tbuckley/cabot-search huggingface dataset:
Glycogen Synthase Kinase-3 Mediates Endothelial Cell Activation by Tumor Necrosis Factor-α
Authors: Masato Eto, Alexei Kouroedov, Francesco Cosentino, Thomas F. Lüscher
Journal: Circulation (2005)

Endothelial cell transformation to a thrombogenic and inflammatory phenotype plays an important role in the pathogenesis of atherothrombosis, but the responsible signaling pathways remain to be elucidated. This study was designed to investigate the regulatory role of glycogen synthase kinase-3 (GSK-3) in tissue factor (TF) and vascular cell adhesion molecule (VCAM)-1 expression in tumor necrosis factor (TNF)-alpha-stimulated endothelial cells.In human endothelial cells, TNF-alpha as well as thrombin induced rapid and transient dephosphorylation and hence, activation of GSK-3. A GSK-3 inhibitor, LiCl, suppressed TNF-alpha- and thrombin-induced TF and VCAM-1 expression, whereas NaCl had no effect. A specific GSK-3 inhibitor, TDZD-8, mimicked the inhibitory effects of lithium. GSK-3 inhibition also significantly suppressed the TNF-alpha-induced increase in TF activity and VCAM-1 cell-surface expression. The luciferase reporter system demonstrated that regulation of TF and VCAM-1 expression by GSK-3 was mediated at the transcriptional level. The TNF-alpha-induced increase in nuclear factor (NF)-kappaB DNA-binding activity was significantly suppressed by TDZD-8. TDZD-8 completely prevented the TNF-alpha-induced inhibitor of NF-kappaB (IkappaB)-alpha degradation but had no effect on IkappaB-kinase-beta phosphorylation.GSK-3 regulates TNF-alpha-induced IkappaB-alpha degradation and NF-kappaB activation independent of IkappaB-kinase-beta and subsequent induction of TF and VCAM-1 expression in human endothelial cells. This study provides the experimental basis for a novel strategy of using GSK-3 inhibition to treat atherothrombotic vascular disease.
Chronic Pain and Risk of Falls in Older Adults
Authors: Scott T. Wilber
Journal: JAMA (2010)

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
Helsinki -20 C
Authors: A. J. Lindford, J. Vuola
Journal: BMJ (2011)

<b>Background:</b> Alveolar hypoventilation and a slower rate of lung emptying may increase end-tidal CO<sub>2</sub> (P<sub>ET</sub>CO<sub>2</sub>) as exercise progresses in COPD. In contrast, alveolar hyperventilation and a low cardiac output (i.e. lung underperfusion) may decrease P<sub>ET</sub>CO<sub>2</sub> in systolic heart failure (HF). The consequences of these opposing influences on exercise P<sub>ET</sub>CO<sub>2</sub> remains unknown in COPD+HF overlap. <b>Methods:</b> 98 patients with COPD (41 with HF (ejection fraction= 35.3 ± 7.4 %) underwent an incremental exercise test. <b>Results:</b> P<sub>ET</sub>CO<sub>2</sub> increased to a greater extent from rest to mid exercise in COPD compared to COPD+HF; subsequently, it further increased in most COPD patients. In contrast, it typically decreased in COPD-HF overlap (median (range)= 4.7 (6.2) vs. -0.1 (6.0) mmHg, respectively; p&lt;0.01). Capillary PCO<sub>2</sub> (PcCO<sub>2</sub>) measurements revealed progressively larger P(c-E<sub>T</sub>)CO<sub>2</sub> differences as exercise evolved in COPD+HF (N= 13) compared to COPD (N= 15); p&lt;0.01) (<b>Figure)</b>. Moreover, while ventilation (VE)/CO<sub>2</sub> output (VCO<sub>2</sub>) ratio for a given PcCO<sub>2</sub> was higher in COPD+HF, between-group differences disappeared when VE /VCO<sub>2</sub> was expressed as a function of P<sub>ET</sub>CO<sub>2</sub> (p&gt;0.05). <b>Conclusion:</b> Heart failure downward shifts exercise P<sub>ET</sub>CO<sub>2</sub> in COPD likely reflecting increased “wasted ventilation” due to underperfusion of relatively well ventilated areas. Exercise P<sub>ET</sub>CO<sub>2</sub> might prove clinically useful to assess the contribution of HF to exercise pathophysiology in COPD+HF overlap.
A Plan for Facilitating the Reduction of Strangulated Hernia by Taxis
Authors: W. C. B. Fifield
Journal: BMJ (1872)

