β-Glucans are valuable functional polysaccharides distributed in nature, especially in the cell walls of fungi, yeasts, bacteria, and cereals. The unique features of β-glucans, such as water solubility, viscosity, molecular weight, and so on, have rendered them to be broadly applied in various food systems as well as in medicine to improve human health. Moreover, inhibition of cancer development could be achieved by an increase in immune system activity via β-glucans. β-glucans, which are part of a class of naturally occurring substances known as biological response modifiers (BRMs), have also shown evidence of being anti-tumorogenic, anti-cytotoxic, and anti-mutagenic. These properties make them attractive candidates for use as pharmaceutical health promoters. Along these lines, they could activate particular proteins or receptors, like lactosylceramide (LacCer), Dickin-1, complement receptor 3 (CR3), scavenge receptors (SR), and the toll-like receptor (TLR). This would cause the release of cytokines, which would then activate other antitumor immune cells, like macrophages stimulating neutrophils and monocytes. These cells are biased toward pro-inflammatory cytokine synthesis and phagocytosis enhancing the elicited immunological responses. So, to consider the importance of β-glucans, the present review introduces the structure characteristics, biological activity, and antitumor functions of fungal β-glucans, as well as their application.

Background. Over the past ten years, the incidence rate of papillary thyroid carcinoma (PTC) worldwide has been increasing rapidly year by year, with the incidence rate increasing 6% annually. PTC has become the malignant tumor with the highest growth rate in the world that fourteen PTC‐related mutant genes have been identified. Whether the BRAF^V600E mutation related to more aggressive clinicopathologic features and worse outcome in PTC remains variable and controversial. We aim to investigate the risk factors that may predict the BRAF^V600E mutation potential of these lesions and new prevention strategies in PTC patients. Methods. A total of 9,908 papillary thyroid carcinoma patients with average 74.6% BRAF^V600E mutations were analyzed (RevMan 5.3 software) in this study. The PubMed, Embase, and ISI Web of Science databases were systematically searched for works published through December 15, 2021. Results. The following variables were associated with an increased risk of BRAF^V600E mutation in PTC patients: age ≥ 45 years (OR = 1.39, 95%CI = 1.21–1.60, p < 0.00001), male gender (OR = 1.13, 95%CI = 0.99–1.28, p = 0.06), multifocality (OR = 1.22, 95%CI = 1.07–1.40, p = 0.004), lymph node metastasis (OR = 1.33, 95%CI = 0.79–2.23, p = 0.28), extrathyroidal extension + (OR = 1.61, 95%CI = 1.06–2.44, p = 0.03), vascular invasion + (OR = 2.04, 95%CI = 1.32–3.15, p = 0.001), and tumor node metastasis stage (OR = 1.61, 95%CI = 1.38–1.88, p < 0.00001). In addition, tumor size (>1 cm) (OR = 0.51, 95%CI = 0.32–0.81, p = 0.005) and distant metastasis (OR = 0.69, 95%CI = 0.22–2.21, p = 0.54) had no association or risk with BRAF^V600E mutation in PTC patients. Conclusion. Our systematic review identified the following significant risk factors of BRAF^V600E mutation in PTC patients: age (≥45 years), gender (male), multifocality, lymph node metastasis, vascular invasion, extrathyroidal extension, and advanced tumor node metastasis stage (stages III and IV). Tumor size (>1 cm) and distant metastasis do not appear to be correlated with BRAF^V600E mutation in PTC patients.

DNA methylation is a work of adding a methyl group to the 5th carbon atom of cytosine in DNA sequence under the catalysis of DNA methyltransferase (DNMT) to produce 5-methyl cytosine. Some current studies have elucidated the mechanism of lung cancer occurrence and causes of lung cancer progression and metastasis from the perspective of DNA methylation. Moreover, many studies have shown that smoking can change the methylation status of some gene loci, leading to the occurrence of lung cancer, especially central lung cancer. This review mainly introduces the role of DNA methylation in the pathogenesis, early diagnosis and screening, progression and metastasis, treatment, and prognosis of lung cancer, as well as the latest progress. We point out that methylation markers, sample tests, and methylation detection limit the clinical application of DNA methylation. If the liquid biopsy is to become the main force in lung cancer diagnosis, it must make efficient use of limited samples and improve the sensitivity and specificity of the tests. In addition, we also put forward our views on the future development direction of DNA methylation.

