tbuckley/cabot-search huggingface dataset:
Authors' response
Authors: R A CHAPMAN, M S SULEIMAN, Y E EARM
Journal: Cardiovascular Research (1993)

Journal Article Authors' response Get access R A CHAPMAN, R A CHAPMAN British Heart Foundation Research Group, School of Veterinary Science, Bristol. UK Search for other works by this author on: Oxford Academic PubMed Google Scholar M S SULEIMAN, M S SULEIMAN British Heart Foundation Research Group, School of Veterinary Science, Bristol. UK Search for other works by this author on: Oxford Academic PubMed Google Scholar Y E EARM Y E EARM British Heart Foundation Research Group, School of Veterinary Science, Bristol. UK Search for other works by this author on: Oxford Academic PubMed Google Scholar Cardiovascular Research, Volume 27, Issue 6, June 1993, Page 1137, https://doi.org/10.1093/cvr/27.6.1137 Published: 01 June 1993
AIR EMBOLISM IN CONNECTION WITH PLACENTA PRÆVIA.
Journal: JAMA (1896)

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
Drug testing in sport: Bayes theorem meets advanced technology
Authors: R. Carlen
Journal: JAMA (1996)

<h3>In Reply.</h3> —Testing for performance-enhancing drugs is designed to be 100% specific, and with respect to the laboratory that produced the data in Tables 2 and 3 of our article, there is no evidence to the contrary. No false-positive results have occurred in 12 years of accreditation and proficiency testing, and despite numerous reviews by experts, none of the positive cases have been found to be in error. This 100% accuracy for positive results is achieved primarily by properly using a definitive analytic technique to identify compounds. Technical measures of test validity are important but are only part of the story. In addition, unlike many workplace drug-testing programs, testing of athletes includes collecting the urine under direct observation, splitting the urine into 2 portions, analyzing 1 sample at least twice (screen and confirmation) on separate occasions before reporting the result of that specimen, and requiring the analysis of the second portion of
Erectile Dysfunction
Authors: Tom F. Lue
Journal: New England Journal of Medicine (2000)

Erectile dysfunction is defined as the inability to achieve and maintain an erection sufficient to permit satisfactory sexual intercourse.1 It has been estimated to affect 20 million to 30 million men in the United States.2,3 It may result from psychological, neurologic, hormonal, arterial, or cavernosal impairment or from a combination of these factors. In this article we provide a brief overview of the physiology of erection and the pathophysiology of erectile dysfunction, followed by a discussion of drug treatment for the disorder.Physiology of Penile ErectionPenile erection is a neurovascular event modulated by psychological factors and hormonal status. . . .
Bacterial Interference: A Warning
Journal: JAMA (1966)

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
Syphilis: Its Treatment by Intra-Muscular Injections of Soluble Mercurial Salts.
Journal: JAMA (1893)

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
Abstract 2062: Evaluating the effect of tumor necrosis on glycolytic flux and cell survival in glioblastoma
Authors: Evan Noch, Isaiah Yim, Lewis Cantley
Journal: Cancer Research (2019)

