鳜早期发育阶段骨骼肌纤维的增生与肥大生长

骨骼肌是鱼体的主要组成部分,也是衡量鱼体生长发育的重要指标。为了解鳜(Siniperca chuatsi)早期发育阶段骨骼肌纤维的生长发育特征,通过制作孵化后1～41日龄个体骨骼肌背右侧第一肌节石蜡切片,利用图像分析软件统计该肌节中肌纤维的数目和面积,分析了鳜骨骼肌纤维的增生和肥大生长特征。结果表明,鳜早期发育阶段骨骼肌生长同时包括数目增加(增生)和面积增大(肥大),背侧第一肌节中肌纤维总数由40个增加到520个,肌纤维总面积由805.30μm2增加到186 422.77μm2。其中,孵化后1～9日龄,肌纤维相对增生数目下降,相对增加面积缓慢上升,相对增加面积中增生生长的贡献率由60.53%降至8.80%,肥大生长则与之相反;9～15日龄,肌纤维相对增生数目呈现上升,相对增加面积相对平缓,相对增加面积中增生生长的贡献率略呈上升(由8.80%上升至20.26%),肥大生长贡献率略有下降;15～41日龄,相对增生数目和相对增加面积均呈上升趋势,相对增加面积中增生生长的贡献率下降并趋于平稳,肥大生长贡献率由79.79%上升到87.41%,成为优势生长。

核因子-κB与炎症性肠病

核因子-κB(NF-κB)是一类具有多向活性的转录调控因子, 参与多种基因的表达和调控,在炎症及免疫反应、细胞生长增生、凋亡及感染等方面起着重要作用.本文重点介绍核因子-κB结构和激活机制,及其在炎症性肠病中的表达及可能的作用机制;NF-κB抑制剂在炎症性肠病治疗上的应用.

Response of seedlings of different tree species to elevated CO2 in Changbai Mountain

Eco-physiological responses of seedlings of eight species, Pinus koraiensis, Picea koraiensis, Larix olgensis, Populus ussuriensis, Betula platyphylla, Tilia amurensis, Traxinus mandshurica and Acer mono from broadleaved/Korean pine forest, to elevated CO2 were studied by using open-top chambers under natural sunlight in Changbai Mountain, China in two growing seasons (1998-1999). Two concentrations of CO2 were designed: elevated CO2 (700 祄olmol-1) and ambient CO2 (400 祄olmol-1). The study results showed that the height growth of the tree seedlings grown at elevated CO2 increased by about 10%-40% compared to those grown at ambient CO2. And the water using efficiency of seedlings also followed the same tendency. However, the responses of seedlings in transpiration and chlorophyll content to elevated CO2 varied with tree species. The broad-leaf tree species were more sensitive to the elevated CO2 than conifer tree species. All seedlings showed a photosynthetic acclimation to long-term elevated CO2.

Expression of angiostatin cDNA in human gallbladder carcinoma cell line GBC-SD and its effect on endothelial proliferation and growth

AIM： To explore the influence of angiostatin up-regulation on the biologic behavior of gallbladder carcinoma cells in vitro and in vitro, and the potential value of angiostatin gene therapy for gallbladder carcinoma. METHODS： A eukaryotic expression vector of pcDNA3.1（＋） containing murine angiostatin was constructed and identified by restriction endonuclease digestion and sequencing. The recombinant vector pcDNA3.1-angiostatin was transfected into human gallbladder carcinoma cell line GBC-SD with Upofectamine 2000, and paralleled with the vector and mock control. The resistant clone was screened by G418 filtration. Angiostatin transcription and protein expression were examined by RT-PCR, immunofluorescence and Western-blot. The supernatant was collected to treat endothelial cells. Cell proliferation and growth in vitro were observed under microscope. RESULTS： Murine angiostatin cDNA was successfully cloned into the eukaryotic expression vector pcDNA3.1 （＋）. AFter 14 d of transfection and selection with G418, macroscopic resistant cell cloning was formed in the experimental group transfected with pcDNA 3.1（＋）-angiostatin and vector control. But untreated cells died in the mock control. Angiostatin was detected by RT-PCR and protein expression was detected in the experimental group by immunofluorescence and Western-blot. Cell proliferation and growth in v/tro in the three groups were observed respectively under microscope. No significant difference was observed in the growth speed of GBC- SD cells between groups that were transfected with and without angiostatin. After treatment with supernatant, significant differences were observed in endothelial cell （ECV-304） growth in vitro. The cell proliferation and growth were inhibited. CONCLUSION： Angiostatin does not directly inhibit human gallbladder carcinoma cell proliferation and growth in vitro, but the secretion of angiostatin inhabits endothelial cell proliferation and growth.

