tbuckley/cabot-search huggingface dataset:
INTERMITTENT LIMPING-INTERMITTENT CLAUDICATION; THEIR DIFFERENTIAL DIAGNOSIS
Authors: ISIDOR  MUFSON
Journal: Annals of Internal Medicine (1941)

Article1 June 1941INTERMITTENT LIMPING-INTERMITTENT CLAUDICATION; THEIR DIFFERENTIAL DIAGNOSISISIDOR MUFSON, M.D.ISIDOR MUFSON, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-14-12-2240 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe symptom "intermittent limping" has become so associated with intermittent claudication that clinically, to many, the terms have become almost synonymous. The term "intermittent limping" describes a sequence of events in which the patient finds repeatedly that, after walking a few blocks, he must come to a complete halt because of a cramp-like pain or sense of exhaustion in one or both legs. The first physician consulted usually refers the patient complaining chiefly of this symptom to a colleague particularly interested in peripheral vascular diseases. However, the complaint is frequently due to non-vascular causes.An analysis of all such cases... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Bronx, New York*Received for publication September 4, 1940.From the Department of Medicine, College of Physicians and Surgeons, Columbia University and the Presbyterian Hospital. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byDescription and Pathogenesis of Symptoms and Signs of Arterial Insufficiency 1 June 1941Volume 14, Issue 12Page: 2240-2245KeywordsHospital medicinePeripheral vascular diseaseSurgeonsWalking ePublished: 1 December 2008 Issue Published: 1 June 1941 PDF downloadLoading ...
Enhanced Tumor Formation in Cyclin D1 × Transforming Growth Factor β1 Double Transgenic Mice with Characterization by Magnetic Resonance Imaging
Authors: Natasha G. Deane, Haakil Lee, Jalal Hamaamen, Anna Ruley, M. Kay Washington, Bonnie LaFleur, Snorri S. Thorgeirsson, Ronald Price, R. Daniel Beauchamp
Journal: Cancer Research (2004)

Abstract Transgenic mice that overexpress cyclin D1 protein in the liver develop liver carcinomas with high penetrance. Transforming growth factor β (TGF-β) serves as either an epithelial cell growth inhibitor or a tumor promoter, depending on the cellular context. We interbred LFABP-cyclin D1 and Alb-TGF-β1 transgenic mice to produce cyclin D1/TGF-β1 double transgenic mice and followed the development of liver tumors over time, characterizing cellular and molecular changes, tumor incidence, tumor burden, and tumor physiology noninvasively by magnetic resonance imaging. Compared with age-matched LFABP-cyclin D1 single transgenic littermates, cyclin D1/TGF-β1 mice exhibited a significant increase in tumor incidence. Tumor multiplicity, tumor burden, and tumor heterogeneity were higher in cyclin D1/TGF-β1 mice compared with single transgenic littermates. Characteristics of cyclin D1/TGF-β1 livers correlated with a marked induction of the peripheral periductal oval cell/stem cell compartment of the liver. A number of cancerous lesions from cyclin D1/TGF-β1 mice exhibited unique features such as ductal plate malformations and hemorrhagic nodules. Some lesions were contiguous with the severely diseased background liver and, in some cases, replaced the normal architecture of the entire organ. Cyclin D1/TGF-β1 lesions, in particular, were associated with malignant features such as areas of vascular invasion by hepatocytes and heterogeneous hyperintensity of signal on T2-weighted magnetic resonance imaging. These findings demonstrate that TGF-β1 promotes stem cell activation and tumor progression in the context of cyclin D1 overexpression in the liver.
Detection of Human Papillomavirus DNA in Cytologically Normal Women and Subsequent Cervical Squamous Intraepithelial Lesions
Authors: K.-L. Liaw, A. G. Glass, M. M. Manos, C. E. Greer, D. R. Scott, M. Sherman, R. D. Burk, R. J. Kurman, S. Wacholder, B. B. Rush, D. M. Cadell, P. Lawler, D. Tabor, M. Schiffman
Journal: JNCI Journal of the National Cancer Institute (1999)

