tbuckley/cabot-search huggingface dataset:
Transbronchial Biopsies in Wegener's Granulomatosis
Authors: ZVI ACKERMAN
Journal: Annals of Internal Medicine (1986)

Letters and Corrections1 November 1986Transbronchial Biopsies in Wegener's GranulomatosisZVI ACKERMAN, M.D., HEDI ORBACH, M.D., MOSHE BURSTEIN, M.D., RAPHAEL BREUER, M.D.ZVI ACKERMAN, M.D.Search for more papers by this author, HEDI ORBACH, M.D.Search for more papers by this author, MOSHE BURSTEIN, M.D.Search for more papers by this author, RAPHAEL BREUER, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-105-5-801_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: Wegener's granulomatosis is a disease of unknown cause that involves the lungs in 94% of patients; paranasal sinuses, nose, and nasopharynx in 91%; and the kidney in 85%. Other sites involved less frequently are the joints, ears, eyes, skin, nervous system, and heart (1). If untreated, the disease is associated with a high mortality rate. Thus, early diagnosis and treatment with cyclophosphamide and prednisone are imperative (1).Diagnosis of Wegener's granulomatosis requires histologic evidence of both necrotizing vasculitis and granulomata in one or more of the affected sites (1). Lung tissue gives the best yield for histologic...References1. FAUCIHAYNESKATZWOLFF ABPS. Wegener's granulomatosis: prospective clinical and therapeutic experience with 85 patients for 21 years. Ann Intern Med. 1983;98:76-85. LinkGoogle Scholar2. GIVENSNEWMANMCCURLEY CJT. Diagnosis of Wegener's granulomatosis by transbronchial biopsy. Chest. 1985;88:794-6. CrossrefMedlineGoogle Scholar3. PINCHINGLOCKWOODRUSSELL ACB. Wegener's granulomatosis: observations in 18 patients with severe renal disease. Q J Med. 1983;52:435-60. MedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Hadassah University Hospital Jerusalem 91120 Israel PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByNon-Malignant Central Airway ObstructionPatología obstructiva no maligna de la vía aérea centralPulmonary Capillaritis in Wegener's Granulomatosis Detected Via Transbronchial Lung BiopsyBronchoscopy in the Diagnosis of Wegener GranulomatosisLate Endobronchial Wegener's GranulomatosisPercutaneous image‐guided biopsy of lung nodules in the assessment of disease activity in Wegener's granulomatosisThe diagnosis of Wegener's granulomatosis from transbronchial biopsy specimensWegener's Granulomatosis Presenting as Acute Respiratory Failure with Anti-neutrophil-cytoplasm AntibodiesGranulomatose de wegener et grossesseune observationWegener's granulomatosis: diagnosis by transbronchial lung biopsy, evaluation by gallium scintigraphy and treatment with sulfamethoxazole/trimethoprimThe necrotising vasculitides. 1 November 1986Volume 105, Issue 5Page: 801-802KeywordsBiopsyCyclophosphamideDeath ratesHeartLungsNervous systemRenal diseasesVasculitisWegener granulomatosis Issue Published: 1 November 1986 PDF DownloadLoading ...
5-aminosalicylic acid inhibits cell cycle progression in a phospholipase D dependent manner in colorectal cancer
Authors: Bart Baan, Ashwin A Dihal, Eva Hoff, Carina L Bos, Philip W Voorneveld, Pim J Koelink, Manon E Wildenberg, Vanesa Muncan, Jarom Heijmans, Hein W Verspaget, Dick J Richel, James C H Hardwick, Daniel W Hommes, Maikel P Peppelenbosch, Gijs R van den Brink
Journal: Gut (2011)

