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Haikou, China

Li Y.,Chinese Academy of Sciences | Fei X.,Chinese Academy of Sciences | Fei X.,Hainan Medical College | Deng X.,Chinese Academy of Sciences
Biomass and Bioenergy | Year: 2012

Microalgae usually accumulate triacylglycerols (TAGs) under stress conditions, especially during nitrogen (N) starvation. However, little information is available regarding the underlying mechanism. In the present study, a green algae Micractinium pusillum accumulated significant amounts of TAGs after 6 d of N starvation. Aiming at fundamental elucidation of the molecular mechanisms involved in N starvation-induced TAG accumulation, the global gene expression changes were identified by using suppression subtractive hybridization (SSH). In total, 290 expressed sequence tags (ESTs) showed significant differential expression between the treated and control samples. The expression profiles of 19 ESTs have been confirmed by quantitative real-time PCR (qPCR). Homology analysis showed that the 174 N deficiency-induced ESTs were mainly involved in carbohydrate metabolism, pyruvate and acetyl-CoA synthesis, isoprenoids biosynthesis, and TAG degradation, as well as a severe down-regulation in the expression of 116 genes related to photosynthesis, cell growth, amino acid synthesis and cell cycle regulation. A significant decrease in carbohydrate content was also observed in the N-deficient algal cells. These results suggested that the carbon sources for TAG biosynthesis were largely derived from carbohydrate metabolism rather than from photosynthesis. The results of the qPCR showed that, compared to the control, the transcript levels of genes related to pyruvate and acetyl-CoA synthesis were dramatically increased over 100 times after N starvation, which suggests that pyruvate and acetyl-CoA play important roles in driving carbon flow into TAG biosynthesis. © 2012 Elsevier Ltd. Source

Zhou H.,Cornell College | Zheng S.,Hainan Medical College | Truong L.D.,Cornell College | Ro J.Y.,Cornell College | And 2 more authors.
Human Pathology | Year: 2014

Summary Clear cell papillary renal cell carcinoma (CCP-RCC) has recently been recognized as a distinct subtype of renal cell carcinoma (RCC) due to its unique morphologic, immunohistochemical, and genetic features and indolent clinical behavior. However, the incidence of this tumor in a nephrectomy series for renal mass has not been fully investigated. Twelve cases of CCP-RCC were identified from a total of 290 consecutive partial (n = 137) or radical nephrectomies (n = 153) for RCC from 2010 to 2012 in our hospital. In this series, CCP-RCC was the fourth most common (4.1%) kidney tumor following clear cell (conventional) (70%), papillary (16.6%), and chromophobe (5.9%) RCCs. The average age of the CCP-RCC patients was 58.2 years (range, 18-81 years), with an equal sex distribution. Four cases (33.3%) were associated with end-stage renal disease. Of the 12 CCP-RCCs, 9 presented as solitary tumors; 2 coexisted with clear cell RCC; and 1 with papillary RCC. The average size of tumors was 2.5 cm (range, 0.8-6.0 cm). All tumors were pT1 (10 pT1a and 2 pT1b). Two cases were initially misclassified as clear cell RCC. Strong positive cytokeratin 7 stain and negative stains with α-methylacyl-CoA racemase and RCC marker differentiate CCP-RCC from low-grade clear cell RCC with similar histologic features. We conclude that CCP-RCC is a common renal neoplastic entity, representing the fourth most common (4.1%) RCC. It can be easily misclassified due to its overlapping features with low-grade clear cell RCC. In equivocal cases, immunohistochemical stains with a small panel of markers (cytokeratin 7, α-methylacyl-CoA racemase, RCC marker, or CD10) are warranted in making the correct histologic classification. © 2014 Elsevier Inc. Source

Liu X.,Sun Yat Sen University | Liu X.,Hainan Medical College | Xie C.,Sun Yat Sen University
Molecular and Cellular Biochemistry | Year: 2012

