tbuckley/cabot-search huggingface dataset:
Superoxide Released to High Intra-arteriolar Pressure Reduces Nitric Oxide–Mediated Shear Stress– and Agonist-Induced Dilations
Authors: An Huang, Dong Sun, Gabor Kaley, Akos Koller
Journal: Circulation Research (1998)

Abstract —It is thought that elevated levels of reactive oxygen metabolites contribute to the dysfunction of vascular endothelium in hypertension. We hypothesized that high intravascular pressure itself elicits production of superoxide, which then interferes with nitric oxide (NO)–mediated responses of arterioles. Thus, isolated arterioles (≈80 μm in diameter) from gracilis muscle of normotensive Wistar rats were cannulated and exposed to 140 mm Hg perfusion pressure for 30 minutes (in the absence of perfusate flow). After high intravascular pressure treatment, dilations to increases in perfusate flow (0 to 30 μL/min) were significantly reduced (from 39±2.2 to 19±2.1 μm at 30 μL/min), eliciting an increase in wall shear stress from ≈20 to ≈60 dyne/cm 2 . N ω -nitro- l -arginine (10 −4 mol/L) did not affect, whereas indomethacin eliminated, flow-induced dilations after pressure treatment. In control, substance P (SP, 10 −9 to 5×10 −8 mol/L), sodium nitroprusside (SNP, 10 −8 to 10 −6 mol/L), and adenosine (ADO, 10 −6 to 5×10 −5 mol/L) elicited dilations (SP: 31.5±1.9 μm, SNP: 45.6±4 μm, and ADO: 37.2±4.1 μm, at maximum concentrations, respectively). After pressure treatment, maximum dilations to SP and SNP were significantly reduced (by 49% and 39%, respectively), whereas responses to ADO were not affected. Presence of superoxide dismutase (120 U/mL) and catalase (80 U/mL), but not catalase alone, in the perfusate solution prevented the reduction in dilation of arterioles to flow and agonists after pressure treatment by restoring NO mediation. We conclude that high intravascular pressure per se elicits the release of superoxide, which then interferes with NO, a mechanism that contributes to the elevation of wall shear stress and peripheral resistance in hypertension.
B-Type Natriuretic Peptides and Ejection Fraction for Prognosis After Myocardial Infarction
Authors: A. Mark Richards, M. Gary Nicholls, Eric A. Espiner, John G. Lainchbury, Richard W. Troughton, John Elliott, Christopher Frampton, John Turner, Ian G. Crozier, Timothy G. Yandle
Journal: Circulation (2003)

Background— A recent landmark report has demonstrated that plasma B-type natriuretic peptide (BNP) measured in acute coronary syndromes independently predicts mortality, heart failure, and new myocardial infarction. After acute cardiac injury, left ventricular ejection fraction (LVEF) is also of prognostic significance and plays a major role in determining the therapeutic response. Methods and Results— The present report is the first from a substantial (n=666) cohort of patients with acute myocardial infarction to test the prognostic utility of concurrent measurements of BNP, amino-terminal BNP (N-BNP), norepinephrine, and radionuclide LVEF. The B-type peptides and LVEF were predictors of death, heart failure, and new myocardial infarction (all P &lt;0.001) independent of patient age, gender, previous myocardial infarction, antecedent hypertension or diabetes, previous heart failure, plasma norepinephrine, creatinine, cholesterol, drug therapy, and coronary revascularization procedures. The combination of N-BNP (or BNP) with LVEF substantially improved risk stratification beyond that provided by either alone. Elevated N-BNP (or BNP) predicted new myocardial infarction only in patients with LVEF &lt;40%. LVEF &lt;40% coupled to N-BNP over the group median conferred substantial 3-year risks of death, heart failure, and new myocardial infarction of 37%, 18%, and 26%, respectively. N-BNP and BNP were equivalent prognostic markers for these clinical outcomes. Conclusions— Plasma N-BNP (or BNP) and LVEF are complementary independent predictors of major adverse events on follow-up after myocardial infarction. Combined measurement provides risk stratification substantially better than that provided by either alone.
Hope and advance care planning in patients with end stage renal disease: qualitative interview study
Authors: Sara N Davison, Christy Simpson
Journal: BMJ (2006)

