tbuckley/cabot-search huggingface dataset:
Colonoscopy with robotic steering and automated lumen centralization: a feasibility study in a colon model
Authors: Hendrikus Pullens, Nanda van der Stap, Esther Rozeboom, Matthijs Schwartz, Ferdi van der Heijden, Martijn van Oijen, Peter Siersema, Ivo Broeders
Journal: Endoscopy (2015)

<b>Background and study aims: </b>We introduced a new platform for performing colonoscopy with robotic steering and automated lumen centralization (RS-ALC) and evaluated its technical feasibility. <b>Participants and methods: </b>Expert endoscopists (n = 8) and endoscopy-naive novices (n = 10) used conventional steering and RS-ALC to perform colonoscopy in a validated colon model with simulated polyps (n = 21). The participants were randomized to which modality they were to use first. End points were the cecal intubation time, number of detected polyps, and subjective evaluation of the platform. <b>Results: </b>Novices were able to intubate the cecum faster with RS-ALC (median 8 minutes [min] 56 seconds [s], interquartile range [IQR] 6 min 46 s – 16 min 34 s vs. median 11 min 47 s, IQR 8 min 19 s – 15 min 33 s, <i>P</i> = 0.65), whereas experts were faster with conventional steering (median 2 min 9 s, IQR 1 min 13 s – 7 min 28 s vs. median 13 min 1 s, IQR 5 min 9 s – 16 min 54 s, <i>P</i> = 0.12). Novices detected more polyps with RS-ALC (median 88.1 %, IQR 79.8 % – 95.2 % vs. median 78.6 %, IQR 75.0 % – 91.7 %, <i>P</i> = 0.17), whereas experts detected more polyps with conventional steering (median 80.9 %, IQR 76.2 % – 85.7 % vs. median 69.0 %, IQR 61.0 % – 75.0 %, <i>P</i> = 0.03). Novices were more positive than experts about the new platform (<i>P</i> = 0.02), noting an easier and faster introduction of the colonoscope with RS-ALC than with conventional steering. <b>Conclusions: </b>Colonoscopy with RS-ALC is technically feasible and appears to be easier and more intuitive than conventional steering for endoscopy-naive novices.
CD40 activation mediates p53-dependent cell cycle regulation in human multiple myeloma cell lines
Authors: G. Teoh, Y.-T. Tai, M. Urashima, S. Shirahama, M. Matsuzaki, D. Chauhan, S. P. Treon, N. Raje, T. Hideshima, Y. Shima, K. C. Anderson
Journal: Blood (2000)
Prevalence of the Metabolic Syndrome in the United States, 2003-2012
Authors: Maria Aguilar, Taft Bhuket, Sharon Torres, Benny Liu, Robert J. Wong
Journal: JAMA (2015)

The metabolic syndrome contributes to cardiovascular morbidity and mortality. 1-4Data from the National Health and Nutrition Examination Survey (NHANES) 1999-2006 reported a metabolic syndrome prevalence of 34%. 5 Understanding updated prevalence trends may be important given the potential effect of the metabolic syndrome and its associated health complications on the aging US population.We investigated trends in the prevalence of the metabolic syndrome through 2012.a Trend comparisons from year ranges listed to 2011-2012.
Red facial pseudochromhidrosis
Authors: G.P. Thami, A.J. Kanwar
Journal: British Journal of Dermatology (2000)

Abstract We describe a 9-year-old girl with pseudochromhidrosis simulating apocrine chromhidrosis. Treatment with topical and systemic erythromycin resulted in complete clearance of the reddish discoloration of the face. No relapse or recurrence was observed over a 3-month period.
NHS Executive promotes prophylaxis
Authors: P. Leech
Journal: BMJ (1995)

EDITOR,—In their paper on appropriate prescribing in asthma in east London Jeannette Naish and colleagues highlight the difficulties in defining and measuring good prescribing.1 In both the paper and the Editor's choice, statements are made that pressure to reduce the cost of prescribing in asthma may lead to a reduction in prophylactic treatment, lower the quality of asthma care, and be cost ineffective. The implication of these statements is …
From hereditary hemorrhagic telangiectasia and the SMAD4/TGF-B pathway to juvenile polyposis syndrome and heritable gastrointestinal malignancies
Authors: Douglas A. Marchuk
Journal: Cancer Research (2005)

