tbuckley/cabot-search huggingface dataset:
Pathogenesis of Rejection of Canine Cardiac Allografts
Authors: K. H. SHUMAK, B. S. GOLDMAN, M. D. SILVER, W. G. BIGELOW, J. H. CROOKSTON
Journal: Circulation (1970)

Cardiac rejection was studied in 25 mongrel dogs receiving heterotopic abdominal cardiac allografts from unrelated donors. Seventeen recipients were not given immunosuppressive therapy; the other eight were treated with antilymphocyte serum. Antibodies cytotoxic to dog lymphocytes were detected in the serum of five dogs after transplantation. Immunofluorescence studies showed the presence of IgG deposits on the sarcolemma of hearts undergoing rejection. In addition, there were focal IgG deposits on many of the recipients' own hearts, including five which showed changes of focal myocarditis when stained with hematoxylin and eosin. In the dogs treated with antilymphocyte serum, rejection was delayed, and the histological changes were modified. However, the development of lymphocytotoxic antibody and the deposition of IgG were unaffected.
Pathophysiology of Nerve Conduction: Relation to Diabetic Neuropathy
Authors: STEPHEN G. WAXMAN
Journal: Annals of Internal Medicine (1980)

Pathophysiologic and clinicopathologic aspects of diabetic nerve disease are reviewed. Abnormal modes of impulse conduction in diseased nerves include decreased conduction velocity, temporal dispersion of impulses, frequency-related and total conduction block, abnormal cross-talk, and impulse reflection. Because structural and electrophysiologic variables (such as fiber geometry, ionic channel density, and properties of the extracellular milieu) vary with diameter, it is suggested that pathophysiologic mechanisms also should vary with diameter. Topographic patterns of clinical deficit, and their pathologic basis, are reviewed; it is suggested that lesions distributed at random along the length of the entire fiber may result in dysfunction that exhibits distinct proximal-distal gradients.
Factor V Leiden and Venous Thromboembolism
Authors: Klaus Juul, Børge G. Nordestgaard, Anne Tybjærg-Hansen
Journal: Annals of Internal Medicine (2004)

