tbuckley/cabot-search huggingface dataset:
(1 → 3)- β -<scp>d</scp>-Glucan and Endotoxin in House Dust and Peak Flow Variability in Children
Authors: JEROEN DOUWES, ARJAN ZUIDHOF, GERT DOEKES, SASKIA van der ZEE, INGE WOUTERS, H. MARIKE BOEZEN, BERT BRUNEKREEF
Journal: American Journal of Respiratory and Critical Care Medicine (2000)

House dust-associated bacterial endotoxins have been shown to be associated with asthma severity, and a similar role has been suggested for fungal (1-->3)-beta-D-glucans. In this study the relation between these agents and peak expiratory flow (PEF) variability was investigated in 148 children 7 to 11 yr of age of whom 50% had self- or parent-reported chronic respiratory symptoms. All children self-monitored twice daily their PEF for a period of 16 wk. Dust samples were collected from mattresses and from living room and bedroom floors, and endotoxin and (1-->3)-beta-D-glucan were measured in dust extracts. The relations with mean daily PEF variability (Ampl%mean) were investigated by linear regression analysis, adjusting for dust mite allergen levels, presence of pets, and type of floor cover. In unadjusted analyses the levels of both endotoxin and (1--> 3)-beta-D-glucan per square meter of living room floor were significantly associated with PEF-variability (but not when expressed per gram of sampled dust), particularly in atopic children with asthma symptoms. Adjusted analyses showed the same association for (1--> 3)-beta-D-glucan but not for endotoxin. Although no associations were found with microbial agent levels in bedroom floor or mattress dust, high levels of (1-->3)-beta-D-glucan in living room floor dust apparently increase PEF variability in asthmatic children.
Tyrosine-Phosphorylated Bacterial Proteins
Authors: Antonello Covacci, Rino Rappuoli
Journal: The Journal of Experimental Medicine (2000)

For over a century, since the discovery by Roux and Yersin that sterile culture supernatants of Corynebacterium diphtheriae contained a potent toxin able to reproduce the lesions caused by diphtheria ([1][1]), most pathogenic bacteria have been considered to be microorganisms able to intoxicate
Androgens in pregnancy: roles in parturition
Authors: Sofia Makieva, Philippa T.K. Saunders, Jane E. Norman
Journal: Human Reproduction Update (2014)

BACKGROUNDUnderstanding the physiology of pregnancy enables effective management of pregnancy complications that could otherwise be life threatening for both mother and fetus. A functional uterus (i) retains the fetus in utero during pregnancy without initiating stretch-induced contractions and (ii) is able to dilate the cervix and contract the myometrium at term to deliver the fetus. The onset of labour is associated with successful cervical remodelling and contraction of myometrium, arising from concomitant activation of uterine immune and endocrine systems. A large body of evidence suggests that actions of local steroid hormones may drive changes occurring in the uterine microenvironment at term. Although there have been a number of studies considering the potential role(s) played by progesterone and estrogen at the time of parturition, the bio-availability and effects of androgens during pregnancy have received less scrutiny. The aim of this review is to highlight potential roles of androgens in the biology of pregnancy and parturition.
Ventilator-induced coagulopathy in experimental Streptococcus pneumoniae pneumonia
Authors: J. J. Haitsma, M. J. Schultz, J-J. H. Hofstra, J. W. Kuiper, J. Juco, R. Vaschetto, M. Levi, H. Zhang, A. S. Slutsky
Journal: European Respiratory Journal (2008)

Pneumonia, the main cause of acute lung injury, is characterised by a local pro-inflammatory response and coagulopathy. Mechanical ventilation (MV) is often required. However, MV can lead to additional injury: so-called ventilator-induced lung injury (VILI). Therefore, the current authors investigated the effect of VILI on alveolar fibrin turnover in Streptococcus pneumoniae pneumonia. Pneumonia was induced in rats, followed 48 h later by either lung-protective MV (lower tidal volumes (L V T ) and positive end-expiratory pressure (PEEP)) or MV causing VILI (high tidal volumes (H V T ) and zero end-expiratory pressure (ZEEP)) for 3 h. Nonventilated pneumonia rats and healthy rats served as controls. Thrombin–antithrombin complexes (TATc), as a measure for coagulation, and plasminogen activator activity, as a measure of fibrinolysis, were determined in bronchoalveolar lavage fluid (BALF) and serum. Pneumonia was characterised by local (BALF) activation of coagulation, resulting in elevated TATc levels and attenuation of fibrinolysis compared with healthy controls. L V T -PEEP did not influence alveolar coagulation or fibrinolysis. H V T -ZEEP did intensify the local procoagulant response: TATc levels rose significantly and levels of the main inhibitor of fibrinolysis, plasminogen activator inhibitor-1, increased significantly. H V T -ZEEP also resulted in systemic elevation of TATc compared with L V T -PEEP. Mechanical ventilation causing ventilator-induced lung injury increases pulmonary coagulopathy in an animal model of Streptococcus pneumoniae pneumonia and results in systemic coagulopathy.
No association between interferon- receptor-1 gene polymorphism and pulmonary tuberculosis in a Gambian population sample
Authors: A A Awomoyi
Journal: Thorax (2004)

