tbuckley/cabot-search huggingface dataset:
Implementing the NHS information technology programme: qualitative study of progress in acute trusts
Authors: Jane Hendy, Naomi Fulop, Barnaby C Reeves, Andrew Hutchings, Simon Collin
Journal: BMJ (2007)

<b>Objectives</b> To describe progress and perceived challenges in implementing the NHS information and technology (IT) programme in England. <b>Design</b> Case studies and in-depth interviews, with themes identified using a framework developed from grounded theory. We interviewed personnel who had been interviewed 18 months earlier, or new personnel in the same posts. <b>Setting</b> Four NHS acute hospital trusts in England. <b>Participants</b> Senior trust managers and clinicians, including chief executives, directors of IT, medical directors, and directors of nursing. <b>Results</b> Interviewees unreservedly supported the goals of the programme but had several serious concerns. As before, implementation is hampered by local financial deficits, delays in implementing patient administration systems that are compliant with the programme, and poor communication between Connecting for Health (the agency responsible for the programme) and local managers. New issues were raised. Local managers cannot prioritise implementing the programme because of competing financial priorities and uncertainties about the programme. They perceive a growing risk to patients9 safety associated with delays and a loss of integration of components of the programme, and are discontented with Choose and Book (electronic booking for referrals from primary care). <b>Conclusions</b> We recommend that the programme sets realistic timetables for individual trusts and advises managers about interim IT systems they have to purchase because of delays outside their control. Advice needs to be mindful of the need for trusts to ensure longer term compatibility with the programme and value for money. Trusts need assistance in prioritising modernisation of IT by, for example, including implementation of the programme in the performance management framework. Even with Connecting for Health adopting a different approach of setting central standards with local implementation, these issues will still need to be addressed. Lessons learnt in the NHS have wider relevance as healthcare systems, such as in France and Australia, look to realise the potential of large scale IT modernisation.
Effect of secretin on release of heterogeneous forms of gastrin.
Authors: E Straus, A J Greenstein, R S Yalow
Journal: Gut (1975)

The effect of an intravenous injection of secretin on plasma gastrin concentration is shown to be dependent upon the relative concentration of the major forms of immunoreactive gastrin present in the plasma at the time of injection. Secretin suppressed gastrin secretion in the fasting state in patients in whose plasma heptadecapeptide and big gastrins predominated and did not suppress when big big gastrin comprised more than 90% of plasma gastrin immunoreactivity. The post-secretin decrease in plasma gastrin was due entirely to the disappearance of the smaller, more rapidly degraded forms. Food-stimulated gastrin response was suppressed by secretin for the initial 40 minutes after a test meal but was greater than usual from 40 to 120 minutes.
Seeding With Omental Cells Prevents Late Neointimal Hyperplasia in Small-Diameter Dacron Grafts
Authors: Miralem Pasic, Werner Müller-Glauser, Bernhard Odermatt, Mario Lachat, Burkhardt Seifert, Marko Turina
Journal: Circulation (1995)

Background The influence of complete endothelialization of a prosthetic graft on development of late neointimal hyperplasia is unknown. This study was designed to investigate the effect of complete coverage with endothelial-like cells on late neointimal hyperplasia in small-diameter Dacron grafts seeded with omental cells in a canine model. Methods and Results Four-mm-ID Dacron grafts were seeded with cells from omentum and implanted in the carotid arteries in 24 mongrel dogs. Each dog received one seeded and one nonseeded graft. The graft patencies were assessed by angiography at 1, 5, 12, 26, and 52 weeks after surgery. The prostheses were explanted at 5, 12, 26, and 52 weeks after surgery and underwent microscopic studies. The actuarial patency rates at 1, 5, 12, 26, and 52 weeks were 100%, 95%, 95%, 95%, and 95% for seeded grafts and 100%, 86%, 49%, 40%, and 13% for nonseeded grafts, respectively. The seeded grafts exhibited a uniform endothelial-like luminal monolayer without the development of late neointimal proliferation or anastomotic neointimal hyperplasia. Neointimal tissue thickness increased up to 6 months; no additional progression of the subendothelial tissue thickness was observed, in fact there was an insignificant decrease. Conclusions Seeding with omental cells prevents development of late neointimal hyperplasia of small diameter prosthetic vascular grafts in a canine model.
Circulating ICAM-1 is increased in septic shock.
Authors: C N Sessler, A C Windsor, M Schwartz, L Watson, B J Fisher, H J Sugerman, A A Fowler
Journal: American Journal of Respiratory and Critical Care Medicine (1995)

