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BACKGROUND To investigate the combination of beraprost sodium (BPS) and aspirin in the treatment of acute ischemic stroke (AIS). MATERIAL AND METHODS 308 patients with acute cerebral infarction were randomly divided into two groups: experimental group (n=154), treated with BPS (40 μg, tid) and aspirin (100 mg, qd); control group (n=154), treated with 100 mg of aspirin, qd). The antiplatelet therapy remained unchangeable until six months after hospital discharge. RESULTS Initially, no significant differences were found between the two groups. After six months, the relapse-free survival rate was similar between the treatment group (98.1%) and the control group (97.4%). One patient died from AIS in the control group. However, glomerular filtration rate was significantly higher; neurological function and functional ability of patients were better in patients treated with BPS plus aspirin (experimental group) than that in aspirin alone group. No significant difference was found in the function of the coagulation system, suggesting that BPS plus aspirin treatment did not increase the risk of bleeding. Serious adverse events did not occur in both groups. Facial flushing (one case) and mild gastrointestinal reaction (one case) were found in the treatment group without influencing treatment. CONCLUSIONS In our trial involving patients with acute cerebral infarction, BPS plus aspirin was not found to be superior to aspirin in reducing the recurrence of cerebral infarction or death. However, BPS plus aspirin treatment could improve renal function and neurological function without increasing the risk of bleeding.

As an autoimmune disease, myasthenia gravis is caused by the dysfunction of neural transmission. Acetylcholine is known to exert its function after entering into synaptic cleft through binding onto postsynaptic membrane. The role of acetylcholine in binding MuSK in myasthenia gravis, however, remains unknown. A total of 38 myasthenia gravis patients and 27 healthy controls were included in this study for the detection of the expression of MuSK using immunofluorescent method. Expression of both MuSK and interleukin-6 (IL-6) were measured by Western blot, followed by the correlation analysis between heat shock protein 90 (HSP90) and IL-6 which were measured by enzyme-linked immunosorbent assay (ELISA). In myasthenia gravis patients, MuSK was co-localized with acetylcholine at the postsynaptic membrane. Such accumulation of MuSK, however, did not occur in normal people. Meanwhile we also observed elevated expression of IL-6 in myasthenia gravis patients (p<0.05). ELISA assay showed higher expression of HSP90 in patients. Further signaling pathway screening revealed the activation of IL-6-mediated pathways including STAT3 and SPH2. In conclusion, MuSK was co-localized with acetylcholine in myasthenia gravis patients, with elevated expression. HSP90 in disease people can activate IL-6 mediated signaling pathways.

Arterial thrombosis in cerebral infarction severely affects patients' lives. Classical treatment including surgery and medication both had significantly adverse effects, making it necessary to find novel strategy. Endothelial progenitor cells (EPCs) have been shown to enhance the recanalization of thrombosis, while leaving its molecular mechanism unclear. EPCs were separated from peripheral blood, and were transfected by microRNA (miR)-145. The growth, proliferation and migration abilities were quantified by MTT, clone formation and Transwell assays, respectively. Cell apoptosis was evaluated by flow cytometry. The activation of JNK signaling pathway was measured by Western blotting, followed by JNK inhibitor SP600125. In a mouse cerebral infarction model, miR-145 transfected EPCs were injected to observe the condition of arterial thrombosis. MiR-145 transfection enhanced growth, migration and proliferation of EPCs without induction of apoptosis. MiR-145 exerts its effects via JNK signaling pathway, as the blocking inhibited cell migration/proliferation. In vivo injection of miR-145 transfected EPCs also potentiated cell proliferation and migration, in addition to the recanalization of arterial thrombosis. MiR-145 facilitates proliferation and migration of EPCs and recanalization of arterial thrombosis in cerebral infarction mice via JNK signal pathway. This study provided new insights regarding infarction treatment.