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1
Pikman, R., S. Kivity, Y. Levy, M.-T. Arango, J. Chapman, H. Yonath, Y. Shoenfeld, and S. G. Gofrit. "Neuropsychiatric SLE: from animal model to human." Lupus 26, no. 5 (April 2017): 470–77. http://dx.doi.org/10.1177/0961203317694261.
Анотація:
Animal models are a key element in disease research and treatment. In the field of neuropsychiatric lupus research, inbred, transgenic and disease-induced mice provide an opportunity to study the pathogenic routes of this multifactorial illness. In addition to achieving a better understanding of the immune mechanisms underlying the disease onset, supplementary metabolic and endocrine influences have been discovered and investigated. The ever-expanding knowledge about the pathologic events that occur at disease inception enables us to explore new drugs and therapeutic approaches further and to test them using the same animal models. Discovery of the molecular targets that constitute the pathogenic basis of the disease along with scientific advancements allow us to target these molecules with monoclonal antibodies and other specific approaches directly. This novel therapy, termed “targeted biological medication” is a promising endeavor towards producing drugs that are more effective and less toxic. Further work to discover additional molecular targets in lupus’ pathogenic mechanism and to produce drugs that neutralize their activity is needed to provide patients with safe and efficient methods of controlling and treating the disease.
2
Andersson, Leif. "Fisher’s quantitative genetic model and the molecular genetics of multifactorial traits." Journal of Animal Breeding and Genetics 135, no. 6 (October 2018): 391–92. http://dx.doi.org/10.1111/jbg.12362.
3
Von Diemen, Vinicius, Eduardo Neubarth Trindade, and Manoel Roberto Maciel Trindade. "Experimental model to induce obesity in rats." Acta Cirurgica Brasileira 21, no. 6 (December 2006): 425–29. http://dx.doi.org/10.1590/s0102-86502006000600013.
Анотація:
The etiology of obesity is multifactorial and is becoming a problem of public health, due to its increased prevalence and the consequent repercussion of its comorbidities on the health of the population. The great similarity and homology between the genomes of rodents and humans make these animal models a major tool to study conditions affecting humans, which can be simulated in rats. Obesity can be induced in animals by neuroendocrine, dietary or genetic changes. The most widely used models to induce obesity in rats are a lesion of the ventromedial hypothalamic nucleus (VMH) by administering monosodium glutamate or a direct electrical lesion, ovariectomy, feeding on hypercaloric diets and genetic manipulation for obesity.
4
Nakhleh-Francis, Yara, Yaseen Awad-Igbaria, Reem Sakas, Sarina Bang, Saher Abu-Ata, Eilam Palzur, Lior Lowenstein, and Jacob Bornstein. "Exploring Localized Provoked Vulvodynia: Insights from Animal Model Research." International Journal of Molecular Sciences 25, no. 8 (April 11, 2024): 4261. http://dx.doi.org/10.3390/ijms25084261.
Анотація:
Provoked vulvodynia represents a challenging chronic pain condition, characterized by its multifactorial origins. The inherent complexities of human-based studies have necessitated the use of animal models to enrich our understanding of vulvodynia’s pathophysiology. This review aims to provide an exhaustive examination of the various animal models employed in this research domain. A comprehensive search was conducted on PubMed, utilizing keywords such as “vulvodynia”, “chronic vulvar pain”, “vulvodynia induction”, and “animal models of vulvodynia” to identify pertinent studies. The search yielded three primary animal models for vulvodynia: inflammation-induced, allergy-induced, and hormone-induced. Additionally, six agents capable of triggering the condition through diverse pathways were identified, including factors contributing to hyperinnervation, mast cell proliferation, involvement of other immune cells, inflammatory cytokines, and neurotransmitters. This review systematically outlines the various animal models developed to study the pathogenesis of provoked vulvodynia. Understanding these models is crucial for the exploration of preventative measures, the development of novel treatments, and the overall advancement of research within the field.
5
Olexová, Lucia, Tomáš Senko, Peter Štefánik, Alžbeta Talarovičová, and Lucia Kršková. "Habituation of exploratory behaviour in VPA rats: animal model of autism." Interdisciplinary Toxicology 6, no. 4 (December 1, 2013): 222–27. http://dx.doi.org/10.2478/intox-2013-0033.
Анотація:
ABSTRACT Autism is a neurodevelopmental disorder with multifactorial aetiology, represented as impairment in social behaviour, communication and the occurrence of repetitive activities, which can be observed in the early life. The core features are frequently accompanied by other manifestations, including limited environmental exploration. The aim of the presented study, realised on an animal model of autism - VPA rats, i.e. animals prenatally affected with valproic acid on gestation day 12.5, was to investigate the habituation process of exploratory activity (manifested by a gradual decrease in the intensity of locomotor activity), which reflects the stage of the central nervous system. VPA rats were tested in open-field in three developmental periods - weaning (postnatal day 21 - PND 21), puberty (PND 42) and adulthood (PND 72). In each period of ontogenesis, the rapidity of habituation was evaluated by using the method of linear regression. Compared to controls, VPA rats showed a significant decrease in the intensity and an increase in the rapidity of exploratory activity habituation during puberty and adulthood. Our results indicate that the animal model of autism, i.e. VPA rats, showed disabilities in the development of the nervous system. These findings can help confirm not only the validity of this animal model of autism but can also help better understand neuronal changes in humans with autism
6
Netto, Cesar de Cesar, Zijun Zhang, Mario Lobao Goncalves, Chris Cychosz, Shuyuan Li, Kyle R. Duchman, Jessica E. Goetz, John E. Femino, Ruth Chimenti, and Lew C. Schon. "Mechanical Overload Followed by Consecutive Collagenase Injections: Developing a Multifactorial and Long-Lasting Animal Model of Induced Achilles Tendinopathy." Foot & Ankle Orthopaedics 5, no. 4 (October 1, 2020): 2473011420S0003. http://dx.doi.org/10.1177/2473011420s00034.
Анотація:
Category: Basic Sciences/Biologics; Hindfoot; Sports Introduction/Purpose: Different animal models of Achilles tendinopathy have been proposed in the literature. They usually involve the induction of tendinopathic findings by either chemical stress (most commonly with one or more injections of collagenase, mimicking intrinsic factors) or mechanical stress (by repetitive exercise-induced stress with treadmill running exercises, simulating extrinsic risk factors). To date, no study has evaluated the combination of a mechanical trigger followed by collagenase injections, replicating the logical and sequential steps involved in the development the human pathology. Our goal was to develop this novel animal model of Achilles tendinopathy and to compare histological and functional findings with animals subjected to isolated mechanical or chemical stress, as well as to controls. Methods: Sixty-four Sprague-Dawley rats were divided into four groups (n=16): isolated treadmill running protocol (15o uphill running, 20meters/minute, 1hour/day, 3 weeks duration, weeks 2-4); isolated injections of collagenase (0.1mg each, 3 injections total, weeks 5-7); treadmill protocol (weeks 2-4) followed by three consecutive collagenase injections (weeks 5-7); and controls, no running and three injections of normal saline (weeks 5-7). Five animals from each group were sacrificed at weeks 8 and 10. Six animals by group were sacrificed at week 12. Gait analysis was performed at weeks one (after acclimation), five (following running protocol), eight (following injection protocol) and twelve (just before latest sacrifice time-point). Histological findings were assessed by the Movin Tendinopathy Score (eight parameters, scored from 0-3, total score 0-24), assessing collagen arrangement, structure, and stainability, cellularity, vascularity, nuclear rounding, hyalinization and presence of glycosaminoglycans. Gait parameters included stand and swing times, stride length, duty cycle and swing length. Results: After 8 weeks, significantly increased tendinopathic scores (p<0.001) were found in animals subjected to collagenase injections (16, CI 13.1-18.9) and to running/collagenase (17.4, CI 14.4-20.3), when compared to controls (1.6, CI -1.3-4.50) and running (3, CI 0.1-5.9). Similarly, after 10 weeks significantly increased scores were found in the same groups, with slight severity regression: controls (1, CI -0.8-2.8), running (2.2, CI 0.4-4.0), collagenase (10, CI 8.2-11.8) and running/collagenase (17.6, CI 15.8- 19.4). After 12 weeks, collagenase group demonstrated reversion of the findings (3.3, CI 1.6-5.1), and wasn’t different than control (2.1, CI 0.4-3.9) and running groups (2.5, CI 0.3-4.7). However, significantly increased pathological findings were noted in the running/collagenase group (20.0, CI 18.2-21.8) consistent with chronic tendinopathic process. Gait analysis results presented in Figure1. Conclusion: When compared to other models of induced Achilles tendinopathy and to controls, the novel animal model induced by a mechanical trigger and sustained by chemical stress demonstrated progressively increased histological tendinopathic scores after 12 weeks. Findings observed after isolated mechanical or chemical stresses were temporary, not maintained at latest follow- up. Steps involved in tendinopathy development, as well as the observed histological results of the combined running/collagenase model, replicate better the findings of human chronic Achilles tendinopathy. Applications for this novel model are promising, potentially supporting a better understanding of early/late findings as well as treatment options for Achilles tendinopathy. [Figure: see text]
7
Ureshino, Rodrigo Portes, Angelica Jardim Costa, Adolfo Garcia Erustes, Gustavo José da Silva Pereira, Rita Sinigaglia-Coimbra, and Soraya Soubhi Smaili. "Effects of Aging in the Striatum and Substantia Nigra of a Parkinson’s Disease Animal Model." Toxicologic Pathology 46, no. 3 (April 2018): 348–58. http://dx.doi.org/10.1177/0192623318767065.