Background: Tuberculosis (TB) is a major global cause of mortality and morbidity, and host genetic factors influence disease susceptibility. Interferon-γ mediates immunity to mycobacteria and rare mutations in the interferon-γ receptor-1 gene ( IFNGR1 ) result in increased susceptibility to mycobacterial infection, including TB, in affected families. The role of genetic variation in IFNGR1 in susceptibility to common mycobacterial diseases such as pulmonary TB in outbred populations has not previously been investigated. Methods: The association between IFNGR1 and susceptibility to pulmonary TB was investigated in a Gambian adult population sample using a case-control study design. The coding and promoter regions of IFNGR1 were sequenced in 32 patients with pulmonary TB, and the frequencies of six common IFNGR1 polymorphisms were determined using PCR based methods in 320 smear positive TB cases and 320 matched controls. Haplotypes were estimated from the genotype data using the expectation-maximisation algorithm. Results: There was no association between the IFNGR1 variants studied and TB in this Gambian population sample. Three common haplotypes were identified within the study population, none of which was associated with TB. Conclusions: These data represent an important negative finding and suggest that, while IFNGR1 is implicated in rare Mendelian susceptibility to mycobacterial disease, the common variants studied here do not have a major influence on susceptibility to pulmonary TB in The Gambian population.
Pathogenesis of Human B Cell Lymphomas
Authors: Arthur L. Shaffer, Ryan M. Young, Louis M. Staudt
Journal: Annual Review of Immunology (2012)

The mechanisms that drive normal B cell differentiation and activation are frequently subverted by B cell lymphomas for their unlimited growth and survival. B cells are particularly prone to malignant transformation because the machinery used for antibody diversification can cause chromosomal translocations and oncogenic mutations. The advent of functional and structural genomics has greatly accelerated our understanding of oncogenic mechanisms in lymphomagenesis. The signaling pathways that normal B cells utilize to sense antigens are frequently derailed in B cell malignancies, leading to constitutive activation of prosurvival pathways. These malignancies co-opt transcriptional regulatory systems that characterize their normal B cell counterparts and frequently alter epigenetic regulators of chromatin structure and gene expression. These mechanistic insights are ushering in an era of targeted therapies for these cancers based on the principles of pathogenesis.
Translocation Carcinomas of the Kidney After Chemotherapy in Childhood
Authors: Pedram Argani, Marick Laé, Edgar T. Ballard, Mahul Amin, Carlos Manivel, Brian Hutchinson, Victor E. Reuter, Marc Ladanyi
Journal: Journal of Clinical Oncology (2006)

Children who survive cancer are at more than 19-fold increased risk of developing another malignancy. Renal cell carcinoma (RCC) occurring as a secondary malignancy is uncommon. Translocation RCC, bearing TFE3 or TFEB gene fusions, are recently recognized entities for which risk factors have not been identified.We describe the clinical, pathologic, cytogenetic, and molecular data on six translocation RCCs that arose in five young patients who had received chemotherapy.The ages at time of diagnosis of the RCC ranged from 6 to 22 years. Histologically, these tumors showed typical features previously described for translocation RCCs. At the molecular level, three tumors contained the ASPL-TFE3 fusion, two contained Alpha-TFEB, and one contained PRCC-TFE3. The intervals between chemotherapy and the diagnosis of RCC ranged from 4 to 13 years. The indications for the antecedent chemotherapy were varied and included acute promyelocytic leukemia, acute myeloid leukemia with t(9;11), bilateral Wilms' tumor, systemic lupus erythematosus, and conditioning regimen of bone marrow transplant for Hurler's syndrome. Only the latter patient had also received radiation. Hence, among 39 genetically confirmed translocation RCCs in our personal experience, six (15%) have arisen in patients who had received cytotoxic chemotherapy.Cytotoxic chemotherapy may predispose to the development of renal translocation carcinomas.
British Society for Rheumatology Biologics Register
Authors: A Silman
Journal: Annals of the Rheumatic Diseases (2003)

