Treating cerebral ischemia continues to be a clinical challenge. Studies have shown that the neurovascular unit (NVU), as the central structural basis, plays a key role in cerebral ischemia. Here, we report that anthocyanin, a safe and natural antioxidant, could inhibit apoptosis and inflammation to protect NVU in rats impaired by middle cerebral artery occlusion/reperfusion (MCAO/R). Administration of anthocyanin significantly reduced infarct volume and neurological scores in MCAO/R rats. Anthocyanin could also markedly ameliorate cerebral edema and reduce the concentration of Evans blue (EB) by inhibiting MMP-9. Moreover, anthocyanin alleviated apoptotic injury resulting from MCAO/R through the regulation of Bcl-2 family proteins. The levels of inflammation-related molecules including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6), which were over-expressed with MCAO/R, were decreased by anthocyanin. In addition, Nuclear factor-kappa B (NF-κB) and the NLRP3 inflammasome pathway might be involved in the anti-inflammatory effect of anthocyanin. In conclusion, anthocyanin could protect the NVU through multiple pathways, and play a protective role in cerebral ischemia/reperfusion injury.

In this study, we investigated incidental parathyroidectomy during total thyroidectomy surgery that required central lymph node dissection and the potential risk factors. Patients requiring total thyroidectomy and tracheoesophageal groove node dissection were enrolled in the study from January 2013 to June 2015 and we obtained all medical information, including pathology reports. Furthermore, we recorded the parathyroid hormone level in all patients prior to operation and then 3 further times: 1 day, 1 week, and 3 months after surgery. A total of 341 patients (66 male and 275 female) were enrolled in the study. Microscopic examination of postoperative specimens revealed that incidental parathyroidectomy existed in 35 (10.3%) cases: 32 (91.4%) patients had 1 parathyroid gland excised, 3 (8.6%) patients had 2 parathyroid glands excised, and no patients had 3 or more parathyroid glands resected. The mean size of the resected glands was 4.6 mm. Parathyroid tissue from 16 (42.1%) cases was located in the intrathyroidal position, 6 glands were located in central lymphatic adipose tissue, and 16 glands were located within or along with thymus tissue. Lateral neck dissection significantly increased the risk of incidental parathyroidectomy (P < 0.001). No other factors including age, sex, and postoperative symptomatic hypocalcemia were significantly associated with incidental parathyroidectomy (all P > 0.05), though incidental parathyroidectomy tended to cause transient hypoparathyroidism (P = 0.051). Therefore, the risk of incidental parathyroidectomy in total thyroidectomy is relatively low; the majority of the resected parathyroid tissue is situated outside the thyroid, therefore we suggest future operations focus on preserving the parathyroid gland when the node dissection is close to the thymus. Incidental parathyroidectomy appears to have an effect on the expression of parathyroid hormone and it is significantly associated with lateral cervical lymph node dissection.

Multimodal learning analytics (MMLA), which has become increasingly popular, can help provide an accurate understanding of learning processes. However, it is still unclear how multimodal data is integrated into MMLA. By following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, this paper systematically surveys 346 articles on MMLA published during the past three years. For this purpose, we first present a conceptual model for reviewing these articles from three dimensions: data types, learning indicators, and data fusion. Based on this model, we then answer the following questions: 1. What types of data and learning indicators are used in MMLA, together with their relationships; and 2. What are the classifications of the data fusion methods in MMLA. Finally, we point out the key stages in data fusion and the future research direction in MMLA. Our main findings from this review are (a) The data in MMLA are classified into digital data, physical data, physiological data, psychometric data, and environment data; (b) The learning indicators are behavior, cognition, emotion, collaboration, and engagement; (c) The relationships between multimodal data and learning indicators are one-to-one, one-to-any, and many-to-one. The complex relationships between multimodal data and learning indicators are the key for data fusion; (d) The main data fusion methods in MMLA are many-to-one, many-to-many and multiple validations among multimodal data; and (e) Multimodal data fusion can be characterized by the multimodality of data, multi-dimension of indicators, and diversity of methods.

Background: miR-155 was up-regulated in natural killer/T-cell lymphoma (NKTCL), an aggressive malignancy, and correlated with disease progression. However, minimal is known on biological activities and underlying mechanisms of miR-155 in NKTCL. In this study, we examined BRG1, a potential target of miR-155, and focused on the miR-155/BRG1 signaling in regulating lymphangiogenesis of NKTCL. Methods: The expression of miR-155, BRG1, VEGFC, and VEGFD was compared between two NKTCL cell lines and normal NK cells. The critical role of miR-155 and STAT3 was assessed using miR-155 inhibitor and STAT3 inhibitor S31-201, respectively. Two biological phenotypes, apoptosis and pro-lymphangiogenesis, were examined in vitro by flow cytometry and lymphatic tube formation, respectively, and in vivo using an NKTCL xenograft model. Results: The miR-155 level negatively correlated with BRG1, but positively with VEGFC in normal NK as well as two NKTCL cell lines. Targeting miR-155 in NKTCL cells significantly boosted BRG1 expression and decreased the activated STAT3 or VEGFC level, leading to enhanced apoptosis and reduced lymphangiogenesis. STAT3 acted downstream of BRG1 and essentially regulated miR-155-mediated up-regulation of VEGFC and pro-lymphangiogenesis. In vivo, targeting miR-155 inhibited primary xenograft growth as well as tumor-associated lymphangiogenesis. Conclusions: By inhibiting BRG1 expression, miR-155 activated STAT3/VEGFC signaling and promoted lymphangiogenesis. In addition, miR-155 also controlled the viability of NKTCL cells. Therefore, targeting miR-155 provides a novel therapy for NKTCL.