Human papillomavirus (HPV) infection has been strongly associated with cervical carcinoma and its cytologic precursors, squamous intraepithelial lesions (SIL). We investigated the risk of SIL prospectively following polymerase chain reaction (PCR)-based DNA testing for a wide range of genital HPV types in a cohort of initially cytologically normal women, to clarify the role of HPV in the etiology of SIL.Starting in April 1989, 17,654 women who were receiving routine cytologic screening at Kaiser Permanente (Portland, OR) were followed for the development of incident SIL. During follow-up, 380 incident case patients and 1037 matched control subjects were eligible for this nested case-control study. Cervical lavages collected at enrollment and, later, at the time of case diagnosis (or the corresponding time for selection of control subjects) were tested for HPV DNA using a PCR-based method. The data were analyzed as contingency tables with two-sided P values or, for multivariable analyses, using odds ratios (ORs) with 95% confidence intervals (CIs).In comparison with initially HPV-negative women, women who tested positive for HPV DNA at enrollment were 3.8 times (95% CI = 2.6-5.5) more likely to have low-grade SIL subsequently diagnosed for the first time during follow-up and 12.7 times more likely (95% CI = 6.2-25.9) to develop high-grade SIL. At the time of diagnosis, the cross-sectional association of HPV DNA and SIL was extremely strong (OR = 44.4 and 95% CI = 24.2-81.5 for low-grade SIL and OR = 67.1 and 95% CI = 19.3-233.7 for high-grade SIL). HPV16 was the virus type most predictive of SIL, even low-grade SIL.These findings are consistent with the hypothesis that HPV infection is the primary cause of cervical neoplasia. Furthermore, they support HPV vaccine research to prevent cervical cancer and efforts to develop HPV DNA diagnostic tests.
332 OCOXIN+VIUSID INDUCES APOPTOSIS OF HEPATOMA AND HEPATIC STELLATE CELLS AND POTENTIATES THE EFFECT OF SORAFENIB ON HEPATOMA CELLS
Authors: E. Arriazu, M. Ruiz de Galarreta, M.P. Perez de Obanos, M. Iraburu
Journal: Journal of Hepatology (2012)
Ten-Year Follow-up of Cluster-based Asthma Phenotypes in Adults. A Pooled Analysis of Three Cohorts
Authors: Anne Boudier, Ivan Curjuric, Xavier Basagaña, Hana Hazgui, Josep M Anto, Jean Bousquet, Pierre O Bridevaux, Elise Dupuis-Lozeron, Judith Garcia-Aymerich, Joachim Heinrich, Christer Janson, Nino Künzli, Bénédicte Leynaert, Roberto de Marco, Thierry Rochat, Christian Schindler, Raphaëlle Varraso, Isabelle Pin, Nicole Probst-Hensch, Jordi Sunyer, Francine Kauffmann, Valérie Siroux
Journal: American Journal of Respiratory and Critical Care Medicine (2013)

The temporal stability of adult asthma phenotypes identified using clustering methods has never been addressed. Longitudinal cluster-based methods may provide novel insights in the study of the natural history of asthma.To compare the stability of cluster-based asthma phenotype structures a decade apart in adults and to address the individuals' phenotypic transition across these asthma phenotypes.The latent transition analysis was applied on longitudinal data (twice, 10 yr apart) from 3,320 adults with asthma who took part in the European Community Respiratory Health Survey, the Swiss Cohort Study on Air Pollution and Lung and Heart Diseases in Adults, or the Epidemiological Study on Genetics and Environment of Asthma. Nine variables covering personal and phenotypic characteristics measured twice, 10 years apart, were simultaneously considered.Latent transition analysis identifies seven asthma phenotypes (prevalence range, 8.4-20.8%), mainly characterized by the level of asthma symptoms (low, moderate, high), the allergic status, and pulmonary function. Phenotypes observed 10 years apart showed strong similarities. The probability of membership in the same asthma phenotype at both times varied across phenotypes from 54 to 88%. Different transition patterns were observed across phenotypes. Transitions toward increased asthma symptoms were more frequently observed among nonallergic phenotypes as compared with allergic phenotypes. Results showed a strong stability of the allergic status over time.Adult asthma phenotypes identified by a clustering approach, 10 years apart, were highly consistent. This study is the first to model the probabilities of transitioning over time between comprehensive asthma phenotypes.
"Swallowed" Endotracheal Tube
Authors: J. S. Crawford
Journal: BMJ (1967)

