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81.
Marwan SM Al-Nimer 《World journal of diabetes》2022,13(5):417-419
Hyperandrogenism and hyperinsulinemia have resulted from dysfunction of the theca cell of the ovary and adipose tissue and each one potentiates the other in patients with androgen excess disorders e.g., polycystic ovary disease and idiopathic hirsutism. Possible external and/or internal triggers can produce such cellular dysfunction. There is evidence that sodium valproate acts as a trigger of cellular dysfunction and produces both hyperinsulinemia and hyperandrogenism. Therefore, the elimination of these triggers can help the patients to recover from hyperinsulinemia, insulin resistance and hyperandrogenism. 相似文献
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Ilias Nikolakopoulos MD James W. Choi MD Khaldoon Alaswad MD Jaikirshan J. Khatri MD Oleg Krestyaninov MD Dmitrii Khelimskii MD Robert W. Yeh MD PhD Farouc A. Jaffer MD PhD Catalin Toma MD Mitul Patel MD Ehtisham Mahmud MD Nicholas J. Lembo MD Manish Parikh MD Ajay J. Kirtane MD SM Ziad A. Ali MD Fotis Gkargkoulas MD Barry Uretsky MD Abdul M. Sheikh MD Evangelia Vemmou MD Iosif Xenogiannis MD Bavana V. Rangan BDS MPH Santiago Garcia MD Shuaib Abdullah MD Subhash Banerjee MD M. Nicholas Burke MD Emmanouil S. Brilakis MD PhD Dimitri Karmpaliotis MD PhD 《Catheterization and cardiovascular interventions》2021,97(4):658-667
84.
85.
Weisdorf DJ; Verfaillie CM; Davies SM; Filipovich AH; Wagner JE Jr; Miller JS; Burroughs J; Ramsay NK; Kersey JH; McGlave PB 《Blood》1995,85(12):3452-3456
Delay in hematologic recovery after bone marrow transplantation (BMT) can extend and amplify the risks of infection and hemorrhage, compromise patients' survival, and increase the duration and cost of hospitalization. Because current studies suggest that granulocyte- macrophage (GM) colony-stimulating factor (CSF) may potentiate the sensitivity of hematopoietic progenitor cells to G-CSF, we performed a prospective, randomized trial comparing GM-CSF (250 micrograms/m2/d x 14 days) versus sequential GM-CSF x 7 days followed by G-CSF (5 micrograms/kg/d x 7 days) as treatment for primary or secondary graft failure after BMT. Eligibility criteria included failure to achieve a white blood cell (WBC) count > or = 100/microL by day +21 or > or = 300/microL by day +28, no absolute neutrophil count (ANC) > or = 200/microL by day +28, or secondary sustained neutropenia after initial engraftment. Forty-seven patients were enrolled: 23 received GM-CSF (10 unrelated, 8 related allogeneic, and 5 autologous), and 24 received GM- CSF followed by G-CSF (12 unrelated, 7 related allogeneic, and 5 autologous). For patients receiving GM-CSF alone, neutrophil recovery (ANC > or = 500/microL) occurred between 2 and 61 days (median, 8 days) after therapy, while those receiving GM-CSF+G-CSF recovered at a similar rate of 1 to 36 days (median, 6 days; P = .39). Recovery to red blood cell (RBC) transfusion independence was slow, occurring 6 to 250 days (median, 35 days) after enrollment with no significant difference between the two treatment groups (GM-CSF: median, 30 days; GM-CSF+G- CSF; median, 42 days; P = .24). Similarly, platelet transfusion independence was delayed until 4 to 249 days (median, 32 days) after enrollment, with no difference between the two treatment groups (GM- CSF: median, 28 days; GM-CSF+G-CSF: median, 42 days; P = .38). Recovery times were not different between patients with unrelated donors and those with related donors or autologous transplant recipients. Survival at 100 days after enrollment was superior after treatment with GM-CSF alone. Only 1 of 23 patients treated with GM-CSF died versus 7 of 24 treated with GM-CSF+G-CSF who died 16 to 84 days (median, 38 days) after enrollment, yielding Kaplan-Meier 100-day survival estimates of 96% +/- 8% for GM-CSF versus 71% +/- 18% for GM-CSF+G-CSF (P = .026). These data suggest that sequential growth factor therapy with GM-CSF followed by G-CSF offers no advantage over GM-CSF alone in accelerating trilineage hematopoiesis or preventing lethal complications in patients with poor graft function after BMT.(ABSTRACT TRUNCATED AT 400 WORDS) 相似文献
86.
87.
