Describing Strong Correlation with Block-Correlated Coupled Cluster Theory

A block-correlated coupled cluster (BCCC) method based on the generalized valence bond (GVB) wave function (GVB-BCCC in short) is proposed and implemented at the ab initio level, which represents an attractive multireference electronic structure method for strongly correlated systems. The GVB-BCCC method is demonstrated to provide accurate descriptions for multiple bond breaking in small molecules, although the GVB reference function is qualitatively wrong for the studied processes. For a challenging prototype of strongly correlated systems, tridecane with all 12 single C-C bonds at various distances, our calculations have shown that the GVB-BCCC2b method can provide highly comparable results as the density matrix renormalization group method for potential energy surfaces along simultaneous dissociation of all C-C bonds

Dysgerminoma in a case of 46, XY pure gonadal dysgenesis (swyer syndrome): a case report

Simple 46, XY gonadal dysgenesis syndrome, also called Swyer syndrome, is known as pure gonadal dysgenesis. Individuals with the syndrome are characterized by 46, XY karyotype and phenotypically female with female genital appearance, normal Müllerian structures and absent testicular tissue. The condition usually first becomes apparent in adolescence with delayed puberty and primary amenorrhea due to the gonads have no hormonal or reproductive potential. Herein, we report a case of dysgerminoma diagnosed in a dysgenetic gonad of a 21-year-old patient with Swyer syndrome

High Expression of DNMT1 was Correlated with beta-catenin Accumulation and Malignant Phynotype of Lung Squamous Cell Carcinoma and Adenocarcinoma

Background and objective DNA methyltransferase 1 (DNMT1) is one of the important molecules regulating DNA methylation. The abnormal expression of DNMT1 was associated with the methylation and inactivation of tumor suppressor gene and tumorigenesis. The aim of this study is to clarify the difference of DNMT1 expression between lung cancer tissues and corresponding normal lung tissues, to analyze the relationships between DNMT1 expression and clinicopathologic characteristics of lung squamous cell carcinoma and adenocarcinoma, and to investigate the correlation between the expressions of DNMT1 and β-catenin. Methods The expressions of DNMT1 and β-catenin were examined in 84 lung squamous cell carcinoma and adenocarcinoma tissues and corresponding normal lung tissues using tissue microarray and immunohistochemistry. Results The average positive rate of DNMT1 was significantly higher in 84 lung cancer tissues [(58.04±35.07)%] than that in corresponding normal lung tissues [(6.88±10.26)%](t=12.835, P < 0.001). The high expression of DNMT1 was positively correlated with adenocarcinoma histological type (r=0.365, P=0.001), poor differentiation (r=0.253, P=0.021) and lymph node metastasis (r=0.246, P=0.024) in lung cancer. The expression of DNMT1 was significantly correlated with the cytoplasmic expression of β-catenin (r=0.571, P < 0.001). Conclusion The high expression of DNMT1 was a common phenomenon in lung squamous cell carcinoma and adenocarcinoma. The high expression of DNMT1 was correlated with the malignant phynotype of lung cancer. DNMT1 may express coordinately with β-catenin in lung cancer

CCL21/CCR7 Promotes G2/M Phase Progression via the ERK Pathway in Human Non-Small Cell Lung Cancer Cells

