tbuckley/cabot-search huggingface dataset:
Pitfalls in Digital Computation of the Impulse Response of Vascular Beds from Indicator-Dilution Curves
Authors: JOHN GAMEL, WILLIAM F. ROUSSEAU, CHARLES R. KATHOLI, EMMANUEL MESEL
Journal: Circulation Research (1973)

Many methods are available for digital computation of the impulse response from indicator-dilution measurements representing input and output signals. In all instances, the only criterion for validity of the computation is comparison of the reconvolution of the computed impulse response and the input with the actual output. In this paper, a model mathematical system was constructed with a known impulse response; noise and time variation could be introduced independently or simultaneously in the input and the output data. Six methods for digital computation of the impulse response were applied to data from this system and to actual dye-dilution data. Precision of reconvolution did not assure that the computed response would resemble the actual response of the system. Some numerical considerations also significantly affected the digital computation of a valid response.
Cadmium the missing link between smoking and increased rheumatoid disease activity?
Authors: Matthew Cates, David Hutchinson
Journal: Annals of the Rheumatic Diseases (2014)

Ospelt et al 1 have observed a number of important and interesting observations in their paper “Smoking induces transcription of the heat shock protein system in the joints”. It was observed that when synovial fibroblasts were incubated with 5% cigarette smoke extract there was a significant upregulation of the heat shock proteins DnaJA4, DnaJB4, DnaJC6, HspB8 and Hsp70. This important scientific work follows on from the overwhelming epidemiological evidence that smoking is associated with rheumatoid arthritis (RA). A meta-analysis of seven case control and …
P776 REDUCTION OF MIR-122 IN IFNL3 CT+TT CARRIERS AND DURING PROGRESSION OF FIBROSIS IN PATIENTS WITH CHRONIC HEPATITIS C
Authors: E. Estrabaud, M. Lapalus, P. Broet, K. Appourchaux, S. De Muynck, O. Lada, M. Martinot-Peignoux, I. Bieche, D. Valla, P. Bedossa, P. Marcellin, M. Vidaud, T. Asselah
Journal: Journal of Hepatology (2014)
Blood lactate recovery at different times of the day and menstrual cycle phases
Authors: Effat Bambaeichi, Nader Rahnama, Akram Khani
Journal: British Journal of Sports Medicine (2010)

Lactate removal of body at the end of practices session is essential for subsequent performance. The aim of this study was to establish the time of day and the effect of menstrual cycle on lactate recovery after a maximal exercise. Twelve physical education female students (mean±SD, aged 20.75±1.60 years, height 164.75±3.62 cm, weight 55.08±5.45 kg) participated in this study. All subjects performed the Bruce test to exhaustion and then walked for 20 min, with 1.7 speed (mph) and 0% grade of slope at recovery period. Blood lactate samples were obtained from the tip of the subjects' index finger immediately after the test and at 5th, 10th and 20th min of recovery period at two times of day (06:00 and 18:00 h) and two phases of the menstrual cycle (mid-luteal and mid-follicular phases). A lactometer was used for analysis. A significant variation in blood lactate concentrations was found at the 5th, 10th and 20th min of recovery between 06:00 and 18:00 (F=2.99, p&lt;0.05). No significant effect of menstrual cycle (F=1.10, p&gt;0.05) and no significant interaction effects (menstrual cycle × time of day) were observed for lactate recovery (F=0.67, p&gt;0.05). It can be concluded that lactate recovery in the afternoon occurred faster compared to that in the morning. But follicular and luteal phases of the menstrual cycle had no effects on the lactate recovery.
Benign Pleural Lesions Simulating Tumour
Authors: L. Tivenius
Journal: Thorax (1963)

Without theaidofthoracotomy itisoften difficult toestablish adiagnosis incases oftumourinthe thorax. Certain formsofbenignpleural changes arelikely tobemisinterpreted asintrapulmonary, andoperation forsuspected lungtumourmaybe carried out.Inthecasesdescribed here, itwas possible toestablish thediagnosis without employingthoracotomy. Asverylittle attention appears tohavebeenpaidtothese lesions intheliterature, a numberofcasesrecently observed havebeen collected.
Changes in Glucose and Cholesterol Levels in Patients With Schizophrenia Treated With Typical or Atypical Antipsychotics
Authors: Jean-Pierre Lindenmayer, Pal Czobor, Jan Volavka, Leslie Citrome, Brian Sheitman, Joseph P. McEvoy, Thomas B. Cooper, Miranda Chakos, Jeffrey A. Lieberman
Journal: American Journal of Psychiatry (2003)

