1.
Effect of Perioperative Glucose-Insulin-Potassium Therapy in Patients Undergoing On-Pump Cardiac Surgery: A Meta-Analysis.
Li, Q, Yang, J, Zhang, J, Yang, C, Fan, Z, Yang, Y, Zheng, T, Yang, J
The heart surgery forum. 2020;(1):E063-E069
Abstract
OBJECTIVE The role of glucose-insulin-potassium (GIK) infusion during cardiac surgery has held interest for so many years without a clear answer. The aim of this meta-analysis was to evaluate the effect of GIK therapy on outcomes in patients undergoing on-pump cardiac surgery. METHODS A comprehensive online review was performed in The Web of Science, Embase, Medline, PubMed, and The Cochrane Library databases from 2000 to 2019. Eligible studies included randomized controlled trials (RCTs) that compared GIK treatment with placebo or standard care during on-pump cardiac surgery. Risk ratios (RR) were used for binary outcomes and mean difference (MD) was used for continuous variables; both with their 95% confidence intervals (CI). RESULTS A total of 18 RCTs involving 2,131 patients met the inclusion criteria. Compared with the control group, the GIK treatment significantly reduced in-hospital mortality (RR = 0.56, 95% CI: 0.32-0.97; P = .04), postoperative myocardial infarctions (MI) (RR = 0.71, 95% CI: 0.56-0.91; P = .006), the use of inotropic support (RR = 0.53, 95% CI: 0.45-0.63; P < .00001), and length of stay in the intensive care unit (ICU) (MD = -0.33, 95% CI: -0.52--0.14; P = .0007). Moreover, GIK treatment seemed to be associated with fewer postoperative atrial fibrillation (AF) (RR = 0.81, 95% CI: 0.64-1.03; P = .09). CONCLUSIONS In patients undergoing on-pump cardiac surgery, GIK infusion has a beneficial role in mortality during hospital stay and demonstrates superior efficacy versus standard care for reduction in postoperative MI, AF, ICU length of stay as well as inotropic agent requirements.
2.
Importance of mitochondrial calcium uniporter in high glucose-induced endothelial cell dysfunction.
Chen, W, Yang, J, Chen, S, Xiang, H, Liu, H, Lin, D, Zhao, S, Peng, H, Chen, P, Chen, AF, et al
Diabetes & vascular disease research. 2017;(6):494-501
Abstract
OBJECTIVE Mitochondrial Ca2+ overload is implicated in hyperglycaemia-induced endothelial cell dysfunction, but the key molecular events responsible remain unclear. We examined the involvement of mitochondrial calcium uniporter, which mediates mitochondrial Ca2+ uptake, in endothelial cell dysfunction resulting from high-glucose treatment. METHODS Human umbilical vein endothelial cells were exposed to various glucose concentrations and to high glucose (30 mM) following mitochondrial calcium uniporter inhibition or activation with ruthenium red and spermine, respectively. Subsequently, mitochondrial calcium uniporter and mitochondrial calcium uniporter regulator 1 messenger RNA and protein expression was measured by real-time polymerase chain reaction and western blotting. Ca2+ concentrations were analysed by laser confocal microscopy, and cytoplasmic and mitochondrial oxidative stress was detected using 2',7'-dichlorofluorescein diacetate and MitoSOX Red, respectively. Apoptosis was assessed by annexin V-fluorescein isothiocyanate/propidium iodide staining, and a wound-healing assay was performed using an in vitro model. RESULTS High glucose markedly upregulated mitochondrial calcium uniporter and mitochondrial calcium uniporter regulator 1 messenger RNA expression, as well as protein production, in a dose- and time-dependent manner with a maximum effect demonstrated at 72 h and 30 mM glucose concentration. Moreover, high-glucose treatment significantly raised both mitochondrial and cytoplasmic Ca2+ and reactive oxygen species levels, increased apoptosis and compromised wound healing (all p < 0.05). These effects were enhanced by spermine and completely negated by ruthenium red, which are known to activate and inhibit mitochondrial calcium uniporter, respectively. CONCLUSION Mitochondrial calcium uniporter plays an important role in hyperglycaemia-induced endothelial cell dysfunction and may constitute a therapeutic target to reduce vascular complications in diabetes.
3.
PET Index of Bone Glucose Metabolism (PIBGM) Classification of PET/CT Data for Fever of Unknown Origin Diagnosis.
Yang, J, Liu, X, Ai, D, Fan, J, Zheng, Y, Li, F, Huo, L, Wang, Y
PloS one. 2015;(6):e0130173
Abstract
OBJECTIVES Fever of unknown origin (FUO) remains a challenge in clinical practice. Fluorine-18 fluorodeoxyglucose (FDG) positron emission tomography/computed tomography (PET/CT) is helpful in diagnosing the etiology of FUO. This paper aims to develop a completely automatic classification method based on PET/CT data for the computer-assisted diagnosis of FUO. METHODS We retrospectively analyzed the FDG PET/CT scan of 175 FUO patients, 79 males and 96 females. The final diagnosis of all FUO patients was achieved through pathology or clinical evaluation, including 108 normal patients and 67 FUO patients. CT anatomic information was used to acquire bone functional information from PET images. The skeletal system of FUO patients was classified by analyzing the standardized uptake value (SUV) and the PET index of bone glucose metabolism (PIBGM). The SUV distributions in the bone marrow and the bone cortex were also studied in detail. RESULTS The SUV and PIBGM of the bone marrow only slightly differed between the FUO patients and normal people, whereas the SUV of whole bone structures and the PIBGM of the bone cortex significantly differed between the normal people and FUO patients. The method detected 43 patients from 67 FUO patients, with sensitivity, specificity, positive predictive value, negative predictive value, and accuracy of 64.18%, 95%, 93.48%, 72.73%, and 83.33%, respectively. CONCLUSION The experimental results demonstrate that the study can achieve automatic classification of FUO patients by the proposed novel biomarker of PIBGM, which has the potential to be utilized in clinical practice.