tbuckley/cabot-search huggingface dataset:
Helmets and Preventing Motorcycleand Bicycle-Related Injuries
Authors: Yank D. Coble, Ronald M. Davis, C. Alvin Head, John P. Howe, Mitchell S. Karlan, William R. Kennedy, Patricia Joy Numann, Monique A. Spillman, W. Douglas Skelton, Richard M. Steinhilber, Jack P. Strong, Henry N. Wagner, Jerod M. Loeb, Robert C. Rinaldi, Theodore C. Doege, James R. Allen
Journal: JAMA (1994)

RESOLUTION 423, as amended and adopted at the 1992 Interim Meeting, asked that the American Medical Association (AMA) evaluate the effectiveness of motorcycle and bicycle helmets in preventing injuries, determine the medical costs of not using helmets, and explore ways of ensuring the use of helmets by instituting incentives or disincentives such as insurance premium adjustments or licensing fees. This report responds to the medical science aspects of the resolution and considers the occurrence and prevention of motorcycle- and bicycle-related injuries and the efficacy of helmet use by motorcyclists and bicyclists. The AMA's Council on Medical Services is studying the use of incentives and disincentives and will report to the House of Delegates at a future meeting.  See also pp 1506 and 1541.  According to age-adjusted data, injuries are the third most common cause of death in the US population, with vehiclerelated deaths causing approximately half of all deaths. 1
Caspase-11 Mediates Oligodendrocyte Cell Death and Pathogenesis of Autoimmune-Mediated Demyelination
Authors: Shin Hisahara, Junying Yuan, Takashi Momoi, Hideyuki Okano, Masayuki Miura
Journal: The Journal of Experimental Medicine (2001)

Multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE), are inflammatory diseases of the central nervous system (CNS) characterized by localized areas of demyelination. The mechanisms underlying oligodendrocyte (OLG) injury in MS and EAE remain unknown. Here we show that caspase-11 plays crucial roles in OLG death and pathogenesis in EAE. Caspase-11 and activated caspase-3 were both expressed in OLGs in spinal cord EAE lesions. OLGs from caspase-11–deficient mice were highly resistant to the cell death induced by cytotoxic cytokines. EAE susceptibility and cytokine concentrations in the CNS were significantly reduced in caspase-11–deficient mice. Our findings suggest that OLG death is mediated by a pathway that involves caspases-11 and -3 and leads to the demyelination observed in EAE.
Confronting the avian influenza threat: vaccine development for a potential pandemic
Authors: Iain Stephenson, Karl G Nicholson, John M Wood, Maria C Zambon, Jacqueline M Katz
Journal: The Lancet Infectious Diseases (2004)

Sporadic human infection with avian influenza viruses has raised concern that reassortment between human and avian subtypes could generate viruses of pandemic potential. Vaccination is the principal means to combat the impact of influenza. During an influenza pandemic the immune status of the population would differ from that which exists during interpandemic periods. An emerging pandemic virus will create a surge in worldwide vaccine demand and new approaches in immunisation strategies may be needed to ensure optimum protection of unprimed individuals when vaccine antigen may be limited. The manufacture of vaccines from pathogenic avian influenza viruses by traditional methods is not feasible for safety reasons as well as technical issues. Strategies adopted to overcome these issues include the use of reverse genetic systems to generate reassortant strains, the use of baculovirusexpressed haemagglutinin or related non-pathogenic avian influenza strains, and the use of adjuvants to enhance immunogenicity. In clinical trials, conventional surfaceantigen influenza virus vaccines produced from avian viruses have proved poorly immunogenic in immunologically naive populations. Adjuvanted or whole-virus preparations may improve immunogenicity and allow sparing of antigen.
Estrogen Stimulates Neuronal Nitric Oxide Synthase Protein Expression in Human Neutrophils
Authors: Margarita García-Durán, Trinidad de Frutos, Joaquín Díaz-Recasens, Gema García-Gálvez, Ana Jiménez, Mercedes Montón, Jerónimo Farré, Lourdes Sánchez de Miguel, Fernando González-Fernández, María del Mar Arriero, Luis Rico, Rosa García, Santos Casado, Antonio López-Farré
Journal: Circulation Research (1999)

