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Search Results: 1 - 10 of 42570 matches for " Huaxi Xu "
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Food Quality Safety Evaluation Model in College Canteens Based on the Improved AHP-taking Bengbu College as an Example
Huaxi Chen,Qingbing Xu
Advance Journal of Food Science and Technology , 2013,
Abstract: Based on the results of investigation and the suggestion from the experts, the factors influencing the college canteen food quality and safety are found and assessment system for university cafeteria food quality and safety is constructed. With the improved Analytic Hierarchy Process (AHP) to the various indexes for the empowerment and the fuzzy comprehensive evaluation method, the university canteen food quality and safety evaluation method is created. Then based on the example from Bengbu College, the solution of the model is provided, thus it is concluded that the process management factors, food factors and environmental factors, make the biggest influence on the canteen food quality and safety. Meanwhile, the extent of the influence of the second level factor on the canteen food quality and safety is identified and further it should be paid a greater attention to the several factors in order to improve the status of the food quality and safety condition.
Identifying an APP-binding protein in neuronal cell death
Zhang Yunwu,Xu Huaxi
Molecular Neurodegeneration , 2012, DOI: 10.1186/1750-1326-7-s1-l22
Abstract:
High Mobility Group Box 1 and Traumatic Brain Injury  [PDF]
Seidu A. Richard, Wu Min, Zhaoliang Su, Huaxi Xu
Journal of Behavioral and Brain Science (JBBS) , 2017, DOI: 10.4236/jbbs.2017.72006
Abstract: Traumatic brain injury (TBI) is a leading cause of death and disability worldwide. We identify High Mobility Group Box 1 (HMGB1) as a novel causative factor in the development of cerebral oedema, mediating coagulation, preventing secondary brain damage as well as serving as a novel therapeutic target to limit secondary neurological injury after TBI. As a prototypical danger associated molecular patterns (DAMP), HMGB1 is released from necrotic neurons via a NR2B-mediated mechanism during TBI. The secretion of HMGB1 requires severe injury and tissue hypoperfusion, and is associated with posttraumatic coagulation abnormalities, activation of complement and severe systemic inflammatory response. HMGB1 is clinically associated with elevated intracranial pressure (ICP) in patients and functionally promoted cerebral edema after TBI. The detrimental effects of HMGB1 is mediated at least in part between activation of microglial toll-like receptor 4 (TLR4) and the subsequent expression of the astrocytic water channel aquaporin-4 (AQP4). Anti-HMGB1mAb remarkably inhibited fluid percussion-induced brain edema by inhibiting HMGB1 translocation, protection of blood-brain barrier (BBB) integrity, suppression of inflammatory molecule expression and improvement of motor function. Our review demonstrates the pathological role of HMGB1 as well as the possible therapeutic valve of HMGB1 in patients with TBI.
Zoom in on neurodegeneration
Guojun Bu, Huaxi Xu, Todd E Golde
Molecular Neurodegeneration , 2006, DOI: 10.1186/1750-1326-1-1
Abstract: We are proud to introduce you to a new home for neurodegeneration research, Molecular Neurodegeneration. Through the open-access format we plan to bring you the most timely and exciting research focusing on the molecular and cellular mechanisms underlying neurodegenerative disease processes and on potential therapeutic interventions for these devastating diseases. Molecular Neurodegeneration will also provide a forum to discuss and review the current research and foster creative thinking in this exciting field.The increased prevalence of certain age-associated neurodegenerative diseases is largely attributable to the increase in average lifespan among individuals who live in industrialized nations. From a patient perspective, diseases such as Alzheimer's, Parkinson's or amyotrophic lateral sclerosis are feared because of their slow and progressive nature and because there are no effective treatments or cures for these diseases. The economic and social burden of neurodegenerative diseases is huge and growing all too rapidly. We have made significant progress with respect to understanding certain aspects of neurodegenerative diseases. However, compared to our understanding of other human diseases such as cancer and cardiovascular disorders, our knowledge on the mechanisms of neurodegeneration is still in its infancy. Indeed, for most neurodegenerative diseases, we can only guess as to why neurons ultimately die.Most existing scientific journals that publish research papers related to neurodegenerative diseases focus on the genetic epidemiology and pathological aspects of these diseases. Molecular Neurodegeneration will uniquely focus on the molecular and cellular aspects of the disease mechanisms, identification of potential therapeutic targets, and preclinical studies evaluating potential therapeutic interventions in model systems. Studies of the physiological and pathophysiological functions of cellular proteins contributing to neurodegeneration are strongly encoura
