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981.
Acute upper airway obstruction is a potentially life-threatening event. The most common causes include foreign body inhalation, thermal injury, inflammation, angioedema and trauma. Airway obstruction caused by submucosal extension of subcutaneous emphysema has only been previously reported once. We report the case of a patient who suffered a respiratory arrest as a result of hypopharyngeal and laryngeal swelling associated with massive subcutaneous emphysema. 相似文献
982.
Rosenwald A Wright G Leroy K Yu X Gaulard P Gascoyne RD Chan WC Zhao T Haioun C Greiner TC Weisenburger DD Lynch JC Vose J Armitage JO Smeland EB Kvaloy S Holte H Delabie J Campo E Montserrat E Lopez-Guillermo A Ott G Muller-Hermelink HK Connors JM Braziel R Grogan TM Fisher RI Miller TP LeBlanc M Chiorazzi M Zhao H Yang L Powell J Wilson WH Jaffe ES Simon R Klausner RD Staudt LM 《The Journal of experimental medicine》2003,198(6):851-862
Using current diagnostic criteria, primary mediastinal B cell lymphoma (PMBL) cannot be distinguished from other types of diffuse large B cell lymphoma (DLBCL) reliably. We used gene expression profiling to develop a more precise molecular diagnosis of PMBL. PMBL patients were considerably younger than other DLBCL patients, and their lymphomas frequently involved other thoracic structures but not extrathoracic sites typical of other DLBCLs. PMBL patients had a relatively favorable clinical outcome, with a 5-yr survival rate of 64% compared with 46% for other DLBCL patients. Gene expression profiling strongly supported a relationship between PMBL and Hodgkin lymphoma: over one third of the genes that were more highly expressed in PMBL than in other DLBCLs were also characteristically expressed in Hodgkin lymphoma cells. PDL2, which encodes a regulator of T cell activation, was the gene that best discriminated PMBL from other DLBCLs and was also highly expressed in Hodgkin lymphoma cells. The genomic loci for PDL2 and several neighboring genes were amplified in over half of the PMBLs and in Hodgkin lymphoma cell lines. The molecular diagnosis of PMBL should significantly aid in the development of therapies tailored to this clinically and pathogenetically distinctive subgroup of DLBCL. 相似文献
983.
Therapeutic approaches for muscle wasting disorders 总被引:1,自引:0,他引:1
Muscle wasting and weakness are common in many disease states and conditions including aging, cancer cachexia, sepsis, denervation, disuse, inactivity, burns, HIV-acquired immunodeficiency syndrome (AIDS), chronic kidney or heart failure, unloading/microgravity, and muscular dystrophies. Although the maintenance of muscle mass is generally regarded as a simple balance between protein synthesis and protein degradation, these mechanisms are not strictly independent, but in fact they are coordinated by a number of different and sometimes complementary signaling pathways. Clearer details are now emerging about these different molecular pathways and the extent to which these pathways contribute to the etiology of various muscle wasting disorders. Therapeutic strategies for attenuating muscle wasting and improving muscle function vary in efficacy. Exercise and nutritional interventions have merit for slowing the rate of muscle atrophy in some muscle wasting conditions, but in most cases they cannot halt or reverse the wasting process. Hormonal and/or other drug strategies that can target key steps in the molecular pathways that regulate protein synthesis and protein degradation are needed. This review describes the signaling pathways that maintain muscle mass and provides an overview of some of the major conditions where muscle wasting and weakness are indicated. The review provides details on some therapeutic strategies that could potentially attenuate muscle atrophy, promote muscle growth, and ultimately improve muscle function. The emphasis is on therapies that can increase muscle mass and improve functional outcomes that will ultimately lead to improvement in the quality of life for affected patients. 相似文献
984.
Two quality of life studies at the University of Nebraska Medical Center and 3 similar studies in the nursing literature were compared regarding family distress to illness scores as reported by long-term cancer survivors. All studies were cross-sectional mail surveys and used City of Hope National Medical Center questionnaires. Participants represented a broad range of survivorship in terms of diagnosis and length of survival (range of means 3Y8 years). Single-item scores were compared among participants regarding the item "How distressing has your illness been for your family?" Significant levels of patient-reported family distress to illness were reported in all 5 studies. Patient survivors may have been able to recall past levels of significant family distress despite prolonged survival or they may have reported significant ongoing family distress as a result of their disease and treatment. Longitudinal assessment of patients' and families' quality of life is essential throughout survivorship. Future studies should identify and compare the types distress experienced by patient survivors and families over time and also measure the intensity of their distress. Interventions designed to meet their individual and collective needs, thereby decreasing their distress, are needed to improve quality of life for survivors and families. 相似文献
985.