Adhesion molecules play a critical role in the interaction of circulating neutrophils with vascular endothelium during inflammation. Increased quantities of soluble, circulating intercellular adhesion molecule-1 (cICAM-1) are present in various inflammatory conditions. The purpose of this investigation was to measure cICAM-1 levels in septic adults, as well as to examine the relationship between this potential marker of endothelial-cell activation and the consequences of sepsis (i.e., multiple organ failure and death). Using a sandwich-type enzyme-linked immunosorbent assay (ELISA), we measured cICAM-1 in blood samples obtained within 12 h of admission to an intensive care unit (ICU) for sepsis and other conditions. We found cICAM-1 levels to be increased in 25 septic patients (1,259 +/- 159 ng/ml, mean +/- SEM) as compared with 12 healthy volunteers (355 +/- 41 ng/ml, p < 0.0001) and four ICU patients without systemic inflammatory response syndrome (SIRS) (585 +/- 76 ng/ml, p < 0.001). Twenty-five patients with SIRS but no evidence of causative infection also had elevated levels of cICAM-1 (937 +/- 144 ng/ml, p = 0.12 versus sepsis). Serial measurements over the first week of sepsis demonstrated persistent elevation in most patients. Day 1 cICAM-1 levels were higher (p = 0.017, ANOVA) in 16 patients with septic shock than in seven with severe sepsis and two with sepsis but without hypotension or hypoperfusion. There was a positive correlation (r = 0.50, p = 0.009) between Day-1 cICAM-1 measurements and severity of shock as determined by the presence of hypotension and vasopressor use.(ABSTRACT TRUNCATED AT 250 WORDS)
HMGB1 Promotes Drug Resistance in Osteosarcoma
Authors: Jun Huang, Jiangdong Ni, Ke Liu, Yan Yu, Min Xie, Rui Kang, Philip Vernon, Lizhi Cao, Daolin Tang
Journal: Cancer Research (2011)

Osteosarcoma is the most commonly occurring bone cancer in children and adolescents. Unfortunately, treatment failures are common due to the development of chemoresistance, for which the underlying molecular mechanisms remain unclear. In this study, we implicate the DNA-binding protein HMGB1, which also exerts immunoregulatory effects in its secreted form, in the development of drug resistance in osteosarcoma. Anticancer agents including doxorubicin, cisplatin, and methotrexate each induced HMGB1 upregulation in human osteosarcoma cells, and RNA interference-mediated knockdown of HMGB1 restored the chemosensitivity of osteosarcoma cells in vivo and in vitro. Mechanistic investigation revealed that HMGB1 increased drug resistance by inducing autophagy, an intracellular self-defense mechanism known to confer drug resistance. We found that HMGB1 bound to the autophagy regulator Beclin1 and regulated the formation of the Beclin1-PI3KC3 [PI3KC3, phosphatidylinositol 3-kinase class 3] complex that facilitates autophagic progression. In addition, we found that interaction between HMGB1 and Beclin1 relied upon the autophagic complex ULK1-mAtg13-FIP200. Therefore, through its role as a regulator of autophagy, HMGB1 is a critical factor in the development of chemoresistance, and it offers a novel target for improving osteosarcoma therapy.
Characterization of a reproducible rat model of hepatic veno-occlusive disease
Authors: Laurie D. DeLeve, Robert S. McCuskey, Xiangdong Wang, Liping Hu, Margaret K. McCuskey, Robert B. Epstein, Gary C. Kanel
Journal: Hepatology (1999)

