ABSTRACT
Introduction: Traumatic optic neuropathy is known to be a critical condition that can cause blindness; however, the specific mechanism underlying optic nerve injury is unclear. Recent studies have reported that artemisinin, considered vital in malaria treatment, can also be used to treat neurodegenerative diseases; however, its precise role and mechanism of action remain unknown. Therefore, in this study, we aimed to investigate the impact and probable mechanism of action of artemisinin in retinal ganglion cells (RGCs) in a mouse model of traumatic optic neuropathy induced by optic nerve crush (ONC). Methods: ONC was induced in the left eye of mice by short-term clamping of the optic nerve; oral artemisinin was administered daily. The neuroprotective effect of the drug was assessed using Tuj-1 staining in RGCs. In addition, the inflammatory response and the expression levels of phosphorylated tau protein and tau oligomers were observed using RT-qPCR, TUNEL assay, and fluorescence staining to investigate the underlying mechanisms. Results: Artemisinin increased the survival rate of RGCs 14 days after ONC. Artemisinin significantly reduced the levels of inflammatory factors such as CXCL10, CXCR3, and IL-1ß in the retina and decreased the apoptosis of RGCs. Moreover, downregulation of the phosphorylation of tau proteins and the expression of tau oligomers were observed after artemisinin treatment. Conclusion: Our results suggest that artemisinin can increase the survival rate of RGCs after ONC and reduce their apoptosis. This effect may be achieved by inhibiting the inflammatory response it triggers and downregulating tau protein phosphorylation and tau oligomer expression. These findings suggest the potential application of artemisinin as a therapeutic agent for neuropathy.
ABSTRACT
Background: Kaposiform hemangioendothelioma (KHE) is a rare and invasive vascular tumor that mainly occurs in children and is rarely seen in adults. We report a case of KHE found on the eyelid of an adult patient. Case report: We present an adult patient in whom KHE recurred 6â months after tumor resection. He underwent second surgical resection and intraoperative chemotherapy. There was no evidence of recurrence at the 3-year follow-up. Conclusion: KHE in adults is easy to be misdiagnosed. KHE can be treated by surgical resection. Complete resection of the tumor and intraoperative chemotherapy may help prevent a recurrence.
ABSTRACT
Cell tracking is critical for the modeling of plant cell growth patterns. A local graph matching algorithm is proposed to track cells by exploiting the tight spatial topology of cells. However, the local graph matching approach lacks robustness in the unregistered images because the feature descriptors are handcrafted. In this paper, we propose a Deep Local Patch Matching Network (DLPM-Net) to track cells robustly, by exploiting local patches' deep similarity information and cells' spatial-temporal contextual information. Furthermore, to reduce the time consumption during the matching process and enhance tracking accuracy, we take two steps to realize the tracking of non-division cells and the detection of cell divisions. In the first step, the DLPM-Net is employed to match the non-division cells by exploiting the cell pair candidates' local patch contextual information, then the non-matched cells are recorded as the cell division candidates. In the second step, the DLPM-Net is used to detect cell divisions from these non-matched cells, by exploiting the local patch contextual similarity between the mother cell's local patch and daughter cells' local patch. Compared with the existing local graph matching method, the experimental results show that the proposed method gains 29.1% improvement in the tracking accuracy.