Abstract —Recent studies have postulated the contribution of nitric oxide (NO) released by the endothelium to the beneficial effects of estrogen. Despite a neuronal-type NO synthase (nNOS) described in neutrophils, less is known about the effect of estrogen in these cells. The aim of the present study was to analyze the expression of nNOS protein in human neutrophils under different estrogenic conditions. We first analyzed nNOS expression in neutrophils obtained from premenopausal women. During the first 2 days of the follicular phase (low circulating estrogen concentrations), nNOS expression in neutrophils was reduced with respect to that found in neutrophils obtained from the same donors during the ovulatory phase (high circulating estrogen concentrations). Moreover, the expression of nNOS protein in neutrophils obtained from postmenopausal women after transdermal estrogen therapy was markedly enhanced with respect to that observed before the treatment. In vitro incubation of neutrophils derived from men for 6 hours with 17β-estradiol (10 −10 to 10 −8 mol/L) upregulated the expression of nNOS protein. The 17β-estradiol receptor antagonists, tamoxifen (10 −8 mol/L) and ICI 182780 (10 −8 mol/L), inhibited the upregulation of nNOS protein induced by 17β-estradiol. The putative functional implication was denoted by a reduced expression of the CD18 antigen on the surface of 17β-estradiol–incubated neutrophils, which was accompanied by a decreased adhesive capacity. Both effects were prevented by an NO antagonist. In conclusion, the in vivo levels of circulating estrogen concentrations seem to be associated with the level of nNOS protein expression in neutrophils from women. Moreover, low doses of 17β-estradiol upregulate nNOS protein expression in neutrophils from men. The increased ability of 17β-estradiol–incubated neutrophils derived from men to produce NO reduced their adhesive properties.
The Vibratory Perception Threshold in Young Diabetic Patients: Associations with Glycemia and Puberty
Authors: Jay M Sosenko, Andrew J M Boulton, Denise B Kubrusly, Jagdish K Weintraub, Jay S Skyler
Journal: Diabetes Care (1985)

The vibratory perception threshold, an indicator of sensory neuropathy, was measured in young type I diabetic patients (N = 55) and nondiabetic control subjects (N = 34) of similar age. Values were significantly higher in the diabetic patients (P less than 0.01), and 20% had values greater than that of any control subject. This difference was most marked among those postpubertal and persisted with allowances for age and gender in an analysis of covariance. Although the vibratory perception threshold was not related to hemoglobin A1 in younger diabetic patients (Tanner stage less than 5), there was a highly significant positive relationship in postpubertal patients (r = 0.72, P less than 0.001). There were also associations of the vibratory perception threshold with age in diabetic and control subjects (r = 0.44 and r = 0.43, respectively, P less than 0.01 for both) and with diabetes duration (r = 0.36, P less than 0.01). These data indicate that vibratory perception threshold abnormalities occur early in the course of type I diabetes mellitus; however, they are more evident in those patients who are postpubertal. In addition, they suggest that the association between the vibratory perception threshold and glycemia may be modified by developmental factors.
Epstein-Barr Virus Binding to CD21 Activates the Initial Viral Promoter via NF-κB Induction
Authors: Naoyuki Sugano, Weiping Chen, M. Luisa Roberts, Neil R. Cooper
Journal: The Journal of Experimental Medicine (1997)

Epstein-Barr virus (EBV), an oncogenic human herpesvirus, binds to and infects normal human B lymphocytes via CD21, the CR2 complement receptor. Studies of the mechanisms that enable EBV to infect nonactivated, noncycling B cells provide compelling evidence for a sequence of events in which EBV binding to CD21 on purified resting human B cells rapidly activates the NF-κB transcription factor, which, in turn, binds to and mediates transcriptional activation of Wp, the initial viral latent gene promoter. Thus, EBV binding to its cellular receptor on resting B cells triggers an NF-κB–dependent intracellular signaling pathway which is required for infection.
Activated Intrinsic Apoptosis Pathway Is a Key Related Prognostic Parameter in Acute Myeloid Leukemia
Authors: Corine J. Hess, Johannes Berkhof, Fedor Denkers, Gert J. Ossenkoppele, Jan P. Schouten, Joost J. Oudejans, Quinten Waisfisz, Gerrit J. Schuurhuis
Journal: Journal of Clinical Oncology (2007)

