tbuckley/cabot-search huggingface dataset:
High-fat diet up-regulates caveolin-1 expression in aorta of diet-induced obese but not in diet-resistant rats
Authors: N YANG, C YING, M XU, X ZUO, X YE, L LIU, Y NARA, X SUN
Journal: Cardiovascular Research (2007)

Caveolin-1 (Cav-1) is considered as a negative regulator of endothelial nitric oxide synthase (eNOS) and influences various cardiovascular functions. The objective of the study is to investigate the effects of high-fat diet on vascular Cav-1 expression and eNOS activities.Male outbred Sprague-Dawley rats were fed with a high-fat diet for 15 weeks to induce obesity. The diet-induced obese (DIO) rats were then divided into two groups. One group (DIO-LF) was fed a normal diet and another group (DIO-HF) along with diet-resistance (DR) rats were fed a high-fat diet for 8 more weeks. Cav-1 expression was determined using reverse transcription (RT)-PCR, Western blotting, and immunohistochemistry techniques. NOS activities were assessed using Griess reagents. Protein kinase B (PKB/Akt) and eNOS expression and phosphorylation were determined by Western blotting.A high-fat diet up-regulated Cav-1 and down-regulated eNOS expression in aorta of DIO rats, but not in that of DR rats. These effects were reversed in DIO rats after switching to a low-fat diet for 8 weeks. Decreased NOS activities in aortas were observed in DIO rats, but not in DR rats. Phosphorylation of PKB/Akt and eNOS (Ser1177) were enhanced in aortas of DIO rats of both DIO-HF and DIO-LF groups.These findings suggest that the decrease of vascular NOS activities in rats fed a high-fat diet were due, at least in part, to the up-regulation of Cav-1 expression.
Epithelial Modulation of Leukotriene-C<sub>4</sub>-induced Human Tracheal Smooth Muscle Contraction
Authors: Mutsuo Yamaya, Kiyohisa Sekizawa, Kohei Yamauchi, Hiroki Hoshi, Takashi Sawai, Hidetada Sasaki
Journal: American Journal of Respiratory and Critical Care Medicine (1995)

We investigated the role of epithelium in smooth muscle contraction induced by leukotriene C4 (LTC4) in isolated human trachea. The contractile response to LTC4 was potentiated by a gamma-glutamyl transpeptidase (gamma-GTP) inhibitor L-serine borate and by removal of the epithelium. Both L-serine borate (4.5 x 10(-2) M) and removal of the epithelium shifted the concentration-response curves to LTC4 to lower concentrations by 1.2 and 1.0 log units, respectively. Incubation of cultured human tracheal epithelial cells with either LTC4 or LTD4 resulted in the formation of LTD4 or LTE4. The isolated epithelial cells and cultured epithelial cells contained gamma-GTP activity. Histochemical study indicated that gamma-GTP-like activity was present in the epithelial, submucosal, and smooth muscle layers. These findings suggest that the epithelium modulates the contractile response to LTC4 in human trachea by LT-degrading enzymes.
Transforming growth factor-β1-induced CD4+CD25+ regulatory T cells in vitro reverse and prevent a murine lupus-like syndrome of chronic graft-versus-host disease
Authors: H. Su, D-Q. Ye, B-L. Wang, X-H. Fang, J. Chen, Q. Wang, W-X. Li, N. Zhang
Journal: British Journal of Dermatology (2008)

