tbuckley/cabot-search huggingface dataset:
Long-Term Follow-Up of Residual Mediastinal–Hilar Ga-67 Uptake After Treatment for Hodgkin’s and Non–Hodgkin’s Lymphomas
Authors: NAYER NIKPOOR, PIRAN ALIABADI, LUIS DIAZ, FINN MANNTING
Journal: Clinical Nuclear Medicine (2000)

Ga-67 planar and SPECT images of 85 patients after treatment for mediastinal-hilar (M-H) lymphoma were reviewed retrospectively. Forty-seven patients had Hodgkin's disease and 38 patients had non-Hodgkin's lymphoma. The entire period was 7 years after diagnosis. The main goal was visual assessment of the significance of mild (grades 1 or 2) Ga-67 uptake in the M-H area as compared with Ga-67 uptake in bone marrow.Residual Ga-67 mediastinal uptake after a complete course of chemotherapy or other treatments was defined as normal (no residual) M-H uptake, borderline (M-H residual uptake with intensity less than that or equal to the sternum, spine, or both), and abnormal (M-H residual uptake with intensity greater than that of the sternum or spine).Among the 38 patients (45%) with no residual M-H uptake, four (one Hodgkin's disease and three non-Hodgkin's lymphoma) experienced recurrence: two in the mediastinum and two in the abdomen. Among the 45 patients (53%) with borderline M-H uptake, five experienced recurrence: two in the mediastinum and three in other sites. The two patients (2%) with abnormal (M-H) uptake never responded to treatment. No significant statistical difference in tumor recurrence was found between no residual and borderline uptake (P = 0.21).Visual assessment of M-H Ga-67 uptake (without quantification) could be useful to differentiate active residual tumor from nonactive residual uptake.
Pathology Working Group review of selected upper respiratory tract lesions in rats and mice.
Authors: R R Maronpot
Journal: Environmental Health Perspectives (1990)

The collected comments and pathologic diagnoses of several pathologists are summarized for 18 cases in which lesions were induced in the upper respiratory tract of rats and mice. Specific neoplastic and nonneoplastic lesions of the nose and trachea are described and discussed, and opinions regarding pathogenesis and biologic significance of the lesions are presented. The anatomic and pathophysiologic complexities of the rodent nose in relation to lesion development following inhalation or systemic exposure to xenobiotics are important considerations in the genesis of pathologic changes in this organ.
Blood Pressure Rhythm
Authors: Jean-François De Plaen
Journal: Annals of Internal Medicine (1991)

Letters15 May 1991Blood Pressure RhythmJean-François De Plaen, MDJean-François De Plaen, MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-114-10-914_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the Editors: In his letter, Rosansky (1) reports evaluating the circadian rhythm of blood pressure in hypertensive patients receiving hemodialysis. He points out that in these patients, blood pressure did not decrease during the night, as it did in a control group of 50 hypertensive patients not receiving dialysis. Both groups were receiving antihypertensive medication. The author suggests that the lack of a normal nocturnal decline in blood pressure in dialyzed patients is related to abnormal renal function or to a condition associated with renal failure.We recently explored the circadian rhythm of blood pressure in eight patients receiving...References1. Rosansky S. Nocturnal hypertension in patients receiving chronic hemodialysis [Letter]. Ann Intern Med. 1991;114:96. LinkGoogle Scholar2. BaumgartWalgerGerkeDorstVetterRahn PPMKHK. Nocturnal hypertension in renal failure, haemodialysis and after renal transplantation. J Hypertens. 1989;7(Suppl 6):S70-1. CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: University of Louvain Medical School B-1200 Brussels, Belgium PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByCircadian blood pressure variation versus renal functionHypertension is Not Adequately Controlled in Hemodialysis Patients 15 May 1991Volume 114, Issue 10Page: 914-914KeywordsBlood pressureMedical dialysisRenal failure Issue Published: 15 May 1991 PDF DownloadLoading ...
The atherogenic lipoprotein Lp(a) is internalized and degraded in a process mediated by the VLDL receptor.
Authors: K M Argraves, K F Kozarsky, J T Fallon, P C Harpel, D K Strickland
Journal: Journal of Clinical Investigation (1997)

