tbuckley/cabot-search huggingface dataset:
Abstract OT2-5-01: Brain metastases in breast cancer network Germany (BMBC, GBG 79): Multicentric, retro- and prospective collection of patient data and biomaterial from breast cancer patients with brain metastases
Authors: Isabell Witzel, Elena Laakmann, Tanja Fehm, Volker Möbus, Gunter vonMinckwitz, Julia Kaiser, Sibylle Loibl, Volkmar Müller
Journal: Cancer Research (2015)

Abstract Background: The incidence of brain metastases in breast cancer patients is rising and has become a major clinical challenge in the last years. So far, limited therapeutic options and insights into the biology of brain metastases exist. Most reports include patients with brain metastases from different tumor entities and few studies so far analyzed exclusively patient data or tumor samples from breast cancer patients. In this context, an open, multicenter registry and biobank should be helpful for analysis of a large number of breast cancer patients with brain metastases. Therefore, we initiated the Brain Metastases in Breast Cancer Network Germany (BMBC; GBG79). Trial design and eligibility criteria: Patients with brain metastases from breast cancer are eligible. Registration of patient data is allowed retrospectively and prospectively. To enable an easy access, an internet-based database was chosen ("MedCodes" by the German Breast Group). Specific aims: Documented data cover incidence, symptoms, number and localization of brain metastases, histopathology, imaging methods, outcome, therapy, and quality of life measurement. Tissue of brain metastases and primary tumors will be collected for translational research projects. Planned analyses include treatment patterns in Germany, patient outcome, as well as validation of prognostic scoring systems in a multicenter setting and in the context of new targeted therapies. Translational research projects investigate the impact of glycosylation, resistance mechanisms against HER2-targeted therapies, role of the blood brain barrier, evaluation of markers of radioresistance and specific genomic alterations associated with brain tropism of breast cancer cells. The registry and biobank should be also open for cooperation with other groups. Present accrual and target accrual: The accrual target is app. 1000 patients in the database and app. 400 tissues of brain metastases from German centers. The study was opened for documentation in April 2014 with more than 50 participating centers as of June 2014. Citation Format: Isabell Witzel, Elena Laakmann, Tanja Fehm, Volker Möbus, Gunter vonMinckwitz, Julia Kaiser, Sibylle Loibl, Volkmar Müller. Brain metastases in breast cancer network Germany (BMBC, GBG 79): Multicentric, retro- and prospective collection of patient data and biomaterial from breast cancer patients with brain metastases [abstract]. In: Proceedings of the Thirty-Seventh Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2014 Dec 9-13; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2015;75(9 Suppl):Abstract nr OT2-5-01.
DEVELOPMENTS IN AVIATION MEDICINE
Authors: Harry G. Armstrong
Journal: Annals of Internal Medicine (1940)

Article1 June 1940DEVELOPMENTS IN AVIATION MEDICINEHARRY G. ARMSTRONGHARRY G. ARMSTRONGSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-13-12-2212 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptA highly specialized field of medical science may normally develop in two directions, either by increasing the information available in its own particular field or by broadening its scope. As a result of the tremendous growth of the aviation industry in this country during the past few years aviation medicine has shown a marked development in both of these directions which has not only brought it into a position of prominence as a medical specialty but has made it a matter of interest and importance to the general medical profession as well.Aviation medicine may be defined as that branch... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: HARRY G. ARMSTRONGAffiliations: U. S. Army*Read at the Cleveland meeting of the American College of Physicians, April 1, 1940. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 June 1940Volume 13, Issue 12Page: 2212-2216 ePublished: 1 December 2008 Issue Published: 1 June 1940 PDF downloadLoading ...
72. Position and Copy Number Dependence of the Central Polypurine Tract (cPPT) Function in Simple and Complex Lentiviral Vectors
Authors: Alex H. Chang, Leszek Lisowski, Matthias Stephan, Isabelle Rivière, Michel Sadelain
Journal: Molecular Therapy (2004)