Background The suppressive mechanism of CD4+CD25+ regulatory T cells (Tregs) is poorly understood. It is also not known how to obtain enough peripheral Tregs, and how to make them effective in ameliorating a murine lupus-like syndrome of chronic graft-versus-host disease (cGVHD). Objectives To confirm the contribution of transforming growth factor (TGF)-β1 in the function of CD4+CD25+ Tregs in vitro, and to identify in vivo suppressive effects of different Tregs generated through TGF-β1. Methods Suppressive effects of freshly isolated CD4+CD25+ Tregs, TGF-β1-expanded CD4+CD25+ Tregs (eTregs) and TGF-β1-induced CD4+CD25+ Tregs (iTregs) in vitro were assessed. Reverse transcription–polymerase chain reaction was used to detect Foxp3. The respective roles that different Tregs might play in controlling murine lupus-like syndrome of cGVHD were analysed. Results TGF-β1 was necessary for expanding the existing CD4+CD25+ Tregs in vitro, as well as converting peripheral CD4+CD25− T cells to CD4+CD25+ Tregs through upregulating CD25 and Foxp3. These eTregs and iTregs had a suppressive effect similar to that of freshly isolated CD4+CD25+ Tregs. The inhibitory function of iTregs could be partially blocked by anti-TGF-β1. Importantly, it was revealed for the first time that both eTregs and iTregs had an inhibitory effect on reversing the morbidity of mice that had already developed anti-dsDNA, and iTregs gave more suppression than eTregs. Besides, iTregs could prevent the onset and slow the progress of disease in a significantly dose-dependent manner. Conclusions Results indicate that TGF-β1 signalling is required to maintain the suppression of CD4+CD25+ Tregs in vitro and in vivo. Together, this study suggests a possible therapeutic role for iTregs in the treatment of murine lupus-like syndrome of cGVHD.
Smart Aid
Authors: Trevor Mundel
Journal: JAMA Internal Medicine (2014)

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
86 REGULATION OF ALTERNATIVE SPLICING BY SLU7 IS ESSENTIAL FOR HCC CELL SURVIVAL
Authors: M. Elizalde, R. Urtasun, M.U. Latasa, M. Azkona, O. García- Irigoyen, J. Muntané, J. Prieto, M.A. Ávila, C. Berasain
Journal: Journal of Hepatology (2013)
P2-221: Adjuvant docetaxel plus carboplatin versus observation in patients with completely resected stage IB-IIIA non-small-cell lung cancer: preliminary results of the Chinese Society of Lung Cancer randomised controlled trial (CSLC201)
Authors: Yi-Long Wu, Xue-Ning Yang, Gang Chen, Li-Jia Gu, Jin-Ji Yang, Wen-Zhao Zhong, Ri-Qiang Liao, Ying-Chang Zhu, Xiao-Song Ben
Journal: Journal of Thoracic Oncology (2007)
The Integral Role of Clinical Research in Clinical Care
Authors: Steven M. Grunberg, William T. Cefalu
Journal: New England Journal of Medicine (2003)

The ethical justification for clinical research as currently conducted has been questioned on the grounds that physicians do not make a strict and unequivocal distinction for their patients between clinical research and clinical care, and their patients may therefore participate in clinical studies with the false impression that they are being cared for to the best of their physicians' ability.1 This issue raises difficult and controversial questions about the intentions, goals, and responsibilities of clinical researchers, as evidenced by the numerous editorials and articles on the subject that have appeared in the Journal in recent decades.26 These are certainly . . .
Estimating Exposure to Environmental Tobacco Smoke
Authors: Christopher R. E. Coggins
Journal: JAMA (1996)

<h3>To the Editor.</h3> —Dr Pirkle and colleagues<sup>1</sup>appear to have overlooked the impact that some of their findings have on recent attempts to regulate smoking in the workplace<sup>2</sup>while overstating the potential impact on other risk assessments.<sup>3</sup>For example, in proposing workplace regulations, the Occupational Safety and Health Administration has assumed that ETS exposure in the workplace (due to working with smokers) is equivalent to or greater than ETS exposure in the home (due to living with smokers). However, as the data of Pirkle et al show (Table 4), living with smokers results in at least a 2-fold increased exposure (as measured by cotinine) compared with working with smokers, which is similar to findings that have been reported by us<sup>4</sup>and others.<sup>5</sup> Furthermore, in discussing their public health implications, Pirkle et al interpret their data as suggesting that there may be considerable ETS exposure within the control groups
Phylogenetic Analysis Under Reticulate Evolution
Authors: Shizhong Xu
Journal: Molecular Biology and Evolution (2000)

