Experimental Study on the Impact of Using FRP Sheets on the Axial Compressive Performance of Short-Circular Composite Columns.

This paper conducts an experimental study on the axial compressive performance of FRP-steel-concrete composite columns. Nine short columns were produced and evaluated in the study, comprising of three concrete-filled steel tube reference columns and six FRP-steel-concrete composite columns, respectively denoted as "reference columns" and "composite columns". Two categories of failure modes, including shear failure and waist drum, were observed from the experiments. The failure mode may trend toward waist drum from shear failure as more FRP layers were used. The number of FRP layers had a direct effect on the level of compressive strength attained, with a greater number of layers resulting in a greater increase in compressive strength. Moreover, a greater tensile strength and higher elastic modulus of CFRP sheets are more effective at improving the compressive stiffness of the columns. Finally, a four-stage confinement mechanism for FRP-wrapped steel tube concrete composite columns is proposed and discussed, through which the damage mechanisms of the composite structures are more rationally characterized.

Effects of Lipid Peroxidation-Mediated Ferroptosis on Severe Acute Pancreatitis-Induced Intestinal Barrier Injury and Bacterial Translocation.

Ferroptosis is a recently recognized type of regulated cell death characterized by iron- and lipid peroxidation-mediated nonapoptotic cell death. However, whether ferroptosis is involved in severe acute pancreatitis- (SAP-) induced intestinal barrier injury is unknown. The aim of this study was to investigate whether ferroptosis is involved in SAP-induced intestinal barrier injury, particularly intestinal epithelial cell (IEC) death, and determine whether the inhibition of ferroptosis would ameliorate intestinal barrier injury and prevent bacterial translocation (BT). Sodium taurocholate (5%) was retrogradely perfused into the biliopancreatic duct to establish a rat model of SAP. The rats were divided into three groups: sham operation (SO), SAP-induced intestinal barrier injury (SAP), and ferroptosis inhibitor liproxstatin-1 (SAP + Lip). Serum indexes were measured in the rats. In addition, the biochemical and morphological changes associated with ferroptosis were observed, including iron accumulation in intestinal tissue, lipid peroxidation levels, and mitochondrial shrinkage. Hematoxylin staining and eosin staining were used to assess histological tissue changes. Western blot, RT-PCR, and immunofluorescent staining were performed to analyze the expression of ferroptosis-related proteins and genes as well as tight junction. BT was detected by 16S rDNA sequencing analysis. The results indicated that ferroptosis was significantly induced in the IECs from rats with SAP and ferroptosis was mediated by lipid peroxidation. The specific lipid peroxidation of IECs clearly upregulated ferroptosis and exacerbated intestinal barrier injury. Furthermore, treatment with liproxstatin-1 lowered the levels of serum damage markers, decreased lipid peroxidation, and alleviated intestinal and acute remote organ injury in SAP rats. In addition, inhibition of ferroptosis reduced BT. Our findings are the first to demonstrate that ferroptosis contributes to SAP-induced intestinal barrier injury via lipid peroxidation-mediated IEC death. These results suggest that ferroptosis is a potential therapeutic target for SAP-induced intestinal barrier injury.

Parallel analysis of global garlic gene expression and alliin content following leaf wounding.

BACKGROUND: Allium sativum (garlic) is an economically important food source and medicinal plant rich in sulfides and other protective substances such as alliin, the precursor of allicin biosynthesis. Cysteine, serine and sulfur is the precursor of alliin biosynthesis. However, little is known about the alliin content under abiotic stress or the mechanism by which it is synthesized. RESULTS: The findings revealed that the content of alliin was lowest in the garlic roots, and highest in the buds. Furthermore, alliin levels decreased in mature leaves following wounding. Transcriptome data generated over time after wounding further revealed significant up-regulation of genes integral to the biosynthetic pathways of cysteine and serine in mature garlic leaves. CONCLUSIONS: The findings suggest that differential expression of cysteine, serine and sulfide-related genes underlies the accumulation of alliin and its precursors in garlic, providing a basis for further analyses of alliin biosynthesis.

