Efficacy of autologous blood patch injection for pneumothorax rate after CT-guided percutaneous transthoracic lung biopsy: a systematic review and meta-analysis.

BACKGROUND: Pneumothorax is the most frequent complication after CT-guided percutaneous transthoracic lung biopsy (CT-PTLB). Many studies reported that injection of autologous blood patch (ABP) during biopsy needle withdrawal could reduce the pneumothorax and chest tube insertion rate after CT-PTLB, but the result is debatable. The aim of this systematic review and meta-analysis is to synthesize evidence regarding the efficacy of ABP procedure in patients receiving CT-PTLB. METHODS: Eligible studies were searched in Pubmed, Embase and Web of Science databases. The inclusion criteria were studies that assessed the relationship between ABP and the pneumothorax and/or chest tube insertion rate after CT-PTLB. Subgroup analyses according to study type, emphysema status and ABP technique applied were also conducted. Odds ratio (OR) with 95% confidence interval (CI) were calculated to examine the risk association. RESULTS: A total of 10 studies including 3874 patients were qualified for analysis. Our analysis suggested that ABP reduced the pneumothorax (incidence: 20.0% vs. 27.9%, OR = 0.67, 95% CI = 0.48-0.66, P < 0.001) and chest tube insertion rate (incidence: 4.0% vs. 8.0%, OR = 0.47, 95% CI = 0.34-0.65, P < 0.001) after CT-PTLB. Subgroup analysis according to study type (RCT or retrospective study), emphysema status (with or without emphysema), and ABP technique applied (clotted or non-clotted ABP) were also performed and we found ABP reduced the pneumothorax and chest tube insertion rate in all subgroups. CONCLUSIONS: Our study indicated that the use of ABP was effective technique in reducing the pneumothorax and chest tube insertion rate after CT-PTLB.

Tumorigenesis of basal muscle invasive bladder cancer was mediated by PTEN protein degradation resulting from SNHG1 upregulation.

BACKGROUND: Phosphatase and tensin homolog deleted on chromosome ten (PTEN) serves as a powerful tumor suppressor, and has been found to be downregulated in human bladder cancer (BC) tissues. Despite this observation, the mechanisms contributing to PTEN's downregulation have remained elusive. METHODS: We established targeted genes' knockdown or overexpressed cell lines to explore the mechanism how it drove the malignant transformation of urothelial cells or promoted anchorageindependent growth of human basal muscle invasive BC (BMIBC) cells. The mice model was used to validate the conclusion in vivo. The important findings were also extended to human studies. RESULTS: In this study, we discovered that mice exposed to N-butyl-N-(4-hydroxybu-tyl)nitrosamine (BBN), a specific bladder chemical carcinogen, exhibited primary BMIBC accompanied by a pronounced reduction in PTEN protein expression in vivo. Utilizing a lncRNA deep sequencing high-throughput platform, along with gain- and loss-of-function analyses, we identified small nucleolar RNA host gene 1 (SNHG1) as a critical lncRNA that might drive the formation of primary BMIBCs in BBN-treated mice. Cell culture results further demonstrated that BBN exposure significantly induced SNHG1 in normal human bladder urothelial cell UROtsa. Notably, the ectopic expression of SNHG1 alone was sufficient to induce malignant transformation in human urothelial cells, while SNHG1 knockdown effectively inhibited anchorage-independent growth of human BMIBCs. Our detailed investigation revealed that SNHG1 overexpression led to PTEN protein degradation through its direct interaction with HUR. This interaction reduced HUR binding to ubiquitin-specific peptidase 8 (USP8) mRNA, causing degradation of USP8 mRNA and a subsequent decrease in USP8 protein expression. The downregulation of USP8, in turn, increased PTEN polyubiquitination and degradation, culminating in cell malignant transformation and BMIBC anchorageindependent growth. In vivo studies confirmed the downregulation of PTEN and USP8, as well as their positive correlations in both BBN-treated mouse bladder urothelium and tumor tissues of bladder cancer in nude mice. CONCLUSIONS: Our findings, for the first time, demonstrate that overexpressed SNHG1 competes with USP8 for binding to HUR. This competition attenuates USP8 mRNA stability and protein expression, leading to PTEN protein degradation, consequently, this process drives urothelial cell malignant transformation and fosters BMIBC growth and primary BMIBC formation.

