OBJECTIVE: To investigate the curative effects of nanometer silver dressing and recombinant bovine basic fibroblast growth factor gel on burn residual wounds.METHODS: Forty burn patients with residual wounds because of deep second degree burn and full-thickness burn, were randomly divided into control group and management group. There were 20 patients in both groups. The patients of management group were treated by nanometer silver dressing and recombinant bovine basic fibroblast growth factor gel. The patients of control group were treated by saline and paraffin absorbent gauze. Healing time, wound healing rates at different time points,cases of infected wound and results of bacterial culture before and 7 days following treatment, and drug adverse reaction were recorded.RESULTS: The healing time of management group was significantly shorter than the control group (P < 0.01). The wound healing rates of management group was significantly higher than the control group at different time points (P< 0.01). The cases of infected wound was significantly fewer than the control group after treating (P < 0.01). The pathogenic bacteria detection rate was significantly lower than the control group after 7 days (P < 0.01).CONCLUSION: There was better antibacterial activity, decurtating the healing time when the management of nanometer silver dressing and recombinant bovine basic fibroblast growth factor gel on burn residual wounds were put into practice.

Background and objective Molecular targeting therapy is the direction of individualized treatment of lung cancer, scholars has been established targeted therapy prediction models which provide more guidance for clinical individual therapy. hTis study investigated the relationship among pulmonary surfactant-associated protein D (SP-D), trans-forming growth factorα(TGF-α), matrix metalloproteinase 9 (MMP-9), tissue polypeptide speciifc antigen (TPS), and Krebs von den Lungen-6 (KL-6) and response as well as survival in the patients with recurrent non-small cell lung cancer, which Erlotinib was as second line treatment atfer failure to chemotherapy. hTis study also established a predictive prognostic model.Methods Serum levels of SP-D, TGF-α, MMP-9, TPS, and KL-6 in 114 patients before erlotinib treatment were detected by ELISA method. Combined with clinical factors, these levels were used to investigate the relationship with effcacy in erlotinib treatment and construct a predicted prognostic model by Kaplan-Meier curve and Cox proportional hazard model multivariate analysis. Results hTe objective response rate (ORR) and disease control rate (DCR) in the 114 patients, were 22.8%(26/114) and 72.8%(83/114), to Erlotinib treatment respectively. hTe median progression-free survival (PFS) and one year survival rate with Erlotinib treatment were 5.13 months and 69.3%, respectively. Patients in the SP-D>110 ng/mL group exhibited more ORR (33.3%vs 13.3%, P=0.011) and DCR (83.3%vs 63.3%, P=0.017) than those in the≤110 ng/mL group. Patients in the MMP-9≤535 ng/mL group showed more DCR (83.9%) than those in the>535 ng/mL group (62.1%) (P=0.009). Patients in the TPS<80 U/L group showed more DCR (82.4%) than those in the≥80 U/L group (55.0%) (P=0.002). hTe SP-D>110 ng/mL (5.95 months vs 3.25 months, P=0.009), MMP-9≤535 ng/mL (5.83 months vs 3.47 months, P=0.046), KL-6<500 U/mL (6.03 months vs 3.40 months, P=0.040), and TPS<80 U/L (6.15 months vs 2.42 months, P=0.014) groups showed better PFS. Multivariate analysis showed that current or ever-smoker, wild style of EGFR status, progression atfer prior chemotherapy, absence of skin rash, elevated serum LDH level, and TPS≥80 U/L were independent adverse prognostic factors for PFS. hTese six factors were used in the prognostic model. Patients were categorized into four prognosis risk groups based on the prog-nostic index from the model, namely, low risk, intermediate low risk, intermediate risk, and high risk groups. hTe median PFS of good, intermediate, poor, and very poor prognosis groups were 9.12, 6.88, 3.52, and 0.93 months (P<0.001), respectively. Conclusion hTe prognostic model based on clinical parameters with TPS will be useful in identifying patients who might be most likely to beneift from Erlotinib therapy in the patients with recurrent non-small cell lung cancer.

Hepatic cholesterol accumulation is an important contributor to hypercholesterolemia, which results in atherosclerosis and cardiovascular disease (CVD). ATP-citrate lyase (ACLY) is a key lipogenic enzyme that converts cytosolic citrate derived from tricarboxylic acid cycle (TCA cycle) to acetyl-CoA in the cytoplasm. Therefore, ACLY represents a link between mitochondria oxidative phosphorylation and cytosolic de novo lipogenesis. In this study, we developed the small molecule 326E with an enedioic acid structural moiety as a novel ACLY inhibitor, and its CoA-conjugated form 326E-CoA inhibited ACLY activity with an IC₅₀ = 5.31 ± 1.2 μmol/L in vitro. 326E treatment reduced de novo lipogenesis, and increased cholesterol efflux in vitro and in vivo. 326E was rapidly absorbed after oral administration, exhibited a higher blood exposure than that of the approved ACLY inhibitor bempedoic acid (BA) used for hypercholesterolemia. Chronic 326E treatment in hamsters and rhesus monkeys resulted in remarkable improvement of hyperlipidemia. Once daily oral administration of 326E for 24 weeks prevented the occurrence of atherosclerosis in ApoE^-/- mice to a greater extent than that of BA treatment. Taken together, our data suggest that inhibition of ACLY by 326E represents a promising strategy for the treatment of hypercholesterolemia.