Antibiotic resistance of cyanobacteria has been a global threat to public health. The widespread presence of cyanobacteria in aquatic environments exposes them to antibiotic contamination. The cyanobacteria are also in direct contact with pathogenic bacteria containing Antibiotic-Resistance Genes (ARGs) that gives them these characteristics. The study aims to the presence of some ARGs in locally isolated cyanobacteria species, Spirulina laxa, Chroococcus minutes, Oscillatoria princeps, Oscillatoria proteus, Oscillatoria terebriformis, Lyngbya epiphytica, and to compare the presence of these genes in two pathogenic bacteria, Escherichia coli and Klebsiella pneumoniae. The results revealed the presence of The ampicillin (Ap) and erythromycin (Em) resistance genes were detected in five algal samples. Meanwhile, the chloramphenicol (Cm) and gentamicin (Gm) resistance genes were apparent in only two species. Genes encoding resistance towards kanamycin (Km) and spectinomycin (Sp) were recorded in three specimens. The results also documented that E. coli possessed the resistance genes for four antibiotics: Ampicillin (Ap), Erythromycin (Em), Gentamicin (Gm), and Kanamycin (Km), whereas K. pneumoniae was resistant towards three anti-biotics: Ampicillin (Ap), Gentamicin (Gm), and Kanamycin (Km). The results show that there are a match in antibiotic resistance genes in both cyanobacteria and pathogenic bacteria. suggesting the possibility that cyanobacteria could acquire ARGs from the environment through horizontal gene transfer. Thus, freshwater cyanobacteria may play an important role in the prevalence of ARGs in their environment.

High-grade gliomas are extremely fatal tumors, marked by severe hypoxia and therapeutic resistance. Autophagy is a cellular degradative process that can be activated by hypoxia, ultimately resulting in tumor advancement and chemo-resistance. Our study aimed to examine the link between autophagy markers expression in low (LGG) and high-grade gliomas (HGG). In 39 glioma cases, we assessed protein expression of autophagy markers LC3B, p62, and DRAM by immunohistochemistry (IHC) and mRNA expression of autophagy genes; PI3K, AKT, m-TOR, PTEN, ULK1, ULK2, UVRAG, Beclin 1 and VPS34 using RT-qPCR. Livak’s method was used to analyze the relative changes in gene expression and multi-variate Anova test and Spearman's correlation tests were performed for statistical significance. LC3B, p62, and DRAM expression were positive in 64.1%, 51.3%, and 28.2% of glioma cases respectively. The expression of LC3B and p62 was notably higher in HGG compared to LGG. VPS34 exhibited a significant differential expression and increased fold change and demonstrated strong positive correlations with Beclin1 (rs=0.768), UVRAG (rs=0.802), and ULK2 (rs=0.786) in HGG compared to LGG, thus highlighting the potential link between autophagy and glioma progression. We Provide preliminary data for functional analysis of autophagy using cell culture model and to identify potential targets for therapeutic interventions

Val-Phe-Val-Arg-Asn (VFVRN) has been identified and screened from lipid-lowering chickpea peptides (ChPs) by using a pharmacokinetic model in our previous experiment. The present study was conducted to investigate its effects and mechanisms on lipid metabolism. A high-fat diet C57BL/6J mice model and 3T3-L1 preadipocyte cell model were used. VFVRN was found to significantly decrease the levels of some blood lipids. The expressions of LDL receptor (LDLR), peroxisome proliferator-activated receptors (PPAR)α, liver X receptor (LXR)α, cholesterol 7α-hydroxylase (CYP7A1) and AMP-activated protein kinase (p-AMPK) in liver were up-regulated by VFVRN treatment. The expressions of 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGR), fatty acid synthetase (FAS), 1-aminocyclopropane-1-carboxylate synthetase (ACC), sterol regulatory element-binding protein (SREBP)-1c and SREBP-2 in liver were significantly (P<0.05) down-regulated. Additionally, the expressions of PPARα and PPARγ in adipose tissues were up-regulated by VFVRN significantly (P<0.05). VFVRN might also contribute to transintestinal cholesterol efflux (TICE) by up-regulating the expressions of LXRα and ATP binding cassette G5/8 transporters (ABGC5/8). Moreover, VFVRN promoted 3T3-L1 preadipocyte apoptosis by up-regulating the expressions of BaX, cleaved Caspase-3 and down-regulating Bcl-2. VFVRN had potent effects in reversing metabolic disorders of blood and liver in a high-fat diet mice model, as well as to promote the apoptosis of 3T3-L1 preadipocytes.