Erlotinib inhibits progression to dysplasia in a colitis-associated colon cancer model

AIM:To investigate the role of epidermal growth factor receptor(EGFR) in colitis-associated dysplasia using the EGFR tyrosine kinase inhibitor erlotinib.METHODS:Sprague-Dawley rats received trinitrobenzene sulfonic acid(TNBS;30 mg in 50% ethanol,ic),followed 6 wk later by reactivation with TNBS(5 mg/kg,iv) for 3 d.To induce colitis-associated dysplasia,rats then received TNBS(iv) twice a week for 10 wk.One group received erlotinib(10 mg/kg,ip) for 1 wk before the start of the reactivation of the colitis and 2 wk after(21 d);the rest received the vehicle.After rats were euthanized,the colons were removed and analyzed for damage and expression of the EGFR downstream effectors Erk1/2 and c-Myc.RESULTS:Ninety percent of the vehicle-treated animals had dysplasia in any region of the colon.Erlotinib-treated animals had a significant decrease in the incidence of dysplasia compared to vehicle-treated animals in all regions of the colon(50.00% ± 11.47% vs 90.00% ± 10.00% in proximal,P < 0.05;15.00% ± 8.19% vs 50.00% ± 16.67% in mid,P < 0.05;and 20.00% ± 9.17% vs 70.00% ± 15.28% in distal,P < 0.01).Erlotinib-treated animals also had reduced cell proliferation,reduced active Erk1/2,and reduced c-Myc in colon epithelium compared with the vehicle-treated animals.In vitro,erlotinib treatment was shown to markedly decrease c-Myc and pErk1/2 levels in rat epithelial cells.Proliferation of rat epithelial cells was stimulated by epidermal growth factor and inhibited by erlotinib(P < 0.05).CONCLUSION:Erlotinib can decrease the development of colitis-associated dysplasia,suggesting a potential therapeutic use for erlotinib in patients with long-standing colitis.

Involvement of 90-kuD ribosomal S6 kinase in collagen type Ⅰ expression in rat hepatic fibrosis

AIM： To investigate the relationship between 90-kuD ribosomal $6 kinase （pg0RSK） and collagen type I expression during the development of hepatic fibrosis in vivo and in vitro.METHODS： Rat hepatic fibrosis was induced by intraperitoneal injection of dimethylnitrosamine. The protein expression and cell location of p90RSK and their relationship with collagen type I were determined by co-immunofluoresence and confocal microscopy.Subsequently, RNAi strategy was employed to silence p90RSK mRNA expression in HSC-T6, an activated hepatic stellate cell （HSC） line. The expression of collagen type I in HSC-T6 cells was assessed by Western blotting and real-time polymerase chainreaction. Furthermore, HSCs were transfected with expression vectors or RNAi constructs of p90RSK to increase or decrease the p90RSK expression, thencollagen type I promoter activity in the transfected HSCs was examined by reporter assay. Lastly HSC-T6 cells transfected with p90RSK siRNA was treated withor without platelet-derived growth factor （PDGF）-BB at a final concentration of 20μg/L and the cell growthwas determined by MTS conversion.RESULTS： In fibrotic liver tissues, p90RSK was over-expressed in activated HSCs and had a significantpositive correlation with collagen type I levels.In HSC-T6 cells transfected with RNAi targeted top90RSK, the expression of collagen type I was down-regulated （61.8% in mRNA, P 〈 0.01, 89.1% inprotein, P 〈 0.01）. However, collagen type ] promoteractivity was not increased with over-expression of p90RSK and not decreased with low expression either,compared with controls in the same cell line （P = 0.076）.Furthermore, p90RSK siRNA exerted the inhibitionof HSC proliferation, and also abolished the effect of PDGF on the HSC proliferation.CONCLUSION： p90RSK is over-expressed in activatedHSCs and involved in regulating the abnormalexpression of collagen type I through initiating theproliferation of HSCs.

