Objective To investigate the effect of galangin on cardiac remodeling and cardiac func-tion after myocardial infarction(MI).Methods A total of 32 male C57/BL6 mice(8-10 weeks old)were subjected for MI modeling,and finally 24 mice were assigned into control group[sham operation+hydroxycellulose sodium(CMC-Na)],model group(MI+CMC-Na),and experimental group(MI+galangin),with 8 mice in each group.After MI modeling,the mice of the experimen-tal group were given 40 mg/kg galangin by gavage for 4 weeks,and those of the control group and the model group were given the same volume(0.4 ml)of CMC-Na solution.HE staining was used to observe the size of the infarct area.The mRNA levels of inflammatory factors in the heart were detected by qRT-PCR,and protein levels of related signaling pathway proteins were measured with Western blotting.Immunofluorescence(IF)assay was applied to detect the infiltration of in-flammatory cells in the infarct border zone.TUNEL staining was employed to detect cell apoptosis in the infarct border zone.Results At 4 weeks after modeling,larger infarct size,enhanced expression levels of IL-1β,IL-6,TNF-α,p-P65,p-IκBα and Bax,elevated apoptotic rate,decreased cardiac function indicators such as FS and LVEF,and reduced Bcl-2 expression level were observed in the model group than the control group(P＜0.05).The experimental group had sig-nificant smaller myocardial infarct size[(11.64±0.64)％vs(21.84±1.94)％],less CD3 positive T cells[(3.10±0.46)％vs(6.28±0.24)％],F4-80 positive macrophages[(1.98±0.50)％vs(5.35±0.62)％]and LY6G positive neutrophils[(6.33±0.67)％vs(11.33±1.77)％],decreased expression levels of IL-1β,IL-6,TNF-α,p-P65,p-IκBα and Bax,reduced apoptotic rate[(21.45± 1.62)％vs(35.68±0.88)％],and increased FS and LVEF values and Bcl-2 expression level when compared with the model group(P＜0.05).Conclusion Galangin improves myocardial remode-ling and cardiac dysfunction after MI by inhibiting inflammatory response and cell apoptosis.

Background::Sepsis is a systemic inflammatory syndrome induced by several infectious agents. Multiple organs are affected by sepsis, including the liver, which plays an important role in metabolism and immune homeostasis. Fibroblast growth factors (FGFs) participate in several biological processes, although the role of FGF5 in sepsis is unclear. Methods::In this study, lipopolysaccharide (LPS) was administrated to mice to establish a sepsis-induced liver injury. A similar in vitro study was conducted using L-02 hepatocytes. Western blot and immunohistochemistry staining were performed to evaluate the FGF5 expression level in liver tissues and cells. Inflammatory cell infiltrations, cleaved-caspase-3 expressions, reactive oxygen species and levels of inflammatory cytokines were detected by immunofluorescence, dihydroethidium staining, and reverse transcription quantitative polymerase chain reaction analysis, respectively. Flow cytometry was used to detect the apoptosis level of cells. In addition, ribonucleic acid (RNA)-sequencing was applied to explore the possible mechanism by which FGF5 exerted effects. Results::LPS administration caused FGF5 down-regulation in the mouse liver as well as in L-02 hepatocytes. Additionally, with FGF5 overexpression, liver injury and the level of hepatocyte apoptosis were ameliorated. Further, RNA sequencing performed in hepatocytes revealed the phosphoinositide-3-kinase/protein kinase B (PI3K/AKT) pathway as a possible pathway regulated by FGF5. This was supported using an inhibitor of the PI3K/AKT pathway, which abrogated the protective effect of FGF5 in LPS-induced hepatocyte injury. Conclusion::The anti-apoptotic effect of FGF5 on hepatocytes suffering from LPS has been demonstrated and was dependent on the activation of the PI3K/AKT signaling pathway.