Lack of a reproducible animal model has hampered progress in understanding hepatic veno-occlusive disease (HVOD). This article characterizes a reproducible model of HVOD. Rats gavaged with monocrotaline, 160 mg/kg, were killed between days 1 and 10. Sections were evaluated by light microscopy with a standardized scoring system, by immunoperoxidase staining with ED-1 (monocytes, macrophages) and ED-2 (Kupffer cells) antibodies, and by transmission (TEM) and scanning electron microscopy (SEM). On days 1 and 2, the earliest manifestations were progressive injury to the sinusoidal wall with loss of sinusoidal lining cells, sinusoidal hemorrhage, and mild damage to central vein (CV) endothelium. On days 3 through 5 (“early HVOD”), there was centrilobular coagulative necrosis, severe injury to sinusoids, severe sinusoidal hemorrhage, and severe CV endothelial damage; inflammation with ED-1–positive cells was most marked on these days. Days 6 and 7 (“late HVOD”) were characterized by subendothelial and advential fibrosis of CVs, damage of the CV endothelium with subendothelial hemorrhage, and some restoration of the sinusoidal wall. Between days 8 and 10, sections showed interindividual variation ranging from mild, residual fibrosis to severe, late HVOD. From days 1 through 10, ED-2–positive cells were decreased in number, and the number of ED-1–positive cells was increased. Sinusoidal damage is the earliest change in HVOD. Coagulative necrosis follows sinusoidal injury and resolves with improvement in sinusoidal endothelial cell (SEC) morphology. Moderate-to-severe CV fibrosis occurs after reappearance of sinusoidal lining cells and resolution of hepatocyte necrosis. The inflammatory response within the lobule and CVs is a result of recruitment of monocytes, whereas Kupffer cells are decreased in number.
The Pediatric Vaccine Controversy: What Should the Doctor Do?
Authors: Alan R. Nelson
Journal: JAMA (1984)

When Senator Paula Hawkins (R, Fla) held hearings on her vaccine injury compensation bill (S. 2117) this summer, videotapes were shown that depicted children who had been injured by pediatric vaccines. The audience watching the video segment was visibly moved. Many may have been led to conclude that diphtheria-tetanus-pertussis (DTP) vaccination causes more problems than it solves. Some parents were bitter because state laws require administration of vaccines that (they allege) killed or maimed their child. Others were critical because their physician had not warned them of the risk of DTP immunization prior to administration. At the same hearing, other parents called for repeal of state laws that require immunization as a condition of entry into school. Vaccine manufacturers were criticized for failing to produce safer vaccines. Pediatricians testified that some of their colleagues are no longer administering vaccines because of concern about being sued (for failure to warn adequately
Halothane Hepatitis in Three Pairs of Closely Related Women
Authors: Richard H. Hoft, John P. Bunker, Harvey I. Goodman, Peter B. Gregory
Journal: New England Journal of Medicine (1981)

AN association between administration of halothane for general anesthesia and postoperative hepatitis is generally believed to exist,1 , 2 although some disagreement continues.3 , 4 An unresolved feature of the assumed association is the mechanism by which halothane damages the liver. The most favored explanation is that halothane induces a hypersensitivity response in the liver.5 It has also been proposed that one or more of the metabolic products of halothane injures the organ6 or that hepatitis occurring after use of halothane is simply viral hepatitis,7 which post-halothane hepatitis resembles clinically and morphologically.We have observed post-halothane hepatitis in three pairs of closely related women . . .
Migrant Populations and the Diffusion of the Sickle-Cell Gene
Authors: A. P. GELPI
Journal: Annals of Internal Medicine (1973)

If we assume that the sickle-cell mutation occurred in equatorial Africa, distribution of the sickle-cell trait in the Middle East and India correlates well with historical evidence of population displacement into these areas as a result of the East African slave trade, and with the distribution of African blood group markers in Asia. The occurrence of the sickle-cell trait in southern Europe parallels the extent of the medieval Arab conquests and is believed to reflect gene flow from the Middle East. Changing endemicity of Plasmodium falciparum malaria; interaction between hemoglobin S, thalassemia, and glucose-6-phosphate dehydrogenase deficiency; and contribution to the gene pool from subjects with mild homozygous sickle-cell disease are thought to be additional reasons for patterns of sickle-cell trait distribution in Eurasian populations.
Corrigendum to “Acute hepatitis caused by a natural lipid-lowering product: When “alternative” medicine is no “alternative” at all” [J Hepatol 50 (2009) 1273–1277]
Authors: Antonio Grieco, Luca Miele, Maurizio Pompili, Marco Biolato, Fabio M. Vecchio, Ignazio Grattagliano, Giovanni Gasbarrini
Journal: Journal of Hepatology (2010)
Inhibition of Complement Activation Decreases Airway Inflammation and Hyperresponsiveness
Authors: Christian Taube, Yeong-Ho Rha, Katsuyuki Takeda, Jung-Won Park, Anthony Joetham, Annette Balhorn, Azzeddine Dakhama, Patricia C. Giclas, V. Michael Holers, Erwin W. Gelfand
Journal: American Journal of Respiratory and Critical Care Medicine (2003)

