816 results match your criteria negative littermates

Ferulic Acid Ameliorates Alzheimer's Disease-like Pathology and Repairs Cognitive Decline by Preventing Capillary Hypofunction in APP/PS1 Mice.

Neurotherapeutics 2021 Mar 30. Epub 2021 Mar 30.

CAS Key Laboratory of Animal Models and Human Disease Mechanisms, and KIZ-SU Joint Laboratory of Animal Model and Drug Development, and Laboratory of Learning and Memory, Kunming Institute of Zoology, the Chinese Academy of Sciences, Kunming, 650223, China.

Brain capillaries are crucial for cognitive functions by supplying oxygen and other nutrients to and removing metabolic wastes from the brain. Recent studies have demonstrated that constriction of brain capillaries is triggered by beta-amyloid (Aβ) oligomers via endothelin-1 (ET1)-mediated action on the ET1 receptor A (ETRA), potentially exacerbating Aβ plaque deposition, the primary pathophysiology of Alzheimer's disease (AD). However, direct evidence is still lacking whether changes in brain capillaries are causally involved in the pathophysiology of AD. Read More

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Transcriptomic data showing differentially expressed genes between Notch3 and Notch4 deleted mice.

Data Brief 2021 Apr 13;35:106873. Epub 2021 Feb 13.

Molecular and integrative physiology, United States.

The Notch signaling pathway is an important conserved pathway for normal homeostasis during development. However, targeted deletion of Notch4 ( ) or Notch3 ( ) in mice is not lethal. In fact, both and mice develop normally and are fertile. Read More

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FOXO1 expression in chondrocytes modulates cartilage production and removal in fracture healing.

Bone 2021 Mar 1:115905. Epub 2021 Mar 1.

Department of Periodontics, School of Dental Medicine, University of Pennsylvania, Philadelphia, PA, USA. Electronic address:

Fracture healing is a multistage process characterized by inflammation, cartilage formation, bone deposition, and remodeling. Chondrocytes are important in producing cartilage that forms the initial anlagen for the hard callus needed to stabilize the fracture site. We examined the role of FOXO1 by selective ablation of FOXO1 in chondrocytes mediated by Col2α1 driven Cre recombinase. Read More

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FoxO1 is required for physiological cardiac hypertrophy induced by exercise but not by constitutively active PI3K.

Am J Physiol Heart Circ Physiol 2021 04 12;320(4):H1470-H1485. Epub 2021 Feb 12.

Baker Heart and Diabetes Institute, Melbourne, Victoria, Australia.

The insulin-like growth factor 1 receptor (IGF1R) and phosphoinositide 3-kinase p110α (PI3K) are critical regulators of exercise-induced physiological cardiac hypertrophy and provide protection in experimental models of pathological remodeling and heart failure. Forkhead box class O1 (FoxO1) is a transcription factor that regulates cardiomyocyte hypertrophy downstream of IGF1R/PI3K activation in vitro, but its role in physiological hypertrophy in vivo was unknown. We generated cardiomyocyte-specific FoxO1 knockout (cKO) mice and assessed the phenotype under basal conditions and settings of physiological hypertrophy induced by ) swim training or ) cardiac-specific transgenic expression of constitutively active PI3K (caPI3K). Read More

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Cardiomyocytes-specific deletion of monoamine oxidase B reduces irreversible myocardial ischemia/reperfusion injury.

Free Radic Biol Med 2021 Mar 18;165:14-23. Epub 2021 Jan 18.

Justus-Liebig-University Giessen, Physiologisches Institut, Giessen, Germany.

Monoamine oxidase B (MAO-B), a protein localized at the outer mitochondrial membrane, catalyzes the oxidative deamination of biogenic amines thereby producing reactive oxygen species (ROS). Increased ROS formation contributes to myocardial ischemia/reperfusion (I/R); however, the importance of different ROS producing enzymes for increased I/R-induced ROS formation and the subsequent I/R injury is still a matter of debate. Here we describe the first cardiomyocytes-specific MAO-B knockout mouse and test the hypothesis that lack of cardiomyocyte MAO-B protects the heart from I/R injury. Read More

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The Presence of Cholesteryl Ester Transfer Protein (CETP) in Endothelial Cells Generates Vascular Oxidative Stress and Endothelial Dysfunction.

