Optimal radiotherapy after breast-conserving surgery for early breast cancer: A network meta-analysis of 23,418 patients.

PURPOSE: In order to explore whether partial breast irradiation can replace hypofractionated whole breast irradiation and whether the former two are superior to conventional fractionated whole breast irradiation, we conducted a network meta-analysis based on the data from the latest randomized controlled trials to evaluate the efficacy of these radiotherapy modalities. MATERIAL AND METHODS: Data from eligible studies were analyzed to determine the published events for ipsilateral breast tumor recurrence, distant metastasis, total deaths, and non-breast cancer-related deaths. In the case of low or high heterogeneity, the fixed-effect or random-effect model was used for statistical analysis respectively. NMA was performed by using the node-splitting model for two-category data among three radiotherapies based on a Bayesian method. RESULTS: A total of 23,418 patients were included in 16 studies. For ipsilateral breast tumor recurrence, both pairwise (OR=1.9; CI95%: 1.2 -2.8; p<0.05) and indirect (OR=1.7; CI95%: 1.2 -2.4; p<0.05) comparison of three radiotherapies by network meta-analysis showed that conventional fractionated whole breast irradiation was significantly better than partial breast irradiation. Indirect comparison of three radiotherapies by network meta-analysis showed that hypofractionated whole breast irradiation was significantly better than partial breast irradiation (OR=1.6; CI95%: 1.0 -2.5; p<0.05). Network and paired meta-analyses found no significant differences in other endpoints among the three radiotherapies. CONCLUSION: Overall, this network meta-analysis showed that partial breast irradiation was related to the increase of ipsilateral breast tumor recurrence compared with hypofractionated or conventional fractionated whole breast irradiation in patients with early-stage breast cancer.

Multiple mechanisms of salidroside on anti-tumor effects.

Salidroside, a kind of natural herb, has the advantages of a wide range of anti-tumor activities with low toxicity and high efficiency. A large number of studies have shown that salidroside can inhibit the proliferation of tumors in different ways and achieve the goal of treating tumors. After summary and analysis of the recent research on anti-tumor mechanisms of salidroside, it can be concluded that salidroside could suppress cancer proliferation by blocking cell cycle, promoting cell differentiation, inducing cell apoptosis or autophagy, and regulating the signal pathways of cancer cells.

A blackberry-dill extract combination synergistically increases skin elasticity.

BACKGROUND: The loss of structural elastin due to intrinsic and extrinsic ageing results in the skin's inability to stretch and recoil (decrease in elasticity) and manifests as loss of skin firmness and sagging. While other extracellular matrix (ECM) components such as collagen and hyaluronic acid are continually synthesized and assembled through life, elastic fibres are not. Elastic fibre assembly and functionality require fibre cross-linking, induced by the lysyl oxidase-like (LOXL) enzymes, which sharply decrease during ageing. OBJECTIVE: To evaluate the enhanced elastogenic effect of a blackberry-dill extract combination, which was hypothesized to induce elastin fibre component synthesis, fibre cross-linking and reduce elastin fibre degradation. METHODS: The blackberry and the dill extracts were tested separately and in combination to confirm single ingredient bioactivity and synergistic benefits. Human skin explants, dermal fibroblasts, elastase assays, ELISAs, quantitative real-time PCRs and spectrofluorometer measurements were used. Moreover, a double-blinded, placebo-controlled clinical study was carried out to assess skin elasticity using Cutometer and histologically from biopsies. RESULTS: The blackberry extract induced elastin gene expression, elastin promoter activity and inhibited elastic fibre degradation by matrix metalloproteinases (MMPs) 9 and 12. The dill extract induced elastin, collagen and LOXL1 gene expression, resulting in enhanced fibre cross-linking in human skin explants. Clinically, the blackberry and dill combination treatment displayed synergistic pro-elasticity activity as compared to each ingredient alone and placebo. CONCLUSION: Taken together, these results demonstrated the two multimodal plant-based extracts complemented each other in terms of bioactivity and resulted in a synergistic elastogenesis induction.