RhoGDIß inhibition via miR-200c/AUF1/SOX2/miR-137 axis contributed to lncRNA MEG3 downregulation-mediated malignant transformation of human bronchial epithelial cells.

Nickel pollution is a recognized factor contributing to lung cancer. Understanding the molecular mechanisms of its carcinogenic effects is crucial for lung cancer prevention and treatment. Our previous research identified the downregulation of a long noncoding RNA, maternally expressed gene 3 (MEG3), as a key factor in transforming human bronchial epithelial cells (HBECs) into malignant cells following nickel exposure. In our study, we found that deletion of MEG3 also reduced the expression of RhoGDIß. Notably, artificially increasing RhoGDIß levels counteracted the malignant transformation caused by MEG3 deletion in HBECs. This indicates that the reduction in RhoGDIß contributes to the transformation of HBECs due to MEG3 deletion. Further exploration revealed that MEG3 downregulation led to enhanced c-Jun activity, which in turn promoted miR-200c transcription. High levels of miR-200c subsequently increased the translation of AUF1 protein, stabilizing SOX2 messenger RNA (mRNA). This stabilization affected the regulation of miR-137, SP-1 protein translation, and the suppression of RhoGDIß mRNA transcription and protein expression, leading to cell transformation. Our study underscores the co-regulation of RhoGDIß expression by long noncoding RNA MEG3, multiple microRNAs (miR-200c and miR-137), and RNA-regulated transcription factors (c-Jun, SOX2, and SP1). This intricate network of molecular events sheds light on the nature of lung tumorigenesis. These novel findings pave the way for developing targeted strategies for the prevention and treatment of human lung cancer based on the MEG3/RhoGDIß pathway.

Characteristics of the microbiome in lung adenocarcinoma tissue from patients in Kunming city of southwestern China.

The purpose of this study is to identify the characteristics of microbial communities in the lung cancer tissues from patients in Kunming sity of southwestern China and to compare the microbial differences at different clinical stages of lung cancer to uncover potential microbial biomarkers. In total, 40 tissue samples of primary lung adenocarcinoma were collected and further performed by 16S rRNA gene sequencing. The subjects were grouped according to TNM stages (T and N group), clinical stage, and smoke status, and the microbial differences in each group were compared. Analysis of sequence data to determine beta diversity, the UniFrac distance was calculated by QIIME and visualized by principal coordinate analysis (PCoA) using R (version 2.15.3). Microbiome abundance and diversity between different groups were calculated by t test or Wilcoxon rank sum test and drawn by R. The linear discriminant analysis effect size (LEfSe) method was utilized to compare relative abundances of all bacterial taxa between groups. A total of 951 OTUs were identified in the cancer tissues. No significant difference has been found in the alpha diversity within all the groups. Beta diversity significantly differed in the N, T, and clinical stage groups. By LEfSe analysis, eight differential taxa including Bifidobacterium were identified in the N group. In the T1 and T2 group, the LEfSe result identified five phyla and ten genera. The differential genera were Moraxella, Dolosigranulum, unidentified_Corynebacteriaceae, and Citrobacter in the T2 group and Bifidobacterium, Alistipes, Akkermansia, Blautia, Lactobacillus, as well as Faecalibaculum in the T1 group. Differential bacterial composition and abundance were also observed in the clinical stage group. This study confirmed that by 16S rRNA sequencing, we identified the dominant microbe of lung cancer tissue in different groups. Bifidobacterium may play an essential role in lymph node metastasis and tumor progression, providing a specific potential microbial biomarker for lung adenocarcinoma. PCR products were subject to vertical electrophoresis on 2% agarose gels, and a colloid recovery kit (Qiagen, Valencia, CA) was applied to recover the target bands. Libraries were generated by the TruSeq DNA PCR-Free Sample Preparation Kit (Illumina, San Diego, USA), and the concentrations were quantitated with a Qubit fluorometer. Finally, the qualified libraries were sequenced by NovaSeq6000 (Illumina).

