tbuckley/cabot-search huggingface dataset:
Contribution of noninvasive evaluation to the diagnosis of pulmonary embolism in hospitalized patients
Authors: MJ Miron, A Perrier, H Bounameaux, P de Moerloose, DO Slosman, D Didier, A Junod
Journal: European Respiratory Journal (1999)

The effectiveness of new diagnostic tools for suspected pulmonary embolism (PE), such as clinical probability assessment, plasma D-dimer (DD) measurement and lower limb venous compression ultrasonography (US), has not been specifically studied in patients with a suspected PE occurring during hospital stay. This study applied a sequential, decision analysis-based strategy adding these instruments to a ventilation/perfusion lung scan in a cohort of 114 consecutive inpatients clinically suspected of PE in order to establish in how many patients a pulmonary angiogram could thereby be avoided. A definitive diagnosis could be established by the noninvasive protocol in 61% of these patients: normal/near-normal lung scan, 14%; high probability lung scan, 19%; clinical probability combined with lung scan result, 18%; and US, 8%. Specificity of DD was only 7% and contributed to the exclusion of PE in only two patients. Pulmonary angiography was required in 39% of patients. The 3-month thromboembolic risk in patients in whom PE was excluded by the diagnostic process was 0% (95% confidence interval 0-4.9%). In conclusion, a noninvasive work-up for suspected pulmonary embolism is effective in hospitalized patients, allowing to forego angiography in 61% of them, and it appears to be safe, although this should be further investigated. In contrast to outpatients, D-dimer measurement appears to be useless in hospitalized patients.
Effects of the angiotensin II antagonist valsartan on blood pressure, proteinuria, and renal hemodynamics in patients with chronic renal failure and hypertension.
Authors: J Plum, B Bünten, R Németh, B Grabensee
Journal: Journal of the American Society of Nephrology (1998)

Angiotensin II receptor antagonists have become clinically available for the treatment of arterial hypertension. Presently, there is little information about their effects on BP, proteinuria, and renal function in patients with moderate or advanced renal failure. This study examines the effects of the angiotensin II antagonist Valsartan (80 mg/d) on proteinuria and glomerular permselectivity in patients with chronic renal failure during a 6-mo treatment, using a double-blind, randomized, placebo-controlled study (treatment group [V-group]: n = 5, age 57 +/- 7 yr, serum creatinine 365 +/- 122 micromol/L; placebo group [P-group]: n = 4, age 62 +/- 11 yr, serum creatinine 346 +/- 61 micromol/L). Study parameters included BP, 24-h proteinuria, GFR, and effective renal plasma flow (ERPF) as determined by inulin and para-aminohippurate clearance. Changes in glomerular permselectivity were assessed by measuring the fractional clearances of neutral dextrans by HPLC gel-permeation chromatography. Valsartan lowered the mean arterial pressure on average by 13 +/- 7 mmHg during the 6-mo treatment (P < 0.05). GFR and ERPF remained almost unchanged. However, after 6 mo of Valsartan treatment, proteinuria was reduced by 396 +/- 323 mg/24 h (26 +/- 18%) and albuminuria by 531 +/- 499 mg/24 h (41 +/- 21%) with regard to baseline values (P < 0.05). In the P-group, both proteinuria and albuminuria increased slightly with time (by 30 +/- 43% and 30 +/- 54%, respectively, NS). The fractional clearances of high molecular weight dextrans >66 A were significantly reduced after 6 mo of Valsartan treatment (P < 0.05), indicating a reduction of the glomerular shunt volume by 54 +/- 20% (P < 0.05) according to the model of Deen et al. (Am J Physiol 249: 347-389, 1985). The mean pore size radius of the glomerular membrane remained unchanged. This effect was independent of glomerular hemodynamic changes. Valsartan persistently lowered proteinuria in patients with chronic renal failure. Although GFR and ERPF remained nearly stable, this effect could be attributed to an improvement in glomerular permselectivity.
Translating the Molecular Message of Triple-Negative Breast Cancer into Targeted Therapy
Authors: Neelima Vidula, Hope S. Rugo
Journal: Clinical Cancer Research (2014)

Triple-negative breast cancer (TNBC) has a poor prognosis with limited treatment options. Genomic analysis of TNBCs offers the opportunity to decode TNBC into biologically relevant subtypes with unique molecular targets. With further research, these findings may be translated into effective targeted therapeutic options.
Use of Positron Emission Tomography Scans in Ovarian Cancer: A Diagnostic Technique in Search of an Indication
Authors: Maurie Markman
Journal: Journal of Clinical Oncology (2005)