the Luntz series are in fact cases listed in Wright's account under the headings " Ocular Hypertension " and " Possible Early Glau- coma," with a combined prevalence of 3 %.The Luntz series clearly excluded any cases of true glaucoma, and indeed all patients with any history of previous eye disease.As the authors give no criteria for their diagnosis of glaucoma, it is impossible to say to what ex- tent their findings can be compared with either survey.They certainly cannot be compared with both.The literature of glaucoma abounds in such comparisons of in- compatible data.It is depressing also to note that the defi- ciencies of a single measurement of ocular pressure as a means of detecting glaucoma still do not appear to be fully appreciated.This aspect of the problem is discussed in the same symposium and more fully in the account of the Royal Society of Medicine's 1966 Annual Symposium on Presymptomatic Screening.2It would be interesting to know if the authors have read these papers and are aware of the objections to tonometric screen- ing.-I am, etc.,
Prognostic Significance of Tumorigenic Cells With Mesenchymal Features in Pancreatic Adenocarcinoma
Authors: Zeshaan A. Rasheed, Jie Yang, Qiuju Wang, Jeanne Kowalski, Irwin Freed, Christopher Murter, Seung-Mo Hong, Jan-Bart Koorstra, N. V. Rajeshkumar, Xiaobing He, Michael Goggins, Christine Iacobuzio-Donahue, David M. Berman, Daniel Laheru, Antonio Jimeno, Manuel Hidalgo, Anirban Maitra, William Matsui
Journal: JNCI Journal of the National Cancer Institute (2010)

Specific populations of highly tumorigenic cells are thought to exist in many human tumors, including pancreatic adenocarcinoma. However, the clinical significance of these tumor-initiating (ie, cancer stem) cells remains unclear. Aldehyde dehydrogenase (ALDH) activity can identify tumor-initiating cells and normal stem cells from several human tissues. We examined the prognostic significance and functional features of ALDH expression in pancreatic adenocarcinoma.ALDH expression was analyzed by immunohistochemistry in 269 primary surgical specimens of pancreatic adenocarcinoma and examined for association with clinical outcomes and in paired primary tumors and metastatic lesions from eight pancreatic cancer patients who had participated in a rapid autopsy program. The clonogenic growth potential of ALDH-positive pancreatic adenocarcinoma cells was assessed in vitro by a colony formation assay and by tumor growth in immunodeficient mice (10-14 mice per group). Mesenchymal features of ALDH-positive pancreatic tumor cells were examined by using quantitative reverse transcription-polymerase chain reaction and an in vitro cell invasion assay. Gene expression levels and the invasive potential of ADLH-positive pancreatic cancer cells relative to the bulk cell population were examined by reverse transcription-polymerase chain reaction and an in vitro invasion assays, respectively. All statistical tests were two-sided.ALDH-positive tumor cells were detected in 90 of the 269 primary surgical specimens, and their presence was associated with worse survival (median survival for patients with ALDH-positive vs ALDH-negative tumors: 14 vs 18 months, hazard ratio of death = 1.28, 95% confidence interval = 1.02 to 1.68, P = .05). Six (75%) of the eight patients with matched primary and metastatic tumor samples had ALDH-negative primary tumors, and in four (67%) of these six patients, the matched metastatic lesions (located in liver and lung) contained ALDH-positive cells. ALDH-positive cells were approximately five- to 11-fold more clonogenic in vitro and in vivo compared with unsorted or ALHD-negative cells, expressed genes consistent with a mesenchymal state, and had in vitro migratory and invasive potentials that were threefold greater than those of unsorted cells.ALDH expression marks pancreatic cancer cells that have stem cell and mesenchymal features. The enhanced clonogenic growth and migratory properties of ALDH-positive pancreatic cancer cells suggest that they play a key role in the development of metastatic disease that negatively affects the overall survival of patients with pancreatic adenocarcinoma.
Models for the pathogenesis of stress fractures in athletes.
Authors: K L Bennell, S A Malcolm, J D Wark, P D Brukner
Journal: British Journal of Sports Medicine (1996)