Biomolecules 2021 Jan 7;11(1). Epub 2021 Jan 7.

Department of Structural and Functional Biology, Institute of Biology, State University of Campinas, Campinas 13083-970, Brazil.

Endothelial dysfunction precedes atherosclerosis and is an independent predictor of cardiovascular events. Cholesterol levels and oxidative stress are key contributors to endothelial damage, whereas high levels of plasma high-density lipoproteins (HDL) could prevent it. Cholesteryl ester transfer protein (CETP) is one of the most potent endogenous negative regulators of HDL-cholesterol. Read More

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January 2021

Lipocalin-2: a role in hepatic gluconeogenesis via AMP-activated protein kinase (AMPK).

J Endocrinol Invest 2021 Jan 9. Epub 2021 Jan 9.

Department of Endocrinology, Jinan Central Hospital, Cheeloo College of Medicine, Shandong University, 105 Jiefang Road, Jinan, 250013, Shandong Province, China.

Purpose: Evidence is accumulating that lipocalin2 (LCN2) is implicated in insulin resistance and glucose homeostasis, but the underlying possible mechanisms remain unclear. This study is to investigate the possible linkage between LCN2 and AMP-activated protein kinase (AMPK) or forkhead transcription factor O1 (FoxO1), which influences insulin sensitivity and gluconeogenesis in liver.

Methods: LCN2 knockout (LCN2KO) mice and wild-type littermates were used to evaluate the effect of LCN2 on insulin sensitivity and hepatic gluconeogenesis through pyruvate tolerance test (PTT), glucose tolerance test (ipGTT), insulin tolerance test (ITT), and hyperinsulinemic-euglycemic clamps, respectively. Read More

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January 2021

Sinomenine protects bone from destruction to ameliorate arthritis via activating p62-Keap1-Nrf2 feedback loop.

Biomed Pharmacother 2021 Mar 1;135:111195. Epub 2021 Jan 1.

State Key Laboratory of Quality Research in Chinese Medicine/Macau Institute for Applied Research in Medicine and Health, Macau University of Science and Technology, Macau, China; Joint Laboratory for Translational Cancer Research of Chinese Medicine of the Ministry of Education of the People's Republic of China, Macau University of Science and Technology, Macau, China; Guangdong-Hong Kong-Macao Joint Laboratory of Respiratory Infectious Disease, Macau University of Science and Technology, Macau, China. Electronic address:

Disease-modifying antirheumatic drugs (DMARDs) are the first line medications to treat rheumatoid arthritis (RA), a chronic and systemic autoimmune disease affecting multiple joints. Sinomenine (SIN) is thought a natural DMARD (nDMARD) and effectively utilized to treat RA in clinic for several decades in China. Here we reported that it is not methotrexate (MTX), a representative drug of DMARDs, but SIN protected joints from destruction to alleviate the symptoms of the mice with arthritis, indicating that the underlying mechanism of SIN is different from MTX to treat arthritis. Read More

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BMP2 Is Required for Postnatal Maintenance of Osteochondral Tissues of the Temporomandibular Joint.

Cartilage 2020 Dec 14:1947603520980158. Epub 2020 Dec 14.

Division of Orthodontics, University of Connecticut Health Center, Farmington, CT, USA.

Objective: Bone morphogenetic protein 2 (BMP2) plays important roles in cartilage growth and development. Paradoxically, elevated levels of BMP2 leads to hypertrophic differentiation and osteoarthritis of cartilage. We examined the loss of BMP2 in cells expressing aggrecan of the mandibular condyle and knee. Read More

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December 2020

Detailed evaluation of the upper airway in the Dp(16)1Yey mouse model of Down syndrome.

Sci Rep 2020 12 7;10(1):21323. Epub 2020 Dec 7.

Sleep and Circadian Neurobiology Laboratory, Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, 3155 Porter Drive, Room 2141, Palo Alto, CA, 94304, USA.

