tbuckley/cabot-search huggingface dataset:
Stratum basale keratinocyte expression of the cell-surface glycoprotein CDCP1 during epidermogenesis and its role in keratinocyte migration
Authors: J.A. McGovern, J.R. Heinemann, L.J. Burke, R. Dawson, T.J. Parker, Z. Upton, J.D. Hooper, K.J. Manton
Journal: British Journal of Dermatology (2012)

Epidermogenesis and epidermal wound healing are tightly regulated processes during which keratinocytes must migrate, proliferate and differentiate. Cell-to-cell adhesion is crucial to the initiation and regulation of these processes. CUB-domain-containing protein (CDCP)1 is a transmembrane glycoprotein that is differentially tyrosine phosphorylated during changes in cell adhesion and survival signalling, and is expressed by keratinocytes in native human skin, as well as in primary cultures.To investigate the expression of CDCP1 during epidermogenesis and its role in keratinocyte migration.We examined both human skin tissue and an in vitro three-dimensional human skin equivalent model to examine the expression of CDCP1 during epidermogenesis. To examine the role of CDCP1 in keratinocyte migration we used a function-blocking anti-CDCP1 antibody and a real-time Transwell™ cell migration assay.Immunohistochemical analysis indicated that in native human skin CDCP1 is expressed in the stratum basale and stratum spinosum. In contrast, during epidermogenesis in a three-dimensional human skin equivalent model, CDCP1 was expressed only in the stratum basale, with localization restricted to the cell-cell membrane. No expression was detected in basal keratinocytes that were in contact with the basement membrane. Furthermore, an anti-CDCP1 function-blocking antibody was shown to disrupt keratinocyte chemotactic migration in vitro.These findings delineate the expression of CDCP1 in human epidermal keratinocytes during epidermogenesis and demonstrate that CDCP1 is involved in keratinocyte migration.
PhysioBank, PhysioToolkit, and PhysioNet
Authors: Ary L. Goldberger, Luis A. N. Amaral, Leon Glass, Jeffrey M. Hausdorff, Plamen Ch. Ivanov, Roger G. Mark, Joseph E. Mietus, George B. Moody, Chung-Kang Peng, H. Eugene Stanley
Journal: Circulation (2000)

The newly inaugurated Research Resource for Complex Physiologic Signals, which was created under the auspices of the National Center for Research Resources of the National Institutes of Health, is intended to stimulate current research and new investigations in the study of cardiovascular and other complex biomedical signals. The resource has 3 interdependent components. PhysioBank is a large and growing archive of well-characterized digital recordings of physiological signals and related data for use by the biomedical research community. It currently includes databases of multiparameter cardiopulmonary, neural, and other biomedical signals from healthy subjects and from patients with a variety of conditions with major public health implications, including life-threatening arrhythmias, congestive heart failure, sleep apnea, neurological disorders, and aging. PhysioToolkit is a library of open-source software for physiological signal processing and analysis, the detection of physiologically significant events using both classic techniques and novel methods based on statistical physics and nonlinear dynamics, the interactive display and characterization of signals, the creation of new databases, the simulation of physiological and other signals, the quantitative evaluation and comparison of analysis methods, and the analysis of nonstationary processes. PhysioNet is an on-line forum for the dissemination and exchange of recorded biomedical signals and open-source software for analyzing them. It provides facilities for the cooperative analysis of data and the evaluation of proposed new algorithms. In addition to providing free electronic access to PhysioBank data and PhysioToolkit software via the World Wide Web (http://www.physionet. org), PhysioNet offers services and training via on-line tutorials to assist users with varying levels of expertise.
AN EXPERIMENTAL STUDY INTO THE CAUSE OF THE INCREASED PORTAL PRESSURE IN PORTAL CIRRHOSIS
Authors: Frederick C. Herrick
Journal: The Journal of Experimental Medicine (1907)

1. In the liver of portal cirrhosis there is a far freer communication between the arterial and portal currents than in the normal liver. 2. Factors contributing to the increased portal pressure in portal cirrhosis are (1) the direct communication of the arterial pressure to the portal vessels through dilated capillaries, (2) the larger volume-flow of the hepatic artery in proportion to the portal flow in cirrhosis as compared to that in the normal liver. 3. A portal cirrhotic liver gives passage to an amount of portal fluid proportionate to .its weight. There is no obstruction to the portal vessels from fibrosis in the large portal cirrhotic liver. 4. From an arterial inflow there is a free return flow through the portal as well as through the hepatic veins in both normal and cirrhotic livers. 5. From a portal inflow the return is through the hepatic vein only. The Gad's theory of valves and the arterial capillary network account for this fact. 6. The portal pressure has a decided influence on the arterial volume-flow and vice versa. This influence is more marked in the cirrhotic than in the normal liver. 7. The communication of the arterial pressure to the portal pressure is an important factor in an explanation of the increased portal pressure in portal cirrhosis.
The level of BLyS (BAFF) correlates with the titre of autoantibodies in human Sjogren's syndrome
Authors: X Mariette
Journal: Annals of the Rheumatic Diseases (2003)