<h3>Background</h3> 5-aminosalicylic acid (5-ASA) may protect against the development of inflammation-associated colorectal cancer. In vitro data suggest that, in colorectal cancer cells, 5-ASA induces cell cycle arrest, but the molecular mechanism leading to this arrest remains to be determined. <h3>Aim</h3> To dissect the signal transduction events that lead to 5-ASA mediated inhibition of proliferation of colorectal cancer cells, focusing on mammalian target of rapamycin (mTOR), a regulator of cell cycle progression. <h3>Methods</h3> The influence of 5-ASA on mTOR signalling was examined in a panel of colorectal cancer cell lines. The effects of 5-ASA on the pathways that control mTOR activity were studied in detail in two different colorectal cancer cell lines, using western blot, siRNA, a phospholipase D (PLD) activity assay, proliferation assays and cell cycle analysis. The phosphorylation status of mTOR and its downstream target, ribosomal protein S6, was studied in colorectal cancers before and after topical 5-ASA treatment. <h3>Results</h3> Treatment of colorectal cancer with 5-ASA inhibited mTOR signalling in vitro and in vivo. 5-ASA had no effect on any of the pathways that regulate the activity of the tuberous sclerosis complex in colorectal cancer cells. Both proliferation and mTOR activity depended on PLD, an enzyme that generates phosphatidic acid (PA). 5-ASA treatment inhibited PLD activity and proliferation; these effects could be rescued with exogenous PA. <h3>Conclusion</h3> 5-ASA interferes with proliferation of colorectal cancer cells via inhibition of PLD-dependent generation of PA and loss of mTOR signalling.
Amiodarone induced lupus
Authors: R. SUSANO, L. CAMINAL, D. RAMOS, B. DIAZ
Journal: Annals of the Rheumatic Diseases (1999)

Cladribine in the treatment of systemic lupus erythematosus nephritisSystemic lupus erythematosus (SLE) nephritis often requires treatment with cyclophosphamide, which carries the risk of major side eVects including infection, ovarian failure and bladder malignancy.Therapeutic strategies that would specifically target lymphocytes are appealing.Following the first report of the use of the purine nucleoside analogue cladribine (2-chloro-2'deoxyadenosine), a selective lymphocyte depleting agent, in the treatment of lupus nephritis, 1 we report our experience in two patients with severe renal involvement.
Reversible Focal Hepatic Steatosis in Type 1 Diabetic Patients Treated With Intraperitoneal Insulin Implantable Pump Therapy
Authors: Laurent Meyer, Jeremy Jeantroux, Jean Pierre Riveline, François Moreau, Sophie Boivin, Thomas Moser, Michel Pinget, Nathalie Jeandidier
Journal: Diabetes Care (2008)

Intraperitoneal insulin infusion (IPII) using implantable devices is used in treatment of hypoglycemia-prone diabetes. A 35-year-old type 1 diabetic woman had been treated with IPII for 3 years when a metabolic degradation occurred. A catheter tip obstruction wassuspected. An enhanced computed tomography (CT) scan was performed showing a subcapsular hypoattenuating region in the left lobe of the liver, consistent with focal steatosis. The catheter tip, surrounded by a thickening of tissue, stuck to the …
Antisense Oligonucleotides to NF- κ B Improve Survival in Bleomycin-induced Pneumopathy of the Mouse
Authors: XIAO YE ZHANG, SANAE SHIMURA, TOHRU MASUDA, HIROKI SAITOH, KUNIO SHIRATO
Journal: American Journal of Respiratory and Critical Care Medicine (2000)