Abstract Glioblastoma continues to rank as one of the most lethal primary human tumors. The degree of necrosis in glioblastoma remains one of the most powerful predictors of poor prognosis, but the relationship between necrosis and poor prognosis is not known. It is unclear whether endogenous tumor necrosis is merely an indicator of an aggressive phenotype or whether tumor necrosis itself propagates the aggressive phenotype. Determining the role of necrosis in mediating the malignant potential of glioblastoma therefore represents an important aspect of therapy. We describe a model of patient-derived glioblastoma spheroids expressing a genetically encoded fluorescent NADH/NAD+ biosensor. This biosensor reports glycolytic flux and can be imaged with fluorescent microscopy. We imaged spheroids using multiphoton microscopy and differentiated cells by high versus low NADH/NAD+ levels. FACS analysis of dissociated spheroids followed by RT-PCR analysis demonstrated increased expression of genes known to be upregulated in peri-necrotic regions, including procollagen-lysine,2-oxoglutarate 5-dioxygenase 2 (PLOD2), activating transcription factor 5 (ATF5), and protein O-fucosyltransferase 2 (POFUT2). These cells also had increased expression of hypoxia-responsive genes, including vascular endothelial growth factor (VEGF) and jumonji domain-containing protein 6 (JMJD6). We created an intracranial glioblastoma patient-derived xenograft model, with cells expressing this NADH/NAD+ biosensor. When imaging these tumors in vivo, we were able to demonstrate that cells with high NADH/NAD+ levels are more likely to survive within the peri-necrotic environment. These findings indicate that increased glycolytic flux facilitates survival from expanding regions of necrosis. Future experiments will focus on biopsy of cellular populations with high versus low NADH/NAD+ levels within the peri-necrotic niche. We will then perform RNAseq and metabolomics analysis to determine the genetic and metabolic adaptations that facilitate survival within this microenvironment. This model to study cell survival within the peri-necrotic region will improve awareness of necrosis-mediated growth proliferation and may lead to treatments targeted to tumor necrosis that could improve patient prognosis. Citation Format: Evan Noch, Isaiah Yim, Lewis Cantley. Evaluating the effect of tumor necrosis on glycolytic flux and cell survival in glioblastoma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 2062.
Abstract 1527: Intraperitoneal myeloid-derived suppressor cells in peritoneal dissemination mouse model
Authors: Yutaka Sugita, Kimihiro Yamashita, Rishu Takimoto, Tomoko Tanaka, Akira Arimoto, Eiji Fukuoka, Tetsu Nakamura, Satoshi Suzuki, Yoshihiro Kakeji
Journal: Cancer Research (2019)

Abstract Background: Myeroid-derived suppressor cells (MDSCs) are heterogeneous cell populations derived from bone marrow, and two subsets of M-MDSC and PMN-MDSC are known in mice. They accumulate in the tumor-bearing host, and suppresse cell-mediated immunity mainly on T cells, and inhibit anti-tumor immune responses. We have previously reported that (1) the increase of MDSCs in lung, peripheral blood, and spleen reflects the cancer progression, (2) MDSCs in peripheral blood would be useful as a marker of recurrence as it increases in recurrent cases after surgical resection. On the other hand, no detailed report on the dynamics of intraperitoneal MDSCs has been made. In this study, we made peritoneal dissemination mouse models and monitored intraperitoneal MDSCs, and investigated whether MDSCs are involved in the progression of peritoneal dissemination. Methods: MC38 colon cancer cell line was intraperitoneally injected to C57BL / 6J mice and the change in the number and ratio of immune cells (MDSC, Macrophage, T-cell, B-cell) in the spleen, peripheral blood and peritoneal cavity was monitored over time. We examined the correlation between transition of immune cells and cancer progression. Results: MDSCs increased with cancer progression in all spleen, peripheral blood, and intraperitoneal cavity. The proportion of PMN-MDSCs in MDSCs increased in peripheral blood. In contrast, the proportion of M-MDSCs increased initially, then the PMN-MDSCs increased in the abdominal cavity. Conclusion: Intraperitoneal MDSCs were thought to reflect the progression of peritoneal dissemination as well as spleen and peripheral blood. The proportion of M-MDSCs reflects the disease state in the microperitoneal dissemination with serous ascitic fluid, and ascites became bloody and the proportion of PMN-MDSCs increased with the progression of seeding. We are examining treatment for peritoneal dissemination with this feature in mind. Citation Format: Yutaka Sugita, Kimihiro Yamashita, Rishu Takimoto, Tomoko Tanaka, Akira Arimoto, Eiji Fukuoka, Tetsu Nakamura, Satoshi Suzuki, Yoshihiro Kakeji. Intraperitoneal myeloid-derived suppressor cells in peritoneal dissemination mouse model [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 1527.
Issue Information ‐ TOC
Journal: Allergy (2019)