Recent evidence that specific molecular abnormalities strongly influence the activity of gefitinib in lung cancer, 1 and trial results demonstrating the effectiveness of trastuzumab employed as breast cancer adjuvant therapy in the presence of HER-2 overexpression, 2 emphasize the relevance of diagnostic testing in influencing cancer patient management. Furthermore, based on existing data, it is reasonable to conclude that the development of novel biologic markers and innovative imaging strategies have the realistic potential to alter substantially the approach oncologists traditionally use to both initiate and modify anticancer treatment. However,asinotherareasofoncology,theenthusiasm forpromisingnewdiagnostictestsmustbeaccompaniedby appropriate and critical analysis of what has been claimed. 3
Aberrant DNA methylation characterizes juvenile myelomonocytic leukemia with poor outcome
Authors: Christiane Olk-Batz, Anna R. Poetsch, Peter Nöllke, Rainer Claus, Manuela Zucknick, Inga Sandrock, Tania Witte, Brigitte Strahm, Henrik Hasle, Marco Zecca, Jan Starý, Eva Bergstraesser, Barbara De Moerloose, Monika Trebo, Marry M. van den Heuvel-Eibrink, Dorota Wojcik, Franco Locatelli, Christoph Plass, Charlotte M. Niemeyer, Christian Flotho
Journal: Blood (2011)
Stratum corneum adhesive tape stripping: influence of anatomical site, application pressure, duration and removal
Authors: H. Loffler, F. Dreher, H.I. Maibach
Journal: British Journal of Dermatology (2004)

Tape stripping is a common method for investigating stratum corneum (SC) physiology as well as bioavailability and bioequivalence of topical drugs.To investigate the influence of procedures (anatomical site, pressure, pressure duration, tape removal rate) inherent in each stripping protocol on changes in skin physiology.Tape stripping was performed using tapes on the forearm, forehead and back. On the forearm different pressures (165 and 330 g cm(-2)), durations of pressure (2 and 10 s), and removal rate (slow and rapid removal) were used. Changes in skin physiology were evaluated by measurement of transepidermal water loss (TEWL) and hydration.A significant influence of all parameters on the TEWL increase as a function of tape strip number was observed. The fastest increase was demonstrated on the forehead, followed by the back and, lastly, the forearm. Rapid removal produced a protracted increase in comparison with slow removal. Pressure for 10 s induced a faster increase in TEWL than 2 s pressure. Likewise, pressure at 330 g cm(-2) induced an earlier increase than pressure at 165 g cm(-2). Skin hydration was not influenced by the variables tested.Tape stripping results are influenced dramatically by all investigated parameters. A dynamic SC stress test to investigate SC cohesion more closely is proposed based on the present observations.
Targeting bone marrow to treat vascular diseases: Accelerated vascular healing by colony stimulating factor
Authors: J SAINZ, M SATA
Journal: Cardiovascular Research (2006)

See article by Yoshioka et al.  [6]  (pages 61–69) in this issue .

It is a generally accepted view that endothelial damage triggers the pathogenesis of various types of vascular diseases [1]. A growing body of evidence suggests that bone marrow (BM)-derived cells may participate in arterial repair after injury [2,3] by homing to the injured vessel and differentiating into endothelial cells (ECs). Walter et al. suggested that the mobilization of endothelial progenitor cells (EPCs) from BM after vascular injury may mediate accelerated reendothelialization and reduced neointima formation by statin therapy [4]. It was reported that granulocyte colony-stimulating factor (G-CSF), a major regulator of haemopoiesis and the innate immune system, potently mobilizes EPCs from BM and accelerates reendothelialization [5].

In the current issue of Cardiovascular Research , Yoshioka et al. examined a hypothesis that G-CSF treatment could reduce neointimal formation by increasing the number of circulating EPCs and thereby accelerating reendothelialization after mechanical vascular injury [6]. Pre-treatment with G-CSF before the vascular injury enhanced reendothelialization and decreased neointimal formation. These favourable effects on the injured artery were associated with an increase in the number of putative EPCs (CD34+ Flk-1+ cells) in peripheral blood and a decrease in serum IL-6 level. To assess the effective contribution of EPCs originating from the BM itself, the investigators replaced the BM cells of wild-type mice with those from GFP- or Tie-2/LacZ-transgenic mice and … 

