Non-protein coding RNA sequences mediate specific colorimetric detection of Staphylococcus aureus on unmodified gold nanoparticles.

Nonprotein coding RNA (npcRNA) is a transcribed gene sequence that is not able to translate into protein, yet it executes a specific function in modulation and regulation mechanisms. As npcRNA is highly resistant to the mutation, the Sau-02 npcRNA gene and its probe oligonucleotide, which are specifically present in Staphylococcus aureus and in methicillin-resistant S. aureus only, used to develop a highly specific and sensitive colorimetric assay on unmodified gold nanoparticles (AuNPs). Hybridization between the npcRNA Sau-02 gene sequences was detected through noncrosslinking AuNP aggregation in salt solution in the presence of probe-target gene sequences. AuNPs of 10 and 15 nm in sizes with monovalent ion salt (NaCl) solution were optimized as the ideal tool for investigating the stability of AuNPs upon the addition of gene sequences. The state dispersed and aggregated forms of 10 nm AuNPs with the presented colorimetric assay were justified through field emission scanning electron microscopy and atomic force microscopy. The particle distribution of two different AuNP states was evaluated through particle distribution analysis. The lowest detection amount of S. aureus npcRNA from the colorimetric assay performed was 6 pg/µL, as the color of AuNPs turned blue with the presence of probe oligonucleotides and target gene sequences.

Genetic Polymorphisms and Diversity in Nonalcoholic Fatty Liver Disease (NAFLD): A Mini Review.

Nonalcoholic fatty liver disease (NAFLD) is a common liver disease with a wide spectrum of liver conditions ranging from hepatic steatosis to nonalcoholic steatohepatitis (NASH), fibrosis, cirrhosis, and hepatocellular carcinoma. The prevalence of NAFLD varies across populations, and different ethnicities have specific risks for the disease. NAFLD is a multi-factorial disease where the genetics, metabolic, and environmental factors interplay and modulate the disease's development and progression. Several genetic polymorphisms have been identified and are associated with the disease risk. This mini-review discussed the NAFLD's genetic polymorphisms and focusing on the differences in the findings between the populations (diversity), including of those reports that did not show any significant association. The challenges of genetic diversity are also summarized. Understanding the genetic contribution of NAFLD will allow for better diagnosis and management explicitly tailored for the various populations.

Nonalcoholic Fatty Liver Disease (NAFLD): Pathogenesis and Noninvasive Diagnosis.

The global prevalence of nonalcoholic fatty liver disease (NAFLD) or metabolic associated fatty liver disease (MAFLD), as it is now known, has gradually increased. NAFLD is a disease with a spectrum of stages ranging from simple fatty liver (steatosis) to a severe form of steatosis, nonalcoholic steatohepatitis (NASH), which could progress to irreversible liver injury (fibrosis) and organ failure, and in some cases hepatocellular carcinoma (HCC). Although a liver biopsy remains the gold standard for accurate detection of this condition, it is unsuitable for clinical screening due to a higher risk of death. There is thus an increased need to find alternative techniques or tools for accurate diagnosis. Early detection for NASH matters for patients because NASH is the marker for severe disease progression. This review summarizes the current noninvasive tools for NAFLD diagnosis and their performance. We also discussed potential and newer alternative tools for diagnosing NAFLD.

Extracellular Vesicles in the Development of the Non-Alcoholic Fatty Liver Disease: An Update.

Non-alcoholic fatty liver disease (NAFLD) is a broad spectrum of liver damage disease from a simple fatty liver (steatosis) to more severe liver conditions such as non-alcoholic steatohepatitis (NASH), fibrosis, and cirrhosis. Extracellular vesicles (EVs) are a heterogeneous group of small membrane vesicles released by various cells in normal or diseased conditions. The EVs carry bioactive components in their cargos and can mediate the metabolic changes in recipient cells. In the context of NAFLD, EVs derived from adipocytes are implicated in the development of whole-body insulin resistance (IR), the hepatic IR, and fatty liver (steatosis). Excessive fatty acid accumulation is toxic to the hepatocytes, and this lipotoxicity can induce the release of EVs (hepatocyte-EVs), which can mediate the progression of fibrosis via the activation of nearby macrophages and hepatic stellate cells (HSCs). In this review, we summarized the recent findings of adipocyte- and hepatocyte-EVs on NAFLD disease development and progression. We also discussed previous studies on mesenchymal stem cell (MSC) EVs that have garnered attention due to their effects on preventing liver fibrosis and increasing liver regeneration and proliferation.