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Abstract Background Gliomas account for the majority of primary human brain tumors and remain a challenging neoplasm for cure due to limited therapeutic options. Cell adhesion molecules play pivotal roles in the growth and progression of glial tumors. Roles of the adhesion molecules on glia (AMOG) and L1CAM (L1) in glioma cells have been shown to correlate with tumorigenesis: Increased expression of L1 and decreased expression of AMOG correlate with degree of malignancy. Methods We evaluated the interdependence in expression of these molecules by investigating the role of AMOG in vitro via modulation of L1 expression and analyzing apoptosis and cell senescence of glioma cells. Results Immunohistochemical staining of normal human cortical and glioma tissue microarrays demonstrated that AMOG expression was lower in human gliomas compared to normal tissue and is inversely correlated with the degree of malignancy. Moreover, reduction of AMOG expression in human glioblastoma cells elevated L1 expression, which is accompanied by decreased cell apoptosis as well as senescence. Conclusion AMOG and L1 interdependently regulate their expression levels not only in U-87 MG cells but also in U251 and SHG44 human glioma cell lines. The capacity of AMOG to reduce L1 expression suggests that methods for increasing AMOG expression may provide a therapeutic choice for the management of glial tumors with high expression of L1.

This study reveals that increases in the global population command an augmented demand for products and services that calls for more effective ways of using existing natural resources and materials. The recent development of information and communication technologies, which had a great impact on many areas, also had a damaging effect on the environment and human health. Therefore, societies are moving toward a greener future by reducing the consumption of nonrenewable materials, raw materials, and resources while at the same time decreasing energy pollution and consumption. Since information technology is considered a tool for solving ecological difficulties, the green Internet of things (G-IoT) is playing a vital role in creating a sustainable home. Extensive data analysis is required to obtain a valuable overview of the large and diverse data generated by the G-IoT. The gathered information will facilitate forecasting, decision-making, and other activities related to smart urban services and then contribute to the incessant development of G-IoT technology. Therefore, even if sustainable and smart cities become an actuality, the G-IoT approach and the knowledge gained through big data (BD) analysis will make cities more sustainable, safer, and smarter. The goal of this article is to combine innovation in technological development with the main focus on resource sharing in creating cities that improve the quality of life while reducing pollution and realizing more efficient use of the raw materials. In the practice of big data science, it is always of interest to provide the best description of the data under consideration. Recent studies have pointed out the applicability of the statistical distributions in modeling data in applied sciences. In this article, we introduce a new family of statistical models to provide the best description of the life span of the wireless sensors network’s data. Based on the proposed approach, a special submodel called new exponent power-Weibull distribution is studied in detail. The applicability of the proposed model is shown by analyzing the life span of the wireless sensors network’s data.

The cell adhesion molecule with homology to L1CAM (close homolog of L1) (CHL1) is a member of the cell adhesion molecule L1 (L1CAM) gene family. Although CHL1 expression and function have been reported in several tumors, the roles of CHL1 in the development of glioma remain unclear. In the present study, we investigated the effects of CHL1 on proliferation indexes and activation of Akt1 and Erk signaling by siRNA in U-87 MG human glioblastoma and human U251 and SHG-44 glioma cells. We found that siRNA targeting CHL1 significantly down-regulated the expression of CHL1 mRNA and protein accompanied by reduced cell proliferation and transmigration invasion in all three cell lines. Down-regulating CHL1 expression also reduced cell survival, as measured by the Bax/Bcl-2 ratio, and increased activation of caspase-3. In subcutaneous U-87 MG cell xenograft tumors in nude mice, intratumoral administration of siRNA targeting CHL1 treatment significantly down-regulated CHL1 expression in vivo, accompanied by increased levels of activated caspase-3. Our combined results confirmed for the first time that in contrast to findings about CHL1 in most other cancer types, CHL1 functions in promoting cell proliferation, metastasis and migration in human glioma cells both in vitro and in vivo. These results indicate that CHL1 is a therapeutic target in the clinical management of glioma/glioblastoma.