Letters21 September 2004Factor V Leiden and Venous ThromboembolismKlaus Juul, MD, Børge G. Nordestgaard, MD, DMSc, and Anne Tybjærg-Hansen, MD, DMScKlaus Juul, MDFrom Herlev University Hospital, DK-2730 Herlev, Denmark, and Copenhagen University Hospital; DK-2100 Copenhagen, Denmark.Search for more papers by this author, Børge G. Nordestgaard, MD, DMScFrom Herlev University Hospital, DK-2730 Herlev, Denmark, and Copenhagen University Hospital; DK-2100 Copenhagen, Denmark.Search for more papers by this author, and Anne Tybjærg-Hansen, MD, DMScFrom Herlev University Hospital, DK-2730 Herlev, Denmark, and Copenhagen University Hospital; DK-2100 Copenhagen, Denmark.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-141-6-200409210-00025 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail IN RESPONSE:As Dr. Murphy points out, the role of smoking in VTE is controversial. In our study, smoking overall was a risk factor for VTE (hazard ratio, 1.7 [95% CI, 1.2 to 2.2]) after adjustment for sex, factor V Leiden, body mass index, myocardial infarction, physical activity, estrogen-containing preparations, menopause, and year of study entry. Because smoking did not interact with factor V Leiden genotype or estrogen-containing preparations to affect risk for VTE, our data can suggest only additive effects of these 3 factors on VTE risk. However, because of limited statistical power, we are unable to provide accurate ...References1. Feder JN, Gnirke A, Thomas W, Tsuchihashi Z, Ruddy DA, Basava A, et al . A novel MHC class I-like gene is mutated in patients with hereditary haemochromatosis. Nat Genet. 1996;13:399-408. [PMID: 8696333] CrossrefMedlineGoogle Scholar2. Andersen RV, Tybjaerg-Hansen A, Appleyard M, Birgens H, Nordestgaard BG. Hemochromatosis mutations in the general population: iron overload progression rate. Blood. 2004;103:2914-9. [PMID: 15070663] CrossrefMedlineGoogle Scholar Author, Article, and Disclosure InformationAffiliations: From Herlev University Hospital, DK-2730 Herlev, Denmark, and Copenhagen University Hospital; DK-2100 Copenhagen, Denmark. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetailsSee AlsoFactor V Leiden and the Risk for Venous Thromboembolism in the Adult Danish Population Klaus Juul , Anne Tybjærg-Hansen , Peter Schnohr , and Børge G. Nordestgaard Factor V Leiden and Venous Thromboembolism Philip T. Murphy Factor V Leiden and Venous Thromboembolism Jan P. Vandenbroucke and Frits R. Rosendaal Metrics 21 September 2004Volume 141, Issue 6Page: 484-485KeywordsEstrogensFactor V LeidenGenetic diseasesHazard ratioHemochromatosisLongitudinal studiesMedical risk factorsPopulation geneticsProspective studiesVenous thromboembolism ePublished: 21 September 2004 Issue Published: 21 September 2004 CopyrightCopyright © 2004 by American College of Physicians. All Rights Reserved.PDF DownloadLoading ...
993 PLASMA APELIN LEVELS ARE ELEVATED IN SUBJECTS WITH NON-ALCOHOLIC FATTY LIVER DISEASE
Authors: C.N. Ercin, T. Dogru, S. Tapan, Y. Karslioglu, N. Karadurmus, S. Kilic, G. Kilciler, Z. Yesilova, A. Uygun, M. Gulsen, S. Bagci
Journal: Journal of Hepatology (2009)
Short‐ and long‐term results of a programme for the prevention of readmissions and mortality in patients with heart failure: Are effects maintained after stopping the programme?
Authors: Soledad Ojeda, Manuel Anguita, Mónica Delgado, Felipe Atienza, Carmen Rus, Amador L. Granados, Federico Ridocci, Federico Vallés, Jose A. Velasco
Journal: European Journal of Heart Failure (2005)
A Case of Multimodality Multiparametric 11C-Choline PET/MR for Biopsy Targeting in Prior Biopsy-Negative Primary Prostate Cancer
Authors: Toshiki Takei, Michael Souvatzoglou, Ambros J. Beer, Alexander Drzezga, Sybille Ziegler, Ernst J. Rummeny, Markus Schwaiger, Matthias Eiber
Journal: Clinical Nuclear Medicine (2012)

We introduce the case of a 70-years-old man with an elevated level of prostate-specific antigen and prior negative biopsy. For targeting rebiopsy, the patient underwent C-choline PET/CT and subsequent PET/MR. Both the high uptake in PET and the abnormal findings in MR gave strong evidence for prostate cancer at the ventral periphery of the right apex. This location is sometimes not covered by routine sextant biopsy. The following targeted rebiopsy was positive for prostate cancer. This case indicates the potential role of PET/MR for identifying primary prostate cancer because of its high soft tissue contrast and the possibility of a multimodality approach.
Case 30-1973
Authors: Richard C. Cabot, Benjamin Castleman, Robert E. Scully, Betty U. McNeely, Robert W. Carey, John C. Long
Journal: New England Journal of Medicine (1973)

Presentation of CaseA 64-year-old woman was admitted to the hospital because of weakness of the extremities.Thirty-two years previously supraclavicular lymphadenopathy developed. A biopsy performed at another hospital revealed Hodgkin's disease, and radiation treatment was given, with a good response. During the next 31 years the patient received radiation treatment to the superior mediastinum, neck, trunk, supraclavicular region and cervical spine (Table 1). Twenty-four years before entry there was the onset of intermittent numbness and paresthesias. Ten years before admission she experienced pain in the right lumbar region and again complained of numbness in the extremities. An x-ray film . . .
A Case of Extra-Uterine Pregnancy: Death of the F tus at Four Months: Intestinal Obstruction from Pressure: Removal of the F tus by Perineal Section: Recovery
Authors: G. J. Robertson
Journal: BMJ (1886)