Cardiovascular disease is the leading cause of morbidity and mortality in patients with moderate-to-severe chronic obstructive pulmonary disease (COPD). More than 44% of these patients present with generalized atherosclerosis at autopsy. It is accepted that endothelial progenitor cells (EPCs) participate in the repair of dysfunctional endothelium and thus protects against atherosclerosis. However, whether COPD affects the repairing capacity of EPCs is unknown. Therefore, the objective of this study was to determine whether and how EPCs are involved in the vascular repair process in patients with COPD. In our study, EPCs from 25 COPD and 16 control patients were isolated by Ficoll density-gradient centrifugation and identified using fluorescence activated cell sorting. Transwell Migratory Assay was performed to determine the number of EPC colony-forming units and the adherent capacity late-EPCs to human umbilical vein endothelial cells. Following arterial damage in NOD/SCID mice, the number of EPCs incorporated at the injured vascular site was determined using a fluorescence microscope. We found that the number of EPC clusters and cell migration, as well as the expression of CXCR4, was significantly decreased in patients with COPD. Additionally, the number of late-EPCs adherent to HUVEC tubules was significantly reduced, and fewer VEGFR2 +-staining cells were incorporated into the injured site in COPD patients. Our study demonstrates that EPC capacity of repair was affected in COPD patients, which may contribute to altered vascular endothelium in this patient population. © 2011 Springer Science+Business Media, LLC. Source

Yang S.,Hubei University | Yang S.,Hainan Medical College | Chen X.,Hubei University
International Journal of Oral and Maxillofacial Surgery | Year: 2012

Epithelial-myoepithelial carcinoma (EMC) is a rare low-grade salivary gland malignancy of presumed intercalated duct origin comprising 1% of all salivary gland tumours. High grade transformation (HGT) in EMC is a recently recognised entity with only a few cases reported in the literature. The authors report an additional case of EMC with HGT involving the submandibular gland. The patient was a 60-year-old woman who requested examination of the rapid growth of a mass in the left submandibular area, which she had first noticed 20 years previously. Histologically, the tumour had two distinct carcinomatous components. One component had features of a low grade EMC. The second component consisted of polygonal cells, arranged in a solid and nested pattern, with marked nuclear pleomorphism, brisk mitotic activity, and frequent necrosis. The Ki-67 labelling index of the EMC component was 9%, and that of the high grade component was 40%. The patient developed multiple pulmonary metastases 15 months after surgery. The aggressive behaviour of EMC with HGT suggests that it is important to recognise this variant of EMC to avoid misdiagnosis and inappropriate treatment. © 2011 International Association of Oral and Maxillofacial Surgeons. Source

Zhang H.,Hainan Medical College | Yang H.,Nanjing Medical University | He S.,Nanjing Medical University
Cellular Physiology and Biochemistry | Year: 2010

Tumor necrosis factor (TNF) is a proinflammatory cytokine which has been shown to be actively involved in the pathogenesis of allergic inflammation. However, little is known of the effects of TNF on cytokine secretion and protease activated receptor (PAR) expression in mast cells. In the present study, we examined potential influence of TNF on IL-4 and IL-12 release from P815 cells and PAR expression in P815 cells by using flow cytometry analysis, quantitative real time PCR, ELISA and cellular activation of signaling ELISA (CASE) techniques. The results showed that TNF induced up to 2.7-fold increase in IL-4, but not IL-12 release from P815 cells, and PAR-2 antagonist peptide FSLLRY-NH 2 and PAR-4 antagonist peptide trans-cinnamoyl (tc)-YPGKF-NH 2 did not affect TNF induced IL-4 release. Approximately up to 2.4 and 2.3 fold increases in expression of PAR-2 and PAR-4 were observed when cells were incubated with TNF. Pretreatment of cells with TNF for 60 min enhanced trypsin and tryptase induced PAR-2 expression by 2.4 and 2.3 fold; PAR-3 expression by 1.6 and 1.7 fold and PAR-4 expression by 1.6 and 1.7 fold, respectively. LY294002, an inhibitor PI3K abolished TNF induced IL-4 release and phosphorylation of Akt in P815 cells, indicating Akt cell signalling pathway is involved in the event. In conclusion, TNF can stimulate IL-4 release from mast cells through an Akt cell signalling pathway dependent, but PAR independent mechanism. TNF may serve as a regulator for IL-4 production and PAR expression, and through which participates in the mast cell related inflammation. © 2010 S. Karger AG, Basel. Source

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