Ecological functions of ciliated protozoa in marine ecosystem： effects of ammonium on the population growth of Euplotes vannus

The effects of ammonium on the population growth of the marine ciliate, Euplotes vannus, were examined using ecotoxicological method, h is showed that ammonium exerts inhibitory effects on the growth of the ciliate populations in a concentration-dependent way. Statistical analvsis reveals that the population growth dynamics exposed to ammoniunt-N concentration over 100mg/L are significantly different from that in the control at P 〈 0.05 level. Linear regression determined that the 24h, 36h, 48h, 60h, 72h and 84h IC50 values of ammonium-N are 19.68, 201.51, 167.49, 47.86, 50.43 and 43.11 concentration over 100mg/L, respectively （ P 〈 0.05; pH 8.2; salinity 28 ppt; temperature, 25℃ ）. The results indicate that the tolerance to ammonium in E. vannus is considerably higher than that of the larvae or juveniles of some metozoa, such as cuhured prawns and oysters. Therefore, it is believed that the high tolerance to ammonium is necessary for eiliated protozoa to play positive roles in maintaining and improving water quality in marine ecosystems, especially in the intensive aquacuhure waters with high-level ammonium. In addition, the correlation between /C50 values and exposure time was discussed.

Insulin promotes sinusoidal endothelial cell proliferation mediated by upregulation of vascular endothelial growth factor in regenerating rat liver after partial hepatectomy

AIM： To determine whether insulin could promote sinusoidal endothelial cell （SEC） proliferation mediated by upregulation of vascular endothelial growth factor （VEGF） in regenerating rat liver after partial hepatectomy （PHx）. METHODS： Adult male Sprague-Dawley rats undergoing 70% PHx were injected with insulin （300 MU/kg） or saline via the tail veins every 8 h after surgery for 7 d and killed at 0, 24, 48, 72, 96, 120, 144, and 168 h after surgery. Proliferation of both hepatocytes and SECs was monitored by evaluating the proliferating cell nuclear antigen （PCNA） labeling index （LI）. The expression of VEGF protein was evaluated by immunohistochemistJv. The mRNA expressions of VEGF and its receptors FIt-1 and FIk-1 were evaluated by semi-quantitative reverse transcription-PCR. RESULTS： Insulin markedly increased the expression of VEGF mRNA between 24 and 120 h after hepatectomy compared to controls. Similarly, insulin significantly increased the expression of Fit-1 between 24 and 96 h. However, insulin had no significant effect on FIk-1. Furthermore, the immunohistochemical staining revealed that expression of VEGF protein increased in the insulin groups. Insulin significantly increased the PCNA LI of hepatocytes and SECs compared to controls. CONCLUSION： Exogenous insulin may promote SEC proliferation with an enhanced expression of VEGF and its receptor Fit-1 in regenerating rat liver after PHx.

