Study on the construction of nomogram prediction model for prognostic assessment of heart failure patients based on serological markers and echocardiography.

OBJECTIVE: We aimed to construct a nomogram prediction model for prognostic assessment of patients with heart failure (HF) based on serological markers and echocardiography. PATIENTS AND METHODS: A total of 200 HF patients admitted to the Second Affiliated Hospital of Nanchang University from January 2018 to January 2020 were selected as the research objects. According to the New York Heart Association (NYHA) cardiac function classification, they were divided into 3 groups, including 65 cases of grade II, 97 cases of grade III, and 38 cases of grade IV. Three groups of echocardiographic parameters were compared [including left ventricular ejection fraction (LVEF), left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD), left ventricular end-systolic volume (LVESV)], differences in serum markers brain natriuretic peptide (BNP), soluble growth-stimulating expression gene 2 (sST2) and the Modified Early Warning Score (MEWS). The patients were divided into two groups according to their clinical outcomes during the follow-up period, including 52 cases in the death group and 148 cases in the survival group. The clinical data of the two groups were compared, and multi-factor logistic regression analysis was performed to screen out the independent risk factors affecting the patient's death. A nomogram model of the patient's mortality risk was constructed based on the independent risk factors. Receiver operating characteristic (ROC) curves and calibration curves were used to evaluate the discrimination and accuracy of the nomogram model. RESULTS: As the cardiac function class of elderly chronic heart failure (CHF) patients increases, LVEDD, LVESD, sST2, and MEWS increase and LVEF decreases (p<0.05). Multifactor analysis results showed that LVEF, LVEDD, sST2, and MEWS were independent factors affecting the clinical outcome of patients. The AUCs predicted using LVEF, LVEDD, sST2, and MEWS alone were 0.738, 0.775, 0.717, 0.831, and 0.768, respectively. There is a certain degree of discrimination, and the model has extremely high accuracy. CONCLUSIONS: MEWS, LVEDD, and sST2 increase as the NYHA cardiac function grade of HF patients increases and LVEF decreases, which can reflect the severity of the disease to a certain extent. Additionally, the nomogram model established based on this has a high predictive value for the long-term prognosis of patients and can formulate effective intervention measures for quantitative values.

Polyoxometalate SbW9 regulates proliferation and apoptosis of NSCLC cells via PTEN-dependent AKT signaling pathway.

The article "Polyoxometalate SbW9 regulates proliferation and apoptosis of NSCLC cells via PTEN-dependent AKT signaling pathway, by H.-B. Sun, L. Xu, Z.-X. Wang, Y. Zheng, Y. Zhao, Y.-Y. Yin, X.-L. Han, Z.-N. Xu, published in Eur Rev Med Pharmacol Sci 2019; 23 (18): 7959-7967-PMID: 31599421" has been withdrawn from the authors due to some technical reasons (there are some evident errors and incorrect data). The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/19012.

MicroRNA-218 regulates the epithelial-to-mesenchymal transition and the PI3K/Akt signaling pathway to suppress lung adenocarcinoma progression by directly targeting BMI-1.

The article "MicroRNA-218 regulates the epithelial-to-mesenchymal transition and the PI3K/Akt signaling pathway to suppress lung adenocarcinoma progression by directly targeting BMI-1, by L. Xu, H.-B. Sun, Z.-N. Xu, X.-L. Han, Y.-Y. Yin, Y. Zheng, Y. Zhao, Z.-X. Wang, published in Eur Rev Med Pharmacol Sci 2019; 23 (18): 7978-7988-DOI: 10.26355/eurrev_201909_19014-PMID: 31599423" has been withdrawn from the authors due to some technical reasons (there are some errors and  incorrect data). The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/19014.

LINC01093 promotes proliferation and invasion of non-small cell lung cancer cells via targeting akt signaling pathway.