Bacterial canker is a devastating disease in kiwifruit production, primarily caused by Pseudomonas syringae pv. actinidiae. In this study, a strain of Bacillus velezensis named JIN4, isolated from a kiwifruit branch, showed antagonistic activity. The B. velezensis JIN4 strain was identified based on its morphological, physiological and biochemical characteristics, 16S rDNA, and gyrA sequences. Furthermore, the complete genome of the strain was elucidated, revealing the presence of three genes that confer resistance to antibiotics, including tetracycline, lincomycin, and streptomycin. Additionally, a cluster of nine secondary metabolite synthesis genes was identified. In the laboratory, the JIN4 strain exhibited nitrogen (N) and phosphorus (P) production, demonstrating plant growth-promoting and broad-spectrum inhibitory activities against pathogenic fungi and bacteria. In the field, the JIN4 strain demonstrated effective colonization of kiwifruit, increased antioxidant enzyme activity, induced resistance in kiwifruit plants, and achieved a control efficiency of 60.22% against kiwifruit bacterial canker. These results indicate that B. velezensis JIN4 is a potential biocontrol agent against kiwifruit bacterial canker. [ABSTRACT FROM AUTHOR]

• Relationships of microbial corrosion and barnacle cement. • Infrared peaks of biofilm were found in the junction of barnacles and shipwreck. • Photoluminescence spectroscopy was used to identify the corrosion regions. Wooden shipwrecks submerged in underwater environments are susceptible to physical and biological corrosion. This study investigates the microscopic morphology and structural composition of barnacles and the wooden surface of the Yangtze Estuary II shipwreck. Analytical techniques, including optical microscopy (OM), scanning electron microscope equipped with an energy dispersive spectrometer (SEM-EDS), X-ray diffraction (XRD), X-ray photoelectron spectroscopy (XPS), Fourier infrared transform spectroscopy (FTIR) and photoluminescence spectroscopy (PL), were employed to analyze the corrosion processes. The findings have unveiled a distinct pattern of black corrosion, prominently concentrated within the interface region where barnacles attach to the wooden shipwreck. This corrosion primarily consists of FeS, FeS 2 and Fe 3 S 4 and exhibits a notable tendency to expand along the wooden surface to interior region. Additionally, a striking ultraviolet fluorescence phenomenon emanates from the barnacle cement within the adhesion region of barnacles and the wooden surface. This observation has led to the hypothesis that the origin of this black corrosion is intricately linked to the barnacle cement, its role in biological corrosion, and subsequent biomineralization processes. To conclude, this study provides an intricate account of the microbial corrosion process influenced by barnacle cement in the context of the wooden shipwreck. The research findings offer valuable insights that can serve as a point of reference in identifying the sources of disease and implementing protective measures for waterlogged wooden cultural relics. [ABSTRACT FROM AUTHOR]

After the excavation and unloading of deep-buried soft rock tunnels, support structures often experience deformation-related disasters such as concrete cracking, steel frame bending and twisting, and primary support instability under different forms of load. Accurately calculating the load borne by the primary support structure is the key to ensuring design rationality and construction safety. Especially in layered soft surrounding rock formations, the magnitude and distribution of the loads are different from those of conventional rock and soil masses, resulting in limited applicability of existing load calculation methods to similar formations. Therefore, based on the measured deformation of the tunnel structure, while considering the different geometric forms of the primary support structure during partial excavation, this paper proposes a deformation-structure (D-S) load calculation method. By comparing the calculation results of this method and a large number of sample data for typical deep-buried layered soft rock tunnels, the reliability of the D-S load calculation method is verified. In addition, the variation law of the loads during the tunnel construction period is enunciated, and the magnitude and distribution of the loads acting on the primary support are clarified. The D-S load calculation method provides a theoretical basis for load calculation in deep-buried layered soft rock tunnels. [ABSTRACT FROM AUTHOR]