Purpose By parallel assessment of multiple apoptosis-related transcripts, we aimed to refine the current concept of apoptosis resistance in acute myeloid leukemia (AML) and identify the combination of genes best predicting overall survival (OS). Patients and Methods The reverse transcriptase multiplex ligation–dependent probe amplification technique was used for simultaneous quantification of 31 apoptosis-related transcripts in viable (7AAD – /AnnexinV – ) blasts (CD45 dim ) from bone marrow aspirates of 120 newly diagnosed AML patients. By forward selection, a prognosis-predicting gene expression profile was constructed. The predictive validity of this profile was assessed by cross validation. Results High transcript levels were associated with poor OS for seven of 31 genes, three of which were proapoptotic. The average expression of all 12 antiapoptotic genes was associated with poor OS (P = .029). A similar association with poor OS was found for the average expression of all 19 proapoptotic genes (P = .009). Forward selection and cross validation revealed the antiapoptotic gene BIRC3 and the proapoptotic genes BAX-(l) and BMF to optimally predict OS. Three equally sized patient groups, constructed by ranking the cross-validated prognoses of the patients, were clearly distinct (median OS times were 8.2, 16.7, and 85.6 months). Conclusion High expression of both pro- and antiapoptotic genes predicted poor OS, which postulates a mechanism of activation of the apoptosis pathway as a whole. This mechanism, which culminates in a three-gene expression signature, allows accurate clinical outcome prediction in AML and puts efforts to target single antiapoptosis genes in a new perspective.
Comparison of dual-chamber pacing versus septal myectomy for the treatment of patients with hypertrophic obstructive cardiomyopathy11There are no financial affiliations to disclose with respect to this article.
Authors: Steve R Ommen, Rick A Nishimura, Ray W Squires, Hartzell V Schaff, Gordon K Danielson, A.Jamil Tajik
Journal: Journal of the American College of Cardiology (1999)
Microenvironmental influences on inflammatory cell differentiation
Authors: J. A. Denburg
Journal: Allergy (1995)

Airways inflammation involves accumulation of inflammatory cells such as eosinophils, basophils and mast cells, which are derived from progenitors in marrow and blood. The inflamed tissue of the airways, through its structural (epithelium, stroma) and inflammatory cell components, produces an array of cytokines which can influence the differentiation of inflammatory cell progenitors. It is particular mechanism that we have investigated, showing that molecules such as GM‐CSF, G‐CSF, IL‐6, IL‐8 and SCF can be produced by airways epithelial cells and fibroblasts in quantities sufficient to induce hemopoietic events, either systemically or locally. Corticosteriods may act therapeutically, at least in part, to block inflammatory cell differentiation, and thus recruitment, into the allergic inflammatory process in the airways.
ELECTROMYOGRAPHIC RECORDING DURING INTERVIEW
Authors: FREDERICK H. DAVIS, ROBERT B. MALMO
Journal: American Journal of Psychiatry (1951)

1. A method for electromyographic study of the interview situation has been described. 2. In the present exploratory study, the close synchronization of physiological recording with sound-tape recording of interview content, which this method provides, has been of value in a number of ways: (a) in providing objective evidence, in Case 1, of the activation of a tensional headache mechanism by psychological stress; (b) in demonstrating the specificity of this mechanism, and its alteration following treatment; and (c) in providing objective evidence of physiological differentiation corresponding to differences in psychotherapeutic productivity in Case 2. 3. This method appears to be a promising one for use in further investigations of this kind.
Radon and COPD mortality in the American Cancer Society Cohort
Authors: Michelle C. Turner, Daniel Krewski, Yue Chen, C. Arden Pope, Susan M. Gapstur, Michael J. Thun
Journal: European Respiratory Journal (2011)

