The structure of anthocyanins and the copigmentation by common micromolecular copigments: A review.

Under natural physiological conditions, anthocyanins can keep bright and stable color for a long time due to the relatively stable acid-base environment of plant vacuoles and the copigmentation from various copigment substances, such as polyphenols, nucleotides, metallic ions and other substances. Therefore, the copigmentation caused by copigments is considered an effective way to stabilize anthocyanins against adverse environmental conditions. This is attributed to the covalent and noncovalent interactions between colored forms of anthocyanins (flavylium ions and quinoidal bases) and colorless or pale yellow organic molecules (copigments). These interactions are usually manifested in both hyperchromic effect and bathochromic shifts. In addition to making anthocyanins more stable, the copigmentation also could make an important contribution to the diversification of their tone. Based on the molecular structure of anthocyanins, this review focuses on the interaction mode of auxochrome groups or copigments with anthocyanins and their effects on the chemical and color stability of anthocyanins.

[Mechanism of miR-186-5p Regulating PRKAA2 to Promote Ferroptosis 
in Lung Adenocarcinoma Cells].

BACKGROUND: Lung adenocarcinoma (LUAD) is the most common type of non-small cell lung cancer, and any change of miRNAs expression will affect the degree of target regulation, thus affecting intracellular homeostasis. This study verified that miR-186-5p could inhibit the proliferation, migration and invasion of LUAD cells by regulating PRKAA2. METHODS: Previous investigations found that the expression of miR-186-5p was markedly suppressed in LUAD. Bioinformatics method is used to predict the target protein related to ferroptosis downstream and inquire about its expression level in LUAD and its influence on the survival of patients. Double luciferase verified the binding site of PRKAA2 and miR-186-5p. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot were used to detect the expression of PRKAA2. The effects of miR-186-5p of LUAD cells as well as the mechanism by which miR-186-5p inhibits Fer-1's sensitivity to ferroptosis were confirmed by EdU, Transwell, and scratch assays. The effect of miR-186-5p on the amount of reactive oxygen species (ROS) in LUAD cells was discovered using ROS experiment. Malondialdehyde (MDA) and glutathione (GSH) experiments were used to detect the effects of miR-186-5p and PRKAA2 on ferroptosis index of LUAD cells. The concentration of lipid ROS (L-ROS) in LUAD cells were measured using the L-ROS tests to determine the effects of miR-186-5p and PRKAA2. RESULTS: The expression of PRKAA2 is up-regulated, and a high level of PRKAA2 expression was associated with a poor prognosis for patients with LUAD. Overexpression of miR-186-5p decreased the gene and protein expression of PRKAA2. By promoting ferroptosis, miR-186-5p overexpression prevented lung cancer cells from proliferating, invading, and migrating. ROS could be produced in higher amounts in LUAD cells due to miR-186-5p. Overexpression of miR-186-5p and knockdown PRKAA2 up-regulated MDA content and reduced GSH content in LUAD cells, respectively. miR-186-5p could increase the content of L-ROS and promote the ferroptosis sensitivity of LUAD cells by targeting PRKAA2. CONCLUSIONS: miR-186-5p promotes ferroptosis of LUAD cells through targeted regulation of PRKAA2, thus inhibiting the proliferation, invasion and migration of LUAD.
.

Effects of fine substance content in soil substrate on the formation of artificial cyanobacteria crusts.

The use of artificial cyanobacteria crusts is one of the effective methods to prevention and control of desertification. Soil fine substance is one of the important factors limiting the colonization and growth of artificial cyanobacteria crusts. We compared the growth of artificial cyanobacterial crusts with different fine substance contents by setting the volume ratios of fine substance to quicksand as 0:1, 1:1, 2:1, 4:1 and 1:0. The results showed that the cover of artificial cyanobacteria crusts increased gradually with the increases of fine substance contents, while the contents of chlorophyll a and extracellular polysaccharide firstly increased and then decreased slightly. The optimum growth of artificial cyanobacterial crusts was achieved under the treatment of 4:1 ratio. Under such treatment after 60 days of incubation, artificial cyanobacteria crusts cover was 70%, and the contents of chlorophyll a, loosely bound exopolysaccharide (LB-EPS), tightly bound exopolysaccharide (TB-EPS), and glycocalyx exopolysaccharide (G-EPS) were 17.5, 70.0, 175.0, and 200.0 µg·cm-2, respectively. Increasing the amount of cyanobacteria under the condition of low fine substance content could promote the formation and growth of artificial cyanobacterial crusts (0.5 g of cyanobacteria per petri dish was the optimal). It could provide a new idea for the large-scale culture of artificial cyanobacterial crusts inoculum.

