tbuckley/cabot-search huggingface dataset:
The possibility of using the level of concentration Fe2 + in the exhaled breath condensate as a diagnostic indicator in pulmonary pathology
Authors: Elena Zaprudnova, Svetlana Soodaeva, Igor Klimanov, Timur Li, Lidiya Nikitina, Fedor Petrovskiy
Journal: European Respiratory Journal (2013)

The aim was to study the level of concentration of Fe2+ in exhaled breath condensate of smokers compared with non-smokers during exercise, as well as in patients with bronchial asthma (BA).

Methods. The control group consisted of healthy (those with no diagnosed respiratory disease), non-smokers aged 25 - 45 years. The second group included smokers aged 25 - 45 years old, diagnosed as those with no respiratory disease. Smoking history of 10 or more years. The third group consisted of non-smokers aged 25 - 45 years of age with asthma. Level of Fe2+ was determined by the ferrozin method at rest and after exercise (at a heart rate of 100-120 beats per minute) in both healthy and smokers than patients with asthma.

Results. The study found that smokers there is an increase in the basal concentration of Fe2+ 2-fold in the lung tissue compared to healthy nonsmokers (p <0.05). Fe2+ content of smokers during exercise is 1.4 times higher than in non-smokers (p <0.05). BA patients also noted a change in the level of Fe2+ EBC. During exacerbation of asthma occurred increase in Fe2+ 1.6-fold compared with healthy subjects (p <0.05).

Conclusion . Thus, the increase in Fe2+ in EBC may signal a change of free radical processes in the lungs, accompanied by the development of pathological processes in them.
Abstract 3474: Cardiac -Specific SOCS3 Dificient Mice Shows Resistance to Lipopolysaccharide-Induced Cardiac Dysfunction
Authors: Futamata Nobuyoshi, Hldeo Yasukawa, Toyoharu Ohba, Kazutoshi Mawatari, Daisuke Fukui, Masahiko Hoshijima, Tsutomu Imaizumi
Journal: Circulation (2008)

Background : Lypopolysaccharide (LPS)-induced left ventricular (LV) dysfunction is a well-established model for sepsis-induced acute heart failure. STAT3 signaling in the heart has been shown to promote cardiomyocyte survival during LPS-induced LV dysfunction. Little is known, however, about the role of negative regulation of STAT3 signaling during LPS-induced LV dysfunction. Suppressor of cytokine signaling 3 (SOCS3) is an intrinsic negative regulator of gp130 cytokine-induced STAT3 signaling that plays an important role in cardiomyocyte survival. In this study, we determined whether STAT3 signaling and its negative regulator SOCS3 would play a role in LPS-induced LV dysfunction. Methods and Results : We examined the activation of STAT3 and inductions of gp130 cytokines and SOCS3 in the wild-type (WT) mice hearts after LPS injection by western blot and real-time PCR (RT-PCR). RT-PCR revealed that gp130 cytokines were markedly increased after AMI. Western blot revealed that STAT3 was markedly phosphorylated and SOCS3 was induced in WT mice hearts after LPS injection. To investigate the role of STAT3 signaling and SOCS3 in LPS-induced LV dysfunction, we generated cardiac-specific SOCS3 knockout mice (SOCS3-CKO). Left ventricular ejection fraction (LVEF) of SOCS3-CKO mice was similar to that of WT mice at baseline (64.2 ± 6.1 vs. 62.4 ± 4.4%). LPS (30mg/kg) elicited a significant and robust reduction of LVEF in both SOCS3-CKO mice and WT mice 3 hr after LPS injection (18 ± 4.5 vs. 16 ± 5.2%, p &lt;0.01). LVEF in WT mice was further reduced 6 hr after LPS injection. On the other hand, interestingly, LVEF was restored to the baseline in SOCS3-CKO mice 6 hr after LPS injection (10.4 ± 3.9 vs. 62.2 ± 8.1%, p &lt;0.01). Also the duration and intensity of STAT3 phosphorylation after LPS injection was greater in SOCS3-CKO mice than WT mice. Furthermore, SOCS3-CKO mice showed greater survival rate than WT mice after LPS injection ( p &lt;0.01). Conclusion : Our data show that the deletion of SOCS3 in cardiomyocytes prevents the LPS-induced LV dysfunction in mice, possibly by augmenting the STAT3-mediated gp130 cytokine signaling.
Abstract 3097: Significance of Delayed Enhancement with Contrast Enhanced Cardiovascular Magnetic Resonance in Hypertrophic Cardiomyopathy
Authors: Martin S Maron, Evan Appelbaum, Caitlin Harrigan, jacki Buros, C. Michael Gibson, Connie Hannah, John R Lesser, James E Udelson, Warren J Manning, Barry J Maron
Journal: Circulation (2007)