About the coverThunderstorm asthma was fi rst described by medical doctors in the UK in 1983.This phenomenon is a sudden increase of acute bronchospasm due to a local thunderstorm during pollen season.Weather condi ons such as wind and torren al rain combined with a high pollen count were suggested to trigger severe asthma among suscep ble people.The largest and most catastrophic thunderstrom-triggered asthma epidemic occured on November 21 st 2016 in Melbourne.In this issue, Hew et al. present an interview of 1435 pa ents aff ected by this event.The authors explored individual suscep bility and summarized compunding risk factors for hospital admission.An editorial wri en by D'Amato describes recent thunderstorm asthma events and their e opathogene c aspects.Thunderstorm-triggered asthma attacks
The BRAF V600E Mutation in Hairy Cell Leukemia and Other Mature B-Cell Neoplasms
Authors: Luca Arcaini, Silvia Zibellini, Emanuela Boveri, Roberta Riboni, Sara Rattotti, Marzia Varettoni, Maria Luisa Guerrera, Marco Lucioni, Annamaria Tenore, Michele Merli, Silvia Rizzi, Lucia Morello, Chiara Cavalloni, Marco Paulli, Mario Cazzola
Journal: Blood (2011)
CHORIONIC CARCINOMA
Authors: W. Salisbury
Journal: BMJ (1933)

rMEDTCAL JOURNAT follows.The liver showed marked fatty changes, with areas of focal necrosis, and around the areas of necrosis infiltration by lymphocytes and polymorphonuclear cells; there was also diffuse necrosis of the cells.The spleen was congested and showed a marked endothelial-celled proliferation, while there was often some flaky lymph to be seen in the peritoneum, and the intestines appeared congested.Cultures from the peritoneum, however, proved sterile.The order in which the various series of mice died was interesting.Three mice were inoculated with the filtered sputum of " S. H." on April 23rd and all died on May
Principles of Economic Zoology.
Journal: JAMA (1913)

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
The "gold-standard," accuracy, and the current concepts: Hepatitis C virus genotype and viremia
Authors: T Ohno
Journal: Hepatology (1996)

A proteotyping approach using high resolution mass spectrometry has been applied, for the first time, to subtype the hepatitis C virus based upon detection of one or more signature peptides derived from the E1 and E2 envelope glycoproteins. These signature peptides represent conserved peptide segments within these proteins for particular subtypes of the virus that are found to be unique in mass when compared with the theoretical masses for all peptide segments of translated HCV proteins within a specifically constructed database. The successful application of the approach to three different subtypes of the virus (i.e., 1a, 1b and 2b) is demonstrated for protein and whole virus proteolytic digests. The approach has the potential to replace existing PCR-based subtyping by offering a more direct and cost comparable strategy that is not challenged by mixed infection scenarios.
Elevated pretreatment serum activin A and progression-free and overall survival in trastuzumab-treated metastatic breast cancer.
Authors: Allan Lipton, Lindsey Zubritsky, Kim Leitzel, Suhail M. Ali, Wolfgang Koestler, Eva-Maria Fuchs, Luis Costa, Robert D. Knight, Abderrahmane Laadem, Matthew L. Sherman
Journal: Journal of Clinical Oncology (2012)

