Radiomics in Kidney Transplantation: A Scoping Review of Current Applications, Limitations, and Future Directions.

Radiomics is increasingly applied to the diagnosis, management, and outcome prediction of various urological conditions. The purpose of this scoping review is to evaluate the current evidence of the application of radiomics in kidney transplantation, especially its utility in diagnostics and therapeutics. An electronic literature search on radiomics in the setting of transplantation was conducted on PubMed, EMBASE, and Scopus from inception to September 23, 2022. A total of 16 studies were included. The most widely studied clinical utility of radiomics in kidney transplantation is its use as an adjunct to diagnose rejection, potentially reducing the need for unnecessary biopsies or guiding decisions for earlier biopsies to optimize graft survival. Technology such as optical coherence tomography is a noninvasive procedure to build high-resolution optical cross-section images of the kidney cortex in situ and in real time, which can provide histopathological information of donor kidney candidates for transplantation, and to predict posttransplant function. This review shows that, although radiomics in kidney transplants is still in its infancy, it has the potential for large-scale implementation. Its greatest potential lies in the correlation with conventional established diagnostic evaluation for living donors and potential in predicting and detecting rejection postoperatively.

Measurements of Two-Particle Correlations in e

Measurements of two-particle angular correlations of charged particles emitted in hadronic Z decays are presented. The archived e^{+}e^{-} annihilation data at a center-of-mass energy of 91 GeV were collected with the ALEPH detector at LEP between 1992 and 1995. The correlation functions are measured over a broad range of pseudorapidity and full azimuth as a function of charged particle multiplicity. No significant long-range correlation is observed in either the lab coordinate analysis or the thrust coordinate analysis, where the latter is sensitive to a medium expanding transverse to the color string between the outgoing qq[over ¯] pair from Z boson decays. The associated yield distributions in both analyses are in better agreement with the prediction from the pythia v6.1 event generator than from herwig v7.1.5. They provide new insights to showering and hadronization modeling. These results serve as an important reference to the observed long-range correlation in proton-proton, proton-nucleus, and nucleus-nucleus collisions.

Leptin increases endothelin type A receptor levels in vascular smooth muscle cells.

Leptin, one of the adipocyte-secreted peptides, is involved in the control of appetite and body weight. Several studies have demonstrated that plasma leptin levels are elevated in obese subjects and are positively correlated with body weight. The arterial endothelin (ET) system plays an important role in the regulation of vascular tone, and ET-1 overexpression may be involved in the pathogenesis of the hypertension associated with insulin resistance. This study was performed to explore the regulatory effects of leptin on ET receptor expression and ET binding in A10 vascular smooth muscle cells (VSMCs) by use of Northern blotting, immunoblotting, and a (125)I-labeled ET-1 binding assay. The effect of leptin on ET receptor-mediated cell proliferation was also tested. The results showed that leptin caused a significant increase in [(125)I]-ET-1 binding, which was time- and dose-dependent. Immunoblotting showed that expression of the ET type A receptor (ET(A)R) in leptin (10(-7) M)-treated cells was increased by up to 2.3-fold compared with controls. Levels of ET(A)R mRNA measured by Northern blotting were also increased by up to 2.2-fold in leptin (10(-7) M)-treated cells. Pretreatment with an ERK inhibitor, PD-98059 (2.5 x 10(-5) M), blocked the leptin-induced increase in (125)I-ET-1 binding. Finally, ET-1 (10(-7) M)-stimulated cell proliferation was enhanced by leptin (10(-7) M) pretreatment, with a maximal increase of twofold compared with controls. In conclusion, leptin increases ET(A)R expression in VSMCs in a time- and dose-dependent manner. This effect is ERK dependent and is associated with increased ET-1-stimulated cell proliferation. These findings provide support for roles for leptin and the ET system in the pathogenesis of obesity-associated hypertension.

Insulin infusion induces endothelin-1-dependent hypertension in rats.

We previously showed that chronic insulin infusion induces insulin resistance, hyperendothelinemia, and hypertension in rats (C. C. Juan, V. S. Fang, C. F. Kwok, J. C. Perng, Y. C. Chou, and L. T. Ho. Metabolism 48: 465-471, 1999). Endothelin-1 (ET-1), a potent vasoconstrictor, is suggested to play an important role in maintaining vascular tone and regulating blood pressure, and insulin increases ET-1 production in vivo and in vitro. In the present study, BQ-610, a selective endothelin A receptor antagonist, was used to examine the role of ET-1 in insulin-induced hypertension in rats. BQ-610 (0.7 mg/ml; 0.5 ml/kg body wt) or normal saline was given intraperitoneally two times daily for 25 days to groups of rats infused with either saline or insulin (2 U/day via sc-implanted osmotic pumps), and changes in plasma levels of insulin, glucose, and ET-1 and the systolic blood pressure were measured over the experimental period, whereas changes in insulin sensitivity were examined at the end of the experimental period. Plasma insulin and ET-1 levels were measured by RIA, plasma glucose levels using a glucose analyzer, systolic blood pressure by the tail-cuff method, and insulin sensitivity by an oral glucose tolerance test. Our studies showed that insulin infusion caused sustained hyperinsulinemia in both saline- and BQ-610-injected rats over the infusion period. After pump implantation (2 wk), the systolic blood pressure was significantly higher in insulin-infused rats than in saline-infused rats in the saline-injected group (133 +/- 3.1 vs. 113 +/- 1.1 mmHg, P < 0.05) but not in the BQ-610-injected group (117 +/- 1.2 vs. 117 +/- 1.8 mmHg). Plasma ET-1 levels in both sets of insulin-infused rats were higher than in saline-infused controls (2.5 +/- 0.6 and 2.5 +/- 0.8 vs. 1.8 +/- 0.4 and 1.7 +/- 0.3 pmol/l, P < 0.05). Oral glucose tolerance tests showed that BQ-610 treatment did not prevent the insulin resistance caused by chronic insulin infusion. No significant changes were found in insulin sensitivity and blood pressure in saline-infused rats treated with BQ-610. In a separate experiment, insulin infusion induced the increase in arterial ET-1 content, hypertension, and subsequent plasma ET-1 elevation in rats. These results suggest that, in the insulin infusion rat model, ET-1 plays a mediating role in the development of hypertension, but not of insulin resistance.