LncRNA-AC009948.5 promotes invasion and metastasis of lung adenocarcinoma by binding to miR-186-5p.

Background: Long non-coding RNAs (LncRNAs) has been confirmed to play a crucial role in the development and progression of various cancer types. Here we evaluated the expression profiles of LncRNAs in Lung adenocarcinoma (LUAD) tissues and identified a novel LncRNA, termed LncRNA-AC009948.5. However, the role and potential molecular mechanisms of this novel LncRNA in LUAD carcinogenesis is unknown. Methods: Regarding the public databases and based on integrating bioinformatics analyses, we determined whether LncRNA-AC009948.5 exerts its oncogenic functions via sponging miR-186-5p in LUAD. Furthermore, we determined whether NCAPG2 was a downstream target of miR-186-5p. Moreover, the expression level and biological function of LncRNA-AC009948.5 in LUAD were determined by qRT-PCR, cell apoptosis, Edu, transwell, wound healing and western blot assays. Besides, xenograft mice were established for validation. We explored the expression of LncRNA-AC009948.5 and its roles in the prognosis of LUAD. Results: LncRNA expression microarray data indicate that LncRNA-AC009948.5 is upregulated in LUAD samples. The present study confirmed the upregulation of LncRNA-AC009948.5 in LUAD tissues and cells. Encreased expression of LncRNA-AC009948.5 was correlated with tumor size, lymph nodes, distant metastasis and histological grade, and poor prognosis.LncRNA-AC009948.5 knockdown significantly inhibited cell proliferation, migration, and invasion in vitro, as well as tumorigenesis and metastasis in vivo. Conversely, LncRNA-AC009948.5 upregulated had opposite effects. Mechanistically, we elucidated that LncRNA-AC009948.5 could directly bind to miR-186-5p and subsequently suppress expression of the target gene of NCAPG2. Conclusions: LncRNA-AC009948.5 promotes lung adenocarcinoma cells metastasis via the miR-186-5p/NCAPG2 axis and activation of the EMT process. Which may serve as potential targets for the treatment of LUAD in the future.

[miR-30b-3p Inhibits the Proliferation and Invasion of Lung Adenocarcinoma 
by Targeting COX6B1].

BACKGROUND: Lung adenocarcinoma (LUAD) is the most common clinical histological subtype of lung cancer and microRNAs (miRNAs) are a type of small non-coding RNAs which play a central role in cells. miR-30b-3p plays a key effect in many types of carcinoma, but there is still very little research on how it works in lung adenocarcinoma. The role and mechanism of miR-30b-3p in the proliferation and invasion of LUAD were explored in this study, to provide new targets for inhibiting the proliferation and invasion of LUAD. METHODS: NCBI database was used to screen out miRNA with obvious differential expression, and the differential expression and survival curve were searched by StarBase database. Real-time fluorescence quantitative polymerase chain reaction (qRT-PCR) was used to detect the relative expression of miR-30b-3p in each lung adenocarcinoma cell line. 5-ethynyl-2'-deoxyuridine (EdU) cell proliferation assay and Transwell invasion assay were used to detect the proliferation and invasion of A549 cells in each group. The target genes of miR-30b-3p were determined by the target gene prediction websites. Western blot assay was used to detect the expression of COX6B1 in each group of A549 cells. Double luciferase assay was used to verify the targeted binding relationship between miR-30b-3p and COX6B1. RESULTS: The expression of miR-30b-3p in lung adenocarcinoma tissues and lung adenocarcinoma cells was downregulated (P<0.05). Low expression levels of miR-30b-3p were associated with poor prognosis in patients with lung adenocarcinoma (P=0.005,8). Overexpression of miR-30b-3p could inhibit the proliferation and the invasion of lung adenocarcinoma cells (P<0.05). Double luciferase assay proved that miR-30b-3p could target and bind to COX6B1 (P<0.05). Western blot analysis showed that the overexpression of miR-30b-3p could downregulate the expression of COX6B1 in A549 cells (P<0.05). EdU cell proliferation assay and Transwell invasion assay showed that the overexpression of miR-30b-3p could reverse the promoting effect of upregulation of COX6B1 on proliferation and invasion in lung adenocarcinoma cells (P<0.05). CONCLUSIONS: miR-30b-3p acts as a tumor suppressor gene in lung adenocarcinoma, and it can inhibit the proliferation and invasion of lung adenocarcinoma by targeting the expression of COX6B1.