* Corresponding author. Department of Cardiovascular Medicine, University of Tokyo, Graduate School of Medicine, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan. Tel.: +81 3 3815 5411; fax: +81 3 3814 0021. Email address: msata-circ{at}umin.ac.jp
LOW ON-TREATMENT REACTIVITY WITH CLOPIDOGREL DOES NOT SIGNIFICANTLY IMPACT BLEEDING COMPLICATIONS IN PATIENTS RECEIVING DUAL ANTI-PLATELET THERAPY
Authors: Marvin Eng, Paul A. Hudson, Sarah Endemann, Colin Barker, Marcus Williams, Justin Levisay, Curtiss Stiniss, Paul S. Teirstein, Matthew J. Price
Journal: Journal of the American College of Cardiology (2011)
P-Cresol, a uremic compound, enhances the uptake of aluminum in hepatocytes.
Authors: K Abreo, M Sella, S Gautreaux, R De Smet, P Vogeleere, S Ringoir, R Vanholder
Journal: Journal of the American Society of Nephrology (1997)

In the end-stage renal disease patient, certain uremic compounds could influence the cellular accumulation of aluminum (Al). In this study, we examined the effect of 15 uremic ultrafiltrate fractions obtained by HPLC on the uptake and toxicity of Al in mouse hepatocytes (MH) in culture, a model system in which Al is taken up bound to transferrin (Tf). Uremic fractions 4 to 8, 12, 14, and 15 increased cellular Al uptake and aspartate aminotransferase release and decreased cell growth when Tf-Al, not Al citrate, was added to culture media. Compounds that have been extracted previously from these ultrafiltrate fractions (p-cresol, xanthine, tryptophan, hippuric acid, and o-hydroxyhippuric acid) were then tested for their effect on Al uptake and toxicity in MH at concentrations found in uremic serum. Significant Al uptake by MH was observed only when p-cresol was added together with Tf-Al. Time-response curves showed increased Al uptake and toxicity at p-cresol concentrations of 3 mg/dl in culture media. Dose-response curves confirmed that Al uptake and cell toxicity were proportional to p-cresol from 1.5 mg/dl to 3 mg/dl in culture media. p-Cresol was not toxic to MH in the absence of Tf-Al in media. p-Cresol increased Tf-associated Al uptake only because there was no effect on Al uptake when Al citrate was substituted, and studies with Tf-I125-Al in the presence of this compound showed increased Tf-I125 taken up by MH. p-Cresol did not increase Tf saturation with Al. p-Cresol also increased Tf-Al uptake in Friend erythroleukemia and neuroblastoma cells in culture. Our studies suggest that p-cresol and uremic fractions 4 to 8, 12, 14, and 15 increase the uptake and toxicity of Al in cultured MH. These compounds may play a role in the accumulation and toxicity of Al in the liver of end-stage renal disease patients and possibly in all cells that express Tf receptors.
A case of hepatoblastoma misdiagnosed as combined hepatocellular carcinoma and cholangiocarcinoma in an adult
Authors: Keun Woo Park, Chang Jin Seo, Dae Young Yun, Min Keun Kim, Byung Seok Kim, Young Seok Han, Hoon Kyu Oh, Chang Hyeong Lee
Journal: Clinical and Molecular Hepatology (2015)

Hepatoblastoma usually occurs in children under the age of 2 years, with very few cases reported in adults. We experienced a case of adult hepatoblastoma in a 36-year-old female with chronic hepatitis B. She had experienced sudden onset abdominal pain. Her serum alpha-fetoprotein level was markedly elevated, and abdominal CT showed a 9-cm mass with internal hemorrhage in the right hepatic lobe with hemoperitoneum, so an emergency hepatic central bisectionectomy was performed. The initial histologic examination revealed that the mass mimicked combined hepatocellular carcinoma and cholangiocarcinoma with spindle-cell metaplasia of the cholangiocarcinoma element. Follow-up abdominal CT performed 3 months later showed a 5.5-cm metastatic mass in the left subphrenic area. Laparoscopic splenectomy with mass excision was performed, and hepatoblastoma was confirmed histologically. A histologic re-examination of previously obtained surgical specimens also confirmed the presence of hepatoblastoma. Metastatic hepatoblastoma was found at multiple sites of the abdomen during follow-up, and so chemotherapy with cisplatin, 5-fluorouracil (5-FU), and vincristine was applied, followed by carboplatin and doxorubicin. Despite surgery and postoperative chemotherapy, she died 12 months after symptom onset. Keywords: Hepatoblastoma; Surgery; Chemotherapy
Association Between Variation in Neuropsychological Development and Trajectory of ADHD Severity in Early Childhood
Authors: Khushmand Rajendran, Joey W. Trampush, David Rindskopf, David J. Marks, Sarah O’Neill, Jeffrey M. Halperin
Journal: American Journal of Psychiatry (2013)