ELANE Promotes M2 Macrophage Polarization by Down-Regulating PTEN and Participates in the Lung Cancer Progression.

BACKGROUND: Macrophages are one of the most important immunoinflammatory cell populations in the tumor microenvironment (TME). In this study, we preliminarily investigated the upstream pathway of M2 macrophage polarization affecting lung cancer progression. METHODS: Bioinformatics analysis was used to evaluate genes closely associated with lung adenocarcinoma and their relationship with immune cells. THP-1 monocytes were induced into M2 macrophages. The expression of markers in M2 macrophages was detected by quantitative reverse transcription-PCR (qRT-PCR), enzyme linked immunosorbent assay (ELISA), and flow cytometry. The effects of neutrophil elastase (ELANE)-mediated M2 macrophages on lung cancer cell proliferation, migration and invasion and tumor growth were investigated by in vitro and in vivo experiments after co-culture of macrophage conditioned medium (CM) and lung cancer cell lines A549 and H1299. The PTEN protein expression was detected by Western blotting. RESULTS: ELANE was significantly positively correlated with M2 macrophages. ELANE up-regulated the expression of the M2 macrophage markers CD206, CCL22, IL-10 and CCL18 and increased the proportion of CD206+ macrophages. Compared with M0-CM, M2-CM promoted cell proliferation, migration, and invasion, and (M2+ELANE)-CM further enhanced this effect. In vivo, ELANE promoted M2 macrophage-induced tumor growth in lung cancer mice model. In vitro experiments showed that ELANE can down-regulate the expression of PTEN and promote the polarization of M2 macrophages. CONCLUSION: ELANE promotes the polarization of M2 macrophages by down-regulating PTEN, thus promoting cell proliferation, migration, and invasion in vitro and growth of lung cancer cells in vivo.

M2 macrophages-derived exosomal miR-3917 promotes the progression of lung cancer via targeting GRK6.

Macrophages in the tumor microenvironment (TME) can serve as potential targets for therapeutic intervention. The aim of this study was to investigate the molecular mechanism by which M2 macrophage-derived exosomes (M2-Ex) affect lung cancer progression through miRNA transport. The THP-1 cells were differentiated into M0 and M2 macrophages. M2-Ex were isolated and identified by transmission electron microscopy (TEM) and nanoparticle tracking analysis (NTA). Cancer tissues and adjacent tissues of non-small-cell lung cancer (NSCLC) patients were collected. H1299 and A549 cells were co-cultured with M2-Ex. Subcutaneous xenograft mouse model was established. miR-3917 is highly expressed in lung cancer tissues and M2-Ex. Interference of miR-3917 in M2-Ex inhibits H1299 cell proliferation, migration and invasion, while overexpression of miR-3917 had the opposite effect in A549 cells. M2-Ex promote tumor growth by delivering miR-3917 in vivo. miR-3917 could target G protein-coupled receptor kinase 6 (GRK6), and interference of miR-3917 in M2-Ex inhibits H1299 cells proliferation, migration and invasion by up-regulating GRK6 level, while overexpression of miR-3917 had the opposite effect in A549 cells. M2-Ex can transfer miR-3917 into lung cancer cells and promote lung cancer progression, providing theoretical basis for the diagnosis and effective treatment of lung cancer.

TTQR: A Traffic- and Thermal-Aware Q-Routing for 3D Network-on-Chip.

