tbuckley/cabot-search huggingface dataset:
The Resistance Factor to<i>Plasmodium vivax</i>in Blacks
Authors: Louis H. Miller, Steven J. Mason, David F. Clyde, Mary H. McGinniss
Journal: New England Journal of Medicine (1976)

Duffy-blood-group-negative human erythrocytes, FyFy, are resistant to invasion in vitro by Plasmodium knowlesi. The FyFy genotype is found predominantly in African and American blacks, who are the only groups completely resistant to infection by P. vivax. To determine if the FyFy genotype is the vivax resistance factor, we performed blood typing on 11 black and six white volunteers who had been exposed to the bites of P. vivax-infected mosquitoes. Only the five FyFy blacks were resistant to erythrocytic infection; the remaining six blacks and all whites had the Duffy-positive determinants (Fya or Fyb or both) and had contracted malaria. We conclude that Duffy determinants (Fya or Fyb or both) on the erythrocyte surface are required for invasion of erythrocytes by vivax merozoites.
Iodine and Thyroid Cancer
Authors: Joan Stephenson
Journal: JAMA (2005)

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 Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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) 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 16638: Effect of Eplerenone According to Qrs Duration and Morphology in Emphasis-HF
Authors: Jane Cannon, Timothy Collier, Karl Swedberg, Henry Krum, Dirk J van Veldhuisen, John Vincent, Stuart Pocock, Bertram Pitt, Faiez Zannad, John McMurray
Journal: Circulation (2014)

Background: The importance of QRS duration (QRSd) and QRS morphology (left and right bundle-branch block [LBBB, RBBB], interventricular conduction defect [IVCD]) as predictors of prognosis and value in selecting patients for device therapy is increasingly recognized. We examined the effect of eplerenone in heart failure with reduced ejection fraction (HF-REF), according to QRSd/morphology in EMPHASIS-HF.

Methods: Patients were categorized as: QRSd (msec) a) <120 (n=1375), b) 120-149 (n=517) and c) 150+ (n=383) and QRS morphology i) normal (n=1252), ii) RBBB/IVCD (n=415) and iii) LBBB (n=608); 462 patients were excluded because of missing or incorrect ECG data. Occurrence of the primary composite outcome of cardiovascular death or heart failure hospitalization was estimated in patients randomized to placebo or eplerenone. The effect of eplerenone was adjusted for the previously described predictors of the primary outcome in EMPHASIS-HF.

Results: Both prolonged QRSd and abnormal QRS morphology were associated with increased risk. Eplerenone reduced the risk of the primary outcome, compared with placebo, in all patients (n=2275) with ECG data (HR 0.71, 95% CI 0.60-0.84 p<0.001) and this beneficial effect was consistent across QRSd and QRS morphology subgroups (Table).

Conclusion: We confirmed the association between QRS prolongation and adverse outcomes in HF-REF. Eplerenone was similarly effective, irrespective of QRSd and morphology.

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Fetal Microchimeric Cells and Breast Cancer—Reply
Authors: Kirby L. Johnson, Kiarash Khosrotehrani, Dong Hyun Cha, Robert N. Salomon, Diana W. Bianchi
Journal: JAMA (2004)

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In vitro chemosensitivity testing in invasive breast cancer: Increased sensitivity of the basal subtype is not independent of the tumor proliferation rate
Authors: Cornelia Liedtke, Jens Packeisen, Hartmut Schmidt, Eberhard Korsching, Pia Wuelfing, Burkhard Brandt, Ludwig Kiesel, Horst Buerger
Journal: Clinical Cancer Research (2006)