The article "LINC01093 promotes proliferation and invasion of non-small cell lung cancer cells via targeting akt signaling pathway, by Z.-X. Wang, Z.-N. Xu, H.-B. Sun, Y. Wang, Z.-F. Han, Y. Yu, X.-L. Han, Y.-Y. Yin, L. Xu, published in Eur Rev Med Pharmacol Sci 2020; 24 (1): 222-229- DOI: 10.26355/eurrev_202001_19914-PMID: 31957835" has been withdrawn from the authors due to some technical reasons (there are some errors and incorrect data). The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/19914.

Nrf2 mediates the neuroprotective effect of isoflurane preconditioning in cortical neuron injury induced by oxygen-glucose deprivation.

OBJECTIVE: To investigate how nuclear factor-E2-related factor 2 (Nrf2) involved in the protective effect of isoflurane (Iso) preconditioning in oxygen glucose deprivation (OGD)-induced cortical neuron injury. METHODS: Primary mouse cortical neurons were divided into Control, ML385 (an Nrf2 inhibitor), Iso, Iso + ML385, OGD, ML385 + OGD, Iso + OGD, and Iso + ML385 + OGD groups. Lactate dehydrogenase activity (LDH) release and oxidative stress indexes were quantified. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was used to detect cell viability, Annexin V-FITC/propidium iodide (PI) staining to measure cell apoptosis, dichloro-dihydro-fluorescein diacetate (DCFH-DA) method to test reactive oxygen species (ROS), and quantitative reverse-transcription polymerase chain reaction (qRT-PCR) and Western blotting to evaluate genes and protein expression. RESULTS: Iso preconditioning reduced LDH release and inhibited cell cytotoxicity in OGD-induced cortical neurons, which was abolished by ML385. Iso preconditioning increased the Nrf2 nuclear translocation in cortical neurons. Meanwhile, Iso decreased the OGD-induced apoptosis with the down-regulations of Bax and Caspase-3 and the up-regulation of Bcl-2, which was reversed by ML385. OGD enhanced the level of ROS and malondialdehyde (MDA) in cortical neurons, but reduced the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), which were aggravated in ML385 + OGD group and mitigated in Iso + OGD group. No observable difference was found between OGD group and Iso + ML385 + OGD group regarding apoptosis-related proteins and oxidative stress-related indexes. CONCLUSION: Iso preconditioning up-regulated Nrf2 level to play its protective role in OGD-induced mouse cortical neuron injury.

Long noncoding RNA SNHG14 exerts oncogenic functions in lung adenocarcinoma through acting as a sponge to miR-613.

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "Long noncoding RNA SNHG14 exerts oncogenic functions in lung adenocarcinoma through acting as a sponge to miR-613, by Z.-N. Xu, Z.-X. Wang, L. Xu, H.-X. Yu, K. Chao, L.-L. Yang, X.-L. Han, H.-B. Sun, published in Eur Rev Med Pharmacol Sci 2019; 23 (24): 10810-10817-DOI: 10.26355/eurrev_201912_19784-PMID: 31858549" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/19784.

CircRNF20 aggravates the progression of non-small-cell lung carcinoma by activating MAPK9.

OBJECTIVE: To explore the clinical significance of circRNF20 in non-small-cell lung carcinoma (NSCLC), and its regulatory effects on NSCLC cell functions by activating MAPK9. PATIENTS AND METHODS: Relative levels of circRNF20 and MAPK9 in NSCLC tissues were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The relationship between circRNF20, MAPK9 and pathological factors in NSCLC patients was analyzed. Prognostic potentials of circRNF20 and MAPK9 in NSCLC were assessed by Kaplan-Meier method. The interaction between circRNF20 and MAPK9 was tested by Dual-Luciferase reporter assay. Regulatory effects of circRNF20 and MAPK9 on proliferative abilities in H358 and SPC-A1 cells were examined by Cell Counting Kit-8 (CCK-8) and colony formation assay. RESULTS: CircRNF20 and MAPK9 were upregulated in NSCLC tissues than normal ones. They were correlated to T stage and poor prognosis in NSCLC patients, while their levels were unrelated to gender, age, and incidences of lymphatic and distant metastasis. Knockdown of circRNF20 attenuated proliferative abilities in H358 and SPC-A1 cells. On the contrary, the overexpression of MAPK9 yielded the opposite results. MAPK9 was the target gene binding circRNF20, which was able to reverse the regulatory effect of circRNF20 on NSCLC proliferation. CONCLUSIONS: CircRNF20 and MAPK9 are upregulated in NSCLC cases, which are closely linked to T stage in NSCLC patients. They are independent prognostic factors for NSCLC. By activating MAPK9, circRNF20 stimulates NSCLC proliferation.