The die-stacking structure of 3D network-on-chips (3D NoC) leads to high power density and unequal thermal conductance between different layers, which results in low reliability and performance degradation of 3D NoCs. Congestion-aware adaptive routing, which is capable of balancing the network's traffic load, can alleviate congestion and thermal problems so as to improve the performance of the network. In this study, we propose a traffic- and thermal-aware Q-routing algorithm (TTQR) based on Q-learning, a reinforcement learning method. The proposed algorithm saves the local traffic status and the global temperature information to the Q1-table and Q2-table, respectively. The values of two tables are updated by the packet header and saved in a small size, which saves the hardware overhead. Based on the ratio of the Q1-value to the Q2-value corresponding to each direction, the packet's output port is selected. As a result, packets are transferred to the chosen path to alleviate thermal problems and achieve more balanced inter-layer traffic. Through the Access Noxim simulation platform, we compare the proposed routing algorithm with the TAAR routing algorithm. According to experimental results using synthetic traffic patterns, our proposed methods outperform the TAAR routing algorithm by an average of 63.6% and 41.4% in average latency and throughput, respectively.

SOX2 Promotes Invasion in Human Bladder Cancers through MMP2 Upregulation and FOXO1 Downregulation.

SOX2, a member of the SRY-related HMG-box (SOX) family, is abnormally expressed in many tumors and associated with cancer stem cell-like properties. Previous reports have shown that SOX2 is a biomarker for cancer stem cells in human bladder cancer (BC), and our most recent study has indicated that the inhibition of SOX2 by anticancer compound ChlA-F attenuates human BC cell invasion. We now investigated the mechanisms through which SOX2 promotes the invasive ability of BC cells. Our studies revealed that SOX2 promoted SKP2 transcription and increased SKP2-accelerated Sp1 protein degradation. As Sp1 is a transcriptionally regulated gene, HUR transcription was thereby attenuated, and, in the absence of HUR, FOXO1 mRNA was degraded fast, which promoted BC cell invasion. In addition, SOX2 promoted BC invasion through the upregulation of nucleolin transcription, which resulted in increased MMP2 mRNA stability and expression. Collectively, our findings show that SOX2 promotes BC invasion through both SKP2-Sp1-HUR-FOXO1 and nucleolin-MMP2 dual axes.

Towards Convolutional Neural Network Acceleration and Compression Based on Simonk-Means.

Convolutional Neural Networks (CNNs) are popular models that are widely used in image classification, target recognition, and other fields. Model compression is a common step in transplanting neural networks into embedded devices, and it is often used in the retraining stage. However, it requires a high expenditure of time by retraining weight data to atone for the loss of precision. Unlike in prior designs, we propose a novel model compression approach based on Simonk-means, which is specifically designed to support a hardware acceleration scheme. First, we propose an extension algorithm named Simonk-means based on simple k-means. We use Simonk-means to cluster trained weights in convolutional layers and fully connected layers. Second, we reduce the consumption of hardware resources in data movement and storage by using a data storage and index approach. Finally, we provide the hardware implementation of the compressed CNN accelerator. Our evaluations on several classifications show that our design can achieve 5.27× compression and reduce 74.3% of the multiply-accumulate (MAC) operations in AlexNet on the FASHION-MNIST dataset.

CircRNA circ_0004370 promotes cell proliferation, migration, and invasion and inhibits cell apoptosis of esophageal cancer via miR-1301-3p/COL1A1 axis.

BACKGROUND: The aim of this study was to investigate the circ_0004370 expression in EC, its effects on cell proliferation, apoptosis, migration, invasion, and epithelial-mesenchymal transition (EMT) process, and the underlying regulatory mechanisms in EC. METHODS: The protein levels of COL1A1 and EMT-related proteins were detected by western blot. The role of circ_0004370 on cell viability, proliferation, and apoptosis was analyzed by Cell Counting Kit-8 (CCK-8) assay, colony formation assay, and flow cytometry, respectively. The transwell assay was used to examine cell migration and invasion. The binding sites between miR-1301-3p and circ_0004370 or COL1A1 were predicted by starbase software and confirmed by dual-luciferase reporter assay and RNA pull-down assay. RESULTS: We discovered that circ_0004370 was remarkably upregulated in EC tissues and cells. Knockdown of circ_0004370 inhibited cell proliferation, migration as well as invasion, and promoted apoptosis in vitro, while its effect was rescued by miR-1301-3p inhibition. And circ_0004370 mediated the EMT process in EC cells. Moreover, we explored its regulatory mechanism and found that circ_0004370 directly bound to miR-1301-3p and COL1A1 was verified as a target of miR-1301-3p. COL1A1 was highly expressed in EC cells and upregulation of COL1A1 reversed the effects of miR-1301-3p on cell proliferation, migration, invasion, and apoptosis. In addition, silencing of circ_0004370 reduced tumor volumes and weights in vivo. We showed that circ_0004370/miR-1301-3p/COL1A1 axis played the critical role in EC to regulate the cell activities. CONCLUSION: Circ_0004370 promotes EC proliferation, migration and invasion, and EMT process and suppresses apoptosis by regulating the miR-1301-3p/COL1A1 axis, indicating that circ_0004370 may be used as a potential therapeutic target for EC.