APP processing in Alzheimer's disease
Yun-wu Zhang, Robert Thompson, Han Zhang, Huaxi Xu
Molecular Brain , 2011, DOI: 10.1186/1756-6606-4-3
Abstract: Alzheimer's disease (AD) is the most prevalent neurodegenerative disorder, afflicting 10% of the population over the age of 65 and 50% of the population over the age of 85. A small subset (<10%) of AD cases result from an inherited autosomal dominant gene mutation and have an early-onset (the fourth to sixth decade). The majority of these familial AD (FAD) mutations are in the genes encoding β-amyloid precursor protein (APP) and presenilins (PS1 and PS2) [1-3]. Significant efforts have gone into understanding the mechanisms underlying the genes tied to FAD as the clinicopathological features are indistinguishable from regular onset AD.AD is characterized in patients by an inexorably progressing dementia. In vulnerable brain regions, such as the hippocampus and cortex, there is an accumulation of extracellular neuritic plaques and intracellular neurofibrillary tangles. The neurofibrillary tangles (NFTs) consist largely of hyperphosphorylated twisted filaments of the microtubule-associated protein tau [4,5]. Extracellular neuritic plaques are deposits of differently sized small peptides called β-amyloid (Aβ) that are derived via sequential proteolytic cleavages of the β-amyloid precursor protein (APP) [6].The APP gene is located on chromosome 21 in humans with three major isoforms arising from alternative splicing [3]. These are APP695, APP751 and APP770 (containing 695, 751, and 770 amino acids, respectively). APP751 and APP770 are expressed in most tissues and contain a 56 amino acid Kunitz Protease Inhibitor (KPI) domain within their extracellular regions. APP695 is predominantly expressed in neurons and lacks the KPI domain [7,8]. There are reports showing that the protein and mRNA levels of KPI-containing APP isoforms are elevated in AD brain and associated with increased Aβ deposition [9]; and prolonged activation of extrasynaptic NMDA receptor in neurons can shift APP expression from APP695 to KPI-containing APP isoforms, accompanied with increased production o
The γ-secretase complex: from structure to function
Xian Zhang,Yanfang Li,Huaxi Xu,Yun-Wu Zhang
Frontiers in Cellular Neuroscience , 2014, DOI: 10.3389/fncel.2014.00427
Abstract: One of the most critical pathological features of Alzheimer’s disease (AD) is the accumulation of β-amyloid (Aβ) peptides that form extracellular senile plaques in the brain. Aβ is derived from β-amyloid precursor protein through sequential cleavage by β- and γ-secretases. γ-secretase is a high molecular weight complex minimally composed of four components: presenilins, nicastrin, anterior pharynx defective 1, and presenilin enhancer 2. In addition to APP, γ-secretase also cleaves many other type I transmembrane protein substrates. As a crucial enzyme for Aβ production, γ-secretase is an appealing therapeutic target for AD. Here, we summarize current knowledge on the structure and function of γ-secretase, as well as recent progress in developing γ-secretase targeting drugs for AD treatment.
Expression of fljB: z66 on a linear plasmid of Salmonella enterica serovar typhi is dependent on FliA and FlhDC and regulated by OmpR
Xu, Shungao;Zou, Xin;Sheng, Xiumei;Zhang, Haifang;Mao, Lingxiang;Du, Hong;Xu, Huaxi;Huang, Xinxiang;
Brazilian Journal of Microbiology , 2010, DOI: 10.1590/S1517-83822010000300025
Abstract: salmonella enterica serovar typhi z66-positive strains have two different flagellin genes, flic:d/j and fljb:z66, located on the chromosome and on a linear plasmid, respectively. to investigate the mechanism underlying the expressional regulation of fljb:z66, gene deletion mutants of the regulators flia, flhdc, and ompr were constructed in this study. the expression levels of flic and fljb:z66 were analyzed by qrt-pcr in the wild-type strain and mutants at high and low osmolarity. the results show that the expression levels of both fljb:z66 and flic were greatly reduced in flia and flhdc mutants under both high and low osmotic conditions. in the ompr mutant, the expression levels of fljb:z66, flic, flia, and flhd were increased at low osmotic conditions. sds-page and western blotting analysis of the secreted proteins revealed that the fljb:z66 was almost absent in the flia and flhdc mutants at both high and low osmolarity. in the wild-type strain, the fljb:z66 was more highly expressed under high-osmolarity conditions than under low-osmolarity conditions. however, this difference in expression disappeared in the ompr mutant. translational expression assay of fljb:z66 showed that the fljb:z66 expression was decreased in ompr mutant at both low and high osmolarity. these results suggest that the expression of fljb:z66 in s. enterica serovar typhi is dependent on flia and flihdc, and ompr can regulate the expression and secretion of fljb:z66 in different osmolarity.