CONTEXTE: la perte de l'élastine structurelle causée par un vieillissement intrinsèque et extrinsèque provoque l'incapacité de la peau à s'étirer et à rebondir (diminution de l'élasticité) et se manifeste comme une perte de fermeté et un relâchement de la peau. Alors que d'autres composants de la matrice extracellulaire (MEC), tels que le collagène et l'acide hyaluronique sont continuellement synthétisés et assemblés tout au long de la vie, les fibres élastiques ne le sont pas. L'assemblage et la fonctionnalité des fibres élastiques nécessitent une réticulation des fibres, causée par les enzymes de type lysyle oxydase (LOXL), qui diminuent fortement au cours du vieillissement. OBJECTIF: évaluer l'effet élastogène amélioré d'une combinaison d'extrait de mûre et d'aneth, qui était supposée induire la synthèse des composants des fibres d'élastine, la réticulation des fibres et réduire la dégradation des fibres d'élastine. MÉTHODES: les extraits de mûre et d'aneth ont été testés séparément et ensemble pour confirmer la bioactivité d'un seul ingrédient et les avantages synergiques. Des explants de peau humaine, des fibroblastes cutanés, des dosages d'élastase, des ELISA, des analyses PCR quantitatives en temps réel et des mesures de spectrofluorimètre ont été utilisés. De plus, une étude clinique en double aveugle, contrôlée par placebo, a été réalisée pour évaluer l'élasticité de la peau à l'aide du cutomètre et histologiquement à partir de biopsies. RÉSULTATS: l'extrait de mûre a induit l'expression génique de l'élastine, l'activité de promoteur de l'élastine et a inhibé la dégradation des fibres élastiques par des métalloprotéinases matricielles (MPM) 9 et 12.L'extrait d'aneth a causé l'expression génique de l'élastine, du collagène et du gène LOXL1, entraînant une amélioration de la réticulation des fibres dans les explants de peau humaine. Cliniquement, le traitement par une combinaison de mûre et d'aneth a montré une activité de pro-élasticité synergique par rapport à chaque ingrédient seul et au placebo. CONCLUSION: ensemble, ces résultats ont démontré que les deux extraits de plantes multimodales se complètent en termes de bioactivité et ont entraîné une induction synergique de l'élastogenèse.

CDKN3 regulates cisplatin resistance to colorectal cancer through TIPE1.

OBJECTIVE: The aim of this study was to investigate the level of cyclin-dependent kinase inhibitor 3 (CDKN3) in colorectal cancer (CRC), to explore the underlying mechanism of CDKN3 in modulating cisplatin resistance and promoting the malignant progression of CRC. PATIENTS AND METHODS: 43 pairs of CRC tissues and para-cancerous tissues were collected from CRC patients. CDKN3 expression was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The relationship between CDKN3 expression and the prognosis of CRC patients was analyzed. Meanwhile, qRT-PCR was performed to verify CDKN3 level in CRC cell lines. Next, CDKN3 knockdown model was constructed in CRC cisplatin-resistant cell lines. The influence of CDKN3 on the biological function of CRC cells was analyzed by Cell Counting Kit-8 (CCK-8) and plate cloning assays. Furthermore, the mechanism of its regulation of TIPE1 affecting cisplatin resistance to CRC was explored. RESULTS: QRT-PCR results showed that CDKN3 level in CRC tissues was remarkably higher than that of the adjacent tissues (p<0.05). Compared with patients with low expression of CDKN3, the prognosis of patients with high expression of CDKN3 was significantly worse (p<0.05). Similarly, the proliferation and colony formation ability of cells in CDKN3 knockdown group remarkably decreased when compared with the sh-NC group (p<0.05). In addition, CDKN3 level was remarkably elevated in CRC patients with cisplatin resistance. In cisplatin-resistant cell lines (including HT28 and HCT-116), the knockdown of CDKN3 remarkably reduced cell viability (p<0.05). Furthermore, TIPE1 expression was remarkably downregulated in CRC tissues (p<0.05). A negative correlation was observed between the expressions of TIPE1 and CDKN3. Cell reverse experiment demonstrated that TIPE1 could reverse the promoting effect of CDKN3 on the malignant progression of CRC. All these findings suggested that there might exist a mutual regulation between CDKN3 and TIPE1. CONCLUSIONS: CDKN3 was highly expressed in CRC, which might be closely correlated with poor prognosis of CRC patients. In addition, CDKN3 regulated cisplatin resistance to CRC by modulating TIPE1, thereby promoting the proliferation of CRC.

Magnon profile on SrRuO3 films studied by inelastic neutron scattering.