This longitudinal study examined if changes in neuropsychological functioning were associated with the trajectory of symptoms related to attention deficit hyperactivity disorder (ADHD) and impairment between preschool and school age. The sample consisted of 3- and 4-year-old children (N=138) who were identified as being at risk for ADHD based on parent and teacher reports. Neuropsychological functioning was measured annually using the NEPSY at four time points (mean ages, 4.19, 5.36, 6.35, and 7.35 years). ADHD symptoms and impairment were assessed with semiannual parent and teacher reports using the ADHD Rating Scale-IV and the Children's Problems Checklist at 10 time points (mean ages at baseline and final assessment, 4.19 and 8.81 years, respectively). Hierarchical linear modeling was used to assess the trajectories of change in neuropsychological functioning and ADHD severity as well as the association of change in neuropsychological functioning with change in ADHD severity over time. Baseline neuropsychological functioning was not significantly associated with the slope of change in ADHD severity. However, the magnitude of change in neuropsychological functioning was linearly associated with the trajectory of ADHD symptom severity and impairment, such that individuals with greater neuropsychological growth over time had a greater diminution of ADHD severity and impairment. Family socioeconomic status at baseline was significantly associated with initial ADHD severity and impairment, but not with change over time. Interventions that enhance neuropsychological functioning at an early age may be beneficial in attenuating long-term ADHD severity and impairment.
Severe combined immunodeficiency (SCID) in man: B cell-negative (B-) SCID patients exhibit an irregular recombination pattern at the JH locus.
Authors: K Schwarz, T E Hansen-Hagge, C Knobloch, W Friedrich, E Kleihauer, C R Bartram
Journal: The Journal of Experimental Medicine (1991)

Human severe combined immunodeficiency (SCID) patients were analyzed by a polymerase chain reaction assay for their recombination capability at the DHQ52-JH region of the immunoglobulin heavy chain locus. Five patients with B cells (B+ SCID) exhibited a recombination pattern also observed in healthy persons. In contrast, six patients lacking B cells (B- SCID) showed a grossly altered rearrangement pattern characterized by the (partial) absence of regular DHQ52-JH recombinations and the presence of abnormal rearrangements. These events were caused by deletions surpassing the boundaries of immunoglobulin coding elements and thus resemble the pattern of deletional recombinations previously described in SCID mice.
Effects of AGI-1067 and Probucol After Percutaneous Coronary Interventions
Authors: Jean-Claude Tardif, Jean Grégoire, Leonard Schwartz, Lawrence Title, Louise Laramée, François Reeves, Jacques Lespérance, Martial G. Bourassa, Philippe L. L’Allier, Mitchell Glass, Jean Lambert, Marie-Claude Guertin
Journal: Circulation (2003)

Background— AGI-1067, a metabolically stable modification of probucol, is an equipotent antioxidant to probucol but is pharmacologically distinct. In a multicenter trial, we studied whether AGI-1067 reduces restenosis assessed by intravascular ultrasound (IVUS) after percutaneous coronary intervention (PCI) compared with placebo and probucol used as a positive control. Methods and Results— Two weeks before PCI, 305 patients were randomly assigned to 1 of 5 treatment groups: placebo, probucol 500 mg BID, or AGI-1067 70, 140, or 280 mg once daily. Patients were treated for 2 weeks before and 4 weeks after PCI. Baseline and 6-month follow-up IVUS were interpreted by a blinded core laboratory. Stents were used in 85% of patients. Luminal area at the PCI site at follow-up was 2.66±1.58 mm 2 for placebo, 3.69±2.69 mm 2 for probucol, 2.75±1.76 mm 2 for AGI-1067 70 mg, 3.17±2.26 mm 2 for AGI-1067 140 mg, and 3.36±2.12 mm 2 for AGI-1067 280 mg ( P =0.02 for the dose-response relationship; P ≤0.05 for AGI-1067 280 mg and probucol versus placebo). There was a mean narrowing of 5.3 mm 3 of reference segment lumen in the placebo group and an enlargement in the AGI-1067 140- and 280-mg groups at follow-up ( P =0.05 for 140 mg). An increase in QTc interval &gt;60 ms occurred in 4.8% of placebo patients, 17.4% of probucol patients, and 4.8%, 2.4%, and 2.5% of patients in the AGI-1067 groups ( P =0.02). Conclusions— AGI-1067 and probucol reduce restenosis after PCI. In contrast to probucol, AGI-1067 did not cause prolongation of the QTc interval and improved lumen dimensions of reference segments, suggestive of a direct effect on atherosclerosis.
Best practices in the management of the psycho-oncologic aspects of head and neck cancer patients: recommendations from the European Head and Neck Cancer Society Make Sense Campaign
Authors: M. Reich, C.R. Leemans, J.B. Vermorken, J. Bernier, L. Licitra, S. Parmar, W. Golusinski, J.L. Lefebvre
Journal: Annals of Oncology (2014)
Manganese superoxide dismutase and aldehyde dehydrogenase deficiency increase mitochondrial oxidative stress and aggravate age-dependent vascular dysfunction
Authors: Philip Wenzel, Swenja Schuhmacher, Joachim Kienhöfer, Johanna Müller, Marcus Hortmann, Matthias Oelze, Eberhard Schulz, Nicolai Treiber, Toshihiro Kawamoto, Karin Scharffetter-Kochanek, Thomas Münzel, Alexander Bürkle, Markus Michael Bachschmid, Andreas Daiber
Journal: Cardiovascular Research (2008)