A high prevalence of obstructive sleep apnea (OSA) has been reported in Down syndrome (DS) owing to the coexistence of multiple predisposing factors related to its genetic abnormality, posing a challenge for the management of OSA. We hypothesized that DS mice recapitulate craniofacial abnormalities and upper airway obstruction of human DS and can serve as an experimental platform for OSA research. This study, thus, aimed to quantitatively characterize the upper airway as well as craniofacial abnormalities in Dp(16)1Yey (Dp16) mice. Read More

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December 2020

MD1 Depletion Predisposes to Ventricular Arrhythmias in the Setting of Myocardial Infarction.

Heart Lung Circ 2020 Nov 27. Epub 2020 Nov 27.

Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China; Cardiovascular Research Institute of Wuhan University, Wuhan, China; Hubei Key Laboratory of Cardiology, Wuhan, China. Electronic address:

Background: Myeloid differentiation protein 1 (MD1) is expressed in the human heart and is a negative regulator of Toll-like receptor 4 (TLR4) signalling. MD1 exerts anti-arrhythmic effects.

Aim: The aim of this study was to determine the role of MD1 in myocardial infarction (MI)-related ventricular arrhythmias (VAs). Read More

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November 2020

Rho Guanine Nucleotide Exchange Factor 4 (Arhgef4) Deficiency Enhances Spatial and Object Recognition Memory.

Exp Neurobiol 2020 Oct;29(5):334-343

Department of Medicine and Microbiology, Graduate Program in Neuroscience, College of Medicine, Chungbuk National University, Cheongju 28644, Korea.

Guanine nucleotide exchange factors (GEFs) play multiple functional roles in neurons. In a previous study, we reported that (Rho guanine nucleotide exchange factor 4) functioned as a negative regulator of the excitatory synaptic function by sequestering postsynaptic density protein 95 (PSD-95). However, the role of in behavior has not been examined. Read More

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October 2020

ADAP1/Centaurin-α1 Negatively Regulates Dendritic Spine Function and Memory Formation in the Hippocampus.

eNeuro 2021 Jan-Feb;8(1). Epub 2021 Jan 6.

Max Planck Florida Institute for Neuroscience, Jupiter, FL 33458

ADAP1/Centaurin-α1 (CentA1) functions as an Arf6 GTPase-activating protein highly enriched in the brain. Previous studies demonstrated the involvement of CentA1 in brain function as a regulator of dendritic differentiation and a potential mediator of Alzheimer's disease (AD) pathogenesis. To better understand the neurobiological functions of CentA1 signaling in the brain, we developed knock-out (KO) mice. Read More

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January 2021

Proper mTORC1 Activity Is Required for Glucose Sensing and Early Adaptation in Human Pancreatic β Cells.

J Clin Endocrinol Metab 2021 Jan;106(2):e562-e572

Department of Endocrine and Metabolic Diseases, Shanghai Institute of Endocrine and Metabolic Diseases, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Context: The mechanistic target of rapamycin complex I (mTORC1) is crucial for β-cell identity and function in rodents. However, its possible relevance to the physiopathology of diabetes in humans remains unclear.

Objective: This work aimed to understand the participation of mTORC1 in human β cells in prediabetes and diabetes. Read More

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January 2021

Retinoid Signaling in Intestinal Epithelial Cells Is Essential for Early Survival From Gastrointestinal Infection.

Front Immunol 2020 8;11:559635. Epub 2020 Oct 8.

Department of Veterinary and Biomedical Sciences, The Pennsylvania State University, University Park, PA, United States.

Vitamin A deficiency (A-) increases morbidity and mortality to gastrointestinal (GI) infection. Blocking retinoid signaling (dominant negative retinoic acid receptor, dnRAR) in intestinal epithelial cells (IEC, dnRAR) had no effect on vitamin A absorption, the expression of tight junction proteins or the integrity of the barrier. Immune cells in the gut were present in normal frequencies in the dnRAR mice, with the exception of the T cell receptor (TCR)αβ+/CD8αα cells, which were significantly lower than in wildtype littermates. Read More

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October 2020

Mouse models of growth hormone deficiency.