In this study, the inelastic neutron scattering probe of SIKA in ANSTO is employed to investigate the magnon dispersion curve in ferromagnetic SrRuO3 single crystal epitaxial films and to better understand the underlying mechanisms. This report presents the successful measurement of a magnon peak from the SrRuO3 films which contained an amount of material of only 0.9 mg. We reveal one significant magnon dispersion curve along [002] following the quadratic E ∝ Q 2 ) relation, which shows a magnon gap of 0.32 meV. We have discussed several possible mechanisms, such as the higher symmetry structure and the impurity levels, which may contribute to this smaller gap.

MiR-96-5p promotes the proliferation, invasion and metastasis of papillary thyroid carcinoma through down-regulating CCDC67.

OBJECTIVE: MicroRNAs (miRNAs) have been identified to play an important regulatory role in various biological behaviors of papillary thyroid carcinoma (PTC). However, the specific role and function of miR-96-5p in PTC remain unclear. Therefore, the aim of this study is to detect the expression of miR-96-5p in PTC, and to explore its exact function. PATIENTS AND METHODS: The relative expression level of miR-96-5p in PTC tissues and cell lines was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). MiR-96-5p mimics or inhibitors were then constructed and transfected into cells to upregulate or downregulate miR-96-5p expression. MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) assay and colony formation assay were employed to evaluate the proliferation of PTC cells. Meanwhile, transwell assay was employed to detect the invasion and metastasis of PTC cells. In addition, the underlying mechanism of miR-96-5p was identified by Luciferase reporter gene assay and Western blot analysis. RESULTS: The expression of miR-96-5p in PTC tissues and PTC-derived cell lines was significantly higher than that of normal controls. The overexpression of miR-96-5p remarkably promoted the proliferation, invasion and migration of PTC cells. However, knockdown of miR-96-5p significantly decreased cell growth and metastasis. CCDC67 was verified as a target gene of miR-96-5p in PTC. Further experiments demonstrated that the restoration of CCDC67 could significantly reduce the carcinogenic function of miR-96-5p. CONCLUSIONS: MiR-96-5p was remarkably upregulated in PTC tumor tissues and cells. In addition, it promoted cell growth, invasion, and migration via repressing CCDC67 expression.

Long non-coding RNA PICART1 inhibits cell proliferation by regulating the PI3K/AKT and MAPK/ERK signaling pathways in gastric cancer.

OBJECTIVE: Gastric cancer (GC) is one of the most frequent malignancies and the second leading cause of cancer-related death in the world. The aim of this work was to illustrate the functional role of long non-coding RNA (lnRNA)-PICART1 (p53-inducible cancer-associated RNA transcript 1) in GC, thereby providing novel insights into biomarkers and therapeutic strategies in GC. PATIENTS AND METHODS: The relative expression level of lncRNA-PICART1 was evaluated by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Cell counting kit-8 (CCK-8) assay and colony formation assay were used to determine the ability of cell proliferation. Flow cytometric analysis was performed to detect cell cycle and cell apoptosis. The protein expressions of ERK, p-ERK, AKT and p-AKT were detected by Western blotting. Furthermore, the transfected cells were used to perform tumor xenograft formation assay. RESULTS: LncRNA-PICART1 was lowly expressed in both GC tissues and cell lines. CCK-8 assay, colony formation assay and flow cytometric analysis validated that up-regulated lncRNA-PICART1 significantly suppressed cell proliferation, whereas promoted cell apoptosis. Besides, the over-expression of lncRNA-PICART1 remarkably inhibited the PI3K/AKT and ERK/MAPK signaling pathways. Tumor xenograft formation assay indicated that lncRNA-PICART1 overexpression significantly inhibited tumor formation. CONCLUSIONS: Our research illustrated that lncRNA-PICART1 functioned as a tumor suppressor in GC. The regulation of the PI3K/AKT and ERK/MAPK signaling pathways might be the underlying mechanism of the tumor suppressor role of lncRNA-PICART1. In addition, our study might bring novel insights into biomarkers and therapeutic strategies for GC.

MicroRNA-124 inhibits colorectal cancer cell proliferation and suppresses tumor growth by interacting with PLCB1 and regulating Wnt/ß-catenin signaling pathway.