The usual assumption that species have evolved from a common ancestor by a simple branching process—where each branch is genetically isolated—has been challenged by the observation of frequent hybridization between species in natural populations. In fact, most plant species are thought to have hybrid origins. This reticulate pattern of species evolution has posed problems in the definition of speciation and in phylogenetic reconstruction, especially when molecular data are used. As a result, hybridization has been largely treated as an evolutionary accident or statistical error in phylogenetic analysis. In this paper, I explicitly incorporate hybridization as an evolutionary occurrence and then conduct phylogenetic reconstruction. I first examine the reticulate evolution under a pure drift model, and then extend the theory to fit a mutation model. A least-squares method is developed for reconstructing a reticulate phylogeny using gene frequency data. The efficacy of the method under the pure drift model is verified via Monte Carlo simulations.
Ventricular Nuclei-DNA Relationships with Myocardial Growth and Hypertrophy in the Rat
Authors: ARTHUR F. GRIMM, LUIS DE LA TORRE, MICHAEL LA PORTA
Journal: Circulation Research (1970)

Rat ventricles, ranging from 306 to 1999 mg, were obtained from normal animals of different ages and from animals subjected to chronic aortic constriction. The concentration of DNA in the paired ventricles (right and left) was found to be closely related to the concentration of nuclei in the left ventricular papillary muscles. Muscle nuclei represented only 10 to 15% of this population of nuclei. In young animals (phase 1), the total ventricular content of muscle nuclei, nonmuscle nuclei, and of DNA were increasing with ventricular growth. In the adult rat (phase 2), the total ventricular content of DNA and of both muscle and nonmuscle nuclei remained relatively constant with ventricular growth. In the enlarged hearts (phase 3), there was a further increase in total ventricular DNA but there was no further increase in the total number of muscle nuclei. Spectrophotometric studies (Feulgen stain), showed that 88% of the muscle nuclei belonged to a single ploidy class (probably diploid). No relation could be demonstrated between the extent of nuclear polyploidy and the weight of the ventricles. It was concluded that polyploidy was not a significant factor in the increased total DNA of phase 3. The increased ventricular DNA of phase 3 was explained by the proliferation of the nonmuscle nuclei.
Ventricular Pacing With Premature Excitation for Treatment of Hypertensive-Cardiac Hypertrophy With Cavity-Obliteration
Authors: David A. Kass, Chen-Huan Chen, Maurice W. Talbot, Carlos E. Rochitte, João A. C. Lima, Ronald D. Berger, Hugh Calkins
Journal: Circulation (1999)

Background —Hypertensive left ventricular hypertrophy with supranormal systolic ejection and distal cavity obliteration (HHCO) can result in debilitating exertional fatigue and dyspnea. Dual-chamber pacing with ventricular preactivation generates discoordinate contraction, which can limit cavity obliteration and thereby increase potential ejection reserve. Accordingly, we hypothesized that pacing may improve exercise tolerance long-term in this syndrome. Methods and Results —Dual-chamber pacemakers were implanted in 9 patients with exertional dyspnea caused by HHCO. Intrinsic atrial rate was sensed, and ventricular preactivation was achieved by shortening the atrial-ventricular delay. Pacing was on or off for successive 3-month periods (randomized, double-blind, crossover design), followed by 6 additional pacing-on months. Metabolic exercise testing, quality-of-life assessment, and rest and dobutamine-stress echocardiographic/Doppler data were obtained. After 3 months of pacing-on, exercise duration rose from 324±133 to 588±238 s (mean±SD; P =0.001, with 7 of 9 patients improving ≥30%), and maximal oxygen consumption increased from 13.6±2.9 to 16.7±3.3 mL of O 2 · min −1 · kg −1 ( P &lt;0.02). Both parameters were little changed from baseline during the pacing-off period. Improved exercise capacity persisted at 1-year follow-up. Clinical symptoms and activities of daily living improved during the pacing-on period and stayed improved at 1 year, but they were little changed during the pacing-off period. Despite similar basal values, stroke volume ( P &lt;0.001) and cardiac output ( P &lt;0.02) increased with dobutamine stimulation 2 to 3 times more after 1 year of follow-up as compared with baseline. Conclusions —Long-term dual-chamber pacing can improve exercise capacity, cardiac reserve, clinical symptoms, and activities of daily living in patients with HHCO. This therapy may provide a novel alternative for patients in whom traditional pharmacological treatment proves inadequate.
The Leech in French
Authors: Jean-Philippe Méry
Journal: Annals of Internal Medicine (1988)