Brain fodrin: substrate for calpain I, an endogenous calcium-activated protease. 总被引:15,自引:3,他引:15
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R Siman M Baudry G Lynch 《Proceedings of the National Academy of Sciences of the United States of America》1984,81(11):3572-3576
The calcium-activated thiol-protease calpain I, which is present in cytosolic and membrane preparations from rat brain, was tested for its capacity to degrade the neuronal spectrin-like protein fodrin. In the presence of micromolar calcium concentrations purified calpain I degraded both purified fodrin and the fodrin present in hippocampal and cerebellar membranes. Fodrin was identified as a high molecular weight protein present in brain membranes by the following criteria: (i) comigration on NaDodSO4/polyacrylamide gels with purified fodrin, (ii) reactivity with antibodies to purified fodrin, and (iii) a proteolytic map following calpain activation comparable to that found after calpain-mediated degradation of purified fodrin. The fodrin breakdown was selective in that calpain I did not affect at least 15 other membrane-associated polypeptides. Fodrin degradation by the protease was rapid and was accompanied by the appearance of a lower molecular weight breakdown product. Calpain I had a high affinity for fodrin, with a Km for degradation of about 50 nM. Purified calpain I also degraded purified spectrin and the spectrin present in erythrocyte membranes. Calpain I-mediated degradation of spectrin-like proteins could provide a mechanism by which brief increases in intracellular free calcium levels modify the structure of the submembraneous cytoskeleton and the distribution of cell surface receptors and alter cell shape. 相似文献
986.
Irreversible inhibitors of the EGF receptor may circumvent acquired resistance to gefitinib 总被引:25,自引:0,他引:25
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Kwak EL Sordella R Bell DW Godin-Heymann N Okimoto RA Brannigan BW Harris PL Driscoll DR Fidias P Lynch TJ Rabindran SK McGinnis JP Wissner A Sharma SV Isselbacher KJ Settleman J Haber DA 《Proceedings of the National Academy of Sciences of the United States of America》2005,102(21):7665-7670
Non-small cell lung cancers (NSCLCs) with activating mutations in the kinase domain of the epidermal growth factor receptor (EGFR) demonstrate dramatic, but transient, responses to the reversible tyrosine kinase inhibitors gefitinib (Iressa) and erlotinib (Tarceva). Some recurrent tumors have a common secondary mutation in the EGFR kinase domain, T790M, conferring drug resistance, but in other cases the mechanism underlying acquired resistance is unknown. In studying multiple sites of recurrent NSCLCs, we detected T790M in only a small percentage of tumor cells. To identify additional mechanisms of acquired resistance to gefitinib, we used NSCLC cells harboring an activating EGFR mutation to generate multiple resistant clones in vitro. These drug-resistant cells demonstrate continued dependence on EGFR and ERBB2 signaling for their viability and have not acquired secondary EGFR mutations. However, they display increased internalization of ligand-activated EGFR, consistent with altered receptor trafficking. Although gefitinib-resistant clones are cross-resistant to related anilinoquinazolines, they demonstrate sensitivity to a class of irreversible inhibitors of EGFR. These inhibitors also show effective inhibition of signaling by T790M-mutant EGFR and killing of NSCLC cells with the T790M mutation. Both mechanisms of gefitinib resistance are therefore circumvented by irreversible tyrosine kinase inhibitors. Our findings suggest that one of these, HKI-272, may prove highly effective in the treatment of EGFR-mutant NSCLCs, including tumors that have become resistant to gefitinib or erlotinib. 相似文献
987.
Who,What, Where: an analysis of private sector family planning provision in 57 low‐ and middle‐income countries
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988.
Assessment of clinical occupational dose reduction effect of a new interventional cardiology shield for radial access combined with a scatter reducing drape
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989.
Coleman Karen J. Lutsky Marta A. Yau Vincent Qian Yinge Pomichowski Magdalena E. Crawford Phillip M. Lynch Frances L. Madden Jeanne M. Owen-Smith Ashli Pearson John A. Pearson Kathryn A. Rusinak Donna Quinn Virginia P. Croen Lisa A. 《Journal of autism and developmental disorders》2015,45(7):1989-1996
Journal of Autism and Developmental Disorders - To identify factors associated with valid Autism Spectrum Disorder (ASD) diagnoses from electronic sources in large healthcare systems. We examined... 相似文献
990.