<b>Background:</b> Increased levels of B lymphocyte stimulator (BLyS) have been detected in serum from patients with systemic lupus erythematosus and rheumatoid arthritis. <b>Objective:</b> To determine the level of BLyS in serum from patients with primary’s Sjögren’s syndrome (SS), another autoimmune disease in which B cell activation is high. <b>Methods:</b> Serum samples from 49 patients with primary SS according to the revised European criteria were assayed for BLyS, quantitative immunoglobulins, and autoantibody levels and compared with samples from 47 healthy control subjects. <b>Results:</b> The median level of BLyS was 5.99 ng/ml (25th-75th centile range 3.20–8.93 ng/ml) in SS <i>v</i> 2.49 ng/ml (25th-75th centile range 1.96–2.96 ng/ml) in healthy controls (p&lt;0.001). More importantly, among patients with SS, the presence of anti-SSA antibodies was associated with significantly higher levels of BLyS (medians 7.90 ng/ml <i>v</i> 3.70 ng/ml; p=0.008) as was the presence of anti-SSB antibodies (medians 7.14 ng/ml <i>v</i> 3.70 ng/ml; p=0.02) and of rheumatoid factor (medians 7.70 ng/ml <i>v</i> 3.80 ng/ml; p=0.016). The level of BLyS in three patients with a monoclonal gammopathy was higher than in the other patients (medians 26.53 ng/ml <i>v</i> 5.92 ng/ml; p=0.13). Higher levels of BLyS were associated with higher levels of gammaglobulins and IgG. There was a strong correlation between BLyS and rheumatoid factor level (<i>r</i>=0.71, p&lt;0.0001), anti-SSA IgG level (<i>r</i>=0.32, p=0.02) and anti-SSA IgM level (<i>r</i>=0.39, p=0.006). <b>Conclusion:</b> In human SS the level of BLyS correlates with the level of autoantibodies. Thus, BLyS may play a part in activating specific autoreactive B cells and modulating the level of production of autoantibodies which are the hallmark of the disease. These findings raise the possibility of a novel therapeutic approach in human SS.
Sternomastoid muscle fatigue and twitch maximum relaxation rate in patients with steroid dependent asthma.
Authors: V H Mak, J R Bugler, S G Spiro
Journal: Thorax (1993)

BACKGROUND--Long term oral corticosteroid treatment is a cause of myopathy of the skeletal muscles. The effect of long term treatment with oral corticosteroids on the respiratory muscles is uncertain. Respiratory muscle function and fatigue in sternomastoid muscle were investigated in a group of patients with chronic severe asthma who were taking oral corticosteroids. The results were compared with those from a group of patients with chronic airflow limitation who were not taking oral steroids. METHODS--Twelve patients with chronic severe asthma, taking a mean daily dosage of 8 mg of prednisolone for a mean (SD) of 16.8 (9.1) years, were compared with patients with chronic airflow limitation and individually matched for sex, age, and severity of airflow limitation. Lung function tests, maximal mouth pressures, and quadriceps and sternomastoid muscle strength were measured. The sternomastoid muscle was fatigued by maximal headlift exercise to 70% of initial headlift force and the endurance time noted. Sternomastoid fatigue was assessed by twitch maximum relaxation rate (TMRR) measured in the fresh state and for 30 minutes after exercise. RESULTS--There was no significant difference between the control group and the corticosteroid group for maximal mouth pressures, fresh state TMRR, and quadriceps and sternomastoid strength. The control group had a significantly longer mean (SD) endurance time than the corticosteroid group (121 (47) s v 86 (24) s), and also had significantly less slowing and faster recovery of the TMRR after exercise. The slowing and recovery of the TMRR in the corticosteroid group, however, was similar to that previously reported for normal subjects. CONCLUSION--Respiratory muscle weakness does not occur more often in patients taking oral corticosteroids. The corticosteroid group was more prone to fatigue than the control group, but was similar to normal subjects. This suggests that chronic airflow limitation may produce a training effect on the respiratory muscles that might be attenuated by long term oral corticosteroid treatment.
Remarks on the Changes in the Spinal Cord in Two Cases of Pernicious Anaemia
Authors: J. M. Clarke
Journal: BMJ (1897)

