BACKGROUND It is still not clear whether native or platelet count adjusted platelet rich plasma (PRP) should be used for platelet aggregation measurements. AIM To evaluate the necessity of using adjusted PRP in platelet function testing. METHODS Platelet aggregation with native PRP and adjusted PRP (platelet count: 250/nl, obtained by diluting native PRP with platelet poor plasma) was perfo...

We aimed to evaluate the effect of activated platelet-rich plasma (PRP) on proliferation and chondrogenic differentiation bone marrow-derived mesenchymal stem cells (BMSCs). Six mature male rabbits were included in this study. PRP was obtained by two-step centrifugation from whole blood, it using CaCl2 solution. BMSCs isolated proliferated marrow characterized flow cytometry. Passage 3 cultured...

An abnormal isoform, PrP(Sc), of the normal cellular prion protein (PrP(C)) is the major component of the causative agent of prion diseases. Both isoforms were found to possess the same covalent structures, including a C-terminal glycosylphosphatidylinositol anchor, but different secondary and tertiary structures. In this study, a variant of full-length PrP with an unpaired cysteine at the C te...

background: plantar fasciitis (pf) is a common foot complaint, affects both active sportsmen and physically inactive middle age group. it is believed that pf results from degenerative changes rather than inflammation. platelet?rich plasma (prp) therapy has been introduced as an alternative therapy for pf. this study is aimed to systematically review to the effectiveness and relevant factors of ...

Prion diseases, or transmissible spongiform encephalopathies, are neurodegenerative diseases, which affect human and many species of animals with 100% fatality rate. The most accepted etiology for prion disease is 'prion', which arises from the conversion from cellular PrP(C) to the pathological PrP(Sc). This review discussed the characteristic structure of PrP, including PRNP gene, PrP(C), PrP...

Molecules that inhibit the formation of an abnormal isoform of prion protein (PrP(Sc)) in prion-infected cells are candidate therapeutic agents for prion diseases. Understanding how these molecules inhibit PrP(Sc) formation provides logical basis for proper evaluation of their therapeutic potential. In this study, we extensively analyzed the effects of the anti-PrP monoclonal antibody (mAb) 44B...

Although prion propagation is well understood, the signaling pathways activated by neurotoxic forms of prion protein (PrP) and those able to mitigate pathological phenotypes remain largely unknown. Here, we identify src-2, a Fyn-related kinase, as a gene required for human PrP with an insertional mutation to be neurotoxic in Caenorhabditis elegans, and the longevity modulator sir-2.1/SIRT1, a s...

The conversion of a ubiquitous cellular protein (PrP(C)), an isoform of the prion protein (PrP), to the pathology-associated isoform PrP(Sc) is one of the hallmarks of transmissible spongiform encephalopathies such as bovine spongiform encephalopathy (BSE). Accumulation of PrP(Sc) has been used to diagnose BSE. Here we describe a quantitative enzyme-linked immunosorbent assay (ELISA) that invol...

Prion protein (PrP) inhibits the activation of proapoptotic Bax in primary human neurons and MCF-7 cells. Because neuronal apoptosis occurs in human prion diseases, here we examine the anti-Bax function of familial PrP mutants. All Creutzfeldt-Jakob disease and fatal familial insomnia-associated prion protein mutations partially or completely lose the anti-Bax function in human neurons and, exc...