Анотація:
Aging is a multifactorial process associated with functional deficits, and the brain is more prone to developing chronic degenerative diseases such as Parkinson’s disease. Several groups have tried to correlate the age-related ultrastructural alterations to the neurodegeneration process using in vivo pharmacological models, but due to the limitations of the animal models, particularly in aged animals, the results are difficult to interpret. In this work, we investigated neurodegeneration induced by rotenone, as a pharmacological model of Parkinson’s disease, in both young and aged Wistar rats. We assessed animal mobility, tyrosine hydroxylase staining in the substantia nigra pars compacta (SNpc), and TdT-mediated dUTP-biotin nick end labeling-positive nuclei and reactive oxygen species production in the striatum. Interestingly, the mobility impairment, dopaminergic neuron loss, and elevated number of apoptotic nuclei in the striatum of aged control rats were similar to young rotenone-treated animals. Moreover, we observed many ultrastructural alterations, such as swollen mitochondria in the striatum, and massive lipofuscin deposits in the SNpc of the aged rotenone-treated animals. We conclude that the rotenone model can be employed to explore age-related alterations in the ontogeny that can increase vulnerability in the striatum and SNpc, which may contribute to Parkinson’s disease pathogenesis.
8
Sauer, Sven W., Silvana Opp, Shoko Komatsuzaki, Anna-Eva Blank, Michel Mittelbronn, Peter Burgard, D. M. Koeller, Jürgen G. Okun, and Stefan Kölker. "Multifactorial modulation of susceptibility to l-lysine in an animal model of glutaric aciduria type I." Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 1852, no. 5 (May 2015): 768–77. http://dx.doi.org/10.1016/j.bbadis.2014.12.022.
9
Perše, Martina, and Anton Cerar. "Dextran Sodium Sulphate Colitis Mouse Model: Traps and Tricks." Journal of Biomedicine and Biotechnology 2012 (2012): 1–13. http://dx.doi.org/10.1155/2012/718617.
Анотація:
Inflammatory bowel disease (IBD) is a complex multifactorial disease of unknown etiology. Thus, dozens of different animal models of IBD have been developed in past decades. Animal models of IBD are valuable and indispensable tools that provide a wide range of options for investigating involvement of various factors into the pathogenesis of IBD and to evaluate different therapeutic options. However, the dextran sulphate sodium (DSS-) induced colitis model has some advantages when compared to other animal models of colitis. It is well appreciated and widely used model of inflammatory bowel disease because of its simplicity. It has many similarities to human IBD, which are mentioned in the paper. In spite of its simplicity and wide applicability, there are also traps that need to be taken into account when using DSS model. As demonstrated in the present paper, various factors may affect susceptibility to DSS-induced lesions and modify results.
10
Zerani, Massimo, Angela Polisca, Cristiano Boiti, and Margherita Maranesi. "Current Knowledge on the Multifactorial Regulation of Corpora Lutea Lifespan: The Rabbit Model." Animals 11, no. 2 (January 25, 2021): 296. http://dx.doi.org/10.3390/ani11020296.
Анотація:
Our research group studied the biological regulatory mechanisms of the corpora lutea (CL), paying particular attention to the pseudopregnant rabbit model, which has the advantage that the relative luteal age following ovulation is induced by the gonadotrophin-releasing hormone (GnRH). CL are temporary endocrine structures that secrete progesterone, which is essential for maintaining a healthy pregnancy. It is now clear that, besides the classical regulatory mechanism exerted by prostaglandin E2 (luteotropic) and prostaglandin F2 (luteolytic), a considerable number of other effectors assist in the regulation of CL. The aim of this paper is to summarize our current knowledge of the multifactorial mechanisms regulating CL lifespan in rabbits. Given the essential role of CL in reproductive success, a deeper understanding of the regulatory mechanisms will provide us with valuable insights on various reproductive issues that hinder fertility in this and other mammalian species, allowing to overcome the challenges for new and more efficient breeding strategies.
11
Baydi, Zineb, Youness Limami, Loubna Khalki, Nabil Zaid, Abdallah Naya, El Mostafa Mtairag, Mounia Oudghiri, and Younes Zaid. "An Update of Research Animal Models of Inflammatory Bowel Disease." Scientific World Journal 2021 (December 13, 2021): 1–12. http://dx.doi.org/10.1155/2021/7479540.
Анотація:
Inflammatory bowel disease (IBD) is a group of chronic disorders that includes two main disease forms, Crohn’s disease, and ulcerative colitis. The understanding of the intestinal inflammation occurring in IBD has been immeasurably advanced by the development of the now numerous murine models of intestinal inflammation. The usefulness of this research tool in IBD arises from a convergence of underlying genetic susceptibility, immune system dysfunction, environmental factors, and shifts in gut microbiota. Due to the multifactorial feature of these diseases, different animal models have been used to investigate the underlying mechanisms and develop potential therapeutic strategies. The results of preclinical efficacy studies often inform the progression of therapeutic strategies. This review describes the distinct feature and limitations of each murine IBD model and discusses the previous and current lessons from the IBD models.
12
Tsai, Teresa, Sabrina Reinehr, Leonie Deppe, Alexandra Strubbe, Nils Kluge, H. Burkhard Dick, and Stephanie C. Joachim. "Glaucoma Animal Models beyond Chronic IOP Increase." International Journal of Molecular Sciences 25, no. 2 (January 11, 2024): 906. http://dx.doi.org/10.3390/ijms25020906.
Анотація:
Glaucoma is a complex and multifactorial disease defined as the loss of retinal ganglion cells (RGCs) and their axons. Besides an elevated intraocular pressure (IOP), other mechanisms play a pivotal role in glaucoma onset and progression. For example, it is known that excitotoxicity, immunological alterations, ischemia, and oxidative stress contribute to the neurodegeneration in glaucoma disease. To study these effects and to discover novel therapeutic approaches, appropriate animal models are needed. In this review, we focus on various glaucoma animal models beyond an elevated IOP. We introduce genetically modified mice, e.g., the optineurin E50K knock-in or the glutamate aspartate transporter (GLAST)-deficient mouse. Excitotoxicity can be mimicked by injecting the glutamate analogue N-methyl-D-aspartate intravitreally, which leads to rapid RGC degeneration. To explore the contribution of the immune system, the experimental autoimmune glaucoma model can serve as a useful tool. Here, immunization with antigens led to glaucoma-like damage. The ischemic mechanism can be mimicked by inducing a high IOP for a certain amount of time in rodents, followed by reperfusion. Thereby, damage to the retina and the optic nerve occurs rapidly after ischemia/reperfusion. Lastly, we discuss the importance of optic nerve crush models as model systems for normal-tension glaucoma. In summary, various glaucoma models beyond IOP increase can be utilized.
13
Sztuka, Katarzyna, Daria Orszulak-Michalak, and Magdalena Jasińska-Stroschein. "Application of animal models in experimental medicine on the basis of pulmonary hypertension." Postępy Higieny i Medycyny Doświadczalnej 72 (July 22, 2018): 686–700. http://dx.doi.org/10.5604/01.3001.0012.2057.