TltE BIITISH IJRDICAi JOURIAL. [Feb.13, 188& to an encysted stone, which was remiioved subsequently.In looking over the cases of multiple stone, I was surprised to find how few present facets, and I believe it may almost be laid down as an axiom tat facets only occur when one or more of the stones is to some ex- tent fixed.The moral to be draw,i is: Always search the bladder thoroughly as a matter of rontine.Group D. -Stones of bladdler formationi duie to chronic cystitis (Nos. 1, 2, 11, 13, 16, 19, 20, 26, 35, 41 A. andl n., 42 A. and n., 45 A. and u.; 16 out of SO cases).The intervals varied from 7
Response to a costly revolution for a subgroup of patients with metastatic melanoma
Authors: A. Hauschild
Journal: British Journal of Dermatology (2013)

Van Akkooi and Nijsten have written a thoughtful review of our phase III trial, which compared dabrafenib, a BRAF inhibitor, with dacarbazine chemotherapy in patients with metastatic BRAF‐mutated melanoma. They bring up a very important point about overpowering clinical trials. I believe they are correct to caution that large randomized trials can detect statistically significant differences that may be too small to be clinically meaningful. In fact, our trial was rather small as phase III trials go because the trial was not powered to detect a difference in overall survival. The primary endpoint was progression‐free survival (PFS). Van Akkooi and Nijsten correctly point out that PFS has not been a validated endpoint in melanoma trials. One exception has been in the case of vemurafenib, the first BRAF inhibitor developed. A previous, larger trial using vemurafenib showed a high response rate (47%), a significant improvement in PFS and a significant, clinically meaningful improvement in overall survival compared with dacarbazine. This led to U.S. Food and Drug Administration (FDA) and European Medicines Agency (EMA) approval of vemurafenib. It also served to validate this magnitude of response and PFS as correlating with overall survival improvement compared with dacarbazine for this class of drugs. Our trial showed that the overall response rate and PFS benefit with dabrafenib was almost identical to that seen with vemurafenib. The assumption is that dabrafenib would also have a similar beneficial effect on overall survival, although this was not tested directly in order to be able to conduct a smaller trial.
935-32 Differing Mechanisms of Late Arterial Responses to Transcatheter Therapy: A Serial Quantitative Angiographic and Intravascular Ultrasound Study
Authors: Gary S. Mintz, Jeffrey J. Popma, Augusto D. Pichard, Kenneth M. Kent, Lowell F. Satler, Theresa A. Bucher, Carol L. Walsh, Jennifer Griffin, Martin B. Leon
Journal: Journal of the American College of Cardiology (1995)
Abstract 5008: Epidermal growth factor downregulates expression of neutrophil gelatinase-associated lipocalin (NGAL) through E-cadherin in pancreatic cancer cells
Authors: Zhimin Tong, Subhankar Chakraborty, Bokyung Sung, Sukhwinder Kaur, Bharat B. Aggarwal, Sendurai Mani, Robert S. Bresalier, Surinder Batra, Sushovan Guha
Journal: Cancer Research (2011)

