[Anatomical and biomechanical characteristics of plantaris tendon and its application in ligament reconstruction].

Objective: To improve the clinical utility of the plantaris tendon mainly by summarizing its anatomical characteristics, biomechanical properties, harvesting methods, and its applications in ligament reconstruction. Methods: The relevant literature from domestic and international databases regarding the anatomical and biomechanical characteristics of the plantaris tendon and its applications in ligament reconstruction was comprehensively reviewed and systematically summarized. Results: The plantaris tendons have an absence. The majority of plantaris tendon forms a fan-shape on the anterior and medial sides of the Achilles tendon and terminates at the calcaneal tuberosity. There are significant differences in biomechanical parameters between plantaris tendon with different numbers of strands, and multi strand plantaris tendon have significant advantages over single strand tendon. The plantaris tendon can be harvested through proximal and distal approaches, and it is necessary to ensure that there are no obvious anatomical variations or adhesions in the surrounding area before harvesting. The plantaris tendon is commonly utilized in ligament reconstruction around the ankle joint or suture reinforcement for Achilles tendon rupture, with satisfactory effectiveness. There is limited research on the use of plantar tendon in the reconstruction of upper limb and knee joint ligaments. Conclusion: The plantaris tendon is relatively superficial, easy to be harvested, and has less impact on local function. The plantaris tendon is commonly utilized in ligaments reconstruction around the ankle joint or suture reinforcement for Achilles tendon rupture. The study on the plantaris tendon for upper limbs and knee joints ligament reconstruction is rarely and require further research.

A new molecular probe: An NRP-1 targeting probe for the grading diagnosis of glioma in nude mice.

Magnetic resonance molecular imaging, as a safe imaging technology, provides a new idea for the early qualitative and hierarchical diagnosis of gliomas. The purpose of this study was to design and evaluate the value of neuropilin-1 (NRP-1) targeting molecular probes in the hierarchical diagnosis of gliomas. First, we created an NRP-1 targeted magnetic resonance molecular probe (USPIO-PEG-tLyP-1) by combining the polypeptide tLyP-1 with ultra-small superparamagnetic iron oxide nanoparticles (USPIONs), detecting the physical properties by transmission electron microscopy (TEM) and dynamic light scattering (DLS). Second, in vivo experiments, we established two different degrees of malignant gliomas in-situ in nude mice by injecting U87 and CHG-5 cells. Then, to detect the binding ability of the probe with different grades of tumour tissues, we injected the probe into the tumour-bearing mice through the tail vein. Next, MRI was performed before injection, and 6 h, 12 h, 24 h after injection, and we found significantly more iron particles in the tumour tissues of U87 tumour-bearing mice than in tumour tissues of CHG-5 tumour-bearing mice. The signal intensities of the T2-weighted images of the tumour tissues of each group as well as microscopic observations by Prussian blue staining indicated that the binding ability of this molecular probe to U87 glioma (HGG) with high NRP-1 expression was significantly greater than that of CHG-5 glioma (LGG) with low NRP-1 expression (P < 0.01). Therefore, this study confirms that the novel molecular probe USPIO-PEG-tLyP-1 can be used for the grading diagnosis by MRI for gliomas of high and low grade with different NRP-1 expression levels.

Wetting mechanism of Sn to Zr50.7Cu28Ni9Al12.3 bulk metallic glass assisted by ultrasonic treatment.

In this work, pure Sn was used to wet Zr50.7Cu28Ni9Al12.3 bulk metallic glasses (BMGs) assisted by ultrasonic treatment. Without ultrasonic treatment, pure Sn showed a non-wetting condition to BMG. Ultrasonic vibration facilitated the wetting of Sn to BMG. Prior to ultrasonication for 30 s, only physical adsorption formed at the Sn/BMG interface. Increasing ultrasonic time led to the alteration of the bond at the Sn/BMG interface from point contact to local surface contact, and to diffusion layer. Two bonding modes of order-order and order-disorder were discovered at the Sn/BMG interface. Cu content was higher than the other elements near the bonding interface. Longer diffusion distances of Sn into the BMG were obtained at high ultrasonic power, high temperature and large dip depth.

Optical Depolarization of DCX-Expressing Cells Promoted Cognitive Recovery and Maturation of Newborn Neurons via the Wnt/ß-Catenin Pathway.

