tbuckley/cabot-search huggingface dataset:
Abstract 923: Association of <i>TGF-β1</i> genetic variants with HPV16-positive oropharyngeal cancer
Authors: Guojun Li, Erich M. Sturgis, Dapeng Lei, Yang Zhang, Qingyi Wei
Journal: Cancer Research (2010)

Abstract Purpose: Transforming growth factor-β1 (TGF-β1) plays an important role in inflammation and immune responses, which control the HPV clearance and escape of immune surveillance, and may contribute to genetic susceptibility to HPV16 infection. Experimental Design: In this case series study, we analyzed the HPV16 status in tumor specimens and genotyped three TGF-β1 polymorphisms using genomic DNA from blood of 200 squamous cell carcinoma of the oropharynx (SCCOP). We calculated odds ratio (OR) and 95% confidence intervals (CIs) in univariate and multivariable logistic regression models to examine the association between the TGF-β1 polymorphisms and HPV16 status in SCCOP. Results: Compared with those with the common homozygous genotype, the TGF-β1 T869C variant genotypes were significantly associated with HPV16-positive tumor status among patients with SCCOP (OR, 1.97; 95% CI, 1.03 − 3.76) but no significant association was observed for the TGF-β1 C509T or G915C polymorphism. However, when all variant genotypes were combined, SCCOP patients carrying genotypes with any of these TGF-β1 variant were more than twice as likely to have an HPV16-positive tumor (OR, 2.28; 95% CI, 1.16-4.50) as patients with no variant genotypes. When stratified by demographic and clinical characteristics, those under 54 years of age, non-Hispanic white patients, never smokers, and never drinkers with any variant TGF-β1 genotypes were also more likely to have HPV16-positive tumors. Conclusions: TGF-β1 polymorphisms may serve as a susceptibility marker for tumor HPV16 status among SCCOP patients, particularly those who were never smokers and never drinkers. Large studies are needed to validate our findings. Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 923.
Benefits of Male Circumcision—Reply
Authors: Aaron A. R. Tobian, Ronald H. Gray
Journal: JAMA (2012)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Evidence for a Continuum of Genetic, Phenotypic, and Biochemical Abnormalities in Children with Growth Hormone Insensitivity
Authors: Alessia David, Vivian Hwa, Louise A. Metherell, Irène Netchine, Cecilia Camacho-Hübner, Adrian J. L. Clark, Ron G. Rosenfeld, Martin O. Savage
Journal: Endocrine Reviews (2011)

GH insensitivity (GHI) presents in childhood as growth failure and in its severe form is associated with dysmorphic and metabolic abnormalities. GHI may be caused by genetic defects in the GH–IGF-I axis or by acquired states such as chronic illness. This article discusses the former category. The field of GHI due to mutations affecting GH action has evolved considerably since the original description of the extreme phenotype related to homozygous GH receptor (GHR) mutations over 40 yr ago. A continuum of genetic, phenotypic, and biochemical abnormalities can be defined associated with clinically relevant defects in linear growth. The role and mechanisms of the GH–IGF-I axis in normal human growth is discussed, followed by descriptions of mutations in GHR, STAT5B, PTPN11, IGF1, IGFALS, IGF1R, and GH1 defects causing bioinactive GH or anti-GH antibodies. These defects are associated with a range of genetic, clinical, and hormonal characteristics. Genetic abnormalities causing growth failure that is less severe than the extreme phenotype are emphasized, together with an analysis of height and serum IGF-I across the spectrum of different types of GHR defects. An overall view of genotype and phenotype relationships is presented, together with an updated approach to the assessment of the patient with GHI, focusing on investigation of the GH–IGF-I axis and relevant molecular studies contributing to this diagnosis.
Second Cancers After Radiotherapy and Chemotherapy for Early Stages of Hodgkin's Disease<xref ref-type="fn" rid="FN2">2</xref>
Authors: M Henry-Amar
Journal: JNCI Journal of the National Cancer Institute (1983)