C-C chemokine receptor 7 (CCR7) contributes to the survival of certain cancer cell lines, but its role in the proliferation of human non-small cell lung cancer (NSCLC) cells remains vague. Proliferation assays performed on A549 and H460 NSCLC cells using Cell Counting Kit-8 indicated that activation of CCR7 by its specific ligand, exogenous chemokine ligand 21 (CCL21), was associated with a significant linear increase in cell proliferation with duration of exposure to CCL21. The CCL21/CCR7 interaction significantly increased the fraction of cells in the G2/M phase of the cell cycle as measured by flow cytometry. In contrast, CCL21/CCR7 had no significant influence on the G0/G1 and S phases. Western blot and real-time PCR indicated that CCL21/CCR7 significantly upregulated expression of cyclin A, cyclin B1, and cyclin-dependent kinase 1 (CDK1), which are related to the G2/M phase transition. The expression of cyclin D1 and cyclin E, which are related to the G0/G1 and G1/S transitions, was not altered. The CCL21/CCR7 interaction significantly enhanced phosphorylation of extracellular signal-regulated kinase (P-ERK) but not Akt, as measured by Western blot. LY294002, a selective inhibitor of PI3K that prevents activation of the downstream Akt, did not weaken the effect of CCL21/CCR7 on P-ERK. Coimmunoprecipitation further confirmed that there was an interaction between P-ERK and cyclin A, cyclin B1, or CDK1, particularly in the presence of CCL21. CCR7 small interfering RNA or PD98059, a selective inhibitor of MEK that disrupts the activation of downstream ERK, significantly abolished the effects of exogenous CCL21. These results suggest that CCL21/CCR7 contributes to the time-dependent proliferation of human NSCLC cells by upregulating cyclin A, cyclin B1, and CDK1 potentially via the ERK pathway

Overexpression of CARMA3 in Non-Small-Cell Lung Cancer Is Linked for Tumor Progression

We aimed to investigate the clinical significance of the expression of novel scaffold protein CARMA3 in non-small-cell lung cancer (NSCLC) and the biological function of CARMA3 in NSCLC cell lines. We observed moderate to high CARMA3 staining in 68.8% of 141 NSCLC specimens compared to corresponding normal tissues. The overexpression of CARMA3 was significantly correlated with TNM stage (P = 0.022) and tumor status (P = 0.013). CARMA3 upregulation also correlated with a shorter survival rate of patients of nodal status N0 (P = 0.042)as well as the expression of epidermal growth factor receptor (EGFR) (P = 0.009). In EGFR mutation positive cases, CARMA3 expression was much higher (87.5%) compared to non-mutation cases (66.1%). In addition, we observed that knockdown of CARMA3 inhibits tumor cell proliferation and invasion, and induces cell cycle arrest at the boundary between the G1 and S phase. We further demonstrated a direct link between CARMA3 and NF-κB activation. The change of biological behavior in CARMA3 knockdown cells may be NF-κB-related. Our findings demonstrated, for the first time, that CARMA3 was overexpressed in NSCLC and correlated with lung cancer progression, EGFR expression, and EGFR mutation. CARMA3 could serve as a potential companion drug target, along with NF-kB and EGFR in EGFR-mutant lung cancers

Expression of p130cas, E-cadherin and β-catenin and their correlation with clinicopathological parameters in non-small cell lung cancer: p130cas over-expression predicts poor prognosis

p130cas (p130 Crk-associated substrate) is a scaffolding protein and plays an important role in regulating focal adhesion and driving cell migration. Also, the destruction of E-cadherin/β-catenin adhesive complex is one of the changes that characterizes the invasive phenotype of tumors. The aim of this study is to evaluate the role of p130cas, E-cadherin, and β-catenin expression in patients with non-small cell lung cancer (NSCLC). We examined the expression of p130cas, E-cadherin, and β-catenin in 105 lung cancer tissues and paired adjacent normal lung tissues using immunohistochemistry. The overexpression of p130cas was observed in 61.9% (65/105) of lung cancer samples. The overexpression of p130cas was correlated with abnormal expression of E-cadherin and β-catenin (P=0.002 and P=0.006, respectively). Chi-square test showed that the overexpression of p130cas correlated positively with lymph node metastasis and high TNM stage. The Log-Rank test revealed that the mean survival time of patients with p130cas overexpression (36.31 ± 5.66 months) was markedly shorter than those with p130cas normal expression (60.57 ± 6.95 months). Multivariable analysis indicated p130cas overexpression (P<0.001) as an independent significant prognostic factor for NSCLC patients’ survival. These results indicate that p130cas may impact a variety of clinicopathological features of NSCLC and may y influence the prognosis of lung cancer patients

CCL21/CCR7 Prevents Apoptosis via the ERK Pathway in Human Non-Small Cell Lung Cancer Cells