OBJECTIVE: Colorectal cancer (CRC) is the most common malignancy for cancer-associated death. This study aimed to investigate the effects of microRNA-124 (miR-124) on tumor proliferation of CRC in vivo and in vitro. MATERIALS AND METHODS: MiR-124 mimics were synthesized and transfected into SW620 cells, which were divided into SW620, microRNA-normal control (miR-NC) and miR-124 mimics group. Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was used to examine miR-124, chemokine (C-C motif) ligand-20 (CCL20), tankyrase-2 (TNKS2), phospholipase Cbeta1 (PLCB1) and Wnt4. Cell counting kit-8 (CCK-8) was employed to evaluate cell proliferation. The interaction between miR-124 and PLCB1 was tested with the Dual-Luciferase assay. Cell cycle, apoptosis and invasion were also evaluated. CRC xenograft mouse model was established and tumor size was measured. Hematoxylin and eosin (HE) was used to examine inflammation. Western blot was utilized to detect Wnt4. RESULTS: MiR-124 was over-expressed in SW620 cells, significantly reduced CCL20 and enhanced TNKS2 compared to that of the miR-NC group (p<0.05). MiR-124 might play roles by initiating PLCB1 expression. MiR-124 significantly decreased cell viability compared to the miR-NC group (p<0.05). MiR-124 regulated cell cycle and markedly induced apoptosis and inhibited cell invasion compared to the miR-NC group (p<0.05). MiR-124 significantly decreased tumor size of CRC models compared to miR-NC mice (p<0.05). MiR-124 remarkably alleviated inflammation of tumor tissues. MiR-124 markedly enhanced Wnt4 expression compared to the miR-NC group (p<0.05). CONCLUSIONS: MiR-124 inhibited tumor cell proliferation in vitro and suppressed tumor growth in vivo by interacting with PLCB1 and regulating the Wnt/ß-catenin signaling pathway.

Using changes in pro-brain natriuretic peptide of plasma amino-terminal and norepinephrine levels as prognostic and diagnostic factors in hand-foot-and-mouth disease.

OBJECTIVE: We explored the possibility of using the variations in the pro-brain natriuretic peptide (NT-proBNP) of serum amino-terminal and norepinephrine (NE) levels as prognostic as well as diagnostic factors in children suffering from severe hand-foot-and-mouth disease (HFMD). PATIENTS AND METHODS: From February 2014 to February 2015, 102 HFMD patients were enrolled in this study. They were divided into the common group (n=55) and the severe group (n=47). During the same period, 30 healthy children were enrolled in the control group. NT-proBNP and NE levels were evaluated in all patients. RESULTS: Our results revealed that NT-proBNP and NE levels in the common group were not evidently different compared with those of the control group. However, these levels in the severe group were significantly higher than other groups. After treatment, NT-proBNP and NE levels in the severe group were lower than those measured before treatment. CONCLUSIONS: We suggest that serum level of NT-proBNP can be used as a valuable index to judge the severity of HFMD and to predict the prognosis. We believe that NT-proBNP and NE levels can be added to other HFMD diagnostic tools.

MiR-877-5p suppresses cell growth, migration and invasion by targeting cyclin dependent kinase 14 and predicts prognosis in hepatocellular carcinoma.

OBJECTIVE: Recent studies reveal that hepatocellular carcinoma (HCC) express aberrant microRNAs. Dysregulation of miR-877-5p has been observed in HCC. The objective of the present study was to explore the clinical significance, function and underlying mechanism of miR-877-5p in HCC. PATIENTS AND METHODS: Quantitative reverse transcription PCR (qRT-PCR) was used to measure the levels of miR-877-5p in HCC specimens and HCC cell lines. Correlations between miR-877-5p expression and the clinicopathological features and prognosis of HCC patients were then evaluated. MTT assays, colony formation assays, scratch test, transwell assays were used to explore the biological function of miR-877-5p in HCC. A luciferase reporter assay and Western blot were conducted to confirm the target gene of miR-877-5p, and the results were validated in HCC cell lines. RESULTS: We found that the expression of miR-877-5p was downregulated in HCC tissues or cell lines. Clinicopathologic analysis revealed that low miR-877-5p expression correlated with histologic grade (p = 0.008) and TNM stage (p = 0.018). The Kaplan-Meier method indicated that low miR-877-5p levels in HCC were associated with shorter overall survival (p = 0.0041) and disease-free survival (p = 0.0005). Multivariate analysis demonstrated that miR-877-5p expression was an independent poor prognostic factor for HCC patients. Functional assay revealed that upregulation of miR-877-5p could inhibit proliferation, migration, and invasion of HCC cells in vitro. We further identified cyclin-dependent kinase 14 (CDK14) as a direct target of miR-877-5p in HCC cells. Ectopic expression of CDK14 reversed the inhibitory effects of miR-877-5p. CONCLUSIONS: Low miR-877-5p expression was a poor prognostic factor for HCC patients, and miR-877-5p functioned as a tumor suppressor in HCC cells via targeting CDK14.