Smad7 suppresses melanoma lung metastasis by impairing Tregs migration to the tumor microenvironment.

Transforming growth factor ß (TGF-ß) signaling plays critical roles in both physiological and pathological conditions. In the tumor microenvironment, TGF-ß are well demonstrated as a tumor inducer, which also promote tumor growth and metastasis. SMAD family is an important TGF-ß signalling transducer, which consists of receptor-regulated SMADs (R-SMADs), common-mediator SMADs (co-SMADs), and inhibitory SMADs (I-SMADs). Smad7 is one of the I-SMADs which has been proved to block TGF-ß signalling transduction in both tumor cells and immune cells. Accumulated evidence has suggested SMAD7 acted as a tumor suppressor in various cancer types, such as colorectal cancer, pancreatic cancer and skin melanoma, etc. However, the role of SMAD7 in melanoma lung metastasis has not been well studied. Here, we first investigated the role of SMAD7 on tumor cell viability by overexpressing SMAD7 in murine melanoma cell line B16-F10. Our results showed that SMAD7 overexpression slightly impaired B16-F10 cells growth, promoted cell apoptosis and arrested the cell cycle at S phase. In vivo study showed that SMAD7 overexpression inhibited B16-F10 lung metastasis. Further mechanism study suggested that SMAD7 promoted T cells activation by decreasing regulatory T cells (Tregs) infiltrating into the tumor microenvironment. In summary, our results proved that tumor cell derived SMAD7 inhibited melanoma lung metastasis by impairing the migration capacity of Tregs.

Inhibition of Ferroptosis Attenuates Acute Kidney Injury in Rats with Severe Acute Pancreatitis.

BACKGROUND: Acute kidney injury (AKI) is a frequent complication of severe acute pancreatitis (SAP). Ferroptosis is involved in a range of diseases. However, the role of ferroptosis in SAP-induced AKI has yet to be elucidated. AIMS: We aimed to investigate whether ferroptosis is induced in the kidney after SAP and whether inhibition of ferroptosis ameliorates AKI in a rat model of SAP. METHODS: Sodium taurocholate (5%) was retrogradely perfused into the biliopancreatic duct to establish a model of SAP with AKI in rats. The levels of serum amylase, lipase, tumor necrosis factor (TNF)-α, interleukin (IL)-6, creatinine (Cr) and blood urea nitrogen (BUN) in rats were measured. We also determined the biochemical and morphological changes associated with ferroptosis in renal tissue, including iron accumulation, lipid peroxidation assays, and mitochondrial shrinkage. H&E staining was used to assess pancreatic and renal histological changes. Western blot analysis, RT-PCR, and immunofluorescence staining were performed to analyze the expression of ferroptosis-related proteins and genes. RESULTS: SAP-induced AKI was followed by iron accumulation, increased lipid peroxidation, and upregulation of ferroptosis-related proteins and genes. Twenty-four hours after SAP, TEM confirmed the presence of typical shrunken mitochondria. Furthermore, treatment with liproxstatin-1 lowered the levels of serum amylase, TNF-α, IL-6, Cr and BUN, decreased kidney lipid peroxidation and alleviated pancreatic and renal histopathology injury in SAP rats. CONCLUSION: Our findings are the first to demonstrate the involvement of ferroptosis in SAP-associated renal damage and present ferroptosis as a therapeutic target for effective treatment of SAP-induced AKI.

Metabolic syndrome and the incidence of lung cancer: a meta-analysis of cohort studies.

