scholarly journals Analysis of Animal Models of Oral Ulcers Based on the Characteristics of Clinical Symptoms of Chinese and Western Medicine

2017 ◽  
Author(s):  
Huan LI ◽  
Ming BAI ◽  
Yan-yan MIAO ◽  
Ming-san MIAO
Keyword(s):  
Animal Models ◽  
Western Medicine ◽  
Clinical Symptoms ◽  
Oral Ulcers

scholarly journals Therapeutic Effects of Hydrogen in Animal Models of Parkinson's Disease

2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
Kyota Fujita ◽  
Yusaku Nakabeppu ◽  
Mami Noda
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Animal Models ◽  
Animal Studies ◽  
Clinical Symptoms ◽  
Therapeutic Effects ◽  
Therapeutic Approaches ◽  
Cellular Apoptosis ◽  
6 Hydroxydopamine

Since the first description of Parkinson's disease (PD) nearly two centuries ago, a number of studies have revealed the clinical symptoms, pathology, and therapeutic approaches to overcome this intractable neurodegenerative disease. 1-methy-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 6-hydroxydopamine (6-OHDA) are neurotoxins which produce Parkinsonian pathology. From the animal studies using these neurotoxins, it has become well established that oxidative stress is a primary cause of, and essential for, cellular apoptosis in dopaminergic neurons. Here, we describe the mechanism whereby oxidative stress evokes irreversible cell death, and propose a novel therapeutic strategy for PD using molecular hydrogen. Hydrogen has an ability to reduce oxidative damage and ameliorate the loss of nigrostriatal dopaminergic neuronal pathway in two experimental animal models. Thus, it is strongly suggested that hydrogen might provide a great advantage to prevent or minimize the onset and progression of PD.

Atherosclerosis and Thrombosis: Lessons from Animal Models

2001 ◽  
Vol 86 (07) ◽  
pp. 356-365 ◽  
Author(s):  
Lina Badimon
Keyword(s):  
Animal Models ◽  
Vascular Disease ◽  
Clinical Symptoms ◽  
Plaque Rupture ◽  
Disease Process ◽  
Renin Angiotensin System ◽  
Experimental Models ◽  
Therapeutic Interventions ◽  
Plaque Disruption ◽  
Progression Of Atherosclerosis

SummaryAtherothrombosis defines the occurrence of thrombosis on athero-sclerotic lesions. Atherosclerosis is the most prevalent disease of our time and its thrombotic complications are responsible for an exceedingly high number of deaths and disabilities. Over the past few years, experimental investigation and clinical and pathologic observations have led to a better understanding of how a thrombus forms and also of its incidence in acute ischemic syndromes. A thrombus is usually found secondary to atherosclerotic plaque disruption. Mural thrombosis, also at the site of plaque rupture, is an important mechanism in the progression of atherosclerosis even when symptoms are absent. Because atherosclerosis is a silent and asymptomatic disease until complications arise with thrombosis producing clinical symptoms, it is necessary to have models that reproduce the human disease in its early stages. Unfortunately, not all the experimental models of vascular disease have human resemblance and validity. Knowledge of the disease process and of what an experimental animal model can offer is a milestone for a successful investigation. Experimental models of vascular disease have enhanced our understanding of the pathophysiological processes leading to vascular obstruction in both spontaneous and accelerated atherosclerosis and thrombosis. Animal models have provided insight into the role of platelets, lipids, renin-angiotensin system (RAS), cytokines and growth factors in the evolution and progression of atherosclerosis and have suggested potential therapeutic interventions. Significant advances in our understanding of the vascular biology and pathology of atherosclerosis and thrombosis, and of the interactions of blood cells, lipids and proteins with the vascular wall, have allowed us to formulate new experimental hypotheses and to test therapeutic strategies, either pharmacological or surgical.

scholarly journals Animal Models in Human Adenovirus Research

Biology ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 1253
Author(s):  
Luca D. Bertzbach ◽  
Wing-Hang Ip ◽  
Thomas Dobner
Keyword(s):  
Animal Models ◽  
Clinical Symptoms ◽  
Cell Transformation ◽  
Human Adenovirus ◽  
Upper Respiratory Tract ◽  
Tree Shrews ◽  
Cotton Rats ◽  
In Vitro Systems ◽  
Tract Disease