Abstract Background: Neutrophil gelatinase-associated lipocalin (NGAL), a member of the lipocalin family, is a secreted protein that is upregulated in multiple cancer types. Our group previously reported that NGAL overexpression significantly blocked invasion and angiogenesis in pancreatic ductal adenocarcinoma (PDAC). We and others have also demonstrated loss NGAL expression in advanced stages of PDAC. However, little is known about mechanisms that regulate NGAL expression in PDAC. As EGF-EGFR axis is significantly upregulated in PDAC, we examined EGF-mediated NGAL regulation in these cells. Methods: NGAL-positive AsPC-1 and BxPC-3 cells were used as model system. Quantitative RT-PCR, western blot analysis, and immunofluorescence studies were used to investigate EGF-mediated effects on NGAL expression. E-cadherin expression was manipulated using lentiviral overexpression or shRNA constructs. NGAL promoter activity was assessed by luciferase-reporter assay and electrophoretic mobility shift assay (EMSA). Results: NGAL expression was positively associated with tumor differentiation and was significantly downregulated after EGF treatment along with a concomitant reduction of E-cadherin expression in PDAC cells. E-cadherin downregulation was partly through the EGF receptor (EGFR)-dependent MEK1/2-ERK1/2 signaling pathway, which was demonstrated using pharmacologic inhibitors of EGFR (AG1478) and MEK1/2 (U0126 and PD98059). In addition, E-cadherin downregulation reduced NGAL expression in PDAC cells, whereas overexpression of E-cadherin led to increased NGAL expression and partly rescued inhibition of NGAL expression by EGF. Furthermore, EGF in part through E-cadherin reduced NGAL promoter activity by blocking NF-κB activation. Conclusion: We demonstrated for the first time that EGF potently blocked NGAL expression in PDAC cells. This effect is partly mediated through activation of the EGFR-MEK1/2-ERK1/2 signaling pathway, which in turn downregulated E-cadherin with a subsequent reduction in NF-κB activation. Our findings illustrate a novel mechanism by which EGF regulates NGAL expression in PDAC. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 5008. doi:10.1158/1538-7445.AM2011-5008
Refusal of transfusions for cardiac surgery was not associated with shorter long-term survival
Authors: John Kepros
Journal: Annals of Internal Medicine (2012)

Source Citation Pattakos G, Koch CG, Brizzio ME, et al. Outcome of patients who refuse transfusion after cardiac surgery: a natural experiment with severe blood conservation. Arch Intern Med. 2012;172:1154-60. 22751620
FDG Uptake in Parahepatic Brown Fat Mimics Peritoneal Carcinomatosis in a Malignant Ovarian Germ Cell Tumor
Authors: In Young Hyun, Soon Gi Kim
Journal: Clinical Nuclear Medicine (2008)

F-18 fluorodeoxyglucose (FDG) PET/CT contributes to the diagnosis of malignancy and the detection of recurrence of malignancy after therapy. However, FDG uptake in physiologic and benign processes is well documented. Misinterpretation of FDG uptake in brown fat may result in an erroneous definition of PET findings as malignant. We present the case of FDG uptake in parahepatic brown fat, which mimicked peritoneal carcinomatosis in a malignant ovarian germ cell tumor. Repeat PET/CT scan after the control of the patient's environmental temperature to 75°C showed resolution of the parahepatic brown fat uptake.
Hypoxia Inducible Factor 1α and Hypoxia Inducible Factor 2α Play Distinct and Functionally Overlapping Roles in Oral Squamous Cell Carcinoma
Authors: Gui-quan Zhu, Ya-ling Tang, Ling Li, Min Zheng, Jian Jiang, Xiao-yu Li, Si-xiu Chen, Xin-hua Liang
Journal: Clinical Cancer Research (2010)

Abstract Purpose: This study aimed to investigate the functional difference between hypoxia inducible factor (HIF)-1α and HIF-2α in oral squamous cell carcinomas (OSCC). Experimental Design: We evaluated the correlations between HIF-1α and HIF-2α expression and the clinical-pathologic characteristics of 97 patients with OSCC by immunohistochemical staining. OSCC cell lines transfected with lentivirus encoding short hairpin RNA against HIF-1α/2α were used to investigate the HIF-1α/2α–dependent target genes. Xenograft tumors in nude mice were established using cells affected by lentivirus, and tumor growth, angiogenesis, proliferation, and apoptosis were measured. Results: HIF-1α expression was significantly associated with T stage (P = 0.004), lymph node involvement (P = 0.006), histologic differentiation (P = 0.013), and microvessel density (P = 0.014), whereas that of HIF-2α was associated with T stage (P = 0.011) and microvessel density (P = 0.005). Patients with positive HIF-1α nuclear staining had a significantly worse overall survival (P &amp;lt; 0.001) and disease-free survival (P &amp;lt; 0.001) than those with negative HIF-1α staining. When OSCC cells were cultured at 5% O2, only HIF-2α contributed to the expression of vascular endothelial growth factor. At 1% O2, vascular endothelial growth factor was regulated by both HIF-1α and HIF-2α, but glucose transporter 1, carbonic anhydrase 9, and urokinase-type plasminogen activator receptor were regulated by HIF-1α rather than by HIF-2α. Knocking down HIF-1α or HIF-2α individually inhibited the xenograft tumor angiogenesis and growth, and knocking them down simultaneously revealed a better inhibitory effect than knocking down either unit alone. Conclusions: HIF-1α and HIF-2α correlated with different clinical-pathologic parameters, stabilized at different oxygen levels, and regulated different genes in OSCC. However, both HIF-1α and HIF-2α showed promoting roles in tumor angiogenesis and growth, and therapeutic outcome may benefit from combined targeting of HIF-1α and HIF-2α. Clin Cancer Res; 16(19); 4732–41. ©2010 AACR.
Thyrotoxicosis Associated with Renal Tubular Acidosis and Acute Pancreatitis: A Case Report
Authors: PHILIP MAY
Journal: Annals of Internal Medicine (1976)