CBX7, a Potential Prognostic Biomarker in Lung Adenocarcinoma.

BACKGROUND: Lung adenocarcinoma (LUAD) is a major type of NSCLC and has high morbidity and mortality. The identification of useful prognostic biomarkers for LUAD is important. CBX7 has been reported in various cancers yet its expression level and potential roles have not been fully understood. METHODS: GEPIA, Oncomine, TCGA, KM plotter and OSluca databases were used to explore the expression profile and prognostic effects of CBX7 mRNA expression in patients with LUAD. TIMER was used to explore the relationship between CBX7 and immune infiltrating cells. GSEA was used to further explore the potential biological process and pathways regulated by CBX7 in LUAD. Lastly, IHC detection of CBX7 in 95 samples was used to validate the result. RESULTS: We found CBX7 was downregulated in LUAD in GEPIA, Oncomine and TCGA databases. TCGA, KM plotter and OSluca databases suggested that CBX7 was associated with poor clinical outcomes and low survival rate. Using TIMER, we found that CBX7 might be associated with immune infiltration. Via gene set enrichment analysis, we found that tumor-associated biological processes and signaling pathways were enriched in the CBX7 downregulated group. Using clinical samples, we found that CBX7 protein has low expression in LUAD and was associated with poor survival. CONCLUSION: CBX7 might serve as a promising biomarker and potential molecular target in LUAD.

An Accelerator Design Using a MTCA Decomposition Algorithm for CNNs.

Due to the high throughput and high computing capability of convolutional neural networks (CNNs), researchers are paying increasing attention to the design of CNNs hardware accelerator architecture. Accordingly, in this paper, we propose a block parallel computing algorithm based on the matrix transformation computing algorithm (MTCA) to realize the convolution expansion and resolve the block problem of the intermediate matrix. It enables high parallel implementation on hardware. Moreover, we also provide a specific calculation method for the optimal partition of matrix multiplication to optimize performance. In our evaluation, our proposed method saves more than 60% of hardware storage space compared with the im2col(image to column) approach. More specifically, in the case of large-scale convolutions, it saves nearly 82% of storage space. Under the accelerator architecture framework designed in this paper, we realize the performance of 26.7GFLOPS-33.4GFLOPS (depending on convolution type) on FPGA(Field Programmable Gate Array) by reducing bandwidth and improving data reusability. It is 1.2×-4.0× faster than memory-efficient convolution (MEC) and im2col, respectively, and represents an effective solution for a large-scale convolution accelerator.

Effect of polysaccharide extract SPSS1 from Apostichopus japonicas spermary on HepG2 cells via iTRAQ-based proteome analysis.

In this study, polysaccharide extract was prepared from Apostichopus japonicus spermary and purified by ion-exchange chromatography and gel filtration chromatography. Two main fractions named SPSS1 and SPSS2 were obtained and analyzed by ultraviolet spectroscopy and mixed with KBr, respectively. Chemical components analysis proved that SPSS1 and SPSS2 were rich in sulfate. Monosaccharide analysis indicated that in addition to the high content of lactose in both kinds of polysaccharides, the highest content of monosaccharide in SPSS1 was galactose, while in SPSS2 it was fucose. Further, the antitumor study of SPSS1 was carried and the results showed that SPSS1 treatment inhibited the proliferation of HepG2 cells. Through the iTRAQ-based proteome analysis, there were 208 differential proteins between control tumor cells and SPSS1 treatment of tumor cells. Compared to control tumor cells, 135 proteins were upregulated and 73 proteins were downregulated in treatment tumor cells. PRACTICAL APPLICATIONS: Our study suggested that polysaccharide from sea cucumbers had the potential to be further developed as antitumor drugs.

