Glioblastoma (GBM) is one of the most malignant and intractable central nervous system tumors with high recurrence, low survival rate, and poor prognosis. Despite the advances of aggressive, multimodal treatment, a successful treatment strategy is still elusive, often leading to therapeutic resistance and fatality. Thus, it is imperative to search for and identify novel markers critically associated with GBM pathogenesis to improve the existing trend of diagnosis, prognosis, and treatment. Seven publicly available GEO microarray datasets containing 409 GBM samples were integrated and further data mining was conducted using several bioinformatics tools. A total of 209 differentially expressed genes (DEGs) were identified in the GBM tissue samples compared to the normal brains. Gene Ontology (GO) enrichment analysis of the DEGs revealed association of the upregulates genes with extracellular matrix (ECM), conceivably contributing to the invasive nature of GBM while downregulated DEGs were found to be predominantly related to neuronal processes and structures. Alongside, Kyoto Encyclopedia of Genes and Genomes (KEGG) and Reactome pathway analyses described the involvement of the DEGs with various crucial contributing pathways (PI3K-Akt signaling pathway, p53 signaling pathway, insulin secretion, etc.) in GBM progression and pathogenesis. Protein-protein interaction (PPI) network containing 879 nodes and 1237 edges revealed 3 significant modules and consecutive KEGG pathway analysis of these modules showed a significant connection to gliomagenesis. Later, 10 hub genes were screened out based on degree and their expressions were externally validated. Surprisingly, only fibronectin 1 (FN1) high expression appeared to be related to poor prognosis. Subsequently, 109 transcription factors and 211 miRNAs were detected to be involved with the hub genes where FN1 demonstrated the highest number of interactions. Considering its high connectivity and potential prognostic value FN1 could be a novel biomarker providing new insights into the prognosis and treatment for GBM, although experimental validation is required.

The aim of the study was to assess the pharmacokinetic and bioavailability of 2 formulations of 5-mg prednisolone tablets, reference product (Teva UK Limited) and Pred (Eskayef Bangladesh Ltd) as test product. The open-label, randomized, 2-way crossover studies were conducted on 14 healthy subjects. Participants were assigned to receive both products as a single dose (20 mg formulations, 4 × 5 mg tablets) followed by a 2 weeks’ washout period. Following oral administration, samples were obtained at various time intervals and analyzed for prednisolone concentrations using a validated high-performance liquid chromatography assay method with ultraviolet detection. The obtained values for test and reference products were 683.00 ± 94.54 ng/mL and 635.16 ± 125.57 ng/mL for C_max; 2716.54 ± 196.28 ng·h/mL and 2780.5 ± 119.73 ng·h/mL for AUC_0-12; 3284.36 ± 138.12 ng·h/mL and 3317.96 ± 133.95 ng·h/mL for AUC_0-∞, respectively. From the paired Student t test, no significant differences between 2 formulations were observed ( P > .05). The 90% confidence intervals of C_max, AUC_0-12, and AUC_0-∞ were found to be 99.0% to 100.9%, 99.4% to 100.5%, and 99.9% to 101.3%, respectively. Finally, it can be concluded that Pred (Test) of Eskayef Bangladesh Ltd and prednisolone (Reference) of Teva UK Limited are bioequivalent and interchangeable.

Alzheimer’s disease (AD) is a neurodegenerative disease with rapid progression. Black cumin (Nigella sativa) is a nutraceutical that has been investigated as a prophylactic and therapeutic agent for this disease due to its ability to prevent or retard the progression of neurodegeneration. Thymoquinone (TQ) is the main bioactive compound isolated from the seeds of black cumin. Several reports have shown that it has promising potential in the prevention and treatment of AD due to its significant antioxidative, anti-inflammatory, and antiapoptotic properties along with several other mechanisms that target the altered signaling pathways due to the disease pathogenesis. In addition, it shows anticholinesterase activity and prevents α-synuclein induced synaptic damage. The aim of this review is to summarize the potential aspects and mechanisms by which TQ imparts its action in AD.