tbuckley/cabot-search huggingface dataset:
A trial of fludarabine and cyclophosphamide combination chemotherapy in the treatment of advanced refractory primary cutaneous T-cell lymphoma
Authors: J.J. Scarisbrick, F.J. Child, A. Clift, R. Sabroe, S.J. Whittaker, M. Spittle, R. Russell-Jones
Journal: British Journal of Dermatology (2001)

Background The combination of fludarabine and cyclophosphamide shows synergistic toxicity in vitro and has been used to treat nodal non‐Hodgkin's lymphoma and relapsed chronic lymphocytic leukaemia. Objectives To test the efficacy of this combination in 12 patients with cutaneous T‐cell lymphoma (CTCL). Methods Nine patients with erythrodermic CTCL were identified for the study, eight of whom met the criteria for Sézary syndrome (SS), and three with tumour‐stage mycosis fungoides (MF). Patients received intravenous fludarabine and cyclophosphamide 3 days monthly for 3–6 months. Results Six patients tolerated at least three cycles. Five with SS had a response (one had a complete clinical response and four a partial response) and one patient with MF had stable disease. The mean duration of the response was 10 months. Six patients had treatment withdrawn, five due to bone marrow suppression and one due to progressive disease. No difference in pretrial parameters were found in those who had treatment withdrawn and those who tolerated at least three courses. Survival since the trial was similar in both groups at 11 months. Conclusions These data indicate that the combination of fludarabine with cyclophosphamide may be of clinical benefit in patients with SS but does not affect patient survival. As with other multiagent chemotherapy regimens, bone marrow toxicity is a common and severe side‐effect. These data suggest that this regimen should be considered palliative and should be reserved for patients with refractory disease without bone marrow suppression.
IgE class-restricted tolerance induced by neonatal administration of soluble or cell-bound IgE.
Authors: S S Chen, D H Katz
Journal: The Journal of Experimental Medicine (1983)

Induction of IgE class-restricted tolerance was studied in high IgE-responder (BALB/c X SJL)F1 mice, of which the parental BALB/c and SJL mice are high and low IgE-responder mice, respectively. 2,4-Dinitrophenyl (DNP)-specific monoclonal IgE was administered to (BALB/c X SJL)F1 mice neonatally in two forms: soluble IgE at 250 micrograms per injection, or 10-100 ng of IgE coupled to 25-50 X 10(6) syngeneic splenocytes by binding to the chemically reactive hapten trinitrobenzene sulfonate (TNBS) or directly conjugated via a heterobifunctional reagent, N-succinimidyl 3-(2-pyridyldithio) propionate (SPDP). Polyclonal induction of IgE class-restricted tolerance was observed in (BALB/c X SJL)F1 mice, neonatally treated with soluble IgE or IgE-conjugated syngeneic splenocytes. Thus these mice failed to mount IgE antibody responses to either keyhole limpet hemocyanin or ovalbumin challenge, assessed by the passive cutaneous anaphylaxis reaction. The IgG antibody responses to these same antigens, however, were not affected by this treatment. The IgE class-restricted tolerance induced by both forms of IgE persisted up to at least 6 mo with repeated antigenic challenges. IgE coupled to syngeneic cells by TNBS or the SPDP method induced prolonged tolerance up to 9 mo. The induction of polyclonal IgE class-restricted tolerance was achieved only by monoclonal IgE, whereas DNP-specific monoclonal IgG1 plus IgG2b coupled to syngeneic splenocytes by the SPDP method failed to modulate either IgE or IgG antibody responses. In contrast, (BALB/c X A/J)F1 mice, of which both parental strains are high IgE responders, developed IgE class-restricted tolerance upon repeated neonatal injection of soluble IgE, but not IgE-conjugated syngeneic splenocytes, indicating that gene products of the low IgE-responder mice contributed to the effective presentation and/or recognition of epsilon heavy chain of the IgE molecules. Taken collectively, these results demonstrated that non-antigen-specific, isotype-restricted tolerance can be induced in the IgE antibody system. The differential induction of IgE class-restricted tolerance by different forms of tolerogen in the strains studied perhaps distinguishes two underlying cellular mechanisms for IgE class-restricted tolerance.
The Impact of Psychiatric Comorbidities on Readmissions for Diabetes in Youth
Authors: Michelle M. Garrison, Wayne J. Katon, Laura P. Richardson
Journal: Diabetes Care (2005)

