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Haiyan Fu

Publications and source records attributed to Haiyan Fu.

4 recordsLinked to original sources

Co-degradation with glucose of four surfactants, CTAB, Triton X-100, SDS and Rhamnolipid, in liquid culture media and compost matrix.

Strengthened biodegradation is one of the key means to treat surfactant pollution in environment, and microorganism and surfactant have significant effects on degradation. In this paper, co-degradation of CTAB, Triton X-100, SDS and rhamnolipid with glucose by Pseudomonas aeruginosa, Bacillus subtilis and compost microorganisms in liquid culture media, as well as the degradation of rhamnolipid in compost were investigated. The results showed that CTAB was recalcitrant to degrade by the three microorganisms and it also inhibited microorganisms from utilizing readily degradable carbon source. Non-ionic surfactant Triton X-100 could also hardly be degraded, but it was not toxic to microorganisms and would not inhibit the growth of the microorganisms. Anion surfactant SDS had no toxicity to microorganisms and could be co-degraded as carbon source with glucose. Biosurfactant rhamnolipid was a kind of particular surfactant, which had no toxicity and could be degraded by Bacillus subtilis and compost microorganisms, while it could not be utilized by its producing bacterium Pseudomonas aeruginosa. Among these three bacteria, the compost consortium had the strongest degradation capacity on the tested surfactants due to their microorganisms' diversity. In compost matrix rhamnolipid could be degraded during composting, but not preferentially utilized.

Bacillus subtilis↗

Transcriptional up-regulation of restin by all-trans retinoic acid through STAT1 in cancer cell differentiation process.

RESTIN, a member of the melanoma-associated antigen superfamily, is a nuclear protein induced by atRA (all-trans retinoic acid) in HL60 cells. HeLa cells stably transfected with restin results in G1 cell cycle arrest. How this gene is regulated by atRA in the cell differentiation process is still unclear. In this study, we observed that up-regulation of restin was present during the atRA-induced HL60 cell differentiation process, suggesting the functional relevance between RESTIN and atRA-induced cellular effects. In order to further define the transcriptional regulation of restin by atRA, we analyzed the promoter region of restin. About 2.1kb 5' flanking sequence of this gene was cloned into vector pGL3 and its core promoter region was identified through systemic deletions. Interestingly, restin promoter containing several potential consensus-binding sites of STAT-1alpha was activated by atRA in ER(+) MCF-7 cells but not in ER(-) MDA-MB-231 cells, over-expression of STAT-1alpha in latter rescued the activation effect of restin promoter in response to atRA and IFNgamma. Our evidence supported that STAT-1alpha plays an important role in the atRA-induced transcriptional up-regulation of restin, which was associated with the atRA-induced HL60 cell differentiation and potentially mediated the downstream effects of atRA signal pathway via STAT-1alpha in some cancer cells.

Antigens, Neoplasm↗

Self-complementary adeno-associated virus serotype 2 vector: global distribution and broad dispersion of AAV-mediated transgene expression in mouse brain.

The blood-brain barrier is the main obstacle to efficient delivery of therapeutic reagents, including viral vectors, into the central nervous system (CNS) for treating global CNS diseases. In this study, the effects of mannitol infusions on global brain gene expression of a novel AAV vector were examined after intravenous (i.v.) or intracisternal injection. Initially, a self-complementary adeno-associated virus serotype 2 vector (scAAV) was compared to traditional single-stranded AAV2 vector for reporter gene expression in the brain of adult mice with or without pretreatment of an i.v. mannitol infusion. One to two months postinjection, analysis of vector-transduced green fluorescent protein (GFP) expression in the brain revealed that vector delivery to the CNS via i.v. injection required pretreatment with mannitol. This expression was observed only when scAAV vectors were used. Using these conditions, transgene expression was observed in various neurons and glial cells throughout the brain. The peripherally administered scAAV vectors also transduced the cells in multiple somatic tissues with efficient expression in liver (20-30% of hepatocytes), but was less efficient in other somatic tissues. Intracisternal injection of scAAV vector produced a broad and intense transgene expression in both neurons and glial cells in the CNS of injected mice ranging from the olfactory area to the brain stem and spinal cord. More than 50% of the Purkinje cells in the cerebellum expressed GFP. Intravenous infusion of mannitol before intracisternal injection of the scAAV vector enhanced the dispersion of the vector in the CNS. Further optimization of these steps combining peripheral and intracisternal scAAV gene delivery should facilitate the development of treatments for global CNS diseases, especially diseases involving both the somatic system and the CNS, such as lysosomal storage disorders.

Animals↗

Neurological correction of lysosomal storage in a mucopolysaccharidosis IIIB mouse model by adeno-associated virus-mediated gene delivery.

Mucopolysaccharidosis (MPS) IIIB is characterized by mild somatic features and severe neurological diseases leading to premature death. No definite treatment is available for MPS IIIB patients. We constructed two recombinant adeno-associated virus (rAAV) vectors containing the human alpha-N-acetylglucosaminidase (NaGlu) cDNA driven by either a CMV or a neuron-specific enolase (NSE) promoter. In vitro, these rAAV vectors mediated efficient expression of recombinant NaGlu in human MPS IIIB fibroblasts and mouse MPS IIIB somatic and brain primary cell cultures. The secreted rNaGlu was taken up by both human and mouse MPS IIIB cells in culture and degraded the accumulated glycosaminoglycans (GAG). A direct microinjection (10(7) viral particles, 1 microl/10 minutes per injection) of vectors containing the NSE promoter resulted in long-term (6 months, the duration of the experiments) expression of rNaGlu in multiple brain structures/areas of adult MPS IIIB mice. Consistent with previous studies, the main target cells were neurons. However, while vector typically transduced an area of 400-500 microm surrounding the infusion sites, the correction of GAG storage involved neurons of a much broader area (1.5 mm) in a 6-month duration of experiments. These results provide a basis for the development of a treatment for neurological disease in MPS IIIB patients using AAV vectors.

Acetylglucosaminidase↗