Feb. io, i872potash of Class No. iII or effete material; as, while in muscular tissue these two substances occur precisely in the right proportions to form pyrophosphate of potash (a very remarkable and interesting result), no such proportion is found to exist between the two corresponding sub- stances in pulmonary tissue, which is clearly shown thus.Mluscular Tissue.Pulmonary Tissue.Theory.Phosphoric acid.. (o.563) 42.4* (0.058) II.4 43 ) Pyroph. of Potash.(0.764) 57.6 (0.45J) 88.6 575 potash.
Hypercholesterolemia Exacerbates Transplant Arteriosclerosis via Increased Neointimal Smooth Muscle Cell Accumulation
Authors: Chengwei Shi, Wen-Sen Lee, Mary E. Russell, Dorothy Zhang, Donald L. Fletcher, John B. Newell, Edgar Haber
Journal: Circulation (1997)

Background Hypercholesterolemia is thought to be a significant risk factor for coronary vasculopathy in cardiac transplant recipients. Methods and Results We examined the development of arteriosclerosis in mouse carotid artery loops allografted from B.10A(2R) (H-2 h2 ) donors to normocholesterolemic C57BL/6J (H-2 b ) recipients and hypercholesterolemic C57BL/6J recipients in which the apolipoprotein (apo) E gene had been knocked out. Luminal occlusion and cross-sectional neointimal area were greater in arteries allografted into hypercholesterolemic recipients at 15 and 30 days after transplantation. We also measured cellular and extracellular matrix components of the neointima by computerized planimetry of the fractional areas subtended by smooth muscle cells (anti–α-actin stain), collagen (Masson’s trichrome), lipid (oil red O), and leukocytes (anti-CD45). The neointimal area stained for smooth muscle cells was significantly greater in hypercholesterolemic recipients than in normocholesterolemic recipients at 15 and 30 days after allografting. Lipid contributed to neointimal area to a lesser degree, and there was no significant increase in the contribution of collagen or leukocytes. Conclusions Smooth muscle cell accumulation appears to be the principal contributor to the increase in neointimal area observed in arteries allografted into hypercholesterolemic mice.
Introducing intermediate filaments: from discovery to disease
Authors: John E. Eriksson, Thomas Dechat, Boris Grin, Brian Helfand, Melissa Mendez, Hanna-Mari Pallari, Robert D. Goldman
Journal: Journal of Clinical Investigation (2009)

It took more than 100 years before it was established that the proteins that form intermediate filaments (IFs) comprise a unified protein family, the members of which are ubiquitous in virtually all differentiated cells and present both in the cytoplasm and in the nucleus. However, during the past 2 decades, knowledge regarding the functions of these structures has been expanding rapidly. Many disease-related roles of IFs have been revealed. In some cases, the molecular mechanisms underlying these diseases reflect disturbances in the functions traditionally assigned to IFs, i.e., maintenance of structural and mechanical integrity of cells and tissues. However, many disease conditions seem to link to the nonmechanical functions of IFs, many of which have been defined only in the past few years.
Postsplenectomy Sepsis and Mortality in Adults
Authors: Paul E. Schwartz
Journal: JAMA (1982)

From 1955 to 1979, in Rochester, Minn, 193 residents with a mean age of 46 years underwent splenectomy. Only two cases of fulminant sepsis were documented during the 1,090 person-years of follow-up (0.18 cases per 100 person-years) in this unselected population. The incidence of any type of serious infection subsequent to splenectomy was estimated at 7.16 infections per 100 person-years of follow-up (78 cases). The incidence of infections was significantly increased among patients undergoing incidental splenectomy in conjunction with abdominal operations for malignant neoplasms or other conditions. Immunosuppression, radiation, and chemotherapy also significantly increased the risk of subsequent infection. The low risk of fulminant sepsis after splenectomy in the general adult population justifies a policy of individualization of each case as to the relative merits of splenectomy<i>v</i>splenic preservation. (<i>JAMA</i>1982;248:2279-2283)
Castor Bean Allergy Among Workers in the Felt Industry
Authors: M. D. Topping, R. T. S. Henderson, Christina M. Luczynska, Alison Woodmass
Journal: Allergy (1982)

We describe occupational allergy to castor bean in workers in a felt manufacturing plant. Twenty-six (37%) of the workers complained they were affected by the felt and were examined by us. Of these, 12 were considered to have occupational allergy. These 12 subjects had raised specific IgE levels to both felt and castor bean extracts. In addition, three subjects without occupational allergy had raised specific IgE. The presence of castor bean allergens in the felt was suggested by the correlation between the RAST scores to the felt and castor bean and confirmed by RAST inhibition experiments. The RAST results correlated well with the results of skin prick tests to felt and castor bean extracts. In addition it was found that atopy did not predispose the workers to castor bean allergy.
<i>GNAL</i>Mutations and Dystonia
Authors: Roberto Erro, Kailash P. Bhatia, John Hardy
Journal: JAMA Neurology (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 Neurology 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 Neurology journal
Nitrazepam: lastingly effective but trouble on withdrawal.
Authors: K Adam, L Adamson, V Brezinova, W M Hunter
Journal: BMJ (1976)