Анотація:
Pulmonary hypertension (PH) is a rare disorder with a severe course. Despite significant progress in diagnosis and therapy, PH is an incurable disease with a high mortality rate. Current pharmacotherapy improves the patient’s quality of life and prolongs his/her longevity, but it does not completely reverse pathological and haemodynamic changes. This might result from the multifactorial pathomechanism of the disease, which includes multiple signaling pathways. There is a need to develop novel therapies. In order to achieve this purpose, preclinical experiments are made, for instance, on animal models. Identification of potentially effective substances for further evaluation in clinical trials is determined by a variety of factors, including the selection of an appropriate test model. An ideal animal model that fully reflects the human form of pulmonary hypertension has not been identified, as yet. Generally, studies are conducted on classical models, including the chronic hypoxia model (CH) and monocrotaline model (MCT). This study presents selected animal models of pulmonary hypertension, which are used in efficiency tests on potentially new drugs as well as a mechanism of action of PH inductors and both haemodynamic and histopathological changes, characteristic for each model. The technique and conditions for the induction of pulmonary hypertension are discussed for selected methods. The authors emphasized interspecific differences in experimental animals. The article also summarizes potential benefits and limitations of animal models of pulmonary hypertension in preclinical studies, with consideration given to the repeatability and predictability of results, the cost of experiments, the toxicity of PH inductors and the comparability between haemodynamic and histopathological changes, induced in animals, and changes in the clinical picture of pulmonary hypertension in humans.
14
Panina, Yulia A., Olga L. Lopatina, Angelina I. Mosyagina, Yulia K. Komleva, Andrey V. Morgun, Yana V. Gorina, and Elena D. Hilazheva. "Neurobehavioral Testing as Cognitive Function Evaluation tool in Experimentally Induced Neurodegeneration in Mice." Annals of Clinical and Experimental Neurology 17, no. 4 (January 5, 2024): 72–81. http://dx.doi.org/10.54101/acen.2023.4.9.
Анотація:
Neurodegeneration is a complex and multifactorial process presenting one of the major issues of fundamental science and clinical medicine due to its high prevalence, multiple nosological entities, and variations in pathogenesis. Translational research contributes to the study of neurodegenerative diseases, with modeling of such pathologies being an important part of this research. Behavioral testing in various animal models of neurodegenerative diseases allows to assess the model validity and reliability, as well as to investigate the potential efficacy of pharmacotherapy and other management approaches. In this overview we present test batteries that evaluate behavior, cognitive performance, and emotional states in animals with experimentally induced neurodegeneration.
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Rahman, Md Mahbubur, Dong Hyun Kim, Chul-Kyu Park, and Yong Ho Kim. "Experimental Models, Induction Protocols, and Measured Parameters in Dry Eye Disease: Focusing on Practical Implications for Experimental Research." International Journal of Molecular Sciences 22, no. 22 (November 9, 2021): 12102. http://dx.doi.org/10.3390/ijms222212102.
Анотація:
Dry eye disease (DED) is one of the major ophthalmological healthcare challenges worldwide. DED is a multifactorial disease characterized by a loss of homeostasis of the tear film, and its main pathogenesis is chronic ocular surface inflammation related with various cellular and molecular signaling cascades. The animal model is a reliable and effective tool for understanding the various pathological mechanisms and molecular cascades in DED. Considerable experimental research has focused on developing new strategies for the prevention and treatment of DED. Several experimental models of DED have been developed, and different animal species such as rats, mice, rabbits, dogs, and primates have been used for these models. Although the basic mechanisms of DED in animals are nearly identical to those in humans, proper knowledge about the induction of animal models is necessary to obtain better and more reliable results. Various experimental models (in vitro and in vivo DED models) were briefly discussed in this review, along with pathologic features, analytical approaches, and common measurements, which will help investigators to use the appropriate cell lines, animal, methods, and evaluation parameters depending on their study design.
16
Lee, Won-Seok, and Bo-Eun Yoon. "Necessity of an Integrative Animal Model for a Comprehensive Study of Attention-Deficit/Hyperactivity Disorder." Biomedicines 11, no. 5 (April 24, 2023): 1260. http://dx.doi.org/10.3390/biomedicines11051260.
Анотація:
Animal models of attention-deficit/hyperactivity disorder (ADHD) have been used to study and understand the behavioral, neural, and physiological mechanisms underlying ADHD. These models allow researchers to conduct controlled experiments and manipulate specific brain regions or neurotransmitter systems to investigate the underlying causes of ADHD and test potential drug targets or treatments. However, it is essential to note that while these models can provide valuable insights, they do not ideally mimic the complex and heterogeneous nature of ADHD and should be interpreted cautiously. Additionally, since ADHD is a multifactorial disorder, environmental and epigenetic factors should be considered simultaneously. In this review, the animal models of ADHD reported thus far are classified into genetic, pharmacological, and environmental models, and the limitations of the representative models are discussed. Furthermore, we provide insights into a more reliable alternative model for the comprehensive study of ADHD.
17
Hoff, Catherine M. "Experimental Animal Models of Encapsulating Peritoneal Sclerosis." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 25, no. 4_suppl (April 2005): 57–66. http://dx.doi.org/10.1177/089686080502504s08.
Анотація:
Encapsulating peritoneal sclerosis (EPS) is an infrequent, but extremely serious complication of long-term peritoneal dialysis. The cause of EPS is unclear, but the low incidence suggests that it is most likely multifactorial. The elucidation of developmental pathways and predictive markers of EPS would facilitate the identification and management of high-risk patients. Animal models are often used to define pathways of disease progression and to test strategies for treatment and prevention in the patient population. Ideally such models could help to define the cause of EPS and its developmental pathways, to facilitate the identification of contributing factors and predictive markers, and to provide a system to test therapeutic strategies. Researchers have studied several rodent models of EPS that rely on chronic chemical irritation (for example, bleach, low-pH solution, chlorhexidine gluconate) to induce peritoneal sclerosis and abdominal encapsulation. Development in all models is progressive, with inflammation giving way to peritoneal fibrosis or sclerosis with accumulating membrane damage, culminating in cocoon formation. Microscopic findings are similar to those proposed as diagnostic criteria for clinical EPS: an initial inflammatory infiltrate and submesothelial thickening, collagen deposition, and activation and proliferation of peritoneal fibroblasts. The potential to block progression of peritoneal sclerosis in these models by anti-inflammatory, antifibrotic, and antiangiogenic agents, and by inhibitors of the renin–angiotensin system have been demonstrated. Animal models based on clinically relevant risk factors (for example, uremia, peritonitis, and long-term exposure to dialysis solutions) now represent the next step in model development.
18
Tkacs, Nancy C., and Hilaire J. Thompson. "From Bedside to Bench and Back Again: Research Issues in Animal Models of Human Disease." Biological Research For Nursing 8, no. 1 (July 2006): 78–88. http://dx.doi.org/10.1177/1099800406289717.
Анотація:
To improve outcomes for patients with many serious clinical problems, multifactorial research approaches by nurse scientists, including the use of animal models, are necessary. Animal models serve as analogies for clinical problems seen in humans and must meet certain criteria, including validity and reliability, to be useful in moving research efforts forward. This article describes research considerations in the development of rodent models. As the standard of diabetes care evolves to emphasize intensive insulin therapy, rates of severe hypoglycemia are increasing among patients with type 1 and type 2 diabetes mellitus. A consequence of this change in clinical practice is an increase in rates of two hypoglycemia-related diabetes complications: hypoglycemia-associated autonomic failure (HAAF) and resulting hypoglycemia unawareness. Work on an animal model of HAAF is in an early developmental stage, with several labs reporting different approaches to model this complication of type 1 diabetes mellitus. This emerging model serves as an example illustrating how evaluation of validity and reliability is critically important at each stage of developing and testing animal models to support inquiry into human disease.
19
Assina, Rachid, Tejas Sankar, Nicholas Theodore, Sam P. Javedan, Alan R. Gibson, Kris M. Horn, Michael Berens, Volker K. H. Sonntag, and Mark C. Preul. "Activated autologous macrophage implantation in a large-animal model of spinal cord injury." Neurosurgical Focus 25, no. 5 (November 2008): E3. http://dx.doi.org/10.3171/foc.2008.25.11.e3.