Expression and significance of vWF, GMP-140 and ADAMTS13 in patients with aneurysmal subarachnoid hemorrhage.

OBJECTIVE: The aim of this study was to investigate the role of the von Willebrand factor (vWF) in patients with aneurysmal subarachnoid hemorrhage (aSAH), platelet membrane glycoprotein-140 (GMP-140). The aim is also to discover the expression and clinical significance of von Willebrand factor (vWF) cleaving protease (ADAMTS13). PATIENTS AND METHODS: 83 patients with aSAH were selected from January 2014 to December 2016. The patients were divided into cerebral vasospasm group (CVS group) (n = 37) and no convulsion group (non-CVS group) (n = 46); delayed cerebral ischemia group (DCI group) (n = 31) and non-delayed cerebral ischemia group (non-DCI group) (n = 52). Also, the different aneurysm diameter group included 43 patients in < 5 mm group, 29 patients in 5-10 mm group, 11 patients in > 10 mm group. The number of patients in the good prognosis group and the poor prognosis group were 49 and 34, respectively. Enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of vWF, GMP-140, and ADAMTS13 in plasma of aSAH patients, and the correlation between the indexes was analyzed. RESULTS: The repeated measures analysis of variance showed that there was no significant difference in plasma vWF, GMP-140, and ADAMTS13 levels in each group of the aSAH patients (p < 0.05). The vWF level of the CVS group was higher than that of the non-CVS group on day 4 and day 10. The GMP-140 level of the CVS group was higher than that of the non-CVS group on day 1, day 4 and day 10. And the ADAMTS13 level was lower than that of the non-CVS group on day 1 and day 10. The difference was statistically significant (p < 0.05). The plasma vWF level of DCI group was higher than that of the non-DCI group on day 1 and day 4. The plasma GMP-140 level at day 4 was higher than that of the non-DCI group. The plasma ADAMTS13 level at day 1 was lower than that in the non-DCI group. The difference was significant (p < 0.05). The plasma vWF level in > 10 mm group was higher than that in < 5 mm group and 5-10 mm group at day 1 and day 4. The plasma vWF level in 5-10 mm group was higher than that in < 5 mm group at day 4. The plasma GMP-140 levels in > 10 mm group were higher than that in < 5 mm group and 5-10 mm group at day 1 and d ay 4. The plasma GMP-140 level in 5-10 mm group was higher than that in < 5 mm group at day 1. The plasma ADAMTS13 level in > 10 mm group was lower than that in < 5 mm group and 5-10 mm group on day 1. Moreover, the plasma ADAMTS13 level in 5-10 mm group was lower than that in < 5 mm group: p < 0.05. The plasma vWF level in the good prognosis group was lower than that in the poor prognosis group on day 4 and day 10. On day 1, day 4, and day 10, the level of GMP-140 was lower than that of the poor prognosis group. The ADAMTS13 level on day 1 and day 4 was higher than that in the poor prognosis group. The difference was statistically significant (p < 0.05). Pearson product moment correlation analysis showed that the plasma vWF level was positively correlated with GMP-140 at day 1 (r = 0.334, p < 0.05), negatively correlated with ADAMTS13 (r = -0.426, p < 0.05), and GMP-140 was negatively correlated with ADAMTS13 (r = -0.398, p < 0.05). At day 4, plasma vWF was positively correlated with GMP-140 (r = 0.278, p < 0.05), negatively correlated with ADAMTS13 (r = -0.311, p < 0.05), and GMP-140 was negatively correlated with ADAMTS13 (r = -0.235, p < 0.05). At day 10, there was no significant correlation between vWF, GMP-140, and ADAMTS13 (p > 0.05). CONCLUSIONS: VWF, GMP-140, and ADAMTS13 were correlated with the diameters and prognoses of CVS, DCI, aneurysms. Combined detection can help to evaluate the condition of patients with aSAH, so as to provide a guide for clinical treatment and prognosis.

Exposure to fine particulate matter associated with senile lentigo in Chinese women: a cross-sectional study.

