Role of animal models in selecting antiviral combinations for clinical studies

1996 ◽  
Vol 29 (1) ◽  
pp. 57-59 ◽  
Author(s):  
Earl R. Kern
2020 ◽  
Vol 7 (4) ◽  
pp. 251-259
Author(s):  
D. A. Leonard ◽  
K. R. Amin ◽  
H. Giele ◽  
J. E. Fildes ◽  
Jason K. F. Wong

Abstract Purpose of Review Skin provides a window into the health of an individual. Using transplanted skin as a monitor can provide a powerful tool for surveillance of rejection in a transplant. The purpose of this review is to provide relevant background to the role of skin in vascularized transplantation medicine. Recent Findings Discrete populations of T memory cells provide distributed immune protection in skin, and cycle between skin, lymph nodes, and blood. Skin-resident TREG cells proliferate in response to inflammation and contribute to long-term VCA survival in small animal models. Early clinical studies show sentinel flap rejection to correlate well with facial VCA skin rejection, and abdominal wall rejection demonstrates concordance with visceral rejection, but further studies are required. Summary This review focuses on the immunology of skin, skin rejection in vascularized composite allografts, and the recent advances in monitoring the health of transplanted tissues using distant “sentinel” flaps.


2002 ◽  
Vol 3 (4) ◽  
pp. 217-231 ◽  
Author(s):  
Subrata Chakrabarti ◽  
Zia Ali Khan ◽  
Mark Cukiernik ◽  
Gen Fukuda ◽  
Shali Chen ◽  
...  

Endothelin (ET) peptides perform several physiological, vascular, and nonvascular functions and are widely distributed in a number of tissues. They are altered in several disease processes including diabetes. Alteration of ETs have been demonstrated in organs of chronic diabetic complications in both experimental and clinical studies. The majority of the effects of ET alteration in diabetes are due to altered vascular function. Furthermore, ET antagonists have been shown to prevent structural and functional changes induced by diabetes in animal models. This review discusses the contribution of ETs in the pathogenesis and the potential role of ET antagonism in the treatment of chronic diabetic complications.


Author(s):  
Abdulmaged M. Traish

AbstractAdvancement in basic and clinical research has provided considerable evidence suggesting a key role of androgens in the physiology and pathophysiology of sexual function. Evidence from clinical studies in men and women with androgen deficiency support a role of androgens in maintaining sexual function in men and women and are integral in maintaining sexual health. Preclinical studies utilizing male animal models demonstrated a role of androgens in maintenance of: (i) penile tissue structural integrity, (ii) penile trabecular smooth muscle growth and function, (iii) integrity of penile nerve fiber network, (iv) signaling pathways in the corpora cavernosa, (v) myogenic and adipogenic differentiation in the corpora cavernosa, (vi) physiological penile response to stimuli, and (vii) facilitating corporeal hemodynamics. These findings strongly suggest a role for androgen in the physiology of penile erection. In addition, clinical studies in hypogonadal men with erectile dysfunction treated with testosterone provided invaluable information on restoring erectile function and improving ejaculatory function. Similarly, clinical studies in surgically or naturally postmenopausal women with androgen deficiency suggested that androgens are important for maintaining sexual desire and testosterone treatment was shown to improve sexual desire, arousal and orgasm. Furthermore, studies in female animal models demonstrated that androgens maintain the integrity of vaginal nerve fiber network, muscularis volume, and enhance genital blood flow and mucification. Based on the biochemical, physiological and clinical findings from human and animal studies, we suggest that androgens are integral for maintaining sexual function and play a critical role in maintaining sexual health in men and women.


2016 ◽  
Author(s):  
M Mannelli ◽  
E Rapizzi ◽  
L Canu ◽  
T Ercolino ◽  
V Giache
Keyword(s):  

2019 ◽  
Vol 26 (5) ◽  
pp. 765-779 ◽  
Author(s):  
Alexios S. Antonopoulos ◽  
Athina Goliopoulou ◽  
Evangelos Oikonomou ◽  
Sotiris Tsalamandris ◽  
Georgios-Angelos Papamikroulis ◽  
...  

Background: Myocardial redox state is a critical determinant of atrial biology, regulating cardiomyocyte apoptosis, ion channel function, and cardiac hypertrophy/fibrosis and function. Nevertheless, it remains unclear whether the targeting of atrial redox state is a rational therapeutic strategy for atrial fibrillation prevention. Objective: To review the role of atrial redox state and anti-oxidant therapies in atrial fibrillation. Method: Published literature in Medline was searched for experimental and clinical evidence linking myocardial redox state with atrial fibrillation pathogenesis as well as studies looking into the role of redoxtargeting therapies in the prevention of atrial fibrillation. Results: Data from animal models have shown that altered myocardial nitroso-redox balance and NADPH oxidases activity are causally involved in the pathogenesis of atrial fibrillation. Similarly experimental animal data supports that increased reactive oxygen / nitrogen species formation in the atrial tissue is associated with altered electrophysiological properties of atrial myocytes and electrical remodeling, favoring atrial fibrillation development. In humans, randomized clinical studies using redox-related therapeutic approaches (e.g. statins or antioxidant agents) have not documented any benefits in the prevention of atrial fibrillation development (mainly post-operative atrial fibrillation risk). Conclusion: Despite strong experimental and translational data supporting the role of atrial redox state in atrial fibrillation pathogenesis, such mechanistic evidence has not been translated to clinical benefits in atrial fibrillation risk in randomized clinical studies using redox-related therapies.