The predictive value of vascular endothelial growth factor and Ki-67 expression on neoadjuvant therapy in rectal cancer

Objective： To investigate the expressions of vascular endothelial growth factor （VEGF） and proliferating cell nuclear antigen （Ki-67） in patients with rectal adenocarcinoma and their associations with neoadjuvant therapy. Methods： The expressions of Ki-67 and VEGF in 32 cases of rectal adenocarcinoma, including both pretreatment tumor biopsies and postoperative specimen, were detected by immunohistochemistry using specific antibodies, and were correlated with clinicopathological factors. Results： The intensity of VEGF staining was significantly correlated with lymph nodal metastasis （P =0.033）, depth of tumor invasion （P =0.007） and tumor stage （P= 0.016）, but not with histological types, tumor sizes, patients＇ ages and genders （P 〉 0.05）. Low level of VEGF expression had significant correlation with the high sensitivity of response to neoadjuvant therapy （P = 0.016）. The transient increase of VEGF expression could be seen after neoadjuvant therapy （P = 0.035）. Ki-67 labeling index （Ki-67-LI） was significantly correlated with lymph node metastasis （P = 0.028）, but not correlated to tumor sizes, patients＇ ages and genders （P 〉 0.05）. Tumors with lower Ki-67-LI were more sensitive to neoadjuvant therapy （P = 0.032）. The Ki-67 level decreased after neoadjuvant therapy, but no statistical significance was found （P 〉 0.05）. Conclusion： Our results demonstrate that the expression of VEGF and Ki-67 in pretreatment rectal adenocarcinoma biopsies may be predictive of tumor response to neoadjuvant therapy.

Matrine inhibits proliferation of mouse skin fibroblasts induced by platelet-derived growth factor-BB

Objective:To studythe effectof matrineon proliferationof mouseskinfibroblastsinducedby platelet-derivedgrowthfactor-BB(PDGF-BB).Methods :MouseskinfibroblastswereobtainedfromnewbornI-CRmiceandpropagatedin vitro.Proliferationof cellwasanalyzedby mitochondrialreductionof tetrazoliumsalt MTT andactualcellcount.Re sults:Matrine(50to500μg/ml)causeddose-dependentreductionof serum-stimu-latedcellgrowth.Growthinhibitionwas totallyreversedafterremovalof the drug.Matrinealso inhibited PDGF-BBinducedcellgrowthdose-dependently.Conclusion:Matrineexhibitspotentanti-proliferationeffecton mouseskinfibroblast.Thiseffectappearsto be mediatedby decreaseof PDGF-inducedgrowth.Theseresultssug-gestthatmatrinemighthavepreventiveandtherapeuticimplicationin skinfibrosis.

Evaluation of the tumor angiogenesis in benign prostate hyperplasia and prostatic cancer with MR perfusion-weighted imaging

Objective： To explore the application of MR perfusion-weighted imaging （PWI） in the benign and malignant prostate diseases, and evaluate the correlations of PWl features with vascular endothelial growth factor （VEGF） and microvessel density （MVD）. Methods： Seventy-four consecutive patients who were diagnosed clinically for the prostate diseases, including forty-four cases with benign prostate hyperplasia and thirty cases with prostatic cancer proved pathologically, were examined by PWI. MVD and VEGF were stained with immunohistochemical methods. Some parameters of PWl, including the steepest slope of signal intensity-time curve （SSmax） and the change in relaxation rate （ΔR2^＊ peak） at lesions, were analyzed. Correlation analysis was used to determine the relationship between the results of PWl and immunohistochemistry. Results： （1） In the benign prostate hyperplasia （BPH）, SSmax and ΔR2^＊ peak of perfusion curve were 34.2 ± 2.9 and 1.49 ± 0.11, respectively; however, in the prostatic cancer （Pca）, they were 58.6± 4.8 and 3.18 ±0.49 respectively; there were statistical differences （t = 2.16 and 2.31, P 〈 0.05）. （2） The VEGF and MVD expressions of thirty Pca patients were significantly higher than those of forty-four BPH patients （x2 = 28.64, P 〈 0.01; t = 21.2, P 〈 0.01）. MVD expressions of Pca and BPH groups showed positive associations with VEGF expressions （P 〈 0.01）. On MR perfusion-weighted imaging, SSmax and ΔR2^＊ peak showed associations with MVD and VEGF expressions （P 〈 0.01）. Conclusion： On MR perfusion-weighted imaging, SSmax and ΔR2^＊ peak can reflect MVD and VEGF expression levels in the benign and malignant prostate diseases and might be implied the tumor angiogenesis so as to distinguish benign from malignant and provide the important information for the surgeon to diagnose and treat the prostatic diseases.