We examined the effect of antisense oligonucleotides to the p65 subunit of NF-kappaB on the survival of bleomycin (BLM)-induced pneumonitis in C57BL/6 mice (female, 8 wk of age, 17 to 20 g body weight). Fifty-three percent and all control mice died within 6 to 9 d after intravenous administration of 150 and 300 mg/kg BLM alone, respectively. The intravenous administration of the antisense oligonucleotides (900 microgram/animal dissolved in 200 microliter saline, 6 h before and 5 d after BLM administration) significantly improved the survival rate to 100 and 40% in 150- and 300-mg/kg-treated animals, respectively. The antisense oligonucleotides also significantly improved the loss of body weight, the increase in lung hydroxyproline, and histologic changes by BLM, whereas the antisense oligonucleotides themselves did not produce any significant changes in the behavior or lung histology. Both peripheral blood monocytes and alveolar macrophages were confirmed to contain large amounts of intracellular antisense oligonucleotides after BLM injection by FITC-labeled fluorescent microscopy. Further, Western blotting confirmed the inhibition of NF-kappaB in macrophages by the antisense oligonucleotides. These findings suggest that the antisense oligonucleotides are incorporated into activated alveolar macrophages and ameleriorate the lung injury and pneumonitis/fibrosis, thereby improving the survival of BLM-induced pneumopathy in mice.
Activation of antigen-specific suppressor T cells by B cells from mice immunized with type III pneumococcal polysaccharide.
Authors: C E Taylor, P W Stashak, G Caldes, B Prescott, T E Chused, A Brooks, P J Baker
Journal: The Journal of Experimental Medicine (1983)

The transfer of B lymphocytes from mice immunized with type III pneumococcal polysaccharide (SSS-III) results in antigen-specific suppression of the antibody response of recipients immunized with SSS-III. Such suppression shares many features associated with low-dose paralysis, a phenomenon mediated by suppressor T cells; it reaches maximal levels 3 d after the transfer of viable or irradiated immune B cells and can be eliminated by the depletion of SSS-III-binding cells from spleen cell suspensions before transfer. In a two-step cell transfer experiment, purified T lymphocytes, isolated from recipients previously given immune B cells, caused suppression upon transfer to other mice immunized with SSS-III. Also, B-cell-induced suppression could be abrogated in a competitive manner by the infusion of amplifier T lymphocytes, as was previously demonstrated in the case of low-dose paralysis. These findings suggest that B cell surface components, presumably the idiotypic determinants of cell-associated antibody specific for SSS-III, are instrumental in activating suppressor T cells involved in regulating the magnitude of the antibody response to SSS-III.
Biomarkers of Cardiovascular Disease
Authors: Ramachandran S. Vasan
Journal: Circulation (2006)

C ardiovascular diseases (CVD) are the leading cause of morbidity and mortality in the United States. 1 Primary prevention and secondary prevention of CVD are public health priorities. 2 Substantial data indicate that CVD is a life course disease that begins with the evolution of risk factors that in turn contribute to the development of subclinical atherosclerosis. 3,4Subclinical disease culminates in overt CVD. 5,6The onset of CVD itself portends an adverse prognosis with greater risk of recurrent events, morbidity, and mortality. 7,8It is also increasingly clear that although clinical assessment is the keystone of patient management, such evaluation has its limitations. 9 -12 Clinicians have used additional tools to aid clinical assessment and to enhance their ability to identify the "vulnerable" patient at risk for CVD, as suggested by a recent National Institutes of Health (NIH) panel. 13,14Biomarkers are one such tool to better identify high-risk individuals, to diagnose disease conditions promptly and accurately, and to effectively prognosticate and treat patients with disease.This review provides an overview of the molecular basis of biomarker discovery and selection and the practical considerations that are a prerequisite to their clinical use.
Congress May Order Breast Cancer Study On Long Island
Authors: T. Reynolds
Journal: JNCI Journal of the National Cancer Institute (1993)

Journal Article Congress May Order Breast Cancer Study On Long Island Get access Tom Reynolds Tom Reynolds Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 85, Issue 7, 7 April 1993, Pages 520–522, https://doi.org/10.1093/jnci/85.7.520 Published: 07 April 1993
Repression of BIM mediates survival signaling by MYC and AKT in high-risk T-cell acute lymphoblastic leukemia
Authors: C Reynolds, J E Roderick, J L LaBelle, G Bird, R Mathieu, K Bodaar, D Colon, U Pyati, K E Stevenson, J Qi, M Harris, L B Silverman, S E Sallan, J E Bradner, D S Neuberg, A T Look, L D Walensky, M A Kelliher, A Gutierrez
Journal: Leukemia (2014)
A restriction fragment of the C2 gene is a unique marker for C2 deficiency and the uncommon C2 allele C2*B (a marker for type 1 diabetes).
Authors: S Simon, Z Awdeh, R D Campbell, P Ronco, S J Brink, G S Eisenbarth, E J Yunis, C A Alper
Journal: Journal of Clinical Investigation (1991)