The sleep of 10 volunteers with an average age of 57 years was recorded electrophysiologically before, during, and after nitrazepam 5 mg nightly for 10 weeks. Sleep was longer and less broken on the drug and no tolerance was obvious after two months' use. Withdrawal of the drug, however, caused sleep to be temporarily worse than before the drug had been taken. Slow-wave sleep was reduced by nitrazepam, but the accompanying secretion of growth hormone was not impaired.
Dose-Response Relationship Between Cumulative Mercury Exposure Index and Specific Uptake Ratio in the Striatum on Tc-99m TRODAT SPECT
Authors: Chun-Yi Lin, Saou-Hsing Liou, Chun-Ming Hsiech, Ming-Chou Ku, Song-Yen Tsai
Journal: Clinical Nuclear Medicine (2011)

Tc-99m TRODAT is an agent for dopamine transporters and measuring dopamine innervation of the striatum. An association between Parkinson disease and body burden mercury level has been reported in the scientific published data. The purpose of this study was to investigate the effect of mercury exposure on dopamine transporters in the striatum measured by Tc-99m TRODAT single-photon emission computed tomography (SPECT).Study subjects included 17 workers who worked in a lamp factory at risk for mercury vapor exposure and 15 age-matched healthy controls. All subjects received Tc-99m TRODAT SPECT, brain computed tomography scan, and neurologic examinations. Biologic urine mercury levels at the end of a work week were assessed for workers.There were significant differences in specific uptake ratio (SUR) in the striatum, caudate, and putamen between mercury exposure workers and healthy controls on Tc-99m TRODAT SPECT (all P < 0.001). The results showed a significantly negative correlation between urine and cumulative mercury levels and SUR in the striatum on Tc-99m TRODAT SPECT by Pearson analysis (r = -0.501, P = 0.040; r = -0.563, P = 0.019). After adjusting for age, gender, and body mass index, cumulative mercury exposure index (Cum Hg) was demonstrated to be the statistically significant predictor for SUR in the striatum, caudate, and putamen on Tc-99m TRODAT SPECT by multiple linear regression analysis (β = -0.543, P = 0.018; β = -0.521, P = 0.033; β = -0.465, P = 0.048).Mercury exposure has significantly negative effect on dopamine transporters in the striatum. There is dose-response relationship between cumulative mercury exposure index (Cum Hg) and SUR in the striatum on Tc-99m TRODAT brain SPECT.
Analysis of 5' flanking regions of the gamma globin genes from major African haplotype backgrounds associated with sickle cell disease.
Authors: S R Month, R W Wood, P T Trifillis, P J Orchowski, B Sharon, S K Ballas, S Surrey, E Schwartz
Journal: Journal of Clinical Investigation (1990)

There are at least three major African haplotype backgrounds on which the beta s mutation arises. Sequence changes in the immediate 5' flanking area of the gamma-globin genes may account for differences in fetal hemoglobin expression among the three haplotypes. We determined the sequence from -350 to 10 bp 5' of the G gamma and A gamma fetal globin genes from one beta s-containing chromosome on each of the three major haplotype backgrounds. The Senegal chromosome had a T at -158 5' to the G gamma gene; the Benin (BEN) chromosome had an A to G change at -309 5' to the G gamma gene; and the Central African Republic (CAR) chromosome had a C to T change at -271 5' to the A gamma gene. Genomic DNA from patients with sickle cell disease was analyzed using the polymerase chain reaction and radiolabeled allele-specific oligonucleotide probes. The -309 G variant 5' to the G gamma gene is associated with BEN chromosomes, and the -271 T variant 5' to A gamma with CAR. The -309 change was also found on beta A-containing chromosomes, while the -271 change was not. The -309 change may have predated the beta s mutation on the BEN chromosome.
Mechanisms of Myocardial Capture and Temporal Excitable Gap During Spiral Wave Reentry in a Bidomain Model
Authors: Takashi Ashihara, Tsunetoyo Namba, Takanori Ikeda, Makoto Ito, Kazuo Nakazawa, Natalia Trayanova
Journal: Circulation (2004)

