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Li Q.,Harbin Medical University | Wu D.,Harbin Veterinary Research Institute | Zhang L.,Harbin Medical University | Zhang Y.,Harbin Medical University
Experimental Gerontology

Galantamine (Gal) is an acetylcholinesterase inhibitor and used to treat the symptoms of Alzheimer's disease (AD). Recent studies show that Gal may affect amyloid precursor protein (APP) metabolism and increase release of secretory APPα (sAPPα). However the effect of Gal on amyloid-Β peptide (AΒ) release and Β-site cleaving enzyme 1 (BACE1) expression is still unknown. Consequently, we investigated the effect of Gal on the level of AΒ and BACE1. In a differentiated human neuroblastoma cell line (SH-SY5Y), Gal (0.3 ΜM) was found to significantly decrease AΒ release and BACE1 expression following treatment for 6, 12, and 24. h. Increasing Gal to 0.9 ΜM or 10 ΜM had no further effect. The effect of Gal (0.3 ΜM for 18. h) was maximal on BACE1 expression but not on AΒ secretion. At higher concentration (0.9 ΜM and 10 ΜM), Gal had no effect on the level of full-length APP but could still stimulate further decrease in AΒ secretion and release of sAPPα. These observations suggested that 0.3 ΜM Gal exerts its effect on AΒ production by inhibiting BACE1 expression, while 0.9 μM or 10 ΜM Gal mainly reduces AΒ production by stimulating the non-amyloidogenic pathway to decrease the amount of APP substrate available for Β-secretase cleavage. In addition, α7 nicotinic acetylcholine receptor (α7nAChR) and multiple second messengers (including PKC, MEK, and p38MAPK) were found to be involved in the regulation of Gal-inhibited AΒ release and BACE1 expression. © 2010 Elsevier Inc. Source

Ye L.,Emory University | Wen Z.,Emory University | Wen Z.,Harbin Veterinary Research Institute | Dong K.,Emory University | And 7 more authors.

Several conserved neutralizing epitopes have been identified in the HIV Env protein and among these, the MPER of gp41 has received great attention and is widely recognized as a promising target. However, little success has been achieved in eliciting MPER-specific HIV neutralizing antibodies by a number of different vaccine strategies. We investigated the ability of HA/gp41 chimeric protein-based vaccines, which were designed to enhance the exposure of the MPER in its native conformation, to induce MPER-specific HIV neutralizing antibodies. In characterization of the HA/gp41 chimeric protein, we found that by mutating an unpaired Cys residue (Cys-14) in its HA1 subunit to a Ser residue, the modified chimeric protein HA-C14S/gp41 showed increased reactivity to a conformation-sensitive monoclonal antibody against HA and formed more stable trimers in VLPs. On the other hand, HA-C14S/gp41 and HA/gp41 chimeric proteins expressed on the cell surfaces exhibited similar reactivity to monoclonal antibodies 2F5 and 4E10. Immunization of guinea pigs using the HA-C14S/gp41 DNA or VLP vaccines induced antibodies against the HIV gp41 as well as to a peptide corresponding to a segment of MPER at higher levels than immunization by standard HIV VLPs. Further, sera from vaccinated guinea pigs were found to exhibit HIV neutralizing activities. Moreover, sera from guinea pigs vaccinated by HA-C14S/gp41 DNA and VLP vaccines but not the standard HIV VLPs, were found to neutralize HIV pseudovirions containing a SIV-4E10 chimeric Env protein. The virus neutralization could be blocked by a MPER-specific peptide, thus demonstrating induction of MPER-specific HIV neutralizing antibodies by this novel vaccine strategy. These results show that induction of MPER-specific HIV neutralizing antibodies can be achieved through a rationally designed vaccine strategy. © 2011 Ye et al. Source

Song Z.,Harbin Veterinary Research Institute | Li Y.,Harbin Veterinary Research Institute | Xin J.,Harbin Veterinary Research Institute | Zou X.,Harbin Veterinary Research Institute | Sun W.,Harbin Veterinary Research Institute

Mycoplasma bovis is the causative agent of Mycoplasma bovis-associated disease (MbAD). Although the mechanisms underlying M. bovis adherence to host cells is not clear, recent studies have shown that the cell surface protein α-enolase facilitates bacterial invasion and dissemination in the infected host. In this study, we cloned, expressed and purified recombinant M. bovis α-enolase and induced polyclonal anti-α-enolase antibodies in rabbits. M. bovis α-enolase was detected in the cytoplasmic and membrane protein fractions by these antibodies. Triple immunofluorescence labeling combined with confocal laser scanning microscopy (CLSM) revealed that the plasminogen (Plg) enhanced the adherence of M. bovis to embryonic bovine lung (EBL) cells; the values obtained for adherence and inhibition are consistent with this finding. Interestingly, we found that trace amounts of trypsin acted as a more effective enhancer of cell adherence than Plg. Hence, our data indicate that surface-associated M. bovis α-enolase is an adhesion-related factor of M. bovis that contributes to adherence by binding Plg. © 2012 Song et al. Source

Wang J.,Harbin Veterinary Research Institute | Wang M.,Heilongjiang Institute of Animal Health Inspection | Wang S.,Harbin Veterinary Research Institute | Liu Z.,Harbin Veterinary Research Institute | And 5 more authors.
Emerging Infectious Diseases

During March 25-May 5, 2014, we investigated 11 outbreaks of peste des petits ruminants in Heilongjiang Province, China. We found that the most likely source of the outbreaks was animals from livestock markets in Shandong. Peste des petits ruminants viruses belonging to lineages II and IV were detected in sick animals. © 2015, Emerging Infectious Diseases. All rights reserved. Source

Xin J.,Harbin Veterinary Research Institute | Li Y.,Harbin Veterinary Research Institute | Nicholas R.A.J.,Veterinary Laboratories Agency | Chen C.,Harbin Veterinary Research Institute | And 3 more authors.
Veterinary Journal

Contagious bovine pleuropneumonia (CBPP), caused by Mycoplasma mycoides subsp. mycoides small colony type, was once the most damaging infectious animal disease in China, second only to rinderpest. Between 1949 and 1989, 178,570 cattle died of CBPP, causing estimated losses of 356. million RMB (1. RMB = approx £0.094, US$0.15, €0.11 at 27th January 2011). In 1956, in an effort to control the disease, a virulent strain of the causative organism (Ben-1) was attenuated by multiple passages in rabbits. The resultant vaccine achieved a high protection rate in cattle with a duration of immunity of 28. months. Vaccines were also prepared in sheep to increase the antigen yield and then in Tibetan sheep because it caused fewer adverse reactions in yaks and related species. The last CBPP infected animal was identified in 1989 since when no more cases have occurred. In 1992, vaccination of cattle was stopped. In 2008 China submitted an application to the World Organization for Animal Health (OIE) to be declared CBPP-free. © 2011. Source

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