There are three common C2 protein alleles in caucasians, C2*C, C2*B, and C2*Q0, with allele frequencies of 0.96, 0.03, and 0.01, as well as Sst I RFLP variants of 2.75, 2.7, 2.65, 2.55, and 2.4 kb, with frequencies of 0.017, 0.533, 0.358, 0.017, and 0.075. Thus, C2*C is informatively split by the RFLP. Of 94 nonrandomly ascertained caucasian complotypes, 77 contained C2*C, four contained C2*Q0, and 13 had C2*B. None of the C2*C-containing complotypes carried the 2.75 kb Sst I fragment and all of the complotypes with C2*B or C2*Q0 carried it. All of the C2*Q0 alleles were associated with C4A*4, C4B*2 in the complotype S042 as previously reported. C2*B was usually (9/13) in the complotype SB42, occasionally (1/13 each) in SB45, SB41, SB(4,3)0, and SB31. Thus, the association of the C2 2.75-kb fragment was with C2*B and C2*Q0, not with C4A*4, C4B*2, or even C4A*4 alone. The complotype SC42 was associated with the 2.65-kb Sst I fragment in four of five instances and in a single example with the 2.7-kb fragment. C2*B and C2*Q0 possibly had a common evolutionary ancestor complotype which carried the 2.75-kb Sst I fragment, and BF*S, C4A*4, and C4B*2. C2*B (particularly as the haplotype HLA-Bw62, SB42, DR4) is associated with type 1 diabetes but C2*Q0 is protective.
Decline of lung function and development of chronic airflow limitation: a longitudinal study of non-smokers and smokers in Busselton, Western Australia.
Authors: J K Peat, A J Woolcock, K Cullen
Journal: Thorax (1990)

Data collected during seven population health surveys over 18 years in Busselton, Western Australia, were examined to determine the effect of smoking on lung function and to investigate the development of chronic airflow limitation. Lung function was measured and details of respiratory illness and smoking histories were collected from subjects attending surveys at three year intervals from 1966 to 1984. Data from ex-smokers and asthmatic patients (diagnosis based on answer to questionnaire) were excluded. Regression of height adjusted forced expiratory volume in one second (FEV1) on age was calculated individually for 759 non-smokers and 225 regular smokers with four or more observations. Decline in height adjusted FEV1 was similar for men and women. In smokers the rate of decline in FEV1 was greater than in non-smokers and was related to the amount smoked, to the extent that a smoker could expect a 20-30% greater rate of decline than a non-smoker of the same age. Chronic airflow limitation (defined as FEV1/FEV less than 65% or FEV1 less than 65% predicted on at least two occasions) was common, occurring in 24% of men and 18% of women who were regular smokers and in 5% of male and 8% of female non-smokers. These figures are higher than those reported in other populations, especially for women and for non-smokers. Not all chronic airflow limitation was associated with respiratory symptoms, confirming that the condition may be unrecognised until it is advanced.
CD3+CD4low and CD3+CD8low are induced by HLA-G: novel human peripheral blood suppressor T-cell subsets involved in transplant acceptance
Authors: Abderrahim Naji, Solene Le Rond, Antoine Durrbach, Irene Krawice-Radanne, Caroline Creput, Marina Daouya, Julien Caumartin, Joel LeMaoult, Edgardo D. Carosella, Nathalie Rouas-Freiss
Journal: Blood (2007)
Why Great Britain's success in Beijing could have been anticipated and why it should continue beyond 2012
Authors: A M Nevill, N J Balmer, E M Winter
Journal: British Journal of Sports Medicine (2009)