Glycyrrhizin improves inflammation and apoptosis via suppressing HMGB1 and PI3K/mTOR pathway in lipopolysaccharide-induced acute liver injury.

OBJECTIVE: Acute liver injury (ALI) is mainly characterized by the symptom of metabolic disorders, homeostasis unbalance, and loss of liver function. There are no effective treatment methods at present stage except the liver transplantation. Effective treatment for early ALI is of great significance for the treatment of liver injury thereof. Glycyrrhizin (GL) is a promising inhibitor of the high-mobility group box-1 gene (HMGB1) which is expressed much higher in an inflammatory injury. However, it is not clear whether GL improves ALI via the inhibition of HMGB1. The present study is to probe the function and mechanism of glycyrrhizin on acute liver injury. MATERIALS AND METHODS: The expression of HMGB1 and inflammation in liver macrophages were analyzed. Lipopolysaccharide (LPS) was used in stimulating the macrophages to activate inflammatory response and recombined human HMGB1 was used to resist the function of GL to explore whether GL acted via the target of HMGB1. Then, LPS injection was utilized to induce ALI in mice, and then we evaluated GL treatment in ALI model. RESULTS: The results showed that the expressions of HMGB1 and inflammatory factors were markedly increased in LPS-activated liver macrophages. GL inhibited the progress of macrophages inflammation by restraining HMGB1, and the administration of GL could reverse the effects of LPS-induced ALI in mice. Moreover, PI3K/mTOR pathway was significantly suppressed by GL application. CONCLUSIONS: These results suggest that GL prevents inflammation in liver macrophages via inhibition of HMGB1. GL restrains inflammation and cell apoptosis by inhibiting HMGB1 via PI3K/mTOR signaling pathway in ALI. GL may become a novel drug for the therapy of ALI in the future.

LINC01093 promotes proliferation and invasion of non-small cell lung cancer cells via targeting akt signaling pathway.

OBJECTIVE: To explore the expression of LINC01093, a long non-coding ribonucleic acid (lncRNA) in non-small cell lung cancer (NSCLC) tissues, and cells and its regulatory role in NSCLC cell proliferation and invasion. PATIENTS AND METHODS: The expression of LINC01093 in NSCLC tissues and cells was detected via quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR) experiment. The specific sequences interfering in LINC01093 were designed and transiently transfected into A549 and SPCA-1 cells using LipofectamineTM 2000, and 48 later, the transfection efficiency was detected. Moreover, the impacts of small interfering (si)-LINC01093 on NSCLC cell proliferation were observed via methyl thiazolyl tetrazolium (MTT) and colony forming assays, the influence of LINC01093 on the cycle distribution of NSCLC cells was determined through flow cytometry, and the changes in the invasion and migration abilities of NSCLC cells were evaluated via transwell assay after interfering in the expression of LINC01093. Finally, the expression changes of the molecular markers in the protein kinase B (Akt) signaling pathway in the downstream of LINC01093 were detected via Western blotting. RESULTS: According to the results of qRT-PCR, the relative expression level of LINC01093 was up-regulated in NSCLC tissues and cells. After interfering in the expression of LINC01093, the results of MTT and colony forming assays revealed that the proliferation ability of NSCLC cells was weakened, according to the findings in the flow cytometry, the cells were arrested in G1/0 phase, the transwell assay results manifested that the cell migration and invasion abilities were weakened, and the results of the Western blotting suggested the changes in the expressions of molecular markers in the Akt signaling pathway. CONCLUSIONS: The expression of LINC01093 is upregulated in NSCLC tissues and cells, and it facilitates the proliferation, invasion, and metastasis of NSCLC cells via the Akt signaling pathway.