Human adenovirus (HAdV) infections cause a wide variety of clinical symptoms, ranging from mild upper respiratory tract disease to lethal outcomes, particularly in immunocompromised individuals. To date, neither widely available vaccines nor approved antiadenoviral compounds are available to efficiently deal with HAdV infections. Thus, there is a need to thoroughly understand HAdV-induced disease, and for the development and preclinical evaluation of HAdV therapeutics and/or vaccines, and consequently for suitable standardizable in vitro systems and animal models. Current animal models to study HAdV pathogenesis, persistence, and tumorigenesis include rodents such as Syrian hamsters, mice, and cotton rats, as well as rabbits. In addition, a few recent studies on other species, such as pigs and tree shrews, reported promising data. These models mimic (aspects of) HAdV-induced pathological changes in humans and, although they are relevant, an ideal HAdV animal model has yet to be developed. This review summarizes the available animal models of HAdV infection with comprehensive descriptions of virus-induced pathogenesis in different animal species. We also elaborate on rodent HAdV animal models and how they contributed to insights into adenovirus-induced cell transformation and cancer.

scholarly journals The Role of Stress Regulation on Neural Plasticity in Pain Chronification

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Xiaoyun Li ◽  
Li Hu
Keyword(s):  
Chronic Pain ◽  
Animal Models ◽  
Neural Plasticity ◽  
Clinical Symptoms ◽  
Brain Plasticity ◽  
Brain Regions ◽  
Stress Regulation ◽  
Pain Chronification ◽  
A Chain

Pain, especially chronic pain, is one of the most common clinical symptoms and has been considered as a worldwide healthcare problem. The transition from acute to chronic pain is accompanied by a chain of alterations in physiology, pathology, and psychology. Increasing clinical studies and complementary animal models have elucidated effects of stress regulation on the pain chronification via investigating activations of the hypothalamic-pituitary-adrenal (HPA) axis and changes in some crucial brain regions, including the amygdala, prefrontal cortex, and hippocampus. Although individuals suffer from acute pain benefit from such physiological alterations, chronic pain is commonly associated with maladaptive responses, like the HPA dysfunction and abnormal brain plasticity. However, the causal relationship among pain chronification, stress regulation, and brain alterations is rarely discussed. To call for more attention on this issue, we review recent findings obtained from clinical populations and animal models, propose an integrated stress model of pain chronification based on the existing models in perspectives of environmental influences and genetic predispositions, and discuss the significance of investigating the role of stress regulation on brain alteration in pain chronification for various clinical applications.

scholarly journals Pathogenesis of Human Metapneumovirus Lung Infection in BALB/c Mice and Cotton Rats

2005 ◽  
Vol 79 (14) ◽  
pp. 8894-8903 ◽  
Author(s):  
Marie-Ève Hamelin ◽  
Kevin Yim ◽  
Katie H. Kuhn ◽  
Rose P. Cragin ◽  
Marina Boukhvalova ◽  
...  
Keyword(s):  
Animal Models ◽  
Viral Replication ◽  
Clinical Symptoms ◽  
Small Animal ◽  
Human Metapneumovirus ◽  
Viral Loads ◽  
Inflammatory Protein ◽  
Cotton Rats ◽  
Tract Infections ◽  
Rats And Mice

ABSTRACT Human metapneumovirus (hMPV) is a newly described member of the Paramyxoviridae family causing acute respiratory tract infections, especially in young children. We studied the pathogenesis of this viral infection in two experimental small animal models (BALB/c mice and cotton rats). Significant viral replication in the lungs of both animals was found following an intranasal challenge of 108 50% tissue culture infectious doses (TCID50) and persisted for <2 and <3 weeks in the case of cotton rats and mice, respectively. Peak viral loads were found on day 5 postinfection in both mice (mean of 1.92 × 107 TCID50/g lung) and cotton rats (mean of 1.03 × 105 TCID50/g). Clinical symptoms consisting of breathing difficulties, ruffled fur, and weight loss were noted in mice only around the time of peak viral replication. Most significant pulmonary inflammatory changes and peak expression of macrophage inflammatory protein 1α, gamma interferon, and RANTES occurred at the time of maximal viral replication (day 5) in both models. Cellular infiltration occurred predominantly around and within alveoli and persisted for at least 21 days in mice, whereas it was more limited in time with more peribronchiolitis in cotton rats. Both animal models would be of great value in evaluating different therapeutic agents, as well as vaccine candidates against hMPV.

scholarly journals Proteomics of Multiple Sclerosis: Inherent Issues in Defining the Pathoetiology and Identifying (Early) Biomarkers

2021 ◽  
Vol 22 (14) ◽  
pp. 7377
Author(s):  
Monokesh K. Sen ◽  
Mohammed S. M. Almuslehi ◽  
Peter J. Shortland ◽  
David A. Mahns ◽  
Jens R. Coorssen
Keyword(s):  
Multiple Sclerosis ◽  
Animal Models ◽  
Demyelinating Disease ◽  
Clinical Symptoms ◽  
Literature Mining ◽  
Targeted Therapeutics ◽  
Single Model ◽  
Human Central Nervous System ◽  
Early Biomarkers ◽  
Analytical Approaches

