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Zeolite ZSM-5 was synthesized from sodium tetrapropylammonium aluminosilicate gels and tetrapropylammonium silicate gel. Effects of varying the ratio SiO,/AI,O, and alkalinity in the starting gels and the reaction temperature were studied. The alkalinity was found to affect the rate of nucleation more than the rate of crystal growth. An optimum alkalinity exists in the synthesis of ZSM-5; the optimum value is closely related to the value of SiO,jAl,O, ratio in the batch composition. The apparent activation energies for nucleation and crystal growth are 38 and 46 kJ mot-', respectively, for the aluminium-free silicate system and 25 and 29 kJ mot-', respectively, for the aluminosilicate system with SiO,/Al,O, = 70. The results are consistent with a complicated solution mechanism of crystallization.A newly synthesized zeolite known as ZSM-5 has interesting applications in fuel and petrochemical processing.l? ZSM-5 possesses a unique channel structure with an aperture of ca. 6 A and an unusually high silica ~o n t e n t . ~ These properties contribute to the excellent shape selectivity and steam and heat stability of ZSM-5.4 This paper reports a study of the mechanism of the formation of ZSM-5. The effects of temperature and alkalinity on the syntheses were investigated by measuring the rates of nucleation and crystal growth for selected batch compositions at various temperatures. Detailed kinetic studies on the growth and Aand near-faujasite zeolites have been reported by K e ~r , ~ Ciric,6 Lechert7 and Culfaz and Sand.H Some of their techniques have been followed in this work.

Fibroblast growth factor 1 (FGF1) has been shown to regulate cell proliferation, cell division, and neurogenesis. Human FGF1 gene 1B promoter (-540 to +31)-driven green fluorescence (F1BGFP) was shown to recapitulate endogenous FGF1 gene expression. It can also be used to isolate neural stem/progenitor cells (NSPCs) and glioblastoma stem cells (GBM-SCs) from developing mouse brains and human glioblastoma tissues, respectively. However, the regulatory mechanisms of FGF-1B promoter and F1BGFP(+) cells are not clear. In this study, we present several lines of evidence to show the roles of ciliogenic RFX transcription factors in the regulation of FGF-1B gene promoter and F1BGFP(+) cells: (i) RFX1, RFX2, and RFX3 transcription factors could directly bind the 18-bp cis-element (-484 to -467), and contribute to the regulation of FGF1 promoter and neurosphere formation. (ii) We demonstrated RFX2/RFX3 complex could only be detected in the nuclear extract of FGF-1B positive cells, but not in FGF-1B negative cells. (iii) Protein kinase C inhibitors, staurosporine and rottlerin, could decrease the percentage of F1BGFP(+) cells and their neurosphere formation efficiency through reducing the RFX2/3 complex. (iv) RNA interference knockdown of RFX2 could significantly reduce the percentage of F1BGFP(+) cells and their neurosphere formation efficiency whereas overexpression of RFX2 resulted in the opposite effects. Taken together, this study suggests ciliogenic RFX transcription factors regulate FGF-1B promoter activity and the maintenance of F1BGFP(+) NSPCs and GBM-SCs.

Nasopharyngeal carcinoma (NPC) is a unique malignancy derived from the epithelium of the nasopharynx. Despite great advances in the development of radiotherapy and chemotherapy, relapse and metastasis in NPC patients remain major causes of mortality. Evidence accumulated over recent years indicates that Epstein-Barr virus (EBV) lytic replication plays an important role in the pathogenesis of NPC and inhibition of EBV reactivation is now being considered as a goal for the therapy of EBV-associated cancers. With this in mind, a panel of dietary compounds was screened and emodin was found to have potential anti-EBV activity. Through Western blotting, immunofluorescence, and flow cytometric analysis, we show that emodin inhibits the expression of EBV lytic proteins and blocks virion production in EBV- positive epithelial cell lines. In investigating the underlying mechanism, reporter assays indicated that emodin represses Zta promoter (Zp) and Rta promoter (Rp) activities, triggered by various inducers. Mapping of the Zp construct reveals that the SP1 binding region is important for emodin-triggered repression and emodin is shown to be able to inhibit SP1 expression, suggesting that it likely inhibits EBV reactivation by suppression of SP1 expression. Moreover, we also show that emodin inhibits the tumorigenic properties induced by repeated EBV reactivation, including micronucleus formation, cell proliferation, migration, and matrigel invasiveness. Emodin administration also represses the tumor growth in mice which is induced by EBV activation. Taken together, our results provide a potential chemopreventive agent in restricting EBV reactivation and NPC recurrence.

FGF1 is involved in multiple biological functions and exhibits the importance in neuroprotective effects. Our previous studies indicated that, in human brain and retina, the FGF1B promoter controlled the expression of FGF1. However, the exact function and regulation of FGF1 in brain is still unclear. Here, we generated F1B-GFP transgenic mice that expressed the GFP reporter gene under the control of human FGF1B promoter (2540 to 131). Using the fresh brain sections of F1B-GFP transgenic mice, we found that the F1B-GFP cells expressed strong fluorescent signals in the ventricular system throughout the brain. The results of immunohistochemistry further showed that two distinct populations of F1B-GFP 1 cells existed in the brains of F1B-GFP transgenic mice. We demonstrated that one population of F1B-GFP 1 cells was ependymal cells, which distributed along the entire ventricles, and the second population of F1B-GFP 1 cells was neuronal cells that projected their long processes into multiple directions in specific areas of the brain. The double labeling of F1B-GFP 1 cells and tyrosine hydroxylase indicated that a subpopulation of F1B-GFP 1 -neuronal cells was dopaminergic neurons. Importantly, these F1B-GFP 1 /TH 1 cells were distributed in the main dopaminergic neuronal groups including hypothalamus, ventral tegmental area, and raphe nuclei. These results suggested that human FGF1B promoter was active in ependymal cells, neurons, and a portion of dopaminergic neurons. Thus, the F1B-GFP transgenic mice provide an animal model not only for studying FGF1 gene expression in vivo but also for understanding the role of FGF1 contribution in neurodegenerative disorders such as Parkinson's disease and Alzheimer's disease. V C 2014 Wiley Periodicals, Inc. Develop Neurobiol 75: 232-248, 2015