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Emulsion stability directly affects the effect of surfactants in driving oil production. In this paper, the influence of crude oil components and the molecular structure of surfactants on the stabi...

Currently, in the background of a large number of distributed photovoltaic and electric vehicle charging stations with access to the distribution network, this paper presents a distribution network planning method with distributed photovoltaic and electric vehicle charging stations based on multi-population traction differential evolution algorithm. Firstly, this paper considers the curve characteristics of photovoltaic and load, and uses cluster analysis to determine the planning scenery, so that the planning results are more accurate. Then, the distribution network planning model is constructed from the aspects of the minimum investment cost, operation cost and performance index. Then, to improve the speed and the accuracy of planning results, the multi-population traction differential evolution algorithm is used to solve the planning model. Finally, a 10kV line is used as an example to verify the reliability of the proposed method. Then, the traditional differential evolution algorithm and the other two algorithms are compared and analyzed to verify the effectiveness of the proposed planning method.

Nonylphenol dodecyl sulfonate (C12NPAS) has been synthesized, and mixed with heavy alkyl benzene sulfonates (HABS) in different proportions. The effects of different mixing ratios on properties suc...

Nonylphenol-substituted dodecyl sulfonate (C12-NPAS) was synthesized via sulfonation-alkylation-neutralization using 1-dodecene, SO3, and nonylphenol as raw materials. The properties such as surfac...

Background: Atherosclerosis progresses later and with fewer complicated plaques in cerebral arteries than in peripheral arteries. The internal elastic lamina has been proposed to be important for the migration of smooth muscle cells into the intima during intimal thickening and atherosclerosis. Methods: A total of 280 segments were retrieved from 14 autopsy specimens. Five sites were selected for analysis in each case: the middle cerebral artery, basilar artery, coronary artery, iliac artery and renal artery. We investigated the differences in the internal elastic lamina of cerebral and peripheral arteries. Results: The average thickness of the internal elastic lamina of the cerebral arteries was larger than that of the peripheral arteries in both the early and advanced atherosclerotic plaque groups. Among the cerebral arteries, the basilar arteries had a thicker internal elastic lamina than the middle cerebral arteries. Among the peripheral arteries, the renal arteries had the thickest internal elastic lamina, followed by the iliac arteries and coronary arteries. Atherosclerosis led to a reduction in the thickness of the internal elastic lamina of the basilar, middle cerebral, and renal arteries. The stratification of the internal elastic lamina of iliac arteries significantly affected its measurement. The internal elastic lamina of coronary arteries was not affected by atherosclerosis, but it appeared fragmented. Conclusion: The results suggest that the characteristics of atherosclerotic plaques in cerebral and peripheral arteries may be related to the characteristics of the internal elastic lamina.

Inflammatory myofibroblastic tumor (IMT) is a distinctive neoplasm composed of myofibroblastic and fibroblastic spindle cells, accompanied by the inflammatory infiltration of plasma cells, lymphocytes and/or eosinophils. Epithelioid inflammatory myofibroblastic sarcoma (EIMS), which primarily consists of cells with a round or epithelioid morphology, is associated with a poor prognosis and rapid development of local recurrence, and has been recognized to be a variant of IMT. Diagnosis of EIMS is difficult owing to its close resemblance to malignant mesothelioma, anaplastic large cell lymphoma, gastrointestinal stromal tumor and other malignant diseases. In the present study, a case of this rare tumor was evaluated in a 26-year-old male who was admitted to hospital after experiencing abdominal pain for ~18 days and abdominal distention for 1 week. The patient's tumor was examined by imaging, gross examination, histology, immunohistochemistry and fluorescence in situ hybridization (FISH). The magnetic resonance imaging enhanced-scanning image revealed that the morphology of the tumor was irregular, and signal was medley consisting of high and low hybrid reinforcement. Tumors were located in the bladder and rectal pit, in the lower part of the lower abdomen, indicating the presence of malignancy and involvement of the small intestine and rectum. Enhanced-scanning imaging revealed notable inhomogeneous enhancement. Gross examination revealed that the tumor was solid and had a variegated appearance with alternating fleshy and mucoid areas in the cut surface. Microscopically, the tumors were dominated by sheets of epithelioid-to-round cells with a prominent inflammatory infiltrate. The majority of the stroma was myxoid. Immunohistochemically, the tumor cells exhibited diffuse strong staining for ALK receptor tyrosine kinase (hereafter ALK), vimentin, tumor protein P53, desmin, Wilms' tumor 1 and programmed death-ligand 1. FISH analysis also revealed the existence of ALK rearrangement. The expression of PD-L1 in EIMS indicates that the immune checkpoint blockade could represent a novel therapy for the treatment of EIMS.

