Search

Amphiphilic cationic peptide (ACP) is a widely studied biofilm-active peptide that has great potential in cancer treatment. However, poor stability, a short half-life, and complex preparation pose significant challenges for practical therapeutic applications. In the current investigation, the amphiphilic peptide Melittin (Mel), recognized for its powerful anticancer properties, was chosen from natural and synthetic ACP, and integrated into a nanostructure by utilizing polyhydroxyalkanoate (PHA) microspheres as carriers to produce Mel-loaded PHA microspheres (Mel@PHA-PhaC). Mel@PHA-PhaC nanostructure was self-assembled in Escherichia coli, simplifying its preparation and making it more convenient and high-yield. Mel@PHA-PhaC were spherical, with a particle size of approximately 300 nm, as observed by scanning electron microscopy (SEM) and transmission electron microscopy (TEM). The concentration of Mel in Mel@PHA-PhaC was 4 μg/mg. Mel@PHA-PhaC still maintained good stability after being treated with pancreatic enzymes. Furthermore, in vitro experiments demonstrated that Mel@PHA-PhaC enhanced the inhibitory effect on cancer cells compared to free Mel. This study provides insights and guidelines for the development and utilization of peptide delivery systems using PHA microspheres to create stable and improved peptides for cancer therapy. [ABSTRACT FROM AUTHOR]

Cerebellar ataxia is a form of ataxia that originates from dysfunction of the cerebellum, but may involve additional neurological tissues. Its clinical symptoms are mainly characterized by the absence of voluntary muscle coordination and loss of control of movement with varying manifestations due to differences in severity, in the site of cerebellar damage and in the involvement of extracerebellar tissues. Cerebellar ataxia may be sporadic, acquired, and hereditary. Hereditary ataxia accounts for the majority of cases. Hereditary ataxia has been tentatively divided into several subtypes by scientists in the field, and nearly all of them remain incurable. This is mainly because the detailed mechanisms of these cerebellar disorders are incompletely understood. To precisely diagnose and treat these diseases, studies on their molecular mechanisms have been conducted extensively in the past. Accumulating evidence has demonstrated that some common pathogenic mechanisms exist within each subtype of inherited ataxia. However, no reports have indicated whether there is a common mechanism among the different subtypes of inherited cerebellar ataxia. In this review, we summarize the available references and databases on neurological disorders characterized by cerebellar ataxia and show that a subset of genes involved in lipid homeostasis form a new group that may cause ataxic disorders through a common mechanism. This common signaling pathway can provide a valuable reference for future diagnosis and treatment of ataxic disorders. [ABSTRACT FROM AUTHOR]