Background. Cardiovascular magnetic resonance (CMR) with delayed enhancement (DE) can provide in vivo assessment of myocardial fibrosis. DE is an independent predictor of cardiovascular morbidity and mortality in ischemic and non-ischemic dilated cardiomyopathy but its clinical significance in hypertrophic cardiomyopathy (HCM) remains unresolved. Methods and Results. Cine and CMR-DE were performed in 202 HCM patients (42±17 years; 71% male). DE was identified in 103 (51%) HCM patients, occupying 9±11% (range 0.2 to 51%) of LV myocardial volume, including 12% with DE &gt; 25%. DE was present all 10 patients with ejection fraction (EF) ≤50% (i.e., end-stage phase), 9/10 (90%) with EF 51–59% and 84/182 (45%) with EF ≥ 60% (p&lt;0.001). %DE was inversely related to EF (r= −0.4; p&lt; 0.001), most extensive in patients with EF ≤50% (27% vs.9% for other patients, p&lt;0.001) and an independent predictor of EF (r= −0.6; p&lt;0.001). Of the 182 patients with normal EF ≥60%, 49 (27%) were both asymptomatic and had DE (7±7% of LV; 51% transmural), including 7 patients ≥60 years. %DE was unassociated with heart failure symptoms (p=0.1) and age (r = 0.05; p = 0.6). Conclusions. In a large HCM cohort, DE was common and occupied substantial areas of LV myocardium. Importantly, DE was a strong and independent predictor of evolution to “end-stage” with systolic dysfunction. However, extensive DE was also present in many patients without heart failure symptoms, suggesting that such HCM patients undergo vigilant clinical surveillance (including serial CMR) for prospective detection of changes in clinical course and LV remodeling.
873. Low Level Hepatocyte Repopulation Corrects Hyperphenylalaninemia in Murine Phenylketonuria
Authors: Cary O. Harding, Kelly Hamman, Heather Clark, Eugenio Montini, Muhsen Al-Dhalimy, Markus Grompe, Milton Finegold
Journal: Molecular Therapy (2004)

Objective: Determine the minimal number of phenylalanine hydroxylase (PAH) positive hepatocytes and minimal level of PAH activity required to correct hyperphenylalaninemia in Pahenu2 mice, a model of human phenylketonuria (PKU).
Abstract 17520: Emerging Prognostic Factors in Patients with Aortic Stenosis -A Report from the CHART-2 Study
Authors: Kenjiro Sato, Yasuhiko Sakata, Kotaro Nochioka, Satoshi Miyata, Msanobu Miura, Soichiro Tadaki, Ryuichi Ushigome, Takeshi Yamauchi, Takeo Onose, Kanako Tsuji, Ruri Abe, Hiroaki Shimokawa
Journal: Circulation (2014)