Lymphoid enhancer-binding factor 1 (LEF1) has been regarded as an important gene for carcinogenesis in many malignancies, however, the role of LEF1 in the progression of human renal cell carcinoma (RCC) has not been well studied. In this study, we investigated the expression of LEF1 in human RCC and the effect on proliferative ability of RCC cells. RCC samples from 138 patients who underwent radical nephrectomy were used in this study, the expression of LEF1 protein was determined by immunohistochemistry and Western blot, mRNA expression was analyzed by RT-PCR and real-time PCR. To investigate the effect of LEF1 on the proliferation of RCC cells, a LEF1 vector was transfected into RCC cells and LEF1 expression was also decreased by using siRNA. Proliferative ability of RCC cells was examined by WST-1 assay and a xenograft study with BALB/C nude mice. Our results indicated that LEF1 expression was significantly increased in stage III, IV and grade 3 RCC than in normal kidney, however, decreased LEF1 expression was found in low-stage and grade RCC compared to that in normal kidney, the expression of LEF1 was correlated to tumor stages, histologic grade, and tumor sizes in RCC. The effect of LEF1 on the proliferation in RCC was also analyzed, our results suggested that RCC cells expressing high levels of LEF1 had significantly increased proliferative ability compared to control cell lines, in contrast, RCC cells with a low LEF1 expression had lower proliferative ability. Moreover, LEF1 promoted proliferation of RCC cells depending on suppressing G2/M cell-cycle arrest. Our study demonstrated that the expression of LEF1 is associated with the progression of RCC and that LEF1 maybe involved in the development of RCC, these suggested LEF1 play a key role and might serve as a therapeutic target in treating advanced RCC.

ALK gene has been identified as a major neuroblastoma (NBL) predisposition gene. But ALK gene copy number and protein expression in ganglioneuroblastoma (GNBL) and ganglioneuroma (GN) are poorly described in the literature. Furthermore, there are controversies on the correlation between ALK protein expression and clinical outcome in NBL.We evaluated MYCN/ALK gene copy number by fluorescence in situ hybridization (FISH) and detected ALK protein expression by immunohistochemistry (IHC) in 188 NBL, 52 GNBL and 6 GN samples and analyzed their association with clinical outcome of the patients.Although ALK gene copy number increase is a recurrent genetic aberration of neuroblastic tumors (NTs) (39.1%, 96/246), ALK amplification was only present in three NBLs (1.2%, 3/246). The frequency of ALK positivity in NBL (50.5%, 51/101) was significantly higher than in GNBL (22.6%, 7/31) and in GN (0.0%, 0/4) (P0.05). In addition, ALK positivity also significantly correlates with MYCN/ALK gene copy number increases (P0.05). Kaplan-Meier survival analysis indicated that MYCN/ALK amplification is correlated with decreased overall survival in NBL. A better prognosis trend was observed in patients with MYCN/ALK gain tumors compared with those with MYCN/ALK normal tumors. Furthermore, ALK positivity significantly correlated with inferior survival in NBL (P=0.044).ALK positivity in NTs correlated with advanced tumor types and MYCN/ALK gene copy number increases. ALK positivity predicts inferior prognosis in NBL and IHC is a simplified strategy to screen ALK positivity in clinical practice.

Anthracosis is the deposition of black dusty material in the pulmonary parenchyma. Previous reports showed anthracosis and p16(ink4a) gene aberrant methylation are closely related to the promotion and progression of small-sized pulmonary adenocarcinoma. In this study, we investigated the influence of anthracosis and p16(ink4a) gene aberrant methylation on clinical samples from patients with small-sized adenocarcinoma.DNA was bisulfite modified and methylation-specific PCR was performed to detect p16(ink4a) gene aberrant methylation; black dusty material was extracted from lung tissues. Anthracotic index (AI) was defined as the absolute absorbance by densitometry. The histopathological diagnosis was concluded according to Noguchi's classification for small-sized pulmonary adenocarcinoma. The mean AI and the frequency of p16(ink4a) gene aberrant methylation of heavy smokers were significantly higher than that of nonsmokers (Ｐ0.01 andＰ0.05, respectively). The frequency of p16(ink4a) gene aberrant methylation of early stage small-sized adenocarcinoma was lower than that of advanced and poorly differentiated, while p16(ink4a) protein expression level of early stage small-sized adenocarcinoma was significantly higher than that of poorly differentiated small-sized adenocarcinoma (P0.05).AI and p16(ink4a) gene aberrant methylation may provide a potential universal biomarker for small-sized adenocarcinoma.