What Life Is and How It Originated

This paper refutes the mechanistic interpretation of cellular dynamics and contends that the life-giving principle is sustained growth a biological system and is uninterrupted growth balanced in a dynamic state by synthesis and dissolution. The process began by an oxidation/reduction reaction on the surface of pyrite energized photovoltaically by sunlight. Hydrogen sulfide was oxidized, carbon dioxide was reduced, and phosphate on the surface of the pyrite was a reactant. The first organic compounds were sulfides and phosphoglycerates. These organophosphates were at the center of the energy cycle of all life where the dehydration of a relatively unreactive ＂low-energy＂ two-phosphoglycerate transforms it into the ＂high-energy＂ phosphoenolpyruvate. Life began as a growth process and continues to grow ceaselessly out of necessity. It cannot discontinue the life-giving energy flow without irreparable loss of the process. All forms of life past and present were and are stabilized systems in which the growth process is contained in metabolic turnover.

Forecasting China's Labor Supply and Demand and the Unemployment Structure in the 13th Five-Year-Plan Period

The changes in labor supply and demand are important factors affecting economic growth.The purpose of this paper is to predict and analyze the trends in China's labor supply and demand during the 13 th Five-Year Plan period and the longer period in the future.The scale and structure of the annual new entrants of labor force are predicted by accounting the numbers who are leaving from various stages of education.while trends of labor demand are predicted according to employment elasticity from the experience of industrialization of developed countries. The results show that, during the 13 th FiveYear Plan period.the scale of the new added labor would decrease slightly, with an average annual increment of around 15.68 million. At the same time.labor demand would increase steadily, with annually 15.42 million employment opportunities. Labor supply and demand would be roughly balanced; however,there would be increasing structural contradictions of the labor market.Based on the analysis of labor supply and demand,we provide an estimation of the unemployment scale of the 40's and 50's generations,migrant workers and college graduates,and discuss policy suggestions on promoting employment of college graduates.

Ecological Footprint and Endogenous Economic Growth in the Poyang Lake Area in China Based on Empirical Analysis of Panel Data Model

In this paper, ecological footprint methods were used to calculate the ecological footprint of six cities （Nanchang, Jingdezhen, Jiujiang, Xinyu, Yingtan and Fuzhou） in the Poyang Lake Area, Jiangxi, China from 1991 to 2010. Ecological footprint was the input factor for ecological resources and the contribution of this and other factors such as labor and capital to economic growth were analyzed. The results showed that, from 1991 to 2010, ecological footprints in the six cities increased year by year. The amount of land for fossil energy, under cultivation and grassland influenced total ecological footprint in each city. The contribution of ecological resources, labor factors and capital factors to economic growth showed regional differences. Nanchang, Jiujiang, Xinyu, and Yingtan are capital-orientated and capital factor had a great influence on the economic growth rates, whereas, Jingdezhen and Fuzhou were labor-orientated. The contribution of ecological resources to economic growth in the six cities was the lowest of all three factors, meaning that efficiency of ecological resource utilization is low. Total productivity plays a key role in economic development; however, the overall level of total factor productivity for the six cities was low and indicates that the technological content of Poyang Lake Area’s economic growth is low and the utilization of input factors extensive. In summary, we suggest changing the mode of economic growth and developing tertiary industry in the region.