Identification of miRNA-Mediated Subpathways as Prostate Cancer Biomarkers Based on Topological Inference in a Machine Learning Process Using Integrated Gene and miRNA Expression Data.

Accurately identifying classification biomarkers for distinguishing between normal and cancer samples is challenging. Additionally, the reproducibility of single-molecule biomarkers is limited by the existence of heterogeneous patient subgroups and differences in the sequencing techniques used to collect patient data. In this study, we developed a method to identify robust biomarkers (i.e., miRNA-mediated subpathways) associated with prostate cancer based on normal prostate samples and cancer samples from a dataset from The Cancer Genome Atlas (TCGA; n = 546) and datasets from the Gene Expression Omnibus (GEO) database (n = 139 and n = 90, with the latter being a cell line dataset). We also obtained 10 other cancer datasets to evaluate the performance of the method. We propose a multi-omics data integration strategy for identifying classification biomarkers using a machine learning method that involves reassigning topological weights to the genes using a directed random walk (DRW)-based method. A global directed pathway network (GDPN) was constructed based on the significantly differentially expressed target genes of the significantly differentially expressed miRNAs, which allowed us to identify the robust biomarkers in the form of miRNA-mediated subpathways (miRNAs). The activity value of each miRNA-mediated subpathway was calculated by integrating multiple types of data, which included the expression of the miRNA and the miRNAs' target genes and GDPN topological information. Finally, we identified the high-frequency miRNA-mediated subpathways involved in prostate cancer using a support vector machine (SVM) model. The results demonstrated that we obtained robust biomarkers of prostate cancer, which could classify prostate cancer and normal samples. Our method outperformed seven other methods, and many of the identified biomarkers were associated with known clinical treatments.

Bibliometric Analysis of Research Articles on Pain in the Elderly Published from 2000 to 2019.

BACKGROUND: Given the rapid growth of the global aging population, pain has become an unneglectable concern amongst the elderly. The quantity of scientific research outputs on pain in the elderly has increased over time, but only a small number of studies have used bibliometric methods to analyze scientific research in this field. This paper aimed to analyze scientific research on pain in the elderly published from 2000 to 2019 in a systematic manner using bibliometric methods. METHODS: Articles on pain in the elderly published from 2000 to 2019 were retrieved from the Web of Science (WoS). Abstracts were coded on the basis of predetermined items (eg, type of article, topic, type of subjects, pain characteristics), and relevant information on the first author, citation scores, and article keywords were collected. RESULTS: A total of 2105 articles were included in this study. Statistical analysis revealed that the publication of articles on pain in the elderly increased in frequency over time (P<0.001). Most of the publications were original articles. Amongst the countries identified, the United States published the largest number of papers on this topic. Pain characteristics (50.21%), pain intervention (35.68%), and pain assessment (9.69%) were the main topics of research on geriatric pain. Back pain (12.30%) appeared to be the most popular pain type described in the included papers. CONCLUSION: This work provides researchers with an in-depth understanding of pain in the elderly by evaluating relevant publications in the past two decades. Researchers in this field are warranted to explore future directions on geriatric pain such as the transition from acute pain to chronic pain and the underlying mechanisms of pain in the elderly.