BACKGROUND: Metabolic syndrome (MetS) has been related to the pathogenesis of variety categories of cancers. This meta-analysis aimed to determine the association between MetS and the incidence of lung cancer. METHODS: Relevant cohort studies were identified by search of PubMed, Embase, and Cochrane's Library databases. Cochrane's Q test and I2 statistic were used to analyze the heterogeneity. Random-effect model which incorporates the potential heterogeneity was used for the meta-analysis. RESULTS: Five cohort studies with 188,970 participants were included. A total of 1,295 lung cancer cases occurred during follow-up. Meta-analyses showed that neither MetS defined by the revised NCEP-ATP III criteria (hazard ratio [HR]: 0.94, 95% confidence interval [CI]: 0.84 to 1.05, p = 0.25; I2 = 0) nor the IDF criteria (HR: 0.82, 95% CI: 0.61 to 1.11, p = 0.20; I2 = 0) was associated with an affected risk of lung cancer. Subgroup analyses showed consistent results in women and in men, in studies performed in Asian and non-Asian countries, and in prospective and retrospective cohorts (p all > 0.05). Meta-analysis limited to studies with the adjustment of smoking status also showed similar results (HR: 0.91, 95% CI: 0.80 to 1.05, p = 0.21; I2 = 0). No publication bias was detected based on the Egger regression test (p = 0.32). CONCLUSIONS: Current evidence from cohort studies does not support that MetS is an independent risk factor for the incidence of lung cancer.

miR-141-3p inhibits vascular smooth muscle cell proliferation and migration via regulating Keap1/Nrf2/HO-1 pathway.

miR-141-3p is proven to play a prominent role in various inflammation-related diseases. Nonetheless, little is known concerning the function of miR-141-3p in vascular smooth muscle cells (VSMCs) dysfunction and the underlying mechanism. ApoE knockdown (ApoE-/- ) C57BL/6 mice and human VSMCs were employed to establish atherosclerosis (AS) animal model and cell model, respectively. The expressions of miR-141-3p and Keap1 mRNA were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Enzyme-linked immunosorbent assay (ELISA) was conducted to determine inflammatory cytokines IL-6, IL-ß and TNF-α. Cell proliferation, migration and apoptosis were analyzed by BrdU assay, Transwell assay and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, respectively. Luciferase reporter assay was carried out to determine the regulatory relationship between miR-141-3p and Keap1. Additionally, Western blot was used to detect the function of miR-141-3p on the expression levels of Keap1, Nrf2 and HO-1 in VSMCs. miR-141-3p was remarkably down-regulated in both AS animal model and cell model while the expression of Keap1 was elevated. Proliferation and migration of VSMCs were suppressed after miR-141-3p mimics transfection and cell apoptosis was promoted. miR-141-3p also inhibited the expressions of IL-6, IL-ß, TNF-α and Keap1 but promoted the expressions of Nrf2 and HO-1. Moreover, the binding site between miR-141-3p and the 3'UTR of Keap1 was confirmed. miR-141-3p is down-regulated during AS, and it can alleviate VSMCs' dysfunction by targeting the Keap1/Nrf2/HO-1 axis.

MicroRNA-544 inhibits esophageal squamous cell carcinoma cell proliferation and enhances sensitivity to cisplatin by repressing E2F transcription factor 5.

Esophageal squamous cell carcinoma (ESCC) is one of the most common malignancies worldwide. MicroRNA (miRNA)-544 is an important cancer-associated RNA that is downregulated in multiple types of cancer. However, the role of miR-544 in ESCC progression remains unknown. In the present study, miR-544 expression level was determined via RT-qPCR in 30 pairs of ESCC and adjacent normal tissues and in a panel of ESCC cell lines. Cell proliferation and cell apoptosis were assessed by MTT and flow cytometry assays. Luciferase reporter assay and western blot analysis were conducted to verify E2F transcription factor 5 (E2F5), an oncogene in ESCC, as a novel target gene of miR-544. The results illustrated that miR-544 is frequently downregulated in ESCC tissues and cell lines. Overexpression of miR-544 in ESCC cells resulted in decreased cell proliferation and increased cell apoptosis. Thus, E2F5 was identified as a target of miR-544, and its expression was negatively correlated with miR-544 expression in clinical ESCC tissues. More importantly, overexpression of miR-544 led to increased sensitivity of ESCC cells to cisplatin, an anticancer drug. Overall, these findings indicate that miR-544 serves as a tumor suppressor by targeting E2F5; thus, miR-544 may be a therapeutic target for the treatment of ESCC.