Although radon gas is a known cause of lung cancer, the association between residential radon and mortality from non-malignant respiratory disease has not been well characterised. The Cancer Prevention Study-II is a large prospective cohort study of nearly 1.2 million Americans recruited in 1982. Mean county-level residential radon concentrations were linked to study participants9 residential address based on their ZIP code at enrolment (mean±sd 53.5±38.0 Bq·m<sup>−3</sup>). Cox proportional hazards regression models were used to estimate adjusted hazard ratios (HR) and 95% confidence intervals (CI) for non-malignant respiratory disease mortality associated with radon concentrations. After necessary exclusions, a total of 811,961 participants in 2,754 counties were included in the analysis. Throughout 2006, there were a total of 28,300 non-malignant respiratory disease deaths. Radon was significantly associated with chronic obstructive pulmonary disease (COPD) mortality (HR per 100 Bq·m<sup>−3</sup> 1.13, 95% CI 1.05–1.21). There was a significant positive linear trend in COPD mortality with increasing categories of radon concentrations (p&lt;0.05). Findings suggest residential radon may increase COPD mortality. Further research is needed to confirm this finding and to better understand possible complex inter-relationships between radon, COPD and lung cancer.
Modulation of cellular calcium stores in the perfused rat heart by isoproterenol and ryanodine.
Authors: D R Hunter, R A Haworth, H A Berkoff
Journal: Circulation Research (1983)

The inhibitory action of procaine on cellular calcium release was utilized to define a new cellular calcium pool which, under physiological conditions, is present only during catecholamine stimulation. Rat hearts labeled with 45Ca++ were perfused with medium containing procaine and EGTA at 23 degrees C to remove extracellular calcium, and then cellular calcium was released by removal of procaine and restoration of calcium. By this method we have identified a cellular calcium pool (pool C) whose release is inhibited by procaine, but which does not require extracellular calcium for its release. Release of pool C can also be triggered by caffeine. [We have previously identified a cellular calcium pool (pool A) whose release is triggered by caffeine, inhibited by procaine, and which does require extracellular calcium for its release.] When hearts were labeled for 3 minutes with perfusate containing 1 mM 45Ca++, 48 +/- 6 nmol Ca++/g wet weight was found in pool A, but only 3 +/- 1 nmol Ca++/g in pool C. However, if isoproterenol was present during labeling, the hearts contained 72 +/- 5 nmol Ca++/g in pool A and 42 +/- 6 nmol Ca++/g in pool C. When calcium concentration in the labeling perfusate was varied, with and without isoproterenol, it was found that pool C does not begin to fill until pool A is almost full. The same effect was seen when excess cellular calcium uptake was induced by removing sodium from the perfusate. Ryanodine (0.2 microM) induced contractile failure (t1/2 = 3.4 +/- 0.4 min) and depleted pool A in control hearts by 85%. Ryanodine also similarly depleted pools A and C in isoproterenol-treated hearts. When contractility was monitored at the same time as the hearts were labeled, a linear relationship between dP/dt and the sum of pools A and C was observed over a wide range of conditions. Pools A and C both selected strongly for calcium over barium. These observations suggest that both pools A and C are located in the sarcoplasmic reticulum and are intimately involved in the regulation of contractility.
Release of prostacyclin from cultured human endothelial cells following prolonged exposure to histamine
Authors: HELEN A. BULL, M.H.A. RUSTIN, PAULINE M. DOWD
Journal: British Journal of Dermatology (1989)

Histamine is an important pro‐inflammatory molecule mediating leukocyte margination, plasma extravasation and vasodilation, but its precise mode of action on vascular endothelium is unclear. We report that histamine is able to induce prolonged release of prostacyclin (PGI2) from human endothelial cells via occupancy of the H1 receptor, without an absolute requirement for the presence of histamine or synthesis of new enzyme protein to facilitate continued release of PGI2.
Pathology of antibiotic-treated human heart valve allografts
Authors: J. B. Gavin, P. B. Herdson, J. L. Monro, B. G. Barratt-Boyes
Journal: Thorax (1973)

<b>Gavin, J. B., Herdson, P. B., Monro, J. L., and Barratt-Boyes, B. G. (1973).</b><i>Thorax</i>, <b>28,</b> 473-481. <b>Pathology of antibiotic-treated human heart valve allografts.</b> Forty-two human heart valves treated with an antibiotic solution were examined by light and electron microscopy up to 168 weeks after grafting in aortic, mitral, and tricuspid positions. There was a progressive degeneration of donor cells and by 40 days both fibroblasts and endothelial cells had vanished, leaving grafts virtually acellular. However, host inflammatory cells, together with fibrin and erythrocytes, infiltrated some regions. After 12 weeks macrophages were present in these focal collections of cells and were associated with the removal of intracuspal fibrin and the disruption of cuspal collagen. Avascular intimal fibrous sheaths of host tissue tapered from the margins of all grafts after six weeks and extended as much as half-way out of the cusp leaflets of some with consequent cusp thickening. Slow, progressive replacement fibrosis occurred along the deep surface of grafts but calcification of donor arterial wall was not observed. There was little invasion of the graft by fibroblasts from the intimal sheaths although macrophages were common along the interface between them and the underlying graft. These changes were qualitatively similar to those following chemical sterilization although intracuspal macrophage activity was generally much less and intimal fibrous sheaths were more extensive.
Detection of occult cardiac invasion by two dimensional echocardiography in patients with bronchial carcinoma.
Authors: P A Corris, P J Kertes, K Jennings, G N Morritt, E Neville, G J Gibson
Journal: Thorax (1986)

