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131.
132.
This study was focused on the immunohistochemical profile of the adenomatoid odontogenic tumor. A Pub/Medline search revealed a number of immunohistochemical studies including cytokeratin profiles, extracellular matrix proteins, Integrins, ameloblast‐associated proteins resorption regulators (RANK, RANKL), p53, PCNA, MDM2 protein, cyclin D1, Ki‐67, Bcl‐2 metallothionein, metalloproteinases, D56 hepatocyte growth factor, c‐met, DNA methyltransferase, podoplanin, TGF‐βI, Smad‐2/3, Smad‐I‐5/‐8, Smad 4, beta‐ catenin, calretinin, and clonality. Careful interpretation of the findings indicates that the adenomatoid odontogenic tumor may be more of a hamartomatous than neoplastic nature. 相似文献
133.
134.
Landry CS Grubbs EG Warneke CL Ormond M Chua C Lee JE Perrier ND 《Annals of surgical oncology》2012,19(4):1269-1274
Background
The purpose of this study was to compare the outcome of robot-assisted transaxillary thyroid surgery (RATS) to the standard open technique for thyroid lobectomy in the U.S. population. 相似文献135.
Comparison of thrombin and ristocetin in the interaction between von Willebrand factor and platelets 总被引:1,自引:0,他引:1
It is known that the antibiotic ristocetin exposes the platelet membrane receptor for factor VIII/von Willebrand glycoprotein (FVIII/vWF). Recent reports suggest that low concentrations of thrombin also cause platelet membrane receptors to become available for FVIII/vWF. As a consequence, the suspicion has been raised that thrombin provides similar or equivalent activity in vivo to that observed for ristocetin under in vitro conditions. In this study, we quantitated the extent to which thrombin promotes the binding of FVII/vWF to platelets and determined whether or not this interaction initiates or complements platelet aggregation. With ristocetin present, the amount of 125I-FVIII/vWF that became platelet-bound correlated closely with the onset, rate, and extent of platelet aggregation. In contrast, at every thrombin concentration tested, the amount of 125I- FVIII/vWF that specifically bound to platelets was about 6% of that observed with ristocetin. Significantly, FVIII/vWF did not augment the rate of aggregation of platelets in response to thrombin or initiate platelet aggregation when subaggregating doses of thrombin were used. These observations indicate that the minimal association that occurs between FVIII/vWF and the platelet membrane in the presence of thrombin does not correlate with platelet aggregation and therefore is not analogous to the effects of ristocetin. Whether the low level of binding relates to another process, such as platelet-endothelial interactions, remains unknown. 相似文献
136.
Pippins JR Gandhi TK Hamann C Ndumele CD Labonville SA Diedrichsen EK Carty MG Karson AS Bhan I Coley CM Liang CL Turchin A McCarthy PC Schnipper JL 《Journal of general internal medicine》2008,23(9):1414-1422
Background Failure to reconcile medications across transitions in care is an important source of potential harm to patients. Little is
known about the predictors of unintentional medication discrepancies and how, when, and where they occur.
Objective To determine the reasons, timing, and predictors of potentially harmful medication discrepancies.
Design Prospective observational study.
Patients Admitted general medical patients.
Measurements Study pharmacists took gold-standard medication histories and compared them with medical teams’ medication histories, admission
and discharge orders. Blinded teams of physicians adjudicated all unexplained discrepancies using a modification of an existing
typology. The main outcome was the number of potentially harmful unintentional medication discrepancies per patient (potential
adverse drug events or PADEs).
Results Among 180 patients, 2066 medication discrepancies were identified, and 257 (12%) were unintentional and had potential for
harm (1.4 per patient). Of these, 186 (72%) were due to errors taking the preadmission medication history, while 68 (26%)
were due to errors reconciling the medication history with discharge orders. Most PADEs occurred at discharge (75%). In multivariable
analyses, low patient understanding of preadmission medications, number of medication changes from preadmission to discharge,
and medication history taken by an intern were associated with PADEs.
Conclusions Unintentional medication discrepancies are common and more often due to errors taking an accurate medication history than
errors reconciling this history with patient orders. Focusing on accurate medication histories, on potential medication errors
at discharge, and on identifying high-risk patients for more intensive interventions may improve medication safety during
and after hospitalization.
Portions of this work were presented as a poster at the 2007 Summer Meeting of the American Society of Health-System Pharmacists,
June 24–27, 2007, San Francisco, CA and as a poster at the 2008 Annual Meeting of the Society of General Internal Medicine,
April 9–12, 2008, Pittsburgh, PA. This study was supported in part by an investigator-initiated grant from the Harvard Risk
Management Foundation, and by internal support from Massachusetts General Hospital, Brigham and Women’s Hospital, and Partners
Healthcare. Dr. Pippins was supported by a National Research Service Award from the Health Resources and Services Administration
(T32 HP11001–18). Dr. Schnipper is supported by a Mentored Clinical Scientist Award from the National Heart, Lung, and Blood
Institute (K08 HL072806). 相似文献
137.
Kaplan LD; Shiramizu B; Herndier B; Hahn J; Meeker TC; Ng V; Volberding PA; McGrath MS 《Blood》1995,85(7):1727-1735
138.
