Ecological application of wavelet analysis in the scaling of spatial distribution patterns of Ceratoides ewersmanniana

Ecological experiments are usually conducted on small scales, but the ecological and environmental issues are usually on large scales. Hence, there is a clear need of scaling. Namely, when we deal with patterns and processes on larger scales, a special connection needs to be established on the small scales that we are familiar with. Here we presented a wavelet analysis method that could build relationships between spatial distribution patterns on different scales. With this method, we also studied how spatial heterogeneity and distribution patterns changed with the scale. We investigated the distribution and the habitat of C. ewersmanniana in two plots (200 m × 200 m; the distance between these two plots is 15 km) at Mosuowan desert. The results demonstrated that spatial heterogeneity and distribution patterns were incorporated into larger scales when the wavelet scale varied from one (5 m) to four (20 m). However, if the wavelet scale was above five (25 m), the spatial distribution patterns varied placidly, the oscillation frequency of landforms stabilized at 110 m, and the dynamic quantity period of C. ewersmanniana stabilized at 115–125 m. We also identified signal mutation points with wavelet analysis and verified the heterogeneity degree of local space with position variance. We found that position variance decomposed the distribution patterns on large scales into small sampling plots, and the position with the largest variance also had the strongest heterogeneity. In a word, the wavelet analysis method could scale-up spatial distribution patterns and habitat heterogeneity. With this method and other methods derived from this one, such as wavelet scale, wavelet variance, position variance and extremely direct-viewing graphs, wavelet analysis could be widely applied in solving the scaling problem in ecological and environmental studies.     

Melatonin alleviates the deterioration of oocytes from mice subjected to repeated superovulation

Induction of repeated superovulation with exogenous hormones is widely used in assisted reproductive technology (ART). Though it is generally safe, emerging evidence has indicated that repeated superovulation may compromise oocyte quality. However, few studies have explored how to ameliorate such impairment. Because melatonin has beneficial influences on oocytes in various detrimental environments, we aimed to explore whether melatonin could protect mouse oocytes after repeated superovulation. We found that repeated superovulation markedly reduced meiotic maturation and disrupted spindle organization and chromosome alignment. Furthermore, we observed reduced mitochondrial content and enhanced early apoptosis in oocytes from mice subjected to repeated superovulation. In addition, 5-methylcytosine (5mc) fluorescence intensity was lower in oocytes from experimental mice than in those from control mice, indicating that repeated superovulation disrupts genomic DNA methylation, and elevations in reactive oxygen species levels indicated that repeated superovulation also induces oxidative stress. Conversely, melatonin administration improved oocyte maturation and attenuated the observed defects. Interestingly, supplementation with melatonin during in vitro maturation had the same protective effects on oocytes as in vivo melatonin administration. In summary, our results show that melatonin can improve oocyte quality after repeated superovulation and thus provide a potential strategy to improve ART efficiency.     

Long noncoding RNA CPS1-IT1 suppresses melanoma cell metastasis through inhibiting Cyr61 via competitively binding to BRG1

Long noncoding RNA CPS1-IT1 is recently recognized as a tumor suppressor in several cancers. Here, we investigate the role of CPS1-IT1 in human melanoma. Presently, our study reveals the low expression of CPS1-IT1 in human melanoma tissues and cell lines, which is significantly associated with metastasis and tumor stage. Besides, the potential of CPS1-IT1 as a prognosis-predictor is strongly indicated. Functionally, CPS1-IT1 overexpression inhibits cell migration, invasion, epithelial–mesenchymal transition, and angiogenesis in melanoma cells. CYR61, an angiogenic factor that participates in tumor metastasis as well as a recognized oncogene in melanoma, is shown to be confined under CPS1-IT1 overexpression in melanoma cells. Furthermore, enforced expression of Cyr61 in CPS1-IT1-silenced melanoma cells dramatically normalized the protein level of Cyr61 and that of its downstream targets vascular endothelial growth factor and matrix metalloproteinase-9, as well as the repressive effect of CPS1-IT1 overexpression on melanoma cell metastasis. BRG1, a core component of SWI/SNF complex, is implied to interact with both CPS1-IT1 and Cyr61 in melanoma cells. Moreover, CPS1-IT1 negatively regulates Cyr61 expression by blocking the binding of BRG1 to Cyr61 promoter. Jointly, CPS1-IT1 controls melanoma metastasis through impairing Cyr61 expression via competitively binding with BRG1, uncovering a novel potential therapeutic and prognostic biomarker for patients with melanoma.     

Identification of EPHX2 and RMI2 as two novel key genes in cervical squamous cell carcinoma by an integrated bioinformatic analysis

Cervical cancer is the fourth most common malignancy in women worldwide and cervical squamous cell carcinoma (CESC) is the most common histological type of cervical cancer. The dysregulation of genes plays a significant role in cancer. In the present study, we screened out differentially expressed genes (DEGs) of CESC in the GSE63514 data set from the Gene Expression Omnibus database. An integrated bioinformatics analysis was used to select hub genes, as well as to investigate their related prognostic signature, functional annotation, methylation mechanism, and candidate molecular drugs. As a result, a total of 1907 DEGs were identified (944 were upregulated and 963 were downregulated). In the protein–protein interaction network, three hub modules and 30 hub genes were identified. And two hub modules and 116 hub genes were screened out from four CESC-related modules by the weighted gene coexpression network analysis. The gene ontology term enrichment analysis and Kyoto encyclopedia of genes and genomes pathway analysis were performed to better understand functions and pathways. Genes with a significant prognostic value were found by prognostic signature analysis. And there were five genes (EPHX2, CHAF1B, KIAA1524, CDC45, and RMI2) identified as significant CESC-associated genes after expression validation and survival analysis. Among them, EPHX2 and RMI2 were noted as two novel key genes for the CESC-associated methylation and expression. In addition, four candidate small molecule drugs for CESC (camptothecin, resveratrol, vorinostat, and trichostatin A) were defined. Further studies are required to explore these significant CESC-associated genes for their potentiality in diagnosis, prognosis, and targeted therapy.     

