tbuckley/cabot-search huggingface dataset:
Abstract 18307: Prevalence, Predictors and Prognostic Impact of High On-treatment Platelet Reactivity to Aspirin and Clopidogrel in Patients With Symptomatic Peripheral Artery Disease in Japanese Population
Authors: KEIKO FUKINO, Koji Hozawa, Takahiro Matsumoto, Hisaaki Ishiguro, Sunao Nakamura
Journal: Circulation (2014)

Introduction: High on-treatment platelet reactivity (HPR) is associated with increased risk of ischemic events and therapeutic failure in patients with coronary artery disease, whereas its role in patients with peripheral artery disease is not widely reported. Purpose: This study aims to investigate the prevalence of HPR in patients with symptomatic peripheral artery disease and its possible predictors in Asian population. Methods: Among patients who underwent endovascular therapy at our institution during September 2013 to April 2014, 125 patients who received aspirin and/or clopidogrel were included. Residual platelet reactivity was assessed with VerifyNow aspirin and P2Y12 assays. HPR was defined as aspirin reaction units (ARU) ≧ 550 for aspirin and P2Y12 reaction units (PRU) ≧ 235 for clopidogrel. Results: The prevalence of HPR to aspirin was not significantly different between patients with intermittent claudication (IMC) and critical limb ischemia patients (22.2% and 23.2%, respectively), whereas the prevalence of HPR to clopidogrel was higher in CLI patients, especially in patients with tissue loss compared to IMC patients (39.3% and 62.5%, respectively, p&lt;0.05). 7.7% of IMC patients and 12.5% of CLI patients showed HPR to both aspirin and clopidogrel. Multivariate analysis revealed that age and diabetes were independent predictors for HPR to clopidogrel. Conclusion: HPR to aspirin and/or clopidogrel was highly prevalent in symptomatic PAD patients in Japanese population. The prevalence of HPR was significantly higher in patients with tissue loss compared with those without. Optimizing antiplatelet regimen according to residual platelet reactivity in CLI patients would be indispensable to avoid repeat revascularization and unexpected amputation.
Abstract B09: Phosphorylation of BRAF by AMPK impairs BRAF-KSR1 association and cell proliferation
Authors: Che-Hung Shen, Ping Yuan, Rolando Perez-Lorenzo, Yaqing Zhang, Sze Xian Lee, Yang Ou, Li Cai, John M. Asara, Lewis C. Cantley, Bin Zheng
Journal: Cancer Research (2015)

Abstract BRAF is an oncogenic protein kinase that drives cell growth and proliferation through the MEK-ERK signaling pathway. BRAF inhibitors have demonstrated antitumor efficacy in melanoma therapy but have also been found to be associated with the development of cutaneous squamous cell carcinomas (cSCCs) in certain patients. Here, we report that BRAF is phosphorylated at Ser729 by AMP-activated protein kinase (AMPK), a critical energy sensor. This phosphorylation promotes the association of BRAF with 14-3-3 proteins and disrupts its interaction with the KSR1 scaffolding protein, leading to attenuation of the MEK-ERK signaling. We also show that phosphorylation of BRAF by AMPK impairs keratinocyte cell proliferation and cell-cycle progression. Furthermore, AMPK activation attenuates BRAF inhibitor-induced ERK hyperactivation in keratinocytes and epidermal hyperplasia in mouse skin. Our findings reveal a mechanism for regulating BRAF signaling in response to energy stress and suggest a strategy for preventing the development of cSCCs associated with BRAF-targeted therapy. Citation Format: Che-Hung Shen, Ping Yuan, Rolando Perez-Lorenzo, Yaqing Zhang, Sze Xian Lee, Yang Ou, Li Cai, John M. Asara, Lewis C. Cantley, Bin Zheng. Phosphorylation of BRAF by AMPK impairs BRAF-KSR1 association and cell proliferation. [abstract]. In: Proceedings of the AACR Special Conference on Advances in Melanoma: From Biology to Therapy; Sep 20-23, 2014; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(14 Suppl):Abstract nr B09.
PERIARTERITIS NODOSA WITH A CASE REPORT
Authors: K. Yardumian, R. Robert Cohen
Journal: Annals of Internal Medicine (1937)