RNA m6 A methylation regulates uveal melanoma cell proliferation, migration, and invasion by targeting c-Met.

N6 -methyladenosine (m6 A) is a novel epitranscriptomic marker that contributes to regulating diverse biological processes through controlling messenger RNA metabolism. However, it is unknown if m6 A RNA methylation affects uveal melanoma (UM) development. To address this question, we probed its function and molecular mechanism in UM. Initially, we demonstrated that global RNA m6 A methylation levels were dramatically elevated in both UM cell lines and clinical specimens. Meanwhile, we found that METTL3, a main m6 A regulatory enzyme, was significantly increased in UM cells and specimens. Subsequently, cycloleucine (Cyc) or METTL3 targeted small interfering RNA was used to block m6 A methylation in UM cells. We found that Cyc or silencing METTL3 significantly suppressed UM cell proliferation and colony formation through cell cycle G1 arrest, as well as migration and invasion by functional analysis. On the other hand, overexpression of METTL3 had the opposite effects. Furthermore, bioinformatics and methylated RNA immunoprecipitation-quantitative polymerase chain reaction identified c-Met as a direct target of m6 A methylation in UM cells. In addition, western blot analysis showed that Cyc or knockdown of METTL3 downregulated c-Met, p-Akt, and cell cycle-related protein levels in UM cells. Taken together, our results demonstrate that METTL3-mediated m6 A RNA methylation modulates UM cell proliferation, migration, and invasion by targeting c-Met. Such a modification acts as a critical oncogenic regulator in UM development.

miR-142-3p suppresses uveal melanoma by targeting CDC25C, TGFßR1, GNAQ, WASL, and RAC1.

Purpose: Uveal melanoma (UM) is the most frequent metastatic ocular tumor in adults. Therapeutic intervention remains ineffective since none of the novel procedures used to treat this disease increased survival rates. To deal with this limitation, additional studies are required to clarify its pathogenesis. The current study focused on describing how epigenetic modulation by miR-142-3p affects changes in some cellular functions underlying UM pathogenesis. Methods and results: Microarray analysis identified 374 miRNAs which were differentially expressed between UM cells and uveal melanocytes. miR-142-3p was one of the 10 most downregulated miRNAs. Quantitative RT-PCR analysis confirmed that miR-142-3p expression levels were significantly decreased in both UM cell lines and clinical specimens. The results of the MTS, clone formation, scratch wound, transwell assays, and in vivo biofluorescence imaging showed that miR-142-3p overexpression significantly inhibited cell proliferation, migration, and invasiveness. Nevertheless, miR-142-3p did not affect cell apoptotic activity or sensitivity to doxorubicin. Cell cycle and EdU analysis showed that miR-142-3p overexpression induced G1/G2 cell cycle arrest and reduced DNA synthesis in UM cells. Microarray analysis showed that miR-142-3p mainly regulates the TGFß signaling pathway, and those in which MAPK and PI3K-Akt are constituents. Functional interactions between miR-142-3p and CDC25C, TGFßR1, GNAQ, WASL, and RAC1 target genes were confirmed based on the results of the luciferase reporter assay and Western blot analysis. CDC25C or RAC1 downregulation is in agreement with cell cycle arrest and DNA synthesis disorder induction, while downregulation of TGFßR1, GNAQ, WASL, or RAC1 accounts for declines in cell migration. Conclusion: miR-143-3p is a potential therapeutic target to treat UM since overriding its declines in expression that occur in this disease reversed the pathogenesis of this disease. Such insight reveals novel biomarker for decreasing UM vitality and for improved tracking of tumor progression.