Recombinant lentiviral vectors derived from human immunodeficiency virus-1 are promising vectors for gene therapy applications. This is due to their ability to transduce nondividing cells, their genomic stability, their relatively large genomic capacity, as well as their ability to stably maintain long term transgene expression. Recent studies have uncovered that the central polypurine tract (cPPT) plays an important role in increasing lentivirus-mediated gene transfer efficiency. The cPPT participates in lentiviral reverse transcription by initiating the synthesis of a downstream plus strand cDNA. Together with the upstream plus strand initiated at the 3' polypurine tract, it forms a central DNA flap that bears in its center a short plus strand overlap. A possible role in nuclear import enhancement of the viral preintegration complex has been suggested (Zennou, Cell, 2000), but the mechanism of cPPT function is still not fully elucidated. It has also been reported that the incorporation of cPPT in lentiviral vectors can increase particle infectivity (Follenzi, Nature Genetics, 2000). However, a systematic evaluation of the cPPT in complex lentiviral vectors has not been reported to date.
Abstract 11585: Is Brachial Flow-Mediated Dilation the Predictor of Development of Cardiac Allograft Vasculopathy in Recipients With Heart Transplantation?
Authors: Takuya Watanabe, Osamu Seguchi, Kunihiro Nishimura, Masanobu Yanase, Takuma Sato, Haruki Sunami, Seiko Nakajima, Eriko Hisamatsu, Takamasa Sato, Kensuke Kuroda, Yoko Nakao, Michikazu Nakai, Misa Takegami, Hiroki Hata, Tomoyuki Fujita, Yoshihiro Miyamoto, Takeshi Nakatani, Takashi Kobayashi, Aya Higashiyama, Makoto Watanabe, Yoshihiro Kokubo
Journal: Circulation (2014)

Introduction: Cardiac allograft vasculopathy (CAV) is one of the main causes of death in heart transplant (HTx) recipients. Usefulness of FMD for predictor of CAV progression is not clear. Methods: Forty three HTx recipients were included and they underwent measurement of FMD at mean 4.8 years after HTx. All recipients were performed three-dimensional intravascular ultrasounds (3D-IVUS) analysis just after HTx (First; mean 0.3 ± 0.5 year after HTx) and at the time (Last; mean 4.8 ± 3.7 year after HTx) when FMD was performed. We defined the impairment of endothelial function (I-EF) as brachial artery FMD&lt;6.0%. The median of plaque volume index (PVI, plaque volume/measured vessel length) at first IVUS was 0.92 mm 3 /mm. The subjects were sub classified according to PVI at first IVUS, the greater PVI group (≧0.92 mm 3 /mm) and the less PVI group (&lt;0.92 mm 3 /mm). Results: Most of HTx recipients were diagnosed as non-ischemic heart disease (95.3%). 16 recipients had impairment of endothelial function (I-EF group). At first and last IVUS, PVI were significantly greater in the I-EF group. Endothelial function was significantly impaired in 10 recipients (45.5%) in the greater PVI group and 6 (28.6%) in the less PVI group. In the greater PVI group, recipients with I-EF had a greater PVI at last IVUS in the comparison with recipients without I-EF (2.23±0.89 vs 3.87±1.84 mm3/mm, p=0.013). In the less PVI group, there were no significant difference in PVI at last IVUS between with and without I-EF (0.81±0.49 vs 1.50±1.25 mm3/mm/year, p=0.075). After multivariate adjustment for the greater PVI(≧0.92 mm 3 /mm) at baseline, time of last IVUS year since HTx and the presence of I-EF, the presence of I-EF was independently associated with PVI at last IVUS (β coefficient=1.16, 95%CI; 0.42 to 1.90, p=0.003). Conclusions: Impairment of endothelial function was associated with the plaque progression in HTx recipients.
Self-injurious behavior: a review of the behavior and biology of self- mutilation
Authors: R M Winchel, M Stanley
Journal: American Journal of Psychiatry (1991)

