Yi Li

Yi Li
Saint Louis University | SLU · Department of Nutrition and Dietetics

M.Sc., Ph.D.

About

39
Publications
11,307
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Introduction
I use nutritional genomics approaches to understand the involvement of nutrition factors and lifestyle factors in development of chronic diseases such obesity and type 2 diabetes. I am also interested in the mechanisms of adipogenesis induced by nutrition factors.

Publications

Publications (39)
Article
Full-text available
Zinc is one of the most important essential trace elements. It is involved in more than 300 enzyme systems and is an indispensable participant in many biochemical processes. Zinc deficiency causes a number of disorders in the human body, the main ones being the delay of growth and puberty, immune disorders, and cognitive dysfunctions. There are ove...
Article
Full-text available
Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL) is triggered by BCR/ABL kinase. Recent efforts focused on the development of more potent tyrosine kinase inhibitors (TKI) that also inhibit mutant tyrosine kinases such as nilotinib and dasatinib. Although major advances in the treatment of this aggressive disease with potent i...
Article
Introduction: We have investigated aberrant methylation of genes CDH1, RASSF1A, MLH1, N33, DAPK, expression of genes hTERT, MMP7, MMP9, BIRC5 (survivin), PTGS2, and activity of telomerase of 106 gastric tumor samples obtained intra-operatively and 53 gastric tumor samples from the same group of patients obtained endoscopically before surgery. Biop...
Article
Retinal adhesion mechanisms in mammals are quite complex and multifactorial in nature. To date, these mechanisms are incompletely understood due to a variety of chemical, physical, and physiological forces impinging upon retinal tissue: retinal pigment epithelium, nearby tissues as sclera and vitreous, the subretinal space, and the highly complex i...
Article
Full-text available
Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL) is triggered by BCR/ABL and SRC family tyrosine kinases. They interact with each other and subsequently activate downstream growth-signaling pathways, including Raf/MEK/ERK, Akt/mTOR, and STAT5 pathways. Although imatinib is the standard treatment for Ph+ leukemia, response rat...
Article
Full-text available
NCS1 (neuronal calcium sensor-1) is a Ca2+-myristoyl switch protein of the NCS protein family involved in synaptic plasticity and neurotransmission via Ca2+-dependent regulation of dopamine D2 receptor and associated G-protein coupled receptor kinase (GRK)-2. Overexpression of NCS1 in synaptic terminals results in accumulation of membrane-bound pro...
Article
Full-text available
Amyloid β25-35 (Aβ25-35) represents a neurotoxic fragment of Aβ1 - 40 or Aβ1 - 42, and is implicated in the progressive neurodegeneration in cases of the Alzheimer disease (AD). Amyloid β25-35 was shown to lyse rat erythrocytes (RBCs) of all ages, and the extent of the RBC toxicity is directly correlated with Aβ25-35 concentration and cell age. Act...
Article
Full-text available
Introduction: APP/PS1 double-transgenic mouse models of Alzheimer’s disease (AD), which overexpress mutated forms of the gene for the human amyloid precursor protein (APP) and presenilin 1 (PS1), have provided robust neuropathological hallmarks of an AD-like pattern at early ages. This study aimed to characterize immunocytochemical patterns of the...
Chapter
It is well known that both oxidative stress and mitochondrial dysfunction play important roles in animal models of brain ischemia. This study was undertaken to test whether oral supplementation of coenzyme Q10 (ubiquinone) or creatine citrate could protect brain ischemia-induced mitochondrial damage in the rats. Brain ischemia was induced for 50 mi...
Chapter
Full-text available
Oxidative stress in the cardiovascular system, including brain microvessels and/or parenchymal cells, results in increased production and damage by reactive oxygen species (ROS) and reactive nitrogen species (RNS) compounds, thus promoting leukocyte adhesion and increasing endothelial permeability. The resulting chronic injury stimulus results in p...
Chapter
Full-text available
The pathogenesis that is primarily responsible for Alzheimer’s disease (AD) and cerebrovascular accidents (CVA) appears to involve chronic hypoperfusioninduced mitochondrial lesions. We studied the ultrastructural features of vascular lesions and mitochondria in brain vascular wall cells from human AD biopsy samples and two transgenic mouse models...
Chapter
Subject age and brain oxidative stress play pivotal roles in Alzheimer's disease (AD) pathology. Erythrocytes (red blood cells: RBC) are considered as passive reporter cells for the oxidative status of the whole organism, not active participants in mechanisms of AD pathogenesis and are not well studied in AD. The aim of this chapter is to assess wh...
Article
Full-text available
APP/PS1 double-transgenic mouse models of Alzheimer’s disease (AD), which overexpress mutated forms of the gene for human amyloid precursor protein (APP) and presenilin 1 (PS1), have provided robust neuropathological hallmarks of AD-like pattern at early ages. This study characterizes immunocytochemical patterns of AD mouse brain as a model for hum...
Data
Full-text available
Nitric oxide-(NO-) dependent oxidative stress results in mitochondrial ultrastructural alterations and DNA damage in cases of Alzheimer disease (AD). However, little is known about these pathways in human cancers, especially during the development as well as the progression of primary brain tumors and metastatic colorectal cancer. One of the key fe...
Article
Full-text available
Nitric oxide- (NO-) dependent oxidative stress results in mitochondrial ultrastructural alterations and DNA damage in cases of Alzheimer disease (AD). However, little is known about these pathways in human cancers, especially during the development as well as the progression of primary brain tumors and metastatic colorectal cancer. One of the key f...