Cardiac invasion by bronchial carcinoma may prevent successful resection but may be undetected before operation. In a retrospective analysis of 100 consecutive thoracotomies nine patients had unsuspected cardiac invasion by tumour. A prospective study of preoperative two dimensional echocardiography was therefore undertaken in patients with bronchial carcinoma who had no clinical evidence of cardiac tumour. Comparison with anatomical findings was possible in 65 patients in whom an echocardiogram of suitable quality had been obtained. There was one false negative among 55 negative echocardiograms and three false positives among 10 positive echocardiograms; non-malignant pericardial disease accounted for the echocardiographic finding in one of the latter. The predictive value of a negative test was 98%, and the predictive value of a positive test was highest (80%) if the echocardiogram suggested atrial invasion.
Murine CD9 Is the Receptor for Pregnancy-specific Glycoprotein 17
Authors: Roseann Waterhouse, Cam Ha, Gabriela S. Dveksler
Journal: The Journal of Experimental Medicine (2002)

Pregnancy-specific glycoproteins (PSGs) are a family of highly similar secreted proteins produced by the placenta. PSG homologs have been identified in primates and rodents. Members of the human and murine PSG family induce secretion of antiinflammatory cytokines in mononuclear phagocytes. For the purpose of cloning the receptor, we screened a RAW 264.7 cell cDNA expression library. The PSG17 receptor was identified as the tetraspanin, CD9. We confirmed binding of PSG17 to CD9 by ELISA, flow cytometry, alkaline phosphatase binding assays, and in situ rosetting. Anti-CD9 monoclonal antibody inhibited binding of PSG17 to CD9-transfected cells and RAW 264.7 cells. Moreover, PSG17 binding to macrophages from CD9-deficient mice was significantly reduced. We then tested whether PSG17 binds to other members of the murine tetraspanin family. PSG17 did not bind to cells transfected with CD53, CD63, CD81, CD82, or CD151, suggesting that PSG17–CD9 binding is a specific interaction. We have identified the first receptor for a murine PSG as well as the first natural ligand for a member of the tetraspanin superfamily.
The autophagy-related protein beclin 1 shows reduced expression in early Alzheimer disease and regulates amyloid β accumulation in mice
Authors: Fiona Pickford, Eliezer Masliah, Markus Britschgi, Kurt Lucin, Ramya Narasimhan, Philipp A. Jaeger, Scott Small, Brian Spencer, Edward Rockenstein, Beth Levine, Tony Wyss-Coray
Journal: Journal of Clinical Investigation (2008)

Autophagy is the principal cellular pathway for degradation of long-lived proteins and organelles and regulates cell fate in response to stress. Recently, autophagy has been implicated in neurodegeneration, but whether it is detrimental or protective remains unclear. Here we report that beclin 1, a protein with a key role in autophagy, was decreased in affected brain regions of patients with Alzheimer disease (AD) early in the disease process. Heterozygous deletion of beclin 1 (Becn1) in mice decreased neuronal autophagy and resulted in neurodegeneration and disruption of lysosomes. In transgenic mice that express human amyloid precursor protein (APP), a model for AD, genetic reduction of Becn1 expression increased intraneuronal amyloid β (Aβ) accumulation, extracellular Aβ deposition, and neurodegeneration and caused microglial changes and profound neuronal ultrastructural abnormalities. Administration of a lentiviral vector expressing beclin 1 reduced both intracellular and extracellular amyloid pathology in APP transgenic mice. We conclude that beclin 1 deficiency disrupts neuronal autophagy, modulates APP metabolism, and promotes neurodegeneration in mice and that increasing beclin 1 levels may have therapeutic potential in AD.