Introduction: Frame-based stereotactic biopsy is well-established to play an essential role in neurosurgery. In recent years, different robotic devices have been introduced in neurosurgery centers. This study aimed to compare the SINO surgical robot-assisted frameless brain biopsy with standard frame-based stereotactic biopsy in terms of efficacy, accuracy and complications.Methods: A retrospective analysis was performed on 151 consecutive patients who underwent stereotactic biopsy at Chongqing Sanbo Jiangling Hospital between August 2017 and December 2021. All patients were divided into the frame-based group (n = 47) and the SINO surgical robot-assisted group (n = 104). The data collected included clinical characteristics, diagnostic yield, operation times, accuracy, and postoperative complications.Results: There was no significant difference in diagnostic yield between the frame-based group and the SINO surgical robot-assisted group (95.74 vs. 98.08%, p > 0.05). The mean operation time in the SINO surgical robot-assisted group was significantly shorter than in the frame-based group (29.36 ± 13.64 vs. 50.57 ± 41.08 min). The entry point error in the frame-based group was significantly higher than in the robot-assisted group [1.33 ± 0.40 mm (0.47–2.30) vs. 0.92 ± 0.27 mm (0.35–1.65), P < 0.001]. The target point error in the frame-based group was also significantly higher than in the robot-assisted group [1.63 ± 0.41 mm (0.74–2.65) vs. 1.10 ± 0.30 mm (0.69–2.03), P < 0.001]. Finally, there was no significant difference in postoperative complications between the two groups.Conclusion: Robot-assisted brain biopsy becomes an increasingly mainstream tool in the neurosurgical procedure. The SINO surgical robot-assisted platform is as efficient, accurate and safe as standard frame-based stereotactic biopsy and provides a reasonable alternative to stereotactic biopsy in neurosurgery.

BACKGROUND:Breast cancer is one of the most malignant tumors worldwide. The natural flavonoid diosmetin has been reported to exhibit various pharmacological activities, including anti-cancer effects. This study aimed to investigate the anti-breast ca...

Background: Type 1 diabetes mellitus (T1D) is a worldwide health priority due to autoimmune destruction and is associated with an increased risk of multiorgan complications. Among these complications, effective interventions for liver injury, which can progress to liver fibrosis and hepatocellular carcinoma, are lacking. Although stem cell injection has a therapeutic effect on T1D, whether it can cure liver injury and the underlying mechanisms need further investigation. Methods: Sprague–Dawley rats with streptozotocin (STZ)-induced T1D were treated with adipose-derived stem cell (ADSC) or PBS via the tail vein formed the ADSC group or STZ group. Body weights and blood glucose levels were examined weekly for 6 weeks. RNA-seq and PCR array were used to detect the difference in gene expression of the livers between groups. Results: In this study, we found that ADSCs injection alleviated hepatic oxidative stress and injury and improved liver function in rats with T1D; potential mechanisms included cytokine activity, energy metabolism and immune regulation were potentially involved, as determined by RNA-seq. Moreover, ADSC treatment altered the fibroblast growth factor 21 (FGF21) and transforming growth factor β (TGF-β) levels in T1D rat livers, implying its repair capacity. Disordered intracellular energy metabolism, which is closely related to mitochondrial stress and dysfunction, was inhibited by ADSC treatment. PCR array and ingenuity pathway analyses suggested that the ADSC-induced suppression of mitochondrial stress is related to decreased necroptosis and apoptosis. Moreover, mitochondria-related alterations caused liver inflammation, resulting in liver injury involving the T lymphocyte-mediated immune response. Conclusions: Overall, these results improve our understanding of the curative effect of ADSCs on T1D complications: ADSCs attenuate liver injury by inhibiting mitochondrial stress (apoptosis and dysfunctional energy metabolism) and alleviating inflammation (inflammasome expression and immune disorder). These results are important for early intervention in liver injury and for delaying the development of liver lesions in patients with T1D.

To investigate the effects of betaine on HeLa cell growth and apoptosis and molecular mechanisms. Concentrations of 0.1, 1.0, 5.0, 20.0, 100.0 mg/ml of betaine were used to evaluate the anticancer efficacy for HeLa cells respectively, and MCF-10A was also detected as a normal diploid cell control. We found that proliferation of HeLa cells was inhibited significantly upon exposure to increasing betaine levels with the MTT test (p5.0mg/ml) significantly promoted the apoptosis of HeLa cells (p<0.01). SOD activities of the low dose groups were slightly higher than the control group (p<0.05) and there were obvious synchronicity and correlation among the expression of promoting apoptosis genes Bax, P53, Caspase 3 and apoptosis suppression gene Bcl-2. In response to an apoptosis-inducing stimulus, p53 and cyclin D1 could be activated with blockage of the cell cycle at G1/S or S/G2 checkpoints. Our data showed that betaine could promote HeLa cells proliferation in vitro at low concentrations.In contrast, high concentrations could significantly inhibit cell growth and migration, and induce apoptosis of HeLa cells through caspase 3 signaling and further promoted necrosis. This might imply that betaine exhibits tumoricidal effects and acts as a biological response modifier in cancer treatment by inducing apoptosis and cell cycle arrest in a dose and time-dependent manner.

Reversine, a purine analog, had been evidenced that it could induce dedifferentiation of differentiated cells into multipotent progenitor cells. Here, we showed that reversine could increase the plasticity of long-term cryopreserved bovine fibroblasts, and reversine-treated cells achieved the ability to differentiate into all three germ layers cells, such as osteoblasts and adipocytes from mesoblast, neurocyte from ectoderm, hepatocytes and smooth muscle cells from endoderm. Moreover, treatment of reversine caused the grow arrest of fibroblasts at G2/M and distinct cell swelling resulting in the formation of polyploid cells. In parallel, reversine treatment induced a multipotency of fibroblasts might be attributed to the activation of histone modifications, especially the degression of DNA methylation. However, molecular and cellular experiments suggested that reversine treatment enhanced selectively the expression of pluripotent marker gene Oct4 and mesenchymal marker genes CD29, CD44 and CD73, but Sox2 and Nanog were not detected. Taken together, these results clearly demonstrate the ability of reversine to dedifferentiation of long-term cryopreserved somatic cells through activation of pluripotent gene Oct4.