Lp(a) is a major inherited risk factor associated with premature heart disease and stroke. The mechanism of Lp(a) atherogenicity has not been elucidated, but likely involves both its ability to influence plasminogen activation as well as its atherogenic potential as a lipoprotein particle after receptor-mediated uptake. We demonstrate that fibroblasts expressing the human VLDL receptor can mediate endocytosis of Lp(a), leading to its degradation within lysosomes. In contrast, fibroblasts deficient in this receptor are not effective in catabolizing Lp(a). Lp(a) degradation was prevented by antibodies against the VLDL receptor, and by RAP, an antagonist of ligand binding to the VLDL receptor. Catabolism of Lp(a) was inhibited by apolipoprotein(a), but not by LDL or by monoclonal antibodies against apoB100 that block LDL binding to the LDL receptor, indicating that apolipoprotein(a) mediates Lp(a) binding to this receptor. Removal of Lp(a) antigen from the mouse circulation was delayed in mice deficient in the VLDL receptor when compared with control mice, indicating that the VLDL receptor may play an important role in Lp(a) catabolism in vivo. We also demonstrate the expression of the VLDL receptor in macrophages present in human atherosclerotic lesions. The ability of the VLDL receptor to mediate endocytosis of Lp(a) could lead to cellular accumulation of lipid within macrophages, and may represent a molecular basis for the atherogenic effects of Lp(a).
Olecranon nodules in a case of Behcet's disease.
Authors: S Yurdakul, H Yazici, N Tüzüner, S Aytac, A.U Müftüoğlu
Journal: Annals of the Rheumatic Diseases (1981)

A 33-year-old male with definite Behçet's disease had rheumatoid-like nodules at his elbows. This finding, we believe, represents another manifestation of vasculitis in Behçet's disease.
The Medical Library as a Patient Aid
Authors: Ellen Rothbaum
Journal: JAMA (1992)

<h3>To the Editor.</h3> —Ms Lindner's<sup>1</sup>overall philosophy about providing consumer medical information is commendable; patients have the right to information. She does not, however, address the problem of financing such services in libraries that do not have grants such as the grant provided by the state of New Jersey. She also minimizes the issue of responsibility for the information or misinformation provided. The economic reality is that many hospital libraries find it difficult to serve their present constituency and are not in a position to add new services. Many libraries are one- or two-person departments and lack the resources to provide consumer health information. Health care personnel need certain levels of assistance and materials while consumers need different materials and often labor-intensive services. Furthermore, Lindner neglects to address the future of the Regional Consumer Health Information Center, if funding by the state of New Jersey ceases. Until hospital accreditation
CYSTIC MYOMA OF THE ILEUM WITH INTESTINAL HEMORRHAGE
Authors: George G. Finney
Journal: JAMA (1933)

The sources of bleeding from the bowel are many, including the relatively common hemorrhage from a bleeding gastric or duodenal ulcer, neoplasm or hemorrhoids. The case here reported illustrates one of the less common causes of intestinal hemorrhage but, in view of the course of events, seemed well worth while reporting.  REPORT OF CASE  M. T. C., a white man, aged 29, was admitted to the Johns Hopkins Hospital, Dec. 29, 1931, with the complaint of persistent blood in the stools. The family history was unimportant, and there was nothing in the past history that had any bearing on the present complaint. A review of the symptoms showed that the patient had never had any gastro-intestinal distress except occasional fulness after eating. There was no history of nausea, vomiting or jaundice at any time. The patient had a congenital clubfoot, and except for two plastic operations he had had no
New mutant and congenic mouse stocks expressing the murine leukemia virus-associated thymocyte surface antigen G(IX)
Authors: E Stockert, EA Boyse, Y Obata, H Ikeda, NH Sarkar, HA Hoffman
Journal: The Journal of Experimental Medicine (1975)

