Breakthrough Mouse Model for Alzheimer's More Like Human Disease

2001 ◽  
Author(s):  
Keyword(s):  
Mouse Model ◽  
Human Disease

Sex and rheumatoid arthritis: Mouse model versus human disease

2006 ◽  
Vol 56 (1) ◽  
pp. 1-3 ◽  
Author(s):  
Maurizio Cutolo
Keyword(s):  
Rheumatoid Arthritis ◽  
Mouse Model ◽  
Human Disease ◽  
Model Versus

scholarly journals Reversible Nerve Damage and Corneal Pathology in Murine Herpes Simplex Stromal Keratitis

2014 ◽  
Vol 88 (14) ◽  
pp. 7870-7880 ◽  
Author(s):  
Hongmin Yun ◽  
Alexander M. Rowe ◽  
Kira L. Lathrop ◽  
Stephen A. K. Harvey ◽  
Robert L. Hendricks
Keyword(s):  
T Cells ◽  
Herpes Simplex ◽  
Mouse Model ◽  
Human Disease ◽  
Sensory Nerve ◽  
Blink Reflex ◽  
Nerve Damage ◽  
Corneal Scarring ◽  
Corneal Nerves ◽  
Stromal Keratitis

ABSTRACTHerpes simplex virus type 1 (HSV-1) shedding from sensory neurons can trigger recurrent bouts of herpes stromal keratitis (HSK), an inflammatory response that leads to progressive corneal scarring and blindness. A mouse model of HSK is often used to delineate immunopathogenic mechanisms and bears many of the characteristics of human disease, but it tends to be more chronic and severe than human HSK. Loss of blink reflex (BR) in human HSK is common and due to a dramatic retraction of corneal sensory nerve termini in the epithelium and the nerve plexus at the epithelial/stromal interface. However, the relationship between loss of BR due to nerve damage and corneal pathology associated with HSK remains largely unexplored. Here, we show a similar retraction of corneal nerves in mice with HSK. Indeed, we show that much of the HSK-associated corneal inflammation in mice is actually attributable to damage to the corneal nerves and accompanying loss of BR and can be prevented or ameliorated by tarsorrhaphy (suturing eyelids closed), a clinical procedure commonly used to prevent corneal exposure and desiccation. In addition, we show that HSK-associated nerve retraction, loss of BR, and severe pathology all are reversible and regulated by CD4+T cells. Thus, defining immunopathogenic mechanisms of HSK in the mouse model will necessitate distinguishing mechanisms associated with the immunopathologic response to the virus from those associated with loss of corneal sensation. Based on our findings, investigation of a possible contribution of nerve damage and BR loss to human HSK also appears warranted.IMPORTANCEHSK in humans is a potentially blinding disease characterized by recurrent inflammation and progressive scarring triggered by viral release from corneal nerves. Corneal nerve damage is a known component of HSK, but the causes and consequences of HSK-associated nerve damage remain obscure. We show that desiccation of the corneal surface due to nerve damage and associated loss of BR severely exacerbates and prolongs inflammation-induced pathology in mice. Preventing corneal desiccation results in a milder and more transient HSK with variable scarring that mirrors HSK seen in most humans. We further show that nerve damage is reversible and regulated by CD4+T cells. Thus, we provide a mouse model that more closely resembles typical human HSK and suggest nerve damage is an important but largely overlooked factor in human disease.

scholarly journals Mouse models of human cancer and the need for more translational research

2008 ◽  
Author(s):  
Martin Fenner
Keyword(s):  
Mouse Model ◽  
Translational Research ◽  
Synovial Sarcoma ◽  
Mouse Models ◽  
Human Disease ◽  
Human Cancer ◽  
Neuropsychiatric Disorders ◽  
International Congress

One of the opening lectures this Saturday of the International Congress of Genetics was held by Mario Capecchi. His talked was entitled Modeling human disease in the mouse: from cancer to neuropsychiatric disorders. In the first half he described his mouse model of synovial sarcoma. ...

