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71.
Ibrahim Aldoss Raju Pillai Dongyun Yang Lixin Yang Shukaib Arslan Sally Mokhtari Monzr M. Al Malki Amandeep Salhotra Shilpa Shahani Haris Ali Matthew Mei Andrew Artz David Snyder Michelle Afkhami Saro Armenian Anthony Stein Guido Marcucci Stephen J. Forman Ryotaro Nakamura Vinod Pullarkat 《Blood cancer journal》2021,11(7)
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74.
TDP-43 in familial and sporadic frontotemporal lobar degeneration with ubiquitin inclusions 总被引:23,自引:0,他引:23
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Cairns NJ Neumann M Bigio EH Holm IE Troost D Hatanpaa KJ Foong C White CL Schneider JA Kretzschmar HA Carter D Taylor-Reinwald L Paulsmeyer K Strider J Gitcho M Goate AM Morris JC Mishra M Kwong LK Stieber A Xu Y Forman MS Trojanowski JQ Lee VM Mackenzie IR 《The American journal of pathology》2007,171(1):227-240
TAR DNA-binding protein 43 (TDP-43) is a major pathological protein of sporadic and familial frontotemporal lobar degeneration with ubiquitin-positive, tau-negative inclusions (FTLD-U) with or without motor neuron disease (MND). Thus, TDP-43 defines a novel class of neurodegenerative diseases called TDP-43 proteinopathies. We performed ubiquitin and TDP-43 immunohistochemistry on 193 cases of familial and sporadic FTLD with or without MND. On selected cases, immunoelectron microscopy and biochemistry were performed. Clinically defined frontotemporal dementias (FTDs) included four groups: 1) familial FTD with mutations in progranulin (n = 36), valosin-containing protein (n = 5), charged multivesicular body protein 2B (n = 4), and linked to chromosome 9p (n = 7); 2) familial cases of FTD with unknown gene association (n = 29); 3) sporadic FTD (n = 72); and 4) familial and sporadic FTD with MND (n = 40). Our studies confirm that the spectrum of TDP-43 proteinopathies includes most cases of sporadic and familial FTLD-U with and without MND and expand this disease spectrum to include reported families with FTD linked to chromosome 9p but not FTD with charged multivesicular body protein 2B mutations. Thus, despite significant clinical, genetic, and neuropathological heterogeneity of FTLD-U, TDP-43 is a common pathological substrate underlying a large subset of these disorders, thereby implicating TDP-43 in novel and unifying mechanisms of FTLD pathogenesis. 相似文献
75.
Garland SM Hernandez-Avila M Wheeler CM Perez G Harper DM Leodolter S Tang GW Ferris DG Steben M Bryan J Taddeo FJ Railkar R Esser MT Sings HL Nelson M Boslego J Sattler C Barr E Koutsky LA;Females United to Unilaterally Reduce Endo/Ectocervical Disease 《The New England journal of medicine》2007,356(19):1928-1943
76.
Valerie L. Forman–Hoffman Kathryn R. Batts Sarra L. Hedden Kathy Spagnola Jonaki Bose 《Annals of epidemiology》2018,28(7):468-474
Purpose
To examine the prevalence and correlates of mental disorder comorbidity in the adult U.S. household population.Methods
Data are from a nationally representative sample of noninstitutionalized, civilian adults aged 18 years or older (n = 5653) who participated in the 2008–2012 Mental Health Surveillance Study. Mental disorders, including substance use disorders, were assessed by clinical interviewers using a semistructured diagnostic instrument. Analyses examined co-occurrence of mental disorders and associations with sociodemographic, functional impairment, and treatment correlates.Results
Approximately one-third of adults (31.1%, or more than 15 million) with a past-year mental disorder had a co-occurring mental disorder. Correlates of comorbidity in adjusted models included being of young age, being of non-Hispanic white race/ethnicity, having low family income, and living in a large metropolitan area. Adults with comorbid mental disorders had lower mean levels of functioning and were more likely to report past-year treatment than adults with a single disorder; they also had higher estimates of past-year perceived unmet need for care (21.7% vs. 11.6%, P < .01).Conclusions
About one in three adults with a mental disorder have a co-occurring mental disorder. Elucidating factors associated with co-occurrence may lend clues to shared etiologies, help improve prevention efforts, facilitate early identification, and improve treatment regimens. 相似文献77.
Use of central venous catheter-related bloodstream infection prevention practices by US hospitals 总被引:3,自引:0,他引:3
Krein SL Hofer TP Kowalski CP Olmsted RN Kauffman CA Forman JH Banaszak-Holl J Saint S 《Mayo Clinic proceedings. Mayo Clinic》2007,82(6):672-678
OBJECTIVE: To examine the extent to which US acute care hospitals have adopted recommended practices to prevent central venous catheter-related bloodstream infections (CR-BSIs). PARTICIPANTS AND METHODS: Between March 16, 2005, and August 1, 2005, a survey of infection control coordinators was conducted at a national random sample of nonfederal hospitals with an intensive care unit and more than 50 hospital beds (n=600) and at all Department of Veterans Affairs (VA) medical centers (n=119). Primary outcomes were regular use of 5 specific practices and a composite approach for preventing CR-BSIs. RESULTS: The overall survey response rate was 72% (n=516). A higher percentage of VA compared to non-VA hospitals reported using maximal sterile barrier precautions (84% vs 71%; P=.01); chlorhexidine gluconate for insertion site antisepsis (91% vs 69%; P<.001); and a composite approach (62% vs 44%; P=.003) combining concurrent use of maximal sterile barrier precautions, chlorhexidine gluconate, and avoidance of routine central line changes. Those hospitals having a higher safety culture score, having a certified infection control professional, and participating in an infection prevention collaborative were more likely to use CR-BSI prevention practices. CONCLUSION: Most US hospitals are using maximal sterile barrier precautions and chlorhexidine gluconate, 2 of the most strongly recommended practices to prevent CR-BSIs. However, fewer than half of non-VA US hospitals reported concurrent use of maximal sterile barrier precautions, chlorhexidine gluconate, and avoidance of routine central line changes. Wider use of CR-BSI prevention practices by hospitals could be encouraged by fostering a culture of safety, participating in infection prevention collaboratives, and promoting infection control professional certification. 相似文献
78.