Effects of lncRNA SNHG20 on proliferation and apoptosis of non-small cell lung cancer cells through Wnt/ß-catenin signaling pathway.

OBJECTIVE: To investigate the influence of long non-coding ribonucleic acid (lncRNA) small nucleolar host gene 20 (SNHG20) on the proliferation and apoptosis of non-small cell lung cancer (NSCLC) cells through the Wnt/ß-catenin signaling pathway. PATIENTS AND METHODS: The human NSCLC cells were cultured and lncRNA SNHG20 was inhibited using si-SNHG20 and overexpressed using SNHG20-OE. Then, flow cytometry was used to detect the apoptotic rate. The targets of lncRNA SNHG20 were detected via dual-luciferase reporter gene assay, and the changes in the protein level were detected via Western blotting. RESULTS: LncRNA SNHG20 was highly expressed in the cancer tissues and serum of patients with NSCLC. LncRNA SNHG20 could promote the proliferation and inhibit the apoptosis of NSCLC cells. LncRNA SNHG20 could bind to micro RNA (miR)-197 in a targeted manner. Besides, nuclear translocation of ß-catenin was significantly enhanced after transfection of miR-197. After the down-regulation of miR-197 by small interfering RNA (siRNA), the key molecules TCF and LEF1 of the Wnt/ß-catenin pathway were significantly down-regulated. CONCLUSIONS: LncRNA SNHG20 promotes the proliferation and inhibits the apoptosis of NSCLC cells by targeting miR-197 through the Wnt/ß-catenin signaling pathway.

Long noncoding RNA SNHG14 exerts oncogenic functions in lung adenocarcinoma through acting as a sponge to miR-613.

OBJECTIVE: Lung adenocarcinoma is one of the most ordinary malignant tumors. Recent researches have proved that long noncoding RNAs (lncRNAs) are vital factors in many diseases. In this work, lncRNA SNHG14 was studied to identify its function in the development of lung adenocarcinoma. PATIENTS AND METHODS: Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was utilized to detect SNHG14 expression in paired lung adenocarcinoma patients' tissue samples and cells. Then, the function of SNHG14 was detected through MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) assay, colony formation assay, and transwell assay in vitro. Besides, mechanism assays and the interaction between SNHG14 and miR-613 were conducted. RESULTS: SNHG14 was remarkably higher-expressed in lung adenocarcinoma tissues than in adjacent samples. Moreover, cell proliferation and invasion of lung adenocarcinoma were promoted via overexpression of SNHG14, while cell proliferation and invasion of lung adenocarcinoma were inhibited via silence of SNHG14. Moreover, RT-qPCR results revealed that miR-613 was downregulated via overexpression of SNHG14, while miR-613 was upregulated via knockdown of SNHG14. Further experiments showed that miR-613 was also a direct target of SNHG14 in lung adenocarcinoma. CONCLUSIONS: Our study suggests that SNHG14 enhances lung adenocarcinoma cell proliferation and invasion via targeting miR-613, which indicates that SNHG14 may be a potential therapeutic target in lung adenocarcinoma.

MicroRNA-218 regulates the epithelial-to-mesenchymal transition and the PI3K/Akt signaling pathway to suppress lung adenocarcinoma progression by directly targeting BMI-1.