Case Reports1 April 1937PERIARTERITIS NODOSA WITH A CASE REPORTK. YARDUMIAN, M.D., R. ROBERT COHEN, M.D.K. YARDUMIAN, M.D.Search for more papers by this author, R. ROBERT COHEN, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-10-10-1582 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptDiffuse vascular lesions with bizarre clinical symptoms of general systemic infection have been reported under various names both in this country and abroad. Because the majority of these cases, unfortunately, have not been diagnosed during the course of the illness, it is apparent that one should keep in mind the possibility of periarteritis nodosa in patients with indefinite symptoms of infection without known etiology and in which all the laboratory studies throw no light on the case.As one of these, we wish to present the following case of periarteritis nodosa which was missed clinically and even on gross postmortem...Bibliography1. BEATTIEDICKSON JMWE: A textbook of pathology, 1926, C. V. Mosby Co., St. Louis, p. 556-555. Google Scholar2. DERICKHASS CLGM: Diffuse arteritis of syphilitic origin, Am. Jr. Path., 1935, xi, 291-307. Google Scholar3. BOYD W: Pathology of internal medicine, 1932, Lea and Febiger, Philadelphia. Google Scholar4. BERNSTEIN A: Case without peripheral nodules, diagnosed antemortem, Am. Jr. Med. Sci., 1935, clxl, 317-325. CrossrefGoogle Scholar5. HAININGKIMBALL RBTS: Polyarteritis nodosa, Am. Jr. Path., 1934, x, 349-360. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Pittsburgh, Pennsylvania*Received for publication January 20, 1937.From the Department of Pathology, Isaac Kaufmann Foundation, Montefiore Hospital Pittsburgh, Pennsylvania. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 April 1937Volume 10, Issue 10Page: 1582-1588KeywordsEtiologyLesionsResearch laboratories ePublished: 1 December 2008 Issue Published: 1 April 1937 PDF downloadLoading ...
LESSONS FROM SERUM CHOLESTEROL STUDIES IN JAPAN, HAWAII AND LOS ANGELES
Authors: A KEYS, N KIMURA, A KUSUKAWA, B BRONTE-STEWART, N LARSEN, M H KEYS
Journal: Annals of Internal Medicine (1958)

ExcerptTwo years ago, at the meeting of the College in Philadelphia, we reported some of our findings in South Africa. These data were in conformity with the hypothesis that dietary fat is an important element in the remarkable differences between populations in the frequency of coronary heart disease.1, 2It is now possible to report related findings in Japan and on Japanese in Hawaii and in Los Angeles.The basic question under investigation is this: What causes the striking differences in the frequency of coronary heart disease in different populations? Research on this question, and related studies on the cholesterol...
Abstract 17555: Prognostic Impact of Tissue Protrusion After Stenting in Patients With Acute Coronary Syndrome: an Optical Coherence Tomography Study
Authors: Benjamin Bonnet, Fiona Ecarnot, Philoktimon Plastaras, Jian-Feng Huang, Marie-France Seronde, Romain Chopard, Francois Schiele, Nicolas F Meneveau
Journal: Circulation (2014)

Background: Optical Coherence Tomography (OCT) has been studied in stent implantation to assess post-procedural results, with a view to optimizing outcomes but the real clinical impact of OCT-defined abnormalities remains unknown. We investigated the prognostic impact of tissue protrusion between stent struts after stent implantation in patients with non-ST elevation acute coronary syndromes (NSTEACS).

Methods: Prospective study of consecutive pts with NSTEACS (≤ 72 h) undergoing PCI for an infarct-related artery presenting a single lesion without diffuse disease on the culprit artery. Patients were treated at the operator’s discretion according to guidelines. OCT was performed after initial angiography and at the end of the angioplasty procedure. Tissue prolapse was defined as projection of tissue (plaque or thrombus) into the lumen between stent struts after implantation. The primary endpoint of procedural complications associated no reflow, and PCI-related myocardial infarction (MI) as defined by a 20% rise in troponin over baseline levels at 24h. Secondary endpoint was the functional result of angioplasty assessed by fractional flow reserve (FFR) measured at the end of the procedure.

Results: 43 patients were included, mean age 63±11 years, 90% men. Tissue protrusion was observed in 35 (81%), with this tissue taking up a median 8.85% [IQR 6.2-14.2%] of the intra-luminal area over a median length of 2.8mm [IQR 1.4-5.2]. Presence of tissue protrusion through the struts was not associated with cardiovascular risk factors or pre-treatment with aspirin, thienopyridines, antiGP IIb/IIIa or anticoagulants. Tissue protrusion had no impact on procedural complications or FFR (Table).

Conclusion: Tissue protrusion through the struts after stent implantation is common on OCT in NSTEACS patients undergoing angioplasty and stenting. It occludes on average 10% of the intra-stent area, but does not seem to limit flow or impact on post-procedural complications.