Анотація:
Object Axonal regeneration may be hindered following spinal cord injury (SCI) by a limited immune response and insufficient macrophage recruitment. This limitation has been partially surmounted in small-mammal models of SCI by implanting activated autologous macrophages (AAMs). The authors sought to replicate these results in a canine model of partial SCI. Methods Six dogs underwent left T-13 spinal cord hemisection. The AAMs were implanted at both ends of the lesion in 4 dogs, and 2 other dogs received sham implantations of cell media. Cortical motor evoked potentials (MEPs) were used to assess electrophysiological recovery. Functional motor recovery was assessed with a modified Tarlov Scale. After 9 months, animals were injected with wheat germ agglutinin–horseradish peroxidase at L-2 and killed for histological assessment. Results Three of the 4 dogs that received AAM implants and 1 of the 2 negative control dogs showed clear recovery of MEP response. Behavioral assessment showed no difference in motor function between the AAM-treated and control groups. Histological investigation with an axonal retrograde tracer showed neither local fiber crossing nor significant uptake in the contralateral red nucleus in both implanted and negative control groups. Conclusions In a large-animal model of partial SCI treated with implanted AAMs, the authors saw no morphological or histological evidence of axonal regeneration. Although they observed partial electrophysiological and functional motor recovery in all dogs, this recovery was not enhanced in animals treated with implanted AAMs. Furthermore, there was no morphological or histological evidence of axonal regeneration in animals with implants that accounted for the observed recovery. The explanation for this finding is probably multifactorial, but the authors believe that the AAM implantation does not produce axonal regeneration, and therefore is a technology that requires further investigation before it can be clinically relied on to ameliorate SCI.
20
Morton, Rochelle, Michelle L. Hebart, and Alexandra L. Whittaker. "Explaining the Gap Between the Ambitious Goals and Practical Reality of Animal Welfare Law Enforcement: A Review of the Enforcement Gap in Australia." Animals 10, no. 3 (March 13, 2020): 482. http://dx.doi.org/10.3390/ani10030482.
Анотація:
Previous research has identified a number of issues arising at all stages of the animal law enforcement process. These issues contribute to an enforcement gap between the written law, as it relates to the penalties laid out in statutes, and the reality of the animal law justice system. This paper identifies and investigates the contributors to this gap. The identified factors discussed are (1) the role of the public in reporting animal cruelty, (2) the ambiguity of the language used in animal welfare legislation, (3) the nature of enforcement authorities, and (4) the role of the courts. Thus, the causes of the enforcement gap are multifactorial, derived from all stages of the enforcement process. Further research on the enforcement model and public education, in addition to debate on legislative reforms, will be needed to address this gap.
21
Estaphan, Suzanne, Alexandrina-Stefania Curpăn, Dalia Khalifa, Laila Rashed, Andrei Ciobica, Adrian Cantemir, Alin Ciobica, Constantin Trus, Mahmoud Ali, and Asmaa ShamsEldeen. "Combined Low Dose of Ketamine and Social Isolation: A Possible Model of Induced Chronic Schizophrenia-Like Symptoms in Male Albino Rats." Brain Sciences 11, no. 7 (July 11, 2021): 917. http://dx.doi.org/10.3390/brainsci11070917.
Анотація:
While animal models for schizophrenia, ranging from pharmacological models to lesions and genetic models, are available, they usually mimic only the positive symptoms of this disorder. Identifying a feasible model of chronic schizophrenia would be valuable for studying the possible underlying mechanism and to investigate emerging treatments. Our hypothesis starts from the observation that combining ketamine with isolation could result in long-lasting neuro-psychological deficits and schizophrenia-like features; thus, it could probably be used as the first model of chronic schizophrenia that emphasizes the characteristic of having a multifactorial etiology. By the means of this study, we investigated the effects of ketamine administration combined with isolation in inducing schizophrenia-like symptoms in male albino rats and the brain reactive oxygen species levels. Our results showed that the number of lines crossings in the open field test, the number of open arm entries in the elevated plus maze, and the spontaneous alternations percentage in the Y-maze were significantly lower in the ketamine + isolation group compared to both the control and ketamine + social housing group (p < 0.05). Furthermore, the ketamine + isolation intervention significantly increased the MDA levels and decreased the GPx levels both in the hippocampus and the cortex of the rats. In addition, our premise of creating a model capable of exhibiting both positive and negative symptoms of schizophrenia was also based on adding the aripiprazole treatment to a group of rats. Therefore, we compared the ketamine + social isolation group with the ketamine + social isolation + aripiprazole group in order to attempt to discover if the antipsychotic drug would significantly decrease the potential positive schizophrenia-like symptoms induced by social isolation and ketamine. Given that we obtained significant results, we cautiously presume that this might be an important step in developing our animal model capable of illustrating both positive and negative symptoms of schizophrenia. This study could be a first step towards the creation of a complex animal model capable of exhibiting the multifactorial origin and manifestation of schizophrenia.
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Yu, Jinyeong, Sanghyuk Choi, Aran Park, Jungbeom Do, Donghyun Nam, Youngjae Kim, Jinok Noh, Kil Yeon Lee, Chi Hoon Maeng, and Ki-Sook Park. "Bone Marrow Homeostasis Is Impaired via JAK/STAT and Glucocorticoid Signaling in Cancer Cachexia Model." Cancers 13, no. 5 (March 2, 2021): 1059. http://dx.doi.org/10.3390/cancers13051059.
Анотація:
Cancer cachexia is a multifactorial systemic inflammation disease caused by complex interactions between the tumor and host tissues via soluble factors. However, whether cancer cachexia affects the bone marrow, in particular the hematopoietic stem cells (HSCs) and mesenchymal stem cells (MSCs), remains unclear. Here, we investigated the bone marrow and bone in a cancer cachexia animal model generated by transplanting Lewis lung carcinoma cells. The number of bone marrow mononuclear cells (BM-MNCs) started to significantly decrease in the cancer cachectic animal model prior to the discernable loss of muscle and fat. This decrease in BM-MNCs was associated with myeloid skewing in the circulation and the expansion of hematopoietic progenitors in the bone marrow. Bone loss occurred in the cancer cachexia animal model and accompanied the decrease in the bone marrow MSCs that play important roles in both supporting HSCs and maintaining bone homeostasis. Glucocorticoid signaling mediated the decrease in bone marrow MSCs in the cancer cachectic environment. The cancer cachexia environment also skewed the differentiation of the bone marrow MSCs toward adipogenic fate via JAK/STAT as well as glucocorticoid signaling. Our results suggest that the bone loss induced in cancer cachexia is associated with the depletion and the impaired differentiation capacity of the bone marrow MSCs.
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Liu Chung Ming, Clara, Kimberly Sesperez, Eitan Ben-Sefer, David Arpon, Kristine McGrath, Lana McClements, and Carmine Gentile. "Considerations to Model Heart Disease in Women with Preeclampsia and Cardiovascular Disease." Cells 10, no. 4 (April 14, 2021): 899. http://dx.doi.org/10.3390/cells10040899.
Анотація:
Preeclampsia is a multifactorial cardiovascular disorder diagnosed after 20 weeks of gestation, and is the leading cause of death for both mothers and babies in pregnancy. The pathophysiology remains poorly understood due to the variability and unpredictability of disease manifestation when studied in animal models. After preeclampsia, both mothers and offspring have a higher risk of cardiovascular disease (CVD), including myocardial infarction or heart attack and heart failure (HF). Myocardial infarction is an acute myocardial damage that can be treated through reperfusion; however, this therapeutic approach leads to ischemic/reperfusion injury (IRI), often leading to HF. In this review, we compared the current in vivo, in vitro and ex vivo model systems used to study preeclampsia, IRI and HF. Future studies aiming at evaluating CVD in preeclampsia patients could benefit from novel models that better mimic the complex scenario described in this article.
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Poznyak, Anastasia V., Andrey V. Grechko, Reinhard Wetzker, and Alexander N. Orekhov. "In Search for Genes Related to Atherosclerosis and Dyslipidemia Using Animal Models." International Journal of Molecular Sciences 21, no. 6 (March 18, 2020): 2097. http://dx.doi.org/10.3390/ijms21062097.