Recent studies have demonstrated that regional capture during cardiac fibrillation is associated with an elevated capture threshold. It is typically assumed that the temporal excitable gap (capture window) during fibrillation reflects the size of the spatial excitable gap (excitable tissue between fibrillation waves). Because capture threshold is high, virtual electrode polarization is expected to be involved in the process. However, little is known about the underlying mechanisms of myocardial capture during fibrillation.To clarify these issues, we conducted altogether 3168 simulations of single spiral wave capture in a bidomain sheet. Unipolar stimuli of strengths 4, 8, 16, and 24 mA and 2-ms duration were delivered at 99 locations in the sheet. We found that cathode-break rather than cathode-make excitation was the dominant mechanism of myocardial capture. When the stimulation site was located diagonally with respect to the core (upper left or lower right if the spiral wave rotates counterclockwise), the cathode-break excitation easily invaded the spatial excitable gap and resulted in a successful capture as a result of the formation of virtual anodes in the direction of the myocardial fibers. Thus, the spatial distribution of the temporal excitable gap did not reflect the spatial excitable gap.The areas exhibiting wide temporal excitable gaps were areas in which the cathode-break excitation wave fronts easily invaded the spatial excitable gap via the virtual anodes. This study provides mechanistic insight into myocardial capture.
Towards Clinical Application of Methylated DNA Sequences as Cancer Biomarkers: A Joint NCI's EDRN and NIST Workshop on Standards, Methods, Assays, Reagents and Tools
Authors: Jacob Kagan, Sudhir Srivastava, Peter E. Barker, Steven A. Belinsky, Paul Cairns
Journal: Cancer Research (2007)

Abstract The workshop report, entitled Towards Clinical Application of Methylated DNA Sequences as Cancer Biomarkers: A Joint National Cancer Institute's Early Detection Research Network and National Institute of Standards and Technology Workshop, presents a summary of the main issues, current challenges, outcomes, and recommendations toward application of methylated DNA sequences as cancer biomarkers. [Cancer Res 2007;67(10):4545–9]
CLOPIDOGREL RELOADING IN PATIENTS WITH ACUTE CORONARY SYNDROME UNDERGOING PCI ON CHRONIC CLOPIDOGREL THERAPY: RESULTS OF THE ARMYDA-8 RELOAD-ACS (ANTIPLATELET THERAPY FOR REDUCTION OF MYOCARDIAL DAMAGE DURING ANGIOPLASTY) RANDOMIZED TRIAL
Authors: Elisabetta Ricottini, Giuseppe Patti, Vincenzo Vizzi, Vincenzo Pasceri, Fabio Mangiacapra, Giuseppe Colonna, Antonio Montinaro, Ilaria Cavallari, Andrea D'Ambrosio, Emanuele Barbato, William Wijns
Journal: Journal of the American College of Cardiology (2013)
17 THE FEASIBILITY AND VALUE OF SHEAR-WAVES ULTRASOUND BASED ELASTOGRAPHIC METHODS FOR LIVER FIBROSIS EVALUATION (TRANSIENT ELASTOGRAPHY – TE, ACOUSTIC RADIATION FORCE IMPULSE ELASTOGRAPHY – ARFI, SUPERSONIC SHEAR IMAGING – SSI)
Authors: I. Sporea, S. Bota, A. Popescu, A. Jurchis, O. Gradinaru-Tascau, R. Sirli
Journal: Journal of Hepatology (2013)
Enhanced Activity of Variant Phospholipase C-δ1 Protein (R257H) Detected in Patients With Coronary Artery Spasm
Authors: Takao Nakano, Tomohiro Osanai, Hirofumi Tomita, Masayuki Sekimata, Yoshimi Homma, Ken Okumura
Journal: Circulation (2002)

Background — We recently demonstrated that phospholipase C (PLC)–δ1 activity in cultured skin fibroblasts obtained from patients with coronary spastic angina (CSA) is enhanced. We tested the hypothesis that structural abnormality in PLC-δ1 isoform is a cause of the enhanced activity. Methods and Results — Sequence analysis of the cDNA coding for PLC-δ1 obtained from fibroblasts revealed that one conversion of guanine to adenine (A) was present at nucleotide position 864 in one CSA patient, resulting in the amino acid replacement of arginine 257 by histidine (R257H). The incidence of 864A/A in genomic DNA, analyzed by single-strand conformation polymorphism, was greater in patients with CSA than in male control subjects (6 of 57 patients with CSA versus 1 of 62 control subjects, P &lt;0.05). The activity of the variant PLC-δ1 protein under free calcium concentration between 10 −8 and 10 −7 mol/L was 2-fold higher than that of the wild-type protein. Baseline intracellular calcium concentration ([Ca 2+ ] i ) in human embryonic kidney 293 cells transfected with the variant PLC-δ1 was higher than that in cells with the wild type. The peak increase in [Ca 2+ ] i in response to acetylcholine at 10 −6 and 10 −5 mol/L was greater in the cells with the variant PLC-δ1 than in those with the wild type. Conclusions — These findings indicate that the R257H variant in the PLC-δ1 gene detected in patients with CSA is associated with enhancement of enzyme activity, and they describe a novel mechanism for the enhanced coronary vasomotility in CSA.
Johns Hopkins Diabetes Guide: Treatment and Management of Diabetes
Authors: Mary Korytkowski
Journal: JAMA (2012)

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 Journals 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 2024 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