Havesheppard6851

Structurally diverse biopolymers, including extracellular polysaccharides (EPS), synthesized by bacteria can possess physicochemical and functional properties that make them important products of microbial synthesis with a broad and versatile biotechnological potential. Leuconostoc spp. belongs to the group of lactic acid bacteria as one of the predominant members and are relevant not only in varied food fermentations, but also can be employed in the production of extracellular homopolysaccharides (HoPS) such as α-glucans (dextran, alternan) and β-fructans (levan,inulin) from the sucrose-containing substrates. EPS are synthesized by specific Leuconostoc spp. Tamoxifen mw extracellular glycosyltransferases [dextran sucrase, alternansucrase (ASR)] and fructosyltransferases (levansucrase, inulosucrase) and enzymatic reactions can be performed in whole culture systems as well as using cell-free enzymes. Both α-glucans and β-fructans have a wide range of properties, mostly depending on their pattern of linkages, which, although differing in some respects, make suitable prerequisites for their versatile application in many fields, especially in the food industry and biomedicine. As a rule, these properties (polymer type, molecular mass, rheological parameters), as well as the overall EPS yield, are strain-specific for the selected producers and depend to a large extent on the nutritional and growth conditions used, which in many cases remain not sufficiently optimized for Leuconostoc spp. This review summarizes the current knowledge on the potential of Leuconostoc spp. to produce commercially relevant EPS, including information on their applications in various fields, producer strains, production methods and techniques used, selected conditions, the productivity of bioprocesses as well as the possible use of renewable resources for their development.

Gangliogliomas are neoplastic lesions composed by a mixed population of neoplastic glial and dysplastic neural cells. They represent around 5% of all CNS tumors in the pediatric population. These usually are well-differentiated, slow-growing tumors, meaning that complete resection could cure most of these patients. Although most lesions remain stable over time after incomplete resection, some patients develop progression of the residual lesions the optimal approach to treat these tumors is still to be defined.

This is a retrospective study in which we obtained data from medical records of pediatric patients who had a histological diagnosis of ganglioglioma following surgical treatment at a single center between 2001 and 2020.

We included 17 pediatric subjects with gangliogliomas. The median age at diagnosis was 6.7 years, and the median follow-up duration was 60 months. The most common clinical presentation was epileptic seizures (41.1%). Hydrocephalus was present in 29.4% of cases. 52.9% of tumors invocally grade I tumors that occasionally affect children. They classically localize in the cerebral hemisphere but may involve deep structures like the basal ganglia, brain stem, and cerebellum, which seems to be particularly frequent in the pediatric population, implying further challenge to achieve adequate oncological control with surgery as the only treatment modality. Although most cases in which GTR could not be performed remained stable over the follow-up, significant progression of the tumor remains was observed in some patients. BRAF inhibitors should be considered as a feasible treatment option in this setting.Although malignant glioblastoma (GBM) treatment has significantly improved in the past few decades, the prognosis of GBM remains unsatisfactory. MicroRNA (miR)-138-5p has been reported as a tumor suppressor in several types of human cancer; however, little is known about the function of miR-138-5p in GBM. The present study aimed to investigate the role of miR-138-5p in GBM as well as the underlying molecular mechanisms. The present study performed bioinformatics analysis, reverse transcription-quantitative (RT-q)PCR, western blotting, cell viability assays, colony formation assays, invasion assays and cell cycle analysis to investigate the biological function of miR-138-5p in both patient tissues and cell lines. In addition, miR-138-5p targets in GBM were predicted using Gene Expression Omnibus website and further validated by a dual luciferase reporter gene assay. The results revealed that miR-138-5p expression levels in patients with GBM from a Gene Expression Omnibus dataset were significantly downregulated. RT-qPCR analysis of miR-138-5p expression levels also revealed similar results in GBM tissues and cell lines. The upregulation of miR-138-5p expression levels using a mimic significantly inhibited the cell viability, colony formation and the G0/G1 to S progression in GBM cell lines, suggesting that miR-138-5p may be a tumor suppressor. Moreover, miR-138-5p was discovered to directly target cyclin D3 (CCND3), a protein that serves an important role in the cell cycle, and inhibited its expression. Finally, silencing CCND3 using small interfering RNA suppressed the viability of GBM cells. In conclusion, the results of the present study suggested that miR-138-5p may function as a tumor suppressor in GBM by targeting CCND3, indicating that miR-138-5p may be a novel therapeutic target for patients with GBM.The mitotic kinase AURORA-A is essential for cell cycle progression and is considered a priority cancer target. Although the catalytic activity of AURORA-A is essential for its mitotic function, recent reports indicate an additional non-catalytic function, which is difficult to target by conventional small molecules. We therefore developed a series of chemical degraders (PROTACs) by connecting a clinical kinase inhibitor of AURORA-A to E3 ligase-binding molecules (for example, thalidomide). One degrader induced rapid, durable and highly specific degradation of AURORA-A. In addition, we found that the degrader complex was stabilized by cooperative binding between AURORA-A and CEREBLON. Degrader-mediated AURORA-A depletion caused an S-phase defect, which is not the cell cycle effect observed upon kinase inhibition, supporting an important non-catalytic function of AURORA-A during DNA replication. AURORA-A degradation induced rampant apoptosis in cancer cell lines and thus represents a versatile starting point for developing new therapeutics to counter AURORA-A function in cancer.