<h3>Abstract</h3> <b>Objective</b> To understand hope in the context of advance care planning from the perspective of patients with end stage renal disease. <b>Design</b> Qualitative in-depth interview study. <b>Setting</b> Outpatient department of a university affiliated nephrology programme. <b>Participants</b> 19 patients with end stage renal disease purposively selected from the renal insufficiency, haemodialysis, and peritoneal dialysis clinics. <b>Results</b> Patients9 hopes were highly individualised and were shaped by personal values. They reflected a preoccupation with their daily lives. Participants identified hope as central to the process of advance care planning in that hope helped them to determine future goals of care and provided insight into the perceived benefits of advance care planning and their willingness to engage in end of life discussions. More information earlier in the course of the illness focusing on the impact on daily life, along with empowerment of the patient and enhancing professional and personal relationships, were key factors in sustaining patients9 ability to hope. This helped them to imagine possibilities for a future that were consistent with their values and hopes. The reliance on health professionals to initiate end of life discussions and the daily focus of clinical care were seen as potential barriers to hope. <b>Conclusions</b> Facilitated advance care planning through the provision of timely appropriate information can positively enhance rather than diminish patients9 hope. Current practices concerning disclosure of prognosis are ethically and psychologically inadequate in that they do not meet the needs of patients.
WHAT THE CLINICIAN SHOULD KNOW ABOUT ELECTROMYOGRAPHY
Authors: O. Leonard Huddleston
Journal: JAMA (1952)

Electromyography is a recognized clinical procedure that supplies laboratory information to assist the physician in making a diagnosis, outlining a treatment program, and formulating a prognosis for the various disorders of the neuromuscular system.<sup>1</sup>The instrument used is called an electromyograph.<sup>2</sup>It is designed specifically for the detection of electrical potentials associated with the activity of skeletal muscle fibers. It is imperative that the proper selection of equipment and techniques should be made in order to obtain reliable information regarding any electrical disturbance of the lower motor neuron or muscular system. This requires the use of needle electrodes, a cathode ray oscillograph, an optical and sound recording system, and a loud-speaker audio system. The curves exhibited or recorded by the electromyograph represent electrical potentials associated with motor activity of skeletal muscles. As a rule the monopolar technique is employed, consisting of a dispersive electrode (percutaneous) that is affixed
Clinical Application of Tissue Engineered Human Heart Valves Using Autologous Progenitor Cells
Authors: Serghei Cebotari, Artur Lichtenberg, Igor Tudorache, Andres Hilfiker, Heike Mertsching, Rainer Leyh, Thomas Breymann, Klaus Kallenbach, Liviu Maniuc, Aurel Batrinac, Oleg Repin, Oxana Maliga, Anatol Ciubotaru, Axel Haverich
Journal: Circulation (2006)

Background— Tissue engineering (TE) of heart valves reseeded with autologous cells has been successfully performed in vitro. Here, we report our first clinical implantation of pulmonary heart valves (PV) engineered with autologous endothelial progenitor cells (EPCs) and the results of 3.5 years of follow-up. Methods and Results— Human PV allografts were decellularized (Trypsin/EDTA) and resulting scaffolds reseeded with peripheral mononuclear cells isolated from human blood. Positive stain for von Willebrand factor, CD31, and Flk-1 was observed in monolayers of cells cultivated and differentiated on the luminal surface of the scaffolds in a dynamic bioreactor system for up to 21 days, indicating endothelial nature. PV reseeded with autologous cells were implanted into 2 pediatric patients (age 13 and 11) with congenital PV failure. Postoperatively, a mild pulmonary regurgitation was documented in both children. Based on regular echocardiographic investigations, hemodynamic parameters and cardiac morphology changed in 3.5 years as follows: increase of the PV annulus diameter (18 to 22.5 mm and 22 to 26 mm, respectively), decrease of valve regurgitation (trivial/mild and trivial, respectively), decrease (16 to 9 mm Hg) or a increase (8 to 9.5 mm Hg) of mean transvalvular gradient, remained 26 mm or decreased (32 to 28 mm) right-ventricular end-diastolic diameter. The body surface area increased (1.07 to 1.42 m 2 and 1.07 to 1.46 m 2 , respectively). No signs of valve degeneration were observed in both patients. Conclusions— TE of human heart valves using autologous EPC is a feasible and safe method for pulmonary valve replacement. TE valves have the potential to remodel and grow accordingly to the somatic growth of the child.
Cell-cell interactions influence survival and differentiation of purified purkinje cells in vitro
Authors: Carlos A. BaptistaMary E.^Hatten, Richard Blazeski, Carol A. Mason
Journal: Neuron (1994)