Imbalance between pro- and antioxidant species (e.g. during aging) plays a crucial role for vascular function and is associated with oxidative gene regulation and modification. Vascular aging is associated with progressive deterioration of vascular homeostasis leading to reduced relaxation, hypertrophy, and a higher risk of thrombotic events. These effects can be explained by a reduction in free bioavailable nitric oxide that is inactivated by an age-dependent increase in superoxide formation. In the present study, mitochondria as a source of reactive oxygen species (ROS) and the contribution of manganese superoxide dismutase (MnSOD, SOD-2) and aldehyde dehydrogenase (ALDH-2) were investigated. Age-dependent effects on vascular function were determined in aortas of C57/Bl6 wild-type (WT), ALDH-2−/−, MnSOD+/+, and MnSOD+/− mice by isometric tension measurements in organ chambers. Mitochondrial ROS formation was measured by luminol (L-012)-enhanced chemiluminescence and 2-hydroxyethidium formation with an HPLC-based assay in isolated heart mitochondria. ROS-mediated mitochondrial DNA (mtDNA) damage was detected by a novel and modified version of the fluorescent-detection alkaline DNA unwinding (FADU) assay. Endothelial dysfunction was observed in aged C57/Bl6 WT mice in parallel to increased mitochondrial ROS formation and oxidative mtDNA damage. In contrast, middle-aged ALDH-2−/− mice showed a marked vascular dysfunction that was similar in old ALDH-2−/− mice suggesting that ALDH-2 exerts age-dependent vasoprotective effects. Aged MnSOD+/− mice showed the most pronounced phenotype such as severely impaired vasorelaxation, highest levels of mitochondrial ROS formation and mtDNA damage. The correlation between mtROS formation and acetylcholine-dependent relaxation revealed that mitochondrial radical formation significantly contributes to age-dependent endothelial dysfunction.
Glomerular Number and Function Are Influenced by Spontaneous and Induced Low Birth Weight in Rats
Authors: Michiel F. Schreuder, Jens R. Nyengaard, Mariann Fodor, Joanna A.E. van Wijk, Henriette A. Delemarre-van de Waal
Journal: Journal of the American Society of Nephrology (2005)

A link exists between low birth weight and diseases in adulthood, such as hypertension, cardiovascular disease, and insulin resistance. Intrauterine growth restriction (IUGR) has been used to explain this association and has been shown to lead to a nephron endowment in humans. A reduction in glomerular number has been described in animal models with induced low birth weight as well but not in animals with spontaneous low birth weight. It therefore is debatable whether the models are suitable. The effect on glomerular number and size was studied in rats with naturally occurring IUGR and experimental IUGR, induced by bilateral uterine artery ligation. Design-based stereologic methods were used. Urinary protein excretion was determined as a measure of renal damage. Results showed a decrease of approximately 20% in glomerular number in both groups of IUGR (control 35,400, naturally occurring IUGR 30,900, and experimental IUGR 28,000 glomeruli per kidney). Mean glomerular volume was increased in both IUGR groups, which was associated with an increased proteinuria. It is concluded that IUGR leads to a nephron endowment with a compensatory glomerular enlargement. This compensation is associated with more proteinuria in the long run. Uterine artery ligation in the pregnant rat is a suitable model to study the effects of IUGR on the kidney.
Systemic and portal haemodynamic changes following triglycyllysine vasopressin plus nitroglycerin administration in patients with hepatitis B-related cirrhosis
Authors: Han-Chieh Lin, Yang-Te Tsai, Fa-Yauh Lee, Ting-Tsung Chang, Sun-Sang Wang, Chii-Shyan Lay, Shou-Dong Lee, Kwang-Juei Lo
Journal: Journal of Hepatology (1990)