THE two following cases afford examples of the changes present in the spinal cord in pernicious anvemia, and also illustrate the fact that in one class of these cases careful examination failed to elicit clinical symptoms of the disease of the cord, a result possibly to be attributed in some instances to the severity of the general symptoms obscuring those due to the spinal cord affection.E. W., aged 46, was admitted into the Bristol General Hospital on November 17th, I896, complaining of great weakness, palpitation, and shortness of breath.Except that one sister had died of consumption the family history was good.The patient had been married twenty-six years andhad one child; no miscarriages.She had rheumatic feverfour- teen years ago, and jaundice one year ago, but had always been strong and healthy.She had suffered from piles but not from hiemorrhage from them.The catamenia ceased twelve months ago; previously to that she Fig i.-Cord at level of first and second cervical roots: Degeneration in posterior, columns.lhad always been regular, and had nevei suffered from menorrhsgia.She dateca her illness from a fall in Juie, 1896, after whic~h she became Vale, lost flesh, and suff'ered fromn increasing Weakness in the legs, with a feeling of deadness in them.Nine weeks before admission she had an attack of "1bronchitis and inflammation of the lUngs," and was very ill for three weeks.This was followed by jaunadice, with pains in the bowels, ~obstinate constipat~ion, and vomiting after food.Her legs became swollen and weak, and either felt very cold or of a burning heat.She kept her (bed during the whole nine weeks until admission.She had never suf fered from meliena or huematuria.On admission she was very pale and rather thin, the skin of a pale lemon colour.She was very weak and had to be fed.
Transvection mediated by the translocated cyclin D1 locus in mantle cell lymphoma
Authors: Hui Liu, Jing Huang, Jin Wang, Shuguang Jiang, Alexis S. Bailey, Devorah C. Goldman, Markus Welcker, Victoria Bedell, Marilyn L. Slovak, Bruce Clurman, Mathew Thayer, William H. Fleming, Elliot Epner
Journal: The Journal of Experimental Medicine (2008)

In mantle cell lymphoma (MCL) and some cases of multiple myeloma (MM), cyclin D1 expression is deregulated by chromosome translocations involving the immunoglobulin heavy chain (IgH) locus. To evaluate the mechanisms responsible, gene targeting was used to study long-distance gene regulation. Remarkably, these targeted cell lines lost the translocated chromosome (t(11;14)). In these MCL and MM cells, the nonrearranged cyclin D1 (CCND1) locus reverts from CpG hypomethylated to hypermethylated. Reintroduction of the translocated chromosome induced a loss of methylation at the unrearranged CCND1 locus, providing evidence of a transallelic regulatory effect. In these cell lines and primary MCL patient samples, the CCND1 loci are packaged in chromatin-containing CCCTC binding factor (CTCF) and nucleophosmin (NPM) at the nucleolus. We show that CTCF and NPM are bound at the IgH 3′ regulatory elements only in the t(11;14) MCL cell lines. Furthermore, NPM short hairpin RNA produces a specific growth arrest in these cells. Our data demonstrate transvection in human cancer and suggest a functional role for CTCF and NPM.
Effect of earlier initiation of antiretroviral treatment and increased treatment coverage on HIV-related mortality in China: a national observational cohort study
Authors: Fujie Zhang, Zhihui Dou, Ye Ma, Yao Zhang, Yan Zhao, Decai Zhao, Shuntai Zhou, Marc Bulterys, Hao Zhu, Ray Y Chen
Journal: The Lancet Infectious Diseases (2011)
Pathogenesis of Marek's Disease: Early Appearance of Marek's Disease Tumor-Associated Surface Antigen in Infected Chickens&lt;xref ref-type="fn" rid="FN2"&gt;2&lt;/xref&gt;
Authors: K. K. Murthy, B. W. Calnek
Journal: JNCI Journal of the National Cancer Institute (1978)

Marek's disease tumor-associated surface antigen (MATSA) appeared in different lymphoid tissues of P-line chickens soon after they were infected with BC-1 strain of Marek's disease virus. MATSA-bearing cells first appeared in spleens by 5 days post infection (PI) and were observed through a 21-day experimental period at mean levels varying from 3.8 to 21.9% of the total cells examined. Lower percentages of MATSA-bearing cells were observed in the thymus, in the bursa of Fabricius, among peripheral blood lymphocytes, and among bone marrow cells beginning 7 days PI. The antigen was not detected on normal lymphocytes from chickens or chicken embryos, nor was it detected on cultured chicken embryo fibroblasts infected or transformed by avian RNA tumor viruses.
Functional role of the soluble guanylyl cyclase α1 subunit in vascular smooth muscle relaxation☆
Authors: S NIMMEGEERS, P SIPS, E BUYS, P BROUCKAERT, J VANDEVOORDE
Journal: Cardiovascular Research (2007)