Introduction: Along with the rapid aging of general population, the prevalence of aortic stenosis (AS) has also been increasing worldwide, especially in the developed countries including Japan. The previous studies showed that NYHA class and the severity of AS are the major classical prognostic factors (e.g. valve anatomy, valve hemodynamics). However, since AS is one of the major degenerative diseases of the elderly, it is conceivable that other prognostic factors are also involved in the current practice of AS. Methods: We examined the prognostic factors for 3-year mortality of 412 consecutive AS patients (mean age 74.9 years, male 52.4%), defined as peak pressure gradient ≥30mmHg, among 10,219 patients with stage B/C/D heart failure (HF) registered in CHART-2 Study (N=10,219). Results: The prevalence of NYHA I, II, III and IV was 37.7%, 50.9%, 10.8%, and 0.7%, respectively. Renin-angiotensin system inhibitors, beta-blockers, and diuretics were prescribed in 66.7%, 26.9%, and 64.6%, respectively. Crude 3-year mortality was 9.5%, 16.5%, and 49.7% in patients with NYH class I, II and III/IV, respectively (PIII, aortic peak flow (APF)&gt;4.5m/s, serum albumin (Alb), chronic kidney disease (CKD) and use of diuretics was the best model to predict the mortality of AS patients (Table). Conclusions: The present study demonstrates that in addition to NYHA class and APF, other factors (age, sex, HR, Alb, CKD, and use of diuretics) could also be associated with mortality of AS patients, suggesting that these new factors should also be taken into consideration when evaluating long-term prognosis of AS patients in the current era.
Distal Left Main Coronary Disease Is a Major Predictor of Outcome in Patients Undergoing Percutaneous Intervention in the Drug-Eluting Stent Era
Authors: Marco Valgimigli, Patrizia Malagutti, Gaston A. Rodriguez-Granillo, Héctor M. Garcia-Garcia, Jawed Polad, Keiichi Tsuchida, Evelyn Regar, Willem J. Van der Giessen, Peter de Jaegere, Pim De Feyter, Patrick W. Serruys
Journal: Journal of the American College of Cardiology (2006)
Abstract 2759: Colorectal cancer cell lines with high BCL-XL and low MCL-1 expression are sensitive to a potent and selective BCL-XL inhibitor
Authors: Lloyd T. Lam, Haichao Zhang, John Xue, Paul Hessler, Stephen K. Tahir, Jun Chen, Sha Jin, Andrew J. Souers, Joel D. Leverson
Journal: Cancer Research (2014)

Abstract Colorectal cancer is the second most deadly type of cancer in the United States and worldwide despite the recent approval of new therapies. The identification of novel agents that are effective against this cancer thus remains a significant goal. One hallmark of cancer is the defective regulation of programmed cell death, or apoptosis. The anti-apoptotic B-cell lymphoma 2 (BCL-2) family members, including BCL-2, BCL-XL, and MCL-1, are known to regulate cell survival and death and have been characterized as key survival factors in multiple cancer types. As BCL-XL is overexpressed in many solid tumors, the sensitivity of a panel of 25 colorectal cancer cell lines to a potent and selective BCL-XL inhibitor was investigated. Colorectal cell lines with high expression of BCL-XL and NOXA, a pro-apoptotic protein that antagonizes MCL-1 activity, were more sensitive to small molecule BCL-XL inhibition. In contrast, cell lines with lower expression of BCL-XL and higher expression of MCL-1 were resistant. Silencing the expression of BCL-XL via siRNA killed the cell lines that were sensitive to small molecule BCL-XL inhibition while having little effect on lines that were resistant. Furthermore, silencing the expression of MCL-1 restored sensitivity of resistant cells to the BCL-XL inhibitor whereas silencing of NOXA abrogated the sensitivity of cells to BCL-XL inhibitor. BCL-XL inhibition could thus be an effective treatment in a subset of colorectal cancer patients showing high BCL-XL expression. Disclosures: All authors are employees of AbbVie. The design, study conduct, and financial support for the research was provided by AbbVie. AbbVie participated in the interpretation of data, review, and approval of the publication. Citation Format: Lloyd T. Lam, Haichao Zhang, John Xue, Paul Hessler, Stephen K. Tahir, Jun Chen, Sha Jin, Andrew J. Souers, Joel D. Leverson. Colorectal cancer cell lines with high BCL-XL and low MCL-1 expression are sensitive to a potent and selective BCL-XL inhibitor. [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 2759. doi:10.1158/1538-7445.AM2014-2759
Is Domestic Violence Screening Helpful?
Authors: T B Cole
Journal: JAMA (2000)