Rev Endocr Metab Disord 2021 Mar 9;22(1):3-16. Epub 2020 Oct 9.

The Edison Biotechnology Institute, Ohio University, 172 Water Tower Drive, Athens, OH, 45701, USA.

Nearly one century of research using growth hormone deficient (GHD) mouse lines has contributed greatly toward our knowledge of growth hormone (GH), a pituitary-derived hormone that binds and signals through the GH receptor and affects many metabolic processes throughout life. Although delayed sexual maturation, decreased fertility, reduced muscle mass, increased adiposity, small body size, and glucose intolerance appear to be among the negative characteristics of these GHD mouse lines, these mice still consistently outlive their normal sized littermates. Furthermore, the absence of GH action in these mouse lines leads to enhanced insulin sensitivity (likely due to the lack of GH's diabetogenic actions), delayed onset for a number of age-associated physiological declines (including cognition, cancer, and neuromusculoskeletal frailty), reduced cellular senescence, and ultimately, extended lifespan. Read More

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Within-litter covariance of allele-specific MHC heterozygosity, coccidian endoparasite load and growth is modulated by sibling differences in starting mass.

Oecologia 2020 Nov 27;194(3):345-357. Epub 2020 Sep 27.

Laboratoire d'Ethologie Expérimentale et Comparée UR 4443, Université Sorbonne Paris Nord, 93430, Villetaneuse, France.

Although littermates in altricial mammals usually experience highly similar environmental conditions during early life, considerable differences in growth and health can emerge among them. In a study on subadults of a European rabbit (Oryctolagus cuniculus) population with low MHC polymorphism, we tested whether litter-sibling differences in endoparasitic coccidia load and body mass at the end of the vegetation period were associated with within-litter differences in starting body mass (measured around 2 weeks prior to weaning) and in immune-genetic (MHC class II DRB) constitution. We hypothesized that siblings with a lighter starting mass might be more susceptible to endoparasite infections and thus, negative effects of a more unfavourable MHC constitution might be particularly pronounced in such individuals. Read More

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November 2020

A role of color vision in emmetropization in C57BL/6J mice.

Sci Rep 2020 09 10;10(1):14895. Epub 2020 Sep 10.

School of Ophthalmology and Optometry and Eye Hospital, Wenzhou Medical University, 270 Xueyuan Road, Wenzhou, 325027, Zhejiang, China.

Spectral composition affects emmetropization in both humans and animal models. Because color vision interacts the effects of chromatic defocus, we developed a method to bypass the effects of longitudinal chromatic aberration by placing a spectral filter behind the optics of the eye, using genetic tools. Newborn C57BL/6J (B6) mice were reared in quasi-monochromatic red (410-510 nm) or blue (585-660 nm) light beginning before eye-opening. Read More

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September 2020

Histone deacetylase 5 regulates interleukin 6 secretion and insulin action in skeletal muscle.

Mol Metab 2020 12 6;42:101062. Epub 2020 Aug 6.

Institute for Clinical Biochemistry and Pathobiochemistry, German Diabetes Center, Leibniz Center for Diabetes Research at Heinrich Heine University, Medical faculty, Düsseldorf, Germany; German Center for Diabetes Research (DZD), München-Neuherberg, Germany.

Objective: Physical exercise training is associated with increased glucose uptake in skeletal muscle and improved glycemic control. HDAC5, a class IIa histone deacetylase, has been shown to regulate transcription of the insulin-responsive glucose transporter GLUT4 in cultured muscle cells. In this study, we analyzed the contribution of HDAC5 to the transcriptional network in muscle and the beneficial effect of muscle contraction and regular exercise on glucose metabolism. Read More

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December 2020

SHP-1 ameliorates nonalcoholic steatohepatitis by inhibiting proinflammatory cytokine production.

FEBS Lett 2020 Sep 17;594(18):2965-2974. Epub 2020 Jul 17.

Department of Gastroenterology, Changzheng Hospital, Second Military Medical University, Shanghai, China.