It would seem that the development of a stress fracture results from unsuccessful adaptation of bone to a change in its mechanical environment caused by repetitive loading. It involves the physiological processes of microdamage production and remodelling. Whether the initiating factor is microdamage production or activation of remodelling through direct effects of strain is unclear. The remodelling process involves both the removal of bone which has become fatigue damaged or is extraneous to the requirements of the new loading environment, and the addition of new bone in an manner that is best suited to withstand the new mechanical strain. Normally this process is well modulated and does not cause symptoms. If the amount of bone removed is not sufficient to unduly weaken bone structure and the addition of new bone occurs sufficiently rapidly to correct any weakness before failure occurs or to repair microdamage, the process will successfully lead to a bone with appropriate material strength and geometry to withstand the new strain environment. However, if there is imbalance between bone removal and replacement, together with accumulation of microdamage, signs and symptoms of a stress fracture may result. Any factors which influence bone load, bone strength, or remodelling have the potential to result in a stress fracture. Attention should be paid to the identification of these factors in an attempt to prevent this overuse injury in athletes.
Irinotecan combined with infusional 5-fluorouracil/folinic acid or capecitabine plus celecoxib or placebo in the first-line treatment of patients with metastatic colorectal cancer. EORTC study 40015
Authors: C.-H. Köhne, J. De Greve, J.T. Hartmann, I. Lang, P. Vergauwe, K. Becker, D. Braumann, E. Joosens, L. Müller, J. Janssens, C. Bokemeyer, P. Reimer, H. Link, E. Späth-Schwalbe, H.-J. Wilke, H. Bleiberg, J. Van Den Brande, M. Debois, U. Bethe, E. Van Cutsem
Journal: Annals of Oncology (2007)
Widespread Myocardial Inflammation and Infarct-Related Artery Patency
Authors: Antonio Abbate, Elena Bonanno, Alessandro Mauriello, Rossana Bussani, Giuseppe G.L. Biondi-Zoccai, Giovanna Liuzzo, Antonio Maria Leone, Furio Silvestri, Aldo Dobrina, Feliciano Baldi, Franco Pandolfi, Luigi M. Biasucci, Alfonso Baldi, Luigi G. Spagnoli, Filippo Crea
Journal: Circulation (2004)

Diffuse coronary vascular inflammation is associated with acute coronary syndromes. However, it is unknown whether inflammation also occurs within the myocardium. Therefore, this study was aimed at assessing the presence of activated cells in unaffected remote myocardium of patients with acute myocardial infarction (AMI), in comparison to the peri-infarct region from the same cases, and in comparison to myocardial specimens from control hearts.Sixteen patients dying 1 to 12 weeks after AMI and 16 control subjects were selected at autopsy. Myocardial specimens were taken at remote unaffected viable regions and at peri-infarct regions in cases with AMI. Confocal microscopy was performed to measure the number of activated cells (DR+), T-lymphocytes (CD3+), and activated T-lymphocytes (CD3+/DR+). Activated cells and activated T-lymphocytes were found in remote unaffected regions in 11 of 16 cases (69%), in peri-infarct zone in all cases (100%), and in none of the control hearts (0%, P<0.001 versus others). A greater myocardial inflammatory burden in remote regions but not in peri-infarct regions was associated with persistent infarct-related artery occlusion (P<0.05).This study for the first time shows the presence of activated T-lymphocytes in remote unaffected myocardial regions in approximately two thirds of patients with recent AMI. Because these cells are associated with persistent infarct-related artery occlusion, our data may suggest that an antigenic stimulus present also in the myocardium triggers an immune response that may be critical to precipitate artery occlusion.
Modification of the carcinogenic process in colorectal cancer by endogenous and exogenous factors: effect of colestipol hydrochloride on tumors induced by dimethylhydrazine.
Authors: J P Daugherty
Journal: Environmental Health Perspectives (1983)

The effect of the bile acid sequestrant, colestipol hydrochloride, on the incidence of dimethylhydrazine-induced tumors of the large intestine was determined in male Swiss mice. The subcutaneous administration of dimethylhydrazine (15 mg/kg) produced tumors in approximately 89% of the animals with an average of 1.70 tumors per tumor-bearing animal. When carcinogen-treated animals received dietary colestipol (0.52%, w/w) from 4 weeks prior to the first injection of dimethylhydrazine until the time of death, there was an increase in the number of tumors per tumor-bearing animal to 2.23. In an attempt to understand the nature of this enhancement, animals were administered dietary colestipol at different times in relation to the administration of the carcinogen. The number of tumors per tumor-bearing animal for the different protocols was: post-initiation colestipol exposure, 1.70; colestipol exposure concomitant with dimethylhydrazine, 1.41; pre-initiation colestipol exposure, 2.23. Thus, colestipol appeared to function both as an anticarcinogen and as a promoter (pre-initiation). Since colestipol has the capacity to bind a number of chemical agents, the different biological effects probably reflect the multifactorial nature of colorectal cancer with the end result dependent on the balance between opposing factors. The selective administration of colestipol in relation to carcinogen administration may prove useful in elucidating the various factors involved in the etiology of this disease.
Simultaneous Infiltration of Polyfunctional Effector and Suppressor T Cells into Renal Cell Carcinomas
Authors: Sebastian Attig, Jörg Hennenlotter, Graham Pawelec, Gerd Klein, Sven D. Koch, Hanspeter Pircher, Susan Feyerabend, Dorothee Wernet, Arnulf Stenzl, Hans-Georg Rammensee, Cécile Gouttefangeas
Journal: Cancer Research (2009)