In a population of 334 patients treated for Hodgkin's disease by the European Organization for Research and Treatment of Cancer between 1964 and 1971, 21 patients with second primary cancers (SC) were observed: 4 patients with acute leukemias, 3 with non-Hodgkin's lymphomas, and 14 with solid tumors. Time to SC ranged from 2 to 16 years after initial treatment. The relative risk (RR) of acute leukemia for the patients with Hodgkin's disease as compared to the general population was 40 (P less than .001). The RR of leukemia in patients treated by polychemotherapy--mechlorethamine, vincristine, procarbazine, and prednisone--for relapse was 300 (P less than .001). However, the RR of leukemia for those patients who did not experience a relapse was 14 (not significant). The RR of other SC in the overall group was 3.76 (P less than .001). For patients whose relapses were treated by polychemotherapy the RR of SC, leukemia excepted, was 26 (P less than .001), whereas for patients not treated by polychemotherapy for relapse the RR was slightly increased (RR = 3.67; P = .027). The cumulative proportions of acute leukemia at 10 years were 0.7% in the "no-relapse" group and 2.7% in the polychemotherapy group. The cumulative proportions of other SC at 10 years was 1.3% in the no-relapse group, 7.2% in the group of patients not treated by polychemotherapy after relapse, and 8.4% in the polychemotherapy group. The first important risk factor for developing an SC was polychemotherapy, and the second was age over 40 years. These data suggest that combination chemotherapy may be responsible for both acute leukemias and other SC.
Regional Myocardial Metabolism of High-Energy Phosphates during Isometric Exercise in Patients with Coronary Artery Disease
Authors: Robert G. Weiss, Paul A. Bottomley, Christopher J. Hardy, Gary Gerstenblith
Journal: New England Journal of Medicine (1990)

The maintenance of cellular levels of high-energy phosphates is required for myocardial function and preservation. In animals, severe myocardial ischemia is characterized by the rapid loss of phosphocreatine and a decrease in the ratio of phosphocreatine to ATP.
scFv-Based “Grababody” as a General Strategy to Improve Recruitment of Immune Effector Cells to Antibody-Targeted Tumors
Authors: Zheng Cai, Ting Fu, Yasuhiro Nagai, Lian Lam, Marla Yee, Zhiqiang Zhu, Hongtao Zhang
Journal: Cancer Research (2013)

Recruitment of immune cells to tumor cells targeted by a therapeutic antibody can heighten the antitumor efficacy of the antibody. For example, p185(her2/neu)-targeting antibodies not only downregulate the p185(her2/neu) kinase (ERBB2) but also trigger complement-dependent cytotoxicity (CDC) and antibody-dependent cellular cytotoxicity (ADCC) through the antibody Fc region. Here, we describe a generalized strategy to improve immune cell recruitment to targeted cancer cells, using a modified scFv antibody we call a "Grababody" that binds the target protein and endogenous immunoglobulins. The model system we used to illustrate the use of this platform recognizes p185(her2/neu) and includes an IgG binding domain. The recombinant scFv Grababody that was created recruited circulating human IgGs and attracted immune cells carrying Fc receptors to tumor cells that expressed p185(her2/neu). The presence of the IgG binding domain significantly enhanced CDC and ADCC activity and improved antitumor activity in vivo. Our results illustrate a novel general approach to improve antibody-like proteins for therapeutic applications.
Observations Concerning Both the Induction and the Regression of Lipid and Cholesterol Infiltration in Ocular Implants of Rabbit Aorta
Authors: MEYER FRIEDMAN, SANFORD O. BYERS
Journal: Circulation Research (1959)

Segments of both normal and atherosclerotic rabbit aortas were placed in the anterior chamber of host rabbits according to the Higginbotham technic. Normal aorta segments placed in the eyes of cholesterol fed rabbits quickly became infiltrated with fat and cholesterol. The intensity of this infiltration exceeded that observed in the host's own aorta. Atherosclerotic aorta segments placed in the eyes of normal rabbits quickly lost both lipid and cholesterol.
Low heterogeneity and peculiarity of HCV quasispecies in liver, PBMCS and serum of patients with HCV-related cryoglobulinemic syndrome
Authors: M. Gerotto, F. Dal Pero, F. Lari, S. Loffreda, P. Pontisso, F. Bianchi, A. Alberti, M. Lenzi
Journal: Journal of Hepatology (2000)
Postmenopausal Hormone Therapy and Systemic Lupus Erythematosus
Authors: Jorge Sanchez-Guerrero
Journal: Annals of Internal Medicine (1995)