Studies in murine models have suggested the involvement of the complement anaphylatoxins (C3a and C5a) in the development of allergic asthma. We investigated the effects of inhibiting complement activation after sensitization but before allergen challenge on the development of allergic airway inflammation and airway hyperresponsiveness. To prevent complement activation, we used a recombinant soluble form of the mouse membrane complement inhibitor complement receptor-related gene y (Crry) fused to the IgG1 hinge, CH2 and CH3 domains (Crry-Ig), which has decay-accelerating activity for both the classic and alternative pathways of complement as well as cofactor activity for factor I-mediated cleavage of C3b and C4b. C57BL/6 mice were sensitized (Days 1 and 14) and challenged (Days 24–26) with ovalbumin. Crry-Ig was administered after allergen sensitization either as an intraperitoneal injection or by nebulization before allergen challenge. Crry-Ig significantly prevented the development of airway hyperresponsiveness, decreased airway and lung eosinophilia as well as the numbers of lung lymphocytes, decreased levels of interleukin (IL)-4, IL-5, and IL-13 in bronchoalveolar lavage fluid and decreased serum ovalbumin-specific IgE and IgG1. These results suggest that prevention of complement activation may have a therapeutic role in the treatment of allergic airway inflammation and asthma in sensitized individuals.
Abstract 4630: Seminal AMACR protein: a non-invasive test in the detection of prostate cancer
Authors: Wei Huang, David Jarrard, Mark Ritter, Michelle Waknitz, Jane Straus, George Wilding
Journal: Cancer Research (2010)

Abstract Introduction: Current prostate cancer screening relies on the PSA test and the digital rectum rectal examination (DRE), which have relatively low specificity. A more specific marker is in need for prostate cancer screening and risk stratification could reduce the burden of unnecessary biopsies. AMACR, has been proven to be an excellent tissue marker for prostate caner, could be an attractive candidate, but. Soso far, serum the detection of AMACR detection in serum has been unsuccessfuldifficult. This study explored the detection of AMACR protein in semen ejaculate and its potential as a non-invasive test in the diagnosis and management of prostate cancer. Methods: Semen ejaculates were analyzed from 23 prostate cancer (biopsy proven) patients, 21 of which had prostatectomy, as well as 15 age-comparable controls (&amp;gt;50y, PSA&amp;lt;2 ng/mL, assumed prostate cancer free). An indirect sandwich ELISA chemiluminescence assay was used to test semen AMACR protein. Tissue AMACR protein was also quantified in 13 corresponding prostatectomy specimens using automated quantitative analysis (AQUATM). Results: AMACR was detected in 19 of 23 (83%) semen ejaculates of prostate cancer patients. Among the other 4 patients with undetectable semen AMACR, one had no residual tumor in the prostatectomy specimen (#40), one had Gleason score of 9 cancer (#37) with no detectable tissue AMACR either, while the other two remaining patients (#31 and #33) had a very small volume of cancer on two separate sextant biopsies biopsy sets and are on watchful waiting list. AMACR was also detected in 7 of 15 (47%) control group. Using 100 ng/mL as a cutoff value, semen AMACR protein was positive in 16 of 23 (70%) cancer patients who had underwent prostatectomy and in 5 of 15 (33%) age-comparable controls. Conclusions: This has been the first study first to demonstrated that AMACR protein is detectable in semen ejaculate. A high semen AMACR detection rate in cancer patients suggested suggests that semen AMACR may be useful, supplemental, as a non-invasive test in addition toto the PSA test for detecting prostate cancer, especially cancer of significant volume. Questions regarding specificity of AMACR are, however, raised. Given the lack of prostate biopsy confirmation, The the age-comparable controls in this study may not be an entirely representative sample of men free of prostate cancer without confirmation by prostate biopsy. This Our study's findings will form the basis for the design of a larger finding need to be further validated in a larger prospective screening trial of AMACR. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 4630.
Junctional epidermolysis bullosa in two siblings: clinical observations, collagen studies and electron microscopy
Authors: C.A. OAKLEY, N. WILSON, J.A. ROSS, R. StC. BARNETSON
Journal: British Journal of Dermatology (1984)

