With the advent of exploration in finding new sources for treating different diseases, one possible natural source is from marine algae. Having an array of potential benefits, researchers are interested in the components which comprise one of these activities. This can lead to the isolation of active compounds with biological activities, such as antioxidation of free radicals, anti-inflammation, antiproliferation of cancer cells, and anticoagulant to name a few. One of the compounds that are isolated from marine algae are sulfated polysaccharides (SPs). SPs are complex heterogenous natural polymers with an abundance found in different species of marine algae. Marine algae are known to be one of the most important sources of SPs, and depending on the species, its chemical structure varies. This variety has important physical and chemical components and functions which has gained the attention of researchers as this contributes to the many facets of its pharmacologic activity. In this review, recent pharmacologic application potentials and updates on the use of SPs from marine algae are discussed.

Delineation of physical factors that contribute to earthquake triggering is a challenging issue in seismology. We analyze hydrological modulation of seismicity in Taiwan using groundwater level data and GNSS time series. In western Taiwan, the seismicity rate reaches peak levels in February to April and drops to its lowest values in July to September, exhibiting a direct correlation with annual water unloading. The elastic hydrological load cycle may be the primary driving mechanism for the observed synchronized modulation of earthquakes, as also evidenced by deep earthquakes in eastern Taiwan. However, shallow earthquakes in eastern Taiwan (<18 km) are anticorrelated with water unloading, which is not well explained by either hydrological loading, fluid transport, or pore pressure changes and suggests other time-dependent processes. The moderate correlation between stacked monthly trends of large historic earthquakes and present-day seismicity implies a modestly higher seismic hazard during the time of low annual hydrological loading.

The phenolic acid and flavonoid profiles in yam peel extract were determined by HPLC. Quercetin, hesperidin, and apigenin were predominant components in yam peel extract. Male Wistar rats were orally treated with yam peel extract (100.02, 266.72, and 433.42 mg/kg) or silymarin (200 mg/kg) daily, with administration of CCl4 (1 mL/kg, 20% CCl4 in olive oil) twice a week. Yam peel extract for 8 weeks significantly reduced the impact of CCl4 toxicity on the serum markers of liver damage, aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP). The overall potential of the antioxidant system was significantly enhanced by the yam peel extract supplements as the plasma and hepatic thiobarbituric acid reactive substances (TBARS) levels were lowered, whereas the hepatic superoxide dismutase (SOD) and catalase (CAT) activities and glutathione peroxidase (GSH-Px) protein level were elevated. Yam peel extract decreased the level of nitric oxide (NO) production, tumor necrosis factor-alpha (TNF-α), and nuclear factor-kappa B (NF-κB) in CCl4. These results point out that yam peel extract can inhibit lipid peroxidation, enhance the activities of antioxidant enzymes, and decrease the TNF-α/NF-κB level, nitric oxide production, and inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expressions. Therefore, it was speculated that yam peel extract protects rats from liver damage through its anti-inflammation capacity.

Long noncoding RNAs (lncRNAs) play crucial roles in carcinogenesis. Myocardial infarction-associated transcript (MIAT), originally isolated as a candidate gene for myocardial infarction, has been found to act as an oncogene in chronic lymphocytic leukaemias and neuroendocrine prostate cancer (NEPC); however, little is known about its expression pattern, biological function, and underlying mechanism in non-small cell lung cancer (NSCLC). In this study, we observed that MIAT expression was upregulated in NSCLC, and its overexpression was associated with advanced tumor stage. Moreover, MIAT knockdown decreased cell proliferation, migration, invasion, and cell cycle arrested in G1 phase. Mechanistic investigation revealed that MIAT could interact with histone methyltransferase mixed-lineage leukemia (MLL). MIAT silencing impeded the binding of MLL on the matrix metalloproteinase 9 (MMP9) promoter region and epigenetically reduced MMP9 transcriptional activity. Overall, our findings suggest that MIAT expression is associated with NSCLC and may be one of the critical targets in progression and metastasis in NSCLC.