The British Society for Rheumatology (BSR) established a register of patients newly treated with biological agents, the BSR Biologics Register (BSRBR), which became active in January 2002. The goal is to register all patients in the United Kingdom with rheumatic diseases, newly starting treatment with these agents and to follow them up to determine the incidence of any short and long term hazards to health. The Register is also recruiting a comparison cohort of patients with rheumatoid arthritis treated with standard disease modifying antirheumatic drugs to determine the relative contributions of disease factors and other treatments apart from biological agents on any risks observed.
Signal Transducer and Activator of Transcription 1 Activation in Endothelial Cells Is a Negative Regulator of Angiogenesis
Authors: Traci E. Battle, Rebecca A. Lynch, David A. Frank
Journal: Cancer Research (2006)

To determine the role of the transcription factor signal transducer and activator of transcription (STAT) 1 on endothelial cell function, human umbilical vein endothelial cells (HUVEC) were treated with IFN-gamma, a potent activator of STAT1. IFN-gamma inhibited cell growth and tube formation of HUVECs. Although the potent proangiogenic protein vascular endothelial growth factor (VEGF) stimulated cell growth and tube formation, IFN-gamma could suppress these effects of VEGF. Transfection of HUVECs with short interfering RNA targeting STAT1 abrogated IFN-gamma-induced inhibition of HUVEC growth and tube formation, and suppressed the inhibition of VEGF-induced tube formation by IFN-gamma, indicating that STAT1 is critical for this process. IFN-gamma blocks the biological activity of VEGF through inhibition of genes necessary for the VEGF response, including angiopoietin-2, urokinase plasminogen activator, tissue inhibitor of matrix metalloproteinase-1, cyclooxygenase-2, and VEGF receptor 2. To extend these findings in vivo, the role of STAT1 in angiogenesis was examined in STAT1-deficient mice using the Matrigel in vivo angiogenesis assay. Substantial cellular infiltration and formation of vascular structures occurred in STAT1-/- mice compared with wild-type controls. These data indicate that STAT1 plays a key role in the inhibition of angiogenesis through its action within endothelial cells, and exploiting this process may be useful in treating cancers and vascular tumors.
The Battered-Child Syndrome
Authors: C. Henry Kempe
Journal: JAMA (1962)

The battered-child syndrome, a clinical condition in young children who have received serious physical abuse, is a frequent cause of permanent injury or death. The syndrome should be considered in any child exhibiting evidence of fracture of any bone, subdural hematoma, failure to thrive, soft tissue swellings or skin bruising, in any child who dies suddenly, or where the degree and type of injury is at variance with the history given regarding the occurrence of the trauma. Psychiatric factors are probably of prime importance in the pathogenesis of the disorder, but knowledge of these factors is limited. Physicians have a duty and responsibility to the child to require a full evaluation of the problem and to guarantee that no expected repetition of trauma will be permitted to occur.
Uberon, an integrative multi-species anatomy ontology
Authors: Christopher J Mungall, Carlo Torniai, Georgios V Gkoutos, Suzanna E Lewis, Melissa A Haendel
Journal: Genome biology (2012)

Abstract We present Uberon, an integrated cross-species ontology consisting of over 6,500 classes representing a variety of anatomical entities, organized according to traditional anatomical classification criteria. The ontology represents structures in a species-neutral way and includes extensive associations to existing species-centric anatomical ontologies, allowing integration of model organism and human data. Uberon provides a necessary bridge between anatomical structures in different taxa for cross-species inference. It uses novel methods for representing taxonomic variation, and has proved to be essential for translational phenotype analyses. Uberon is available at http://uberon.org
Response to Comment on Genuth. Should Sulfonylureas Remain an Acceptable First-Line Add-on to Metformin Therapy in Patients With Type 2 Diabetes? No, It’s Time to Move On! Diabetes Care 2015;38:170–175
Authors: Saul Genuth
Journal: Diabetes Care (2015)

I appreciate the attention Schrijnders et al. (1) have given to the Counterpoint article on use of sulfonylureas as an add-on to metformin (2). Several sulfonylureas were compared …
Low-dose glucocorticoid therapy decreases risk for treatment-limiting infusion reaction to infliximab in patients with rheumatoid arthritis
Authors: J. Augustsson, S. Eksborg, S. Ernestam, E. Gullstrom, R. van Vollenhoven
Journal: Annals of the Rheumatic Diseases (2007)