Home advantage in the summer Olympic Games is well known. What is not so well known is that countries that host the Olympic Games perform better in the games before and after the games in which they were hosts.To model/quantify the significance associated with these "hosting" effects and to explain the likely causes of Great Britain's improved medals haul in Beijing, while examining implications for London 2012 and beyond.Using all hosting cities/countries since World War II and analysing the number of medals awarded to competitors as a binomial proportion (p) response variable within a logit model, we identified a significant increase in the probability/odds of a country obtaining a medal in the Olympic Games before, during and after hosting the Olympics.Funding appears to be an important factor when explaining these findings. Almost all countries that have been awarded the games after World War II would appear to have invested heavily in sport before being awarded the games. A second factor in Great Britain's success is the legacy of hosting the Commonwealth Games in 2002 (a post-hosting games effect) that undoubtedly provided an infrastructure that benefited, in particular, cycling. Whether the International Olympics Committee either consciously or subconsciously take these factors into account is unclear when awarding the games to a city. What is clear is that based on these findings, Great Britain's prospects of maintaining the Olympic success achieved in Beijing is likely to continue to London 2012 and beyond.
Kallikrein messenger RNA in rat arteries and veins.
Authors: G M Saed, O A Carretero, R J MacDonald, A G Scicli
Journal: Circulation Research (1990)

Glandular kallikrein (EC 3.4.21.8) belongs to a subgroup of serine proteases coded by a multigene family. A kininogenase resembling glandular kallikrein has been identified in vascular tissue; however, it is not clear whether it is synthesized by vascular tissue or taken up from plasma. To determine the potential for kallikrein synthesis in vascular tissues, we tested whether messenger RNA (mRNA) for glandular kallikrein is present in rat arteries and veins. Poly(A+) RNA was isolated from pools of arteries or veins (n = 3, 30 rats each). Poly(A+) RNA from the kidney and liver was used as a positive and negative control, respectively. As a probe, we used rat pancreatic kallikrein 32P-labeled complementary DNA, which recognizes mRNA of the entire rat kallikrein family. Slot-blot analysis indicated that kallikrein mRNA was present in mRNA from the arteries, veins, and kidney but not from the liver. Poly(A+) RNA from arteries and veins contained approximately 1% as much kallikrein mRNA as that from the kidney. To confirm the slot-blot results and determine whether the mRNA for true glandular kallikrein was present in vascular tissue, we employed a polymerase chain reaction assay, first using primers specific for the entire kallikrein family (which amplify a 430-bp fragment) and then using primers specific for true glandular kallikrein mRNA (which amplify a 370-bp fragment). After the polymerase chain reaction assay, both arteries and veins showed fragments of these sizes when tested with rat kallikrein complementary DNA probe, thus confirming the presence of glandular kallikrein mRNA.(ABSTRACT TRUNCATED AT 250 WORDS)
Derivation and Validation of a Clinical Diagnostic Model for Chlamydial Cervical Infection in University Women
Authors: Betty A. Johnson
Journal: JAMA (1990)

We developed and prospectively tested a logistic regression model for chlamydial cervical infection. Study subjects included 2271 women receiving gynecologic care in our student health clinic. Clinical data were collected in a standardized fashion. We identified cell culture--isolated Chlamydia trachomatis from 133 (9%) of 1458 subjects in the derivation set and 73 (10%) of 729 subjects in the validation set. Model variables included a new sexual partner within 2 months or more than one sexual partner within 6 months; cervical ectopy; cervical friability; at least 20 polymorphonuclear leukocytes per high-power field in cervical secretions; white blood cells in vaginal secretions; and use of an antibiotic active against C trachomatis within a month. This model can distinguish women with low, medium, and high risks of chlamydial infection (on derivation set: receiver operating characteristic curve area, 0.710; SE, 0.026; on validation set: area, 0.698; SE, 0.035) using simple clinical information obtained in the office.
High-dosage short-term corticotrophin therapy in acute asthma
Authors: I. W. Glick, M. Friedman
Journal: Thorax (1969)