Article
Full-text available
APP/PS1 double-transgenic mouse models of Alzheimer’s disease (AD), which overexpress mutated forms of the gene for human amyloid precursor protein (APP) and presenilin 1 (PS1), have provided robust neuropathological hallmarks of AD-like pattern at early ages. This study characterizes immunocytochemical patterns of AD mouse brain as a model for hum...
Article
Full-text available
бумагапринимает во внимание, что увлекательные отношениямежду массой и использованием энергии для любого живого существастрого подчиняется математическому универсальному фор-мула всех живых существ, действующая в мельчайшихбактерий до самых больших китов и секвойи.Впервые мы сообщаем о емкости для мам-малая эукариотическая клетка расщепляет, разрыв...
Article
Full-text available
Subject age and brain oxidative stress play pivotal roles in Alzheimer disease (AD) pathology. Erythrocytes (red blood cells: RBC) are considered as passive "reporter cells" for the oxidative status of the whole organism, not active participants in mechanisms of AD pathogenesis and are not well studied in AD. The aim of this work is to assess wheth...
Article
Full-text available
Subject age and brain oxidative stress play pivotal roles in Alzheimer disease (AD) pathology. Erythrocytes (red blood cells: RBC) are considered as passive "reporter cells" for the oxidative status of the whole organism, not active participants in mechanisms of AD pathogenesis and are not well studied in AD. The aim of this work is to assess wheth...
Data
It is known that oxidative stress and mitochondrial dysfunction both play an important role in animal models of brain ischemia. The present study was undertaken to test whether oral supplementation of coenzyme Q10 (ubiquinone) or creatine citrate could protect against brain ischemia-induced mitochondrial damage in the rats model. Brain ischemia was...
Article
Full-text available
Oxidative stress in the cardiovascular system, including brain microvessels and/or parenchymal cells results in an accumulation of reactive oxygen species (ROS) and reactive nitrogen species (RNS) compounds thus promoting leukocyte adhesion and increasing endothelial permeability. The resulting chronic injury stimulus results in progressive cellula...
Article
Full-text available
Abstract: Oxidative stress in cardiovascular system including brain microvessels and/or parenchymal cells results in an accumulation of reactive oxygen species (ROS), thus promoting leukocyte adhesion and increasing endothelial permeability. In this regard, chronic injury results in progressive cellular hypometabolism, which is responsible for Alzh...
Article
Full-text available
It is known that oxidative stress and mitochondrial dysfunction both play an important role in animal models of brain ischemia. The present study was undertaken to test whether oral supplementation of coenzyme Q10 (ubiquinone) or creatine citrate could protect against brain ischemia-induced mitochondrial damage in the rats model. Brain ischemia was...
Article
Full-text available
There is growing scientific agreement that antioxidants, particularly the polyphenolic forms, may help lower the incidence of disease, such as certain cancers, cardiovascular and neurodegenerative diseases, DNA damage, or even have anti-aging properties. On the other hand, questions remain as to whether some antioxidants or phytochemicals potential...
Article
Full-text available
Expression of the Cat-1 gene (cationic amino acid transporter-1) is induced in proliferating cells and in response to a variety of stress conditions. The expression of the gene is mediated via a TATA-less promoter. In the present study we show that an Sp1 (specificity protein 1)-binding site within a GC-rich region of the Cat-1 gene controls its ba...
Article
Full-text available
The accumulation of unfolded proteins in the endoplasmic reticulum (ER) triggers a stress response program that protects cells early in the response and can lead to apoptosis during prolonged stress. The basic leucine zipper transcription factor, CCAAT/enhancer-binding protein beta (C/EBPbeta), is one of the genes with increased expression during E...
Article
Full-text available
The accumulation of unfolded proteins in the endoplasmic reticulum (ER) triggers a stress response program that protects cells early in the response and can lead to apoptosis during prolonged stress. The basic leucine zipper transcription factor, CCAAT/enhancer-binding protein beta (C/EBPbeta), is one of the genes with increased expression during E...
Article
Full-text available
Whole body protein synthesis is reduced during the fed-to-fasted transition and in cases of chronic dietary restriction; however, less is known about tissue-specific alterations. We have assessed the extent to which protein synthesis in cardiac muscle responds to dietary perturbations compared with liver and skeletal muscle by applying a novel (2)H...
Article
Full-text available
The adaptive response to amino acid limitation in mammalian cells inhibits global protein synthesis and promotes the expression of proteins that protect cells from stress. The arginine/lysine transporter, cat-1, is induced during amino acid starvation by transcriptional and post-transcriptional mechanisms. It is shown in the present study that the...
Article
Full-text available
Apoptosis has been shown to be associated with altered glycosylation patterns and biosynthesis of glycoproteins. A major cell surface receptor involved in the induction of apoptosis is Fas that is activated by binding Fas ligand but can also be activated by binding anti-Fas antibody. In order to determine whether the Fas receptor is glycosylated, t...
Article
Full-text available
Changes in free intracellular Ca2+ are thought to regulate several major processes during Dictyostelium development, including cell aggregation and cell type-specific gene expression, but the mechanisms involved are unclear. To learn more about Ca2+ signaling and Ca2+ homeostasis in this organism, we used suppression subtractive hybridization to id...