BACKGROUND: Skin ageing especially senile lentigo directly affects self-esteem. For decades, senile lentigo has been associated with chronic exposure to solar radiation. However, a study conducted recently in Caucasian subjects suggested that exposure to air pollution was significantly correlated with extrinsic skin ageing, in particular senile lentigines. OBJECTIVE: To investigate the association between fine particulate matter (PM2.5 ) and skin ageing, particularly senile lentigo and seborrheic keratosis. METHODS: The study enrolled 400 Chinese women aged 40-90 years including 210 from the Yanqing county in Beijing (low PM2.5 exposure group) and 190 from the Xuanwumen in Beijing (high PM2.5 exposure group). Skin ageing symptoms, particularly senile lentigines and seborrheic keratoses, were clinically assessed using scores of intrinsic and extrinsic skin ageing. An ordinal logistic regression model was used to analyse the effect of PM2.5 on skin ageing adjusted for factors underlying skin ageing. RESULTS: In the study population of Xuanwumen, we found that senile lentigo on cheeks and back of hands was 1.48 times and 2.8 times higher, respectively, compared with those from Yanqing county. However, no association was found between PM2.5 and seborrheic keratosis. We found that other variables such as smoking, second-hand smoking, contact with fossil fuels and skin types were significantly associated with skin ageing. CONCLUSION: These results indicate that PM2.5 was another extrinsic factor promoting skin ageing.

Applied analysis of humanized nursing combined with wet healing therapy to prevent bedsore.

OBJECTIVE: To analyze and evaluate the effects of humanized nursing combined with wet healing therapy to treat the stage II and III bedsores in hospitalized patients. PATIENTS AND METHODS: From March 2013 to July 2014 we enrolled fifty patients with stage II and III bedsores. They were randomly divided into control group and experimental group, with 25 cases in each group. For the control group, we adopted a traditional method of treatment for pressure ulcer treatment, while the experimental group was treated with humanized nursing in combination with wet healing therapy. After 28 days, the treatment results in both groups were evaluated. RESULTS: The improvement rate for patients in the experimental group was significantly higher than that of the control group. In the experimental group, the improvement rates for patients suffering from stage II and III pressure ulcers were significantly higher than those of the control group. The Branden score and the area of pressure ulcer were significantly decreased in the experimental group. The frequency of dressing change, the dressing time and the average cost of hospitalization in the experimental group were significantly lower. CONCLUSIONS: The effect of wet healing therapy combined with humanized nursing in preventing and treating the bedsore is promising, and it is worthy of clinical promotion.

Correlation research on the protein expression (p75NTR, bax, bcl-2, and caspase-3) and cortical neuron apoptosis following mechanical injury in rat.

OBJECTIVE: In this study, we aimed to survey the role of p75NTR, bax, bcl-2, and caspase-3 in the progress of traumatic brain injury (TBI). MATERIALS AND METHODS: A mechanical trauma model of vital neurons was established by putting external pressure, contusion and centrifugal acceleration on neurons. Morphological change, survival rate, assay of LDH activity, and apoptosis rate were evaluated for mild, medium and severe injury models. The expression of bax, bcl-2, caspase-3, p75NTR, p75NTR mRNA was determined by immunohistochemistry, immunofluorescence, Western blotting and RT-PCR. RESULTS: There was a transient high level Bcl-2 protein within 2 h after injury to increase neuronal tolerance and avoid apoptosis. Subsequently p75NTR, Bax/Bcl-2, and Caspase-3 reached their peaks from 48 to 72 h accompanied with the maximum apoptosis rate. CONCLUSIONS: Our results suggest that apoptosis ratio in varying degree injury groups are correlated with the expression level of p75NTRmRNA, p75NTR, Caspase-3, Bax/Bcl-2 ratio.

HoxB7 PROMOTES GROWTH AND METASTASIS OF LUNG ADENOCARCINOMA CELLS THROUGH REGULATION OF THE TGF-ß/SMAD3 SIGNALING.