Letters15 December 1995Postmenopausal Hormone Therapy and Systemic Lupus ErythematosusJorge Sanchez-Guerrero, MD, Matthew H. Liang, MD, and Graham A. Colditz, MBBSJorge Sanchez-Guerrero, MDBrigham and Women's Hospital Boston, MA 02115Search for more papers by this author, Matthew H. Liang, MDBrigham and Women's Hospital Boston, MA 02115Search for more papers by this author, and Graham A. Colditz, MBBSBrigham and Women's Hospital Boston, MA 02115Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-123-12-199512150-00017 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail IN RESPONSE:Despite anecdotal clinical and experimental evidence in various animal models of lupus, which support the belief that estrogens and systemic lupus erythematosus do not mix, the sex hormone hypothesis has not been proved in humans. We agree with Dr. Buyon and colleagues. Our study widens the scope of potential side effects of postmenopausal estrogens and underscores the dilemma of prescribing hormone replacement in normal women and the need to balance the risks and benefits. A distinction must be made between prescribing estrogens to healthy women and prescribing them to women with established lupus. Our study addresses the former ... Author, Article, and Disclosure InformationAuthors: Jorge Sanchez-Guerrero, MD; Matthew H. Liang, MD; Graham A. Colditz, MBBSAffiliations: Brigham and Women's Hospital Boston, MA 02115 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byReproductive health in SLE 15 December 1995Volume 123, Issue 12 Page: 962 Keywords Estrogens Hormonal therapy Hormone replacement therapy Hormones Lupus erythematosus Menopause Pregnancy Risk ratio Sex hormones Steroids ePublished: 15 August 2000 Issue Published: 15 December 1995 Copyright & PermissionsCopyright © 1995 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Early Diagnosis of Slipping of the Upper Femoral Epiphysis
Authors: John J. Joyce, B. David Grant
Journal: JAMA (1964)

In 26 cases of femoral epiphysiolysis the commonest complaints were a peculiar gait following minor trauma, often with accompanying knee pain. A Frölich habitus, limping, and diminished hip motions were the most frequently encountered clinical defects. A delayed diagnosis was made in 12 of 14 children having a history of trauma. Familial or patient reluctance to consult a physician, examiners' inaccuracies and low index of suspicion, and roentgenographic errors contributed to diagnostic delays. Since the duration of the slip, as well as severity and trauma, is important to the prognosis, the diagnosis of epiphysiolysis femoris must be excluded in the limping teenager.
Molecular cloning and characterization of the vasopressin-regulated urea transporter of rat kidney collecting ducts.
Authors: C Shayakul, A Steel, M A Hediger
Journal: Journal of Clinical Investigation (1996)

