Background Anti-retropulsive devices are often used to prevent stone migration in the treatment of proximal ureteral calculi. They are helpful. However, in the meantime, they also add extra expenses. This study was carried out to investigate the best criteria for treating proximal ureteral stones with anti-retropulsive devices. Methods Data from all patients who underwent ureteroscopic holmium: YAG laser lithotripsy for solitary upper ureteral stones in 2018 were collected. Patients who encountered stone retropulsion during the process of inserting the ureteroscope were excluded. Patients were divided into either group URS or group URS + ARD depending on whether the anti-retropulsive device was used. Then, the stone-free rate, expenses and other criteria were compared between groups according to stone location. Stone-free was defined as no stones present. Results For stones located ≤ 30 mm from the ureteropelvic junction (UPJ), the stone-free rates for the URS group were 80% and 80% at one day and one month after the operation, respectively. Those for the URS + ARD group were 71.4% and 78.6% at one day and one month, respectively. For stones located 31–90 mm from the UPJ, the stone-free rates were 84.7% and 84.7% for the URS group and 89.6% and 95.5% for the URS + ARD group at one day and one month, respectively. A statistically significant difference occurred at one month. For stones located > 90 mm from the UPJ, the two groups were both stone free. In the URS + ARD group, expenses were higher. In addition, the mean diameter of residual stones derived from stones located at 31–90 mm from the UPJ was statistically smaller, and 4 of 7 residual stones passed spontaneously within one month, which was obviously more than that in other locations and the URS group. Other outcomes, including operation time and postoperative stay, showed no significant difference between the groups. Conclusion Anti-retropulsive devices are indeed helpful, but they might be cost-effective for stones located solely in the middle part of the upper ureter, not for those too close to or far from the ureteropelvic junction.
In patients suffering from inflammatory bowel diseases (IBDs), the immune system is disrupted and the intestinal barrier function is compromised. Here, six zinc-flavonoid particles were produced by one-step reaction via changing flavonoids (myricetin, quercetin, and rutin) and solvent (water and ethanol), and then their cytocompatibility and ability to scavenge H 2 O 2 , free radicals, and LPS-induced ROS were compared. Zinc-rutin particles (W-ZnRT) composed of rutin (78.92 wt %), Na 12 [ZnPO 4 ] 12 •12H 2 O (6.76 wt %), and crystal water were screened out because W-ZnRT exhibited 80.8 ± 15% cell viability against RAW264.7, could rapidly scavenge 78.1 ± 1% of H 2 O 2 and 71.6 ± 2% of DPPH within 30 min, and reduced LPS-increased intracellular ROS to normal levels. In addition, the therapeutic effects of rutin and W-ZnRT were also compared in dextran sulfate sodium (DSS)-induced acute and chronic colitis in mice. W-ZnRT was superior to rutin alone in chronic colitis (n = 9), although they were equally effective in acute colitis (n = 7). Compared to rutin, 11 oral doses of W-ZnRT (40 mg kg −1 ) significantly improved intestinal permeability (p = 0.0299) and colon length (p = 0.0025), reduced intestinal proinflammatory factors (IL-6, IL-1β, and TNF-α), and upregulated tight junction proteins to maintain intestinal barrier function. Taken together, these results identified W-ZnRT as an efficient and safe therapeutic strategy for IBD.
Hyperoxaluria is a risk factor for urolithiasis and can cause renal epithelial cell injury secondary to oxidative stress. Reactive oxygen species (ROS) produced during cell damage originate from different sources and play different roles. Here, we explored the potential sources of ROS production and investigated the role of ROS from various sources in oxalate-induced oxidative stress and cell injury in normal rat kidney-52 epithelial (NRK-52E) cells. Oxalate-induced injury was assessed by lactate dehydrogenase (LDH) release experiments. 2,7-dichlorodihydrofluorescein diacetate and mitoSOX Red were used to determine the intracellular and mitochondrial ROS (mtROS) production, respectively. The expression level of Nox4, Nox2, and p22 protein was detected by Western blotting to observe the effect of oxalate on nicotinamide adenine dinucleotide phosphate oxidase (NADPH) oxidase (Nox). Furthermore, a specific NADPH oxidase subtype inhibitor and targeted mitochondrial antioxidants were used to preliminarily identify the role of ROS from different sources in renal tubular epithelial cell injury induced by oxalate. We found that oxalate inhibited cell viability, induced LDH release, and prompted intracellular and mitochondrial ROS (mtROS) production. Oxalate also decreased the protein expression level of Nox4 and increased the protein expression level of p22. Mitochondria were also a source of ROS production. In addition, Nox2 inhibitor or mtROS scavenging prevented oxalate-induced cell injury, reversed by an inhibitor of Nox4/1. We concluded that ROS from different sources might play different roles in oxalate-induced renal tubular epithelial cell injury. We also identified new potential targets for preventing or alleviating oxalate-induced renal tubular epithelial cell injury. Graphic abstract
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