OBJECTIVE: To investigate the role of miR-218 in the development of lung adenocarcinoma (LA) and its underlying mechanism. PATIENTS AND METHODS: Fifty-two pairs of human LA samples and adjacent para-carcinoma tissue samples were collected from our hospital between June 2015 and March 2017. Meanwhile, one normal human pulmonary epithelial cell line BEAS-2B and four human LA cell lines (H1299, PC-9, A549, and SPC-A1) were cultured. The cells' ability of proliferation and migration was detected by MTT assays and Transwell assays, respectively. The target gene was clarified by dual-luciferase reporter assay. The related protein and mRNA expression levels were detected by immunohistochemistry (IHC), Western blot and quantitative real-time polymerase chain reaction (qRT-PCR), respectively. At last, the tumor xenograft model was made for further exploring the mechanism. RESULTS: MiR218 expressions were notably reduced in LA tissues in comparison with controls. In addition, the declined miR218 expressions were correlated with the poor OS and worse clinicopathological parameters of LA patients. Furthermore, miR218 overexpression could suppress the proliferation, migration and invasion capacities of LA cells via regulation of PI3K/Akt signaling pathway and epithelial-mesenchymal transition (EMT) respectively. Results in the current study also revealed that miR-218 upregulation could suppress the tumor growth rate and tumor size of LA mice. B-lymphoma Moloney murine leukemia virus insertion region-1 (BMI-1) was confirmed to be a direct target for miR-218 and upregulated in LA tissues, which indicated the poor prognosis of LA patients. CONCLUSIONS: MiR-218 exerted anti-tumor functions in LA partially via the regulation of BMI-1, suggesting that BMI-1/miR-218 axis may provide a novel insight into tumorigenesis and the basis for the development of miRNA-targeting therapies against LA.

Polyoxometalate SbW9 regulates proliferation and apoptosis of NSCLC cells via PTEN-dependent AKT signaling pathway.

OBJECTIVE: To explore the influence of polyoxometalate SbW9 on proliferation and apoptosis of non-small cell lung cancer (NSCLC) cells and its mechanism. MATERIALS AND METHODS: NSCLC cell lines A549 and PC9 were treated with 50 µM polyoxometalate. Then, the proliferation of NSCLC cells was detected via 2,3-bis(2-methoxy-4-nitro-5-sulfophenyl)-5-[(phenylamino)carbonyl]-2H-t tetrazolium hydroxide (XTT) assay and colony formation assay; the apoptosis of NSCLC cells was detected via flow cytometry and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL); and the expression of apoptosis-related proteins, B-cell lymphoma-2 (Bcl-2), and Bcl-2 associated X protein (Bax), was detected via Western blotting. Moreover, the protein expression levels of phosphatase and tensin homolog deleted on chromosome ten (PTEN), phosphorylated-protein kinase B (P-AKT) and total AKT (T-AKT) were detected via Western blotting. RESULTS: The polyoxometalate inhibited the proliferation of A549 and PC9 cells in a concentration-dependent manner (5-100 µM) (p<0.05), and it (50 µM) also inhibited the proliferation of both cells in a time-dependent manner (0-72 h) (p<0.05). The results of colony formation assay revealed that the polyoxometalate (50 µM) could significantly inhibit the colony formation of A549 and PC9 cells (p<0.05). The results of flow cytometry and TUNEL staining showed that the polyoxometalate (50 µM) significantly induced the apoptosis of A549 and PC9 cells (p<0.05). According to further studies, the polyoxometalate (50 µM) inhibited the expression of anti-apoptotic gene Bcl-2 and promoted the expression of pro-apoptotic gene Bax. Besides, the Western blotting results manifested that the polyoxometalate could activate the expression of PTEN and inhibit the phosphorylation of downstream AKT (p<0.05). CONCLUSIONS: The polyoxometalate can activate the expression of PTEN to inhibit the phosphorylation of AKT, ultimately inhibiting the proliferation and inducing the apoptosis of NSCLC cells. Therefore, the polyoxometalate is expected to become a novel drug for the clinical treatment of NSCLC.

MiR-200c regulates apoptosis of placental trophoblasts in preeclampsia rats through Wnt/ß-catenin signaling pathway.