B15   Background:Advances in adjuvant breast cancer treatment have contributed to decreasing numbers of breast cancer deaths in developed countries. However, decision making on whether to opt for adjuvant chemotherapy regimens in a given patient and on which regimen to choose has long been restricted to evidence derived from clinical trials as well to single prognostic and predictive markers. A putative relationship between different molecular and phenotypic breast cancer subgroups and neoadjuvant chemotherapy response has recently been proposed. In vitro chemotherapy sensitivity and resistance assays (CSRAs) as a means to directly evaluate a tumors response to a given drug have been proposed repeatedly as a novel important tool in a more patient-tailored chemotherapeutic approach.Materials and Methods:In order to reveal correlations between in vitro chemosensitivity and different phenotypic breast cancer subgroups, tissue microarrays of 550 invasive breast cancers were composed and investigated for the expression of the estrogen receptor (ER), the progesterone receptor (PR), bcl-2, Cyclin D1, Epithelial Membrane Antigen (EMA), p53, EGFR, vimentin, Ck 5, Ck 14, Ck 19, erbB2 and Mib-1. All carcinomas have been subjected to 4 different  in vitro  chemotherapy protocols (DOCET, EC, MIT, PAEP) and sensivity had been established based on adenosine triphosphate bioluminescence assay technique.Results:Our results show that the expression of EGFR, Ck 5, vimentin and to a lesser degree of p53 and Ck 14 were significantly associated with a clearly increased in vitro chemosensitivity. In contrast, proteins described to characterize the luminal subtype, including ER and bcl-2 were inversely correlated with in vitro chemosensitivity. However, a more detailed analysis showed that these results were not independent of the proliferation rate i.e. increased Mib-1 expression.DISCUSSION:Other groups have already found evidence for an altered sensitivity towards various chemotherapy regimens based on luminal or basal tumor features. In our approach we could make the same observation, however, differences in response to chemotherapy were not independent of Mib-1 expression levels. We see these results as an important indicator, that the increased chemosensitivity in basal and the reduced chemosensitivity in luminal breast cancers, respectively, are mainly determined by the differing proliferation rate rather than to the phenotypic subtypes.
The Three-Legged Stool
Authors: Harold W Horowitz
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
Sibling Exposure and Risk of Juvenile Idiopathic Arthritis
Authors: Jessica Miller, Anne‐Louise Ponsonby, Angela Pezic, Andrew Kemp, Susan E. Piper, Jonathan D. Akikusa, Roger C. Allen, Jane E. Munro, Justine A. Ellis
Journal: Arthritis & Rheumatology (2015)

Objective Susceptibility to juvenile idiopathic arthritis (JIA) is presumed to be determined by both genes and environment. However, the environmental factors remain largely unknown. The hygiene hypothesis suggests that exposure to siblings, as a marker of exposure to microbes in early life, may protect against the development of later immune disorders. Some prior evidence suggests this may also be true for JIA. The present study was undertaken to test this hypothesis in detail. Methods We conducted a comprehensive analysis of the role of sibling exposure in JIA risk within the Childhood Arthritis Risk Factor Identification Study JIA case–hospital control sample (302 cases and 676 controls) from Victoria, Australia. Results We found that, compared to being an only child, having any siblings was protective against JIA, with an adjusted odds ratio (OR) of 0.46 (95% confidence interval [95% CI] 0.28–0.74) ( P = 0.001). The protective association appeared to increase with increasing number of siblings (e.g., for ≥3 siblings, adjusted OR 0.25 [95% CI 0.13–0.48], P &lt; 0.001). A protective association of siblings was also observed when we considered cumulative sibling years by age 6 (e.g., for ≥3 years of exposure versus no exposure, adjusted OR 0.49 [95% CI 0.30–0.79], P = 0.003). We also compared cases to a second control sample (n = 341) collected from the community and weighted to represent the child population of Victoria. Data remained supportive of an association between sibling exposure and protection against JIA, particularly for exposure to younger siblings. Conclusion Increased exposure to siblings is associated with a reduced risk of disease in our sample. This suggests that increased microbial exposure in childhood may confer protection against the development of JIA.
Abstract P131: Association between Marijuana Exposure and Cognitive Function in Middle Age: the Coronary Artery Risk Development in Young Adults (CARDIA) study.
Authors: Reto Auer, Eric Vittinghoff, Kristine Yaffe, Stefan G Kertesz, Deborah A Levine, Steve Sidney, M. Maria Glymour, Mark J Pletcher
Journal: Circulation (2014)