Up-regulation of CKAP2L expression promotes lung adenocarcinoma invasion and is associated with poor prognosis.

AIM: The purpose of this study is to consider the function of cytoskeleton-associated protein 2-like (CKAP2L) in lung adenocarcinoma (LAD) development and its prognostic value. METHODS: The mRNA expression of CKAP2L and its correlation with clinical factors in LAD patients were analyzed from the data taken from The Cancer Genome Atlas and The First Affiliated Hospital of Kunming Medical University. We constructed H460 and A549 cell lines with silenced CKAP2L using RNA interference. Cell counting kit-8 assay and colony formation assays were carried out to determine the function of CKAP2L in H460 and A549 cell proliferation. Transwell and wound healing assays were applied to determine the effect of CKAP2L on H460 and A549 cell invasion and migration. The influences of CKAP2L on mitogen-activated protein kinase signaling pathway-related proteins were tested by Western blotting. RESULTS: CKAP2L expression is enhanced in LAD tissues and is predictive of poor prognosis in LAD patients. High expression of CKAP2L is associated with stage (P<0.001), lymph node status (P=0.002), and metastasis (P=0.025). Depletion of CKAP2L dramatically suppressed the proliferation, migration, and invasion of H460 and A549 cells. Moreover, the ratio of p-MEK/ MEK and p-ERK/ERK reduced obviously in A549 cells after depleting CKAP2L. CONCLUSION: Our findings implied that CKAP2L might be a promoter of LAD and could serve as a predictor for LAD patients.

Phytochemical and bioactive profile of Coriandrum sativum L.

Coriandrum sativum L. is well known around the world because of its food and medicine uses. The main bioactive constituents in C. sativum are essential oil, fatty acids, tocol, sterol and carotenoids, their yields and chemical compositions being influenced by genotype, variety, planting season, ecotype, planting condition, growth stage, plant part, harvesting time, extracting process and other factors. Coriander and its different extracts possess varying degrees of antioxidative and antimicrobial activities on account of different active constituents. The general usages, chemical compositions and bioactivities of coriander are summarized in this review, along with safety considerations.

One surgeon's learning curve for video-assisted thoracoscopic esophagectomy for esophageal cancer with the patient in lateral position: how many cases are needed to reach competence?

BACKGROUND: Minimally invasive esophagectomy is a feasible technique shown to be safe and oncologically adequate for the treatment of esophageal cancer. This study aimed to describe one surgeon's learning curve for video-assisted thoracoscopic esophagectomy with the patient in lateral position. METHODS: From May 2010 to June 2012, 89 thoracoscopic esophagectomies for esophageal cancer were performed by one surgeon. The patients were divided into three groups. Group A included the first 30 cases. Group B comprised cases 31 to 60, and group C included the final 29 cases. The demographic characteristics and the intra- and postoperative variables were collected retrospectively and analyzed. RESULTS: One postoperative death occurred. Eight patients required conversion. No significant difference in background or clinicopathologic factors among the three groups was observed. Compared with group A, a significant decrease in intrathoracic operative time (107.7 ± 16.2 min; P = 0.0000), total operative time (326.3 ± 40.7 min; P = 0.0002), and blood loss (290.8 ± 114.3 ml; P = 0.0129) was observed in group B, whereas more retrieved nodes were harvested (20.1 ± 9.5; P = 0.0002). The last 29 patients (group C) involved significantly less intrathoracic operative time (82.8 ± 18.4 min; P = 0.0386), total operative time (294.7 ± 37.4 min; P = 0.0009), and blood loss (234.7 ± 87.8 ml; P = 0.0125) as well as a shorter postoperative hospital stay (12.4 ± 3.7 days; P = 0.0125) compared with group B. A significant decline in the overall morbidity from group A to group C (P = 0.0005) also was observed. CONCLUSIONS: The results of this study suggest that at least 30 cases were needed to reach the plateau of thoracoscopic esophagectomy. After more than 60 cases of thoracoscopic esophagectomies had been managed, lower morbidity could be obtained.