Browsing by Author "Yu, Qing"
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Item Early Treatment of Acetabular Fractures via an Anterior Approach Increases Blood Loss but not Packed Red Blood Cell Transfusion(Wolters Kluwer, 2024-01) Mullis, Brian H.; Chang, Joshua H.; Shah, Nihar; Sabbagh , Ramsey S.; Yu, Qing; Archdeacon, Michael T.; Sagi, H. Claude; Natoli, Roman M.; Orthopaedic Surgery, School of MedicineOBJECTIVE: The objective of this study was to determine whether time from hospital admission to surgery for acetabular fractures using an anterior intrapelvic (AIP) approach affected blood loss. METHODS: Design: Retrospective review. Setting: Three level 1 trauma centers at 2 academic institutions. Patient Selection Criteria: Adult (18 years or older) patients with no pre-existing coagulopathy treated for an acetabular fracture via an AIP approach. Excluded were those with other significant same day procedures (irrigation and debridement and external fixation were the only other allowed procedures). Outcome Measures and Comparisons: Multiple methods for evaluating blood loss were investigated, including estimated blood loss (EBL), calculated blood loss (CBL) by Gross and Hgb balance methods, and packed red blood cell (PRBC) transfusion requirement. Outcomes were evaluated based on time to surgery. RESULTS: 195 patients were studied. On continuous linear analysis, increasing time from admission to surgery was significantly associated with decreasing CBL at 24 hours (−1.45 mL per hour by Gross method, P = 0.003; −0.440 g of Hgb per hour by Hgb balance method, P = 0.003) and 3 days (−1.69 mL per hour by Gross method, P = 0.013; −0.497 g of Hgb per hour by Hgb balance method, P = 0.010) postoperative, but not EBL or PRBC transfusion. Using 48 hours from admission to surgery to define early versus delayed surgery, CBL was significantly greater in the early group compared to the delayed group (453 [IQR 277–733] mL early versus 364 [IQR 160–661] delayed by Gross method, P = 0.017; 165 [IQR 99–249] g of Hgb early versus 143 [IQR 55–238] g Hgb delayed by Hgb balance method, P = 0.035), but not EBL or PRBC transfusion. In addition, in multivariate linear regression, neither giving tranexamic acid nor administering prophylactic anticoagulation for venous thromboembolism on the morning of surgery affected blood loss at 24 hours or 3 days postoperative (P > 0.05). CONCLUSION: There was higher blood loss with early surgery using an AIP approach, but early surgery did not affect PRBC transfusion and may not be clinically relevant. LEVEL OF EVIDENCE: Therapeutic Level III. See Instructions for Authors for a complete description of levels of evidence.Item Improving Graduate Medical Education in China: Leading Teaching Hospitals Engage in Self-Analysis(Accreditation Council for Graduate Medical Education, 2018-04) Zhang, Shuyang; Yan, Zuoqin; Wan, Xuehong; Shen, Ye; Lei, Guanghua; Kuang, Ming; Pan, Hui; Yu, Qing; Wang, Xingyue; Jiang, Guoping; Peng, Jie; Tang, Lina; Guo, Chao; Zhu, Jiming; Inui, Thomas S.; Medicine, School of MedicineItem Mitochondrial connexin 43 in sex-dependent myocardial responses and estrogen-mediated cardiac protection following acute ischemia/reperfusion injury(Springer, 2019-11-18) Wang, Meijing; Smith, Kwynlyn; Yu, Qing; Miller, Caroline; Singh, Kanhaiya; Sen, Chandan K.; Surgery, School of MedicinePreserving mitochondrial activity is crucial in rescuing cardiac function following acute myocardial ischemia/reperfusion (I/R). The sex difference in myocardial functional recovery has been observed after I/R. Given the key role of mitochondrial connexin43 (Cx43) in cardiac protection initiated by ischemic preconditioning, we aimed to determine the implication of mitochondrial Cx43 in sex-related myocardial responses and to examine the effect of estrogen (17β-estradiol, E2) on Cx43, particularly mitochondrial Cx43-involved cardiac protection following I/R. Mouse primary cardiomyocytes and isolated mouse hearts (from males, females, ovariectomized females, and doxycycline-inducible Tnnt2-controlled Cx43 knockout without or with acute post-ischemic E2 treatment) were subjected to simulated I/R in culture or Langendorff I/R (25-min warm ischemia/40-min reperfusion), respectively. Mitochondrial membrane potential and mitochondrial superoxide production were measured in cardiomyocytes. Myocardial function and infarct size were determined. Cx43 and its isoform, Gja1-20k, were assessed in mitochondria. Immunoelectron microscopy and co-immunoprecipitation