BACKGROUND Stepwise progression of peripheral-type lung adenocarcinoma was characterized morphologically and was related to prognosis. Expression of the tumor suppressor gene p16 in pulmonary adenocarcinoma decreased, mainly as a result of aberrant methylation of the CpG islands of the promoter region. METHODS Aberrant methylation status of the p16 promoter region, the expression of its product, and loss of heterozygosity (LOH) on 9p21 were examined in surgically resected lung specimens from 57 patients (28 males and 29 females) with peripheral-type lung adenocarcinoma measuring ≤ 2 cm in diameter. RESULTS Aberrant methylation of the p16 promoter region, negative p16 protein expression, and LOH of the 9p21 region were detected in 40.4%, 50.9%, and 40.4% of tumor samples, respectively. The alterations of the p16 gene were associated with poor prognosis, and in particular the prognosis of patients with aberrant p16 methylation was significantly worse than that of patients without aberrant methylation. These alterations also were associated with morphologic classification into bronchioloalveolar carcinoma (BAC) and non-BAC adenocarcinoma. Both aberrant methylation and LOH of 9p21 were associated with negative protein expression, but the former was correlated more closely with loss of function than was the latter. Cases with both alterations were completely negative for expression of the p16 gene product. CONCLUSIONS Aberrant methylation of the promoter region of the p16 gene and loss of expression of its product were in accord with the multistep progression of peripheral-type lung adenocarcinoma, and these alterations were associated closely with poor prognosis of the disease. Cancer 2005. © 2004 American Cancer Society.

We investigated the role of protein tyrosine phosphatase ζ (Ptprz1) in human renal cell carcinoma (RCC) cells’ proliferation and associations between Ptprz1 expression and von Hippel-Lindau (VHL) activation. A normal human renal cell line and four human RCC cell lines were used in this study. VHL or Ptprz1 expression in RCC cells was increased by transfection with a VHL or Ptprz1 vector. VHL or Ptprz1 expression was decreased in these cells by siRNA using Lipofectamine 2000. Cells’ proliferative activity was assessed by WST-1 assay. Our results suggested that Ptprz1 was a target of VHL, and a loss of VHL activation increased Ptprz1 expression in RCC cells. Ptprz1 enhanced β-catenin protein expressions in the nuclear fractions of RCC cells and participated in regulating proliferation by activating β-catenin and its downstream genes. In addition, a loss of VHL activity may enhance the proliferative activity of RCC cells by increasing Ptprz1 expression. Ptprz1-enhanced RCC cells’ proliferation depends on VHL inactivation, and the Ptprz1/β-catenin pathway may be a potential target for treating RCC with inactive VHL.

Anthracosis is black dust matter deposition in the pulmonary parenchyma, which can cause bronchial deformity and destruction. Previously reported, anthracosis is closely correlated to the oncogenesis and progression of small pulmonary adenocarcinoma and p16(ink4a) gene aberrant methylation was closely associated with lung carcinogenesis. In this study, we want to characterize the influence of anthracosis and p16(ink4a) gene aberrant methylation on small adenocarcinoma.DNA was bisulfite modified and then Methylation Specific PCR was used to detect p16(ink4a) gene aberrant methylation, and black dust matter was extracted from lung tissues, the absolute absorbance (A) detected by densitometry was defined as anthracotic index (AI). The histopathologic diagnosis was according to Noguchi's classification for small pulmonary adenocarcinoma.For heavy smokers, the mean AI was significantly higher than that of nonsmokers (P =0.005) and the frequency of p16(ink4a) gene aberrant methylation was also significantly higher than that of nonsmokers (P =0.023). The frequency of p16(ink4a) gene aberrant methylation of early stage small adenocarcinoma was lower than that of advanced and poor differentiated small adenocarcinoma, otherwise p16(ink4a) protein expression of early stage small adenocarcinoma was significantly higher than that of poor differentiated small adenocarcinoma (P =0.032).AI and p16(ink4a) gene aberrant methylation detection could be used as a combined potential biomarker of small adenocarcinoma.

In order to characterize the relationship between background anthracosis and pulmonary adenocarcinogenesis, surgically resected tissues of 66 cases of stage I pulmonary adenocarcinoma, 4 cm or less at their greatest dimension, were examined. These cases were diagnosed based on the classification of small-sized adenocarcinoma of the lung (Noguchi et al., Cancer 75, 1995). Thirteen cases were diagnosed as types A (localized bronchioloalveolar adenocarcinoma, LBAC) and B (LBAC with alveolar collapse), 40 cases as type C (LBAC with a focus of fibroblastic proliferation), 8 as type D (poorly differentiated adenocarcinoma) and 5 as types E (bronchial gland type adenocarcinoma) and F (true papillary adenocarcinoma). The 5-year survival rate of types A and B cases was 100%, while those of type C, type D and types E and F were 52%, 48% and 39%, respectively. Nuclear accumulation of abnormal p53 protein in non-replacement type adenocarcinomas (types D, E and F) was detected more frequently than that in replacement type adenocarcinomas (types A, B and C) (P < 0.05). In each case, black dusty material was extracted from tumorous lesions and non-tumorous regions and blotted onto a nitrocellulose membrane. The anthracotic index (AI) was calculated with a densitometer. AIs of non-tumorous regions in early and replacement type adenocarcinomas (types A and B) were significantly less than in relatively advanced (type C) and poorly differentiated (type D) adenocarcinomas (P < 0.05). These results indicated that adenocarcinoma developing in heavily anthracotic lungs readily progresses to an advanced stage, or that adenocarcinoma with a less favorable prognosis tends to develop in severely anthracotic lungs.