Identification and Characterization of a Cis-Encoded Antisense RNA Associated with the Replication Process of Salmonella enterica Serovar Typhi
Isaac Dadzie, Shungao Xu, Bin Ni, Xiaolei Zhang, Haifang Zhang, Xiumei Sheng, Huaxi Xu, Xinxiang Huang
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0061308
Abstract: Antisense RNAs that originate from the complementary strand of protein coding genes are involved in the regulation of gene expression in all domains of life. In bacteria, some of these antisense RNAs are transcriptional noise whiles others play a vital role to adapt the cell to changing environmental conditions. By deep sequencing analysis of transcriptome of Salmonella enterica serovar Typhi, a partial RNA sequence encoded in-cis to the dnaA gene was revealed. Northern blot and RACE analysis confirmed the transcription of this antisense RNA which was expressed mostly in the stationary phase of the bacterial growth and also under iron limitation and osmotic stress. Pulse expression analysis showed that overexpression of the antisense RNA resulted in a significant increase in the mRNA levels of dnaA, which will ultimately enhance their translation. Our findings have revealed that antisense RNA of dnaA is indeed transcribed not merely as a by-product of the cell's transcription machinery but plays a vital role as far as stability of dnaA mRNA is concerned.
Notch Signaling Mediates TNF-α-Induced IL-6 Production in Cultured Fibroblast-Like Synoviocytes from Rheumatoid Arthritis
Zhijun Jiao,Wenhong Wang,Jie Ma,Shengjun Wang,Zhaoliang Su,Huaxi Xu
Clinical and Developmental Immunology , 2012, DOI: 10.1155/2012/350209
Abstract: It has been reported that Notch family proteins are expressed in synovium tissue and involved in the proliferation of synoviocyte from rheumatoid arthritis (RA). The aim of this paper was to investigate whether Notch signaling mediated TNF-α-induced cytokine production of cultured fibroblast-like synoviocytes (FLSs) from RA. Exposure of RA FLSs to TNF-α (10 ng/ml) led to increase of Hes-1, a target gene of Notch signaling, and a marked upregulation of Notch 2, Delta-like 1, and Delta-like 3 mRNA levels. Blockage of Notch signaling by a γ-secretase inhibitor (DAPT) inhibited IL-6 secretion of RA FLSs in response to TNF-α while treatment with recombinant fusion protein of Notch ligand Delta-like 1 promoted such response. TNF-α stimulation also induced IL-6 secretion in OA FLSs; however, the Hes-1 level remained unaffected. Our data confirm the functional involvement of Notch pathway in the pathophysiology of RA FLSs which may provide a new target for RA therapy.
Fis Is Essential for the Stability of Linear Plasmid pBSSB1 and Affects the Motility of Salmonella enterica Serovar Typhi
Haifang Zhang, Bin Ni, Xin Zhao, Isaac Dadzie, Hong Du, Qiang Wang, Huaxi Xu, Xinxiang Huang
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0037462
Abstract: pBSSB1 is a 27 kb non-bacteriophage-related linear plasmid first found in Salmonella enterica serovar Typhi (S. Typhi), but the mechanism underlying the replication of pBSSB1 is currently unknown. Previous reports showed that the factor for inversion stimulation (Fis) encoded by fis can affect the replication, transcription and other processes through binding DNA. Here, a fis deletion mutant of S. Typhi (Δfis) was prepared through the homologous recombination mediated by suicide plasmid and the loss of pBSSB1 in Δfis was observed surprisingly by pulsed field gel electrophoresis (PFGE). Subsequently, the loss of pBSSB1 was verified by PCR and Southern blot. In addition, the motility of Δfis was deficient and the flagellin of Δfis could not be detected by 2-dimensional polyacrylamide gel electrophoresis. All these results show that Fis is essential for the stability of pBSSB1 and affects the motility of S. Typhi.
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