<h3>Background and objective:</h3> Treatment-limiting infusion reactions to infliximab have not been fully explained in rheumatoid arthritis patients. Our main objective is to investigate the role of daily oral glucocorticoids use on such reactions. <h3>Method:</h3> Forty-three patients with immediate-type infusion reactions were identified in a large registry-based cohort. These patients were then compared with the entire cohort (n = 639) and, in a separate analysis, to a nested matched control group (n = 43). The following base-line variables were compared: use of oral glucocorticoids, health-assessment questionnaire, 28-joint count-based disease activity score, duration of disease and number of failed disease-modifying antirheumatic drugs. <h3>Results:</h3> The proportion of infusions associated with infusion reactions decreased significantly during the study period (p = 0.0024). Fifty per cent of the patients in the cohort were treated with daily low-dose glucocorticoids at baseline. 15/326 (4.6%) patients had an infusion reaction as compared with 28/324 (8.6%) of patients without glucocorticoid treatment (p = 0.057). In the matched comparison, 15/43 (35%) of the cases were on low-dose glucocorticoids as compared with 27/43 (64%) of the controls (p = 0.017). The use of low-dose glucocorticoids was associated with a significantly lower risk for a treatment-limiting infusion reactions in a Kaplan–Meier analysis (p = 0.04). The number needed to treat to prevent a treatment-limiting infusion reaction was 25 (95% CI: 13 to 527) in the cohort. <h3>Conclusion:</h3> The use of daily low-dose glucocorticoids is associated with a lower risk for treatment-limiting infusion reactions to infliximab. Overall, treatment-limiting infusion reactions have become significantly less common during the past 5 years.
Therapy for Pediatric Brain Tumors and the Risk of Growth Hormone Deficiency
Authors: Charles Sklar, Suzanne Wolden
Journal: Journal of Clinical Oncology (2011)

REFERENCES 1. Breuer B, Fleishman SB, Cruciani RA, et al: Medical oncologists’ attitudes and practice in cancer pain management: A national survey. J Clin Oncol 29:4769-4775, 2011 2. von Gunten CF: Arrogance ignorance paradox. J Palliat Med 8:898-899, 2005 3. Cleeland CS, Gonin R, Hatfield AK, et al: Pain and its treatment in outpatients with metastatic cancer. N Engl J Med 330:592-596, 1994 4. Cleeland CS, Portenoy RK, Rue M, et al: Does an oral analgesic protocol improve pain control for patients with cancer? An intergroup study coordinated by the Eastern Cooperative Oncology Group. Ann Oncol 16:972-980, 2005 5. Buss MK, Lessen DS, Sullivan AM, et al: A study of oncology fellows’ training in end-of-life care. J Support Oncol 5:237-242, 2007
The natural history of conduction system disease in myotonic muscular dystrophy as determined by serial electrophysiologic studies.
Authors: E N Prystowsky, E L Pritchett, A D Roses, J Gallagher
Journal: Circulation (1979)

To evaluate the progression of conduction system disease in myotonic muscular dystrophy, nine patients underwent serial electrophysiologic studies at a mean of 35 months apart. At the initial study, seven patients had first-degree atrioventricular block and three of these seven had disease in the His-Purkinje system (HV greater than 55 msec). At the second study, seven patients had prolonged HV intervals, and during the almost 3-year period, HV intervals increased by at least 5 msec in all seven patients. No electrophysiologic or electrocardiographic measures could be found that correlated with progression of conduction disease in these patients. Because of the failure of electrophysiologic measures to predict progression of conduction disease in these patients, electrophysiologic studies are recommended only for symptomatic patients. If significant disease is found in either impulse formation or conduction, permanent pacemaker therapy is warranted.
Unconscious influences on decision making: A critical review
Authors: Ben R. Newell, David R. Shanks
Journal: Behavioral and Brain Sciences (2014)

