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.

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.

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.

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.

Objective: To analyze the role of frequency of heterotypic neutrophil-in-tumor structure (FNiT) in the prognosis of patients with buccal mucosa squamous cell carcinoma (BMSCC). Methods: In vitro, we cocultured BMSCC cell line-H157 with neutrophils to form heterotypic neutrophil-in-tumor structures, which were then subject to fluorescence staining. Clinically, 145 patients were retrospectively enrolled. Associations between FNiT and clinicopathological variables including age, sex, smoking history, drinking history, betel nut chewing, tumor stage, node stage, metastasis, disease stage, lymphovascular invasion, extranodal extension, perineural invasion, and tumor grade were analyzed by chi-square test, and the main endpoints of interest were recurrence-free survival (RFS) and disease-specific survival (DSS) which were analyzed by the Kaplan-Meier method and Cox model. Results: Fluorescent staining results of typical heterotypic neutrophil-in-tumor structure showed that well-differentiated H157 cells had a stronger ability to internalize more neutrophils than poorly-differentiated H157 cells, with the latter often internalizing only one neutrophil or nothing. The mean FNiT was 4.2‰, with a range from 2.3‰ to 7.8‰. A total of 80 patients relapsed and 84 patients died of the disease. The 5-year RFS and DSS rate was 42% and 42%, respectively. Patients with an FNiT≥4.2‰ had a significantly higher risk for locoregional recurrence and cancer-caused death than those with an FNiT<4.2‰ (p=0.001 and p<0.001, respectively). The FNiT alone was independently significant in predicting poor RFS, and the FNiT along with tumor grade was an independent predictor for DSS. Conclusion: The FNiT as a novel predictor is significantly negatively associated with both the RFS and DSS of patients with BMSCC.

The hot topics are as follows: (1) anti-inflammatory activity, antioxidant activities, anticancer activity of phytogenic antineoplastic agents, and neuroprotective effects of Chinese herbal drugs; (2) common diseases treated with Chinese herbal drugs include hepatocirrhosis, diabetes, angina, chronic hepatitis B in China, and diabetes, asthma, prostate cancer, and hepatocirrhosis outside of China; (3) Chinese herbal nephropathy and acute hepatitis induced by Chinese herbal drugs; (4) PC-SPES (PDQ) for the treatment of prostate cancer, which was a hot topic for researchers located outside of China; (5) research on extraction of active components from medicinal plants; and finally (6) research related to the identification of the Chinese herbal drugs component with state-of-the-art technologies in China.

Background Natural Killer T–Cell Lymphoma (NKTCL) is a subtype of Non‐Hodgkin's Lymphoma, and its morbidity is ranked the first of T‐Cell Lymphoma. Hippo signaling pathway is involved in the pathogenesis of tumors. However, the role of Hippo signaling pathway in the oncogenesis of NKTCL still remains unclear. Methods The expressions of mammalian sterile 20‐like kinase 1 (MST1) and Yes‐associated protein (YAP) were investigated by RT‐PCR and Western blotting. Cell viability was detected by MTT assays. Cell cycle and cell apoptosis were determined by flow cytometry. Cell proliferative capacity was detected by colony formation assay. Nude mice xenograft models were established and the tumor sections were analyzed by immunohistochemistry (IHC) staining. Results The expression of MST1 was significantly down‐regulated in NKTCL tissues (n = 30) and cell lines, while the expression of YAP was significantly up‐regulated, and the phosphorylation of YAP was inhibited. Overexpression of MST1, knockdown of YAP, or verteporfin (VP) treatment could inhibit cell proliferation, and promote cell cycle arrest and apoptosis in NKTCL cells, while knockdown of MST1 and overexpression of YAP promoted cell proliferation. Additionally, Bcl‐2/Bax ratio and downstream effectors of Hippo signaling pathway (c‐myc, survivin, cyclinD1, CTGF, and TEAD) were significantly decreased when MST1 was overexpressed and YAP was knocked down or after VP treatment. Furthermore, our mice model demonstrated that activation of Hippo signal pathway suppressed the tumorigenesis of NKTCL. Conclusion The activation of Hippo signal pathway via overexpressing MST1 or down‐regulating YAP can inhibit the tumorigenesis of NKTCL.

BackgroundlncRNA-ATB plays an oncogenic role in various types of malignancies, but its involvement in papillary thyroid carcinoma (PTC) cells, which is a main type of thyroid cancer, is unknown.Material/MethodsA total of 76 patients with PTC and 28 people with normal physiological conditions were included in this study. Tumor tissues and adjacent healthy tissues were collected from PTC patients and blood was extracted from both patients and healthy controls. Expression of lncRNA-ATB in those tissues was detected by qRT-PCR. All patients were followed up for 5 years and diagnostic and prognostic values of serum lncRNA-ATB for PTC were investigated by ROC curve analysis and survival curve analysis, respectively. lncRNA-ATB overexpression PTC cell lines were established and effects of lncRNA-ATB overexpression on cell migration and invasion were investigated by Transwell cell migration and invasion assay, respectively. Effects of lncRNA-ATB overexpression on TGF-β1 expression were investigated by Western blot.ResultslncRNA-ATB expression level was higher in tumor tissues than in adjacent healthy tissues in most PTC patients. Serum level of lncRNA-ATB was higher in cancer patients than in healthy control. Serum lncRNA-ATB can be used to accurately predict PTC and its prognosis. lncRNA-ATB overexpression promoted tumor cell migration and invasion, lncRNA-ATB overexpression showed no significant effects on TGF-β1 expression, and TGF-β1 treatment increased the expression level of lncRNA-ATB.ConclusionUpregulation of lncRNA-ATB by TGF-β1 promotes migration and invasion of PTC cells.