Letters and Corrections1 December 1988The Leech in FrenchJean-Philippe Méry, MDJean-Philippe Méry, MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-109-11-930 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the Editor:I read with great interest the extremely well-documented article by Adams (1) on the medicinal leech and was amused to learn that the wordleechhas been used previously as a sobriquet for doctor. I noticed an error in the legend of Figure 1, a lithograph by the French painter and engraver Louis Léopold Boilly (1761-1845). The French word for leech is notsanguebutsangsue. This word comes from the Latin wordsanguisuga(fromsanguis[blood] andsugere[to suck], and is thought to have been first used by Pliny the Elder (23 to 79 AD)....Reference1. Adams S. The medicinal leech: a page from the annelids of internal medicine. Ann Intern Med. 1988;109:399-405. LinkGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: Jean-Philippe Méry, MDAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 December 1988Volume 109, Issue 11Page: 930-930KeywordsBlood ePublished: 1 December 2008 Issue Published: 1 December 1988 PDF downloadLoading ...
A Role for Ca2+ Stores in Kainate Receptor-Dependent Synaptic Facilitation and LTP at Mossy Fiber Synapses in the Hippocampus
Authors: Sari E Lauri, Zuner A Bortolotto, Robert Nistico, David Bleakman, Paul L Ornstein, David Lodge, John T.R Isaac, Graham L Collingridge
Journal: Neuron (2003)
Will doctors now take a lead on climate change?
Authors: F. Godlee
Journal: BMJ (2012)

Last week was Climate Week in the UK, featuring a host of awareness raising activities across the country. And next Wednesday, 28 March, is NHS Sustainability Day (http://doc2doc.bmj.com/forums/off-duty\_general\_nhs-sustainability-day-of-action). So it seems a good moment to be publishing our Spotlight on climate change. The seven articles have been specially commissioned from among the speakers at last year’s high level conference on climate change, hosted by the BMJ in partnership with a consortium of other organisations (http://climatechange.bmj.com).

In case there are any remaining doubters reading the BMJ , we begin with the science. “No science is ever completely settled,” writes Chris …
Lead Increases Lipopolysaccharide-Induced Liver Injury through Tumor Necrosis Factor-α Overexpression by Monocytes/Macrophages: Role of Protein Kinase C and p42/44 Mitogen-Activated Protein Kinase
Authors: Yu-Jung Cheng, Bei-Chang Yang, Ming-Yie Liu
Journal: Environmental Health Perspectives (2005)

Although lead and lipopolysaccharide (LPS), both important environmental pollutants, activate cells through different receptors and participate in distinct upstream signaling pathways, Pb increases the amount of LPS-induced tumor necrosis factor-alpha (TNF-alpha). We examined the cells responsible for the excess production of Pb-increased LPS-induced TNF-alpha and liver injury, and the roles of protein kinase C (PKC) and p42/44 mitogen-activated protein kinase (MAPK) in the induction of TNF-alpha. Peritoneal injection of Pb alone (100 micromol/kg) or a low dose of LPS (5 mg/kg) did not affect serum TNF-alpha or liver functions in A/J mice. In contrast, coexposure to these noneffective doses of Pb plus LPS (Pb+LPS) strongly induced TNF-alpha expression and resulted in profound liver injury. Direct inhibition of TNF-alpha or functional inactivation of monocytes/macrophages significantly decreased the level of Pb+LPS-induced serum TNF-alpha and concurrently ameliorated liver injury. Pb+LPS coexposure stimulated the phosphorylation of p42/44 MAPK and the expression of TNF-alpha in CD14+ cells of cultured mouse whole blood, peritoneal macrophages, and RAW264.7 cells. Moreover, blocking PKC or MAPK effectively reduced Pb+LPS-induced TNF-alpha expression and liver injury. In summary, monocytes/macrophages were the cells primarily responsible for producing, through the PKC/MAPK pathway, the excess Pb-increased/LPS-induced TNF-alpha that caused liver injury. alpha.
Mitochondrial DNA and bindin gene sequence evolution among allopatric species of the sea urchin genus Arbacia
Authors: E. C. Metz, G. Gomez-Gutierrez, V. D. Vacquier
Journal: Molecular Biology and Evolution (1998)