Multiple Sclerosis (MS) is a demyelinating disease of the human central nervous system having an unconfirmed pathoetiology. Although animal models are used to mimic the pathology and clinical symptoms, no single model successfully replicates the full complexity of MS from its initial clinical identification through disease progression. Most importantly, a lack of preclinical biomarkers is hampering the earliest possible diagnosis and treatment. Notably, the development of rationally targeted therapeutics enabling pre-emptive treatment to halt the disease is also delayed without such biomarkers. Using literature mining and bioinformatic analyses, this review assessed the available proteomic studies of MS patients and animal models to discern (1) whether the models effectively mimic MS; and (2) whether reasonable biomarker candidates have been identified. The implication and necessity of assessing proteoforms and the critical importance of this to identifying rational biomarkers are discussed. Moreover, the challenges of using different proteomic analytical approaches and biological samples are also addressed.

scholarly journals Bioactivities and mechanisms of natural medicines in the management of pulmonary arterial hypertension

2022 ◽  
Vol 17 (1) ◽  
Author(s):  
Zhijie Yu ◽  
Jun Xiao ◽  
Xiao Chen ◽  
Yi Ruan ◽  
Yang Chen ◽  
...  
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Animal Models ◽  
Arterial Hypertension ◽  
Clinical Symptoms ◽  
Treatment Strategies ◽  
Terminal Phase ◽  
Pharmacokinetic Studies ◽  
Natural Medicine ◽  
Pulmonary Arterial ◽  
Natural Medicines

AbstractPulmonary arterial hypertension (PAH) is a progressive and rare disease without obvious clinical symptoms that shares characteristics with pulmonary vascular remodeling. Right heart failure in the terminal phase of PAH seriously threatens the lives of patients. This review attempts to comprehensively outline the current state of knowledge on PAH its pathology, pathogenesis, natural medicines therapy, mechanisms and clinical studies to provide potential treatment strategies. Although PAH and pulmonary hypertension have similar pathological features, PAH exhibits significantly elevated pulmonary vascular resistance caused by vascular stenosis and occlusion. Currently, the pathogenesis of PAH is thought to involve multiple factors, primarily including genetic/epigenetic factors, vascular cellular dysregulation, metabolic dysfunction, even inflammation and immunization. Yet many issues regarding PAH need to be clarified, such as the “oestrogen paradox”. About 25 kinds monomers derived from natural medicine have been verified to protect against to PAH via modulating BMPR2/Smad, HIF-1α, PI3K/Akt/mTOR and eNOS/NO/cGMP signalling pathways. Yet limited and single PAH animal models may not corroborate the efficacy of natural medicines, and those natural compounds how to regulate crucial genes, proteins and even microRNA and lncRNA still need to put great attention. Additionally, pharmacokinetic studies and safety evaluation of natural medicines for the treatment of PAH should be undertaken in future studies. Meanwhile, methods for validating the efficacy of natural drugs in multiple PAH animal models and precise clinical design are also urgently needed to promote advances in PAH. Graphical Abstract

scholarly journals Decompressive Pathology in Cetaceans Based on an Experimental Pathological Model

2021 ◽  
Vol 8 ◽  
Author(s):  
Alicia Velázquez-Wallraf ◽  
Antonio Fernández ◽  
Maria José Caballero ◽  
Andreas Møllerløkken ◽  
Paul D. Jepson ◽  
...  
Keyword(s):  
Animal Models ◽  
Experimental Animal ◽  
Clinical Symptoms ◽  
Decompression Sickness ◽  
Rabbit Model ◽  
Clinical Syndrome ◽  
Histopathological Analysis ◽  
Gas Embolism ◽  
Diving Medicine ◽  
Beaked Whales

Decompression sickness (DCS) is a widely known clinical syndrome in human medicine, mainly in divers, related to the formation of intravascular and extravascular gas bubbles. Gas embolism and decompression-like sickness have also been described in wild animals, such as cetaceans. It was hypothesized that adaptations to the marine environment protected them from DCS, but in 2003, decompression-like sickness was described for the first time in beaked whales, challenging this dogma. Since then, several episodes of mass strandings of beaked whales coincidental in time and space with naval maneuvers have been recorded and diagnosed with DCS. The diagnosis of human DCS is based on the presence of clinical symptoms and the detection of gas embolism by ultrasound, but in cetaceans, the diagnosis is limited to forensic investigations. For this reason, it is necessary to resort to experimental animal models to support the pathological diagnosis of DCS in cetaceans. The objective of this study is to validate the pathological results of cetaceans through an experimental rabbit model wherein a complete and detailed histopathological analysis was performed. Gross and histopathological results were very similar in the experimental animal model compared to stranded cetaceans with DCS, with the presence of gas embolism systemically distributed as well as emphysema and hemorrhages as primary lesions in different organs. The experimental data reinforces the pathological findings found in cetaceans with DCS as well as the hypothesis that individuality plays an essential role in DCS, as it has previously been proposed in animal models and human diving medicine.

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