HoxB7 is involved in cell migration and metastasis in many malignant tumors. But, the role of HoxB7 in lung adenocarcinoma has not been elucidated. In the present study, we aimed to clarify the function of HoxB7 in the progression of lung adenocarcinoma. The protein expression of HoxB7 was examined by immunohistochemical assay in human lung adenocarcinoma tissues, and lentivirus-mediated HoxB7 shRNA (Lv-shHoxB7) was transfected into lung adenocarcinoma cells to evaluate cell proliferation and invasive potential indicated by MTT and Transwell assays. As a result, the protein expression level of HoxB7 was increased in lung adenocarcinoma tissues compared with the adjacent non-tumor tissues (56.25% vs 31.25%, P=0.014), and was positively correlated with the lymph node metastasis in patients with lung adenocarcinoma (P=0.036). Moreover, knockdown of HoxB7 decreased the proliferation and invasion of lung adenocarcinoma cells followed by decreased expression of TGF-ß/SMAD3, vascular endothelial growth factor A (VEGFA) and matrix metalloproteinase-2 (MMP-2). Taken together, our findings demonstrate that increased expression of HoxB7 is associated with tumor metastasis in patients with lung adenocarcinoma and HoxB7 may be implicated in promoting the development of lung adenocarcinoma through activation of the TGF-ß/SMAD3 signaling.

Exon 19 deletion was associated with better survival outcomes in advanced lung adenocarcinoma with mutant EGFR treated with EGFR-TKIs as second-line therapy after first-line chemotherapy: a retrospective analysis of 128 patients

Objective. To determine whether the specific genotype of exon 19 deletion has a better survival outcome than that of exon 21 substitution in advanced lung adenocarcinoma with EGFR mutant patients that were treated with EGFR-TKIs as second-line therapy after first-line chemotherapy. Methods. Between April 1, 2010 and December 31, 2012, the detailed clinical information of 128 patients was screened from the hospital information database of the First Affiliated Hospital and the Third Affiliated Hospital of Kunming Medical University by inclusion/exclusion criteria. Then, a telephone follow-up and a review of all patients’ image data were done to obtain the survival information of all patients. After that, all patients’ data were processed by IBM® SPSS® version 19.0. Results. There were correlations between EGFR mutation status, gross tumor type and PFS or OS according to the Kaplan–Meier survival analyses and log-rank tests. The exon 19 deletions had significantly better survival outcomes in comparison to exon 21 substitutions (median PFS: 8.1 vs. 6.8 months, P = 0.002; median OS: 17.6 vs. 12.5 months, P = 0.000). Stratification analyses of PFS and OS revealed that exon 19 deletions had a survival superior to exon 21 substitutions. Conclusion. Compared with L858R mutation, the genotype of exon 19 deletion had a better survival outcome in terms of PFS and OS in patients with advanced lung adenocarcinoma treated with EGFR-TKIs as second-line therapy after first-line chemotherapy (AU)

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Impact of stent over-expansion at distal edge: insights from a 12-month follow-up study.

OBJECTIVE: Although the use of drug-eluting stents has significantly reduced the incidence of restenosis and target lesion revascularization, in-stent and in-segment restenosis remain clinically challenging problems, the underlying mechanisms of which remain unknown. This study aimed to explore the outcomes of different stenting strategies in target vessels with different proximal and distal reference diameters (∆D ≥ 0.25 mm). PATIENTS AND METHODS: In this prospective clinical study, 167 patients undergoing percutaneous coronary intervention with ∆D ≥ 0.25 mm according to QCA results were randomized into 2 groups. Group A (n = 85) was treated by a single stent with high-pressure balloon inflation. Group B (n = 82) was treated by a single stent, with high- and low-pressure balloon inflation at the proximal and distal segment, respectively. The target vessel size and late lumen loss were determined by angiographic analysis. RESULTS: Compared with normal expansion, overexpansion increased the early minimum lumen diameter (A: 2.40 ± 0.18 mm vs. 2.89 ± 0.21 mm; B: 2.45 ± 0.14 mm vs. 2.49 ± 0.24 mm, p < 0.001), but also increased the percentage of late lumen loss (A: 18.22 ± 0.56%; B: 5.63 ± 0.41%, p < 0.001). Although the total restenosis ratio was similar in 2 groups, the incidence of late lumen loss of group A was higher than that of group B. CONCLUSIONS: Stent overexpansion increased the early minimum lumen diameter, but also increased the occurrence of late lumen loss at the distal edge of the stent.

Knockdown of PTTG1 inhibits the growth and invasion of lung adenocarcinoma cells through regulation of TGFB1/SMAD3 signaling.