To determine the role of cell-cell interactions in Purkinje cell survival and dendritic differentiation, perinatal mouse Purkinje cells were purified, and their development was analyzed in vitro. In isolation at low density, Purkinje cell survival was poor, improved by neuronal contacts, either with purified granule neurons or with Purkinje cells themselves. Moreover, coculture with specific cell populations led to widely different degrees of Purkinje cell differentiation. Purified Purkinje cells cultured alone or with an inappropriate afferent, the mossy fibers, did not progress beyond immature forms. With astroglia, Purkinje cells had thin smooth processes. Proper Purkinje cell differentiation was driven only by coculture with granule cells, resulting in dendrites with spines receiving synapses. These results suggest that Purkinje cell differentiation is regulated by local epigenetic factors, provided in large part by the granule neuron.
Leukotriene C4 Synthase Gene A(-444) C Polymorphism and Clinical Response to a CYS-LT(1) Antagonist, Montelukast, in Japanese Children with Asthma
Authors: A. Terada, A. Ueda, H. Murai, T. Tanaka, Y. Hirabayashi, M. Hoshino, K. Ban, S. Shimizu, T. Kobayashi, T. Ichiki, T. Yokoyama, H. Maniwa, M. Ouchi, M. Miyachi, Y. Kokubo, T. Yoshida, H. Tanaka, T. Ito, H. Togari
Journal: Journal of Allergy and Clinical Immunology (2009)
Manslaughter by Fake Artesunate in Asia—Will Africa Be Next?
Authors: Paul N Newton, Rose McGready, Facundo Fernandez, Michael D Green, Manuela Sunjio, Carinne Bruneton, Souly Phanouvong, Pascal Millet, Christopher J. M Whitty, Ambrose O Talisuna, Stephane Proux, Eva Maria Christophel, Grace Malenga, Pratap Singhasivanon, Kalifa Bojang, Harparkash Kaur, Kevin Palmer, Nicholas P. J Day, Brian M Greenwood, François Nosten, Nicholas J White
Journal: PLoS Medicine (2006)

Genuine hologram has the legend 'GUILIN PHARMA' here.Visible with the naked eye, as a thin strip below the waves.Letters are ~ 0.1mm high The photograph, left, is of the genuine hologram attached to the blister packs and packets of the genuine 'Guilin Pharma' artesunate.Below are pictures of 11 types of fake artesunate stickers & holograms with their distinguishing features.As hologram colour depends on the light, please do not use the colours printed here to judge whether artesunate is genuine or fake Guilin Pharmaceutical Co., Ltd.developed their hologram as a security device in response to the first type ('Type 1') of counterfeit artesunate circulated which had no hologram attached.As a result, any 'Guilin Pharma' artesunate now circulating without a blister pack hologram is almost certainly counterfeit or expired.Subsequently, at least 11 different types of counterfeit 'Guilin Pharma artesunate' have been found in Southeast Asia [Burma (Myanmar), Cambodia, China, Lao PDR, Thailand (only on the western border) and Vietnam] with counterfeit stickers or holograms, and there are probably more types circulating.Genuine and counterfeit holograms are ~ 13 mm in diameter.The genuine and 'Type 10' holograms have 'X-52' visible across the mountains when viewed under UV light.Other features of the counterfeit artesunate that differ from the genuine product include -poor printing of bar codes on packets,poor printing of codes on blister packs, codes on blister packs printed with the font made of numerous small dots, poor stamping of code 'AS' and score line on tablets, raised edges of tablets, very hard tablets, blisterpack abbreviations in capital letters ('MFG' and 'EXP') and unusually late expiry date in relation to date of manufacture (>3years).Counterfeits tend to be cheaper than the genuine product.This update has been issued following the discovery that counterfeit artesunate 'Types 4' and '9' contain small quantities of artesunate (~ 10mg) which will not be efficacious but may give misleading positive result on the Fast Red TR dye test and may facilitate the selection of artesunate-resistant malaria parasites.Although, regrettably, the counterfeiters have targeted the 'Guilin Pharma' product, it is possible that other fake artesunate products exist in Asia.Therefore, drug regulatory authorities should be vigilant and regularly monitor the quality of artesunate available on the market.If you are uncertain as the authenticity of any artesunate sample based on the characteristics of the packaging, please check by chemical analysis of the tablet Genuine hologram under UV light with 'X-52' at mountain base
Should surgery be carried out in patients with hepatocellular carcinoma with portal hypertension?
Authors: Tian Yang, Wan Yee Lau, Han Zhang, Mengchao Wu, Feng Shen
Journal: Hepatology (2015)