Absorption of urea in the renal inner medullary collecting duct (IMCD) contributes to hypertonicity in the medullary interstitium which, in turn, provides the osmotic driving force for water reabsorption. This mechanism is regulated by vasopressin via a cAMP-dependent pathway and activation of a specialized urea transporter located in the apical membrane. We report here the cloning of a novel urea transporter, designated UT1, from the rat inner medulla which is functionally and structurally distinct from the previously reported kidney urea transporter UT2. UT1 expressed in Xenopus oocytes mediated passive transport of urea that was inhibited by phloretin and urea analogs but, in contrast to UT2, was strongly stimulated by cAMP agonists. Sequence comparison revealed that the coding region of UT1 cDNA contains the entire 397 amino acid residue coding region of UT2 and an additional 1,596 basepair-stretch at the 5' end. This stretch encodes a novel 532 amino acid residue NH2-terminal domain that has 67% sequence identity with UT2. Thus, UT1 consists of two internally homologous portions that have most likely arisen by gene duplication. Studies of the rat genomic DNA further indicated that UT1 and UT2 are derived from a single gene by alternative splicing. Based on Northern analysis and in situ hybridization, UT1 is expressed exclusively in the IMCD, particularly in its terminal portion. Taken together, our data show that UT1 corresponds to the previously characterized vasopressin-regulated urea transporter in the apical membrane of the terminal IMCD which plays a critical role in renal water conservation.
TCT-543 Partial strut fracture in everolimus-eluting stents: An intravascular ultrasound study
Authors: Shinji Inaba, Gary Mintz, Kyeong Yun, Tadayuki Yakushiji, Takehisa Shimizu, Giora Weisz, Martin Leon, Jeffrey Moses, Gregg Stone, Akiko Maehara
Journal: Journal of the American College of Cardiology (2012)
Investigation of the Cause of Death in a Gene-Therapy Trial
Authors: Karen M. Frank, D. Kyle Hogarth, Jonathan L. Miller, Saptarshi Mandal, Philip J. Mease, R. Jude Samulski, Glen A. Weisgerber, John Hart
Journal: New England Journal of Medicine (2009)

We present a case of disseminated histoplasmosis, complicated by retroperitoneal bleeding and leading to death, in a patient who was receiving systemic immunosuppressive therapy for rheumatoid arthritis and who was enrolled in a gene-therapy trial. This trial was designed to evaluate intraarticular delivery of a tumor necrosis factor alpha (TNF-alpha) antagonist, through an adeno-associated virus (AAV) type 2 delivery system, for inflammatory arthritis. The patient's receipt of concurrent anti-TNF-alpha therapy and other immunosuppressive therapy while she was living in an area where histoplasmosis was endemic was thought to be the most likely explanation for the infection; the evidence presented suggests that this fatal infection was unlikely to have been related to exposure to the agent administered in the gene-therapy trial. This case reinforces the importance of considering infectious complications, such as those from endemic mycoses, in patients receiving treatment with a TNF-alpha antagonist and the importance of having a well-designed monitoring plan when subjects in a research study become ill. (ClinicalTrials.gov number, NCT00126724.)
Spatial Resolution of Atrial Pace Mapping as Determined by Unipolar Atrial Pacing at Adjacent Sites
Authors: K. Ching Man, K.K. Chan, Paul Kovack, Rajiva Goyal, Frank Bogun, Mark Harvey, Emile Daoud, S. Adam Strickberger, Fred Morady
Journal: Circulation (1996)

Background The purpose of this study was to examine the spatial resolution of unipolar atrial pace mapping by pacing at adjacent sites within the coronary sinus and the right atrium. Methods and Results Unipolar pacing from each pole of a quadripolar catheter was performed in the coronary sinus (n=29) and in the right atrium (n=10). Pacing from the distal electrode was used to simulate the site of origin of an atrial tachycardia. These P waves were compared with the P waves generated by unipolar pacing from each of the three proximal electrodes. The P waves were analyzed for changes in amplitude, duration, and configuration. Pacing within the coronary sinus resulted in significant changes in amplitude and duration at distances of 17 and 21 mm from the distal pole, respectively. Similarly, pacing in the right atrium resulted in significant changes in amplitude and duration at distances of 17 and 32 mm from the distal pole, respectively. No significant changes in configuration were noted in the coronary sinus in any lead at pacing sites ≤32 mm from the distal pole. Configurational changes were noted in the right atrium at pacing sites 17 mm from the distal pole. Conclusions The spatial resolution of unipolar atrial pace mapping is ≈17 mm. These findings indicate that mapping techniques that depend on the accurate discrimination of P-wave morphology, such as pace mapping or concealed entrainment, are likely to be imprecise when used in the atria.
Comparative evaluation of naturally occurring Pneumocystis carinii pneumonia (PCP) and PCP despite primary chemoprophylaxis in patients with AIDS
Authors: S. Bonora, M. Lanzafame, B. Allegranzi, F. Soldani, S. Vento, A. Cazzadori, G. Di Perri, E. Concia
Journal: Journal of Infection (1997)
Combination Chemotherapy (CISCA) for Advanced Urinary Tract Carcinoma
Authors: Jack J. Sternberg
Journal: JAMA (1977)