607 Background: About half of HER2-positive metastatic breast cancer patients will respond tofirst-line trastuzumab-containing therapy, but most will progress within a year. Trastuzumab resistance remains a vexing clinical problem, and better predictive and prognostic biomarkers are needed. Activin A is a TGF-B superfamily member and regulates cell proliferation, apoptosis, differentiation, and immune response. Methods: Serum activin A was measured using ELISA (R&amp;D Systems, Minneapolis, MN) in 60 metastatic breast cancer patients before starting first-line trastuzumab-containing therapy. Progression-free survival (PFS) and overall survival (OS) were analyzed using the Kaplan-Meier method and Cox modeling with both continuous and dichotomous (median) serum activin A analyses. Results: Pretreatment serum activin A levels averaged 2376 pg/ml, and had a median of 629 pg/ml and 25 th and 75 th quartile values of 406 and 1791 pg/ml, respectively. Patients who were hormone receptor negative had significantly higher activin A levels (median 1287 vs 450 pg/ml, p=0.002). Higher serum activin A was significant on a continuous basis for predicting reduced PFS to first-line trastuzumab-containing therapy (p&lt;0.003), and for predicting shorter OS (p&lt;0.0001). When analyzed using a dichotomous (median) cutpoint, the elevated serum activin A cohort had a significantly reduced PFS (HR 2.79, p &lt;0. 002) (median 6.6 mo vs. 31.1 mo) and OS (HR 5.24, p &lt;0.0001) (median 19.6 mo vs. median not reached). In multivariate analysis for PFS with other covariates (age, line of therapy, CA 15-3, and hormone receptor status), activin A was the only significant covariate (p=0.021). In multivariate analysis for OS, activin A (p=0.002) and CA 15-3 (p=0.03) remained significant as prognostic factors. Conclusions: Elevated pretreatment serum activin A predicts reduced PFS and overall survival in metastatic breast cancer patients treated with first-line trastuzumab-containing therapy. Activin A deserves further study as an adverse biomarker, and to select patients most likely to respond to activin A-targeted therapy.
Speaking Diseases
Authors: Gail Ghai
Journal: JAMA (2002)

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
Plant tumors
Authors: M. P. Gordon
Journal: JAMA (1983)

Crown gall is a plant tumor incited on dicotyledonous plants by infection with a bacterium,<i>Agrobacterium tumefaciens</i>. During this process, a portion of a large plasmid contained in the bacterial cell is transferred and incorporated into the genome of the host plant cell. The transferred plasmid DNA, the T-DNA, carries information for products that either control or code for the synthesis of plant hormones. The increased level of phytohormones causes the transformed cells to escape from host control mechanisms and proliferate limitlessly, thus causing a tumor. The T-DNA also contains information that codes for the synthesis of a number of unusual compounds, which can be utilized only by strains of agrobacteria that contain the large tumor-inciting plasmid. Thus, the bacterium has transformed its host plant into an ever-expanding factory producing materials that only the inciting organisms can use. In some agrobacteria the tumor-inciting plasmid has DNA genes that are related
Markers of Exposure to Carcinogens
Authors: Gerald N. Wogan
Journal: Environmental Health Perspectives (1989)

Methods have been developed for the detection of exposure to carcinogens and other DNA damaging agents in experimental animals and man through the detection of carcinogens or their metabolic derivatives in body fluids, or through adducts bound covalently to DNA or hemoglobin. The successful use of urinary markers of genotoxic exposures has been reported with respect to nitrosoproline as an indicator of exposure to N-nitroso compounds. The same approach has been used to detect AFB1 and AFB1-N7-Gua as markers of exposure to aflatoxin B1; of 3-methyladenine produced as a result of exposure to methylating agents; and thymine glycol as an indicator of exposure to agents causing oxidative damage to DNA. Detection of adducts formed between genotoxic agents and hemoglobin has been reported in studies of populations occupationally exposed to ethylene oxide, in which 3-hydroxyhistidine and 3-hydroxyvaline have been measured, and in smokers, whose hemoglobin has been found to contain levels of 4-aminobiphenyl and 3-hydroxyvaline that were correlated with the frequency of cigarette smoking. Detection of DNA adducts of genotoxic agents in the cells and tissues of exposed individuals has also been accomplished through the use of several types of analytical methods. Immunoassays and physicochemical methods have been applied to detect adducts formed through the major intermediate in the activation of benzo(a)pyrene, the 7,8-diol-9,10-epoxide (BPDE). This adduct has been found in the DNA of peripheral leukocytes of workers in foundries, aluminum manufacturing plants, roofers, and coke oven plants, and also in cigarette smokers.(ABSTRACT TRUNCATED AT 250 WORDS)