Spatial Variability and Co-acclimation of Phytoplankton and Bacterioplankton Communities in the Pearl River Estuary, China

Phytoplankton and bacterioplankton play significant roles in estuarine systems. It is important to demonstrate the spatial variability of bacterial and microalgal communities and understand the co-acclimation of these organisms to different environmental factors. In this study, MiSeq sequencing and morphological identification were applied to analyze the variations in bacterial and microalgal communities in the Pearl River Estuary, respectively. Molecular ecological network analysis was used to investigate the potential interactions between microalgae and bacteria and illustrate the responses of these interactions to environmental gradients. The results revealed that microalgal/bacterial communities in freshwater samples were distinct from those in mesohaline water samples. Microalgae affiliated to the genus Skeletonema dominated the mesohaline water phytoplankton communities, while Melosira was the more abundant genus in freshwater communities. Actinobacteria, Alphaproteobacteria, Betaproteobacteria, and Acidimicrobiia dominated bacterial communities in freshwater samples, while Gammaproteobacteria, Bacilli, and Synechococcophycideae were more abundant in mesohaline water samples. Tightly correlations were observed between phytoplankton and bacterioplankton. These interactions were regarded to be key factors in shaping the community structures. Further, the KEGG database and PICRUSt were used to predict the functions of bacterioplankton in the process of nitrogen cycling. The results indicated that denitrification could play an important role in nitrogen loss and might alleviate the eutrophication in the Pearl River Estuary. Collectively, the results in this study revealed that substantial changes in phytoplankton and bacterioplankton communities were correlated with the gradients of environmental parameters in the Pearl River Estuary. The results also demonstrated that the interactions between phytoplankton and bacterioplankton were important for these organisms to acclimate to changing environments

Prevalence and Genotypic Distribution of Hepatitis C Virus in Peshawar KPK, Pakistan

This present study was planned to obtain an up-to-date picture of Hepatitis C virus (HCV) infection and its genotypes distribution in Peshawar, Khyber Pakhtunkhwa, Pakistan, as well as of the relationship between HCV genotypes and demographic and clinical parameters, and the risk factors in patients with an HCV subtype. Samples (blood) from 1978 individuals were collected and were tested using a strip-based method called the immunochromatographic test (ICT) for the existence of antibodies against HCV. It was observed that 158 of the 1978 individuals (7.9%) harbored antibodies in their blood against HCV, among which the female percentage (53.2%) was higher than that of the male (46.8%). Among the different age groups, the highest number of incidences of HCV antibodies was found in the age group of 31–40 years (26.6%). ICT positive samples were further screened by polymerase chain reaction (PCR) to determine the existence of active HCV-RNA, and it was found that 6.21% (123) of the total population (1978) tested, was positive, among which the female rate (56.91%) was observed to be higher than that of the male (43.09%). The highest incidence recorded was in the age group of 41–50 years (33.3%). HCV RNA positive individuals were genotyped: genotype 3a (45.5%) was dominant among the other detected genotypes, followed by 1a (11.4%), 3b (4.9%), and 2a (4.1%). It was concluded that the highest prevalence of HCV was found in females, and that the dominant genotype of the screened individuals was 3a genotype

Autophagy-mediated degradation of NOTCH1 intracellular domain controls the epithelial to mesenchymal transition and cancer metastasis

Backgound Autophagy controls levels of cellular components during normal and stress conditions; thus, it is a pivotal process for the maintenance of cell homeostasis. In cancer, autophagy protects cells from cancerous transformations that can result from genomic instability induced by reactive oxygen species or other damaged components, but it can also promote cancer survival by providing essential nutrients during the metabolic stress condition of cancer progression. However, the molecular mechanism underlying autophagy-dependent regulation of the epithelial to mesenchymal transition (EMT) and metastasis is still elusive. Methods The intracellular level of NOTCH1 intracellular domain (NICD) in several cancer cells was studied under starvation, treatment with chloroquine or ATG7-knockdown. The autophagy activity in these cells was assessed by immunocytochemistry and molecular analyses. Cancer cell migration and invasion under modulation of autophagy were determined by in vitro scratch and Matrigel assays. Results In the study, autophagy activation stimulated degradation of NICD, a key transcriptional regulator of the EMT and cancer metastasis. We also found that NICD binds directly to LC3 and that the NICD/LC3 complex associates with SNAI1 and sequestosome 1 (SQSTM1)/p62 proteins. Furthermore, the ATG7 knockdown significantly inhibited degradation of NICD under starvation independent of SQSTM1-associated proteasomal degradation. In addition, NICD degradation by autophagy associated with the cellular level of SNAI1. Indeed, autophagy inhibited nuclear translocation of NICD protein and consequently decreased the transcriptional activity of its target genes. Autophagy activation substantially suppressed in vitro cancer cell migration and invasion. We also observed that NICD and SNAI1 levels in tissues from human cervical and lung cancer patients correlated inversely with expression of autophagy-related proteins. Conclusions These findings suggest that the cellular level of NICD is regulated by autophagy during cancer progression and that targeting autophagy-dependent NICD/SNAI1 degradation could be a strategy for the development of cancer therapeutics

On the upside or flipside: Where is venture capital positioned in the era of digital disruptions?