were also used to examine mitochondrial Cx43 and its interaction with estrogen receptor-α by E2 in mitochondria, respectively. There were sex disparities in stress-induced cardiomyocyte mitochondrial function. E2 partially restored mitochondrial activity in cardiomyocytes following acute injury. Post-ischemia infusion of E2 improved functional recovery and reduced infarct size with increased Cx43 content and phosphorylation in mitochondria. Ablation of cardiac Cx43 aggravated mitochondrial damage and abolished E2-mediated cardiac protection during I/R. Female mice were more resistant to myocardial I/R than age-matched males with greater protective role of mitochondrial Cx43 in female hearts. Post-ischemic E2 usage augmented mitochondrial Cx43 content and phosphorylation, increased mitochondrial Gja1-20k, and showed cardiac protection.Item Sex as Biological Variable in Cardiac Mitochondrial Bioenergetic Responses to Acute Stress(MDPI, 2022-08-18) Scott, Susan R.; Singh, Kanhaiya; Yu, Qing; Sen, Chandan K.; Wang, Meijing; Surgery, School of MedicineCardiac dysfunction/damage following trauma, shock, sepsis, and ischemia impacts clinical outcomes. Acute inflammation and oxidative stress triggered by these injuries impair mitochondria, which are critical to maintaining cardiac function. Despite sex dimorphisms in consequences of these injuries, it is unclear whether mitochondrial bioenergetic responses to inflammation/oxidative stress are sex-dependent. We hypothesized that sex disparity in mitochondrial bioenergetics following TNFα or H2O2 exposure is responsible for reported sex differences in cardiac damage/dysfunction. Methods and Results: Cardiomyocytes isolated from age-matched adult male and female mice were subjected to 1 h TNFα or H2O2 challenge, followed by detection of mitochondrial respiration capacity using the Seahorse XF96 Cell Mito Stress Test. Mitochondrial membrane potential (ΔΨm) was analyzed using JC-1 in TNFα-challenged cardiomyocytes. We found that cardiomyocytes isolated from female mice displayed a better mitochondrial bioenergetic response to TNFα or H2O2 than those isolated from male mice did. TNFα decreased ΔΨm in cardiomyocytes isolated from males but not from females. 17β-estradiol (E2) treatment improved mitochondrial metabolic function in cardiomyocytes from male mice subjected to TNFα or H2O2 treatment. Conclusions: Cardiomyocyte mitochondria from female mice were more resistant to acute stress than those from males. The female sex hormone E2 treatment protected cardiac mitochondria against acute inflammatory and oxidative stress.Item Th17 cells demonstrate stable cytokine production in a proallergic environment(The American Association of Immunologists, 2014-09-15) Glosson-Byers, Nicole L.; Sehra, Sarita; Stritesky, Gretta L.; Yu, Qing; Awe, Olufolakemi; Pham, Duy; Bruns, Heather A.; Kaplan, Mark H.; Department of Pediatrics, IU School of MedicineTh17 cells are critical for the clearance of extracellular bacteria and fungi, but also contribute to the pathology of autoimmune diseases and allergic inflammation. After exposure to an appropriate cytokine environment, Th17 cells can acquire a Th1-like phenotype, but less is known about their ability to adopt Th2 and Th9 effector programs. To explore this in more detail, we used an IL-17F lineage tracer mouse strain that allows tracking of cells that formerly expressed IL-17F. In vitro-derived Th17 cells adopted signature cytokine and transcription factor expression when cultured under Th1-, Th2-, or Th9-polarizing conditions. In contrast, using two models of allergic airway disease, Th17 cells from the lungs of diseased mice did not adopt Th1, Th2, or Th9 effector programs, but remained stable IL-17 secretors. Although in vitro-derived Th17 cells expressed IL-4Rα, those induced in vivo during allergic airway disease did not, possibly rendering them unresponsive to IL-4-induced signals. However, in vitro-derived, Ag-specific Th17 cells transferred in vivo to OVA and aluminum hydroxide-sensitized mice also maintained IL-17 secretion and did not produce alternative cytokines upon subsequent OVA challenge. Thus, although Th17 cells can adopt new phenotypes in response to some inflammatory environments, our data suggest that in allergic inflammation, Th17 cells are comparatively stable and retain the potential to produce IL-17. This might reflect a cytokine environment that promotes Th17 stability, and allow a broader immune response at tissue barriers that are susceptible to allergic inflammation.