The effect of corticotrophin suspended in gelatin in doses varying from 40 to 400 i.u. on the plasma 11-hydroxycorticosteroid response has been investigated in volunteer subjects in order to determine the optimum dose required to produce prolonged and continuous adrenocortical stimulation using this preparation. Increasing the dose of corticotrophin beyond 200 i.u. did not produce a greater intensity or prolongation of adrenocortical stimulation; 300 i.u. corticotrophin in 7·5 ml. of gelatin produced the same effect as 310 i.u. in 1 ml. gelatin. In order to achieve prolonged and continuous adrenal stimulation the optimum dose of corticotrophin would appear to be 200 i.u., which could be suspended in 1 ml. of gelatin for ease of administration, and which produced adrenal stimulation for approximately 36 hours. The effect of the administration of a single large dose of corticotrophin has been investigated in 13 asthmatic patients during an exacerbation. All had failed to respond to conventional therapy but responded to corticotrophin with one exception. Five patients required no more than two injections for a sustained remission. Seven were discharged needing prolonged corticotrophin in conventional doses. The advatage of using this form of corticotrophin therapy over a short course of high-dosage corticosteroid therapy is discussed.
Blockage of 2-Deoxy-<scp>d</scp>-Ribose-Induced Angiogenesis with Rapamycin Counteracts a Thymidine Phosphorylase-Based Escape Mechanism Available for Colon Cancer under 5-Fluorouracil Therapy
Authors: Hendrik Seeliger, Markus Guba, Gudrun E. Koehl, Axel Doenecke, Markus Steinbauer, Christiane J. Bruns, Christine Wagner, Erika Frank, Karl-Walter Jauch, Edward K. Geissler
Journal: Clinical Cancer Research (2004)

Abstract Purpose: Colorectal neoplasms remain a leading cause of cancer-related deaths. A recognized weakness of conventional 5-fluorouracil (5-FU) therapy relates to expression of the intracellular enzyme, thymidine phosphorylase (TP). Although TP promotes 5-FU cytotoxicity, TP-derived 2-deoxy-d-ribose (dRib) counterproductively stimulates tumor angiogenesis. Here, the newly discovered antiangiogenic drug rapamycin was combined with 5-FU to counteract the potential escape mechanism of dRib-induced angiogenesis. Experimental Design: Orthotopic tumor growth was assessed in rapamycin and 5-FU-treated BALB/c mice with TP-expressing CT-26 colon adenocarcinoma cells. To examine liver metastasis, green-fluorescent protein-transfected CT-26 cells were visualized by fluorescence microscopy after intraportal injection. Cell counting and Ki67 staining were used to determine in vitro and in vivo cell expansion, respectively. In vitro angiogenic effects of dRib were assessed with endothelial cell migration and aortic ring assays. Western blotting detected dRib effects on p70/S6 kinase activation. Results: Rapamycin treatment of mice bearing orthotopic tumors inhibited tumor growth more than did 5-FU, and mice treated with both drugs typically developed no tumors. In the liver metastasis assay, combination therapy blocked metastatic expansion of solitary tumor cells. Interestingly, complex drug activities were suggested by tumor-cell proliferation being more sensitive to 5-FU than to rapamycin in vitro, but more sensitive to rapamycin in vivo. With regard to angiogenesis, dRib-induced endothelial cell migration and aortic ring formation were completely abrogated by rapamycin, correlating with blockage of dRib-induced p70/S6 kinase activation in endothelial cells. Conclusions: Inhibition of dRib-induced angiogenesis with rapamycin counteracts a potential TP-based escape mechanism for colorectal cancer under 5-FU therapy, introducing a novel, clinically feasible, combination treatment option for this common neoplasm.