Background: Smoking marijuana is increasingly common, and understanding whether it is associated with long-term cognitive dysfunction has important implications for public health messaging. Aims: We estimated associations between cumulative exposure to marijuana and cognitive function (CF), adjusted for current marijuana use, cigarette smoking and other determinants of CF. Methods: Participants in the CARDIA Study, a population-based study of African Americans and European Americans recruited in 1985/6 at age 18-30 and followed over 25 years. Marijuana use was assessed at clinical visits at years 0, 2, 5, 7, 10, 15, 20 and 25 (2010/11); and cigarette smoking each year. Lifetime exposure to marijuana was expressed in joint-years, with 1 joint-year equivalent to smoking 365 joints. CF at year 25 was assessed with the Rey Auditory Verbal Learning Test (RAVLT), the Digit Symbol Substitution Test (DSST) and the Stroop Interference Test, each expressed as standardized z-scores. We estimated associations between current and lifetime marijuana exposure and each CF score using linear regressions, adjusted for baseline demographics, current smoking and diabetes and cumulative exposure to cigarette smoking, alcohol, illicit drugs, cardiovascular risk factors, physical activity and depression (see Table footnote). Results: Of 3385 participants with CF data, 24% had never reported marijuana use, 43% had smoked &lt;0.5 joint-year during their lifetime, 22% 0.5 to 5 joint-years and 11% ≥5 joint-years; 9% had smoked marijuana within the last 30 days. In adjusted models, current marijuana use was significantly associated with a worse RAVLT test score, but we found no association between cumulative exposure to marijuana use and CF (Table). In contrast, current and cumulative exposure to cigarette smoking were associated with lower CF. Conclusion: Cigarette smoking (current and cumulative) and current marijuana use are associated with lower CF, but we found no evidence of an association with cumulative lifetime exposure of marijuana on CF.
Abstract 3934: Angiogenin and PlexinB2 promote glioblastoma progression by stimulating tumor angiogenesis, cancer cell survival and invasion
Authors: Hailing Yang, Guo-fu Hu
Journal: Cancer Research (2014)

Abstract Glioblastoma (GBM) tumors secrete high level of angiogenic factors and feature vascular abnormality. Targeted therapy, such as Bevacizumab, which neutralizes VEGF and normalizes tumor vasculature, has been approved to treat recurrent GBM. However, it only marginally increases patients' overall survival with inevitable resistance. It suggests that therapy targeting complementary angiogenic pathway in GBM could suppress Bevacizumab resistance and extend patients' survival. Angiogenin (ANG) is involved in tumor angiogenesis where it regulates ribosomal RNA transcription and functions downstream of VEGF and other related angiogenic factors. Like VEGF, ANG is also up-regulated in GBM patients. Inhibition of ANG by neutralizing monoclonal antibody delays U87 human GBM xenografts on nude mice. My preliminary data have shown that ANG is essential for GBM cell line s.c. vessel formation and tumor proliferation. In Rcas/tva orthotropic GBM model, Ang1 knockout mice show lower penetration and better survivals. ANG knockdown increases apoptosis during GBM cell line colony formation in agarose. Notably, ANG's role in tumor proliferation might extend beyond GBM, since oncogenic KRas transformed Ang1 knockout MEFs also fail to grow in agarose. Lastly, I have shown that PlexinB2, ANG cellular receptor, can mediate ANG cellular uptake and also modulate GBM apoptosis in agarose. In conclusion, inhibition of ANG inhibits GBM progression both in vitro and in vivo and thus represents a new molecular target for GBM treatment. Citation Format: Hailing Yang, Guo-fu Hu. Angiogenin and PlexinB2 promote glioblastoma progression by stimulating tumor angiogenesis, cancer cell survival and invasion. [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 3934. doi:10.1158/1538-7445.AM2014-3934
High court upholds GMC's rejection of case against neurologist
Authors: Clare Dyer
Journal: BMJ (2007)

The General Medical Council has comprehensively defeated a challenge in the High Court by the Singapore Medical Council to the GMC's decision to drop a disciplinary case against the British neurologist Simon Shorvon over a research project he headed in Singapore ( BMJ 2003;326:839). 