Comorbid psychiatric disorders have been associated with poorer disease outcomes in diabetic youth. Less is known, however, about the relationship between psychiatric disorders and repeat hospitalizations for youth with diabetes.We performed a retrospective cohort study using data from the Pediatric Health Information System, which included detailed discharge data from 37 non-competing children's hospitals in the U.S. Using logistic regression, we examined whether the presence of coded diagnoses for internalizing or externalizing disorders at an index hospitalization for diabetes was associated with increased risk for rehospitalization during follow-up (duration of follow-up ranged from 3 to 24 months). The analysis was stratified by age-groups, and we controlled for potential confounders including sex, age, race/ethnicity, type 1 versus type 2 diabetes, Medicaid status, intensive care unit utilization, length of stay during index admission, and duration of follow-up.Among adolescents aged 13-18, internalizing disorders were associated with significantly increased odds of rehospitalization (odds ratio 1.79 [95% CI 1.27-2.52]); the point estimate for externalizing disorders was similar, but the finding was not statistically significant at the alpha = 0.05 level (1.74 [0.96-3.15]). No significant association between psychiatric diagnoses and odds of repeat hospitalization was observed in diabetic children aged 5-12 years.Internalizing disorders are associated with increases in repeat hospitalizations for diabetes among adolescents. Future research is needed to explore the reasons for this finding, such as degree to which treatment nonadherence mediates this relationship and whether appropriate treatment of internalizing disorders results in improved diabetes outcomes and decreased readmissions.
Foundation trusts could take over other trusts by next year, government warns
Authors: A. O'Dowd
Journal: BMJ (2009)

NHS trusts that do not meet the 2010 deadline to achieve foundation trust status in England could be merged or taken over by existing foundation trusts, the government has said.

Speaking as a witness at a parliamentary session this week, the health secretary, Alan Johnson, said that 19 trusts were currently considered to be unlikely to achieve foundation trust status, which grants hospitals more clinical and financial independence. The government’s target is to have all acute and mental health trusts achieve such status before December 2010. Currently, about half have done so.

MPs on the parliamentary health …
A Health Care Cooperative Extension Service
Authors: Kevin Grumbach, James W. Mold
Journal: JAMA (2009)

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
Binding of Urethan With Macromolecules From Cell Organelles
Authors: B. G. Chavan, S. Y. Bhide
Journal: JNCI Journal of the National Cancer Institute (1973)

Journal Article Binding of Urethan With Macromolecules From Cell Organelles Get access B. G. Chavan, B. G. Chavan Biology Division, Cancer Research Institute, Tata Memorial Centre, Parel, Bombay 12, India Search for other works by this author on: Oxford Academic PubMed Google Scholar S. Y. Bhide S. Y. Bhide Biology Division, Cancer Research Institute, Tata Memorial Centre, Parel, Bombay 12, India Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 50, Issue 6, June 1973, Pages 1459–1461, https://doi.org/10.1093/jnci/50.6.1459 Published: 01 June 1973 Article history Received: 31 August 1972 Accepted: 12 February 1973 Published: 01 June 1973
Comparative aspects of oxytocin in baboon (Papio hamadryus anubis) and human corpora lutea
Authors: F S Khan-Dawood, M Y Dawood
Journal: Human Reproduction Update (1998)

In spite of the importance of the corpus luteum in human reproduction, little is known about its formation after ovulation and during regression in the absence of conception. This is largely due to constraints on the availability of normal human tissue: therefore an appropriate model which could be studied and provide information applicable to the human was sought. The baboon (Papio), a non-human primate, has been determined to be one such model. Thus, in the past several years our studies have examined the role of luteal peptides in corpus luteum function, and, when possible, we have attempted to examine corpora lutea from the human and baboon in parallel. Although a milk-ejection factor was recognized to be present in luteal tissue in 1910 (Ott and Scott, Proc. Soc. Exp. Biol. Med., Vol. 8, p 49), the role of oxytocin in luteal physiology has not been easy to ascertain. This is in part due to the methodologies employed to assess its role. Our studies summarized below suggest that oxytocin does not directly affect luteal steroidogenesis, but that it may play a role in cell to cell communication involving the expression of the gap junction proteins, the connexins. In view of the fact that oxytocin, its receptor, gap junctions and associated proteins are not unique to the human and non-human primates, the model of luteal development and demise proposed may be applicable to most species. Key words: baboon/cell-cell interaction/corpus luteum/human/oxytocin
Geoepidemiology of systemic vasculitis: comparison of the incidence in two regions of Europe
Authors: R A Watts
Journal: Annals of the Rheumatic Diseases (2001)

