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61.
Direct demonstration that autologous bone marrow transplantation for solid tumors can return a multiplicity of tumorigenic cells 总被引:5,自引:2,他引:5
Rill DR; Santana VM; Roberts WM; Nilson T; Bowman LC; Krance RA; Heslop HE; Moen RC; Ihle JN; Brenner MK 《Blood》1994,84(2):380-383
Patients with solid tumors are increasingly being treated by autologous bone marrow transplantation (BMT). Although response rates appear to be increased, disease recurrence is the commonest cause of treatment failure. Whether relapse is entirely due to residual disease in the patient or arises also from infiltrating malignant cells contained in the autologous marrow transplant has not been resolved. If the latter explanation is correct, then purging would be required as part of the transplantation procedure. We used retrovirally mediated transfer of the neomycin-resistance gene to mark BM harvested from eight patients with neuroblastoma in clinical remission. The marked marrow cells were subsequently reinfused as part of an autologous BMT. At relapse, we sought the marker gene in malignant cell populations. Three patients have relapsed, and in each the marker gene was detected by phenotypic and genetic analyses of resurgent malignant cells at medullary and extramedullary sites. Analysis of neuroblast DNA for discrete marker gene integration sites suggested that at least 200 malignant cells, each capable of tumor formation, were introduced with the autologous marrow transplant and contributed to relapse. Thus, autologous BMTs administered to patients with this solid tumor may contain a multiplicity of malignant cells that subsequently contribute to relapse. The marker-gene technique we describe should permit evaluation of the mechanisms of relapse and the efficacy of purging in patients receiving autologous marrow transplantation for other solid tumors that infiltrate the marrow. 相似文献
62.
L Laval R Martin JN Natividad F Chain S Miquel C Desclée de Maredsous S Capronnier H Sokol EF Verdu JET van Hylckama Vlieg LG Bermúdez-Humarán T Smokvina P Langella 《Gut microbes》2015,6(1):1-9
Impaired gut barrier function has been reported in a wide range of diseases and syndromes and in some functional gastrointestinal disorders. In addition, there is increasing evidence that suggests the gut microbiota tightly regulates gut barrier function and recent studies demonstrate that probiotic bacteria can enhance barrier integrity. Here, we aimed to investigate the effects of Lactobacillus rhamnosus CNCM I-3690 on intestinal barrier function. In vitro results using a Caco-2 monolayer cells stimulated with TNF-α confirmed the anti-inflammatory nature of the strain CNCM I-3690 and pointed out a putative role for the protection of the epithelial function. Next, we tested the protective effects of L. rhamnosus CNCM I-3690 in a mouse model of increased colonic permeability. Most importantly, we compared its performance to that of the well-known beneficial human commensal bacterium Faecalibacterium prauznitzii A2-165. Increased colonic permeability was normalized by both strains to a similar degree. Modulation of apical tight junction proteins expression was then analyzed to decipher the mechanism underlying this effect. We showed that CNCM I-3690 partially restored the function of the intestinal barrier and increased the levels of tight junction proteins Occludin and E-cadherin. The results indicate L. rhamnosus CNCM I-3690 is as effective as the commensal anti-inflammatory bacterium F. prausnitzii to treat functional barrier abnormalities. 相似文献
63.
Pierre Lantelme Hélène Eltchaninoff Muriel Rabilloud Géraud Souteyrand Marion Dupré Marco Spaziano Marc Bonnet Clément Becle Benjamin Riche Eric Durand Erik Bouvier Jean-Nicolas Dacher Pierre-Yves Courand Lucie Cassagnes Eduardo E. Dávila Serrano Pascal Motreff Loic Boussel Thierry Lefèvre Brahim Harbaoui 《JACC: Cardiovascular Imaging》2019,12(1):123-132
Objectives
The aim of this study was to develop a new scoring system based on thoracic aortic calcification (TAC) to predict 1-year cardiovascular and all-cause mortality.Background
A calcified aorta is often associated with poor prognosis after transcatheter aortic valve replacement (TAVR). A risk score encompassing aortic calcification may be valuable in identifying poor TAVR responders.Methods
The C4CAPRI (4 Cities for Assessing CAlcification PRognostic Impact) multicenter study included a training cohort (1,425 patients treated using TAVR between 2010 and 2014) and a contemporary test cohort (311 patients treated in 2015). TAC was measured by computed tomography pre-TAVR. CAPRI risk scores were based on the linear predictors of Cox models including TAC in addition to comorbidities and demographic, atherosclerotic disease and cardiac function factors. CAPRI scores were constructed and tested in 2 independent cohorts.Results
Cardiovascular and all-cause mortality at 1 year was 13.0% and 17.9%, respectively, in the training cohort and 8.2% and 11.8% in the test cohort. The inclusion of TAC in the model improved prediction: 1-cm3 increase in TAC was associated with a 6% increase in cardiovascular mortality and a 4% increase in all-cause mortality. The predicted and observed survival probabilities were highly correlated (slopes >0.9 for both cardiovascular and all-cause mortality). The model’s predictive power was fair (AUC 68% [95% confidence interval [CI]: 64% to 72%]) for both cardiovascular and all-cause mortality. The model performed similarly in the training and test cohorts.Conclusions
The CAPRI score, which combines the TAC variable with classical prognostic factors, is predictive of 1-year cardiovascular and all-cause mortality. Its predictive performance was confirmed in an independent contemporary cohort. CAPRI scores are highly relevant to current practice and strengthen the evidence base for decision making in valvular interventions. Its routine use may help prevent futile procedures. 相似文献64.
65.
The inappropriate expression of c-myc in cells deprived of growth factors has recently been implicated in the activation of programmed cell death (apoptosis). The studies described here examine the ability of interleukin-3 (IL-3) or erythropoietin (Epo) to suppress apoptosis that occurs in association with enforced myc expression during cell cycle arrest of a murine IL-3-dependent myeloid progenitor cell line, 32D. G1 arrest was observed when culturing 32D cells to high density in medium supplemented with IL-3, or at subconfluent densities in medium supplemented with Epo. Under both conditions, endogenous c-myc expression was downregulated and viability was maintained. In clones of cells in which c-myc is constitutively expressed from a retroviral vector, enforced c-myc expression was associated with the activation of apoptosis at high cell densities. Similarly, enforced c-myc expression was deleterious to cell survival when these cells were cultured in Epo, as apoptosis was evident within 6 hours. The results support the concept that inappropriate c-myc expression activates apoptosis and that neither IL-3 nor Epo can suppress this program under these conditions. 相似文献
66.
Wong Tatiana Pressat-Laffouilhre Thibaut Fresse Karine Warin Bejar Sofiane Michelin Paul Bauer Fabrice Dacher Jean-Nicolas 《The international journal of cardiovascular imaging》2022,38(5):1133-1143
The International Journal of Cardiovascular Imaging - To investigate the feasibility and accuracy of cardiac multidetector computed tomography (MDCT) prosthesis sizing prior to ostium secundum... 相似文献
67.
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69.
In a preterm infant, chest tubes were inserted for treatment of bilateral pneumothoraces. Hemorrhagic pericardial effusion with cardiac tamponade developed, probably resulting from traumatic injury by the left chest tube. The infant survived due to timely diagnostic and therapeutic intervention. No recurrence of pericardial effusion was seen and follow-up showed normal psychomotor development. 相似文献
70.