Objective:To analyze the genetic mutations and clinical features of the subtypes of classical BCR-ABL-negative myeloproliferative neoplasm (MPN) .Methods:Mutations of 108 newly diagnosed BCR-ABL-negative MPN patients [including 55 patients with essential thrombocytopenia (ET) , 24 with polycythemia vera (PV) , and 29 with primary myelofibrosis (PMF) ] were identified using next-generation sequencing with 127-gene panel, and the relationship between gene mutations and clinical features were analyzed.Results:Total 211 mutations in 32 genes were detected in 100 MPN patients (92.59% ) , per capita carried (1.96±1.32) mutations. 85.19% (92/108) patients carried the driver gene (JAK2, CALR, MPL) mutations, 69.56% (64/92) of these patients carried at least 1 additional gene mutation. In descending order of mutation frequency, the highest frequency was for activation signaling pathway genes (42.2% , 89/211) , methylation genes (17.6% , 36/211) , and chromatin-modified genes (16.1% , 34/211) . There was a significant difference in the number of mutations in the activation signaling pathway genes, epigenetic regulatory genes, spliceosomes, and RNA metabolism genes among the three MPN subgroups. The average number of additional mutations in PMF patients was higher than that in ET and PV patients (1.69±1.39, 0.67±0.70, 0.87±1.22, χ2=13.445, P=0.001) . MPN-SAF-TSS (MPN 10 score) ( P=0.006) and myelofibrosis level ( P=0.015) in patients with ≥ 3 mutant genes were higher and the HGB level ( P=0.002) was lower than in those with<3 mutations. Twenty-six patients (24.1% ) carried high-risk mutation (HMR) , and patients with HMR had lower PLT ( P=0.017) , HGB levels ( P<0.001) , and higher myelofibrosis level ( P=0.010) and MPN10 score ( P<0.001) . The frequency of ASXL1 mutations was higher in PMF than in PV patients (34.5% vs. 4.2% , P=0.005) . PMF patients with ASXL1 had lower levels of PLT and HGB ( P=0.029 and 0.019) . Conclusion:69.56% of MPN patients carry at least one additional mutation, and 24.1% patients had HMR. Each subgroup had different mutation patterns. PMF patients had a higher average number of additional gene mutations, especially a higher frequency of ASXL1 mutation; PLT and HGB levels were lower in ASXL1 mutation PMF patients.

OBJECTIVE: To analyze the clinical features of chronic myeloid leukemia (CML) with T315 I mutation (CML-T315I) and compare the effectiveness of different treatments. METHODS: We retrospectively analyzed the clinical data and outcomes of 19 patients with CML-T315I receiving different treatments. The T315 I mutations in these patients were detected by examination of BCR-ABL kinase domain (KD) mutation by RTQ-PCR and Sanger sequencing. The relapse following the treatments, defined as hematological, cytogenetic and molecular biological recurrences, were analyzed in these patients. RESULTS: Of the 19 patients with CML-T315I, 14 (73.7%) were in CML-CP stage at the initial diagnosis, and 13 (81.2%) were high-risk patients based on the Sokal scores. All the 19 patients were treated with TKI after the initial diagnosis, and during the treatment, 15 (78.9%) patients were found to have additional chromosomal aberrations, and 10 (52.6%) had multiple mutations; 13 (68.4%) of the patients experienced disease progression (accelerated phase/blast crisis) before the detection of T315I mutation, with a median time of 40 months (5-120 months) from the initial diagnosis to the mutation detection. After detection of the mutation, 12 patients were treated with ponatinib and 7 were managed with the conventional chemotherapy regimen, and their overall survival rates at 3 years were 83.3% and 14.2%, respectively ( < 0.001). CONCLUSIONS CML patients resistant to TKI are more likely to have T315I mutations, whose detection rate is significantly higher in the progressive phase than in the chronic phase. These patients often have additional chromosomal aberrations and multiple gene mutations with poor prognoses and a high recurrence rate even after hematopoietic stem cell transplantation. Long-term maintenance therapy with ponatinib may improve the prognosis and prolong the survival time of the patients.
Drug Resistance, Neoplasm ; Fusion Proteins, bcr-abl ; Humans ; Imidazoles ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; Mutation ; Pyridazines ; Retrospective Studies

Magnetic resonance imaging (MRI) data of 87 patients with suspected cervical posterior longitudinal ligament (PLL) rupture,who underwent cervical spine surgery in Luoyang Orthopedic Hospital from January 2015 to September 2017,were analyzed retrospectively.The criteria of MRI diagnosis for PLL rupture were the low signal image of the PLL on the posterior margin of the vertebral body,the discontinuity or continuous interruption,or the local highlighting signal on the T2 weighted image.According to intraoperative findings,the diagnostic accuracy of MRI for PLL rupture was examined.Among 87 patients,31 cases were diganosed as PLL rupture by preoperative MRI;and 38 cases were confirmed by intraoperative exploration,of whom 30 were diagnosed with MRI,and 8 were missed by MRI.The accuracy,sensitivity and specificity of MRI in the diagnosis of ruptured PLL were 0.90,0.79 and 0.98 respectively.MRI has a good diagnostic efficiency in PLL rupture,which can be used for preoperative investigation.

Objective To evaluate the effect of duration of subcutaneous injection on the extent of bruising at injection sites among patients receiving low- molecular weight heparin. Methods Randomized clinical trials and quasi-experimental within-subject design that assessed the effect of subcutaneous duration on the bruising of injection sites were selected in Cochrane library, JBI evidence-based practice medical and nursing database, PubMed biomedical information retrieval platform, Medline general medical literature retrieval database. RevMan5.3 software was used to analyze the data after quality assessment, and data extraction were made for eligible trials. Results A total of 9 trials were included. The results of Meta-analysis supported the 30 s duration injection technique on reducing the rate of bruising of injection sites than 10 s duration injection technique (odds ratio was 0.34,95%confidence interval 0.25-0.47, P<0.01).While it was failed to support the effect on reducing the bruising area 48 and 72 hours after injection (P > 0.05). Conclusions Increasing the length of low-molecular weight heparin subcutaneous injection can reduce the rate of bruising. While it could not effectively reduce the area.