Soluble guanylyl cyclase (sGC), the predominant receptor for nitric oxide (NO), exists in 2 active isoforms (alpha(2)beta(1) and alpha(1)beta(1)). In vascular tissue sGCalpha(1)beta(1) is believed to be the most important. The aim of our study was to investigate the functional importance of the sGCalpha(1)-subunit in vasorelaxation.Aortic and femoral artery segments from male and/or female sGCalpha(1)(-/-) mice and wild-type littermates were mounted in a small-vessel myograph for isometric tension recording. This was supplemented with biochemical measurements of the cGMP concentration and sGC enzyme activity.The functional importance of sGCalpha(1)beta(1) was demonstrated by the significantly decreased relaxing effects of acetylcholine (ACh), sodium nitroprusside (SNP), S-nitroso-N-acetylpenicillamine (SNAP), NO gas, YC-1, BAY 41-2272 and T-1032 in the sGCalpha(1)(-/-) mice of both genders. Moreover, the basal and SNP-stimulated cGMP levels and basal sGC activity were significantly lower in the sGCalpha(1)(-/-) mice. However, the relaxing effects of NO, BAY 41-2272 and YC-1 seen in blood vessels from sGCalpha(1)(-/-) mice indicate a role for an sGCalpha(1)beta(1)-independent mechanism. The increase in sGC activity after addition of BAY 41-2272 and the inhibition of the ACh-, SNP-, SNAP- and NO gas-induced response by the sGC inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) in the sGCalpha(1)(-/-) mice are observations suggesting that the sGCalpha(2)beta(1) isoform is also functionally active. However, the insignificant increase in cGMP in response to SNP and the non-upregulated sGCalpha(2) expression level in the sGCalpha(1)(-/-) mice suggest rather the involvement of (an) sGC-independent mechanism(s).We conclude that sGCalpha(1)beta(1) is involved in the vasorelaxation induced by NO-dependent and NO-independent sGC activators in both genders. However, the remaining relaxation seen in the sGCalpha(1)(-/-) mice suggests that besides sGCalpha(1)beta(1) also the minor isoform sGCalpha(2)beta(1) and/or (an) sGC-independent mechanism(s) play(s) a substantial role.
Thymic stromal lymphopoietin is released by human epithelial cells in response to microbes, trauma, or inflammation and potently activates mast cells
Authors: Zoulfia Allakhverdi, Michael R. Comeau, Heidi K. Jessup, Bo-Rin Park Yoon, Avery Brewer, Suzanne Chartier, Nicole Paquette, Steven F. Ziegler, Marika Sarfati, Guy Delespesse
Journal: The Journal of Experimental Medicine (2007)

Compelling evidence suggests that the epithelial cell-derived cytokine thymic stromal lymphopoietin (TSLP) may initiate asthma or atopic dermatitis through a dendritic cell-mediated T helper (Th)2 response. Here, we describe how TSLP might initiate and aggravate allergic inflammation in the absence of T lymphocytes and immunoglobulin E antibodies via the innate immune system. We show that TSLP, synergistically with interleukin 1 and tumor necrosis factor, stimulates the production of high levels of Th2 cytokines by human mast cells (MCs). We next report that TSLP is released by primary epithelial cells in response to certain microbial products, physical injury, or inflammatory cytokines. Direct epithelial cell-mediated, TSLP-dependent activation of MCs may play a central role in "intrinsic" forms of atopic diseases and explain the aggravating role of infection and scratching in these diseases.
Ironing Out Cancer
Authors: Suzy V. Torti, Frank M. Torti
Journal: Cancer Research (2011)

Abstract New insights into the roles of proteins that regulate cellular iron in cancer growth, angiogenesis, and metastasis have recently emerged. Discoveries of the roles of ferroportin, hepcidin, lipocalin 2, and members of the six transmembrane epithelial antigen of the prostate (STEAP) and iron regulatory protein (IRP) families in cancer have provided specificity and molecular definition to the role of iron homeostasis in cancer growth and metastasis. A number of studies directly support a role of these proteins in modifying bioavailable iron, whereas other studies suggest that at least some of their effects are independent of their role in iron biology. Cancer Res; 71(5); 1511–4. ©2011 AACR.
Excimer laser-facilitated coronary angioplasty. Relative risk analysis of acute and follow-up results in 200 patients.
Authors: J A Bittl, T A Sanborn
Journal: Circulation (1992)