SY27-3   Juvenile Polyposis (JP) and Hereditary Hemorrhagic Telangiectasia (HHT) are two uncommon autosomal dominant disorders characterized by distinct and essentially non-overlapping clinical features. JP, an inherited gastrointestinal malignancy predisposition, is caused by mutations in either  SMAD4  or  BMPR1A . HHT is a vascular malformation disorder caused by mutations in either  Endoglin  or  ALK1 . All four of these genes encode proteins involved in the TGF- β signaling pathway. We recently reported 7 families segregating both JP and HHT phenotypes where all of the affected members have mutations in the COOH-terminus of  SMAD4  and none had mutations in either  Endoglin  or  ALK1 . This established  SMAD4  as the molecular link between these hitherto separate diseases. To further elucidate the clinical and genetic parameters of this syndrome, we collected DNA samples from additional individuals and families exhibiting the combined JP-HHT syndromic phenotype and from patients with only some of the features of each disease. The coding exons of  SMAD4 ,  BMPR1A ,  Endoglin,  and  ALK1  were sequenced in affected patients. Five more instances of mutations in  SMAD4  were found, all in patients exhibiting the full range of JP-HHT symptoms. None of these patients had mutations in any of the other three genes examined. This mirrors the results of our first set of patients both in range of symptoms and types and locations of  SMAD4  mutations. Only one family displays the full complement of symptoms found in other JP-HHT families but shows no mutation. It is possible that this family has a  SMAD4  mutation, such as is a large deletion which would not be observed by sequencing, or a change within a regulatory region which was not analyzed. In the families and individuals not showing the typical symptoms of JP-HHT, no mutations were found in  SMAD4,  BMPR1A ,  Endoglin,  or  ALK1 . At least three of these five new JP-HHT cases are  de novo  mutations in  SMAD4  bringing the total of documented  de novo  cases of this syndrome to 6 out of our total of 12 instances. This high incidence of  de novo  cases could have important implications for both genetic screening and counseling of the patients and their families. All of the mutations found to date in this combined syndrome are in the COOH-terminus of the SMAD4 protein. It will be necessary to ascertain JP patients with mutations in other regions of  SMAD4  for HHT symptoms to confirm this emerging genotype:phenotype correlation. To begin to establish clinical benchmarks for diagnosis of this syndrome, we have summarized the major symptoms of both diseases found in our  SMAD4  mutation positive JP-HHT syndrome patients. We will continue to collect and analyze patients with symptoms of JP and HHT to better delineate the clinical presentation of JP-HHT syndrome.
Low Serum Insulin-Like Growth Factor I Is Associated With Increased Risk of Ischemic Heart Disease
Authors: Rainer H. Böger
Journal: Circulation (2003)

In a recent interesting paper by Juul et al 1 and an accompanying editorial by Frystyk et al, 2 an association between low insulin-like growth factor I (IGF-I) serum levels and the incidence of ischemic heart disease was reported.The inverse nature of this relationship was unexpected by these authors, and a number of possible mechanisms were discussed.However, in addition to these authors' hypotheses about the molecular mechanisms behind this finding, one mechanism that may contribute to the reported role of IGF-I in coronary heart disease was not mentioned: There is experimental evidence that endothelial cells possess high-affinity binding sites for IGF-I, and that the vasodilator effect of IGF-I is abrogated by the NO synthase inhibitor N G -monomethyl-L-arginine (L-NMMA). 3 These data suggest that IGF-I induces NO-dependent vasodilation.In humans, IGF-I induces endothelium-dependent vasodilation as well, which can also be blocked by co-infusion of L-NMMA. 4Furthermore, we found that the increase in serum IGF-I induced by growth hormone supplementation results in elevated urinary excretion of nitrite/nitrate and cyclic GMP, markers of systemic NO production, in adult patients with acquired growth hormone-deficiency 5 and in patients with cardiomyopathy.In parallel, total peripheral resistance was reduced in both studies, indicating that peripheral vasodilation occurred.Thus, there is evidence that NO may mediate the cardiovascular effects of IGF-I.Administration of IGF-I has an immediate positive effect on NO formation by endothelial cells.This NO release, given the well-known antiproliferative and antiatherogenic effects of NO, may antagonize many of the proproliferative effects of IGF-I in the cardiovascular system.Reduced endothelial NO elaboration caused by reduced stimulation of endothelial cells by IGF-I may therefore be responsible for many of the detrimental cardiovascular changes associated with low IGF-I levels and may help to explain the inverse relationship between low IGF-I and an increased incidence of coronary heart disease.
Collagenous colitis patients demonstrate a Th1/CTL-associated gene expression profile with increased frequencies of Ki67+ proliferating and CD45RO+ activated/ memory CD8+ and CD4+8+ mucosal T cells
Authors: Ashok Kumar Kumawat, H. Strid, K. Elgbratt, Nils Nyhlin, Curt Tysk, J. Bohr, Elisabet Hultgren Hörnquist
Journal: Gut (2011)