This work was supported by grants from the National Natural Science Foundation of China (No. 81472284, 81172020 and 81372262 for Tian Yang) Potential conflict of interest: Nothing to report. To the Editor: We read with great interest the meta‐analysis by Berzigotti et al.1 This study revealed that clinically significant portal hypertension (CSPH) significantly increased the 3‐ and 5‐year mortality rates and risks of clinical liver decompensation after surgery on hepatocellular carcinoma (HCC) patients with cirrhosis and portal hypertension. We appreciate their hard work in coming up with this systematic review and meta‐analysis. However, as hepatic surgeons, we would like to raise the following points: Postoperative outcomes should include not only long‐term (e.g., recurrence and survival), but also short‐term outcomes (e.g., postoperative morbidity and mortality). This meta‐analysis hardly touches on sufficient variables of short‐term outcomes or recurrence as study endpoints. We consider the investigators' conclusion on the absolute necessity to use hepatic venous pressure gradient (HVPG) in the diagnosis of CSPH debatable. HVPG is an invasive procedure performed by blood vessel. Given that endoscopic finding of varices is sufficient to diagnose CSPH,2 why is a less‐invasive procedure of endoscopy not used as the first‐line diagnostic modality for CSPH? We agree with the investigators that: "Even if the presence of CSPH should not be regarded as an absolute contraindication to surgery, our results demonstrate that it has to be considered a major negative prognostic factor," which was also admitted by other scholars.3 However, we would like to point out that the majority of clinicians may be more interested in understanding the prognostic difference between surgery and other treatment modalities (e.g., transcatheter arterial chemoembolizaion or sorafenib), provided that they are comparable for this specific, but not uncommon, group of patients. A prospective study, or even better, a prospective, randomized trial would be required.
The role of fatty acid saturation on plasma lipids, lipoproteins, and apolipoproteins: I. Effects of whole food diets high in cocoa butter, olive oil, soybean oil, dairy butter, and milk chocolate on the plasma lipids of young men
Authors: P.M. Kris-Etherton, Janice Derr, Diane C. Mitchell, Vikkie A. Mustad, Mary E. Russell, Elaine T. McDonnell, Deborah Salabsky, Thomas A. Pearson
Journal: Metabolism (1993)

The present studies were conducted to evaluate the cholesterolemic effects of whole-food diets high in stearic acid. In study no. 1, normocholesterolemic young men were fed diets high in stearic acid provided by cocoa butter (CB); oleic acid provided by olive oil (OO); linoleic acid provided by soybean oil (SO); and myristic acid (and lauric acid) provided by dairy butter (B). In study no. 2, different subjects with similar baseline characteristics were fed diets high in stearic acid provided by milk chocolate (C), CB, CB + B (4:1, MIX), and myristic (and lauric) acid provided by B. Both studies used a randomized, crossover, double-blind experimental design, and experimental subjects (n = 18 for study no. 1 and n = 15 for study no. 2) in each study consumed every diet for 26 days with a 1-month wash-out period between each experimental period. The diets provided 37% of calories from fat, of which 81% was provided by the test fat. Ten ounces (280 g) C was provided daily by the C diet. In study no. 1, the B diet was hypercholesterolemic, whereas the SO diet was hypocholesterolemic, compared with the other diets. The OO and SO diets were hypocholesterolemic compared with the CB diet. Low-density lipoprotein (LDL) cholesterol levels, in general, paralleled the changes in plasma total cholesterol levels. SO significantly decreased apolipoprotein (apo) B levels compared with the other diets. Plasma very-low-density lipoprotein (VLDL) cholesterol, high-density lipoprotein (HDL) cholesterol, and apo A-I levels were unaffected by the experimental diets. Compared with baseline, the CB diet elicited a neutral cholesterolemic response, whereas the B diet was hypercholesterolemic and the OO and SO diets were hypocholesterolemic. In study no. 2, the C, MIX, and CB diets elicited a similar and neutral cholesterolemic response; however, all were hypocholesterolemic compared with the B diet. Since the CB and B diets had virtually identical quantities of long-chain saturated fatty acids (SFA; C12:0 to C18:0), we believe that CB is hypocholesterolemic compared with B because of its high proportion of stearic acid. Thus, stearic acid has unique effects on plasma total cholesterol levels compared with other long-chain saturated fatty acids; the mechanism by which stearic acid exerts this effect is not clear. We also have shown that linoleic acid has a more potent hypocholesterolemic effect than oleic acid and does not affect HDL cholesterol levels or HDL composition.
GROUP THERAPY ON AN ACUTE SERVICE
Authors: M. P. GRAEBER, G. C. BROWN, RUTH M. PILLSBURY, J. D. ENTERLINE
Journal: American Journal of Psychiatry (1954)