Mechanisms of AIDS-related cytomegalovirus retinitis

2019 ◽  
Vol 14 (8) ◽  
pp. 545-560 ◽  
Author(s):  
Jessica Carter ◽  
Christine I Alston ◽  
Jay Oh ◽  
Lauren-Ashley Duncan ◽  
Judee Grace Esquibel Nemeno ◽  
...  
Keyword(s):  
Mouse Model ◽  
Human Cytomegalovirus ◽  
Human Disease ◽  
Cytomegalovirus Retinitis ◽  
Murine Cytomegalovirus ◽  
Opportunistic Pathogens ◽  
Aids Patients ◽  
Clinical Burden ◽  
Antiretroviral Therapies ◽  
Murine Aids

Human cytomegalovirus (HCMV) generates a significant clinical burden worldwide, particularly among the immune compromised. In approximately 30% of untreated HIV/AIDS patients without access or sufficient response to antiretroviral therapies, for example, HCMV causes a sight-threatening retinitis. To study the mechanisms of AIDS-related HCMV retinitis, our lab has for many years used a mouse model in which a mixture of mouse retroviruses induces murine AIDS after approximately 10 weeks, rendering otherwise resistant mice susceptible to opportunistic pathogens. This immunodeficiency combined with subretinal inoculation of murine cytomegalovirus yields a reproducible model of the human disease, facilitating the discovery of many clinically relevant virologic and immunologic mechanisms of retinal destruction which we summarize in this review.

scholarly journals TFE3 Xp11.2 Translocation Renal Cell Carcinoma Mouse Model Reveals Novel Therapeutic Targets and Identifies GPNMB as a Diagnostic Marker for Human Disease

2019 ◽  
Vol 17 (8) ◽  
pp. 1613-1626 ◽  
Author(s):  
Masaya Baba ◽  
Mitsuko Furuya ◽  
Takanobu Motoshima ◽  
Martin Lang ◽  
Shintaro Funasaki ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Mouse Model ◽  
Cell Carcinoma ◽  
Human Disease ◽  
Renal Cell ◽  
Diagnostic Marker ◽  
Therapeutic Targets ◽  
Xp11.2 Translocation ◽  
Novel Therapeutic

scholarly journals A missense mutation in Grm6 reduces but does not eliminate mGluR6 expression or rod depolarizing bipolar cell function

2017 ◽  
Vol 118 (2) ◽  
pp. 845-854 ◽  
Author(s):  
Neal S. Peachey ◽  
Nazarul Hasan ◽  
Bernard FitzMaurice ◽  
Samantha Burrill ◽  
Gobinda Pangeni ◽  
...  
Keyword(s):  
Mouse Model ◽  
Missense Mutation ◽  
Mouse Models ◽  
Human Disease ◽  
Bipolar Cell ◽  
Night Blindness ◽  
Cell Function ◽  
Congenital Stationary Night Blindness ◽  
Depolarizing Bipolar Cell

This article describes a mouse model of the human disease complete congenital stationary night blindness in which the mutation reduces but does not eliminate GRM6 expression and bipolar cell function, a phenotype distinct from that seen in other Grm6 mouse models.

scholarly journals A new mouse model for stationary night blindness with mutant Slc24a1 explains the pathophysiology of the associated human disease

2015 ◽  
Vol 24 (20) ◽  
pp. 5915-5929 ◽  
Author(s):  
Frans Vinberg ◽  
Tian Wang ◽  
Robert S. Molday ◽  
Jeannie Chen ◽  
Vladimir J. Kefalov
Keyword(s):  
Mouse Model ◽  
Human Disease ◽  
Night Blindness

scholarly journals A gene signature identified using a mouse model of androgen receptor-dependent prostate cancer predicts biochemical relapse in human disease

2012 ◽  
Vol 131 (3) ◽  
pp. 662-672 ◽  
Author(s):  
Vanessa C. Thompson ◽  
Tanya K. Day ◽  
Tina Bianco-Miotto ◽  
Luke A. Selth ◽  
Guangzhou Han ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Mouse Model ◽  
Human Disease ◽  
Gene Signature ◽  
Biochemical Relapse
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