Sea urchins of the genus Arbacia (order Stirodonta) have discontinuous allopatric distributions ranging over thousands of kilometers. Mitochondrial DNA (mtDNA) sequences were used to reconstruct phylogenetic relationships of four Arbacia species and their geographic populations. There is little evidence of genetic structuring of populations within species, except in two cases at range extremes. The mtDNA sequence differentiation between species suggests that divergence occurred about 4-9 MYA. Gene sequences encoding the sperm protein bindin and its intron were obtained and compared with the mtDNA phylogeny. Sea urchins among the well-studied echinoid order Camarodonta, with degrees of mtDNA divergence similar to those of Arbacia species, are known to have remarkable variation in bindin. However, in Arbacia, little variation in deduced amino acid sequences of bindin was found, indicating that purifying selection acts on the protein. In contrast, bindin intron sequences showed much differentiation, including numerous insertion/deletions. Fertilization experiments performed between a divergent pair of Arbacia species from the Atlantic and Pacific Oceans revealed no evidence of blocks to gamete recognition. In Arbacia, fertilization specificities may have evolved relatively slowly as a result of extensive gene flow within species, greater functional constraint on the bindin polypeptide, or reduced selective pressure for species recognition in singly occurring species.
Note of a Case in which Severe Constitutional Effects Followed the Application of Cantharidine Blister
Authors: J. A. Campbell
Journal: BMJ (1870)

THE BRITISH MEDICAL 7OURNAL.569 nicotine, will also stand in the some relation.Another an& not uncom.mon cause is distant local hyperaemia, exampled especially in children who suffer from convulsive disease, as an affection secondary to dis- turbance of the digestive organs and the irritation of worms; exempli- fied also in the dentition of infancy; but in this latter case, as perhaps also in a minor degree in the former, the element of peripheral irritation must be somewhat taken into account.Irritation of the peripheral extremity of a nerve will produce epilepsy.A remarkable case was quoted by Dr.
Absent Aldosterone Response to ACTH in Familial Glucocorticoid Deficiency
Authors: Richard F. Spark, James R. Etzkorn
Journal: New England Journal of Medicine (1977)

The syndrome of familial glucocorticoid deficiency is characterized by cutaneous pigmentation, muscular weakness, hypoglycemia and convulsions. Hormonal evaluation of patients afflicted with this syndrome reveals elevated endogenous ACTH levels and low levels of plasma and urinary glucocorticoids that do not respond to stimulation with exogenous ACTH.1 2 3 4 Salt wasting is not a feature of this syndrome, and patients are able to conserve sodium normally in response to a low sodium diet. When measured, aldosterone secretion has been found to be normal.4 Pathological studies have demonstrated degeneration of adrenal zona fasiculata and reticularis, with preservation of the zona glomerulosa.4 The reason for . . .
Bendamustine, etoposide, cytarabine, melphalan, and autologous stem cell rescue produce a 72% 3-year PFS in resistant lymphoma
Authors: Giuseppe Visani, Pietro Maria Stefani, Saveria Capria, Lara Malerba, Piero Galieni, Francesco Gaudio, Giorgina Specchia, Giovanna Meloni, Filippo Gherlinzoni, Roberta Gonella, Marco Gobbi, Armando Santoro, Felicetto Ferrara, Marco Rocchi, Enrique M. Ocio, Maria Dolores Caballero, Federica Loscocco, Alessandro Isidori
Journal: Blood (2014)
Outcomes at 6 months for the direct comparison of tirofiban and abciximab during percutaneous coronary revascularisation with stent placement: the TARGET follow-up study
Authors: David J Moliterno, Steven J Yakubov, Peter M DiBattiste, Howard C Herrmann, Gregg W Stone, Carlos Macaya, Franz-Josef Neumann, Diego Ardissino, Jean-Pierre Bassand, Lynn Borzi, Alan C Yeung, Katherine A Harris, Laura A Demopoulos, Eric J Topol
Journal: The Lancet (2002)