Research Trends on Greenhouse Engineering Using a Science Mapping Approach

Horticultural protected cultivation has spread throughout the world as it has proven to be extremely effective. In recent years, the greenhouse engineering research field has become one of the main research topics within greenhouse farming. The main objectives of the current study were to identify the major research topics and their trends during the last four decades by analyzing the co-occurrence network of keywords associated with greenhouse engineering publications. A total of 3804 pertinent documents published, in 1981-2021, were analyzed and discussed. China, the United States, Spain, Italy and the Netherlands have been the most active countries with more than 36% of the relevant literature. The keyword cluster analysis suggested the presence of five principal research topics: energy management and storage; monitoring and control of greenhouse climate parameters; automation of greenhouse operations through the internet of things (IoT) and wireless sensor network (WSN) applications; greenhouse covering materials and microclimate optimization in relation to plant growth; structural and functional design for improving greenhouse stability, ventilation and microclimate. Recent research trends are focused on real-time monitoring and automatic control systems based on the IoT and WSN technologies, multi-objective optimization approaches for greenhouse climate control, efficient artificial lighting and sustainable greenhouse crop cultivation using renewable energy

Directed growth and fusion of membrane-wall microdomains requires CASP-mediated inhibition and displacement of secretory foci.

Casparian strips (CS) are aligned bands of lignin-impregnated cell walls, building an extracellular diffusion barrier in roots. Their structure profoundly differs from tight junctions (TJ), analogous structures in animals. Nonetheless, CS membrane domain (CSD) proteins 1-5 (CASP1-5) are homologues of occludins, TJ components. CASP-marked membranes display cell wall (matrix) adhesion and membrane protein exclusion. A full CASP knock-out now reveals CASPs are not needed for localized lignification, since correctly positioned lignin microdomains still form in the mutant. Ultra-structurally, however, these microdomains are disorganized, showing excessive cell wall growth, lack of exclusion zone and matrix adhesion, and impaired exocyst dynamics. Proximity-labelling identifies a Rab-GTPase subfamily, known exocyst activators, as potential CASP-interactors and demonstrate their localization and function at the CSD. We propose that CASP microdomains displace initial secretory foci by excluding vesicle tethering factors, thereby ensuring rapid fusion of microdomains into a membrane-cell wall band that seals the extracellular space

Identification of novel proteins binding the AU-rich element of \u3b1-prothymosin mRNA through the selection of open reading frames (RIDome)

We describe here a platform for high-throughput protein expression and interaction analysis aimed at identifying the RNA-interacting domainome. This approach combines the selection of a phage library displaying "filtered" open reading frames with next-generation DNA sequencing. The method was validated using an RNA bait corresponding to the AU-rich element of \u3b1-prothymosin, an RNA motif that promotes mRNA stability and translation through its interaction with the RNA-binding protein ELAVL1. With this strategy, we not only confirmed known RNA-binding proteins that specifically interact with the target RNA (such as ELAVL1/HuR and RBM38) but also identified proteins not previously known to be ARE-binding (R3HDM2 and RALY). We propose this technology as a novel approach for studying the RNA-binding proteome

Construction of chromosome segmen substitution lines in peanut (Arachis hypogaea L.) using a wild synthetic and QTL mapping for plant morphology.

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Both ghrelin deletion and unacylated ghrelin overexpression preserve muscles in aging mice

Sarcopenia, the decline in muscle mass and functionality during aging, might arise from age-associated endocrine dysfunction. Ghrelin is a hormone circulating in both acylated (AG) and unacylated (UnAG) forms with antiatrophic activity on skeletal muscle. Here, we show that not only lifelong overexpression of UnAG (Tg) in mice, but also the deletion of ghrelin gene (Ghrl KO) attenuated the age-associated muscle atrophy and functionality decline, as well as systemic inflammation. Yet, the aging of Tg and Ghrl KO mice occurs with different dynamics: while old Tg mice seem to preserve the characteristics of young animals, Ghrl KO mice features deteriorate with aging. However, young Ghrl KO mice show more favorable traits compared to WT animals that result, on the whole, in better performances in aged Ghrl KO animals. Treatment with pharmacological doses of UnAG improved muscle performance in old mice without modifying the feeding behavior, body weight, and adipose tissue mass. The antiatrophic effect on muscle mass did not correlate with modifications of protein catabolism. However, UnAG treatment induced a strong shift towards oxidative metabolism in muscle. Altogether, these data confirmed and expanded some of the previously reported findings and advocate for the design of UnAG analogs to treat sarcopenia

Genomic organization and evolution of double minutes/homogeneously staining regions with MYC amplification in human cancer

The mechanism for generating double minutes chromosomes (dmin) and homogeneously staining regions (hsr) in cancer is still poorly understood. Through an integrated approach combining next-generation sequencing, single nucleotide polymorphism array, fluorescent in situ hybridization and polymerase chain reaction-based techniques, we inferred the fine structure of MYC-containing dmin/hsr amplicons harboring sequences from several different chromosomes in seven tumor cell lines, and characterized an unprecedented number of hsr insertion sites. Local chromosome shattering involving a single-step catastrophic event (chromothripsis) was recently proposed to explain clustered chromosomal rearrangements and genomic amplifications in cancer. Our bioinformatics analyses based on the listed criteria to define chromothripsis led us to exclude it as the driving force underlying amplicon genesis in our samples. Instead, the finding of coexisting heterogeneous amplicons, differing in their complexity and chromosome content, in cell lines derived from the same tumor indicated the occurrence of a multi-step evolutionary process in the genesis of dmin/hsr. Our integrated approach allowed us to gather a complete view of the complex chromosome rearrangements occurring within MYC amplicons, suggesting that more than one model may be invoked to explain the origin of dmin/hsr in cancer. Finally, we identified PVT1 as a target of fusion events, confirming its role as breakpoint hotspot in MYC amplification