Collagenous colitis patients demonstrate a Th1/CTL-associated gene expression profile with increased frequencies of Ki67+ proliferating and CD45RO+ activated/memory CD8+ and CD4+8+ mucosal T cells
Talactoferrin Alfa, a novel immunomodulatory agent with anti-cancer activity in phase II clinical trials.
Authors: Atul Varadhachary, Michela Spadaro, Jose Engelmayer, Claudia Curcio, Paul Blezinger, Margalit B. Mokyr, Yenyun Wang, Ve ’ted’ Valli, Guido Forni, Federica Pericle
Journal: Cancer Research (2006)

Proc Amer Assoc Cancer Res, Volume 47, 2006

5579 

Clinical Background: Talactoferrin alfa (talactoferrin) is a novel, orally administered immunomodulatory agent that appears to be safe and well tolerated and has anti-cancer activity in human clinical trials. Talactoferrin met its primary efficacy endpoints in multi-center Phase II clinical trials in RCC and NSCLC. In a 44-patient RCC trial, patients receiving talactoferrin monotherapy had an apparent increase in their median PFS. In a 110-patient placebo-controlled, multi-center Phase II trial in patients with advanced NSCLC, addition of oral talactoferrin to carboplatin/paclitaxel in first-line NSCLC substantially enhanced both response rate and PFS. Confirmed BOR in the 110 ITT patients increased from 27% to 42% (15% absolute increase, 56% relative increase; p=0.08). Confirmed RR in the 100 prospectively defined evaluable patients increased from 29% to 47% (18% absolute improvement, 62% relative improvement; p=0.05). Median PFS increased by 2.8 months from 4.2 months to 7 months (61% improvement). Talactoferrin will soon be entering Phase III trials. . Immunomodulatory Mechanism: Talactoferrin is an orally active protein that acts at the gut and the Gut Associated Lymphoid Tissue (GALT) through a novel mechanism involving chemokine and cytokine modulation. Talactoferrin binds enterocyte receptors and immune cells in the Peyer's patches, and initiates an immunostimulatory cascade in the GALT. This results in an increase in key cytokines including IFN-g and IL-18, and activation of both innate and adaptive immunity. In animal experiments, we see increased numbers of NK-T cells and CD8+ T-lymphocytes in small intestinal Peyer's patches, a systemic increase in Natural Killer (NK) and Cytotoxic T-lymphocyte (CTL) activity, and cellular infiltration of distant tumors. The essential role of IFN-g and immune effector cells in talactoferrin's anti-cancer activity has been demonstrated in knockout and depletion experiments. Talactoferrin induced increases in NK-T cells and CD8+ lymphocytes in Peyer's patches was abolished in IFN-g knockout mice, as was talactoferrin's anti-cancer activity. Talactoferrin activity was also lost in animals lacking NK-T or CD8+ cells. . Conclusion: Talactoferrin is a first-in-class molecule with promising Phase II anti-cancer activity, and a novel immunomodulatory mechanism.
Possible role of IL-33 in the pathophysiology of asthma: A cross-sectional study
Authors: Hideki Inoue, Isao Ito, Akio Niimi, Hisako Matsumoto, Tsuyoshi Oguma, Hitoshi Nakaji, Tomoko Tajiri, Toshiyuki Iwata, Tadao Nagasaki, Michiaki Mishima
Journal: European Respiratory Journal (2011)