The association of hyperglycemia and hypercholesterolemia with use of atypical antipsychotics has been documented in case reports and uncontrolled studies. The authors' goal was to assess the effects of clozapine, olanzapine, risperidone, and haloperidol on glucose and cholesterol levels in hospitalized patients with schizophrenia or schizoaffective disorder during a randomized double-blind 14-week trial.One hundred fifty-seven patients with schizophrenia or schizoaffective disorder who were inpatients at four hospitals were originally included in the study. The 14-week trial consisted of an 8-week fixed-dose period and a 6-week variable-dose period. Planned assessments included fasting glucose and cholesterol, which were collected at baseline and at the end of the 8-week period and the following 6-week period.One hundred eight of the 157 patients provided blood samples at baseline and at least at one point after random assignment to clozapine, olanzapine, risperidone, or haloperidol during the treatment trial. Seven of these patients had diabetes; their glucose levels were >125 mg/dl at baseline. Data from 101 patients were used for statistical analyses. During the initial 8-week period there was an overall significant increase in mean glucose levels. There were significant increases in glucose levels at the end of the 8-week fixed-dose period for patients given clozapine (N=27) and those given haloperidol (N=25). The olanzapine group showed a significant increase of glucose levels at the end of the 6-week variable-dose period (N=22). Fourteen of the 101 patients developed abnormal glucose levels (>125 mg/dl) during the trial (six with clozapine, four with olanzapine, three with risperidone, and one with haloperidol). Cholesterol levels were increased at the end of the 8-week fixed-dose period for the patients given clozapine (N=27) and those given olanzapine (N=26); cholesterol levels were also increased at the end of the 6-week variable-dose period for patients given olanzapine (N=22).In this prospective randomized trial, clozapine, olanzapine, and haloperidol were associated with an increase of plasma glucose level, and clozapine and olanzapine were associated with an increase in cholesterol levels. The mean changes in glucose and cholesterol levels remained within clinically normal ranges, but approximately 14% of the patients developed abnormally high glucose levels during the course of their participation in the study.
The role of the adventitia in vascular inflammation
Authors: K MAIELLARO, W TAYLOR
Journal: Cardiovascular Research (2007)

Journal Article The role of the adventitia in vascular inflammation Get access Kathryn Maiellaro, Kathryn Maiellaro aWallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology, United StatesbDivision of Cardiology, Department of Medicine, Emory University, 101 Woodruff Circle, Suite 319 WMB, Atlanta, GA 30322, United States Search for other works by this author on: Oxford Academic PubMed Google Scholar W. Robert Taylor W. Robert Taylor * aWallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology, United StatesbDivision of Cardiology, Department of Medicine, Emory University, 101 Woodruff Circle, Suite 319 WMB, Atlanta, GA 30322, United StatescVeterans Affairs Medical Center, Atlanta, GA 30033, United States * Corresponding author. Emory University School of Medicine, Cardiology Division, 101 Woodruff Circle, Suite 319 WMB, Atlanta, GA 30322, United States. Tel.: +1 404 727 8921; fax: +1 404 727 3572. [email protected][email protected] Search for other works by this author on: Oxford Academic PubMed Google Scholar Cardiovascular Research, Volume 75, Issue 4, September 2007, Pages 640–648, https://doi.org/10.1016/j.cardiores.2007.06.023 Published: 01 September 2007 Article history Received: 05 April 2007 Revision requested: 19 June 2007 Accepted: 21 June 2007 Published: 01 September 2007
Developmentally regulated herpesvirus plaque formation in arterial smooth muscle cells.
Authors: R J Kaner, J Medina, A C Nicholson, R Ursea, S M Schwartz, D P Hajjar
Journal: Circulation Research (1993)