Increased ventral striatal volume in college-aged binge drinkers

BACKGROUND Binge drinking is a serious public health issue associated with cognitive, physiological, and anatomical differences from healthy individuals. No studies, however, have reported subcortical grey matter differences in this population. To address this, we compared the grey matter volumes of college-age binge drinkers and healthy controls, focusing on the ventral striatum, hippocampus and amygdala. METHOD T1-weighted images of 19 binge drinkers and 19 healthy volunteers were analyzed using voxel-based morphometry. Structural data were also covaried with Alcohol Use Disorders Identification Test (AUDIT) scores. Cluster-extent threshold and small volume corrections were both used to analyze imaging data. RESULTS Binge drinkers had significantly larger ventral striatal grey matter volumes compared to controls. There were no between group differences in hippocampal or amygdalar volume. Ventral striatal, amygdalar, and hippocampal volumes were also negatively related to AUDIT scores across groups. CONCLUSIONS Our findings stand in contrast to the lower ventral striatal volume previously observed in more severe forms of alcohol use disorders, suggesting that college-age binge drinkers may represent a distinct population from those groups. These findings may instead represent early sequelae, compensatory effects of repeated binge and withdrawal, or an endophenotypic risk factor

Estimation of the incubation period and generation time of SARS-CoV-2 Alpha and Delta variants from contact tracing data

Quantitative information on epidemiological quantities such as the incubation period and generation time of SARS-CoV-2 variants is scarce. We analyzed a dataset collected during contact tracing activities in the province of Reggio Emilia, Italy, throughout 2021. We determined the distributions of the incubation period for the Alpha and Delta variants using information on negative PCR tests and the date of last exposure from 282 symptomatic cases. We estimated the distributions of the intrinsic generation time using a Bayesian inference approach applied to 9724 SARS-CoV-2 cases clustered in 3545 households where at least one secondary case was recorded. We estimated a mean incubation period of 4.9 days (95% credible intervals, CrI, 4.4-5.4) for Alpha and 4.5 days (95%CrI 4.0-5.0) for Delta. The intrinsic generation time was estimated to have a mean of 7.12 days (95% CrI 6.27-8.44) for Alpha and of 6.52 days (95%CrI 5.54-8.43) for Delta. The household serial interval was 2.43 days (95%CrI 2.29-2.58) for Alpha and 2.74 days (95%CrI 2.62-2.88) for Delta, and the estimated proportion of pre-symptomatic transmission was 48-51% for both variants. These results indicate limited differences in the incubation period and intrinsic generation time of SARS-CoV-2 variants Alpha and Delta compared to ancestral lineages

Phosphorylation by Aurora B kinase regulates caspase-2 activity and function

Abstract: Mitotic catastrophe (MC) is an important oncosuppressive mechanism that serves to eliminate cells that become polyploid or aneuploid due to aberrant mitosis. Previous studies have demonstrated that the activation and catalytic function of caspase-2 are key steps in MC to trigger apoptosis and/or cell cycle arrest of mitotically defective cells. However, the molecular mechanisms that regulate caspase-2 activation and its function are unclear. Here, we identify six new phosphorylation sites in caspase-2 and show that a key mitotic kinase, Aurora B kinase (AURKB), phosphorylates caspase-2 at the highly conserved residue S384. We demonstrate that phosphorylation at S384 blocks caspase-2 catalytic activity and apoptosis function in response to mitotic insults, without affecting caspase-2 dimerisation. Moreover, molecular modelling suggests that phosphorylation at S384 may affect substrate binding by caspase-2. We propose that caspase-2 S384 phosphorylation by AURKB is a key mechanism that controls caspase-2 activation during mitosis

Phosphorylation by Aurora B kinase regulates caspase-2 activity and function.

Mitotic catastrophe (MC) is an important oncosuppressive mechanism that serves to eliminate cells that become polyploid or aneuploid due to aberrant mitosis. Previous studies have demonstrated that the activation and catalytic function of caspase-2 are key steps in MC to trigger apoptosis and/or cell cycle arrest of mitotically defective cells. However, the molecular mechanisms that regulate caspase-2 activation and its function are unclear. Here, we identify six new phosphorylation sites in caspase-2 and show that a key mitotic kinase, Aurora B kinase (AURKB), phosphorylates caspase-2 at the highly conserved residue S384. We demonstrate that phosphorylation at S384 blocks caspase-2 catalytic activity and apoptosis function in response to mitotic insults, without affecting caspase-2 dimerisation. Moreover, molecular modelling suggests that phosphorylation at S384 may affect substrate binding by caspase-2. We propose that caspase-2 S384 phosphorylation by AURKB is a key mechanism that controls caspase-2 activation during mitosis