Wang Y Xu M Che M Von Hofe E Abbas A Kallinteris NL Lu X Liss ZJ Forman JD Hillman GG 《Human gene therapy》2005,16(2):187-199
Transfecting genes into tumors, to upregulate major histocompatibility complex (MHC) class I and class II molecules and inhibit MHC class II associated invariant chain (Ii), induces a potent anti-tumor immune response when preceded by tumor irradiation, in murine RM-9 prostate carcinoma. The transfected genes are cDNA plasmids for interferon-gamma (pIFN-gamma), MHC class II transactivator (pCIITA), an Ii reverse gene construct (pIi-RGC), and a subtherapeutic dose of adjuvant IL-2 (pIL-2). Responding mice rejected challenge with parental tumor and demonstrated tumor-specific cytotoxic T lymphocytes (CTLs). We have extended our investigation to determine the relative roles of each one of the four plasmids pIFN-gamma, pCIITA, pIi-RGC, and pIL-2 in conjunction with radiation for the induction of a curative immune response. Upregulation of MHC class I with pIFN-gamma or class II with pCIITA, separately, does not lead to a complete response even if supplemented with pIL-2 or pIi-RGC. An optimal and specific antitumor response is achieved in more than 50% of the mice when, after tumor irradiation, tumor cells are converted in situ to a MHC class I+/class II+/Ii- phenotype with pIFN-gamma, pCIITA, pIi-RGC, and pIL-2. We demonstrate further that both CD4+ helper T cells and CD8+ cytotoxic T cells are essential for induction of an antitumor response because in vivo depletion of either subset abrogates the response. The radiation contributes to the gene therapy by causing tumor debulking and increasing the permeability of tumors to infiltration of inflammatory cells. 相似文献
79.
Schmitz JE Lifton MA Reimann KA Montefiori DC Shen L Racz P Tenner-Racz K Ollert MW Forman MA Gelman RS Vogel CW Letvin NL 《AIDS research and human retroviruses》1999,15(2):195-202
Cobra venom factor (CVF)-induced consumption of complement proteins was used to investigate the role of complement in vivo in the immunopathogenesis of simian immunodeficiency virus of macaques (SIVmac) infection in rhesus monkeys. Repeated administration of CVF was shown to deplete complement to <5% of baseline hemolytic activity of serum complement for 10 days in a normal monkey. Three groups of SIVmac-infected animals were then evaluated: monkeys treated with CVF resulting in complement depletion from days -1 to 10 postinfection, monkeys treated with CVF resulting in complement depletion from days 10 to 21 postinfection, and control monkeys that received no CVF. CD8+ SIVmac-specific cytotoxic T lymphocyte (CTL) generation and CD4+ T lymphocyte depletion during primary infection were not affected by CVF treatment. Viral load, assessed by measurements of plasma p27gag antigen and viral RNA, was transiently higher during the first 4 weeks following infection in the CVF-treated monkeys and the subsequent clinical course in these treated animals was accelerated. These results suggest that complement proteins may participate in immune defense mechanisms that decrease virus replication following the initial burst of intense viremia during primary SIVmac infection. However, we cannot rule out that the observed increased virus replication was induced by immune activation resulting from the administration of a foreign antigen to these monkeys. 相似文献
80.
Impact of time to therapy and reperfusion modality on the efficacy of adenosine in acute myocardial infarction: the AMISTAD-2 trial. 总被引:6,自引:0,他引:6
Robert A Kloner Mervyn B Forman Raymond J Gibbons Allan M Ross R Wayne Alexander Gregg W Stone 《European heart journal》2006,27(20):2400-2405
AIMS: The purpose of this analysis was to determine whether the efficacy of adenosine vs. placebo was dependent on the timing of reperfusion therapy in the second Acute Myocardial Infarction Study of Adenosine (AMISTAD-II). METHODS AND RESULTS: Patients presenting with ST-segment elevation anterior AMI were randomized to receive placebo vs. adenosine (50 or 70 microg/kg/min) for 3 h starting within 15 min of reperfusion therapy. In the present post hoc hypothesis generating study, the results were stratified according to the timing of reperfusion, i.e. > or = or < the median 3.17 h, and by reperfusion modality. In patients receiving reperfusion < 3.17 h, adenosine compared with placebo significantly reduced 1-month mortality (5.2 vs. 9.2%, respectively, P = 0.014), 6-month mortality (7.3 vs. 11.2%, P = 0.033), and the occurrence of the primary 6-month composite clinical endpoint of death, in-hospital CHF, or rehospitalization for CHF at 6 months (12.0 vs. 17.2%, P = 0.022). Patients reperfused beyond 3 h did not benefit from adenosine. CONCLUSION: In this post hoc analysis, 3 h adenosine infusion administered as an adjunct to reperfusion therapy within the first 3.17 h onset of evolving anterior ST-segment elevation AMI enhanced early and late survival, and reduced the composite clinical endpoint of death or CHF at 6 months. 相似文献