Abstract Renal cell carcinoma is frequently infiltrated by cells of the immune system. This makes it important to understand interactions between cancer cells and immune cells so they can be manipulated to bring clinical benefit. Here, we analyze subsets and functions of T lymphocytes infiltrating renal cell tumors directly ex vivo following mechanical disaggregation and without any culture step. Subpopulations of memory and effector CD4+ Th1, Th2, and Th17 and CD8+ Tc1 cells were identified based on surface phenotype, activation potential, and multicytokine production. Compared with the same patient's peripheral blood, T lymphocytes present inside tumors were found to be enriched in functional CD4+ cells of the Th1 lineage and in effector memory CD8+ cells. Additionally, several populations of CD4+ and CD8+ regulatory T cells were identified that may synergize to locally dampen antitumor T-cell responses. [Cancer Res 2009;69(21):8412–9]
Natural Killer (NK) Cell Lytic Dysfunction and Putative NK Cell Receptor Expression Abnormality in Members of a Family With Chromosome 3p-Linked von Hippel-Lindau Disease
Authors: J R Ortaldo, G M Glenn, H A Young, J L Frey
Journal: JNCI Journal of the National Cancer Institute (1992)

BACKGROUND. Using antibodies to a putative natural killer (NK) cell receptor (pNKR), we recently cloned a novel cDNA and localized this gene to the short arm of human chromosome 3, region 3p21-3p24. Individuals susceptible to or clinically manifesting von Hippel-Lindau disease (VHL) have a genetic defect telomeric to this region on chromosome 3. This defect, resulting in VHL, is manifested by a high incidence of certain tumors.Based on the location of this gene, we sought to determine if VHL patients have a defect in gene expression of pNKR.Because of the proximity of the VHL and pNKR genetic regions, the variable expression of VHL tumors, and the ability of NK cells to target tumor cells, we investigated NK cell activity and other aspects of the immunologic status in 40 members (four branches) of a family with a high incidence of VHL tumors.Individuals affected with VHL and lacking in normal surface expression of pNKR had virtually no NK cell lytic activity. Analysis of genotypes and phenotypes of all subjects revealed that the greatest difference in NK cell lytic activity (P = .0002) was seen when family members exhibited both VHL and pNKR surface expression defects, compared with normal relatives who had neither defect. Furthermore, the lack of NK cell activity strongly correlated (P = .0005) with abnormal pNKR protein surface expression. Of particular interest, individuals who lacked NK cell activity had normal numbers of NK cells. In addition, analysis of leukocyte subsets indicated normal numbers of T and B cells, monocytes, and NK cells in both affected and normal individuals.These data indicate that although all affected individuals have the cell population responsible for NK cell activity, many have cells low in expression of pNKR and lack functional NK cell activity. Overall, these results indicate that, in addition to a predisposition to the development of neoplasms, VHL patients have a defect in a specific mechanism of natural immunosurveillance that correlates with a defect in expression of a novel large granular lymphocyte pNKR protein.
Psychotropic Drug Use and the Risk of Hip Fracture
Authors: Wayne A. Ray, Marie R. Griffin, William Schaffner, David K. Baugh, L.Joseph Melton
Journal: New England Journal of Medicine (1987)

To assess the risk of hip fracture associated with the use of four classes of psychotropic drugs, we performed a case-control study of 1021 patients with hip fractures and 5606 controls among elderly Medicaid enrollees. Persons treated with hypnotics–anxiolytics having short (≤24 hours) elimination half-lives had no increased risk of hip fracture. By contrast, a significantly increased risk was associated with current use of hypnotics–anxiolytics having long (>24 hours) elimination half-lives (odds ratio, 1.8; 95 percent confidence interval, 1.3 to 2.4), tricyclic antidepressants (odds ratio, 1.9; 95 percent confidence interval, 1.3 to 2.8), and antipsychotics (odds ratio, 2.0; 95 percent confidence interval, 1.6 to 2.6). The risk increased in relation to the doses of drugs in these three classes. An analysis for possible confounding by dementia did not alter the results. Previous but noncurrent use of drugs in these classes conferred no increase in risk. Although a cause- and-effect relation was not proved, these data support the hypothesis that the sedative and autonomic effects of psychotropic drugs increase the risk of falling and fractures in elderly persons. The results suggest the need for studies of this association in other populations and for evaluation of newer psychotropic drugs with fewer undesirable sedative and autonomic effects. (N Engl J Med 1987; 316:363–9.)