The authors describe the clinical characteristics of self-injurious behavior, giving special emphasis to self-injurious behavior occurring among individuals with character disorders.They review data suggesting the involvement of serotonergic, dopaminergic, and opiate neurotransmitter systems in the expression of self-injurious behavior.Self-injurious behavior occurs among mentally retarded individuals, psychotic patients, prison populations, and individuals with severe character disorders. Although theoretical psychological models of self-injurious behavior are helpful in understanding the patient's experience of self-injury, no generally useful therapeutic approach has yet evolved from these models. Data derived from animal models and treatment studies suggest the involvement of opiatergic and dopaminergic mechanisms in self-injury among the mentally retarded. Serotonergic influences on self-injurious behavior may be present in varying forms of this behavior. The scientific literature on the benefits of pharmacological agents for mentally retarded individuals is beset with a number of problems. Support is emerging, however, for the use of lithium and carbamazepine with self-injuring mentally retarded patients, and some behavioral interventions appear to be successful for mentally retarded individuals. Self-injuring patients with borderline personality disorder may benefit from milieu treatment.Although no form of treatment has yet been demonstrated to be of general benefit, the literature suggests that therapeutic trials with dopamine antagonists, serotonin reuptake inhibitors, and opiate antagonists may be of value.
ABL1 Methylation Is a Distinct Molecular Event Associated With Clonal Evolution of Chronic Myeloid Leukemia
Authors: Fotis A. Asimakopoulos, Pesach J. Shteper, Svetlana Krichevsky, Eitan Fibach, Aaron Polliack, Eliezer Rachmilewitz, Yinon Ben-Neriah, Dina Ben-Yehuda
Journal: Blood (1999)
Incident heart failure in relation to vascular disease: Insights from the Health, Aging, and Body Composition Study
Authors: Hassan Khan, Andreas P. Kalogeropoulos, Faiez Zannad, Catherine N. Marti, Peter W.F. Wilson, Vasiliki V. Georgiopoulou, Alka M. Kanaya, Anne B. Newman, Erik Schelbert, Tamara B. Harris, Stephen Kritchevsky, Clyde Yancy, Mihai Gheorghiade, Gregg C. Fonarow, Javed Butler
Journal: European Journal of Heart Failure (2014)
582. Detection of Enhanced Serum Antibody Production to Renal Cell Cancer Proteins and Identification of Serological Tumor Antigens in Patients Treated with the GM-CSF-Gene Transduced-Autologous Tumor Vaccines (GVAX®)
Authors: Takao Hashiguchi, Yukoh Nakazaki, Shirley Clift, Dale G. Ando, Shigetaka Asano, Kenzaburo Tani
Journal: Molecular Therapy (2004)

Vaccination of GM-CSF-transduced tumor cells (GVAX®) have been demonstrated to induce cellular and humoral immune response to tumors in animal studies as well as human clinical trials. We have recently done clinical trials of GVAX® using autologous renal cell cancer (RCC) cells in Japan. Four out of six advanced RCC who were entered to our clinical gene therapy trial were injected with GVAX. First of all, to examine whether the therapeutic regimen induced antitumor antibody responses in them, we compared the serum antibody reactivity against autologous tumor cell lysates before and after the vaccinations by immunoblot analysis. Using post-therapy serum as probes, high molecular weight proteins of around 250 kDa generated clear signals, whereas the pre-vaccination serum showed no or only weak signals at the same position, suggesting that the gene therapy induced an antibody response in them. In three of them (Cases 2–4), the induction of antibodies immunoreactive with the 250 kDa proteins was significant, while the results were less clear in Case 1. The suspected common antigen was actually demonstrated in both RCC lysates and normal renal cell lysates, and in human lip-derived fibroblasts, but not in H69 lung cancer cells. Furthermore, the changes in the magnitude of the antibody immunoreactivity over time were analyzed using serum from Case 2. The strongest signal was observed in serum obtained at 67 days after the initial vaccination, between the 5th and 6th vaccinations. This response was maintained from day 67 until day 281, just after the 17th vaccination, although it decreased slightly. After the last vaccination, the immunoreactivity remained at a lower level, although it did not disappear completely. Secondly, based on the results of Western blot analysis, we applied SEREX, the serological identification of antigens by recombinant expression cloning, using patient's serum. We constructed RCC cDNA-expression library on lambda phage vector, and screened the plaques with Case 2 serum pooled between days 25 and 80 after the first vaccination. The mRNA source was Case 2 autologous cultured tumor cells. Sequencing analysis of isolated positive clones (twelve in total) revealed some of them were reported as SEREX defined antigen in previous studies but others were not. Recombinant antigen proteins, fused to epitope tags, were expressed in E. coli and the antibody titration of sera from patients or healthy donner is now going on. The identification of the new anti-RCC antigen might cast a new light on the treatment of patients suffered from advanced RCC.
Impaired prostate tumorigenesis in Egr1-deficient mice
Authors: Sarki A. Abdulkadir, Zhican Qu, Emily Garabedian, Sheng-Kwei Song, Thomas J. Peters, John Svaren, Joseph M. Carbone, Cathy K. Naughton, William J. Catalona, Joseph J.H. Ackerman, Jeffrey I. Gordon, Peter A. Humphrey, Jeffrey Milbrandt
Journal: Nature Medicine (2001)
Abstract 19019: Costs and Diagnostic Yield of Exercise Treadmill Testing vs. Exercise SPECT in Symptomatic Patients at Intermediate Risk of CAD
Authors: Nishant R Shah, Michael K Cheezum, Marcio S Bittencourt, Vikas Veeranna, Viviany R Taqueti, Takashi Kato, Jon Hainer, Courtney Foster, Mariya Gaber, Sharmila Dorbala, Ron Blankstein, Marcelo F Di Carli
Journal: Circulation (2014)