Objective To observe the effect of smoking cessation intervention combined with salmeterol and fluticasone pro‐pionate powder for inhalation on chronic obstructive pulmonary disease (COPD) patients with clinical symptoms and pulmonary function .Methods Totally 78 male long‐term smoking cases were randomly divided into control group(n= 40)and observation group(n=38) .The control group was treated with the ophylline sustained‐release tablets ,shah mette lo fluticasone;observation group received smoking cessation intervention .The smoking rate ,symptoms ,acute exacerbation ,life score and lung function (FEV1 ,FEV1/FVC) ,adverse reactions of two groups were observed .Results Two groups of symptoms were all improved ,but the observation group was better (P<0 .05) .FEV1 ,FEV1/FVC ,acute exacerbation ,scores were improved ,but the observation group was better(all P<0 .05);quit rates in the observation group was better than that of the control group(P<0 .05);and did not found adverse reactions .Conclusion The effect of smoking cessation intervention combined with salmeterol and fluticasone propionate powder for inhalation efficacy in the treatment of COPD is distinct ,can improve the pulmonary function and symptoms .

To effectively screen treating pigmentation disorders drug, a new transgenic zebrafish drug screening model was constructed. Green fluorescent protein(GFP)were drived by tyrosinase-related protein 1a (tyrp1a)promoter specific expression in melanocyte. Effect of N-Phenylthiourea(PTU)and alpha-melanaocyte stimulating hormone(α-MSH)on the GFP expression and melanogenic of tyrp1a: eGFP zebrafish were photographed under the steromicroscope. Results showed that PTU could significantly inhibit the melanogenic and expression of GFP of zebrafish. As compared with control group, α-MSH treatment resulted in marked stimulation of body pigmentation and expression of GFP. In conclusion, a new transgenic zebrafish drug screening model was successfully established, which can be used for treating pigmentation disorders.

ObjectiveTo explore the expression of miR-130b and RUNX3mRNA in human gastric carcinoma and the clinical significance. MethodsThe expression of miR-130b and RUNX3mRNA were detected by RT-PCR in 40 cases of gastric carcinoma and corresponding normal mucosa tissue. The expression of RUNX3protein was determined by immunohistochemistry SP method. ResultsThe expression of miR-130b was significantly up-regulated in gastric carcinoma than that in the adjacent normal gastric mucosa tissues (2.18 ± 3.75 ) vs.( 2.59 ± 3.45 ),P ＜ 0.05 ; The expression of RUNX3mRNA in gastric carcinoma tissues was significantly lower than that in adjacent normal gastric mucosa tissues( 8.76 ±2.82) vs.( 7.58 ± 2.87 ),P ＜ 0.05.The expression of miR-130b and RUNX3mRNA were positively correlated with lymph node metastasis and clinical stage ( P ＜ 0.05 ) ; No significant association was found between the expression and age,gender,tumor size,distant metastasis and depth of tumor invasion ( P ＞0.05 ).The expression of miR-130b was negatively correlated with RUNX3 protein expression in nuclei and cytoplasm (P ＜ 0.05 ).ConclusionsAbnormal expression of miR-130b and RUNX3mRNA correlates with prognosis of gastric carcinoma; Decreased RUNX3 protein expression may contribute to tumourigenesis.

Objective To investigate the relationship between p27 gene methylation and pathology of colorectal carcinoma. Methods p27 gene methylation promotor region and p27 protein expression were detected respectively by methylation specificity polymerase chain reaction and immunohistochemical staining SP in 106 cases of colorectal carcinoma and each adjacent normal mucous membrane tissue and 22 cases of colorectal adenoma tissue. Results The positive expression rate of p27 gene methylation was statistically different in colorectal carcinoma tissue compared with normal mucous membrane and colorectal adenoma tissue (P＜0.05). Their positive expression rate were 59.4% (63/106), 18.2% (4/22) and 3.8%(4/106) respectively in colorectal carcinoma tissue,colorectal adenoma and normal mucous membrane tissue (P ＜ 0. 05). p27 gene methylation in poorly differentiated group was significantly higher than that in welldifferentiated group (48.0% vs. 24. 7%, P ＜0. 05), in Dukes-A + B stage group was significantly lower than that in Dukes C + D stage group(20. 0% vs. 41.2%, P ＜ 0. 05 ), and it was higher in lymph nodes metastases group than that in lymph nodes negative group(41.5% vs. 23. 1%, P ＜0. 05), that in positive serosa infiltration group was higher than negative serosa infiltration group(32. 5% vs. 24. 1%, P ＞ 0. 05 ).Conclusions Methylated p27 gene protein expression in colorectal carcinoma was significantly higher than normal mucous membrane and colorectal adenoma tissue. The methylation rate of p27 gene in colorectal carcinoma was significantly associated with tumor differentiation, invasive depth, Dukes stage, lymph node metastasis.