Previous studies of age-related susceptibility to viral infection have focused largely on the effects of aging on the immune response. Little attention has been given to age-related changes in the infectivity of target cells. We show here a fourfold greater plating efficiency of herpes simplex virus type 1 (HSV-1) for cultured vascular smooth muscle cells derived from adult rats compared with cells from genetically identical pup rats. The difference in plating efficiency appeared to be due to differences in initial attachment of the virion to the cell surface. There were no differences in the rate of viral entry or the efficiency of viral replication at high multiplicities of infection and no resistant "subpopulation" of pup cells. The pup cells did not release a soluble inhibitor of infection. Infection in both cell types was inhibited similarly by basic fibroblast growth factor (bFGF). Although adult cells exhibited a more vigorous mitogenic response to bFGF than did pup cells, binding studies did not demonstrate significant differences in the binding of bFGF to the cell surface, suggesting that differential expression of high-affinity FGF receptors could not be correlated with the difference in infectivity. We speculate that differences in the distribution of heparan sulfate in the cell surface, which serves as the initial attachment site for HSV-1, may explain the observed differences in plating efficiency. Since age is a risk factor for the development of atherosclerosis, these results have potential implications for susceptibility of the vasculature to herpesviral infections as a function of the development of the vessel wall.
Lactose absorption in patients with glucose 6-phosphate dehydrogenase deficiency with and without favism.
Authors: T Meloni, C Colombo, A Ogana, M C Mannazzu, G F Meloni
Journal: Gut (1996)

It has recently been suggested that primary lactase deficiency might have been selected for by malaria, as has been previously shown to occur for thalasaemia and glucose 6-phosphate dehydrogenase (G6PD) deficiency.To test this hypothesis, the prevalence of primary lactase deficiency in G6PD deficient subjects and in controls from the area of Sassari (Northern Sardinia) was determined, which in the past was characterised by an intermediate malarial endemicity.70 adult subjects with G6PD deficiency, 34 of whom had a past history of favism, and 50 age matched control subjects.The capacity to absorb lactose was assessed by measuring breath hydrogen production after oral administration of lactose (50 g) by a gas chromatographic method.Twenty per cent of G6PD deficient subjects with a positive history of favism and 22% of G6PD deficient subjects without a positive history of favism were lactose absorbers compared with 14% lactose absorbers in the control group. The differences were not statistically significant.These data show that the prevalence of primary lactase deficiency in the area of Sassari is relatively high, but comparable to that seen in the adult population from another area of southern Italy (Naples) where malaria was less endemic.
Multivariable Model for Time to First Treatment in Patients With Chronic Lymphocytic Leukemia
Authors: William G. Wierda, Susan O'Brien, Xuemei Wang, Stefan Faderl, Alessandra Ferrajoli, Kim-Anh Do, Guillermo Garcia-Manero, Jorge Cortes, Deborah Thomas, Charles A. Koller, Jan A. Burger, Susan Lerner, Ellen Schlette, Lynne Abruzzo, Hagop M. Kantarjian, Michael J. Keating
Journal: Journal of Clinical Oncology (2011)

The clinical course for patients with chronic lymphocytic leukemia (CLL) is diverse; some patients have indolent disease, never needing treatment, whereas others have aggressive disease requiring early treatment. We continue to use criteria for active disease to initiate therapy. Multivariable analysis was performed to identify prognostic factors independently associated with time to first treatment for patients with CLL.Traditional laboratory, clinical prognostic, and newer prognostic factors such as fluorescent in situ hybridization (FISH), IGHV mutation status, and ZAP-70 expression evaluated at first patient visit to MD Anderson Cancer Center were correlated by multivariable analysis with time to first treatment. This multivariable model was used to develop a nomogram-a weighted tool to calculate 2- and 4-year probability of treatment and estimate median time to first treatment.There were 930 previously untreated patients who had traditional and new prognostic factors evaluated; they did not have active CLL requiring initiation of treatment within 3 months of first visit and were observed for time to first treatment. The following were independently associated with shorter time to first treatment: three involved lymph node sites, increased size of cervical lymph nodes, presence of 17p deletion or 11q deletion by FISH, increased serum lactate dehydrogenase, and unmutated IGHV mutation status.We developed a multivariable model that incorporates traditional and newer prognostic factors to identify patients at high risk for progression to treatment. This model may be useful to identify patients for early interventional trials.
Internal Cardioversion of Chronic Atrial Fibrillation During Percutaneous Mitral Commissurotomy
Authors: Katherine Fan, Kathy L. Lee, Wing-Hing Chow, Elaine Chau, Chu-Pak Lau
Journal: Circulation (2002)

