AIM: To investigate the influences of native and oxidized lipoprotein(a) on human arterial smooth muscle cell (SMC) proliferation, change of intracellular free calcium concentration ([Ca 2+ ] i) and the protective effect of sodium ferulate(SF). METHODS: Lp(a) was oxidized by Cu 2+ and the extent of oxidation was assessed by the MDA content.Human SMC were incubated in culture media with SF for 12 h, then exposed to Lp(a) and oxidized-Lp(a), respectively. MTT colorimetry and flow cytometry were used to evaluated the proliferation of SMC and flurorescent indicator Fura-2/AM was used to determined [Ca 2+ ] i. RESULTS: ox-Lp(a) significantly promoted proliferation of SMC and increased[Ca 2+ ] i compared with Lp(a). SF(40,80 mg/L) remarkedly inhibited SMC proliferation and decreased the rising of [Ca 2+ ] i induced by ox-Lp(a) in a dose-dependent manner, but no effect on SMC proliferation and the increase in [Ca 2+ ] i induced by Lp(a).CONCLUSION: ox-Lp(a) induces the strong growth-promoting effect in SMC through increasing in [Ca 2+ ] i, which might be one of the cellular mechanisms responsible for the higher atherogenic potential of ox-Lp(a) compared with Lp(a), and this process can be prevented by inhibiting of oxidation by SF.

Acute traumatic cervical spinal cord injury (TCSCI) is one of the most common severe injuries, and is often accompanied by complications like respiratory infection due to different degrees of paralysis of respiratory muscles, decreased cough function, increased bronchial secretions and bronchial spasm, which seriously affects the respiratory function recovery and enhances mortality rate. The authors review the respiratory management in patients with TCSCI from mechanical ventilation, tracheotomy, oxygen therapy, aerosolized inhalation, assisted sputum extraction, and respiratory function training, in order to provide a reference for clinical nursing work and improve the treatment effect.

Objective:To analyze survival in patients with advanced oral cancer from prospective clinical trials. Methods:From 2008 to 2010, 256 patients with oral cancer at clinical stage III/IVA were randomly categorized into two groups. Patients in the experi-mental group received neo-adjuvant chemotherapy, surgery, and post-operative radiation, and patients in the control group underwent surgery and post-operative radiation. All patients were routinely followed-up after treatments. Survival was analyzed using Kaplan–Meier method and log-rank test, and differences were considered statistically significant at P value lower than 0.05. Results: Each group was composed of 128 patients. With the median follow-up period of 60 months, the 5-year overall survival rate was 61.7%and the disease-free survival rate was 53.9%. The overall survival rate (P=0.350) and the disease-free survival rate (P=0.160) were not sig-nificantly different between the experimental and control groups. Patients with positive pathological response to neo-adjuvant chemo-therapy exhibited significantly improved overall survival (P＜0.05). Conclusion:Radical surgery should be emphasized to improve the prognosis of oral cancer. Functional reconstruction could also improve the quality of life and survival of patients. Despite that neo-adju-vant chemotherapy could not improve the survival of patients with advanced oral cancer in entirety, it could benefit patients exhibiting positive treatment responses.

Although NPM1 mutations are frequently found in acute myeloid leukemia patients, therapeutic strategies are scarce and unsuitable for those who cannot tolerate intensive chemotherapy. Here we demonstrated that heliangin, a natural sesquiterpene lactone, exerts favorable therapeutic responses in NPM1 mutant acute myeloid leukemia cells, with no apparent toxicity to normal hematogenous cells, by inhibiting their proliferation, inducing apoptosis, causing cell cycle arrest, and promoting differentiation. In-depth studies on its mode of action using quantitative thiol reactivity platform screening and subsequent molecular biology validation showed that the ribosomal protein S2 (RPS2) is the main target of heliangin in treating NPM1 mutant AML. Upon covalent binding to the C222 site of RPS2, the electrophilic moieties of heliangin disrupt pre-rRNA metabolic processes, leading to nucleolar stress, which in turn regulates the ribosomal proteins-MDM2-p53 pathway and stabilizes p53. Clinical data shows that the pre-rRNA metabolic pathway is dysregulated in acute myeloid leukemia patients with the NPM1 mutation, leading to a poor prognosis. We found that RPS2 plays a critical role in regulating this pathway and may be a novel treatment target. Our findings suggest a novel treatment strategy and lead compound for acute myeloid leukemia patients, especially those with NPM1 mutations.