Recent studies have found that disruptive technologies, such as FinTech, have the potential to overturn existing business models and overthrow incumbents. These studies have demonstrated that newly emerging digital platforms financing early-stage ventures threaten traditional venture capital (VC). We argue that, conversely, VC benefits from advances in information and communication technology (ICT), as ICT fosters entrepreneurship and mitigates agency issues in VC deals. This paper examines the impact of digitization on VC investments from 23 European countries spanning 2007–2019 using a dynamic panel two-step system generalized method of moments (GMM) estimation technique. The results show that the factors “ICT penetration” (a general measure of societal internet and computer access and use) and “digital economy” (a measure of ICT-powered economic activity) exert significant and positive effects on early-stage, later-stage, and total VC investments. Moreover, availability of bank credit moderates the effect of digital economy on VC investment. Finally, this study reveals that it is digital entrepreneurship (as reflected in our “digital economy” measure), and not total entrepreneurial activity, that attracts VC investment. We conclude that the VC industry is aligned with rather than threatened by the newly emerging digital environment. The empirical results are robust to different control variables and data sources. This paper offers useful implications for policy and contributes to the literature on digital entrepreneurship and venture capital

Proteogenomics: New Emerging Technology

The term proteogenomics is basically the integration of proteomics with genomics and transcriptomics. Today, proteogenomics is developing on the way to combined understanding about overall cellular functions. At present globally, structure of genes, expression of genes (in the form of mRNA synthesis), synthesis of proteins (translation of mRNA) and post-translational modification (structural modification of proteins) have turn out to be technically practicable and act as a novel viewpoint to molecular procedures. Current research has proved the importance of proteogenomics technology in cancer for studying molecular signature of tumors particularly in human beings, and its treatment and prevention. Proteogenomics is not restricted to oncology but it also plays a vital role in other areas of life sciences and biomedicines and anticipation can make up these areas. Here in this minireview, we will discuss the latest progress made in recent years, challenges and viewpoints about proteogenomics technology

Transcriptional Regulation of Autophagy Genes via Stage-Specific Activation of CEBPB and PPARG during Adipogenesis: A Systematic Study Using Public Gene Expression and Transcription Factor Binding Datasets

Autophagy is the cell self-eating mechanism to maintain cell homeostasis by removing damaged intracellular proteins or organelles. It has also been implicated in the development and differentiation of various cell types including the adipocyte. Several links between adipogenic transcription factors and key autophagy genes has been suggested. In this study, we tried to model the gene expression and their transcriptional regulation during the adipocyte differentiation using high-throughput sequencing datasets of the 3T3-L1 cell model. We applied the gene expression and co-expression analysis to all and the subset of autophagy genes to study the binding, and occupancy patterns of adipogenic factors, co-factors and histone modifications on key autophagy genes. We also analyzed the gene expression of key autophagy genes under different transcription factor knockdown adipocyte cells. We found that a significant percent of the variance in the autophagy gene expression is explained by the differentiation stage of the cell. Adipogenic master regulators, such as CEBPB and PPARG target key autophagy genes directly. In addition, the same factor may also control autophagy gene expression indirectly through autophagy transcription factors such as FOXO1, TFEB or XBP1. Finally, the binding of adipogenic factors is associated with certain patterns of co-factors binding that might modulate the functions. Some of the findings were further confirmed under the knockdown of the adipogenic factors in the differentiating adipocytes. In conclusion, autophagy genes are regulated as part of the transcriptional programs through adipogenic factors either directly or indirectly through autophagy transcription factors during adipogenesis

Control of the Epithelial-to-Mesenchymal Transition and Cancer Metastasis by Autophagy-Dependent SNAI1 Degradation

Autophagy, an intracellular degradation process, is essential for maintaining cell homeostasis by removing damaged organelles and proteins under various conditions of stress. In cancer, autophagy has conflicting functions. It plays a key role in protecting against cancerous transformation by maintaining genomic stability against genotoxic components, leading to cancerous transformation. It can also promote cancer cell survival by supplying minimal amounts of nutrients during cancer progression. However, the molecular mechanisms underlying how autophagy regulates the epithelial-to-mesenchymal transition (EMT) and cancer metastasis are unknown. Here, we show that starvation-induced autophagy promotes Snail (SNAI1) degradation and inhibits EMT and metastasis in cancer cells. Interestingly, SNAI1 proteins were physically associated and colocalized with LC3 and SQSTM1 in cancer cells. We also found a significant decrease in the levels of EMT and metastatic proteins under starvation conditions. Furthermore, ATG7 knockdown inhibited autophagy-induced SNAI1 degradation in the cytoplasm, which was associated with a decrease in SNAI1 nuclear translocation. Moreover, cancer cell invasion and migration were significantly inhibited by starvation-induced autophagy. These findings suggest that autophagy-dependent SNAI1 degradation could specifically regulate EMT and cancer metastasis during tumorigenesis

Ghana: Agricultural Information Network System (GAINS)

The Agricultural Information Network System (GAINS) was established in 1991 as a component of the National Agricultural Research Project (NARP). With 18 participating libraries (universities, the Ministry of Food and Agriculture and research institutes), GAINS is building a network system for collecting, processing, repackaging and sharing information, in any format, to support agricultural R&D in Ghana. The GAINS partners aim to market agricultural information services via a website that will become an agricultural portal (reviewed by Simon K. Osei).The Agricultural Information Network System (GAINS) was established in 1991 as a component of the National Agricultural Research Project (NARP)