Parkinson's disease (PD) is the second most predominant neurodegenerative disease worldwide. It is recognized clinically by severe complications in motor function caused by progressive degeneration of dopaminergic neurons (DAn) and dopamine depletion. As the current standard of treatment is focused on alleviating symptoms through Levodopa, developing neuroprotective techniques is critical for adopting a more pathology-oriented therapeutic approach. Regenerative cell therapy has provided us with an unrivalled platform for evaluating potentially effective novel methods for treating neurodegenerative illnesses over the last two decades. Mesenchymal stem cells (MSCs) are most promising, as they can differentiate into dopaminergic neurons and produce neurotrophic substances. The precise process by which stem cells repair neuronal injury is unknown, and MSC-derived exosomes are suggested to be responsible for a significant portion of such effects. The present review discusses the application of mesenchymal stem cells and MSC-derived exosomes in PD treatment.

Glioblastoma belongs to the most aggressive type of cancer with a low survival rate that is characterized by the ability in forming a highly immunosuppressive tumor microenvironment. Intercellular communication are created via exosomes in the tumor microenvironment through the transport of various biomolecules. They are primarily involved in tumor growth, differentiation, metastasis, and chemotherapy or radiation resistance. Recently several studies have highlighted the critical role of tumor-derived exosomes against immune cells. According to the structural and functional properties, exosomes could be essential instruments to gain a better molecular mechanism for tumor understanding. Additionally, they are qualified as diagnostic/prognostic markers and therapeutic tools for specific targeting of invasive tumor cells such as glioblastomas. Due to the strong dependency of exosome features on the original cells and their developmental status, it is essential to review their critical modulating molecules, clinical relevance to glioma, and associated signaling pathways. This review is a non-clinical study, as the possible role of exosomes and exosomal microRNAs in glioma cancer are reported. In addition, their content to overcome cancer resistance and their potential as diagnostic biomarkers are analyzed.

Objective: This study was performed to systematically review the current literature on the effects of transcutaneous tibial nerve stimulation and percutaneous tibial nerve stimulation on multiple sclerosis-induced neurogenic lower urinary tract dysfunction. Materials and methods: Medical databases including PubMed, Scopus, Embase, and Web of Science were systematically searched from inception to September 2022. Meta-analysis was carried out using the comprehensive meta-analysis tool. Results: Our inclusion criteria were met by 12 studies evaluating the effects of percutaneous tibial nerve stimulation/transcutaneous tibial nerve stimulation on multiple sclerosis-induced neurogenic lower urinary tract dysfunction. Comparing the post-intervention results to the baseline showed that the rate of frequency was decreased in both percutaneous tibial nerve stimulation and transcutaneous tibial nerve stimulation groups after intervention. The overall mean change of tibial nerve stimulation on frequency was –2.623 (95% CI: –3.58, –1.66; P < .001, I 2 : 87.04) among 6 eligible studies. The post-void residual was decreased after treatment in both methods of tibial nerve stimulation, with an overall mean difference of –31.13 mL (95% CI: –50.62, –11.63; P = .002, I 2 : 71.81). The other urinary parameters, including urgency (mean difference: –4.69; 95% CI: –7.64, –1.74; P < .001, I 2 : 92.16), maximum cystometric capacity (mean difference: 70.95; 95% CI: 44.69, 97.21; P < .001, I 2 : 89.04), and nocturia (mean difference: –1.41; 95% CI: –2.22, 0.60; P < .001, I 2 : 95.15), were improved after intervention, too. However, the results of subgroup analysis showed no effect of transcutaneous tibial nerve stimulation on urinary incontinence (mean difference: –2.00; 95% CI: –4.06, 0.06; P = .057, I 2 : 95.22) and nocturia (mean difference: –0.39; 95% CI: –1.15, 0.37; P = .315, I 2 : 84.01). In terms of mean voided volume, the evidence was related to only percutaneous tibial nerve stimulation with a mean change of 75.01 mL (95% CI: –39.40, 110.61; P < .001, I 2 : 85.04). Conclusion: Although the current literature suggests that tibial nerve electrostimulation might be an effective method for treating neurogenic lower urinary tract dysfunction, the evidence base is poor and derived from small, mostly nonrandomized trials with a high risk of bias and confounding.

Background and Purpose: Rutin (RUT) is one of the phenolic compounds found in the invasive plant species, Carpobrotus edulis. Several studies have confirmed numerous pharmacological properties of RUT, including antioxidant, antidiabetic, anti-inflammatory, antimicrobial and anticancer activities. As a result, the goal of this work was to make RUT-loaded PCL-PEG and test its anti-cancer effects against the Skov3 human ovarian cancer cell line. Materials and Methods: The NPs were made using the W1/O/W2 process, and their physicochemical properties were assessed by FE-SEM, FTIR, and DLS. MTT assay were used to investigate the anti-proliferative characteristics of drug-loaded NPs. Real-time PCR was also utilized to examine the expression levels of apoptotic genes including caspase-8, -9, -3, and Bax, as well as anti-apoptotic genes like Bcl-2. Results: Cytotoxicity testing revealed that RUT-loaded PCL-PEG improved cytotoxicity in a dose-and time-dependent manner. In treated MDA-MB-231 cells with RUT-loaded PCL-PEG, there was a significant up-regulation of caspase-8, -9, -3, and Bax genes compared to treated cells with free RUT. Conclusion: Finally, RUT-loaded PCL-PEG NPs are recommended as ideal delivery nanocarriers for enhancing RUT's anticancer characteristics for ovarian cancer treatment.

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