Анотація:
Atherosclerosis is a multifactorial chronic disease that affects large arteries and may lead to fatal consequences. According to current understanding, inflammation and lipid accumulation are the two key mechanisms of atherosclerosis development. Animal models based on genetically modified mice have been developed to investigate these aspects. One such model is low-density lipoprotein (LDL) receptor knockout (KO) mice (ldlr−/−), which are characterized by a moderate increase of plasma LDL cholesterol levels. Another widely used genetically modified mouse strain is apolipoprotein-E KO mice (apoE−/−) that lacks the primary lipoprotein required for the uptake of lipoproteins through the hepatic receptors, leading to even greater plasma cholesterol increase than in ldlr−/− mice. These and other animal models allowed for conducting genetic studies, such as genome-wide association studies, microarrays, and genotyping methods, which helped identifying more than 100 mutations that contribute to atherosclerosis development. However, translation of the results obtained in animal models for human situations was slow and challenging. At the same time, genetic studies conducted in humans were limited by low sample sizes and high heterogeneity in predictive subclinical phenotypes. In this review, we summarize the current knowledge on the use of KO mice for identification of genes implicated in atherosclerosis and provide a list of genes involved in atherosclerosis-associated inflammatory pathways and their brief characteristics. Moreover, we discuss the approaches for candidate gene search in animals and humans and discuss the progress made in the field of epigenetic studies that appear to be promising for identification of novel biomarkers and therapeutic targets.
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Muthuvel vijayan K, Prabhu K, and Rajasankar S. "Aromatic spice Nutmeg attenuates memory deficits in Rotenone model of Parkinson’s disease." International Journal of Research in Pharmaceutical Sciences 11, no. 4 (September 26, 2020): 5441–47. http://dx.doi.org/10.26452/ijrps.v11i4.3173.
Анотація:
PD is a multifactorial neurodegenerative disorder with features such as tremor, rigidity, bradykinesia, postural instability, and dementia. Neuropathologically, selective loss or death of dopaminergic neurons is the hallmark of PD. In PD, elevated oxidative stress, mitochondrial dysfunction and neuroinflammation were reported. Rotenone (an isoflavone obtained from Fabaceae associated vegetation such as the jicama vine plant) induces oxidative stress, mitochondrial dysfunction, inflammation and apoptosis in cell line and animal models. It was useful in the evaluation of neuroprotective properties on cell line and animal models of PD. Drugs with anti-oxidant potential helped to control the cellular stress, free radical formation, neurotransmitter level in PD animal models. Nutmeg, an aromatic spice exhibited memory enhancing, anti-oxidant, anticonvulsant properties. It is an excellent body detoxifier and stimulator of the brain due to the presence of pharmacologically active compounds such as eugenol, isoelemicin, isoeugenol, methoxyeugenol, myristic acid, myristicin, saponins and lignin. Macelignan (a compound present in nutmeg) having the low molecular weight and hydrophobic nature could pass beyond the blood-brain barrier. In this study, we explored the cognitive profile of rotenone-induced model of PD treated with MFSE extract (MFSE) by behavioural tests (Morris water maze test, T-maze test and Elevated plus maze Test). Rotenone was injected to male Wistar albino rats by intra-peritoneal route (2.5mg/kg daily) for 30days. MFSE treated rats showed significant improvement in cognition in rotenone-induced PD model. It might be due to its neuroprotective and anti-cholinesterase properties.
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Mir, Franco Rafael, and María Angélica Rivarola. "Sex Differences in Anxiety and Depression: What Can (and Cannot) Preclinical Studies Tell Us?" Sexes 3, no. 1 (February 22, 2022): 141–63. http://dx.doi.org/10.3390/sexes3010012.
Анотація:
In recent years, the gender perspective in scientific research and sex differences in biological studies on emotional disorders have become increasingly important. However, sex bias in basic research on anxiety and depression is still far from being covered. This review addresses the study of sex differences in the field of anxiety and depression using animal models that consider this issue so far. What can preclinical studies tell us and what are their main limitations? First, we describe the behavioral tests most frequently used in preclinical research to assess depressive-like and anxiety-like behaviors in rodents. Then, we analyze the main findings, strengths, and weaknesses of rodent models of anxiety and depression, dividing them into three main categories: sex chromosome complement-biased sex differences; gonadal hormone-biased sex differences; environmental-biased sex differences. Regardless of the animal model used, none can reproduce all the characteristics of such complex and multifactorial pathologies as anxiety and depressive disorders; however, each animal model contributes to elucidating the bases that underlie these disorders. The importance is highlighted of considering sex differences in the responses that emerge from each model.
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Rubattu, Speranza, Rosita Stanzione, and Massimo Volpe. "Mitochondrial Dysfunction Contributes to Hypertensive Target Organ Damage: Lessons from an Animal Model of Human Disease." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–10. http://dx.doi.org/10.1155/2016/1067801.
Анотація:
Mechanisms underlying hypertensive target organ damage (TOD) are not completely understood. The pathophysiological role of mitochondrial oxidative stress, resulting from mitochondrial dysfunction, in development of TOD is unclear. The stroke-prone spontaneously hypertensive rat (SHRSP) is a suitable model of human hypertension and of its vascular consequences. Pathogenesis of TOD in SHRSP is multifactorial, being determined by high blood pressure levels, high salt/low potassium diet, and genetic factors. Accumulating evidence points to a key role of mitochondrial dysfunction in increased susceptibility to TOD development of SHRSP. Mitochondrial abnormalities were described in both heart and brain of SHRSP. Pharmacological compounds able to protect mitochondrial function exerted a significant protective effect on TOD development, independently of blood pressure levels. Through our research efforts, we discovered that two genes encoding mitochondrial proteins, one (Ndufc2) involved in OXPHOS complex I assembly and activity and the second one (UCP2) involved in clearance of mitochondrial ROS, are responsible, when dysregulated, for vascular damage in SHRSP. The suitability of SHRSP as a model of human disease represents a promising background for future translation of the experimental findings to human hypertension. Novel therapeutic strategies toward mitochondrial molecular targets may become a valuable tool for prevention and treatment of TOD in human hypertension.
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Smulders, D., V. Hautekiet, G. Verbeke, and R. Geers. "Tail and ear biting lesions in pigs: an epidemiological study." Animal Welfare 17, no. 1 (February 2008): 61–69. http://dx.doi.org/10.1017/s0962728600031997.
Анотація:
AbstractTail and ear biting lesions have a negative effect both on the animal welfare status of pigs (Sus scrofus) and the economical revenue of the pig farm. Tail biting behaviour is an unpredictable, abnormal behaviour that is thought to have a multifactorial origin. On-farm factors influencing tail biting have been described, but the real triggers are poorly understood. Much of the research into tail biting has been done on a small scale within a well-controlled environment and small sample sizes. This well-controlled environment is not always representative of the contemporary commercial conditions. Therefore, an observational epidemiological approach at farm level was adopted to gain a better insight into the factors influencing the occurrence of tail and ear biting lesions. Tail and ear biting lesions were observed at pen level three times a year on sixty farms across Belgium. A questionnaire was conducted to build a multifactorial model indicating different risk factors concerning the lesions scored. The temperature and the number of feeding places per animal in the nursery, the percentage of floor space covered with slats in the farrowing unit, the feed type in the growing unit and the overall hygiene policy were the most important indicators for the appearance of tail and ear biting lesions during fattening. The leave-one-out cross validation of the model demonstrated an intraclass correlation coefficient of 0.55 between the predicted model outcomes and the observed data. This epidemiological study provides important potential risk factors in relation to the incidence of tail and ear biting lesions. However, experimental and/or longitudinal studies have to confirm that the correlations found in this work are causal factors.
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Bourdy, Romain, and Katia Befort. "The Role of the Endocannabinoid System in Binge Eating Disorder." International Journal of Molecular Sciences 24, no. 11 (May 31, 2023): 9574. http://dx.doi.org/10.3390/ijms24119574.
Анотація:
Eating disorders are multifactorial disorders that involve maladaptive feeding behaviors. Binge eating disorder (BED), the most prevalent of these in both men and women, is characterized by recurrent episodes of eating large amounts of food in a short period of time, with a subjective loss of control over eating behavior. BED modulates the brain reward circuit in humans and animal models, which involves the dynamic regulation of the dopamine circuitry. The endocannabinoid system plays a major role in the regulation of food intake, both centrally and in the periphery. Pharmacological approaches together with research using genetically modified animals have strongly highlighted a predominant role of the endocannabinoid system in feeding behaviors, with the specific modulation of addictive-like eating behaviors. The purpose of the present review is to summarize our current knowledge on the neurobiology of BED in humans and animal models and to highlight the specific role of the endocannabinoid system in the development and maintenance of BED. A proposed model for a better understanding of the underlying mechanisms involving the endocannabinoid system is discussed. Future research will be necessary to develop more specific treatment strategies to reduce BED symptoms.