The patterns of cell proliferation and cell migration were studied in three patients with the Sezary syndrome using autoradiographic techniques. Cell labeling patterns following pulse labeling with tritiated thymidine in vivo indicated that Sezary cells proliferate actively in skin and in lymph nodes but that few if any Sezary cells proliferate in the peripheral blood. In two of the patients serial samples were obtained. Label dilution patterns in skin and blood over time suggested that circulating Sezary cells originated in extracutaneous sites where cells were proliferating more rapidly than in the skin. Cells labeled in extracutaneous sites of proliferation appear rapidly in the blood, and their transit time through the peripheral blood compartment is short. Circulating Sezary cells may then be deposited in the skin where they resume proliferation at a low rate. Thus, while Sezary cells proliferate in both cutaneous and extracutaneous sites, proliferation appears to be more rapid in extracutaneous sites such as lymph nodes. This suggests that trials of systemic therapeutic approaches should be undertaken. 相似文献
139.
Biallelic neutrophil Na-antigen system is associated with a polymorphism on the phospho-inositol-linked Fc gamma receptor III (CD16) 总被引:3,自引:0,他引:3
Neutrophils express two distinct types of receptor for the Fc region of IgG, FcRII and FcRIII, in amounts of 10,000 to 20,000 FcRII (40 Kd) and 100,000 to 200,000 FcRIII (50 to 80 Kd) per neutrophil. We showed that the FcRIII exhibits genetically determined heterogeneity, detectable by differences in electrophoretic mobility with sodium dodecyl sulfate (SDS) as well as by reaction with antibodies against the biallelic neutrophil-specific antigen system NA. FcRIII was precipitated with an FcRIII-specific monoclonal antibody (MoAb) from the neutrophils of 35 donors. NA1NA1 donors expressed an FcRIII with a molecular weight (mol wt) of 50 to 65 Kd, NA1NA2 donors expressed an FcRIII with a mol wt of 50 to 80 Kd, and NA2NA2 donors expressed an FcRIII with a mol wt of 65 to 80 Kd. Statistical analysis showed that the electrophoretic heterogeneity corresponds with the NA polymorphism (k = 1). Sequential immunoprecipitation with a MoAb against NA1 and a MoAb against anti- FcRIII, followed by SDS-polyacrylamide gel electrophoresis (PAGE), showed that NA1-FcRIII is distinct from NA2-FcRIII. Moreover, immunoprecipitation with a MoAb against NA1 yielded a protein of 50 to 65 Kd, and immunoprecipitation with human anti-NA2 sera or an MoAb against NA2 yielded a protein of 65 to 80 Kd. Preincubation of NA1NA2 neutrophils with F(ab')2 fragments of an MoAb against anti-NA1 reduced binding of IgG dimers to these cells with about 50%, whereas it completely prevented binding of the dimers to NA1NA1 neutrophils. Inhibition experiments with the MoAb against NA2 yielded the same results for NA1NA2 cells, whereas binding of IgG dimers to NA2NA2 cells was completely prevented. Thus, the products of both NA alleles bind IgG. Immunoprecipitation from the medium of neutrophils either stimulated with formyl- methionyl-leucyl-phenylalanine (FMLP) or treated with glycosyl-phosphatidyl-inositol-specific phospholipase C (GPI- PLC) showed that both the NA1-FcRIII and the NA2-FcRIII are released from the cell surface, indicating that both forms of FcRIII have some structural features in common. Deglycosylation of FcRIII from homozygous donors yielded material that showed several bands on SDS- PAGE. GPI-PLC treatment of neutrophils indicated that all of this material is phosphatidyl-inositol linked. 相似文献
140.
The influence of heparin on the reaction between thrombin and plasminogen activator inhibitor-1 (PAI-1) has been examined. With a 50- fold excess of PAI-1, the rate constant for the inhibition of thrombin was 458 mol/L-1s-1, which increased to 5,000 mol/L-1s-1 in the presence of 25 micrograms/mL unfractionated heparin or heparin with low affinity for antithrombin. The effect of low affinity heparin was then examined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, using close to equimolar concentrations of reactants. Thrombin and PAI-1 formed a stable stoichiometric complex in the absence of heparin, which did not dissociate after the addition of 25 micrograms/mL low-affinity heparin. In contrast, when low-affinity heparin was added at the beginning of the reaction, there was an initial increase in PAI-1- thrombin complex formation, but this was rapidly followed by substantial proteolytic cleavage of unreacted PAI-1 and of the thrombin- PAI-1 complex. The idea that the relative concentrations of thrombin and PAI-1, and the presence of low affinity heparin, could influence the products of the reaction was examined in detail. Quantitative zymographic analysis of tissue plasminogen activator and PAI-1 activities and chromogenic substrate assay of thrombin activity showed that low-affinity heparin stimulated the inactivation of PAI-1 by an equimolar amount of thrombin, but caused only a minimal stimulation of thrombin inhibition. It is concluded that low-affinity heparin stimulates thrombin inhibition when PAI-1 is in excess, but, unexpectedly, that low-affinity heparin enhances PAI-1 inactivation when thrombin is equimolar to PAI-1. 相似文献