OBJECTIVE: To investigate the influence of micro ribonucleic acid 200c (miR-200c) on the apoptosis of placental trophoblasts in a rat model of preeclampsia (PE). MATERIALS AND METHODS: PE model in rats was established for extracting placental trophoblasts. Overexpression or knockdown of miR-200c was achieved by transfection of miR-200c mimics or inhibitor. Flow cytometry was carried out to detect the apoptotic rate of placental trophoblasts. Dual-luciferase reporter gene assay was performed to detect the interaction of miR-200c with WNT1. Western blotting was applied to determine the changes of protein levels in placental trophoblasts. RESULTS: The expression level of miR-200c in placental trophoblasts of PE group was significantly higher than that in control group. The apoptosis rate was (22.45 ± 2.62)%, (6.58 ± 1.28)%, and (9.57 ± 1.35)% in miR-200c mimic group, miR-200c inhibitor group, and control group, respectively, showing statistically significant differences. MiR-200c overexpression downregulated the expression level of anti-apoptotic protein B-cell lymphoma 2 (Bcl-2), but upregulated expression levels of apoptotic proteins Bcl-2-associated X protein (Bax) and active Caspase-3. MiR-200c suppressed WNT1 expression through the interaction with the 3'-untranslated region (3'-UTR) of WNT1. The expressions of WNT1 and ß-catenin were up-regulated after miR-200c overexpression, which was reversed by the Wnt/ß-catenin pathway activator. CONCLUSIONS: MiR-200c is involved in the development and progression of PE through the Wnt/ß-catenin signaling pathway.

LncRNA HOTAIR inhibited osteogenic differentiation of BMSCs by regulating Wnt/ß-catenin pathway.

OBJECTIVE: This study aims to investigate whether HOX transcript antisense RNA (HOTAIR) can participate in the osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) by regulating the Wnt/ß-catenin pathway, thereby participating in the pathogenesis of osteoporosis. PATIENTS AND METHODS: We detected the expression level of HOTAIR in 60 osteoporosis patients and 60 normal controls by Quantitative Real-Time Polymerase Chain Reaction (qRT-PCR). Meanwhile, BMSCs derived from human or rats were subjected to determination of HOTAIR level. Subsequently, the effects of HOTAIR on osteogenic differentiation were evaluated by the activity of Alkaline Phosphatase (ALP), Alizarin Red S (ARS) staining, ALP staining and osteogenic-specific gene expression. The expression level of proteins related to the Wnt/ß-catenin was determined by Western blot, and ALP activity was detected by ALP activity determination kit and alizarin red staining after knockdown or overexpression of HOTAIR, as well as the treatment of DKK1 or the Wnt pathway antagonist. Finally, osteoporosis model in rats was established by ovariectomy (OVX). We examined protein levels of HOTAIR, ß-catenin, CyclinD, C-myc, and Runx2 in rat bone tissues. Bone morphology was observed in each group as well. RESULTS: The serum and BMSCs levels of HOTAIR in patients with osteoporosis were remarkably higher than that in normal people. Inhibition of HOTAIR induced increased ALP activity increased osteogenic marker genes and enhanced number of calcified nodules in BMSCs. However, the overexpression of HOTAIR exhibited the opposite effects. HOTAIR inhibited the expression level of Wnt/ß-catenin pathway-related protein. Also, Wnt pathway antagonist DKK1 partially reversed the regulatory effects of HOTAIR on Wnt/ß-catenin. DKK1 treatment markedly reduced the promotive effect of HOTAIR knockdown on ALP activity, ALP content and calcification ability of BMSCs. DKK1 administration in rats undergoing OVX showed worse bone morphology relative to controls. Protein levels of HOTAIR, ß-catenin, CyclinD, C-myc and Runx2 remarkably downregulated in OVX rats administrated with DKK1. CONCLUSIONS: HOTAIR inhibits osteoblast differentiation of rat BMSCs. The underlying mechanism of which may be related to the mediation of Wnt/ß-catenin pathway.