Inflammation is the main contributor for the pathogenesis of nonalcoholic steatohepatitis (NASH). Src homology region 2 domain-containing phosphatase 1 (SHP-1, also known as PTPN6) is regarded as a negative regulator of inflammation, but its role in NASH remains unknown. Here, hepatocyte-specific Ptpn6 knockout mice (Ptpn6 ) and adenovirus vector-mediated ectopic expression of SHP-1 (AdSHP1) were used to evaluate the role of SHP-1 in a methionine- and choline-deficient diet-induced NASH model. Read More

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September 2020

Zinc finger and BTB domain-containing protein 46 is essential for survival and proliferation of acute myeloid leukemia cell line but dispensable for normal hematopoiesis.

Chin Med J (Engl) 2020 Jul;133(14):1688-1695

Department of Hematology, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing 400038, China.

Background: Zinc finger and BTB domain-containing protein 46 (Zbtb46) is a transcription factor identified in classical dendritic cells, and maintains dendritic cell quiescence in a steady state. Zbtb46 has been reported to be a negative indicator of acute myeloid leukemia (AML). We found that Zbtb46 was expressed at a relatively higher level in hematopoietic stem and progenitor cells (HSPCs) compared to mature cells, and higher in AML cells compared to normal bone marrow (BM) cells. Read More

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Up-Regulation of Matrix Metalloproteinase-2 by Scleral Monocyte-Derived Macrophages Contributes to Myopia Development.

Am J Pathol 2020 09 16;190(9):1888-1908. Epub 2020 Jun 16.

School of Optometry and Ophthalmology and Eye Hospital, Wenzhou Medical University, Wenzhou, China; The State Key Laboratory of Optometry, Ophthalmology and Vision Science, Wenzhou, China. Electronic address:

Myopia is a leading cause of visual impairment worldwide. This sight-compromising condition is associated with scleral thinning, extracellular matrix remodeling, and inappropriate optical axial length elongation. Although macrophages are present in the sclera, their involvement in this condition is unknown. Read More

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September 2020

Gestational poly(I:C) attenuates, not exacerbates, the behavioral, cytokine and mTOR changes caused by isolation rearing in a rat 'dual-hit' model for neurodevelopmental disorders.

Brain Behav Immun 2020 10 30;89:100-117. Epub 2020 May 30.

School of Life Sciences, University of Nottingham, Medical School, Queen's Medical Centre, Nottingham NG7 2UH, UK. Electronic address:

Many psychiatric illnesses have a multifactorial etiology involving genetic and environmental risk factors that trigger persistent neurodevelopmental impairments. Several risk factors have been individually replicated in rodents, to understand disease mechanisms and evaluate novel treatments, particularly for poorly-managed negative and cognitive symptoms. However, the complex interplay between various factors remains unclear. Read More

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October 2020

Impact of Key Nicotinic AChR Subunits on Post-Stroke Pneumococcal Pneumonia.

Vaccines (Basel) 2020 May 28;8(2). Epub 2020 May 28.

Institute for Medical Immunology, Charité-Universitätsmedizin Berlin, Corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin Institute of Health, 13353 Berlin, Germany.

Pneumonia is the most frequent severe medical complication after stroke. An overactivation of the cholinergic signaling after stroke contributes to immunosuppression and the development of spontaneous pneumonia caused by Gram-negative pathogens. The α7 nicotinic acetylcholine receptor (α7nAChR) has already been identified as an important mediator of the anti-inflammatory pathway after stroke. Read More

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Maternal separation-induced increases in vascular stiffness are independent of circulating angiotensinogen levels.

J Appl Physiol (1985) 2020 07 14;129(1):58-65. Epub 2020 May 14.

Department of Pharmacology and Nutritional Sciences, University of Kentucky, Lexington, Kentucky.

The renin-angiotensin system (RAS) precursor angiotensinogen (AGT) has been implicated in the functional and mechanical alterations of the vascular wall in response to high-fat diet (HFD). Previously, we showed that HFD exacerbates angiotensin II-induced constriction in isolated aortic rings from male rats exposed to maternal separation (MatSep), a model of early-life stress. Thus, the aim of this study was to investigate whether MatSep increases AGT secretion promoting vascular stiffness in rats fed a HFD. Read More

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Transcriptomic data indicating differential expressed genes between HIV-1 Associated Nephropathy (HIVAN) mouse model (Tg26) and wildtype mice.