Optogenetic is a technique that combines optics and genetics to control specific neurons. This technique usually uses adenoviruses that encode photosensitive protein. The adenovirus may concentrate in a specific neural region. By shining light on the target nerve region, the photosensitive protein encoded by the adenovirus is controlled. Photosensitive proteins controlled by light can selectively allow ions inside and outside the cell membrane to pass through, resulting in inhibition or activation effects. Due to the high precision and minimally invasive, optogenetics has achieved good results in many fields, especially in the field of neuron functions and neural circuits. Significant advances have also been made in the study of many clinical diseases. This review focuses on the research of optogenetics in the field of neurobiology. These include how to use optogenetics to control nerve cells, study neural circuits, and treat diseases by changing the state of neurons. We hoped that this review will give a comprehensive understanding of the progress of optogenetics in the field of neurobiology.

The study aimed to identify the key active components in Silybum marianum (S. marianum) and determine how they protect against nonalcoholic fatty liver disease (NAFLD). TCMSP, DisGeNET, UniProt databases, and Venny 2.1 software were used to identify 11 primary active components, 92 candidate gene targets, and 30 core hepatoprotective gene targets in this investigation, respectively. The PPI network was built using a string database and Cytoscape 3.7.2. The KEGG pathway and GO biological process enrichment, biological annotation, as well as the identified hepatoprotective core gene targets were analyzed using the Metascape database. The effect of silymarin on NAFLD was determined using H&E on pathological alterations in liver tissues. The levels of liver function were assessed using biochemical tests. Western blot experiments were used to observe the proteins that were expressed in the associated signaling pathways on the hepatoprotective effect, which the previous network pharmacology predicted. According to the KEGG enrichment study, there are 35 hepatoprotective signaling pathways. GO enrichment analysis revealed that 61 biological processes related to the hepatoprotective effect of S. marianum were identified, which mainly involved in response to regulation of biological process and immune system process. Silymarin was the major ingredient derived from S. marianum, which exhibited the hepatoprotective effect by reducing the levels of ALT, AST, TC, TG, HDL-C, LDL-C, decreasing protein expressions of IL-6, MAPK1, Caspase 3, p53, VEGFA, increasing protein expression of AKT1. The present study provided new sights and a possible explanation for the molecular mechanisms of S. marianum against NAFLD. GRAPHICAL ABSTRACT

Background: Whether metformin is related to nonalcoholic fatty liver disease (NAFLD) is controversial. Our aim was to investigate the relationship between metformin and NAFLD that may predict the metformin potential of these lesions and new prevention strategies in NAFLD patients. Methods: The meta-analysis was analyzed by Revman 5.3 softwares systematically searched for works published through July 29, 2022. Network pharmacology research based on databases, Cytoscape 3.7.1 software and R software respectively. Results: The following variables were associated with metformin in NAFLD patients: decreased of alanine aminotransferase (ALT) level (mean difference [MD] = −10.84, 95% confidence interval [CI] = −21.85 to 0.16, P = .05); decreased of aspartate amino transferase (AST) level (MD = −4.82, 95% CI = −9.33 to −0.30, P = .04); decreased of triglyceride (TG) level (MD = −0.17, 95% CI = −0.26 to −0.08, P = .0002); decreased of total cholesterol (TC) level (MD = −0.29, 95% CI = −0.47 to −0.10, P = .003); decreased of insulin resistance (IR) level (MD = −0.42, 95% CI = −0.82 to −0.02, P = .04). In addition, body mass index (BMI) (MD = −0.65, 95% CI = −1.46 to 0.16, P = .12) had no association with metformin in NAFLD patients. 181 metformin targets and 868 NAFLD disease targets were interaction analyzed, 15 core targets of metformin for the treatment of NAFLD were obtained. The effect of metformin on NAFLD mainly related to cytoplasm and protein binding, NAFLD, hepatitis B, pathway in cancer, toll like receptor signaling pathway and type 2 diabetes mellitus (T2DM). The proteins of hypoxia inducible factor-1 (HIF1A), nuclear factor erythroid 2-related factor (NFE2L2), nitric oxide synthase 3 (NOS3), nuclear receptor subfamily 3 group C member 1 (NR3C1), PI3K catalytic subunit alpha (PIK3CA), and silencing information regulator 2 related enzyme 1 (SIRT1) may the core targets of metformin for the treatment of NAFLD. Conclusion: Metformin might be a candidate drug for the treatment of NAFLD which exhibits therapeutic effect on NAFLD patients associated with ALT, AST, TG, TC and IR while was not correlated with BMI. HIF1A, NFE2L2, NOS3, NR3C1, PIK3CA, and SIRT1 might be core targets of metformin for the treatment of NAFLD.