Previously, we confirmed that C-C chemokine receptor 7 (CCR7) promotes cell proliferation via the extracellular signal-regulated kinase (ERK) pathway, but its role in apoptosis of non-small cell lung cancer (NSCLC) cell lines remains unknown. A549 and H460 cells of NSCLC were used to examine the effect of CCL21/CCR7 on apoptosis using flow cytometry. The results showed that activation of CCR7 by its specific ligand, exogenous chemokine ligand 21 (CCL21), was associated with a significant decline in the percent of apoptosis. Western blot and real-time PCR assays indicated that activation of CCR7 significantly caused upregulation of anti-apoptotic bcl-2 and downregulation of pro-apoptotic bax and caspase-3, but not p53, at both protein and mRNA levels. CCR7 small interfering RNA significantly attenuated these effects of exogenous CCL21. Besides, PD98059, a selective inhibitor of MEK that disrupts the activation of downstream ERK, significantly abolished these effects of CCL21/CCR7. Coimmunoprecipitation further confirmed that there was an interaction between p-ERK and bcl-2, bax, or caspase-3, particularly in the presence of CCL21. These results strongly suggest that CCL21/CCR7 prevents apoptosis by upregulating the expression of bcl-2 and by downregulating the expression of bax and caspase-3 potentially via the ERK pathway in A549 and H460 cells of NSCLC

Hsa-miR-125a-3p and hsa-miR-125a-5p are downregulated in non-small cell lung cancer and have inverse effects on invasion and migration of lung cancer cells

<p>Abstract</p> <p>Background</p> <p>Two mature microRNAs (miRNAs), hsa-miR-125a-3p and hsa-miR-125a-5p (collectively referred to as hsa-miR-125a-3p/5p), are derived from 3' and 5' ends of pre-miR-125a, respectively. Although impaired regulation of hsa-miR-125a-5p has been observed in some tumors, the role of this miRNA in invasion and metastasis remains unclear, and few studies have examined the function of hsa-miR-125a-3p. In order to characterize the functions of hsa-miR-125a-3p/5p in invasion and metastasis of non-small cell lung cancer (NSCLC), we investigated the relationships between hsa-miR-125a-3p/5p expression and lymph node metastasis in NSCLC tissues. We also explored the impact of expression of these miRNAs on invasive and migratory capabilities of lung cancer cells.</p> <p>Methods</p> <p>Expression of hsa-miR-125a-3p/5p in NSCLC tissues was explored using real-time PCR. The relationships between hsa-miR-125a-3p/5p expression and pathological stage or lymph node metastasis were assessed using the Spearman correlation test. For in vitro studies, lung cancer cells were transfected with sense and antisense 2'-O-methyl oligonucleotides for gain-of-function and loss-of-function experiments. Transwell experiments were performed to evaluate cellular migration and invasion.</p> <p>Results</p> <p>Expression of hsa-miR-125a-3p/5p was lower in NSCLC tissues than in adjacent normal lung tissues (LAC). Furthermore, the results from the Spearman correlation test showed a negative relationship between hsa-miR-125a-3p expression and pathological stage or lymph node metastasis and an inverse relationship between hsa-miR-125a-5p expression and pathological stage or lymph node metastasis. In vitro gain-of-function experiments indicated that hsa-miR-125a-3p and hsa-miR-125a-5p function in an opposing manner, suppressing or enhancing cell migration and invasion in A549 and SPC-A-1 cell lines, respectively. These opposing functions were further validated by suppression of hsa-miR-125a-3p and hsa-miR-125a-5p expression in loss-of-function experiments.</p> <p>Conclusion</p> <p>Hsa-miR-125a-3p and hsa-miR-125a-5p play distinct roles in regulation of invasive and metastatic capabilities of lung cancer cells, consistent with the opposing correlations between the expression of these miRNAs and lymph node metastasis in NSCLC. These results provide new insights into the roles of miR-125a family members in the development of NSCLC.</p

dynamic noise texture generation on fpgas

Ministry of Education of PR China; Hong Kong University of Science and Technology; University of Electronic Science and Technology of China; City University of Hong Kong; IEEEFPGA technology provides a fast prototyping way to implement various algorithms on its reconfigurable hardware platform. It can flexibly handle with different applications. In this paper, procedural texture mapping based on Perlin noise function is imple