Background:  IL-33 and its receptor ST2 have been recognized as key molecules in Th2 inflammation. Clinical roles of serum levels of IL-33/ST2 have not been well evaluated in asthmatic patients.   Aims:  To investigate relationships between serum IL-33/ST2 levels and clinical measurements in patients with stable asthma.   Methods:  Seventy-two patients with stable, mild-to-severe asthma aged 55.0±18.4 (mean ± SD) years were analyzed cross-sectionally. Serum levels of IL-33 and ST2 were measured by ELISA. Relationships between serum levels of IL-33/ST2 and clinical measurements were evaluated. Clinical measurements include spirometric values, exhaled nitric oxide (FeNO) levels, induced sputum cell differentials, blood eosinophil count and serum total and specific IgE results.   Results:  Forty-nine patients were positive for at least one IgE CAP RAST. Serum levels of IL-33 were positively correlated with disease duration (r = 0.34, p    Conclusions:  Serum levels of IL-33 may reflect atopic status as represented by serum total IgE levels as well as degree of airway inflammation as assessed by peripheral blood eosinophilia and FeNO levels.
Inhibition of Dectin-1 Signaling Ameliorates Colitis by Inducing Lactobacillus-Mediated Regulatory T Cell Expansion in the Intestine
Authors: Ce Tang, Tomonori Kamiya, Yang Liu, Motohiko Kadoki, Shigeru Kakuta, Kenshiro Oshima, Masahira Hattori, Kozue Takeshita, Takanori Kanai, Shinobu Saijo, Naohito Ohno, Yoichiro Iwakura
Journal: Cell Host & Microbe (2015)
Eosinophil peroxidase induces expression of cholinergic genes via cell surface neural interactions
Authors: Nadim Akasheh, Marie-Therese Walsh, Richard Costello
Journal: European Respiratory Journal (2014)

Eosinophils localize to and release their granule proteins in close association with nerves in patients with asthma and rhinitis. These conditions are associated with increased neural function. In this study the effect of the individual granule proteins on cholinergic neurotransmitter expression was investigated. Eosinophil peroxidase (EPO) upregulated choline acetyltransferase (ChAT) and vesicular acetylcholine transporter (VAChT) gene expression. MBP caused upregulation of VAChT but had no effect on ChAT expression. EDN failed to upregulate either gene. Fluorescently labeled EPO was seen to bind to the IMR-32 cell surface. Both Poly-L-glutamate (PLG) and Heparinase-1 reversed the up-regulatory effect of EPO on ChAT and VAChT expression and prevented EPO adhesion to the cell surface. Poly-L-arginine (PLA) had no effect on expression of either gene, suggesting that charge is necessary but insufficient to alter gene expression. EPO induced activation of NF-κB and ERK inhibition led to reversal of all up-regulatory effects of EPO. These data indicate a preferential role of EPO signaling via a specific surface receptor that leads to neural plasticity.
Glycosyltransferases in human blood
Authors: Y. S. Kim, J. Perdomo, J. S. Whitehead, K. J. Curtis
Journal: Journal of Clinical Investigation (1972)

Serum galactosyltransferase activity was found to be elevated in patients with alcoholic and other liver disorders but remained at a normal level in patients with a variety of nonhepatic diseases. The properties of the galactosyltransferase in patients with liver disease were compared with those of the enzyme in the serum of normal subjects. The possible presence of inhibitors or activators in the serum was examined. Results indicated that in patients with liver disease, the rise in the serum galactosyltransferase was due to an increase in the level of the enzyme present in normal serum and not due to the appearance of a new enzyme. In the cases examined, the level of the enzyme increased with the deterioration of liver function and declined in a patient recovering from acute alcoholic hepatitis. Another glycosyltransferase, an N-acetylgalactosaminyltransferase, was not elevated in the serum of liver disease patients and, unlike the galactosyltransferase, was not detected in normal liver. The results suggest that the serum galactosyltransferase originates from the liver and that an abnormal rise in the level of this enzyme in serum is due to hepatocellular damage.
Raloxifene as a multifunctional medicine?
Authors: V C. Jordan, M Morrow
Journal: BMJ (1999)

Recent developments in the new endocrinology of selective oestrogen receptor modulators (SERMs) seem to have the potential to transform therapeutics. The emerging data on the multiple effects of raloxifene have generated great excitement that this might be the first multifunctional medicine. Raloxifene was developed for preventing osteoporosis and, like oestrogen, may reduce the risk of cardiovascular disease. In addition, raloxifene may reduce the incidence of breast cancer without increasing that of endometrial cancer. Selective oestrogen receptor modulators such as raloxifene introduce important new concepts for the physician, but how did we get to this point and what is the evidence to support the claims?