Lisa G. Suter MD Shu-Xia Li PhD Jacqueline N. Grady MS Zhenqiu Lin PhD Yongfei Wang MS Kanchana R. Bhat MPH Dima Turkmani DrPH MBA Steven B. Spivack MPH Peter K. Lindenauer MD MSc Angela R. Merrill PhD Elizabeth E. Drye MD SM Harlan M. Krumholz MD SM Susannah M. Bernheim MD MHS 《Journal of general internal medicine》2014,29(10):1333-1340
BACKGROUND
The Centers for Medicare & Medicaid Services publicly reports risk-standardized mortality rates (RSMRs) within 30-days of admission and, in 2013, risk-standardized unplanned readmission rates (RSRRs) within 30-days of discharge for patients hospitalized with acute myocardial infarction (AMI), heart failure (HF), and pneumonia. Current publicly reported data do not focus on variation in national results or annual changes.OBJECTIVE
Describe U.S. hospital performance on AMI, HF, and pneumonia mortality and updated readmission measures to provide perspective on national performance variation.DESIGN
To identify recent changes and variation in national hospital-level mortality and readmission for AMI, HF, and pneumonia, we performed cross-sectional panel analyses of national hospital performance on publicly reported measures.PARTICIPANTS
Fee-for-service Medicare and Veterans Health Administration beneficiaries, 65 years or older, hospitalized with principal discharge diagnoses of AMI, HF, or pneumonia between July 2009 and June 2012. RSMRs/RSRRs were calculated using hierarchical logistic models risk-adjusted for age, sex, comorbidities, and patients’ clustering among hospitals.Results
Median (range) RSMRs for AMI, HF, and pneumonia were 15.1% (9.4–21.0%), 11.3% (6.4–17.9%), and 11.4% (6.5–24.5%), respectively. Median (range) RSRRs for AMI, HF, and pneumonia were 18.2% (14.4–24.3%), 22.9% (17.1–30.7%), and 17.5% (13.6–24.0%), respectively. Median RSMRs declined for AMI (15.5% in 2009–2010, 15.4% in 2010–2011, 14.7% in 2011–2012) and remained similar for HF (11.5% in 2009–2010, 11.9% in 2010–2011, 11.7% in 2011–2012) and pneumonia (11.8% in 2009–2010, 11.9% in 2010–2011, 11.6% in 2011–2012). Median hospital-level RSRRs declined: AMI (18.5% in 2009–2010, 18.5% in 2010–2011, 17.7% in 2011–2012), HF (23.3% in 2009–2010, 23.1% in 2010–2011, 22.5% in 2011–2012), and pneumonia (17.7% in 2009–2010, 17.6% in 2010–2011, 17.3% in 2011–2012).Conclusions
We report the first national unplanned readmission results demonstrating declining rates for all three conditions between 2009–2012. Simultaneously, AMI mortality continued to decline, pneumonia mortality was stable, and HF mortality experienced a small increase. 相似文献88.
Holly C. Gooding MD MS Shannon McGinty MD Tracy K. Richmond MD MPH Matthew W. Gillman MD SM Alison E. Field ScD 《Journal of general internal medicine》2014,29(8):1098-1104
BACKGROUND
Young adults are less likely than older adults to be aware they have hypertension or to be treated for hypertension.OBJECTIVE
To describe rates of hypertension awareness and control in a cohort of young adults and understand the impact of health insurance, utilization of preventive care, and self-perception of health on rates of hypertension awareness and control in this age group.DESIGN AND PARTICIPANTS
Cross-sectional study of 13,512 young adults participating in Wave IV of the National Longitudinal Study of Adolescent Health in 2007–2008.MAIN MEASURES
We defined hypertension as an average of two measured systolic blood pressures (SBP) ≥ 140 mmHg, diastolic blood pressures (DBP) ≥ 90 mmHg, or self-report of hypertension. We defined hypertension awareness as reporting having been told by a health care provider that one had high blood pressure, and assessed awareness among those with uncontrolled hypertension. We considered those aware of having hypertension controlled if their average measured SBP was < 140 mmHg and DBP was < 90 mmHg.KEY RESULTS
Of the 3,303 young adults with hypertension, 2,531 (76 %) were uncontrolled, and 1,893 (75 %) of those with uncontrolled hypertension were unaware they had hypertension. After adjustment for age, sex, race/ethnicity, weight status, income, education, alcohol and tobacco use, young adults with uncontrolled hypertension who had (vs. didn’t have) routine preventive care in the past 2 years were 2.4 times more likely (95 % confidence interval [CI] 1.68–3.55) to be aware, but young adults who believed they were in excellent (vs. less than excellent) health were 64 % less likely to be aware they had hypertension (OR 0.36, 95 % CI 0.23–0.57). Neither preventive care utilization nor self-rated health was associated with blood pressure control.CONCLUSIONS
In this nationally representative group of young adults, rates of hypertension awareness and control were low. Efforts to increase detection of hypertension must address young adults’ access to preventive care and perception of their need for care. 相似文献89.
Infant oral mutilation is the practice of removing developing tooth germs, commonly the mandibular canine, in infants up to the age of 1 year. Subsequent complications include missing, impacted or hypoplastic permanent anterior and canine teeth. We report on a case of bilaterally missing lower canines thought to be due to infant oral mutilation. It is important that general dental practitioners are aware of this practice and resulting complications when treating families from sub‐Saharan East Africa. 相似文献
90.
Lydie Boussicault Anne-Sophie Hérard Noel Calingasan Fanny Petit Carole Malgorn Nicolas Merienne Caroline Jan Marie-Claude Gaillard Rodrigo Lerchundi Luis F Barros Carole Escartin Thierry Delzescaux Jean Mariani Philippe Hantraye M Flint Beal Emmanuel Brouillet Céline Véga Gilles Bonvento 《Journal of cerebral blood flow and metabolism》2014,34(9):1500-1510
Huntington''s disease (HD) is caused by cytosine-adenine-guanine (CAG) repeat expansions in the huntingtin (Htt) gene. Although early energy metabolic alterations in HD are likely to contribute to later neurodegenerative processes, the cellular and molecular mechanisms responsible for these metabolic alterations are not well characterized. Using the BACHD mice that express the full-length mutant huntingtin (mHtt) protein with 97 glutamine repeats, we first demonstrated localized in vivo changes in brain glucose use reminiscent of what is observed in premanifest HD carriers. Using biochemical, molecular, and functional analyses on different primary cell culture models from BACHD mice, we observed that mHtt does not directly affect metabolic activity in a cell autonomous manner. However, coculture of neurons with astrocytes from wild-type or BACHD mice identified mutant astrocytes as a source of adverse non-cell autonomous effects on neuron energy metabolism possibly by increasing oxidative stress. These results suggest that astrocyte-to-neuron signaling is involved in early energy metabolic alterations in HD. 相似文献