Electrical excitability by membrane depolarization is crucial for survival and maturation of newborn cells in the dentate gyrus of the hippocampus. However, traditional technology for membrane depolarization lacks temporal and spatial precision. Optogenetics can be used to activate channelrhodopsin-2 (ChR2), allowing cationic current to depolarize genetically targeted cells. In this study, we used ChR2-EGFP driven by doublecortin (DCX) to promote survival and maturation of newborn cells in the dentate gyrus after traumatic brain injury (TBI). C57BL/6 mice underwent lateral fluid percussion TBI. TBI mice were transfected with a lentivirus carrying the DCX-ChR2-EGFP gene. We observed that not only immature neurons but also type-2b intermediate progenitor (IPs) and neuroblasts expressed DCX-EGFP, indicating that DCX-expressing newborn cells could provide a long time window for electrical activity regulation. Quantitative results showed that the number of EGFP-expressing cells began to rise at 3 days after TBI and peaked at 9 days after TBI. By optical depolarization of DCX-EGFP-expressing cells between 3 and 12 days, we observed significantly improved cognitive deficits after TBI with enhanced survival and maturation of newborn cells in the dentate gyrus. We also investigated the role of optical depolarization in neural stem cells transfected with a lentivirus carrying the ChR2-DCX-EGFP gene in vitro. By administrating verapamil to block L-type calcium channels, we verified that the up-regulation of MAP2, NeuN, Neurog2, NeuroD1 and GluR2 in newborn cells was mediated by ChR2-elicted depolarization. By using ß-catenin inhibitor Dkk1, we demonstrated that optical depolarization of DCX-EGFP-expressing cells facilitated survival and maturation probably through the Wnt/ß-catenin signaling cascade.

Combined intranasal nerve growth factor and ventricle neural stem cell grafts prolong survival and improve disease outcome in amyotrophic lateral sclerosis transgenic mice.

Amyotrophic lateral sclerosis (ALS) is a fatal disease that selectively involves motor neurons. Neurotrophic factor supplementation and neural stem cell (NSC) alternative therapy have been used to treat ALS. The two approaches can affect each other in their pathways of action, and there is a possibility for synergism. However, to date, there have been no studies demonstrating the effects of combined therapy in the treatment of ALS. In this study, for the first time, we adopted a method involving the intranasal administration of nerve growth factor combined with lateral ventricle NSC transplantation using G93A-SOD1 transgenic mice as experimental subjects to explore the treatment effect of this combined therapy in ALS. We discover that the combined therapy increase the quantity of TrkA receptors, broaden the migration of exogenous NSCs, further promote active proliferation in neurogenic regions of the brain and enhance the preservation of motor neurons in the spinal cord. Regarding physical activity, the combined therapy improved motor functions, further postponed ALS onset and extended the survival time of the mice.

MicroRNA-134 modulates glioma cell U251 proliferation and invasion by targeting KRAS and suppressing the ERK pathway.

Dysregulated microRNA-134 (miR-134) has been observed in glioma carcinogenesis, and studies suggested that the ERK pathway plays vital roles in glioma cell growth and proliferation. However, the fundamental relationship between miR-134 and the ERK pathway in glioma has not been fully explained. As a result, this study was aimed to explore the underlying functions of miR-134 in human glioma. Intentionally overexpressed or inhibited miR-134 expression resulted from the transfection of miR-134 mimics, or miR-134 inhibitor within glioma cell line U251 was detected using RT-PCR. Both cell counting kit-8 (CCK-8) assays and Transwell assays were carried out to clarify the proliferation and invasion of U251 cells transfected with miR-134 mimics or miR-134 inhibitors. Our findings showed that miR-134 was significantly downexpressed in glioma tissues, and low miR-134 expression was significantly related to high histopathological grades. However, upregulated miR-134 expression restrained the proliferation and invasion of U251 cells in vitro. Kirsten rat sarcoma viral oncogene (KRAS), a vital factor for the ERK pathway, was directly targeted by miR-134 through its binding with the 3'-UTR of KRAS in glioma. Furthermore, KRAS expression exhibited a positive correlation with the activity of the ERK pathway. Overexpression of KRAS without 3'-UTR partly offsets the suppressive effect of miR-134 on glioma progression. Our data also indicated that miR-134 negatively modulated glioma progression and upregulated miR-134 triggered aberrant activation of the ERK pathway by targeting KRAS. Therefore, miR-134 might be considered as a benign therapeutic target of glioma.