Data Brief 2020 Jun 17;30:105562. Epub 2020 Apr 17.

Department of Internal Medicine, University of Kansas Medical Center, Kansas City, KS 66160, United States.

Tg26 mice are robust models of human immunodeficiency virus 1 associated nephropathy (HIVAN). These mice are useful for HIVAN pathology analysis, and recent studies suggest that the Tg26 mouse model is an excellent model of other chronic kidney diseases. We performed RNA seq analysis of differential gene expression in the kidneys of Tg26 mice. Read More

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In vitro and in vivo roles of glucocorticoid and vitamin D receptors in the control of neonatal cardiomyocyte proliferative potential.

J Mol Cell Cardiol 2020 05 11;142:126-134. Epub 2020 Apr 11.

Cardiovascular Research Institute and Department of Physiology, University of California, San Francisco, San Francisco, CA 94158, USA; Eli and Edythe Broad Center for Regeneration Medicine and Stem Cell Research, University of California, San Francisco, San Francisco, CA 94158, USA. Electronic address:

Cardiomyocyte (CM) proliferative potential varies considerably across species. While lower vertebrates and neonatal mammals retain robust capacities for CM proliferation, adult mammalian CMs lose proliferative potential due to cell-cycle withdrawal and polyploidization, failing to mount a proliferative response to regenerate lost CMs after cardiac injury. The decline of murine CM proliferative potential occurs in the neonatal period when the endocrine system undergoes drastic changes for adaptation to extrauterine life. Read More

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CDKN2a/p16 Antagonizes Hepatic Stellate Cell Activation and Liver Fibrosis by Modulating ROS Levels.

Front Cell Dev Biol 2020 24;8:176. Epub 2020 Mar 24.

Department of Cell Biology, Municipal Laboratory for Liver Protection and Regulation of Regeneration, School of Basic Medical Sciences, Capital Medical University, Beijing, China.

The lipid-storage hepatic stellate cells (HSC) play as pivotal role in liver fibrosis being able to differentiate into myofibroblasts in response to various pro-fibrogenic stimuli. In the present study we investigated the role of CDKN2a/p16, a negative regulator of cell cycling, in HSC activation and the underlying mechanism. Levels of p16 were significantly down-regulated in activated HSCs isolated from mice induced to develop liver fibrosis compared to quiescent HSCs isolated from the control mice . Read More

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Runx2 (Runt-Related Transcription Factor 2)-Mediated Microcalcification Is a Novel Pathological Characteristic and Potential Mediator of Abdominal Aortic Aneurysm.

Arterioscler Thromb Vasc Biol 2020 05 26;40(5):1352-1369. Epub 2020 Mar 26.

Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, China (Z.L., Z.C., L.Y., Y.F., W.K.).

Objective: Abdominal aortic aneurysms (AAAs) are highly lethal diseases without effective clinical predictors and therapeutic targets. Vascular microcalcification, as detected by fluorine-18-sodium fluoride, has recently been recognized as a valuable indicator in predicting atherosclerotic plaque rupture and AAA expansion. However, whether vascular microcalcification involved in the pathogenesis of AAA remains elusive. Read More

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Immune and Inflammatory Determinants Underlying Alzheimer's Disease Pathology.

J Neuroimmune Pharmacol 2020 12 24;15(4):852-862. Epub 2020 Feb 24.

Division of Basic and Clinical Immunology, Department of Medicine, University of California, Irvine, Irvine, CA, 92697, USA.

This study examines the link between peripheral immune changes in perpetuation of the Alzheimer's disease (AD) neuropathology and cognitive deficits. Our research design using human AD patients and rodent model is supported by past evidence from genomic studies. We observed an active immune response against Aβ as indicated by the increased Aβ specific IgG antibody in the serum of AD and patients with mild cognitive impairments as compared to healthy controls. Read More

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December 2020