The aetiopathogenesis of the primary systemic vasculitides (PSV) is unknown but includes both environmental and genetic factors. The development of classification criteria/definitions for PSV allows comparison of the epidemiology between different regions.The same methods and the American College of Rheumatology (1990) criteria or Chapel Hill definitions were used to compare the epidemiology of Wegener's granulomatosis, Churg-Strauss syndrome, microscopic polyangiitis, and polyarteritis nodosa in Norwich (east England population 413 500) and Lugo (northwest Spain population 204 100). Patients with PSV were identified between 1 January 1988 and 31 December 1998.Overall, the incidence of PSV in adults was almost equal in Norwich (18.9/million) and Spain (18.3/million). The incidence of Wegener's granulomatosis in Norwich (10.6/million) was greater than in Spain (4.9/million). There was a marked age-specific increase in incidence in Norwich with a peak age 65-74 years (52.9/million), but a virtually equal age distribution between ages 45 and 74 in Lugo (34.1/million). There was no significant increase with time in either population, or evidence of cyclical changes in incidence.These data support the suggestion that environmental factors may be important in the pathogenesis of PSV.
The Paracetamol (Acetaminophen) In Stroke (PAIS) trial: a multicentre, randomised, placebo-controlled, phase III trial
Authors: Heleen M den Hertog, H Bart van der Worp, H Maarten A van Gemert, Ale Algra, L Jaap Kappelle, Jan van Gijn, Peter J Koudstaal, Diederik WJ Dippel
Journal: The Lancet Neurology (2009)
IgA Fc Receptors
Authors: Renato C. Monteiro, Jan G. J. van de Winkel
Journal: Annual Review of Immunology (2003)

The IgA receptor family comprises a number of surface receptors including the polymeric Ig receptor involved in epithelial transport of IgA/IgM, the myeloid specific IgA Fc receptor (FcalphaRI or CD89), the Fcalpha/muR, and at least two alternative IgA receptors. These are the asialoglycoprotein receptor and the transferrin receptor, which have been implicated in IgA catabolism, and tissue IgA deposition. In this review we focus on the biology of FcalphaRI (CD89). FcalphaRI is expressed on neutrophils, eosinophils, monocytes/macrophages, dendritic cells, and Kupffer cells. This receptor represents a heterogeneously glycosylated transmembrane protein that binds both IgA subclasses with low affinity. A single gene encoding FcalphaRI has been isolated, which is located within the leukocyte receptor cluster on chromosome 19. The FcalphaRI alpha chain lacks canonical signal transduction domains but can associate with the FcR gamma-chain that bears an activation motif (ITAM) in the cytoplasmic domain, allowing activatory functions. FcalphaRI expressed alone mediates endocytosis and recyling of IgA. No FcalphaRI homologue has been defined in the mouse, and progress in defining the in vivo role of FcalphaRI has been made using human FcalphaRI transgenic (Tg) mice. FcalphaRI-Tg mice demonstrated FcalphaRI expression on Kupffer cells and so defined a key role for the receptor in mucosal defense. The receptor functions as a second line of antibacterial defense involving serum IgA rather than secretory IgA. Studies in FcalphaRI-Tg mice, furthermore, defined an essential role for soluble FcalphaRI in the development of IgA nephropathy by formation of circulating IgA-FcalphaRI complexes. Finally, recent work points out a role for human IgA in treatment of infectious and neoplastic diseases.
Adjunct low-molecular-weight heparin to improve live birth rate after recurrent implantation failure: a systematic review and meta-analysis
Authors: N. Potdar, T. A. Gelbaya, J. C. Konje, L. G. Nardo
Journal: Human Reproduction Update (2013)

