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This is the diagnostic experiences as well as the surgical mode of treatment used in a 31 years old women suffering diversion of the inferior vena cava into the left atrium associated with atrial septal defect. The patient had been previously studied and operated thrice under conventional circumstances at different institutions in order to solve the septal defect. The hemodynamic solution had not been reached due to a missing pathological definition. The cineangiogram through the saphenous vein specified the left atrium form the inferior vena cava. Some considerations are made on the surgical methods used for the fourth operation, and in regard of the fact that the patient refused blood transfusion because of religious convictions (Jehova Witness).  相似文献   
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ObjectiveSocial isolation and loneliness are associated with morbidity and mortality in older adults. Limited evidence exists regarding which interventions improve connectedness in this population.Design/Setting/ParticipantsIn this pre-post study we assessed community-based group health class participants’ (age ≥50) loneliness and social isolation. Participants (n = 382) were referred by a Cedars-Sinai Medical Network (Los Angeles, California) healthcare provider or self-referred from the community (July 2017–March 2020).InterventionParticipants met with a program coordinator and selected Arthritis Exercise, Tai Chi for Arthritis, EnhanceFitness, or the Healthier Living Workshop.MeasurementsWe measured social isolation using the Duke Social Support Index (DSSI) and loneliness using the UCLA 3-item Loneliness Scale at baseline, class completion, and 6 months.ResultsMean age was 76.8 years (standard deviation, SD = 9.1); 315 (83.1%) were female; 173 (45.9%) were Non-Hispanic white; 143 (37.9%) were Non-Hispanic Black; 173 (46.1%) lived alone; mean baseline DSSI score was 26.9 (SD = 4.0) and mean baseline UCLA score was 4.8 (SD = 1.8). On multivariable analysis adjusted for gender, race/ethnicity, income, self-rated health, and household size, DSSI improved by 2.4% at 6-week compared to baseline (estimated ratio, ER: 1.024; 95% confidence interval [CI]: 1.010–1.038; p-value = 0.001), and 3.3% at 6-month (ER: 1.033; 95% CI: 1.016–1.050; p-value <0.001). UCLA score after adjusting for age, gender, race/ethnicity, live alone, number of chronic conditions, income, and self-rated health, did not change at 6-week (ER: 0.994; 95% CI: 0.962–1.027; p-value = 0.713), but decreased by 6.9% at 6-months (ER: 0.931; 95% CI: 0.895–0.968; p-value <0.001).ConclusionCommunity-based group health class participants reported decreased loneliness and social isolation at 6-month follow-up.  相似文献   
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Lineage-restricted regulation of the murine SCL/TAL-1 promoter   总被引:10,自引:2,他引:10  
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Galli  SJ; Arizono  N; Murakami  T; Dvorak  AM; Fox  JG 《Blood》1987,69(6):1661-1666
The normal skin and other tissues of adult mast cell-deficient WBB6F1- W/Wv or WCB6F1-Sl/Sld mice contain less than 1.0% the number of mast cells present in the corresponding tissues of the congenic normal (+/+) mice. As a result, genetically mast cell-deficient WBB6F1-W/Wv or WCB6F1-Sl/Sld mice are widely used for studies of mast cell differentiation and function. We found that mast cells developed at sites of idiopathic chronic dermatitis in WBB6F1-W/Wv mice and that the number of mast cells present in the skin of WBB6F1-W/Wv mice was proportional to the severity of the dermatitis (in ear skin, there were 33 +/- 4 mast cells/mm2 of dermis at sites of severe dermatitis v 9 +/- 3 at sites of mild dermatitis, 0.8 +/- 0.3 in skin without dermatitis, and 100 +/- 7 in the normal skin of congenic WBB6F1-+/+ mice; in back skin, the corresponding values were 2.0 +/- 0.6, 1.1 +/- 0.9, 0.025 +/- 0.025, and 26.2 +/- 3.2). The development of mast cells was a local, not systemic, consequence of the dermatitis. Thus, WBB6F1-W/Wv mice with severe dermatitis lacked mast cells in skin not showing signs of dermatitis and also in the peritoneal cavity, stomach, cecum, and tongue. Idiopathic chronic dermatitis was not associated with the local development of mast cells in WCB6F1-Sl/Sld mice, a mutant whose mast cell deficiency is due to a mechanism distinct from that of WBB6F1-W/Wv mice. These findings may have implications for understanding the nature of the mast cell deficiency in WBB6F1-W/Wv and WCB6F1-Sl/Sld mice and for the use of these mutants to analyze mast cell differentiation and function.  相似文献   
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