For several reasons the G(IX) antigen (1) has a prominent place in current work on murine leukemia virus (MuLV): In the prototype G(IX+) mouse strain 129, the G(IX) trait is mendelian, and is expressed selectively (though not exclusively) on thymocytes. Thus, expression of this cell surface component is under the control of cellular genes and is subject to the controls governing the differentiation of T lymphocytes (2). Although the 129 mouse produces no demonstrable leukemia virus such as that found in the AKR strain, it was soon realized that G(IX) antigen must in some way be related to MuLV, because productive infection with MuLV is frequently associated with appearance of G(IX) antigen on cells that are genotypically G(IX-), most notably on MuLV-infected rat cells, or cells that belong to other differentiation pathways (1). The basis of this connection between G(IX) and MuLV has recently become clear from the demonstration that G(IX) is one of MuLV envelope. Therefore, our working hypothesis is that the presence of G(IX) is one of the antigens present on gp69/71 (3,4), the major glycoprotein component of the MuLV envelope. Therefore, our working hypothesis is that the presence of G(IX) antigen always denotes the presence of gp69/71 (though not all variants of gp69/71 need necessarily carry G(IX)). Study of the circumstances under which G(IX) is expressed on the cell surface is thus potentially a powerful approach to understanding how the expression of C-type viral genomes is controlled. Such studies are greatly facilitated by the availability of mutant and congenic strains of inbred mice which differ from the nonmutant or partner strains only with respect to one or another manifestation of the viral genome. It is for this reason that we record here (Table I) some details of two G(IX) mutant and two G(IX) congenic stocks derived in our colonies at Memorial Sloan-Kettering Cancer Center (MSKCC). In addition, to these four strains, Table I includes data for the three relevant partner strains, and for strain AKR, for comparison. These eight strains all differ from one another with respect to one or more MuLV-related traits.
Internal Medicine and Family Medicine
Authors: Gary M. Onady
Journal: Annals of Internal Medicine (1996)

Letters15 September 1996Internal Medicine and Family MedicineGary M. Onady, MD, PhDGary M. Onady, MD, PhDWright State University, Dayton, OH 43409Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-125-6-199609150-00047 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:Dr. Saultz [1] makes realistic comparisons and contrasts between family medicine and internal medicine in terms of educational experience and practice style and philosophy. Concerns about practical aspects of cross-coverage, redistribution of patient demographic characteristics, and internists caring for children within these practices are relevant and remotely feasible. The prospect of involving pediatricians in this collaboration, however, is less than likely. Pediatrics has never had a close relationship with family medicine, and it diverged on its own primary care path 15 years before the American Academy of General Practice was formed in 1947.In 1967, the boards ...References1. Saultz JW. Reflections on internal medicine and family medicine. Ann Intern Med. 1996; 124:600-3. Google Scholar2. The future of family practice implications of the changing environment of medicine. Council on Long Range Planning and Development in Cooperation with the American Academy of Family Practice. JAMA. 1988; 260:1272-9. Google Scholar3. Onady GM. Community based Med/Peds—family medicine collaborative practice experiences [Abstract]. In: Proceedings of the Rush Primary Care Institute. The Challenge of Collaborative Primary Care Practice: Making It Work. 20 October 1995. Google Scholar Author, Article, and Disclosure InformationAuthors: Gary M. Onady, MD, PhDAffiliations: Wright State University, Dayton, OH 43409 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byOutcomes of Combined Internal Medicine—Pediatrics Residency Programs 15 September 1996Volume 125, Issue 6Page: 525KeywordsChildrenData managementGraduate medical educationPediatricsPrimary careSub-specialty care ePublished: 15 August 2000 Issue Published: 15 September 1996 Copyright & PermissionsCopyright © 1996 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Lead poisoning from homemade wine: a case study.
Authors: S Mangas, R Visvanathan, M van Alphen
Journal: Environmental Health Perspectives (2001)