Increased expression of pituitary tumor-transforming gene 1 (PTTG1) is expressed in many tumors and regulates tumor growth and progression. However, the precise function of PTTG1 in the tumorigenesis of lung adenocarcinoma (LAC) is not defined yet. Here, we examined the expression of PTTG1 in human LAC tissues by immunohistochemical assay using a tissue microarray procedure. A loss-of-function experiment was carried out to investigate the effects of lentiviral vector-mediated PTTG1 shRNA (shPTTG1) on cell growth and invasive potential in LAC cell lines (A549 and LETPα-2), assessed by MTT and Transwell assays. As a consequence, we found that the expression of PTTG1 protein was markedly upregulated in LAC tissues compared with the adjacent non-cancerous tissues (ANCT) (54.0% vs. 28.0%, P = 0.008), and was positively associated with the lymphatic invasion of the tumor (P = 0.01). Moreover, knockdown of PTTG1 expression inhibited tumor proliferation and invasion of LAC cells, companied by the decreased expression of CyclinD1 and MMP-2 and increased expression of p-TGFß1 and p-SMAD3. Collectively, our findings indicate that high expression of PTTG1 is correlated with the tumor metastasis of LAC patients, and knockdown of PTTG1 suppresses the growth and invasion of LAC cells through upregulation of the TGFß1/SMAD3 signaling, suggesting that PTTG1 may be a potential target for developing an effective immunotherapeutic strategy for LAC.

Clinical outcome of drug-eluting versus bare-metal stents in patients with calcified coronary lesions: a meta-analysis.

BACKGROUND: The relative safety and efficacy of drug-eluting stents (DES) versus bare-metal stents (BMS) in patients with calcified coronary lesions is still debated. AIMS: To evaluate clinical outcome of DES versus BMS in patients with calcified coronary lesions using a meta-analysis of the current literature. METHODS: We performed a systematic literature search using Medline, Embase, Cochrane and several other databases. Randomised controlled trials, prospective and retrospective cohort studies with a mean follow-up period >6 months were included. Primary efficacy was target lesions revascularisation (TLR) and primary end-point for safety was stent thrombosis. Secondary end-points were cardiac death and recurrent myocardial infarction (MI). RESULTS: Five trials were included in the meta-analysis, including 2440 patients (1230 in the DES group, 1210 in the BMS group). TLR was significantly lower in patients treated with DES as compared with patients treated with BMS (8.5% vs 16.0%; odds ratio (OR) = 0.50; 95% confidence interval (CI) 0.38-0.65; P < 0.00001). There were no significant differences in the incidence of stent thrombosis (0.9% vs 0.3%; OR = 2.01; 95% CI 0.34-11.88; P = 0.44), cardiac death (3.3% vs 4.2%; OR = 0.81; 95% CI 0.50-1.30; P = 0.38) and recurrent MI (5.0% vs 5.2%; OR = 0.99; 95% CI, 0.66-1.49; P = 0.97) between the two groups. Subgroup analysis by the sample size and follow-up duration showed that the associations were similar between DES versus BMS. CONCLUSIONS: DES significantly reduces TLR rates as compared with BMS in patients with calcified coronary lesions, with non-significant differences in terms of stent thrombosis, cardiac death and MI.

Effect analysis of early bedside hemo-filtration in treatment of severe pneumonia with acute renal failure of children.

OBJECTIVE: To investigate the best opportunity for bedside continuous blood purification (CBP) to treat severe pneumonia with acute renal failure (ARF) of children and look for the sensitive marker to evaluate the clinical effects and prognosis. PATIENTS AND METHODS: 54 children patients that were diagnosed as severe pneumonia with ARF by Pediatric Intensive Care Unit (PICU) were enrolled in our study as experimental group. In the meanwhile, 46 children patients that were diagnosed as severe pneumonia with ARF by PICU were enrolled as a normal control group. Patients in the experimental group started CBP treatment within 24 h after onset while patients in the control group started CBP treatment 24h after onset. The differences of clinical effects between two groups were compared for statistical significance. RESULTS: The survival rates of the observation group in day 7, day 28 and 6 months were significantly higher than those in the control group. After treatment for 7 days, IL-6 and TNF-α, YKL-40 and Annexin A1 levels of the experimental group were significantly lower than those of the control group. 7-day infection-related organ failure score (SOFA) of the experimental group was significantly lower than that of the control group. CONCLUSIONS: CBP therapy for treating severe pneumonia with acute renal failure of children within 24 hours could significantly improve the survival rate and reduce the inflammatory reactions.