SUMMARY Tonguesquamouscellcarcinoma(TSCC)isthemostcommontypeoforalcancerandis well known for its high rate of proliferation and lymph nodal metastasis.Exploring the underlying path-ways regulating TSCC could provide novel ideas for diagnosis and prognosis of TSCC patients,as well as molecular targets for treatment of TSCC.MicroRNAs (miRNAs)are small noncoding RNAs that inhibit gene expression through the 3′untranslated regions (3′UTRs)of their target messenger RNAs.They play crucial roles in numerous biological processes,including cancer progression.Although great efforts have been made,what role miRNAs may play in the early detection and diagnosis of TSCC is not fully under-stood .Recently,our team has performed a series of basic and clinical researches in an attempt to investi-gate the relationships between miRNA expressions and prognosis of patients with TSCC and the mecha-nisms under regulation of TSCC.The results showed that miR-1 95,miR-34a,miR-29b,miR-375 and miR-26a could inhibit TSCC cells progression and development via a sophisticated network of genes.Spe-cifically,the anti-tumor effects of miR-1 95 in TSCC may be partially mediated by its inhibition of Cy-clinD1 and Bcl-2 expression.The expression of miR-34a could inhibit migration and invasion of TSCC cell lines via targeting MMP9 and MMP1 4.The function of miR-29b may be through the miR-29b/Sp1 /PTEN/AKT axis.Overexpression of miR-375 inhibited Sp1 expression by targeting the 3′untranslated re-gion of the Sp1 transcript.MEG3 and miR-26a inhibited TSCC cell proliferation,cycle progression and promoted cell apoptosis and miR-26a could increase the MEG3 expression through reduction of the ex-pression of DNMT3B in TSCC.In light of the role of those miRNAs in diagnosis and prognosis of TSCC, we reported that decreased miR-1 95 and miR-375 expression was associated with poor overall survival rate of the TSCC patients,while miR-34a expression was negatively correlated with cervical lymph node me-tastases.Furthermore,combined low expression levels of miR-26a and MEG3 emerged as an independent prognostic factor for poor clinical outcomes in TSCC patients,suggesting that combined miR-26a and MEG3 expression might prove useful as an independent biomarker of clinical prognosis among TSCC pa-tients.

Objective To investigate the dynamic changes of platelets (PLT) and white blood cells (WBC) after traumatic brain injury (TBI) and discuss its clinical significance. Methods The number of PLT and WBC were examined in 63 patients with TBI by using cytoanalyze and also analyzed together with Glasgow Outcome Scale and concurrent infection, in the meantime, enzyme-linked immu-nosorbent was used to investigate concentration changes of C reactive protein (CRP) and thrombospondin 1 (TSPI) and analyze the correlation between CRP and TSP1. Results The number of WBC in all pa-tients, whether concurred with infection or not, was significantly increased within 24 hours after TBI (P < 0.01), with no statistical difference between patients without infection at day 4 and normal patients (P >0.05). However, the number of WBC was decreased to below 10 × 109/L in patients without infec-tion, which was significantly higher than that in normal patients (P < 0.05). In patients with infection and unfavorable prognosis, the number of WBC was increased again ay days 7-14, whereas that of PLT rose significantly at days 14-21 (P <0. 01). The concentration of TSPI was positively correlated with that of CRP (r = 0.720, P < 0.01). Conclusions Monitoring the dynamic changes of PLT and WBC is promising. The change of WBC at day 4 post injury is a key indicator to provide evidences of prophylactic antibiotic usage. Much attention should be paid to the dynamic change of PLT at days 14-21 post injury so as to evaluate the condition of hypercoagulability that can be potentially caused by inflammation response. Secondary increase of WBC and later increase, of PLT may affect prognosis of the patients. TSP1 and CRP may participate in thrombosis formation induced by inflammation.

Objective To study the protective effect of human urinary kallidinogenase (HUK) on focal cerebral ischemia-reperfusion injury in rats via phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling pathway.Methods Eighty adult male SD rats were randomly divided into sham-operated group,model group,HUK group and LY294002 group (n=20).The rat focal cerebral ischemia-reperfusion models in the latter three groups were established by suture-occluded method;model group and HUK group were,respectively,injected with sterile saline or HUK 1.0 mL/kg via tail vein 3 h after reperfusion;rats in the LY294002 group accepted intraventricular injection of 10 nmol LY294002 before cerebral ischemia and caudal vein injection of 1.0 mL/kg HUK three h after reperfusion.Twenty-four h after reperfusion,Neurological Deficit Scale was performed,cerebral infarct volumes were detected by 2,3,5-triphenyltetrazolium chloride (TTC) staining,and protein expressions of Akt,phosphorylated (p)-Akt and Caspase-3 were assessed by Western blotting.Results As compared with those in the model group,the Neurological Deficit Scale scores were significantly lower,cerebral infarct volumes were significantly smaller,p-Akt expression was significantly increased,and Caspase-3 expression was significantly decreased in the HUK group (P＜0.05).As compared with those in the HUK group,Neurological Deficit Scale scores were significantly higher,infarction volumes were significantly increased,p-Akt expression was significantly decreased,and Caspase-3 expression was significantly increased in the LY294002 group (P＜0.05).Conclusion HUK has neuro-protective effect through up-regulating p-Akt expression in the PI3K/Akt signaling pathway and down-regulating Caspase-3 expression.