Stroke results in the disruption of tissue architecture and is the third leading cause of death in the United States1. Transplanting scaffolds containing stem cells into the injured areas of the brain has been proposed as a treatment strategy2, and carbon nanotubes show promise in this regard, with positive outcomes when used as scaffolds in neural cells3,4 and brain tissues5. Here, we show that pretreating rats with amine-modified single-walled carbon nanotubes can protect neurons and enhance the recovery of behavioural functions in rats with induced stroke. Treated rats showed less tissue damage than controls and took longer to fall from a rotating rod, suggesting better motor functions after injury. Low levels of apoptotic, angiogenic and inflammation markers indicated that aminemodified single-walled carbon nanotubes protected the brains of treated rats from ischaemic injury.
Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by mitochondrial dysfunction, Lewy body formation, and loss of dopaminergic neurons. Parkin, an E3 ubiquitin ligase, is thought to inhibit PD progression by removing damaged mitochondria and suppressing the accumulation of α-synuclein and other protein aggregates. The present study describes a protein-based therapy for PD enabled by the development of a cell-permeable Parkin protein (iCP-Parkin) with enhanced solubility and optimized intracellular delivery. iCP-Parkin recovered damaged mitochondria by promoting mitophagy and mitochondrial biogenesis and suppressed toxic accumulations of α-synuclein in cells and animals. Last, iCP-Parkin prevented and reversed declines in tyrosine hydroxylase and dopamine expression concomitant with improved motor function induced by mitochondrial poisons or enforced α-synuclein expression. These results point to common, therapeutically tractable features in PD pathophysiology, and suggest that motor deficits in PD may be reversed, thus providing opportunities for therapeutic intervention after the onset of motor symptoms.
The purpose of this study was to evaluate the time-dependent probability and risk factors of pancreatogenic diabetes mellitus (PDM) in patients who underwent minimally invasive subtotal distal pancreatectomy.Changes in glucose metabolic consequence of 34 patients (laparoscopic: 31, robotic: 3) who underwent surgery from December 2005 to December 2014 were estimated by assessing impaired fasting glucose, PDM, and PDM-free time analysis.A total of 22 patients showed glucose intolerance, including 13 (38.2%) with impaired fasting glucose and 9 (26.5%) with PDM. The median onset time of PDM was 6.8 months (range 5.3–13.2 months). The PDM-free time probability according to time interval was 94.1% (6 months), 75.9% (12 months), and 72.6% (18 months). It was shown that body mass index>23 kg/m2 (49.9 vs 87.9 months, P = .020) and preoperative cholesterol >200 mg/dL (40.9 vs 85.2 months, P = .003) adversely influenced PDM-free time. Preoperative cholesterol >200 mg/dL (hazard ratio = 6.172; 95% confidence interval, 1.532–24.865; P = .010) was significantly associated with short PDM-free time in Cox proportional hazards model.Patients with high cholesterol levels and high BMI should be closely monitored for the development of PDM.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.