1. Group therapy when used as the basic organization of a ward is effective in controlling hyperactivity and acting-out. 2. Nurses and aides can be used both effectively and economically in such a program. 3. Providing a choice and variety of group leaders has seemed to increase therapeutic relationships.
Carnitine palmitoyl transferase-I inhibition prevents ventricular remodeling and delays decompensation in pacing-induced heart failure
Authors: V LIONETTI, A LINKE, M CHANDLER, M YOUNG, M PENN, S GUPTE, C DAGOSTINO, T HINTZE, W STANLEY, F RECCHIA
Journal: Cardiovascular Research (2005)

Experimental evidence suggests that modulation of myocardial substrate metabolism can markedly affect the progression of chronic heart failure (HF). We tested whether the inhibition of carnitine palmitoyl transferase-I (CPT-I), the enzyme regulating mitochondrial fatty acid oxidation, slows left ventricular remodeling and deterioration of function in pacing-induced HF.Normal dogs (n=9) were compared to untreated dogs with pacing-induced HF (n=9) and HF dogs treated with 65 mg/kg/day of oxfenicine (HF+Oxf, n=9), a CPT-I inhibitor.HF+Oxf reached terminal failure (LV end-diastolic pressure=25 mm Hg) 6 days later than untreated HF (P<0.05). At 28 days of pacing, hemodynamic alterations and LV dilation were significantly attenuated and the 25% decrease in LV wall thickness was completely prevented in HF+Oxf vs. untreated HF, as was the activation of matrix metalloproteinase-2 and -9, markers of tissue remodeling. Oxfenicine also prevented HF-induced transcriptional down-regulation of CPT-I, medium chain acyl-CoA dehydrogenase, GAPDH and citrate synthase, key enzymes of cardiac energy metabolism. In addition, mRNA, but not protein levels of the nuclear receptor peroxisome proliferator-activated receptor-alpha were reduced in untreated HF, while they did not change significantly in HF+Oxf, as compared to control.CPT-I inhibition early in the development of HF prevented LV wall thinning and delayed the time to end-stage failure. While these results are limited to an experimental model of disease, they nevertheless suggest that CPT-I inhibition might be effective for slowing the progression of clinical HF.
Abnormal Cytogenetics at Date of Morphologic Complete Remission Predicts Short Overall and Disease-Free Survival, and Higher Relapse Rate in Adult Acute Myeloid Leukemia: Results From Cancer and Leukemia Group B Study 8461
Authors: Guido Marcucci, Krzysztof Mrózek, Amy S. Ruppert, Kellie J. Archer, Mark J. Pettenati, Nyla A. Heerema, Andrew J. Carroll, Prasad R.K. Koduru, Jonathan E. Kolitz, Lisa J. Sterling, Colin G. Edwards, John Anastasi, Richard A. Larson, Clara D. Bloomfield
Journal: Journal of Clinical Oncology (2004)

Purpose As most patients with acute myeloid leukemia (AML) with morphologic complete remission (CR) ultimately relapse, better predictors for outcome are needed. Recently, Cheson et al suggested using cytogenetic remission (CRc) as part of the criteria for CR. To our knowledge, ours is the first relatively large study evaluating the usefulness of CRc attained immediately following induction chemotherapy. Patients and Methods We included AML patients treated on Cancer and Leukemia Group B front-line studies with cytogenetic samples obtained at diagnosis and at the first day of documented CR following induction. Patients with abnormal cytogenetics at diagnosis, and normal cytogenetics at CR (NCR; n = 103) were compared with those with abnormal cytogenetics both at diagnosis and at CR (ACR; n = 15) for overall survival (OS), disease-free survival (DFS), and cumulative incidence of relapse (CIR). Cox proportional hazards models determined the prognostic significance of cytogenetics at CR, adjusting for other covariates. Results Clinical features were similar for both groups, with the exception of favorable cytogenetics [t(8;21), inv(16)/t(16;16), t(15;17)] at diagnosis, which was more frequent (P = .03) in the NCR group. Median follow-up was 3.1 years (range, 1.0 to 11.4 years). ACR patients had significantly shorter OS (P = .006) and DFS (P = .0001), and higher CIR (P = .0001). In multivariable models, the NCR and ACR groups were predictors for OS (P = .03), DFS (P = .02), and CIR (P = .05). The relative risk of relapse or death was 2.1 times higher for ACR patients than for NCR patients (95% CI, 1.1 to 3.9). Conclusion Our data suggest that converting to normal karyotype at the time of first CR is an important prognostic indicator and support the use of CRc as a criterion of CR in AML.