Mechanoelectrical feedback caused by atrial dilatation plays an important role in atrial fibrillation (AF). To test the hypothesis that remodeling is reversible by reducing atrial stretch, we investigated electrophysiological changes after a reduction of left atrial (LA) pressure in patients undergoing percutaneous balloon mitral commissurotomy (PBMC).In 22 patients with chronic AF who were undergoing PBMC for mitral stenosis, internal cardioversion was successful in 19 patients (86%). Twelve patients with sinus rhythm acted as controls. Mean LA pressure was significantly reduced after PBMC (18.5+/-5.9 mm Hg versus 10.2+/-4.1 mm Hg; P<0.001). The effective refractory period (ERP), conduction delay (CD), and the index of heterogeneity (CoV) of the ERP and CD were compared. Changes in LA pressure were only significantly correlated with AF vulnerability (r=0.7; P=0.02) and CoV of CD (r=0.3; P=0.03). There were no significant changes in ERP and CD immediately after PBMC in the AF group. However, the overall CoV of ERP was reduced in the AF group after PBMC. There were homogenous, although not significant, increases in regional ERP in the control group immediately after PBMC. Atrial CD and CoV of CD were significantly reduced after PBMC in the control group; this was most prominent within the regions of the LA.AF vulnerability and CoV of CD correlated significantly with LA pressure. A homogenous increase in regional ERPs could be demonstrated in the control group after an immediate reduction of atrial stretch, whereas the recovery course of electrical remodeling was prolonged and heterogenous in the AF group. Regional conductions were irreversible in patients with preexisting AF.
Enhanced Formation and Disordered Regulation of NETs in Myeloperoxidase-ANCA–Associated Microscopic Polyangiitis
Authors: Daigo Nakazawa, Haruki Shida, Utano Tomaru, Masaharu Yoshida, Saori Nishio, Tatsuya Atsumi, Akihiro Ishizu
Journal: Journal of the American Society of Nephrology (2014)

Microscopic polyangiitis (MPA) is an ANCA-associated vasculitis that affects small vessels, especially renal glomeruli. We recently demonstrated that the abnormal formation and impaired degradation of neutrophil extracellular traps (NETs) may be crucially involved in the generation of myeloperoxidase (MPO)-ANCA and subsequent development of MPA. This study assessed the formation and regulation of NETs in patients with MPO-ANCA-associated MPA. Peripheral blood samples were obtained from 38 patients with MPO-ANCA-associated MPA, 23 patients with systemic lupus erythematosus (SLE), and 8 healthy controls. IgG eluted from MPO-ANCA-associated MPA sera demonstrated the highest ability to induce NETs, and this ability correlated with disease activity and paralleled ANCA affinity for MPO. Moreover, addition of recombinant human MPO to these IgG samples reduced NET induction. Additionally, MPO-ANCA-associated MPA sera exhibited lower rates of NET degradation that recovered partially upon depletion of IgG. The activity of DNase I, an important regulator of NETs, was also lower in MPO-ANCA-associated MPA and SLE sera. IgG depletion from MPO-ANCA-associated MPA sera partially restored the rate of NET degradation, and addition of DNase I synergistically enhanced this restoration. Addition of anti-MPO antibodies did not inhibit DNase I activity, and some MPO-ANCA-associated MPA sera contained anti-NET antibodies at levels not correlated with MPO-ANCA titers, suggesting the involvement of unidentified autoantibodies as well. The collective evidence suggests a vicious cycle involving MPO-ANCA and the regulation of NETs could be critically involved in the pathogenesis of MPO-ANCA-associated MPA.
Adaptation during surgical stress. A reevaluation of the role of glucocorticoids.
Authors: R Udelsman, J Ramp, W T Gallucci, A Gordon, E Lipford, J A Norton, D L Loriaux, G P Chrousos
Journal: Journal of Clinical Investigation (1986)

Pharmacologic doses of glucocorticoids are administered to patients with adrenal insufficiency during operative procedures to prevent hemodynamic instability, cardiovascular collapse, and death. Since these supraphysiologic doses might not be necessary and might have adverse effects, we examined the effects of different doses of glucocorticoids on hemodynamic adaptation during surgical stress in adrenalectomized primates. Sham-adrenalectomized placebo-treated animals served as controls. Adrenalectomized monkeys were maintained for 4 mo on physiologic glucocorticoid and mineralocorticoid replacement. The adrenalectomized monkeys were then stratified into three groups receiving, respectively, subphysiological (one-tenth the normal cortisol production rate), physiological, or supraphysiological (10 times the normal cortisol production rate) cortisol (hydrocortisone) treatment. 4 d later a cholecystectomy was performed. The intraoperative hemodynamic and metabolic parameters, perioperative survival rates, and postoperative wound healing were compared. The subphysiologically treated group was hemodynamically unstable before, during, and after surgery and had a significantly higher mortality rate than control. In this group, arterial blood pressure was low, and the cardiac index, systemic vascular resistance index, and left ventricular stroke work index were all reduced, suggesting decreased cardiac contractility and blood vessel tone. In contrast, the physiologically replaced group was indistinguishable from either supraphysiologically treated animals or sham-operated controls. All groups had similar metabolic profiles and normal wound healing. These findings suggest that the permissive actions of physiologic glucocorticoid replacement are both necessary and sufficient for primates to tolerate surgical stress. Supraphysiological glucocorticoid treatment has no apparent advantage during this form of stress in the primate.
Antiangiogenic Activity of rPAI-1 <sub>23</sub> Promotes Vasa Vasorum Regression in Hypercholesterolemic Mice Through a Plasmin-Dependent Mechanism
Authors: Jessica Mollmark, Saranya Ravi, Baiming Sun, Samantha Shipman, Maarten Buitendijk, Michael Simons, Mary Jo Mulligan-Kehoe
Journal: Circulation Research (2011)