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Synthetic Thyroxine vs Dessicated Thyroid—Reply
Authors: Patrick W. Clyde, Amir E. Harari, K. M. Mohamed Shakir
Journal: JAMA (2004)

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 molecular basis of glucocorticoid-induced skin atrophy: topical glucocorticoid apparently decreases both collagen synthesis and the corresponding collagen mRNA level in human skin<i>in vivo</i>
Authors: None Oikarinen, None Haapasaari, None Sutinen, None Tasanen
Journal: British Journal of Dermatology (1998)

The effects of topical betamethasone‐17‐valerate on collagen propeptide levels, collagen mRNA level, lysyl oxidase mRNA and matrix metalloproteinase (MMP)‐1 and MMP‐2 mRNA levels were studied in human skin. Three days' treatment of healthy skin with topical betamethasone caused a 70–80% decrease in type I and III collagen propeptides in suction blister fluid. A similar decrease was found in type I collagen mRNA when assayed by either slot‐blot hybridization or a quantitative polymerase chain reaction method, indicating that the decrease in collagen synthesis after topical glucocorticoid treatment is apparently due to a decrease in corresponding mRNA. mRNA of lysyl oxidase, which is an important enzyme catalysing the cross‐linking of collagen chains, and collagen‐degrading enzyme MMP‐1 and MMP‐2 mRNAs were not decreased in the same skin samples. This suggests that in vivo, glucocorticoids modulate variably the genes involved in collagen synthesis and degradation. Our study provides a solid molecular basis for glucocorticoid‐induced dermal atrophy, which results from the decrease in functional collagen mRNA in the skin.
Sir William Pepperrell and His Family
Authors: M. Therese Southgate
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
Primary refractory disease in non-Hodgkin lymphoma (NHL): Occurence, clinico-pathological features, and outcome
Authors: Francesco d'Amore, Peter de Nully Brown, Lars Møller Pedersen, Bjarne Bach Pedersen, Michael Pedersen, Ole Vestergaard Gadeberg, Anne Bukh, Mads Hansen, Stanislav Pulczinsky, Steen Ingerslev, Torben Mouritz Andersen, Mikael Frederiksen, Michael Boe Møller, Leif Spange Mortensen
Journal: Annals of Oncology (2008)
The relationship between smoking habit and tuberculosis in patients under anti-TNF-α treatment
Authors: Sermin Borekci, Berna Duman, Nejdiye Mazican, Ersan Atahan, Benan Musellim, Gul Ongen, Vedat Hamuryudan
Journal: European Respiratory Journal (2013)

Aim: There are studies on smoking increases the risk of tuberculosis(TB),but this relationship is unclear.TNF-α inhibitors used in the treatment of various immune-related diseases,and are known to increase the risk of development TB.In this study,we investigated the effect of smoking habit on the risk of TB in patients under the anti-TNF-α treatment.

Method: Between October 2003 and January 2013,in accordance with the criteria of RAED II Consensus Report of TNF-α inhibitors in total 2930 patients with various diagnoses were retrospectively evaluated.Smoker and nonsmoker patients were compared according to risk of TB. Statistical analysis was done by using SPSS15.0 software.

Results: 1494(%51) patients were male, 1436(%49) were female, mean age was 40,1±14,4 years. At admision the distribution of primary diseases was: ankylosing spondylitis (n=1130, 36.8%), rheumatoid arthritis (n=951,32.0%), psoriatic arthritis (n=251,8.6%), juvenile rheumatoid arthritis (n=153,5.2%), Behcet’s disease (n=118,0.4%), Crohn disease (n=100,3.6%). 1279 patients (43.7%, male=856, female=423) were smoker (mean 15.2 ±13.3 packet-year). 10 patients (male=6, female=4) developed TB (341/100.000)[3 miliary TB,3 TB pleurisy,1 TB of ear,1 TB of intestine,2 pulmonary TB;8 patients of 10 TB cases (80%);and all of 5 extrapulmonary TB cases (100%) were smoker ]. TB was statistically significantly higher(P<0.05) in patients who are smoker.

Conclusion :The risk of tuberculosis especially extrapulmonary tuberculosis is increased in patients under anti-TNF-α treatment,this risk is higher in patients who are smoker.The patients using TNF-α inhibitors should be monitored closely for tuberculosis and encouraged for smoking cessation.
Risks and Benefits of Resumption of Anticoagulation Following Traumatic Brain Injury Remain Complex and Uncertain
Authors: Ramesh Grandhi, Lori A. Shutter, David O. Okonkwo
Journal: JAMA Internal Medicine (2015)

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 Internal Medicine HomeNew OnlineCurrent IssueFor Authors Podcast 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 Internal Medicine journal
Overexpression of Protein Kinase C Isoform  but not δ in Human Interleukin-3–Dependent Cells Suppresses Apoptosis and Induces bcl-2 Expression
Authors: E. Gubina, M.S. Rinaudo, Z. Szallasi, P.M. Blumberg, R.A. Mufson
Journal: Blood (1998)
Abstract 07: Trajectories of Weight Change and Their Association with Barriers to Healthy Eating during 18-month Weight Loss Treatment
Authors: Yaguang Zheng, Susan M Sereika, Christopher C Imes, Lei Ye, Meghan Mattos, Juliet M Mancino, Cynthia Danford, Lora E Burke
Journal: Circulation (2014)