A comparative study of thoracoscopic and open surgery of congenital diaphragmatic hernia in neonates.

BACKGROUND: An increasing number of hospitals have carried out neonatal thoracoscopic assisted repair of congenital diaphragmatic hernia (CDH). METHODS: The 26 cases received thoracoscopic-assisted repair (observation group) and 44 cases open repair (control group). General anesthesia was performed with endotracheal intubation using a trachea cannula without cuff. The general preoperative data, intraoperative hemodynamic parameters, intraoperative surgical conditions, postoperative complications, postoperative recovery condition, postoperative survival rate and recurrence rate were recorded. RESULTS: The intraoperative mean arterial pressure and heart rate at each time point in observation group were more stable and effective than those in control group (all P <  0.001). The number of manual ventilation, SpO2 < 90% and hypercapnia cases were significantly lower than those in control group (all P <  0.05). Intraoperative bleeding, incision length and operation duration were significantly lower in observation group compared with control group (all P <  0.001). No significant differences were seen between the two groups in postoperative complications including pulmonary infection, incision infection, pulmonary hypertension, hemorrhage, and scleredema (all P > 0.05). The duration of postoperative mechanical ventilation, antibiotic use and hospitalization in observation group was significantly shorter than those in control group (all P < 0.05). There was no significant difference in postoperative survival rate and recurrence rate between the two groups (both P > 0.05). CONCLUSION: The intraoperative hemodynamic parameters of CDH repair under thoracoscopy were more stable, the duration of postoperative mechanical ventilation, antibiotic use and hospitalization were shortened, and the therapeutic effect was better.

MicroRNA-664 Targets Insulin Receptor Substrate 1 to Suppress Cell Proliferation and Invasion in Breast Cancer.

A large number of microRNAs (miRNAs) have been previously demonstrated to be dysregulated in breast cancer (BC), and alterations in miRNA expression may affect the initiation and progression of BC. This study showed that miR-664 expression was obviously reduced in BC tissues and cell lines. Resumption of the expression of miR-664 attenuated the proliferation and invasion of BC cells. The molecular mechanisms underlying the inhibitory effects of BC cell proliferation and invasion by miR-664 were also studied. Insulin receptor substrate 1 (IRS1) was identified as a novel and direct target of miR-664. In addition, siRNA-mediated silencing of IRS1 expression mimicked the suppressive effects of miR-664 overexpression in BC cells. Rescue experiments demonstrated that recovered IRS1 expression partially antagonized the inhibition of proliferation and invasion of BC cells caused by miR-664 overexpression. Thus, miR-664 may serve as a tumor suppressor in BC by directly targeting IRS1. Moreover, miR-664 downregulation in BC may contribute to the occurrence and development of BC, suggesting that miR-664 may be a novel therapeutic target for patients with BC.

miR-329 inhibits papillary thyroid cancer progression via direct targeting WNT1.

Dysregulated microRNA-329 (miR-329) serves an important role in the progression of certain types of tumor. However, the exact function and mechanisms of miR-329 in papillary thyroid cancer (PTC) remain unknown. The present study investigated the function and mechanisms of miR-329 in regulating PTC cell progression. The results revealed that the expression of miR-329 was significantly downregulated in PTC tissues and cell lines compared with adjacent normal tissues and a human immortalized follicular cell line. miR-329 mimics notably decreased PTC cell proliferation, colony formation and WNT1 expression in vitro, as well as suppressing PTC tumor growth in vivo. In addition, luciferase assays determined that miR-329 was able to directly bind with the 3'untranslated region of WNT1. Furthermore, short interfering RNA-WNT1-induced downregulation of WNT1, which demonstrated similar effects to miR-329 overexpression. WNT1 overexpression rescued the tumor suppressive effects of miR-329 in PTC cells. The present study provided new insights into the role of miR-329 in PTC progression and suggests the potential application of miR-329 as a therapy for PTC.

