Shear wave elastography: A noninvasive approach for assessing acute kidney injury in critically ill patients.

Traditional markers, such as serum creatinine and blood urea nitrogen, frequently show delayed elevations following acute kidney injury (AKI), limiting their utility for prompt detection and timely intervention in AKI management. Shear wave elastography (SWE) exhibits potential for AKI diagnosis by measuring tissue stiffness. Our study aimed to evaluate the diagnostic performance of SWE in detecting AKI by measuring the stiffness of kidney tissue. Between July 2022 and December 2022, a total of 103 consecutive participants who met the eligibility criteria were prospectively enrolled, underwent SWE measurements, and were classified into AKI or non-AKI groups based on the 2012 Kidney Disease: Improving Global Outcomes (KDIGO) criteria. A receiver operating characteristic (ROC) curve was drawn to examine the feasibility of differentiating between AKI and non-AKI patients and assessing diagnostic performance. The effects of tissue anisotropy on SWE measurements were also examined. Our results revealed that patients in the AKI group exhibited significantly increased stiffness values in specific kidney regions compared with those in the non-AKI group. For the diagnosis of AKI, the optimal cut-off values were identified as 9.9 kPa, 2.9 kPa, and 4.4 kPa for the upper pole medulla, middle cortex, and middle medulla, respectively, in the longitudinal plane. Correspondingly, the areas under the ROC curves for these regions were 0.737 (95% confidence interval [CI]: 0.637, 0.822), 0.736 (95% CI: 0.637, 0.821), and 0.784 (95% CI: 0.688, 0.861). Additionally, we observed a significant variability in stiffness values due to tissue anisotropy, specifically in the segments of the upper pole cortex, and medulla across both longitudinal and transverse planes. SWE serves as a noninvasive approach for the quantification of tissue stiffness and shows promise as an adjunctive tool for the assessment of AKI.

Evaluation of Serum miR-216a, miR-216b, miR-217, miR-92b, miR-375 and miR-148a as Potential Biomarkers for Acute Pancreatitis and the Role of miR-92b in Attenuating Caerulein-induced Injury and Inflammatory Responses in AR42J Cells.

BACKGROUND: Acute pancreatitis can eventually lead to morbidity and mortality. The present study aimed to identify the differentially expressed microRNAs (miRNAs) that are related to acute pancreatitis and explore the in vitro functional role of miR-92b in acute pancreatitis. METHODS: Bioinformatics analysis was used to identify differentially expressed miRNAs in caerulein- induced acute pancreatitis samples when compared to normal controls. The role of miR-92b in acute pancreatitis was examined by in vitro functional assays. RESULTS: MiRNA-network analysis revealed 12 miRNAs that function as "core regulatory miRNAs". Further validation studies revealed that six miRNAs (miR-216a, miR-216b, miR-217, miR- 92b, miR-375 and miR-148a) were differentially expressed in the serum samples from patients with acute pancreatitis. These six miRNAs have fair diagnostic potential for severe acute pancreatitis. Caerulein induced cell injury and inflammatory response and repressed miR-92b expression in AR42J cells. MiR-92b overexpression attenuated caerulein-induced cell injury and inflammatory responses in AR42J cells. Luciferase reporter assay showed that mitogen-activated protein kinase 4 (MAP2K4) was a direct target of miR-92b. MiR-92b overexpression repressed MAP2K4 expression, while caerulein up-regulated MAP2K4 expression in AR42J cells. The rescue experiments showed that enforced expression of MAP2K4 partially reversed the miR-92b-mediated protective effects on caerulein-induced AR42J cell injury. CONCLUSION: In conclusion, we identified miR-216a, miR-216b, miR217, miR-92b, miR-375 and miR-148a as new candidate biomarkers for acute pancreatitis. Further in vitro functional studies revealed that miR-92b attenuated caerulein-induced cell injury and inflammatory responses in AJ42R cells partially via targeting MAP2K4.

Tiliacora triandra attenuates cisplatin triggered hepatorenal and testicular toxicity in rats by modulating oxidative inflammation, apoptosis and endocrine deficit.

PURPOSE: Cisplatin (CIS) is a platinum based anticancer drug that has demonstrated significant efficacy against various types of cancers. Unfortunately, this drug is also famous for its severe side effects on delicate organs. Herein this study examined the hepatorenal and testicular protective effects of TiTE against CIS-induced hepatorenal and testicular insults. METHODS: Rats were administered with TiTE (250 and 500 mg/kg body weight) for 4 weeks, while a single dose of CIS (2.5 mg/kg body weight) was injected once per week from week 2 to week 4. RESULTS: Treatment with TITE significantly attenuated CIS-induced increases in serum creatinine, blood urea nitrogen (BUN), uric acid, alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Furthermore, TiTE treatment also decreased oxidative stress (MDA) inflammations (TNF-α, IL-1ß, IL-6, NF-κB) and apoptosis (caspase-3 activity) and restored hepatorenal and testicular antioxidant defense (SOD, CAT and GPx) in CIS treated rats. Additionally, the TiTE improved sperm count, motility and viability, and ameliorated the reduced serum levels of testosterone, follicle stimulating hormone (FSH) and luteinizing hormone (LH) in CIS-injected rats. TiTE also curtailed hepatorenal and testicular histological changes in CIS treated rats. CONCLUSION: The findings from the study indicated that TiTE displayed hepatorenal and testicular protective effects via inhibition of oxidative stress-mediated inflammation and endocrine imbalance in rats.