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Pommergaard, Hans-Christian, Michael Patrick Achiam, Jakob Burcharth, and Jacob Rosenberg. "Impaired Blood Supply in the Colonic Anastomosis in Mice Compromises Healing." International Surgery 100, no. 1 (January 1, 2015): 70–76. http://dx.doi.org/10.9738/intsurg-d-13-00191.1.
Анотація:
Abstract Colon anastomotic leakage has a multifactorial etiology and ischemia is considered one of the most important single factors. However, no existing animal models have established a direct link between ischemia and anastomotic leakage. The aim of this study was to establish a model of colon anastomotic leakage as a result of tissue ischemia. In colon anastomoses of 53 C57BL/6 mice, varying degrees of ischemia were induced. Supplying vessels were divided with bipolar coagulation in order to reduce anastomotic breaking strength and create clinical anastomotic leakage. Breaking strength of all the ischemic anastomoses were significantly lower compared with controls. Increasing ischemia resulted in higher rates of large bowel obstruction without creating anastomotic leakage. Healing was compromised as a result of impaired blood supply. However, clinical leakage was absent. Pure ischemia in otherwise healthy experimental animals may be too simple of an approach to create clinical leakage.
31
Khalifa, D., L. Rashed, A. Shamseldeen, and S. Stephan. "Combined Low Dose of Ketamine and Social Isolation: A Possible Model of Induced Chronic Schizophrenia-Like Symptoms." European Psychiatry 65, S1 (June 2022): S192. http://dx.doi.org/10.1192/j.eurpsy.2022.505.
Анотація:
Introduction Identifying a feasible model of chronic schizophrenia would be valuable for studying the possible underlying mechanism and to investigate emerging treatments. Our hypothesis starts from the observation that combining ketamine with isolation could result in long-lasting neuro-psychological deficits and schizophrenia-like features; thus, it could probably be used as the first model of chronic schizophrenia that emphasizes the characteristic of having a multifactorial etiology Objectives creation of a complex animal model capable of exhibiting the multifactorial origin and manifestation of schizophrenia. Methods we investigated the effects of ketamine administration combined with isolation in inducing schizophrenia-like symptoms in male albino rats and the brain reactive oxygen species levels. Results Our results showed that the number of lines crossings in the open field test, the number of open arm entries in the elevated plus maze, and the spontaneous alternations percentage in the Y-maze were significantly lower in the ketamine + isolation group compared to both the control and ketamine + social housing group (p < 0.05). Furthermore, the ketamine + isolation intervention significantly increased the MDA levels and decreased the GPx levels both in the hippocampus and the cortex of the rats. In addition, our premise of creating a model capable of exhibiting both positive and negative symptoms of schizophrenia was also based on adding the aripiprazole treatment to a group of rats Conclusions combining ketamine with isolation could result in long-lasting neuro-psychological deficits and schizophrenia-like features Disclosure No significant relationships.
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Kaledin, A. P., Yu A. Yuldashbaev, A. I. Filatov, A. M. Ostapchuk, D. V. Zhukov, V. M. Makeeva, and O. N. Golubeva. "Predicting the number of hunting animals in the State complex “Zavidovo” based on a mathematical model." Glavnyj zootehnik (Head of Animal Breeding), no. 11 (October 12, 2022): 3–14. http://dx.doi.org/10.33920/sel-03-2211-01.
Анотація:
It is necessary to predict the number of hunting animals under the conditions of the impact of endogenous and exogenous factors the habitat and economic use, for rational and inexhaustible their use. Understanding changes in the number of hunting animals is an important tool for managing hunting resources. Predicting of the number of hunting animals in the region as a rule, is based on trend models of population dynamics. In practice, the calculation and constructive method and the method of mathematical modeling have become the most widespread in predicting the population of hunting animals in dynamics. The computational and constructive method is based on the use of correlation and regression models, but it does not take into account the main indicators of population size formation: the fertility rate, which is formed on the basis of the specic weight of males, the percentage of yeldness and the number of calves (young animals) in the calving (litter), and the livability depending on the percentage of natural death and losses from poaching. The method of mathematical modeling involves the compilation of mathematical models and conducting model experiments to predict the number of species of hunting animals in dynamics. The relevance of this mathematical analysis lies in its multifactorial nature and rather high reliability. In the eld of predicting the number of hunting animals the modied P. H. Leslie model is of particular interest. The purpose of the work was to predict the number of wild ungulates (roe deer, elk, maral and spotted deer) in the Zavidovo State Complex in the Tver region until 2035. The use of the modied P. H. Leslie model makes it possible to predict the development of hunting animal populations both in the Zavidovo State Complex as a whole and in individual hunting areas with precise adjustment of models according to area parameters.
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KRYLIK, LYUDMILA. "DETERMINATION OF THE QUALITATIVE INFLUENCE OF FACTORS ON THE SENSITIVITY OF THE CAPACITIVE HUMIDITY SENSOR OF A TWO-LAYER STRUCTURE BASED ON MULTIFACTOR DISPERSION ANALYSIS." Herald of Khmelnytskyi National University. Technical sciences 319, no. 2 (April 27, 2023): 175–80. http://dx.doi.org/10.31891/2307-5732-2023-319-1-175-180.
Анотація:
A multifactorial dispersion analysis was applied in order to qualitatively assess the influence of the following factors: thickness of the moisture-sensitive layer; the thickness of the polymer coating as a protective layer; the concentration of the NaCl salt solution as an adsorbent material and their combined effect on the sensitivity of the capacitive humidity sensor of the two-layer structure. Capacitive humidity sensors of a two-layer structure, made on a sitall substrate, served as experimental samples. The copper film, which forms the covers of the capacitive humidity sensors, is applied to the surface of the sitall substrate in the form of a meander. In the developed design, the moisture-sensitive layer is hygroscopic salt, which performs the function of a dielectric. A moisture-absorbing film of polymethylmethacrylate serves as a protective layer. A multifactorial plan is developed for the case of three qualitative factors. Using multifactorial dispersion analysis, it was proved that the response of the model, that is, the sensitivity of the capacitive humidity sensor of the two-layer structure, is influenced by such factors as the thickness of the protective layer, the concentration of the NaCl salt solution, as well as the combined effect of factors such as the thickness of the moisture-sensitive layer + the concentration of the salt solution; the thickness of the protective layer + concentration of the salt solution. That is, the difference in the response values of the model is related to the change in the value of the factor and cannot be caused only by its random nature. However, the response of the model is significantly affected by the combined effect of the factor − the thickness of the protective layer + the concentration of the salt solution. In this case, the value of Fisher’s criterion, which is observed in the experiment, significantly exceeds the critical value of Fisher’s criterion F >Fkr (13.01>4.49). The influence of such factors as the thickness of the moisture-sensitive layer; the thickness of the moisture-sensitive layer + the thickness of the protective layer; the thickness of the moisture-sensitive layer + the thickness of the protective layer + the concentration of the salt solution is insignificant, that is, the difference in the response values of the model is due to its random nature. Using the dispersion analysis of the influence of the factor, it was proved that the sensitivity of capacitive humidity sensors is affected not only by the concentration of the NaCl salt solution, which was used to create a moisture-sensitive layer, but also by the design of the sensor.
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Tsai, Teresa, Pia Grotegut, Sabrina Reinehr, and Stephanie C. Joachim. "Role of Heat Shock Proteins in Glaucoma." International Journal of Molecular Sciences 20, no. 20 (October 18, 2019): 5160. http://dx.doi.org/10.3390/ijms20205160.
Анотація:
Glaucoma, one of the most common causes of blindness worldwide, is a multifactorial neurodegenerative disease characterized by damage of retinal ganglion cells and optic nerve degeneration. However, the exact mechanism leading to glaucoma is still not understood. Evidences suggest an immunological involvement in the pathogenesis. Among other immune responses, altered autoantibody patterns were found in glaucoma patients. Especially elevated antibody levels against heat shock proteins (HSPs), like HSP27 or HSP60, were identified. In an animal model, an immunization with these HSPs induced a pressure-independent retinal ganglion cell degeneration and axon loss, hence mimicking glaucoma-like damage. In addition, development of autoreactive antibodies, as well as a glia and T-cell activation, were described in these animals. Recently, we noted that intravitreal HSP27 injection likewise led to a degeneration of retinal ganglion cells and their axons. Therefore, HSP27 might have a direct damaging effect on retinal cells, and might play a key role in glaucoma.