The antiangiogenic activity of rPAI-1(23), a truncated plasminogen activator inhibitor-1 (PAI-1) protein, induces vasa vasorum collapse and significantly reduces plaque area and plaque cholesterol in hypercholesterolemic low-density lipoprotein receptor-deficient/apolipoprotein B48-deficient mice.The objective of this study was to examine rPAI-1(23)-stimulated mechanisms that cause vasa vasorum collapse.The rPAI-1(23) protein opposed PAI-1 antiproteolytic function by stimulating a 1.6-fold increase in plasmin activity compared with the saline-treated counterpart. The increased proteolytic activity corresponded to increased activity of matrix metalloproteinase-3 and degradation of fibrin(ogen), nidogen, and perlecan in the adventitia of descending aortas. PAI-1 activity was reduced by 48% in response to rPAI-1(23); however, PAI-1 protein expression levels were similar in the rPAI-1(23)- and saline-treated hypercholesterolemic mice. Coimmunoprecipitation assays demonstrated a novel PAI-1-plasminogen complex in protein from the descending aorta of rPAI-1(23)- and saline-treated mice, but complexed PAI-1 was 1.6-fold greater in rPAI-1(23)-treated mice. Biochemical analyses demonstrated that rPAI-1(23) and PAI-1 binding interactions with plasminogen increased plasmin activity and reduced PAI-1 antiproteolytic activity.We conclude that rPAI-1(23) causes regression or collapse of adventitial vasa vasorum in hypercholesterolemic mice by stimulating an increase in plasmin activity. The rPAI-1(23)-enhanced plasmin activity was achieved through a novel mechanism by which rPAI-1(23) and PAI-1 bound plasminogen in a cooperative manner to increase plasmin activity and reduce PAI-1 activity.
Lipid mediators from pollen act as chemoattractants and activators of polymorphonuclear granulocytes
Authors: Claudia Traidl-Hoffmann, Anna Kasche, Thilo Jakob, Michael Huger, Sabine Plötz, Ivo Feussner, Johannes Ring, Heidrun Behrendt
Journal: Journal of Allergy and Clinical Immunology (2002)
Autosomal-dominant hemochrom-atosis is associated with a mutation in the ferroportin (SLC11A3) gene
Authors: Giuliana Montosi, Adriana Donovan, Angela Totaro, Cinzia Garuti, Elisa Pignatti, Stefano Cassanelli, Cameron C. Trenor, Paolo Gasparini, Nancy C. Andrews, Antonello Pietrangelo
Journal: Journal of Clinical Investigation (2001)

Hemochromatosis is a progressive iron overload disorder that is prevalent among individuals of European descent. It is usually inherited in an autosomal-recessive pattern and associated with missense mutations in HFE, an atypical major histocompatibility class I gene. Recently, we described a large family with autosomal-dominant hemochromatosis not linked to HFE and distinguished by early iron accumulation in reticuloendothelial cells. Through analysis of a large pedigree, we have determined that this disease maps to 2q32. The gene encoding ferroportin (SLC11A3), a transmembrane iron export protein, lies within a candidate interval defined by highly significant lod scores. We show that the iron-loading phenotype in autosomal-dominant hemochromatosis is associated with a nonconservative missense mutation in the ferroportin gene. This missense mutation, converting alanine to aspartic acid at residue 77 (A77D), was not seen in samples from 100 unaffected control individuals. We propose that partial loss of ferroportin function leads to an imbalance in iron distribution and a consequent increase in tissue iron accumulation.