Abstract To what extent do we know our own minds when making decisions? Variants of this question have preoccupied researchers in a wide range of domains, from mainstream experimental psychology (cognition, perception, social behavior) to cognitive neuroscience and behavioral economics. A pervasive view places a heavy explanatory burden on an intelligent cognitive unconscious, with many theories assigning causally effective roles to unconscious influences. This article presents a novel framework for evaluating these claims and reviews evidence from three major bodies of research in which unconscious factors have been studied: multiple-cue judgment, deliberation without attention, and decisions under uncertainty. Studies of priming (subliminal and primes-to-behavior) and the role of awareness in movement and perception (e.g., timing of willed actions, blindsight) are also given brief consideration. The review highlights that inadequate procedures for assessing awareness, failures to consider artifactual explanations of “landmark” results, and a tendency to uncritically accept conclusions that fit with our intuitions have all contributed to unconscious influences being ascribed inflated and erroneous explanatory power in theories of decision making. The review concludes by recommending that future research should focus on tasks in which participants' attention is diverted away from the experimenter's hypothesis, rather than the highly reflective tasks that are currently often employed.
Relation between ventricular and myocyte function with tachycardia-induced cardiomyopathy.
Authors: F G Spinale, B M Fulbright, R Mukherjee, R Tanaka, J Hu, F A Crawford, M R Zile
Journal: Circulation Research (1992)

Chronic supraventricular tachycardia (SVT) causes left ventricular (LV) dilatation and dysfunction. Changes in myocyte function and structure may be important factors in the development of SVT cardiomyopathy. Accordingly, LV function and isolated myocyte structure and function were examined in six pigs with pacing-induced SVT cardiomyopathy (3 weeks at 240 beats per minute) and six control pigs. LV function was examined by simultaneous echocardiography and catheterization, and isolated myocyte function was studied using computer-assisted video microscopy. Indexes of isolated myocyte contractile performance were examined in the unloaded, unattached state (31 control and 24 SVT cells) and after attachment to a basement membrane substrate (65 control and 45 SVT cells). LV fractional shortening and peak +dP/dt significantly decreased in SVT cells compared with control cells (12 +/- 2% versus 28 +/- 2%, and 842 +/- 61 versus 1,216 +/- 119 mm Hg/sec, respectively; p less than 0.05). Isolated myocyte percent shortening and normalized peak velocity of shortening of SVT myocytes adherent to a basement membrane were significantly lower than attached control myocytes (1.2 +/- 0.2% versus 4.3 +/- 0.3%, and 15 +/- 2 versus 37 +/- 5% resting cell length/sec, respectively; p less than 0.05). Similarly, in the unattached state, the extent and velocity of shortening of SVT myocytes were reduced by over 50% from control values. Contractile properties of attached and unattached cardiocytes were also examined in the presence of 2-8 mM extracellular Ca2+. For both attached and unattached SVT myocytes, responsiveness to increases in extracellular Ca2+ were significantly blunted from control values. Ultrastructural examination of SVT myocytes revealed that the percent volume of myofibrils within isolated myocytes was reduced from control values (46 +/- 7% versus 65 +/- 2%, p less than 0.05). In summary, SVT cardiomyopathy is probably due to a primary defect in isolated myocyte contractile performance. The reduced contractile function of SVT cardiomyopathic myocytes was associated with abnormalities in cytoarchitecture and Ca2+ responsiveness.
Dispatcher-Directed Bystander Initiated Cardiopulmonary Resuscitation
Authors: David G. Benditt, MaryAnn Goldstein, Richard Sutton, Demetris Yannopoulos
Journal: Circulation (2009)

A pproximately 330 000 out-of-hospital cardiac arrests (OHCAs) occur annually in the United States; in essence, there are nearly 1000 OHCA events each day. 1 However, despite the presence of extensive emergency medical response systems (especially in heavily populated regions) and aggressive steps by both professional organizations and private industry to enhance public awareness of the magnitude of the problem and the need for cardiopulmonary resuscitation (CPR) training, 1,2 overall OHCA survival rates generally remain dismal and highly variable from location to location.[5][6] Article see p 91Improving OHCA survival should be a healthcare priority, but effecting substantial improvement is complex.Experience suggests that altering current outcomes requires a wellorganized, multifaceted treatment strategy.It is unlikely that introduction of any single intervention, no matter how novel, will do the trick.In fact, as the course of events that followed the introduction of portable automatic external defibrillators (AEDs) illustrates, excessive reliance on any single innovative technology might be detrimental.In that case, AED availability was initially accompanied by a seemingly paradoxical decline in resuscitation success. 7Only later did it become evident that failure to initiate basic CPR while waiting for an AED to arrive undermined patient viability.Thus, although early defibrillation is now advocated if available quickly after a witnessed OHCA event, in most cases, CPR should be initiated first to "prime" the pump with oxygenated blood and increase the chances for a successful defibrillation. 1,2,7