A 66-year-old man suffered the symptoms of severe lead poisoning for 2 years before diagnosis. The man had a blood lead level (PbB) on admission to hospital of 98 microg/dL. A detailed investigation revealed that the poisoning occurred as a result of drinking a homemade red wine, for which analyses showed a lead concentration up to 14 mg/L--70 times the Australian maximum limit for lead in wine. The source of the lead was a highly corroded enamel bathtub in which grape crushings and juice were stored for a week prior to bottling. The corrosion of the enamel surface of the bathtub had resulted in pitted patches up to 1 mm in depth along the side of the bathtub. Powdering of the tub surface was evident below a level where wine had been in contact with the sides of the tub. The homemade wine had a pH of 3.8, which would have greatly contributed to the solubilization of metals from the glaze. We conducted a test in which commercial red wine of similar pH and containing < 0.2 mg/L lead was placed in this tub for 7 days. Subsequent testing revealed a lead level of 310 mg/L. This high lead concentration is consistent with the surface area of enamel on the bathtub being in contact with a small liquid volume as in the case of the leaching test using commercial red wine. This case study highlights the importance of the use of food-grade materials for the preparation and storage of homemade beverages or food.
Increased adsorption of cytoplasmic proteins to the erythrocyte membrane in ATP‐depleted normal and pyruvate kinase‐deficient mature cells and reticulocytes
Authors: David W. Allen, Jerome D. Groat, Barbara Finkel, Brian H. Rank, Patricia A. Wood, John W. Eaton
Journal: American Journal of Hematology (1983)

Abstract How the metabolic defect of pyruvate kinase deficiency (PK(–)) accelerates red blood cell (RBC) destruction is not established, but may be related to RBC membrane abnormalities associated with altered cellular metabolism. Furthermore, it has been shown that PK(–) reticulocytes are especially sensitive to metabolic depletion. Therefore, we compared the membranes of reticulocyte‐rich PK(–) RBC, both fresh and ATP depleted, with membranes of fresh and ATP depleted normal mature RBC and reticulocytes. There was no difference between the specific gravity (SG) of the membranes of normal mature RBC (SG 1.152 ± 0.004) and membranes of reticulocyte‐rich RBC from several anemias (SG 1.150 ± 0.002). However, membranes from fresh, reticulocyte‐rich PK(–) RBC were dense with SG of 1.165 ± 0.004 which correlated with a corresponding increase of protein to lipid phosphorus ratio of 66 ± 8 μg protein/μg lipid phosphorus (normal 52 ± 6 μg/μg). The membrane density of PK(–) RBC was further increased when the PK(–) RBC ATP was depleted by anaerobic incubation (SG 1.188 ± 0.004) or cyanide inhibition (SG 1.182 ± 0.001). When ATP was depleted in normal RBC and in non‐PK(–) reticulocytes, corresponding increases in membrane SG occurred. A distinctive 50,000 MW peptide is adsorbed from the cytoplasm to the membranes of reticulocytes (both normal and PK(–) when these cells were depleted of ATP. The increased membrane adsorption of cytoplasmic proteins by PK(–) RBC was not associated with increased RBC calcium uptake, sulfhydryl oxidation, or altered membrane protein phosphorylation. All the observed abnormalities of PK(–) RBC membranes could by reproduced by ATP depletion of reticulocyte‐enriched non‐PK(–) RBC.
A COMBINED NEEDLE ADAPTER AND THERMOMETER FOR INTRAVENOUS INFUSIONS
Authors: Paul Titus
Journal: JAMA (1934)

A thermometer with a limited range of from 90 to 120 Fahrenheit, which is sufficient for intravenous infusions of various sorts, has been inserted within the lumen of an enlarged but otherwise ordinary glass adapter the tip of which is ground for intravenous needles with a standard Luer hub. This is a spirit thermometer with a colored (red) fluid and thus is easily read. Glass adapters for the attachment of the needles are used for practically all intravenous injections. The use of the usual large infusion thermometers involves the addition of an extra breakable part and an extra piece of rubber tubing. Consequently the combination of these two parts in one makes for simplicity, at the same time allowing for more accurate information regarding the actual temperature of an intravenous infusion, as the thermometer is located near to the point of entry of the fluid into the vein. When an
Assessing the exercise response to a bronchodilator in COPD: time to get off your bike?
Authors: M D L Morgan, S J Singh
Journal: Thorax (2007)