BACKGROUNDPoor fertility outcomes in women with recurrent implantation failure (≥RIF) present significant challenges in assisted reproduction, and various adjuncts, including heparin, are used for potential improvement in pregnancy rates. We performed this systematic review and meta-analysis to evaluate the effect of low-molecular-weight heparin (LMWH) on live birth rates (LBRs) and implantation rates (IRs) in women with RIF and undergoing IVF.
Evolution of radiographic joint damage in rituximab-treated versus TNF-treated rheumatoid arthritis cases with inadequate response to TNF antagonists
Authors: Axel Finckh, Burkhard Möller, Jean Dudler, Ulrich A Walker, Diego Kyburz, Cem Gabay
Journal: Annals of the Rheumatic Diseases (2012)

<h3>Background</h3> Observational studies have suggested that patients with rheumatoid arthritis (RA) who experience inadequate response to anti-tumour necrosis factor (anti-TNF) agents respond more favourably to rituximab (RTX) than to an alternative anti-TNF agent. However, the relative effectiveness of these agents on long-term outcomes, particularly in radiographic damage, remains unclear. <h3>Objective</h3> To compare the effectiveness of RTX against anti-TNF agents in preventing joint damage in patients with RA who have experienced inadequate response to at least one prior anti-TNF agent. <h3>Methods</h3> This is a prospective cohort study within the Swiss registry of patients with RA who discontinued at least one anti-TNF agent and subsequently received either RTX or an alternative anti-TNF agent. The primary outcome, progression of radiographic joint erosions (Ratingen erosion score)over time, and the secondary outcome, functional disability (Health Assessment Questionnaire Disability Index), were analysed using regression models for longitudinal data and adjusted for potential confounders. <h3>Results</h3> Of the 371 patients included, 104 received RTX and 267 received an alternative anti-TNF agent. During the 2.6-year median follow-up period, the rates of Ratingen erosion score progression were similar between patients taking RTX and patients taking an alternative anti-TNF agent (p=0.67). The evolution of the Health Assessment Questionnaire score was statistically significantly better in the RTX group (p=0.016), but the magnitude of the effect was probably not clinically relevant. <h3>Conclusion</h3> This observational study suggests that RTX is as effective as an alternative anti-TNF agent in preventing erosions in patients with RA who have previously experienced inadequate response to anti-TNF agents.
CD133+ liver tumor-initiating cells promote tumor angiogenesis, growth, and self-renewal through neurotensin/interleukin-8/CXCL1 signaling
Authors: Kwan Ho Tang, Stephanie Ma, Terence K. Lee, Yuen Piu Chan, Pak Shing Kwan, Carol M. Tong, Irene O. Ng, Kwan Man, Ka-Fai To, Paul B. Lai, Chung-Mau Lo, Xin-Yuan Guan, Kwok Wah Chan
Journal: Hepatology (2011)

A novel theory in the field of tumor biology postulates that cancer growth is driven by a population of stem-like cells, called tumor-initiating cells (TICs). We previously identified a TIC population derived from hepatocellular carcinoma (HCC) that is characterized by membrane expression of CD133. Here, we describe a novel mechanism by which these cells mediate tumor growth and angiogenesis by systematic comparison of the gene expression profiles between sorted CD133 liver subpopulations through genome-wide microarray analysis. A significantly dysregulated interleukin-8 (IL-8) signaling network was identified in CD133+ liver TICs obtained from HCC clinical samples and cell lines. IL-8 was found to be overexpressed at both the genomic and proteomic levels in CD133+ cells isolated from HCC cell lines or clinical samples. Functional studies found enhanced IL-8 secretion in CD133+ liver TICs to exhibit a greater ability to self-renew, induce tumor angiogenesis, and initiate tumors. In further support of these observations, IL-8 repression in CD133+ liver TICs by knockdown or neutralizing antibody abolished these effects. Subsequent studies of the IL-8 functional network identified neurotensin (NTS) and CXCL1 to be preferentially expressed in CD133+ liver TICs. Addition of exogenous NTS resulted in concomitant up-regulation of IL-8 and CXCL1 with simultaneous activation of p-ERK1/2 and RAF-1, both key components of the mitogen-activated protein kinase (MAPK) pathway. Enhanced IL-8 secretion by CD133+ liver TICs can in turn activate an IL-8-dependent feedback loop that signals through the MAPK pathway. Further, in its role as a liver TIC marker CD133 also plays a functional part in regulating tumorigenesis of liver TICs by way of regulating NTS, IL-8, CXCL1, and MAPK signaling. Conclusion : CD133+ liver TICs promote angiogenesis, tumorigenesis, and self-renewal through NTS-induced activation of the IL-8 signaling cascade.
Molecular Imaging of Cardiac Cell Transplantation in Living Animals Using Optical Bioluminescence and Positron Emission Tomography
Authors: Joseph C. Wu, Ian Y. Chen, Gobalakrishnan Sundaresan, Jung-Joon Min, Abhijit De, Jian-Hua Qiao, Michael C. Fishbein, Sanjiv S. Gambhir
Journal: Circulation (2003)