Effects of Ulinastatin on myocardial oxidative stress and inflammation in severely burned rats.

OBJECTIVE: By constructing the severe burns model in rat, we explored the effects of different doses of Ulinastatin (UTI) on protecting myocardium from oxidative stress and inflammatory reaction. MATERIALS AND METHODS: The severe burns model in rat was first constructed. Burned rats were intervened with different doses of UTI. Contents of cardiac troponin I (cTnI), Interleukin-1 (IL-1), Interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) in rat serum and heart homogenate were detected by enzyme-linked immunosorbent assay (ELISA). Activities of SOD (superoxide dismutase), CAT (catalase), GSH-Px (glutathione peroxidase), and MDA (malondialdehyde) were detected by commercial kits. The inflammation and pathological changes in rat heart were observed by HE (Hematoxylin-Eosin) staining. Protein expressions of Cox-2, iNOS, NF-κB, Nrf2, and HO-1 in rat myocardium were detected by Western blot. RESULTS: Higher levels of cTnI, IL-1, IL-6, and TNF-α were found in model group than those of control group (p<0.05). Besides, decreased contents of cTnI, IL-1, IL-6, and TNF-α were observed in both UTI 50 ku/kg group and UTI 100 ku/kg group compared with those of model group (p<0.05). Decreased activities of SOD, CAT, and GSH-Px, as well as increased MDA level were observed in model group than those of control group (p<0.05). However, UTI treatment remarkably elevated SOD, CAT, and GSH-Px activities, whereas downregulated MDA level in burned rats (p<0.05). Abundant infiltration of inflammatory cells was found in the rat's myocardium of model group, which was alleviated in UTI group in a dose-dependent manner. Upregulated Cox-2, iNOS, and NF-κB, as well as downregulated Nrf2 and HO-1 were found in model group compared with those of control group (p<0.05). UTI pretreatment remarkably reversed the above-mentioned trends. CONCLUSIONS: Ulinastatin alleviates myocardial injury induced by severe burns. It exerts a protective role in myocardium via inhibiting oxidative stress and inflammatory response.

miR-192 prevents renal tubulointerstitial fibrosis in diabetic nephropathy by targeting Egr1.

OBJECTIVE: Diabetic nephropathy (DN), as the most common and serious diabetic microvascular complication, has become the first cause of end-stage renal disease (ESRD) in many countries and regions. However, the pathogenesis of renal fibrosis during the development of DN remains unknown. MATERIALS AND METHODS: The expression levels of miR-192 and early growth response factor 1 (Egr1) were determined by quantitative Real-Time Polymerase Chain Reaction (qRT-PCR) and Western blotting in the renal tissues of Otsuka-Long-Evans-Tokushima-Fatty (OLETF) and Long-Evans-Tokushima-Otsuka (LETO) rats. The diabetic kidney environment was simulated by a high-sugar medium. The expression levels of miR-192 and Egr1 were further measured in the HK-2 cell line. Egr1 was verified as a potential target of miR-192 by using bioinformatics analysis and luciferase activity assay. The expression level of Egr1 was determined by overexpressing and knocking down the expression of miR-192. In addition, Western blotting was used to determine changes in Transforming growth factor-beta 1 (TGF-ß1) and fibronectin (FN). RESULTS: Compared with the kidney tissue of LETO rats, the expression of miR-192 was decreased in OLETF rats, whereas the expression of Egr1 was increased. We found the same phenomenon in the HK-2 cell line cultured in the high-glucose medium. Next, miR-192 can act on Egr1 through 3'-UTR to reduce the expression of Egr1 verified by luciferase assay. In addition, the expression levels of TGF-ß1 and FN changed significantly, as the expression level of Egr1 increased or decreased. CONCLUSIONS: MiR-192 causes degradation of TGF-ß1 and FN through targeting Egr1 and affects the progression of TIF and even DN.

Validation of a nomogram for selecting patients for chemotherapy after D2 gastrectomy for cancer.

