To develop and validate a novel 6-dye STR(short tandem repeat) 25-plex DNA typing system for forensic DNA profiling and databases. In this study, a novel STR 25-plex DNA typing system that includes 24 autosomal STRs (D1S1656, D2S1338, D2S441, D3S1358, D5S818, D6S1043, D7S820, D8S1179, D10S1248, D12S391, D13S317, D16S539, D18S51, D19S433, D21S11, D22S1045, CSF1PO, FGA, Penta D, Penta E, TH01, TPOX, vWA, D11S4463) and Amelogenin was developed. Validation studies demonstrated the sensitivity, accuracy, and reproducibility of our novel STR 25-plex DNA typing system. The sensitivity of the STR 25-plex DNA typing system was demonstrated by the ability to obtain complete profiles from as little as 0.125ng of human DNA. Specificity testing was demonstrated by the lack of cross-reactivity to a variety of commonly encountered animal species and microbial pool. For stability testing, full profiles were obtained with humic acid concentration ≤60ng/μL and hematin ≤600μM. For forensic evaluation, the selected 24 autosomal STRs followed the Hardy–Weinberg equilibrium. Since 24 autosomal STRs were independent from one another, PM (Probability matching) was 3.5434×10-28, TDP (Total Probability of Discrimination Power) was 0.999999999999999999999999969863, and CEP (Cumulative probability of exclusion) was 0.99999999375. The new STR 25-plex typing system is sensitive, reproducible, and stable, therefore it is highly applicable for use in national DNA database and can help to facilitate international data sharing.

Bipolar Disorder ; blood ; immunology ; metabolism ; Depressive Disorder ; blood ; immunology ; metabolism ; Humans ; Proteomics

BACKGROUND: Pathological cardiac hypertrophy is one of the main activators of heart failure. Currently, no drug can completely reverse or inhibit the development of pathological cardiac hypertrophy. To this end, we proposed a silicate ion therapy based on extract derived from calcium silicate (CS) bioceramics for the treatment of angiotensin II (Ang II) induced cardiac hypertrophy. METHODS: In this study, the Ang II induced cardiac hypertrophy mouse model was established, and the silicate ion extract was injected to mice intravenously. The cardiac function was evaluated by using a high-resolution Vevo 3100 small animal ultrasound imaging system. Wheat germ Agglutinin, Fluo4-AM staining and immunofluorescent staining was conducted to assess the cardiac hypertrophy, intracellular calcium and angiogenesis of heart tissue, respectively. RESULTS: The in vitro results showed that silicate ions could inhibit the cell size of cardiomyocytes, reduce cardiac hypertrophic gene expression, including atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and b-myosin heavy chain (b-MHC), decrease the content of intracellular calcium induced by Ang II. In vivo experiments in mice confirmed that intravenous injection of silicate ions could remarkably inhibit the cardiac hypertrophy and promote the formation of capillaries, further alleviating Ang II-induced cardiac function disorder. CONCLUSION This study demonstrated that the released silicate ions from CS possessed potential value as a novel therapeutic strategy of pathological cardiac hypertrophy, which provided a new insight for clinical trials.