2019 ◽  
Vol 24 (45) ◽  
pp. 5367-5374 ◽  
Author(s):  
Xiaoyun Li ◽  
Seyed M. Moosavi-Basri ◽  
Rahul Sheth ◽  
Xiaoying Wang ◽  
Yu S. Zhang

The role of endovascular interventions has progressed rapidly over the past several decades. While animal models have long-served as the mainstay for the advancement of this field, the use of in vitro models has become increasingly widely adopted with recent advances in engineering technologies. Here, we review the strategies, mainly including bioprinting and microfabrication, which allow for fabrication of biomimetic vascular models that will potentially serve to supplement the conventional animal models for convenient investigations of endovascular interventions. Besides normal blood vessels, those in diseased states, such as thrombosis, may also be modeled by integrating cues that simulate the microenvironment of vascular disorders. These novel engineering strategies for the development of biomimetic in vitro vascular structures will possibly enable unconventional means of studying complex endovascular intervention problems that are otherwise hard to address using existing models.


2021 ◽  
Vol 14 ◽  
Author(s):  
Mohammad Najim Uddin ◽  
Mohammad Injamul Hoq ◽  
Israt Jahan ◽  
Shafayet Ahmed Siddiqui ◽  
Chayan Dhar Clinton ◽  
...  

: Thymoquinone (TQ) is one of the leading phytochemicals, which is abundantly found in Nigella sativa L. seeds. TQ exhibited various biological effects such as antioxidant, anti-inflammatory, antimicrobial, and anti-tumoral in several pre-clinical studies. Parkinson's disease (PD) is a long-term neurodegenerative disease with movement difficulties, and the common feature of neurodegeneration in PD patients is caused by dopaminergic neural damage in the substantia nigra pars compacta. The neuroprotective activity of TQ has been studied in various neurological disorders. TQ-mediated neuroprotection against PD yet to be reported in a single frame; therefore, this review is intended to narrate the potentiality of TQ in the therapy of PD. TQ has been shown to protect against neurotoxins via amelioration of neuroinflammation, oxidative stress, apoptosis, thereby protects neurodegeneration in PD models. TQ could be an emerging therapeutic intervention in PD management, but mechanistic studies have been remained to be investigated to clarify its neuroprotective role.


2021 ◽  
Vol 10 (5) ◽  
pp. 1081
Author(s):  
Mikkel Parsberg Werge ◽  
Adrian McCann ◽  
Elisabeth Douglas Galsgaard ◽  
Dorte Holst ◽  
Anne Bugge ◽  
...  

The prevalence of non-alcoholic fatty liver disease (NAFLD) is increasing and approximately 25% of the global population may have NAFLD. NAFLD is associated with obesity and metabolic syndrome, but its pathophysiology is complex and only partly understood. The transsulfuration pathway (TSP) is a metabolic pathway regulating homocysteine and cysteine metabolism and is vital in controlling sulfur balance in the organism. Precise control of this pathway is critical for maintenance of optimal cellular function. The TSP is closely linked to other pathways such as the folate and methionine cycles, hydrogen sulfide (H2S) and glutathione (GSH) production. Impaired activity of the TSP will cause an increase in homocysteine and a decrease in cysteine levels. Homocysteine will also be increased due to impairment of the folate and methionine cycles. The key enzymes of the TSP, cystathionine β-synthase (CBS) and cystathionine γ-lyase (CSE), are highly expressed in the liver and deficient CBS and CSE expression causes hepatic steatosis, inflammation, and fibrosis in animal models. A causative link between the TSP and NAFLD has not been established. However, dysfunctions in the TSP and related pathways, in terms of enzyme expression and the plasma levels of the metabolites (e.g., homocysteine, cystathionine, and cysteine), have been reported in NAFLD and liver cirrhosis in both animal models and humans. Further investigation of the TSP in relation to NAFLD may reveal mechanisms involved in the development and progression of NAFLD.


Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 1197
Author(s):  
Klaus Ley

This 11-chapter Special Issue of Cells spans the gamut from basic science in mechanistic animal models to translational science to outcomes of clinical trials, all focused on the role of inflammation in atherosclerosis [...]


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