Excimer laser coronary angioplasty has been reported to be a promising treatment for complex coronary artery disease. The purpose of this study was to define the predictors of acute success and restenosis after this experimental intervention.A cohort of 200 consecutive patients had a minimum of 6 months of follow-up evaluation after treatment of 215 coronary stenoses that were carefully selected for excimer laser coronary angioplasty. At the time of the initial procedure, the laser catheter alone produced a residual stenosis of less than or equal to 50% at 119 of 215 lesions (55.4%). For complete dilatation, 87.9% of the lesions required adjunctive balloon angioplasty. Clinical success was achieved in 183 of the 200 patients (91.5%), as indicated by a reduction by at least 20% of the narrowing of the vessel diameter, less than or equal to 50% residual stenosis, and no in-hospital complication. Complications included abrupt closure (5.0%), myocardial infarction (3.5%), bypass surgery (3.0%), perforation (2.0%), and death (0.0%). Logistic regression analysis showed that lesions at vessel bifurcations (success rate, 66%; adjusted odds ratio [OR] = 0.16; p = 0.002) or in tortuous vessels (success rate, 82%; OR = 0.48; p = 0.004) were associated with decreased clinical success. However, acceptable success rates were achieved in patients with lesions in saphenous vein grafts more than 3 years old (success rate, 94%; OR = 1.40; p = 0.75), in ostial lesions (success rate, 100%; OR = 3.36; p = 0.43), and in lesions longer than 10 mm (success rate, 93.5%; OR = 1.50; p = 0.39). Clinical follow-up was available in 197 of the 200 patients (98.5%) a mean of 5.9 +/- 1.9 months after angioplasty, at which time 31.0% of patients had developed symptoms or evidence of ischemia. No patient died during the study. Follow-up angiography was obtained in 83.1% of eligible patients after a mean [+/- SD] of 5.2 +/- 2.0 months. Angiographic restenosis, defined by greater than 50% stenosis, appeared at 78 of 164 lesions (47.6%). By logistic regression analysis, only lesions in saphenous vein grafts were associated with a decreased rate of restenosis (restenosis rate, 20%; OR = 0.18; p = 0.01).This analysis, which defines the profile of risk for excimer laser angioplasty, provides a sound basis for rigorous comparison of adjunctive excimer laser with balloon angioplasty for ostial narrowings, long lesions, and saphenous vein graft stenoses.
Calcineurin Is Activated in Rat Hearts With Physiological Left Ventricular Hypertrophy Induced by Voluntary Exercise Training
Authors: Yoko Eto, Katsunori Yonekura, Makoto Sonoda, Naoto Arai, Masataka Sata, Seiryo Sugiura, Katsu Takenaka, Antonio Gualberto, Mary L. Hixon, Mark W. Wagner, Teruhiko Aoyagi
Journal: Circulation (2000)

Calcineurin may play a pivotal role in the signaling of cardiac hypertrophy; since this hypothesis was first put forward, controversial reports have been published using various experimental models. This study was designed to compare the physiological left ventricular hypertrophy (LVH) induced by voluntary exercise with LVH induced by aortic constriction and to determine whether calcineurin participates in the signaling of exercise-induced LVH.Wistar rats were assigned to 1 of the following 5 groups: 10 weeks of voluntary exercise (EX), a sedentary regimen, a 1-week (AC1) or 4-week (AC4) ascending aortic constriction period, or a sham operation. EX rats ran 2.4+/-0.7 km/day voluntarily in specially manufactured cages; this was associated with an increase of LV diastolic dimension and stroke volume. Myocardial calcineurin activity markedly increased in EX rats (46.4+/-8.3 versus 18.4+/-0.5 pmol. min(-1). mg(-1) in sedentary rats; P<0.001) and in AC1 rats (44.9+/-6.7 versus 22.1+/-3.7 pmol. min(-1). mg(-1) in sham-operated rats; P<0.001), but not in AC4 rats (29.0+/-3.4 pmol. min(-1). mg(-1)). Treatment with cyclosporin A completely inhibited the development of LVH in EX rats, but it only partially attenuated the development of LVH in AC4 rats.Calcineurin was activated in exercise-induced physiological LVH and in the developing phase of LVH (AC1), but not in decompensated pressure-overload hypertrophy (AC4). Cyclosporin therapy for the prevention of LVH may be harmful because it does not block the development of pathological hypertrophy but rather that of favorable adaptive hypertrophy.