Enhanced hyperplasia in muscles of transgenic zebrafish expressing Follistatin1

Myostatin is a member of the transforming growth factor-β(TGF-β) super-family and functions as a negative regulator of muscle growth.Binding of the specific receptor,Activin receptor IIB(Act RIIB),with myostatin or other related TGF-β members,could be inhibited by the activin-binding protein follistatin(Fst) in mammals.Overexpressing Fst in mouse skeletal muscle leads to muscle hypertrophy and hyperplasia.To determine if Fst has similar roles in fish,we generated transgenic zebrafish expressing high levels of zebrafish Fst1 using the promoter of the zebrafish skeletal muscle-specific gene,myosin,light polypeptide 2,skeletal muscle(Mylz2).Independent transgenic zebrafish lines exhibited elevated expression levels of myogenic regulatory genes MyoD and Pax7 in muscle cells.Adult Fst1 overexpressing transgenic zebrafish exhibited a slight body weight increase.The high level of Fst1 expression dramatically increased myofiber numbers in skeletal muscle,without significantly changing the fiber size.Our findings suggest that Fst1 overexpression can promote zebrafish muscle growth by enhancing myofiber hyperplasia.

The inhibitory activities of Urtica fissa to BPH

In the present study, the BPH inhibitory activities of Urtica fissa were systematically investigated. Firstly, inhibitory activities of 5α reductase of the alcoholic extracts from different parts(root, stem, leaf, flower and fruit) were evaluated. The results indicated that the root possessed the most significant action. Subsequently, U. fissa root(UFR) was subjected to further pharmacological evaluation using the benign prostate hyperplasia(BPH) model rats induced by testosterone propionate. The results revealed that UFR could significantly decrease the prostate index, alter the hyperplasia tissue morphology, suppress the prostatic growth factors of VEGF, EGF, bF GF and KGF, decrease the inflammation factor levels of TNF-α, IL-1β and IL-6, improve the activities of GSH-Px, CAT and SOD and decrease the MDA level in the prostate of the model rats. Moreover, UFR also significantly suppressed the hormone levels of testosterone and dihydrotestosterone. These results indicated that the possible BPH inhibitory mechanisms of UFR were growth factor suppression, hormone level modulation, anti-inflammation, and anti-oxidative stress.

Endostatin inhibits fibrosis by modulating the PDGFR/ERK signal pathway:an in vitro study

Accumulating evidence indicates that endostatin inhibits fibrosis. However, the mechanism is yet to be clarified. The aim of this study is to evaluate the effect of endostatin on platelet-derived growth factor-BB （PDGF-BB）- or transforming growth factor β1 （TGF-β1）-induced fibrosis in cultured human skin fibroblasts, and to further examine the molecular mechanisms involved. Human dermal flbroblasts were cultured in Dulbecco＇s modified Eagle＇s medium （DMEM） and serum-starved for 48 h before treatment. Cells were grouped as follows： ＂PDGF-BB＂, ＂PDGF-BB＋ endostatin＂, ＂TGF-β1＂, ＂TGF-β1＋endostatin＂, ＂endostatin＂, and ＂blank control＂. The fibroblasts were stimulated with either TGF-β1 or PDGF-BB for 72 h in order to set up the fibrosis model in vitro. The cells were co-cultured with either TGF-β1 or PDGF-BB and endostatin and were used to check the inhibiting effect of endostatin. A blank control group and an endostatin group were used as negative control groups. The biomarkers of fibrosis, including the expression of collagen I, hydrroxyproline, and α-smooth muscle actin （a-SMA）, were evaluated using an enzyme-linked immune- sorbent assay （ELISA） and Western blot. The expression of phosphorylated PDGF receptor β （p-PDGFRβ）, PDGFRβ, phosphorylated extracellular signal-regulated kinase （p-ERK）, and ERK was detected using Western blot and im- munofiuorescent staining was used to explore the mechanisms. Both PDGF-BB and TGF-β1 significantly up-regulated the expression of collagen I, hydroxyproline, and a-SMA. Endostatin significantly attenuated both the PDGF-BB- and TGF-β1-induced over-expression of collagen I, hydroxyproline, and a-SMA. PDGF-BB and TGF-β1 both promoted the expression of PDGFR, ERK, and p-ERK. Endostatin inhibited the expression of PDGFR and p-ERK but did not affect the expression of total ERK. Endostatin inhibited hypertrophic scar by modulating the PDGFRI3/ERK pathway. En- dostatin could be a promising multi-target drug in future fibrosis therapy.