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Kelt, Douglas A. "Academics, academia, and intellectual fulfilment: lessons from the career of an eminent mammalogist." Therya 14, no. 3 (September 29, 2023): 395–402. http://dx.doi.org/10.12933/therya-23-5264.
Анотація:
Dr. William (Bill) Lidicker, Jr., was a classically trained mammal biologist who played an important role in pushing the field of mammalogy from largely descriptive beginnings into conceptual arenas soundly rooted in theory and principles. Whereas many readers will know Bill primarily as the architect of a “multifactorial approach” to understanding population cyclicity in arvicoline rodents, less well-known is how Bill’s thematic focus shifted over the years. In an career that often prioritizes high-level productivity, I argue that Bill’s willingness to pursue novel themes provides an compelling model of how to live a rich and fulfilling life in academia.
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Nicas, Thalia I., and Barbara H. Iglewski. "The contribution of exoproducts to virulence of Pseudomonas aeruginosa." Canadian Journal of Microbiology 31, no. 4 (April 1, 1985): 387–92. http://dx.doi.org/10.1139/m85-074.
Анотація:
Pseudomonas aeruginosa produces a large number of extracellular products which may contribute to its virulence. We have employed a genetic approach to determine the contribution of toxin A, exoenzyme S, elastase and alkaline protease to the pathogenesis of P. aeruginosa. Mutations have been introduced with chemicals or transposons. Mutants have been identified using immunological, chemical, or toxicity assays. Mutants were extensively characterized in vitro to ascertain that they were identical to their parent strain except for the production of the desired product. Appropriate mutants were compared with their parent strains in several animal models: the burned mouse model, the mouse corneal infection model, and a rat model of chronic lung infection. The data indicate that virulence of P. aeruginosa is multifactorial. Further, the relative contribution of a given P. aeruginosa product may vary with the type of infection.
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Bonifacino, Tiziana, Roberta Arianna Zerbo, Matilde Balbi, Carola Torazza, Giulia Frumento, Ernesto Fedele, Giambattista Bonanno, and Marco Milanese. "Nearly 30 Years of Animal Models to Study Amyotrophic Lateral Sclerosis: A Historical Overview and Future Perspectives." International Journal of Molecular Sciences 22, no. 22 (November 12, 2021): 12236. http://dx.doi.org/10.3390/ijms222212236.
Анотація:
Amyotrophic lateral sclerosis (ALS) is a fatal, multigenic, multifactorial, and non-cell autonomous neurodegenerative disease characterized by upper and lower motor neuron loss. Several genetic mutations lead to ALS development and many emerging gene mutations have been discovered in recent years. Over the decades since 1990, several animal models have been generated to study ALS pathology including both vertebrates and invertebrates such as yeast, worms, flies, zebrafish, mice, rats, guinea pigs, dogs, and non-human primates. Although these models show different peculiarities, they are all useful and complementary to dissect the pathological mechanisms at the basis of motor neuron degeneration and ALS progression, thus contributing to the development of new promising therapeutics. In this review, we describe the up to date and available ALS genetic animal models, classified by the different genetic mutations and divided per species, pointing out their features in modeling, the onset and progression of the pathology, as well as their specific pathological hallmarks. Moreover, we highlight similarities, differences, advantages, and limitations, aimed at helping the researcher to select the most appropriate experimental animal model, when designing a preclinical ALS study.
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Rhoads, Megan K., Slavina B. Goleva, William H. Beierwaltes, and Jeffrey L. Osborn. "Renal vascular and glomerular pathologies associated with spontaneous hypertension in the nonhuman primate Chlorocebus aethiops sabaeus." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 313, no. 3 (September 1, 2017): R211—R218. http://dx.doi.org/10.1152/ajpregu.00026.2017.
Анотація:
Hypertension is a complex, multifactorial disease affecting an estimated 78 million adults in the United States. Despite scientific gains, the etiology of human essential hypertension is unknown and current experimental models do not recapitulate all the behavioral and physiological characteristics of the pathology. Researchers should assess the translational capacity of these models and look to other animal models for the discovery of new therapies. Chlorocebus aethiops sabaeus, the African Green Monkey (AGM), is a nonhuman primate that develops spontaneous hypertension and may provide a novel translational model for the study of hypertension and associated diseases. In a randomly selected group of 424 adult AGMs, 37% (157/424) exhibited systolic blood pressures (SBP) >140 mmHg (SBP: 172.0 ± 2.2 mmHg) and were characterized as hypertensive (HT). 44% (187/424) were characterized as normotensive with SBP <120 mmHg (NT, SBP: 99.6 ± 1.0 mmHg) and the remaining 18% (80/424) as borderline hypertensive (BHT, SBP: 130.6 ± 0.6 mmHg). When compared with NT animals, HT AGMs are older (8.7 ± 0.6 vs. 12.4 ± 0.7 yr, P < 0.05) with elevated heart rates (125.7 ± 2.0 vs. 137.7 ± 2.2 beats/min, P < 0.05). BHT animals had average heart rates of 138.2 ± 3.1 beats/min ( P < 0.05 compared with NT) and were 11.00 ± 0.9 yr old. NT and HT animals had similar levels of angiotensinogen gene expression, plasma renin activity, and renal cortical renin content ( P > 0.05). HT monkeys exhibit renal vascular remodeling (wall-to-lumen ratio NT 0.11 ± 0.01 vs. HT 0.15 ± 0.02, P < 0.05) and altered glomerular morphology (Bowman’s capsular space: NT 30.9 ± 1.9% vs. HT 44.4 ± 3.1%, P < 0.05). The hypertensive AGM provides a large animal model that is highly similar to humans and should be studied to identify novel, more effective targets for the treatment of hypertension.
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Gallager, Ian, Jasmine Torres, Raniel Alcantara-Lee, Chirag Thadani, Rachel Britton, Eva Czirr, Steven P. Braithwaite, and Viktoria Kheifets. "Beneficial Effects of a Plasma Fraction on Inflammation and Synaptic Deficits for Age-Related Cognitive Disorders." Innovation in Aging 5, Supplement_1 (December 1, 2021): 677. http://dx.doi.org/10.1093/geroni/igab046.2549.
Анотація:
Abstract The process of aging is multifactorial, and therefore single agent interventions would be unlikely to attenuate the myriad pathologies associated with advancing age. Plasma contains many beneficial factors which have been shown in animal models to ameliorate multiple age-related deficits across varied organ systems, including the brain. We confirmed that human plasma from young (18-22-year-old) donors reverses age-related cognitive decline and enhances hippocampal neurogenesis and cell survival in aged immunocompromised mice, while plasma from aged individuals (62-68 years old) has detrimental effects in young mice. We examined PF in a high-fat diet (HFD) mouse model, a surrogate for a western diet, which expresses many characteristics of aging within the CNS in an accelerated manner: decreased cell proliferation, synaptic connectivity and increased inflammation compared to normal diet (NC) controls. We demonstrate that PF administration in HFD mice resulted in decreased brain inflammation, increased synaptic connectivity, improved neural progenitor cell survival, as well as amelioration of behavioral endpoints without impacting the underlying metabolic changes induced by HFD. In summary, we demonstrate that PF is a multifactorial and multimodal intervention for the treatment of global changes induced by the process of aging.
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Rakic, Dejana, Jovana Joksimovic Jovic, Vladimir Jakovljevic, Vladimir Zivkovic, Maja Nikolic, Jasmina Sretenovic, Marina Nikolic, et al. "High Fat Diet Exaggerate Metabolic and Reproductive PCOS Features by Promoting Oxidative Stress: An Improved EV Model in Rats." Medicina 59, no. 6 (June 7, 2023): 1104. http://dx.doi.org/10.3390/medicina59061104.