Objective:  To analyze direct costs and early revascularization rates among intermediate risk symptomatic patients undergoing exercise treadmill testing (ETT) vs. exercise myocardial perfusion SPECT.   Methods:  Intermediate risk patients (Morise score 9-15) clinically referred for ETT or exercise SPECT between January 2006-December 2010 were retrospectively analyzed. Patients were excluded for prior CAD evaluation within 5 years, uninterpretable baseline ECG, cardiac surgery, cardiomyopathy, or valvular disease. One-year direct costs were based on Medicare reimbursement rates and included all non-invasive and invasive diagnostic testing for CAD. Patients were followed for early (   Results:  The study cohort included 1,930 patients, in whom ETT was performed in 1,029 (53%) and exercise SPECT in 901 (47%). The exercise SPECT group was older (60± 10 yrs) than the ETT group (57±9 yrs), p = 0.01. 88% of the ETT group and 94% of the exercise SPECT group did not undergo any downstream testing (p  Figure 1a ). Finally, exercise SPECT resulted in more early revascularizations than ETT, suggesting that the higher initial cost is accompanied by a higher diagnostic yield  (Figure 1b) .   Conclusion:  ETT is associated with lower 1-year costs, but also lower diagnostic yield, than exercise SPECT in intermediate risk symptomatic patients. The downstream cost-benefit of exercise SPECT is limited to intermediate-high risk patients, in whom ETT results in increased test layering.
Abstract 1907: Wnt pathway antagonist OMP-54F28 (FZD8-Fc) inhibits tumor growth and reduces tumor-initiating cell frequency in patient-derived hepatocellular carcinoma and ovarian cancer xenograft models
Authors: Pete Yeung, Lucia Beviglia, Belinda Cancilla, Cristina Dee-Hoskins, James W. Evans, Marcus M. Fischer, Wan-Ching Yen, Austin Gurney, John Lewicki, Timothy Hoey, Ann M. Kapoun
Journal: Cancer Research (2014)