Letters1 May 1976Thyrotoxicosis Associated with Renal Tubular Acidosis and Acute Pancreatitis: A Case ReportPHILIP MAY, M.D., RICHARD P. LEVY, M.D.PHILIP MAY, M.D.Search for more papers by this author, RICHARD P. LEVY, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-84-5-569 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptHypercalcemia as a feature of thyrotoxicosis is well known, as is the association of pancreatitis with hypercalcemia and hyperparathyroidism (1). The case that we report is the first, to our knowledge, in which hyperthyroidism and acute pancreatitis were associated. Furthermore, renal tubular acidosis accompanied the hyperthyroidism; only two other similar cases have been reported (2, 3). In our patient, the tubular acidosis was shown to be of the distal type. Of additional interest are the autopsy findings for this patient, who sustained accidental death shortly after study.The patient was healthy until age 18, when an 11 kg-weight loss in...References1. RASMUSSEN H: Parathyroid hormone, calcitonin, and the calciferols, in Williams Textbook of Endocrinology. Philadelphia, W. B. Saunders Co., 1974, p. 736 Google Scholar2. HUTH E, MAYOCK R, and KERR R: Hyperthyroidism associated with renal tubular acidosis. Am J Med 26:818-826, 1959 CrossrefMedlineGoogle Scholar3. ZISMAN E, BUCCIND R, and GORDON P: Hyperthyroidism and renal tubular acidosis. Arch Intern Med 121:118-122, 1968 CrossrefMedlineGoogle Scholar4. SALLIN O: Hypercalcemic nephropathy in thyrotoxicosis. Acta Endocrinol (Kbh) 29:425-434, 1958 CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: PHILIP MAY, M.D.; RICHARD P. LEVY, M.D.Affiliations: University Hospitals Case Western Reserve University School of Medicine Cleveland, OH 44106 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byParathyroid hormone levels, hyperparathyroidism and acute pancreatitisPancreatitis and hyperparathyroidismMilk–Alkali Syndrome and PancreatitisA Case of Leiomyosarcoma Associated with Humoral Hypercalcemia of Malignancy: Demonstration of Biological and Immunological Activities of Parathyroid Hormone-related Protein in the Tumor ExtractCase Report Renal Tubular Acidosis in PregnancyThe Thyroid 1 May 1976Volume 84, Issue 5Page: 569-570KeywordsAcute pancreatitisAutopsyHypercalcemiaHyperparathyroidismHyperthyroidismPancreatitis ePublished: 1 December 2008 Issue Published: 1 May 1976 PDF downloadLoading ...
Appeals court rules that Nigerian families can sue Pfizer in US
Authors: J. Lenzer
Journal: BMJ (2009)

A US federal appellate court has ruled that 88 Nigerian families can continue their lawsuit in the United States against Pfizer, the world’s largest drug maker. The 2-1 decision, issued by the Second Circuit Court in New York on 30 January, will allow the plaintiffs to reinstate their suit claiming that Pfizer conducted an illegal drug trial in 1996 during an outbreak of bacterial meningitis in Kano state, Nigeria.

