In patients with a minor ischaemic stroke or transient ischaemic attack (TIA), separate trials have shown that dual antiplatelet therapy with clopidogrel plus aspirin (clopidogrel-aspirin) or ticagrelor plus aspirin (ticagrelor-aspirin) are more effective than aspirin alone in stroke secondary prevention. However, these two sets of combination have not been directly compared. Since clopidogrel was less effective in stroke patients who were loss-of-function (LOF) allele carriers, whether ticagrelor-aspirin is clinically superior to clopidogrel-aspirin in this subgroup of patients with stroke is unclear. To describe the rationale and design considerations of the Clopidogrel in High-risk patients with Acute Non-disabling Cerebrovascular Events (CHANCE-2) trial. CHANCE-2 is a randomised, double-blind, double-dummy, placebo-controlled, multicentre trial that compares two dual antiplatelet strategies for minor stroke or TIA patients who are allele carriers ticagrelor (180 mg loading dose on day 1 followed by 90 mg twice daily on days 2-90) or clopidogrel (300 mg loading dose on day 1 followed by 75 mg daily on days 2-90), plus open-label aspirin with a dose of 75-300 mg on day 1 followed by 75 mg daily on day 2-21. selleck inhibitor All will be followed for 1 year. The primary efficacy outcome is any stroke (ischaemic or haemorrhagic) within 3 months and the primary safety outcome is any severe or moderate bleeding event within 3 months. The CHANCE-2 trial will evaluate whether ticagrelor-aspirin is superior to clopidogrel-aspirin for minor stroke or TIA patients who are LOF allele carriers. NCT04078737.NCT04078737. Rapid genotyping is useful for guiding early antiplatelet therapy in patients with high-risk nondisabling ischaemic cerebrovascular events (HR-NICE). Conventional genetic testing methods used in genotype-guided antiplatelet therapy for patients with HR-NICE did not satisfy the needs of the Clopidogrel in High-Risk Patients with Acute Nondisabling Cerebrovascular Events (CHANCE)-2 trial. Therefore, we developed the rapid-genotyping GMEX (point-of-care) system to meet the needs of the CHANCE-2 trial. Healthy individuals and patients with history of cardiovascular diseases (n=408) were enrolled from six centres of the CHANCE-2 trial. We compared the laboratory-based genomic test results with Sanger sequencing test results for accuracy verification. Next, we demonstrated the accuracy, timeliness and clinical operability of the GMEX system compared with laboratory-based technology (YZY Kit) to verify whether the GMEX system satisfies the needs of the CHANCE-2 trial. Genotypes reported by the GMEX system showed 100% agreement with those determined by using the YZY Kit and Sanger sequencing for all three alleles (*2, *3 and *17) tested. The average result's turnaround times for the GMEX and YZY Kit methods were 85.0 (IQR 85.0-86.0) and 1630.0 (IQR 354.0-7594.0) min (p<0.001), respectively. Our data suggest that the GMEX system is a reliable and feasible point-of-care system for rapid genotyping for the CHANCE-2 trial or related clinical and research applications.Our data suggest that the GMEX system is a reliable and feasible point-of-care system for rapid CYP2C19 genotyping for the CHANCE-2 trial or related clinical and research applications.The gut bacterial community prevents many pathogens from colonizing the intestine. Previous studies have associated specific bacteria with clearing Clostridioides difficile colonization across different community perturbations. However, those bacteria alone have been unable to clear C. difficile colonization. To elucidate the changes necessary to clear colonization, we compared differences in bacterial abundance between communities able and unable to clear C. difficile colonization. We treated mice with titrated doses of antibiotics prior to C. difficile challenge, resulting in no colonization, colonization and clearance, or persistent colonization. Previously, we observed that clindamycin-treated mice were susceptible to colonization but spontaneously cleared C. difficile Therefore, we investigated whether other antibiotics would show the same result. We found that reduced doses of cefoperazone and streptomycin permitted colonization and clearance of C. difficile Mice that cleared colonization had antibioticm colonizing and causing infection. However, antibiotics can disturb the gut microbiota, which allows C. difficile to colonize. C. difficile infections (CDI) are primarily treated with antibiotics, which frequently leads to recurrent infections because the microbiota has not yet returned to a resistant state. The recurrent infection cycle often ends when the fecal microbiota from a presumed resistant person is transplanted into the susceptible person. Although this treatment is highly effective, we do not understand the mechanism. We hope to improve the treatment of CDI through elucidating how the bacterial community eliminates CDI. We found that C. difficile colonized susceptible mice but was spontaneously eliminated in an antibiotic treatment-specific manner. These data indicate that each community had different requirements for clearing colonization. Understanding how different communities clear colonization will reveal targets to improve CDI treatments.Prior work has shown that parenterally administered anti-CD20 (5D2) inhibits CD4+ T cell priming in response to challenge with Pneumocystis murina and predisposes to pneumonia. In this study, we investigated the effect of subcutaneous anti-CD20 antibody and Pneumocystis infection. In mice with primary infection, anti-CD20 antibody treatment depleted both CD19+ and CD27+ CD19+ cells but not T cells in the lung at days 14 and 28 after Pneumocystis inoculation. Although anti-CD20 antibody treatment impaired fungal clearance at day 14 postinfection, fungal burden in the lungs was substantially reduced at day 28 in both depleted and control mice in the low-dose group. Subcutaneous anti-CD20 antibody treatment did not alter antigen-specific serum immunoglobulin levels in mice compared with control mice, and there were no significant differences in the numbers of lung gamma interferon-positive (IFN-γ+) CD4+, interleukin 4-positive (IL-4+) CD4+, IL-5+ CD4+, and IL-17A+ CD4+ cells between depleted and control mice after infection.