一株虾池来源的螺旋拟柱孢藻藻株的分离鉴定及重金属离子Cu~(2+)、Cd~(2+)和Pb~(2+)对其生长的影响

【目的】探讨凡纳滨对虾养殖水体中入侵蓝藻拟柱孢藻的生长生理特性。【方法】从汕头澄海人工对虾养殖池分离纯化藻株,通过形态及其16SrRNA基因鉴定,之后在CT与BG11两种蓝藻通用培养基的基础上优化最佳培养条件,最后分析了不同浓度的3种重金属离子即Cu~(2+)(0–0.8 mg/L)、Cd~(2+)(0–4 mg/L)和Pb~(2+)(0–80 mg/L)对藻株生长的影响。【结果】澄海虾池来源的分离纯化藻株形态呈卷曲螺旋型,16S rRNA基因序列与多株其他来源的拟柱孢藻相似度均达98%以上。实验室培养,藻株最佳生长状态的培养条件是在BG11培养基的基础上调整氮浓度及氮磷比分别为N 62 mg/L,N︰P=9︰1,在此条件下,藻丝生物量可达(0.632±0.170)×107/L,藻丝比平均生长速率最高为(0.063±0.001)/d。本分离藻株活体对重金属Cu~(2+)、Cd~(2+)和Pb~(2+)具有一定的耐受性,其耐受浓度范围分别为0–0.2、0–0.5和1–40 mg/L,其中,Cu~(2+)和Cd~(2+)对藻的生长具有抑制作用,而且此抑制作用随着金属离子剂量的增加及作用时间的延长更加显著,Cu~(2+)和Cd~(2+)对藻体的半数抑制浓度(96 h EC50)分别为0.125和0.551 mg/L;而浓度范围为0–80 mg/L的Pb~(2+)对藻体的生长则表现为低剂量(≤40 mg/L)呈促进,高剂量(≥80 mg/L)则抑制。【结论】从凡纳滨对虾养殖池中分离鉴定出一株形态呈螺旋型的拟柱孢藻,命名为螺旋拟柱孢藻(Cylindrospermopsis raciborskii helix),本藻株活体能够在一定浓度的Cu~(2+)、Cd~(2+)和Pb~(2+)中生长,为螺旋拟柱孢藻活藻生物吸附重金属离子而改善虾池水体环境提供了可能性。     

Sodium butyrate ameliorates lipopolysaccharide-induced cow mammary epithelial cells from oxidative stress damage and apoptosis

This study investigated the molecular mechanism by which sodium butyrate (NaB) causes oxidative stress damage induced by lipopolysaccharide (LPS) on cow mammary epithelial cells (MAC-T). We found that NaB significantly increased the activities of antioxidant enzymes, including superoxide dismutase, glutathione peroxidase, catalase, peroxidase, and total antioxidant capacity and decreased the reactive oxygen species production in LPS-induced MAC-T cells. NaB attenuated protein damage and reduced apoptosis in LPS-induced MAC-T cells. The messenger RNA (mRNA) levels of caspase-3, caspase-9, and Bax decreased, while the Bcl-2 mRNA level increased in LPS-induced MAC-T cells treated with NaB. Our results showed that NaB treatment increased the phosphoinositide 3-kinase (PI3K) and phospho-AKT (P-AKT) protein levels, whereas it decreased the Bax, caspase-3, and caspase-9 protein levels in LPS-induced MAC-T cells. However, the increase in PI3K and P-AKT protein levels and the decrease in Bax, caspase-3, and caspase-9 protein levels induced by NaB treatment were reversed when the cells were pretreated with LY294002 (PI3K inhibitor). These results indicate that NaB ameliorates LPS-induced oxidative damage by increasing antioxidative enzyme activities and ameliorating protein damage in MAC-T cells. In addition, NaB decreased apoptosis by inhibiting caspase-3, caspase-9, and Bax protein levels, and this action was mainly achieved via activation of the PI3K/AKT signaling pathways in LPS-induced MAC-T cells. These results provide substantial information for NaB as a chemical supplement to treat oxidative stress and its related diseases in ruminants.     

Ipriflavone as a non‐steroidal glucocorticoid receptor antagonist ameliorates diabetic cognitive impairment in mice

Diabetic cognitive impairment (DCI) is a common diabetic complication with hallmarks of loss of learning ability and disorders of memory and behavior. Glucocorticoid receptor (GR) dysfunction is a main reason for neuronal impairment in brain of diabetic patients. Here, we determined that ipriflavone (IP) a clinical anti‐osteoporosis drug functioned as a non‐steroidal GR antagonist and efficiently ameliorated learning and memory dysfunction in both type 1 and 2 diabetic mice. The underlying mechanism has been intensively investigated by assay against the diabetic mice with GR‐specific knockdown in the brain by injection of adeno‐associated virus (AAV)‐ePHP‐si‐GR. IP suppressed tau hyperphosphorylation through GR/PI3K/AKT/GSK3β pathway, alleviated neuronal inflammation through GR/NF‐κB/NLRP3/ASC/Caspase‐1 pathway, and protected against synaptic impairment through GR/CREB/BDNF pathway. To our knowledge, our work might be the first to expound the detailed mechanism underlying the amelioration of non‐steroidal GR antagonist on DCI‐like pathology in mice and report the potential of IP in treatment of DCI.