[mRNA and Protein Expression of AXIN,ß-Catenin, MMP7 and MMP9 and Their Relationship in Lymphoma Cells].

OBJECTIVE: To investigate the mRNA and protein expression of axin inhibitor (AXIN), ß-chain protein (ß-catenin), matrix metalloproteinase-7 (MMP-7) and matrix metalloproteinase-9 (MMP-9), and their relationship in lymphoma cells. METHODS: The expressions of MMP-7, MMP-9, ß-catenin and AXIN in lymphoma cell lines were detected by Western blot and RT-PCR. Moreover, the lymphoma cells with relatively low expression of AXIN were grouped and were transiently transfected by using pcDNA5-His-ß-catenin and pCMV5-HA-AXIN; the protein and mRNA expression of MMP-7, MMP-9 and ß-catenin in lymphoma cells was detected by Western blot and RT-PCR, respectively; the cell infiltration and migration ability in group with stable ligh expression of AXIN, group of interfering stable high expression of AXIN and blank control group were analyzed by transwell experiment. RESULTS: The AXIN negatively correlated with MMP-7, MMP-9 and ß-catenin expression in lymphoma cell lines. After the up-regulation of AXIN, the mRNA expression of MMP7, MMP-9 and ß-catenin in Raji cells all not significantly changed, while the pratein expression of MMP-7, MMP-9 and ß-catenin all significantly decreased (P<0.05); after the up-regulation of ß-catenin, the mRNA and protein expression of MMP-7, MMP-9 was also up-regulated significantly (P<0.05). After interfering the AXIN, the mRNA expression of MMP-7, MMP-9 and ß-catenin in group with stable high expression of AXIN all not changed significantly, while protein expression of MMP-7, MMP-9 and ß-catenin was down-regulated significantly (P<0.05); after interfering the ß-catenin, the protein and mRNA expression of MMP-7 and MMP-9 in group with stable high expression of AXIN all were down-regulated significantly(P<0.05). CONCLUSION: The up-regulation of AXIN expression in lymphoma cells can lead to decrease of ß-catenin expression and the resuts in significant decrease of MMP-7 and MMP-9 expression, there by plays a role to block the infiltration and migration of lymphoma cells.

MicroRNA­376a inhibits cell proliferation and invasion in glioblastoma multiforme by directly targeting specificity protein 1.

Glioblastoma multiforme (GBM), a World Health Organization grade IV glioma, is the most common and aggressive primary brain tumor in humans. microRNAs (miRNAs) are aberrantly expressed in numerous cancer types, including GBM. Abnormally expressed miRNAs are commonly associated with malignant characteristics of GBM, including malignant growth, proliferation, apoptosis, invasion, metastasis and resistance to chemotherapy. miRNA (miR)­376a is abnormally expressed in multiple human cancers; however, the expression pattern and role of miR­376a in GBM, and the underlying molecular mechanisms by which miR­376a exerts its functions remain to be elucidated. Therefore, the aim of this study was to measure miR­376a expression and determine its biological roles in GBM as well as its associated molecular mechanism. In the present study, miR­376a expression was markedly downregulated in GBM tissues and cell lines. Overexpression of miR­376a markedly decreased the proliferation and invasion of GBM cells in vitro. In the present study, specificity protein 1 (SP1) was demonstrated to be a direct target of miR­376a. In addition, a negative association between SP1 mRNA and miR­376a expression was observed in GBM tissues. SP1 upregulation reduced the effects of miR­376a overexpression on GBM cell proliferation and invasion. miR­376a may be a therapeutic target for the treatment of patients with GBM.