A comparison of exercise tests

Progressive irreversible airway obstruction is the defining characteristic of chronic obstructive pulmonary disease (COPD). However, people with COPD do not complain of airway obstruction but, more usually, about the associated restriction of physical activity. The disability resulting from COPD may also be compounded by peripheral muscle dysfunction that further limits exercise capacity. Traditionally, we have used tests of whole body exercise performance to reflect this process. However, as we learn more about COPD, it is revealed as a complex condition where apparently straightforward truths are neither pure nor simple. The relationship between airway function and exercise capacity is a good example of this complexity, since it may naively be expected that the decline in physical activity may mirror the progression of airway obstruction. Furthermore, it might also be reasonable to expect that an improvement in airway function may lead to a similar gain in physical activity. In fact, neither of these phenomena is necessarily observed. The relationship between static lung function and exercise capacity is not predictive in COPD and, in addition, the forced expiratory volume in 1 s (FEV1) alone cannot be used to judge disability. Furthermore, the effects of short-term improvements in airway function by bronchodilation do not reliably lead to improved exercise capacity. This is clearly a source of frustration—both for patients whose performance may not improve and for those who seek to demonstrate the benefits of a therapeutic intervention. There are several possible explanations for the apparent disconnection between changes in lung function and exercise performance. One explanation lies in understanding the nature of exercise capacity limitation in COPD, which may vary with the stage of the disease. Another factor may be the method chosen to assess activity limitation. We usually use formal, standardised whole body exercise tests as a …
Abstract 2170: The SWI/SNF nucleosome-remodeling gene PBRM1 - Another tumor suppressor gene in renal cell carcinomas
Authors: Hans Krause, Odiljon Ikromov, Eymad All Kamal, Kurt Miller, Martin Schostak, Burkhard Jandrig
Journal: Cancer Research (2012)

Abstract The polybromodomain containing gene PBRM1 was recently discovered to harbor 41% truncating somatic mutations in clear cell renal cell carinomas (ccRCC). Next to the VHL tumor suppressor gene this gene is thought to be the second major cancer gene in ccRCCs. PBRM1 (also called BAF180) belongs to the SWI/SNF-B or PBAF complex and provides functional specificity to this class of chromatin remodelers by binding to acetylated histones via its six bromodomains, two BAH domains, and one HMG domain (the latter binding to nucleosomal DNA). PBRM1 is located on chromosome 3p21 in close vicinity to VHL and SETD2 genes arguing for a putative gatekeeper function in cases where VHL loss alone is insufficient for ccRCCs tumorigenesis. PBRM1 codes for at least three major transcripts of about 7500nt in length whose expression was measured by Q-PCR in 49 cases of paired normal and tumor tissue samples of RCC patients who underwent radical tumor nephrectomy at our clinic between 06/2009 and 10/2010. 20/49 cases showed a marked upregulation of PBRM1 expression whereas in 29/49 cases PBRM1 was clearly downregulated. To assess the contribution of somatic mutations for PBRM1 downregulation we resequenced 29 PBRM1 exons of 48 tumor tissues. Specific truncating mutations were detected in 6 (15.4%) of 39 ccRCCs. These mutations include 5 deletions in exons 1, 10, 16, 23, and 24, as well as one insertion in exon 16. All these heterozygous mutations lead to a decrease of PBRM1 mRNA expression, that was verified by Q-PCR measurements. In addition, 6 coding SNPs (cSNPs) were revealed as well as 5 SNPs in intronic regions, one of the latter is in close vicinity to the splice acceptor site of exon 9. Concurrent expression of three major transcripts (var. 1,2, and 4) is seen in all 46 matched normal and tumor samples analyzed so far. In 22 (47.8%) samples we detected a dominance of var.1 (NM_018165) in normal tissue when compared to the corresponding tumor sample, that preferentially expresses var.4 (NM_181042). So far our data set of 15.4% truncating mutations in 39 cases of ccRCC could not match the exceptional high number of 41% reported in the initial report by the Sanger Institute. Truncating mutations of PBRM1 have been described in breast cancers but were absent in lung carcinomas, despite the fact that LOH at 3p21 is frequently seen in these cancers. Understanding the contribution of PBRM1 expression changes, be it on the genomic level (mutation) and/or mRNA (differential splicing), to clinical disease progression and outcome in kidney cancer needs further investigation. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 2170. doi:1538-7445.AM2012-2170