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A photovoltaic (PV) health diagnostic system for solar power systems is presented. The system consists of two levels of embedded platforms, including the Data Acquisition Module (DAM) and the Control Module (CM). Each DAM is connected to two series-connected PV panels under test. When testing the PV panels, it will inject large-signal disturbances into their panel voltages. Then, the terminal voltage and current of each panel are sampled and, thus, the dynamic current-voltage characteristics of the PV panel are obtained. The CM has a Real-coded Jumping Gene Genetic Algorithm (RJGGA) programmed and a dedicated Field Programmable Gate Array (FPGA) accelerator designed to evaluate objective functions. Its function is to extract the intrinsic parameters of the panels with the dynamic current-voltage characteristics. Panel degradation can thus be observed with the variation of the estimated intrinsic parameters. Prototypes designed for diagnosing four 80W PV panels have been built and evaluated on panels with different degradation levels.

Background Cranial metastasis of thyroid cancer is rare. The aim of this study was to analyse the clinical characteristics, treatments and outcomes of thyroid cancer patients with cranial metastasis and to identify the associated prognostic factors. Materials and methods Between January 1977 and August 2017, a total of 4683 patients were histologically confirmed to have thyroid cancer. Among them, 25 patients (0.53%) were identified as having cranial metastases, and their medical records were reviewed. The Kaplan-Meier method with a log-rank test was performed with cancer-specific survival as the main outcome. Cox regression analysis was used to examine the potential prognostic factors influencing patient survival. Results Of the 25 patients, 21 were female, and 4 were male. The median age at the time of diagnosis of cranial metastasis was 63 years. Sixteen patients had metastases to the brain, and nine patients had metastases involving the skull only. Papillary carcinoma and follicular carcinoma accounted for 84.0% of cases. Twenty-four cases (96.0%) had extracranial metastases at the time of diagnosis of cranial metastases. Twenty patients received surgery, and 4 patients received palliative radiotherapy. One patient received supportive care only. The median cancer-specific survival after the diagnosis of cranial metastases was 27 months. According to the Kaplan-Meier test, 3 factors had a significant impact on survival, the metastatic site, histological types and surgical resection. According to the Cox regression analysis, skull metastases (HR: 0.274, 95% CI: 0.083–0.904, p = 0.033) and surgical resection (HR: 0.134, 95% CI: 0.019–0.929, p = 0.042) were identified as independent prognostic factors for a better outcome. Conclusions Surgical resection is the mainstay therapy for thyroid cancer patients with cranial metastasis. Cranial metastases involving the skull only are associated with a better outcome.

Background Hypoxia could lead to microglia activation and inflammatory mediators’ overproduction. These inflammatory molecules could amplify the neuroinflammatory process and exacerbate neuronal injury. The aim of this study is to find out whether harpagoside could reduce hypoxia-induced microglia activation. Methods In this study, primary microglia cells harvested from neonatal ICR mice were activated by exposure to hypoxia (1 % O2 for 3 h). Harpagoside had been shown to be no cytotoxicity on microglia cells by MTT assay. The scavenger effect of harpagoside on hypoxia-enhanced microglial cells proliferation, associated inflammatory genes expression (COX-II, IL-1β and IL-6 genes) and NO synthesis were also examined. Results Hypoxia enhances active proliferation of microglial cells, while harpagoside can scavenge this effect. We find that harpagoside could scavenge hypoxia-enhanced inflammatory genes expression (COX-2, IL-1β and IL-6 genes) and NO synthesis of microglial cells. Under 3 h’ hypoxic stimulation, the nuclear contents of p65 and hypoxia inducible factor-1α (HIF-1α) significantly increase, while the cytosol IκB-α content decreases; these effects can be reversed by 1 h’s pre-incubation of 10−8 M harpagoside. Harpagoside could decrease IκB-α protein phosphorylation and inhibit p65 protein translocation from the cytosol to the nucleus, thus suppress NF-κB activation and reduce the HIF-1α generation. Conclusion These results suggested that the anti-inflammatory mechanism of harpagoside might be associated with the NF-κB signaling pathway. Harpagoside protect against hypoxia-induced toxicity on microglial cells through HIF-α pathway.