[Efficacy Analysis of GEMOX Regimen for Treatment of Refractory Non-Hodgkin's Lymphoma].

OBJECTIVE: To explore the clinical efficacy of GEMOX regimen on patients with refractory non-hodgkin's lymphoma. METHODS: Eighty-two cases of non-Hodgkin's lymphoma were divided into 2 groups: gemcitabine+oxaliplation(Gem+Oxa) group (42 cases) and vinorelbine+oxaliplatin(Vin+Oxa) group (40 cases) according to chemotherapy regimens. The clinical efficacy, side effects, progression-free survival situation in 2 groups were compared. RESULTS: There was no significant difference on the clinical effects of 2 groups (P>0.05); The therapeutic efficacy for B cell lymphoma was higher than that for T cell lymphoma(P<0.05); The therapeutic effects for I-II stages was lower than that for III-IV stages(P<0.05); The incidences of platelet decline, nausea and vomit, peripheral nerve symptoms in Gem+Oxa group were lower than those in Vin+Oxa group(P<0.05); There was no significant difference in the median progression free survival(P>0.05). CONCLUSION: The efficacy of GEMOX regimen for refractory non-Hodgkin's lymphoma has been confirmed to be good, it has distinct clinical curative effect, it can prolong the progression-free survival time in patients with B cell lymphoma, specially for III-IV stages. It can be used as the preferred method for the treatment of patients with refractory NHL.

Clinical implications of vasohibin-1 in esophageal carcinoma cells: Inhibition of cell growth and migration.

As one of the first-established negative feedback regulators of angiogenesis, mesenchymal vasohibin-1 (VASH1) serves important roles in the progression and prognosis of various types of tumor. However, the clinical implications of VASH1 in esophageal carcinoma (EC) cells have not been reported and the direct effects of VASH1 on EC cells remain unknown. In the present study, the expression of VASH1 in EC cells was observed using immunohistochemistry and western blotting; a χ2 test was used to analyze the correlation of VASH1 with clinical parameters, and it was observed that VASH1 was negatively-correlated with tumor size (r=­0.399; P<0.01) and invasion depth (r=­0.318; P<0.01). Survival analysis demonstrated that VASH1 was positively­correlated with increased overall survival (P=0.039) and disease free survival (P=0.012). The direct effects of VASH1 on EC cells were analyzed by altering VASH1 expression, and it was observed that downregulation of VASH1 increased proliferation, clone formation and the migratory ability of EC9706 cells, whereas upregulation of VASH1 inhibited proliferation, clone formation and the migratory ability of EC1 cells. The results of the present study demonstrated that VASH1 in EC cells was negatively­correlated with progression and poor prognosis of patients with EC. VASH1 was able to directly inhibit the growth and migration of EC cells.

Vasohibin2 promotes adriamycin resistance of breast cancer cells through regulating ABCG2 via AKT signaling pathway.

As a well­known angiogenic factor in different histology and pathological conditions, the pro­progressive role of vasohibin2 (VASH2) has been reported in various types of tumors. However, its role in drug resistance of breast cancer has not been reported so far. The present study demonstrated that MCF­7 cells with increased expression of VASH2 demonstrate stronger adriamycin (ADM) resistance compared with MDA­MB­231 cells with decreased expression of VASH2. Overexpression of VASH2 in MDA­MB­231 cells increased ADM resistance and silencing VASH2 in MCF­7 cells inhibited ADM resistance. Furthermore, in newly established ADM resistant cell lines, VASH2 was significantly upregulated. These results revealed the promotive role of VASH2 in the ADM resistance of breast cancer cells. In addition, overexpression of VASH2 in MDA­MB­231 cells significantly upregulated ATP­binding cassette sub­family G member 2 (ABCG2), however silencing VASH2 in MCF­7 cells inhibited ABCG2 significantly. Silencing ABCG2 abrogated increase of ADM resistance induced by VASH2 overexpression in MDA­MB­231 cells. This proved that VASH2 induced ADM resistance through promoting expression of ABCG2, at least in part. Further study regarding the underlying molecular mechanism demonstrated that VASH2 promoted ABCG2 via the protein kinase B (AKT) signaling pathway. Overall, VASH2 may promote drug resistance of breast cancer cells through regulating ABCG2 via the AKT signaling pathway. This suggests a novel therapeutic target to inhibit drug resistance in breast cancer, for a more efficient therapeutic outcome.