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 Return of the Prodigal Son
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
Abstract 19339: ROCK2 Mediates the Uptake of Fatty Acids through the Transcriptional Regulation of CD36
Authors: Christina J Park, Eltayeb Karrar, Phetcharat Chen, James K Liao
Journal: Circulation (2014)

Background: Basal metabolic rate has a profound effect on the development of obesity and protects against cold intolerance in living organisms. Rho-activated kinase 2 (ROCK2), an important mediator of the actin cytoskeleton, is also necessary for maintaining energy homeostasis. There is a particularly high expression of ROCK2 found in both the brown and white adipocytes. Adipocytes, endocrine organs for fat storage, play a major role in regulating the balance between energy storage and expenditure with the maintenance of fatty acids. Fatty acid uptake by the adipocytes is mediated through a number of fatty acid transporters. One such transporter, called fatty acid translocase (CD36), is found present in a variety of processes including inflammation, atherosclerosis, as well as lipid metabolism. Upon cold exposure, there is a continuous uptake of free fatty acids from the blood in order to maintain heat production through fatty acid oxidation in brown adipocytes. To date, the precise mechanism as to how fatty acid transporters are regulated in response to environmental cues is unknown.

Methods and Results: ROCK2 depleted mouse embryonic fibroblasts (MEF) display significantly decreased luciferase activity under the control of the CD36 promoter. Mutant mice with adipocyte-specific deletion of ROCK2 (ROCK2adipoQ-/-) exhibit a lower expression of CD36. When these mice are exposed to cold temperatures for 6 hours, electron microscopy and immunohistochemistry have demonstrated that the lipid droplets in their brown adipocytes are nearly absent as compared to control littermates. The mutant mice are unable to maintain lipid reserves in their adipose tissue, suggesting a defect in their ability to replenish or uptake fatty acids. This also led to an observation in reduced basal metabolic rate. Conversely, mutant mice with adipocyte-specific expression of the constitutively active form of ROCK (CA-ROCK) exhibit an increased expression of CD36 and enhanced adaptive capabilities.

Conclusion: Our findings indicate a critical role of ROCK2 in mediating the uptake and storage of fatty acids through the transcriptional regulation of CD36 expression and suggest that modulation of ROCK2 activity in adipocytes may have therapeutic benefits in metabolic diseases.
Cystic Fibrosis Treatment Trial
Authors: Marsha F. Goldsmith
Journal: JAMA (2001)

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 4504: Urokinase plasminogen activator-dependent tumor penetrating peptide
Authors: Tambet Teesalu, Kazuki N. Sugahara, Gary B. Braun, Venkata Ramana Kotamraju, Erkki Ruoslahti
Journal: Cancer Research (2014)

Abstract Activity of tumor penetrating peptides depends on C-end Rule (CendR) peptide motif (R/KXXR/K) that must be C-terminally exposed for tissue and cell penetration. We describe here a cryptic CendR peptide (uCendR; amino acid sequence: RPARSGR↓SAGGSVA) that is proteolytically activated by urokinase-type plasminogen activator (uPA), a protease overexpressed in human tumors. uPA cleavage unmasks the cryptic CendR element of uCendR peptide and triggers its binding and internalization to the neuropilin-expressing cultured cancer cells. Intradermally injected post-cleavage mimic of uCendR peptide (RPARSGR) increases permeability of skin microvessels to tracer compounds. Phage and silver nanoparticles functionalized with uCendR peptide in combination with angiogenic integrin-recruitment motif (CRGDC) home to tumor blood vessels, extravasate, and trigger vascular exit of co-injected tracer compounds. This study shows that modular tumor penetrating peptides that are specifically activated by a tumor derived protease can be developed for tumor-targeted drug delivery. Citation Format: Tambet Teesalu, Kazuki N. Sugahara, Gary B. Braun, Venkata Ramana Kotamraju, Erkki Ruoslahti. Urokinase plasminogen activator-dependent tumor penetrating peptide. [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 4504. doi:10.1158/1538-7445.AM2014-4504
Website of the week: http://www.pbs.org/wgbh/pages/frontline/shows/syndrome/
Authors: R. Harling
Journal: BMJ (1999)