The Singapore council found Professor Shorvon guilty of professional misconduct in February 2004 over the $S10m (£3.3m; €5m; $6.5m) project, which was halted amid allegations that researchers breached confidentiality, failed to obtain informed consent, and disregarded the best interests of vulnerable patients. 

The GMC was alerted to the allegations by an article in the Guardian newspaper in January 2003 (www.guardian.co.uk/uk_news/story/0,,878047,00.html) and by Professor Shorvon, who referred his own case to the council. When the case reached the investigation committee of the fitness to practise panel, the chairman decided …
Abstract # 12275: Determination of the Myocardial Area at Risk after Reperfused Acute Myocardial Infarction with Different Imaging Techniques: Cardiac Magnetic Resonance
Authors: Nathan Mewton, Stanislas Rapacci, Lionel Augeul, Rene Ferrera, Joseph Loufouat, Alejandra Micolich, Loic Boussel, Gilles Rioufol, Didier Revel, Pierre Croisille, Creatis Lrmn, Michel Ovize
Journal: Circulation (2010)

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Nathan Mewton, 2010 Finalist and Presenting Author

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Promoter activation of 15-Lipoxygenase-2 by radiation in prostate cancer cells
Authors: Ying Feng, Qiuhui Yang, Dian Wang
Journal: Cancer Research (2006)

Proc Amer Assoc Cancer Res, Volume 47, 2006

4396 

Purpose: Radiation treatment is one of the main therapeutic modalities for prostate cancer. 15-Lipoxygenase-2 (15-Lox-2) is found to be a negative cell-cycle regulator in normal prostate epithelial cells and a functional prostate tumor suppressor. In this study, we investigate if therapeutic doses of radiation are able to activate 15-LOX-2 promoter. Methods: We first cloned upstream promoter structure fragments of 715 bp and 340 bp using fetal skin genomic DNA as a template. The PCR products were gel purified and cloned respectively into the T/A vector pCRII, which were transformed into OneShot cells. Target DNAs were then cloned into pGAW expression vector, which were called pLox2/715 and pLox2/314. These two 15-Lox-2 expression vectors were then transfected into prostate cancer cells LNCAP, which is a known hormone sensitive cells. Twenty four hours later, these transfected cells then received external beam radiation treatment with a dose of 2, 4, 6, 8 Gy in triplicates, respectively. Cells were harvested into lysis buffer 48 hours after radiation. Lysates containing equal amounts of protein were assayed for luciferase activity using luciferase assay kit. After subtracting the baseline values, the relative luciferase unit (RLU) activity was determined as the ratio of luciferase/ - gal activities. The relative promoter activities were expressed as either RLU or relative values (i.e. % or fold increase). DNA binding factors PPARγ and CEBP-α were also measured in the transfected cells when compared with control cells using Western blotting analysis. Results: Luciferase activities of 15-Lox-2 promoter fragments significantly increased up to approximately 150% by therapeutic doses of radiation. 715bp-fragment was maximally induced by radiation of 4 Gy. PPARγ significantly increased while CEBP-α significantly decreased in the transfected cells treated by radiation of 4 Gy. Conclusion: Results from this study suggested that therapeutic doses of radiation activated the promoter of 15-LOX-2. This suggested a potential role of radiation induced gene therapy involving 15-Lox-2. In addition, DNA binding factors PPARγ and CEBP-α may play an important role in mechanisms of the promoter activation of 15-Lox-2 by radiation.
The Limitations of Heliotherapy in Pulmonary Tuberculosis
Authors: Bernard Langdon Wyatt
Journal: Annals of Internal Medicine (1930)