The families allege that Pfizer conducted the study of its experimental drug trovafloxacin (Trovan) without obtaining informed consent ( BMJ 2006;332:1233, doi:10.1136/bmj.332.7552.1233-a). According to court documents, the families claim that Pfizer gave the experimental …
Clinical and Laboratory Studies with Rubella Vaccines in Adults
Authors: J. A. Dudgeon, W. C. Marshall, C. S. Peckham, G. T. Hawkins
Journal: BMJ (1969)

Three live attenuated rubella vaccines were tested in adult volunteers. Clinical reactions were mild, but were more noticeable in vaccinated non-immune subjects than in control subjects. With the exception of two individuals, all of the remaining 54 subjects developed an immune response; the level of antibodies found was somewhat lower than that resulting from natural infection. Though virus could be isolated from some of the seronegative volunteers after vaccination, no evidence was found of transmission of infection.
Quantification of the normal Frank and McFee-Parungao orthogonal electrocardiogram at ages two to ten years.
Authors: J S Kan, J Liebman, M H Lee, A Whitney
Journal: Circulation (1977)

A quantification of the Frank and McFee-Parungao orthogonal electrocardiogram of 175 normal children, ages 2-10 years is presented. There are significant differences in age groups 2-5 and 6-10. The QRS voltages of the younger group demonstrate 1) greater Z anterior, 2) greater initial X right, 3) greater terminal X right, 4) smaller Y inferior, and 5) the T vector is oriented more posteriorly. There are significant differences between the two lead systems. 1) Frank spatial voltages are 70% of those of McFee. 2) Frank X left is 70% of McFee, but terminal X right is 75% and initial X right is 60% of McFee. 3) Frank Y inferior is 78% of McFee, but initial Y superior is 83% and terminal Y superior 61% of McFee. 4) Frank Z anterior is 64% and Frank Z posterior is 70% of McFee. 5) In terms of ratios the Frank is relatively less inferior, about equally posterior and more terminally right. 6) The T vector is more posterior in Frank than McFee.
Remodeling Rather Than Neointimal Formation Explains Luminal Narrowing After Deep Vessel Wall Injury
Authors: Henning Rud Andersen, Michael Mæng, Martin Thorwest, Erling Falk
Journal: Circulation (1996)

Background Oversized balloon dilatation of normal porcine coronary arteries usually heals without stenosis formation. Methods and Results With the purpose of developing a stenotic model and examining the mechanisms of luminal narrowing after angioplasty, we produced a circumferential deep vessel wall injury by inflating and withdrawing an oversized chain-encircled angioplasty balloon in the left anterior descending coronary artery (LAD) of 20 pigs. Three pigs died and did not complete the study. In 8 pigs (group 1), serial coronary arteriography was performed. The lumen diameter (mean±SD) before dilatation was 3.4±0.4 mm; after dilatation, 4.2±0.6 mm; and at follow-ups 2 and 4 weeks later, 1.6±0.4 mm ( P &lt;.0001). In 9 pigs (group 2) examined postmortem 3 weeks after dilatation, histology revealed that the injury was deep (out to adventitia) in all arteries and completely circumferential (360°) in all but two arteries. Adventitia was markedly thickened as a result of neoadventitial formation. Injury correlated strongly with neointimal formation (middle LAD, r =.71, P =.00001), but neither injury nor neointima correlated with lumen size ( r =.14, P =.46 and r =.34, P =.07, respectively); ie, neointimal formation did not explain late luminal narrowing. Lumen size, however, did correlate strongly with vessel size ( r =.74, P =.000005). The late loss in lumen diameter observed angiographically in group 1 substantially exceeded that caused by neointimal formation seen by histology in group 2. Conclusions The chain-encircled angioplasty balloon produced a circumferential deep vessel wall injury that healed by luminal narrowing. In this porcine model, arterial remodeling was more important than neointimal formation in late luminal narrowing.