Journal Article Junctional epidermolysis bullosa in two siblings: clinical observations, collagen studies and electron microscopy Get access C.A. OAKLEY, C.A. OAKLEY University Department of Dermatology, Royal Infirmary, Edinburgh, and Royal Hospital for Sick Children, Edinburgh Search for other works by this author on: Oxford Academic Google Scholar N. WILSON, N. WILSON University Department of Dermatology, Royal Infirmary, Edinburgh, and Royal Hospital for Sick Children, Edinburgh Search for other works by this author on: Oxford Academic Google Scholar J.A. ROSS, J.A. ROSS University Department of Dermatology, Royal Infirmary, Edinburgh, and Royal Hospital for Sick Children, Edinburgh Search for other works by this author on: Oxford Academic Google Scholar R. StC. BARNETSON R. StC. BARNETSON University Department of Dermatology, Royal Infirmary, Edinburgh, and Royal Hospital for Sick Children, Edinburgh Dr R. StC.Barnetson, University Department of Dermatology, Royal Infirmary, Edinburgh. Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 111, Issue 5, 1 November 1984, Pages 533–543, https://doi.org/10.1111/j.1365-2133.1984.tb06622.x Published: 01 November 1984 Article history Accepted: 14 May 1984 Published: 01 November 1984
Polaroid Photography as a Practical Method of Providing Illustrations of Radiographs for Clinical Records
Authors: Edwin J. Euphrat
Journal: New England Journal of Medicine (1955)

ESSENTIAL for good medical practice is the maintenance of clear and concise medical records. That photographs of appropriate scale add immeasurably to the clarity and completeness of most clinical charts is simply to paraphrase the ancient adage, "One picture is worth a thousand words." This is particularly true of radiologic findings. Unillustrated verbal descriptions and interpretations, even when prepared by the most articulate radiologist, frequently leave too much to the imagination of the clinician. It is remarkable, in this golden age of graphic arts, that illustrative reproductions of significant radiographs are conspicuous chiefly by their absence in clinical records kept . . .
Cyclosporine, Methotrexate, and Prednisone Compared with Cyclosporine and Prednisone for Prophylaxis of Acute Graft-versus-Host Disease
Authors: Nelson J. Chao, Gerhard M. Schmidt, Joyce C. Niland, Michael D. Amylon, Andrew C. Dagis, Gwynn D. Long, Auayporn P. Nademanee, Robert S. Negrin, Margaret R. O'Donnell, Pablo M. Parker, Eileen P. Smith, David S. Snyder, Anthony S. Stein, Ruby M. Wong, Karl G. Blume, Stephen J. Forman
Journal: New England Journal of Medicine (1993)

Acute graft-versus-host disease (GVHD) following allogeneic bone marrow transplantation remains a serious problem. In a clinical trial, we tested the combination of cyclosporine and prednisone with and without methotrexate for the prevention of GVHD.One hundred fifty patients with either acute leukemia in first complete remission, chronic myelogenous leukemia in first chronic phase, or lymphoblastic lymphoma in first complete remission were enrolled in the study. All the patients were given fractionated total-body irradiation (1320 cGy) and etoposide (60 mg per kilogram of body weight) in preparation for transplantation, and received bone marrow from genotypically histocompatible donors. To prevent GVHD, they were randomly assigned to prophylactic treatment with either cyclosporine, methotrexate, and prednisone or cyclosporine and prednisone without methotrexate. All the patients received standardized supportive care after transplantation, including intravenous gamma globulin.Patients receiving cyclosporine, methotrexate, and prednisone had a significantly lower incidence of acute GVHD of grades II to IV (9 percent) than those receiving cyclosporine and prednisone (23 percent, P = 0.02). Multivariate regression analysis demonstrated that an increased risk of acute GVHD was associated with an elevated serum creatinine concentration (P = 0.006) and treatment with cyclosporine and prednisone alone (P = 0.02). The lower incidence of acute GVHD was not associated with a higher rate of relapse of leukemia or lymphoma. There was no significant difference in disease-free survival at three years between the two treatment groups (64 percent with the three-drug regimen vs. 59 percent with the two-drug regimen, P = 0.57).The combination of cyclosporine, methotrexate, and prednisone was more effective in preventing acute GVHD of grades II to IV than was the combination of cyclosporine and prednisone without methotrexate.