BACKGROUND: According to some guidelines for the management of gastric cancer, adjuvant chemotherapy is recommended for patients with pT3-4 or node-positive disease. The aim of this study was to define low- and high-risk groups in terms of survival, and to predict the benefit of adjuvant fluoropyrimidine plus oxaliplatin (F-OX) chemotherapy. METHODS: Patients with pT3-4 or node-positive gastric cancer after gastrectomy with D2 lymphadenectomy between 2000 and 2013 were included. The performance of a previously published nomogram was assessed by discrimination and calibration. Patients were stratified into risk groups on the basis of the nomogram-predicted overall survival probability. The efficacy of F-OX within each risk subgroup was assessed using the log rank test and Cox regression analysis weighted by inverse propensity score. RESULTS: Some 1464 patients were included. The nomogram showed better discrimination than the seventh AJCC staging classification (concordance index 0·72 versus 0·68 respectively; P = 0·008) and accurate calibration. F-OX was not associated with improved survival in patients in the low-risk group, whereas it reduced the risk of death by over 20 per cent in the intermediate- and high-risk groups (P = 0·036 and P < 0·001 respectively) (P for interaction = 0·014). CONCLUSION: A nomogram can aid in individualized decision-making regarding the administration of F-OX after gastrectomy for cancer.

Liver Transplantation for Biliary Rhabdomyosarcoma With Liver Metastasis: Report of One Case.

BACKGROUND: Liver transplantation in combination with chemotherapy in postoperative biliary rhabdomyosarcoma recurrence of children was evaluated. METHODS: An 8-year-old girl with biliary rhabdomyosarcoma underwent pancreatico-duodenectomy with postoperative vincristine (VCR), adriamycin (Act-D), and cyclophosphamide (CTX) (VAC chemotherapy) (VCR, 1 mg; Act-D, 0.7 mg; CTX, 1500 mg). Two years later, liver metastasis in the left and right lobes was found and was followed by VAC chemotherapy (CTX, 1800 mg; Act-D, 0.9 mg; VCR, 1.2 mg), with no change of the tumor size. One and a half years later, liver transplantation performed with postoperative pathology confirmed embryonal rhabdomyosarcoma recurrence and was followed by VAC chemotherapy (CTX, 1400 mg; Act-D, 0.7 mg; VCR, 1.9 mg) and immunosuppression treatment. RESULTS: The liver transplantation went well, with no major complications. At the time of this report, the patient had survived for 6 months, with a good quality of life and no tumor recurrence. CONCLUSIONS: For unresectable biliary rhabdomyosarcoma without extra-hepatic metastases, liver transplantation could be an effective treatment. Liver transplantation completely removes the tumor and reduces the long-term side effects of chemotherapy drugs.

Cryopreservation of Schisandra chinensis (Turcz.) Baill callus and subsequent plant regeneration.

Cryopreservation has been proven significance as a technique for promising the long-term conservation of plant germplasms. This study aimed to establish a cryopreservation protocol for calli of Schisandra chinensis (Turcz.) Baill, and to explore the effects of different process parameters on callus viability. Effects of desiccation duration, cryoprotectants and cryopreservation methods, thawing temperature, and post-culture conditions on the viability of cryopreserved calli were assessed. Among different cryoprotectants and freezing procedures, the highest survival was recorded when the water content of callus after 30 min desiccation was 57.3%, were loaded into a cryoprotectant containing 10% ethylene glycol, 8% glucose, and 10% DMSO, and frozen slowly (-1°C/min). Rapid thawing at 40°C for 2 min demonstrated the best recovery of cryopreserved S. chinensis calli. Post-culturing in darkness for one week before transfer to light conditions (under 16 h photoperiod at 36 µmol·m-2·s-1) was beneficial to callus regeneration. Plants regenerated through somatic embryogenesis from cryopreserved calli remained ploidy stable after cryopreservation. The callus cryopreservation procedure established in this study is a promising tool for the conservation of S. chinensis resources.