[Clinical Efficacy of L-Asparaginasum Combined with CHOP for Treating Patients with Extranodal Natural Killer/T Cell Lymphoma].

OBJECTIVE: To investigate the clinical efficacy of L-asparginasum, ASP) combined with CHOP for treating patients with extranodal natural killer/T-cell lymphoma. METHODS: A total of 68 patients with extranodal natural killer/T-cell lymphoma in our hospital from August 2007 to May 2009 were enrolled in this study, out of them 34 patients received CHOP regimen (CHOP group) and other 34 patients received CHOP regimen combined with L-Asparaginasum (ASP+CHOP group). The clinical efficacy of both groups was analyzed and compared after treatment. RESULTS: In CHOP group 16 patients achieved CR+PR, the total remission rate (TRR) was 47.06%; in ASP+CHOP group 24 patients achieved CR+PR, the TRR was 70.58%, and the TRR in ASP+CHOP group was higher than that in CHOP group, there was statistical significance between these 2 groups (X(2) = 3.886, P < 0.05). The time of PFS in CHOP group was 24.7 months, and the time of PFS in ASP+CHOP group was 47.5 months which was significantly longer than that in CHOP group, and there was statistical siguificance between these 2 groups (P < 0.05). The incidence of anemia with grade I-II and III-IV blood cell reduction in ASP+CHOP group was higher than that in CHOP group (P < 0.05). The incidence of fever with grade I-II and albumin decrease in ASP+CHOP group was higher than that in CHOP group (P < 0.05). The abnormality of coagulation function in ASP+CHOP group was higher than that in CHOP group (P < 0.05). The anaphylactic reaction was found in 6 cases. The increase of serum amylase was observed in 1 case of aggressive NK/T cell lymphoma, the acute pancreatitis occured in 1 case who was inproved after treatment, but this patients died due to rapid progression of disease caused by poor general condition and untolerance to chemotherapy. The incomplete intestinal obstruction was found in 3 patients who recovered after conservative treatment. The grade II serum creatinine was elevated in 2 cases of ASP+CHOP group and in 1 case of CHOP group who was inproved after symptomatic therapy. CONCLUSION: L-Asparaginasum combined with CHOP for treating patients with extranodal natural killer/T-cell lymphoma is effective, and may be used in clinic.

Clinical significance of circulating tumor cells in breast cancer patients.

Circulating tumor cells (CTCs) are defined as tumor cells circulating in the peripheral blood of patients, shed from either the primary tumors or its metastases. Many techniques have been developed in the recent years to identify CTCs in breast cancer patients, and trials have proved the prognostic significance of CTCs. In this study, we validated the CTC detection method of combining cell filtration and laser scanning cytometry (LSC), which was highly reproducible with increased sensitivity and accuracy. In 134 non-metastatic breast cancer patients analyzed, HER2 was found to be the only primary tumor characteristics that correlated with the presence of CTCs. 85 patients with definitive stage information were selected for association study between the disease stages and CTC numbers. The detection rate and the number of CTCs were correlated with the disease stages. Moreover, assessment of CTCs in 92 metastatic breast cancer patients was found to be able to predict the efficacy of chemotherapy. Increase in CTC numbers was an independent prognostic factor for treatment outcomes. Our results suggested that CTC assessment could be an indication of the disease progression and analysis of the properties of CTCs is likely to provide new insights into the biology of breast cancer and contribute to defining novel treatments and better prediction of clinical outcomes.