Introduction: Obesity research has typically focused on the overall weight change pattern in randomized clinical trials (RCTs), ignoring the clustering of individuals with distinct weight change patterns (e.g., continuing to lose, maintain weight loss, or regain weight). The study aim was to identify trajectories of weight change and their associated predictors. Methods: This was a secondary analysis of longitudinal weight data pooled from two RCTs using standard behavioral treatment for weight loss. Weight was measured using a digital scale at baseline, 6, 12 and 18 mos. Group-based trajectory modeling was used to identify distinct classes of trajectories of percent weight change. Percent change in Barriers to Healthy Eating (BHE) subscale scores (emotions, daily mechanics and social support) were simultaneously added in the final trajectory model to examine their associations with weight change trajectories. Results: The pooled sample included 338 adults, which was mostly female (85.2%), White (73.7 %), 45.7±9.0 years old with 15.6±2.8 years of education, and a BMI of 33.9±4.3 kg/m2. As shown in the graph, three trajectory groups were identified: maintainers, regainers, and non-responders. Percent weight change was associated with BHE emotions (b=.053, p&lt;.001) as well as social support (b=0.029, p=.003) for maintainers, emotions for regainers (b=0.071, p&lt;.001), and daily mechanics for nonresponders (b=0.059, p &lt;.001). Conclusions: This is the first study to identify distinct weight loss trajectories during active weight loss treatment for adults. What distinguished the maintainers from the regainers was the level of perceived barriers related to managing emotions and the availability of social support, while the group that was unsuccessful at achieving a clinically significant weight loss was challenged by the daily mechanics of adopting a healthy diet. The dimensions of barriers to healthy eating associated with weight change trajectories vary and should be considered in future weight loss programs.
216. Gene Therapy of Huntington Disease Using RNA Interference and Sleeping Beauty Transposon
Authors: Zongyu J. Chen, Xiaoming Ma, Philip Wong, Mikel Roe, Chang-won Park, Betsy T. Kren, Walter C. Low, Clifford J. Steer
Journal: Molecular Therapy (2004)

Huntington Disease (HD) is a devastating neurologic disorder that is characterized by the abnormal expansion of a CAG repeat in the first exon of the huntingtin gene. This expansion results in the expression of a mutant huntingtin protein with an elongated polyglutamine stretch. The presence and aggregation of this mutant protein is responsible for the characteristic loss of the striatal neurons in HD leading to the clinically observed motor, psychiatric and cognitive deficits. Currently there is no effective treatment to prevent the neuronal loss associated with HD. The aim of this study was to evaluate an innovative gene therapy strategy combining RNA interference (RNAi) and gene transfer via the nonviral Sleeping Beauty (SB) transposon (Tn) system to mitigate the detrimental effects of the mutant huntingtin protein. While RNAi has been successfully used to suppress mammalian gene expression, a major shortcoming is the transient nature of the effect due to the intracellular degradation of the synthetic small interfering RNA (siRNA) molecules and/or the vector encoding the siRNA. By integration of the siRNA construct into the host genome via SB-mediated transposition, long-term suppression of gene expression can be achieved. SB is a functional vertebrate class II Tn element that mediates successful chromosomal insertion and long-term expression of its cargo transgenes in both cell culture and in vivo. We have constructed SB-Tns carrying siRNA transgenes targeting Exons 1, 7 and 62 of the human huntingtin gene. Real-time RT-PCR was used to quantify the huntingtin mRNA transcript levels in human neuroblastoma cells following transfection of the siRNA SB-Tns. In addition, DNA was isolated and subjected to bisulfite-mediated genomic sequencing to determine changes in methylation patterns. The results indicated that significant decreases up to 80% in huntingtin mRNA transcript levels relative to control were observed with several of the siRNA constructs. Interestingly, there was no evidence of increased methylation of CpGs in the regions of the hungtingtin sequence targeted by the siRNAs, suggesting that these specific siRNAs do not invoke epigenetic genomic modification. In addition, stereotaxic injection of an SB-Tn DsRed2 vector into the brains of HD transgenic mice resulted in significant expression of the reporter construct. In conclusion, huntingtin-specific siRNA constructs can down regulate huntingtin gene expression in cell culture. When delivered by the nonviral SB transposon, such constructs can potentially lead to long-term suppression of the mutant huntingtin gene expression, thus obliterating the harmful effects of the mutant protein. The combination of siRNAs, the SB transposon and an accurate transgenic mouse model now allows us to pursue a gene therapy approach for the treatment of HD.
Two weeks of postsurgical therapy may be enough for high-risk cases of endocarditis caused by Streptococcus viridans or Streptococcus bovis
Authors: P. Muñoz, M. Giannella, F. Scoti, M. Predomingo, D. Puga, A. Pinto, J. Roda, M. Marin, E. Bouza
Journal: Clinical Microbiology and Infection (2011)