The description of the target site specificity of tamoxifen and raloxifene opened the door for novel applications of the drugs originally known as non-steroidal antiestrogens.1 2 Until then the drugs had been considered only as treatments for breast cancer,3 but then tamoxifen was advanced as a breast cancer preventive agent in high risk women.4 Tamoxifen would never have been acceptable as a preventive agent if it had had an antioestrogenic action on bone, resulting in an increased incidence of osteoporosis. …
Abstract 19528: Biomechanical Properties of Patient-specific Aortas and Pulmonary Arteries According to Aortic Valve Phenotype: Relevance to the Ross Procedure
Authors: Pierre Olivier Dionne, Evan Wener, Rosaire Mongrain, Richard Leask, Nancy Poirier, Raymond Cartier, Ismail El-Hamamsy
Journal: Circulation (2014)

Background:  Long-term outcomes of the Ross procedure can be limited by late autograft dilatation requiring reoperation. It has been suggested that bicuspid aortic valve is a risk factor for autograft dilatation. The aim of this study is to compare the biomechanical properties of pulmonary arteries according to aortic valve phenotype.   Methods:  At the time of surgery, segments of aortic and pulmonary artery wall were harvested according to aortic valve phenotype (n=29 patients). The segments were subjected to displacement-controlled biaxial stretch testing within 8 hours of surgery, in a physiological solution (37 C). Tissue stiffness at an engineering strain of 60% was evaluated, using engineering stress. Histological analyses were performed on the specimens to assess the number of elastic lamellae. Aortic valve phenotype was bicuspid in 18 patients (62%), unicuspid in 7 patients (24%) and tricuspid in 4 patients (14%).   Results:  Pulmonary artery circumferential and longitudinal elastic moduli were similar among the 3 populations (Unicuspid: 0.11±0.05 and 0.09±0.03 MPa, bicuspid: 0.10±0.05 and 0.11±0.05 MPa, tricuspid:0.14±0.07 and 0.09±0.05 MPa, p=0.462 and p=0.621 respectively). Aortic circumferential and longitudinal elastic moduli were also similar among the 3 populations (Unicuspid: 0.13±0.01 and 0.12±0.05 MPa , bicuspid: 0.17±0.06 MPa and 0.14±0.06 MPa, tricuspid: 0.09 MPa and 0.11 MPa , p=0.188 and p=0.720 respectively).  Aortic and pulmonary artery thickness were also similar among the 3 populations (Unicuspid: 1.53±0.16 mm and 1.22±0.29 mm, bicuspid: 1.65±0.33 mm and 1.20±0.32 mm, tricuspid: 2.12 and 1.38±0.15, p=0.248 and p=0.566, respectively).  Pulmonary artery lamellae unit count was also similar among the 3 populations (tricuspid: 30 units, bicuspid: 43±9 units and unicuspid: 30 units, p=0.10). The number of elastic lamellae was also similar in aortic specimens (tricuspid: 52 units, bicuspid: 60±11 units, unicuspid: 52 units, p=0.640).   Conclusion:  Current findings suggest that the biomechanical properties of pulmonary arteries obtained from patients undergoing the Ross procedure are independent of aortic valve phenotype. These results may have significant impact on the long-term clinical outcomes following this procedure.
Abstract 338: Determining the Timeliness of Key Resuscitative Interventions Among Pediatric Patients Treated for Septic Shock at a Pediatric Tertiary Care Hospital
Authors: Blair L Bigham, Emilio Aguirre, Karen Choong, Melissa J Parker
Journal: Circulation (2014)

Introduction: Severe sepsis and septic shock (SS) are associated with high mortality and morbidity, and interventions are time-sensitive. Adherence to evidence based guidelines is poor. Objective: To evaluate the time required to deliver components of the American College of Critical Care Medicine guidelines for SS; vascular access, isotonic fluid bolus of 20mL/kg within 15 min, antibiotics within 15 min, and vasoactive medications. Method: A retrospective case series to determine when SS criteria were met (Time Zero) and the timing of recommended therapies for children 29 days to 17 yrs with SS admitted to the intensive care unit at a pediatric hospital. Descriptive statistics are reported as median and ranges. Results: Of 498 admissions between 01/06/2010 and 30/06/2011, 28 (6%) met criteria for SS; 13 (46.4%) in the emergency department, 7 (25%) on a ward and 8 (28.6%) in the ICU. Half (14) were males, median age and weight were 4.4yrs (0-17) and 19kg (2.9-85.9) and 4 (14.3%) patients died. Septic shoc...
Scientists Probe Roles of Mitochondria in Neurological Disease and Injury
Authors: M J Friedrich
Journal: JAMA (2004)

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