Abstract The Wnt/beta-catenin pathway, which signals through the Frizzled (FZD) receptor family and several co-receptors, has long been implicated in cancer. We have developed OMP-54F28, a recombinant fusion protein consisting of the ligand-binding domain of FZD8 and a human IgG1 Fc fragment. OMP-54F28 acts as a decoy receptor in sequestering Wnts and preventing them from binding to FZD receptors and thereby inhibiting Wnt signaling. The Wnt pathway is important for stem cell self renewal, differentiation, tumorigenicity, and epithelial-mesenchymal transition (EMT). Using minimally passaged human patient-derived xenograft tumors, we demonstrate that OMP-54F28 is efficacious as a single agent and in combination with standard of care in four hepatocellular carcinoma (HCC) and two ovarian cancer models. In the HCC models, OMP-54F28 shows tumor growth inhibition (TGI) as a single agent (average of 46%, p&amp;lt;0.05 vs. control) and displays additive TGI in combination with Sorafenib (average of 78%, p&amp;lt;0.05; 48% Sorafenib alone). Also, in the ovarian cancer models, treatment with OMP-54F28 results in TGI as a single agent (average of 32% vs. control) and shows additive TGI in combination with Paclitaxel (average of 78%, p&amp;lt;0.05; 48% with Paclitaxel alone). We also performed in vivo serial transplantation assays and found that OMP-54F28 as a single agent and in combination with standard of care reduces tumor-initiating cell frequency in both HCC and ovarian cancer xenografts. The anti-tumor effect was associated with a decrease in cell proliferation, induction of cell differentiation, and modulation of target Wnt pathway genes. Our data demonstrate the potential therapeutic benefit of targeting Wnt signaling in HCC and ovarian cancer. OMP-54F28 is being tested in Phase 1b clinical studies in these indications. Citation Format: Pete Yeung, Lucia Beviglia, Belinda Cancilla, Cristina Dee-Hoskins, James W. Evans, Marcus M. Fischer, Wan-Ching Yen, Austin Gurney, John Lewicki, Timothy Hoey, Ann M. Kapoun. Wnt pathway antagonist OMP-54F28 (FZD8-Fc) inhibits tumor growth and reduces tumor-initiating cell frequency in patient-derived hepatocellular carcinoma and ovarian cancer xenograft models. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 1907. doi:10.1158/1538-7445.AM2014-1907
Hospitals to spend £200m to prevent spread of vCJD
Authors: Owen Dyer
Journal: BMJ (2001)

British hospitals have been told to update their sterilisation equipment amid fears that surgical instruments could transmit variant Creutzfeldt-Jakob disease (vCJD).

The government has allocated £200m ($300m) for the purchase of new sterilisation equipment and has ordered hospitals to perform all future tonsillectomies with single use instruments, at a cost of £25m annually.

The Spongiform Encephalopathy Advisory Committee (SEAC) first recommended increased …
Science, medicine, and the future: DNA microarrays in medical practice
Authors: T. J Aitman
Journal: BMJ (2001)

The completion of the draft sequence of the human genome 1 2 has raised public awareness of "genomics" and of the ways in which the emerging technologies of the genomics "revolution" will have direct applications to patient care. 3DNA microarrays, or biochips, are prominent among these new technologies.The past five years have seen a dramatic rise in the use of DNA microarrays for biomedical research, in some cases with immediate applicability to clinical practice.The uses of microarrays for gene expression profiling, genotyping, mutation detection, and gene discovery are leading to remarkable insights into the function of thousands of genes previously known only by their gene sequence.This review discusses ways in which microarrays have started to affect clinical practice and research and how this role will develop in the next five to 10 years. MethodsThe data for this review reflect my personal views from 10 years of research in molecular medicine and five years on DNA microarrays.My views have developed over this period from discussions with colleagues in my own laboratory and at basic science and biotechnology meetings and from regular reading of Nature Genetics, Nature, Science, and other journals.
Tuberculosis Theses; Diagnostic, Prognostic, Therapeutic
Authors: Lawrason Brown
Journal: Annals of Internal Medicine (1929)

Article1 September 1929Tuberculosis Theses; Diagnostic, Prognostic, TherapeuticLAWRASON BROWNLAWRASON BROWNSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-3-3-206 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptArticles of faith to which one may subscribe or from which one may dissent are of value in many activities of life. To the beginner in an art they point out a ford across troublous and swift waters. That other easier and safer fords are not to be found or, indeed, do not already exist is not denied but here at least is one. To him who has long practised the art they seem, in part at least, axiomatic and tiresome, or else not to be accepted. Their power to arouse discussion, to lead to thought, to foster healthy disagreement... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Saranac Lake, N. Y.*These theses appeared in part in the American Review of Tuberculosis, 1917, 1; 193-205. Read before the American College of Physicians, April 8, 1929, Boston, Mass. As they now stand they have been revised and augmented. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 September 1929Volume 3, Issue 3Page: 206-215 Issue Published: 1 September 1929 PDF downloadLoading ...