The current method of analyzing myocardial cell transplantation relies on postmortem histology. We sought to demonstrate the feasibility of monitoring transplanted cell survival in living animals using molecular imaging techniques.For optical bioluminescence charged-coupled device imaging, rats (n=20) underwent intramyocardial injection of embryonic rat H9c2 cardiomyoblasts (3x10(6) to 5x10(5)) expressing firefly luciferase (Fluc) reporter gene. Cardiac bioluminescence signals were present for more than 2 weeks with 3x10(6) cells: day 1 (627 000+/-15%), day 2 (346 100+/-21%), day 4 (112 800+/-20%), day 8 (78 860+/-24%), day 12 (67 780+/-12%), and day 16 (62 200+/-5% p x s(-1) x cm(2-1) x sr(-1)). For micro-positron emission tomography imaging, rats (n=20) received cardiomyoblasts (3x10(6)) expressing mutant herpes simplex type 1 thymidine kinase (HSV1-sr39tk) reporter gene. Detailed tomography of transplanted cells is shown by 9-(4-[18F]-fluoro-3hydroxymethylbutyl)guanine ([18F]-FHBG) reporter probe and nitrogen-13 ammonia ([13N]-NH3) perfusion images. Within the transplanted region, there was a 4.48+/-0.71-fold increase of in vivo [18F]-FHBG activity and a 4.01+/-0.51-fold increase of ex vivo gamma counting compared with control animals. Finally, the in vivo images of cell survival were confirmed by ex vivo autoradiography, histology, immunohistochemistry, and reporter protein assays.The location(s), magnitude, and survival duration of embryonic cardiomyoblasts were monitored noninvasively. With further development, molecular imaging studies should add critical insights into cardiac cell transplantation biology.
The impact of ReoPro illegible??? or lower speeds on platelet aggregation during rotational atherectomy
Authors: M. Retsman, S. Speck, J.L. Petersen, R.J. Westcott, R. Fei, V. Harms, S. Bogosian, D. Dillard, B. Shuman
Journal: Journal of the American College of Cardiology (1998)
Martin Arrowsmith's clinical trial: scientific precision and heroic medicine
Authors: Ilana Löwy
Journal: Journal of the Royal Society of Medicine (2010)

For a while, Martin Arrowsmith, the hero of Sinclair Lewis's 1925 eponymous novel1 – written in close collaboration with the scientist turned writer, Paul de Kruif – became the iconic image of a medical researcher, and a source of inspiration for generations of American medical students and young doctors.2 One of the central elements of the plot is a dramatic account of a trial of an anti-plague prophylactic during an epidemic on a Caribbean island. In all probability, the description of such a trial in an important novel (Lewis was awarded the Pulitzer Prize for Arrowsmith, although he declined it) favoured the diffusion of the concept of scientific testing of putative preventive and therapeutic interventions. It also popularized the idea of controlled clinical experimentation, while depicting it as a dramatic endeavour. Physician-scientists, Lewis's book proposed, need to overcome the natural tendency of physicians to try to provide immediate succour to sufferers seeking their help, and yet to be willing to expose the few to unknown risks for the greater benefit of mankind.3,4 Arrowsmith is an iconic image of scientist as hero, and the field trial an iconic display of his heroism.5