize the disposition of total and free serum digoxin following the administration of digoxin Fab antibody in patients with varying degrees of renal function. Design: Observational study of pharmacokinetics and pharmacodynamics. Setting: Critical care and telemetry units of two university-affiliated teaching institutions, Hartford Hospital and Henry Ford Hospital. Patients: Fourteen digoxin-intoxicated patients (baseline total digoxin > 3.2 nmol/mL) with mean (SD) serum creatinine of 380.1 212.2 mol/L who received digoxin Fab antibody therapy. Measurements: Serum was drawn every 12 to 24 hours for 80 to 327 hours after Fab administration. Total and free digoxin were assayed in serum by fluorescence polarization immunoassay or modified immunofluorometric assay. Results: Before Fab was administered, total digoxin ranged from 3.5 to 10.5 nmol/mL. After treatment with Fab, total digoxin increased rapidly to a mean (SD) maximum of 51.8 22.7 nmol/mL and decreased to 7.2 4.7 nmol/mL at the last measurement. Total digoxin was eliminated in a two-phase fashion. The half-life of the initial phase of total digoxin decline was 11.6 4.1 hours, and the half-life of the second or terminal elimination phase was 118 57 hours. Free digoxin levels decreased rapidly following Fab therapy, to a mean nadir of 0.6 1.1 nmol/mL, but rebounded to a mean maximum free digoxin concentration of 1.7 1.3 nmol/mL in 77 46 hours. The time to maximum free digoxin rebound occurred later in patients with end-stage renal disease (n = 4) compared with other patients (127 40 hours compared with 55 28 hours). Conclusion: Elimination of digoxin following Fab therapy is prolonged in digoxin-toxic patients with renal dysfunction. In addition, rebound of free digoxin is delayed in anephric patients. Monitoring free digoxin following the administration of Fab may be of value in selected patients to guide additional Fab dosing, confirm possible rebound toxicity, or guide the reinitiation of digoxin therapy.
1091 TISSUE ENGINEERING VASCULARIZED HUMAN LIVER ORGANOIDS: STUDY OF MORPHOLOGY, METABOLOMICS AND PHENOTYPIC EXPRESSION OF TRANSITIONAL 2D/3D CO-CULTURES OF HEPATIC C3A CELLS WITH ENDOTHELIAL PROGENITORS
Authors: L.J. Nelson, K. Burgess, O. Tura, M. Navarro, K. Samuel, P.C. Hayes, M. Turner, J.N. Plevris
Journal: Journal of Hepatology (2011)
HORMONAL INFLUENCES ON MAMMARY TUMORS OF THE RAT
Authors: Charles Huggins, Klaus Mainzer
Journal: The Journal of Experimental Medicine (1957)

Many members of the androstane series profoundly retarded the growth of a transplanted benign mammary fibroadenoma of the rat; the restraint of tumor growth was in direct proportion to the amount of the administered compound until its maximal effect was achieved. Certain steroids closely related to the androstane inhibitors accelerated the growth of the tumor. These effects of divergent sort depend on the molecular structure of the steroid. The molecular structure of androstane derivatives, which is of high significance in modifying the rate of growth of the benign mammary tumor, consists of multiple components. These include (a) the presence and number of ketone and hydroxyl groups in special orientation at specific sites, (b) the sites of dehydrogenation in the molecule, and (c) the presence, number, and state of hydrogenation of alkyl groups at designated molecular positions. These multiple factors determine whether androstane compounds will inhibit growth of the tumor, enhance it, or fail to influence its growth. The androstane compounds which caused either the restraint or the promotion of tumor growth had the common property of inducing proliferation of the normal mammary epithelium. Two mechanisms are involved in the restraint of growth of mammary fibroadenoma by androstane inhibitors. The primary effect is the abolition of action of phenolic estrogens and progesterone when dihydrotestosterone is administered concurrently, presumably through direct action at the tumor cell level A secondary contributory suppressive effect is the depression of ovarian activity, and consequently of the production of phenolic estrogens and progesterone, by these compounds. Transplanted mammary fibroadenoma in the rat possesses neoplastic traits and also some growth properties of normal mammary epithelium; inhibition of these latter by hormonal methods commonly retarded the growth of the tumor. But in hypophysectomized rats dihydrotestosterone failed to inhibit the growth of a mammary fibroadenoma with unusually low hormonal dependence as determined by functional tests of its growth.
Vibration during high frequency ventilation in neonates
Authors: P-Y CHEUNG
Journal: Thorax (2001)

seem to be specific to PCH, demonstrating the usefulness of HRCT scanning for diagnosis of this disease.Other previously reported CT findings of the disease include increased soft tissue density of the mediastinum 1 2 and mediastinal and hilar lymph adenopathies, 7 but such findings were absent in our case.Possible explanations for the stable condition of our case over a long period are either that it was a chance discovery of an early phase of the disease by HRCT scanning or that PCH has separate subtypes with diVering speeds of progression.Wider use of HRCT scanning and more extensive understanding of PCH would resolve this issue in the future.
Intraoperative clinical practice and risk of early complications after cataract extraction in the United States, Canada, Denmark, and Spain
Authors: Jens Christian Norregaard, Peter Bernth-Petersen, Lorne Bellan, Jordi Alonso, Charlyn Black, Elaine Dunn, Tavs Folmer Andersen, Mireia Espallargues, Gerard F Anderson
Journal: Ophthalmology (1999)