www.netlink.de/gen/home.html Biotechnology companies trying to introduce genetically modified food into Europe have found themselves up against well organised resistance. The battle for minds and stomachs continues, and on the internet the environmental and food safety lobby seem to be winning.

The Campaign to Ban Genetically Engineered …
The receptor NLRP3 is a transcriptional regulator of TH2 differentiation
Authors: Mélanie Bruchard, Cédric Rebé, Valentin Derangère, Dieudonnée Togbé, Bernhard Ryffel, Romain Boidot, Etienne Humblin, Arlette Hamman, Fanny Chalmin, Hélène Berger, Angélique Chevriaux, Emeric Limagne, Lionel Apetoh, Frédérique Végran, François Ghiringhelli
Journal: Nature Immunology (2015)
Abstract 14000: miR-322/503 Cluster Drives Cardiac Differentiation by Inhibiting CUG-binding Protein 1
Authors: Xiaopeng Shen, Ashley Benham, Benjamin Soibam, Wei Yu, Robert J Schwartz, Yu Liu
Journal: Circulation (2014)

Understanding the mechanisms of early cardiac fate determination may lead to better approaches in promoting heart regeneration after injury. MicroRNAs (miRNAs) involved in the process are particularly interesting due to their small profile and relatively shorter path to clinic. With Mesp1 as the marker, we used a Mesp1-Cre/Rosa-EYFP reporter system to track the earliest cardiac progenitors, and identified the miRNAs enriched in these cells. Among them, the miR-322/503 cluster is found to be a powerful regulator of the cardiac program: (1) in a screening of more than 20 CPC-enriched miRNAs, miR-322/503 was the most powerful in driving calcium flux activity in mouse embryonic stem cells (mESCs) differentiation; (2) induced ectopic expression of miR-322/503 to mimic the natural course in mESCs led to α-actinin expression and significant increases of cardiac transcription factors (Tbx5, Mef2C, Nkx2-5 and α-MHC); (3) inhibitors of miR-322 and miR-503 significantly reduced expression of α-actinin and the above cardiac TFs. Remarkably, miR-322/503 regulates the cardiac program by inhibiting an RNA-alternative splicing/decay factor, CUG-binding protein 1 (Celf1), which is also known for a role in myotonic dystrophy pathogenesis. The evidences include (i) miR-322 and miR-503 had a shared target site at 3’UTR of Celf1; (ii) expression patterns of miR-322/503 and Celf1 were mutually exclusive, with the highest Celf1 expression in the brain; (iii) miR-322/503 repressed Celf1 protein expression in a dose-dependent manner; (iv) Celf1-shRNA induced up-regulation of cardiac transcription factors and α-actinin, mimicking the function of miR-322/503; (v) ectopic Celf1 expression repressed expression of cardiac transcription factors, while promoted expressions of early neural markers, including Sox1, Zic1, Nestin and Pax6. In summary, we have identified a miR-322/503-Celf1 pathway that promotes cardiac differentiation by preventing activation of other lineages. This new regulatory mechanism may be used to direct cardiac regeneration after heart injury, and treat myotonic dystrophy where Celf1 up-regulation is responsible for skeletal muscle wasting and other symptoms.