Article1 October 1930The Limitations of Heliotherapy in Pulmonary TuberculosisBERNARD LANGDON WYATTBERNARD LANGDON WYATTSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-4-4-376 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptIn this discussion of heliotherapy in pulmonary tuberculosis from the standpoint of its limitations, it must be emphasized at the beginning that reference is made primarily to personal experiences under meteorologic conditions that prevail in Southern Arizona. No attempts at "generalizations" will be made for a number of obvious reasons, among which only one will be noted; i.e., that qualitatively and quantitatively these solar radiations are not identical with those at other latitudes and altitudes, not to mention the meteorologic variables peculiar to the desert.Not only will all generalizations be omitted, but also, there will be no discussion of... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Tucson, Arizona*Presented at the Fourteenth Annual Clinical Session of the American College of Physicians, February 14, 1930, Minneapolis, Minn. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 October 1930Volume 4, Issue 4Page: 376-378 ePublished: 1 December 2008 Issue Published: 1 October 1930 PDF downloadLoading ...
Keratinocyte growth factor facilitates alloengraftment and ameliorates graft-versus-host disease in mice by a mechanism independent of repair of conditioning-induced tissue injury
Authors: Angela Panoskaltsis-Mortari, Patricia A. Taylor, Jeffrey S. Rubin, Aykut Uren, Lisbeth A. Welniak, William J. Murphy, Catherine L. Farrell, David L. Lacey, Bruce R. Blazar
Journal: Blood (2000)
Abstract 15881: Delayed Enhancement in Hypertrophic Cardiomyopathy Is Related to Perfusion Abnormalities: An Ischemia-Fibrosis Connection
Authors: Paco E Bravo, Miguel Santaularia, Stefan Zimmerman, Aurélio Pinheiro, Takahiro Higuchi, Richard L Wahl, Roselle M Abraham, Frank M Bengel, Theodore Abraham
Journal: Circulation (2011)

Paco E Bravo, 2011 Finalist and Presenting Author
Skin self-examination and the ABCDE rule in the early diagnosis of melanoma: is the game over? Reply from author
Authors: L. Titus
Journal: British Journal of Dermatology (2013)

We thank De Giorgi et al. for their letter,1 and for the opportunity to clarify our findings and conclusions.2 It is challenging to interpret the influence of screening on melanoma incidence and mortality rates. Recent data from developed areas, including the U.S.A. and much of Europe, generally show increases in melanoma incidence, with the greatest increases affecting older age groups.3, 4 Mortality rates have stabilized or decreased in the younger age groups, and increased in the older age groups.3, 4 In Australia, incidence is increasing overall, but stabilizing in the youngest age groups,5 whereas melanoma mortality is decreasing in the youngest age groups, levelling in the middle age groups and increasing in those aged ≥ 80 years.6 Worldwide, mortality rates have not kept pace with increasing incidence, giving rise to the notion of overdiagnosis – the unnecessary removal of indolent melanomas that are not life threatening. In support of overdiagnosis, De Giorgi et al. cite a recent U.S. ecological study showing elevated rates of biopsy and melanoma incidence in older age groups (≥ 65 years).7 Under the assumption that melanoma incidence rates are stable, these authors propose that rising biopsy rates are responsible for a spurious spike in incidence.7 It is impossible, of course, to determine the extent to which increasing melanoma incidence is due to excessive biopsy, or due to true increases in underlying incidence rates. However, we do know that melanoma mortality rates in the U.S.A.3 are increasing sharply in the same ≥ 65 years age group, especially among men, suggesting that true increases of incidence are responsible for the increased biopsy rates, rather than the other way around. Further evidence supporting true elevations in incidence is provided by a recent U.S. study showing rising incidence for deeper tumours, and increasing incidence across all socio‐economic strata, considered a surrogate for access to screening.4 Although the question of overdiagnosis will likely remain controversial, improvements in survival and mortality, where evident, may reflect a true benefit of early detection.4, 5, 8