Twelve patients with metastatic transitional cell carcinoma from the urinary bladder were treated with a combination chemotherapy program consisting of cisplatinum, cyclophosphamide, and doxorubicin hydrochloride (CISCA). Ten patients had conditions for which a response to therapy could be determined, and nine achieved an objective response (one complete response, eight partial responses). Two additional patients with metastatic transitional cell carcinoma from the renal pelvis were also treated, and one achieved a partial response. In our experience, CISCA combination chemotherapy has given the highest response rate of any protocol thus far tested in advanced, metastatic urinary tract carcinoma.
NOBORI FEMALE STUDY- CLINICAL OUTCOMES AT 12 MONTHS
Authors: Gian Battista Danzi, Marie Claude Maurice, Fina Mauri, Marcus Wiemer, Dragan Sagic, Farzin Fath-Ordoubadi, Antonio Serra, David Hildick-Smith, René Konig, Didier Carrie, Javier Goicolea Ruigomez, Miodrag Ostojic, Marcus Hennersdorf, Stefan Hoffmann
Journal: Journal of the American College of Cardiology (2010)
Airway responsiveness to histamine in man: effect of atropine on in vivo and in vitro comparison.
Authors: J A Roberts, I W Rodger, N C Thomson
Journal: Thorax (1985)

Airway responsiveness to histamine in man may be determined by the smooth muscle sensitivity to histamine or to the interaction between vagal nerve input and smooth muscle sensitivity. We have compared in vivo responsiveness to histamine with in vitro smooth muscle sensitivity to histamine in 20 non-asthmatic patients and one asthmatic patient undergoing thoracic surgery. Histamine responsiveness was assessed in the first 10 non-asthmatics without atropine pretreatment, in the second 10 after atropine pretreatment, and in the asthmatic patient both with and without atropine. In vivo responsiveness was also measured in 10 normal subjects and 10 asthmatic patients not undergoing surgery. Results were expressed as the provocation concentration (PC) causing a decrease in FEV1 of 20% (PC20FEV1) and in specific airways conductance of 35% (PC35SGaw), and in terms of maximal expiratory flow at 35% vital capacity, measured from the partial (V35(P] and complete (V35(C] flow volume curves of 35% (PC35V35(P); PC35V35(C]. In vitro smooth muscle sensitivity to histamine of bronchial tissue obtained at thoracotomy was expressed as the concentration causing a 50% maximum contraction (EC50) and as the maximum tension generated. There was considerable variation between patients in the in vivo responsiveness but a relatively narrow range for in vitro responses. There was no significant correlation between in vivo responsiveness, either with or without atropine pretreatment, and in vitro results. The asthmatic patient showed hyperresponsiveness in vivo but but not in vitro. These results suggest that in vitro airway smooth muscle sensitivity to histamine is not the sole determinant of in vivo airway responsiveness and that this lack of relationship is not explained by the influence of vagal nerve input on in vivo measurements. The results in the asthmatic patient suggest that airway hyperresponsiveness may be an in vivo phenomenon which is not related to a primary abnormality of airway smooth muscle.
Immune thrombocytopenia complicating pulmonary tuberculosis: case report and investigation of mechanisms.
Authors: R J Boots, A W Roberts, D McEvoy
Journal: Thorax (1992)

Of 72 patients with radiological evidence of pulmonary emphysema, emphysema occurred either alone or in association with bronchitis in 61, and 8 of these (13%) were found to have α<sub>1</sub>-antitrypsin deficiency. The main features of this condition are: exertional dyspnoea of relatively early onset (generally between 30 and 45 years of age), severely impaired FEV<sub>1</sub> and T<sub>L</sub>CO, and radiological emphysema predominantly affecting the lower zones of the lungs. It is probable that any patient with all the above abnormalities has α<sub>1</sub>-antitrypsin deficiency. There is evidence to suggest that cigarette smoking may hasten the onset of this type of emphysema.