Анотація:
Background and Objectives: Polycystic ovary syndrome (PCOS) is a frequent multifactorial endocrinopathy affecting women in the reproductive period, often associated with infertility and metabolic disorders. The use of animal models helps to better understand etiopathogenesis, enabling the examination of the effects of certain drugs in order to discover the best possible therapeutic approach. We tried to investigate the additional effect of estradiol-valerate (EV) and high-fat diet (HFD) in female rats to explore PCOS-related alterations with special focus on oxidative stress. Materials and Methods: Animals were divided into three groups: control group (CTRL, n = 6), estradiol-valerate group (EV, n = 6), and estradiol-valerate group on HFD (EV + HFD, n = 6). PCOS was induced by single subcutaneous injection of long-acting EV in a dose of 4 mg/per rat. We tried to improve the metabolic characteristics of the PCOS animal model by adding HFD, so the CTRL and EV group had a regular diet, while the EV + HFD group had HFD during the induction period of 60 days. Results: We observed alterations of anthropometric parameters and hormonal disturbances, along with estrus cycle impairment reassembly to obese-type PCOS phenotype. Moreover, glucose metabolism was impaired after addition of HFD to EV protocol, contrary to EV administered alone. Histological analysis confirmed more numerous cystic follicles after the combination of EV and HFD protocol. The alterations of oxidative stress markers could be related to and serve as the mechanistic base for development of PCOS-related endocrine, reproductive, and metabolic properties. Conclusions: The additive effect of EV and HFD was obvious in the majority of the parameters observed. Our study strongly demonstrated metabolic as well as reproductive properties of PCOS in rats.
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Pallàs, Mercè. "Senescence-Accelerated Mice P8: A Tool to Study Brain Aging and Alzheimer's Disease in a Mouse Model." ISRN Cell Biology 2012 (November 14, 2012): 1–12. http://dx.doi.org/10.5402/2012/917167.
Анотація:
The causes of aging remain unknown, but they are probably intimately linked to a multifactorial process that affects cell networks to varying degrees. Although a growing number of aging and Alzheimer’s disease (AD) animal models are available, a more comprehensive and physiological mouse model is required. In this context, the senescence-accelerated mouse prone 8 (SAMP8) has a number of advantages, since its rapid physiological senescence means that it has about half the normal lifespan of a rodent. In addition, according to data gathered over the last five years, some of its behavioral traits and histopathology resemble AD human dementia. SAMP8 has remarkable pathological similarities to AD and may prove to be an excellent model for acquiring more in-depth knowledge of the age-related neurodegenerative processes behind brain senescence and AD in particular. We review these facts and particularly the data on parameters related to neurodegeneration. SAMP8 also shows signs of aging in the immune, vascular, and metabolic systems, among others.
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Antounians, Lina, Rebeca Lopes Figueira, Lourenço Sbragia, and Augusto Zani. "Congenital Diaphragmatic Hernia: State of the Art in Translating Experimental Research to the Bedside." European Journal of Pediatric Surgery 29, no. 04 (July 31, 2019): 317–27. http://dx.doi.org/10.1055/s-0039-1693993.
Анотація:
AbstractCongenital diaphragmatic hernia (CDH) is a devastating disease that still carries a high mortality and morbidity rate. Poor outcomes for fetuses and infants with CDH are mainly related to pulmonary hypoplasia (PH) and pulmonary vascular remodeling that leads to pulmonary hypertension (PHTN). Over the last five decades, research efforts have focused on modeling CDH not only to study the pathophysiology of the diaphragmatic defect, pulmonary hypoplasia, and pulmonary hypertension, but also to identify therapies that would promote lung growth and maturation, and correct vascular remodeling. As CDH is a multifactorial condition whose etiology remains unknown, there is not a single model of CDH, rather several ones that replicate different aspects of this disease. While small animals like the mouse and the rat have mainly been used to uncover biological pathways underlying the diaphragmatic defect and poor lung growth, larger animals like the lamb and the rabbit models have been instrumental for pursuing medical and surgical interventions. Overall, the use of animal models has indeed advanced our knowledge on CDH and helped us test innovative therapeutic options. For example, the lamb model of CDH has been the paradigm for testing fetal surgical procedures, including tracheal occlusion, which has been translated to clinical use. In this review, we outline the induction protocols of CDH in animals with the use of chemicals, dietary changes, genetic alterations, and surgical maneuvers, and we describe the studies that have translated experimental results to the bedside.
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Dong, Jing, Yifan Lai, Xiaofeng Zhang, Yunyun Yue, Hui Zhong, and Jing Shang. "Optimization of Monobenzone-Induced Vitiligo Mouse Model by the Addition of Chronic Stress." International Journal of Molecular Sciences 24, no. 8 (April 10, 2023): 6990. http://dx.doi.org/10.3390/ijms24086990.
Анотація:
Vitiligo is a common primary, limited or generalized skin depigmentation disorder. Its pathogenesis is complex, multifactorial and unclear. For this reason, few animal models can simulate the onset of vitiligo, and studies of drug interventions are limited. Studies have found that there may be a pathophysiological connection between mental factors and the development of vitiligo. At present, the construction methods of the vitiligo model mainly include chemical induction and autoimmune induction against melanocytes. Mental factors are not taken into account in existing models. Therefore, in this study, mental inducement was added to the monobenzone (MBEH)-induced vitiligo model. We determined that chronic unpredictable mild stress (CUMS) inhibited the melanogenesis of skin. MBEH inhibited melanin production without affecting the behavioral state of mice, but mice in the MBEH combined with CUMS (MC) group were depressed and demonstrated increased depigmentation of the skin. Further analysis of metabolic differences showed that all three models altered the metabolic profile of the skin. In summary, we successfully constructed a vitiligo mouse model induced by MBEH combined with CUMS, which may be better used in the evaluation and study of vitiligo drugs.
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Egro, Francesco Maria. "Why is type 1 diabetes increasing?" Journal of Molecular Endocrinology 51, no. 1 (June 3, 2013): R1—R13. http://dx.doi.org/10.1530/jme-13-0067.
Анотація:
A series of studies have reported a constant global rise in the incidence of type 1 diabetes. Epidemiological and immunological studies have demonstrated that environmental factors may influence the pathogenesis, leading to a cell-mediated pancreatic β-cell destruction associated with humoral immunity. The search for the triggering factor(s) has been going on for the past century, and yet they are still unknown. This review provides an overview of some of the most well-known theories found in the literature: hygiene, viral, vitamin D deficiency, breast milk and cow's milk hypotheses. Although the hygiene hypothesis appears to be the most promising, positive evidence from animal, human and epidemiological studies precludes us from completely discarding any of the other hypotheses. Moreover, due to contrasting evidence in the literature, a single factor is unlikely to cause an increase in the incidence of diabetes all over the world, which suggests that a multifactorial process might be involved. Although the immunological mechanisms are still unclear, there seems to be some overlap between the various hypotheses. It is thought that the emphasis should be shifted from a single to a multifactorial process and that perhaps the ‘balance shift’ model should be considered as a possible explanation for the rise in the incidence of type 1 diabetes.
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Gates, George A. "Ménière's Disease Review 2005." Journal of the American Academy of Audiology 17, no. 01 (January 2006): 016–26. http://dx.doi.org/10.3766/jaaa.17.1.3.
Анотація:
Ménière's disease (MD) is a complex, multifactorial disorder of the inner ear that is the most common cause of the syndrome of episodic vertigo combined with fluctuating hearing loss. In spite of a century of investigation, the etiology and pathophysiology of MD remain controversial and incompletely understood. Among the factors that have contributed to these controversies are the absence of (1) a validated clinical test, (2) an appropriate animal model, and (3) a specific treatment. Nonetheless, physicians are able to assist MD patients with a variety of tailored, symptom-specific medications and therapies. Given that the vertigo induced by MD, in general, is self-limited, the long-term outlook for balance function is good. The same cannot be said for the hearing dysfunction of MD.
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Vissarionov, Sergey V., Timofey S. Rybinskikh, Marat S. Asadulaev, and Nikita O. Khusainov. "Modeling spinal cord injuries: advantages and disadvantages." Pediatric Traumatology, Orthopaedics and Reconstructive Surgery 8, no. 4 (January 9, 2021): 485–94. http://dx.doi.org/10.17816/ptors34638.
Анотація:
Background. Spinal cord injuries have diverse characteristics and associated traumatic changes; they are known as the most severe injuries of locomotorium. The creation of an optimal experimental model of spinal cord injuries using experimental animals, which would have similar changes in humans, is important to assess and analyze the pathological processes, as well as to develop complex treatment methods.
Aim. This study aimed to analyze various experimental models of spinal cord injury using laboratory animals by assessing its advantages and disadvantages for further research and implementation in clinical practice.
Materials and methods. A literature review was performed on the capabilities of experimental models of traumatic spinal cord injury in laboratory animals. A literature search was carried out using databases of PubMed, Science Direct, E-library, and Google Scholar for the period from 1981 to 2019; the keywords are shown below. In total, 105 foreign and 37 domestic articles were identified, 59 articles were analyzed after exclusion, and 75% of studies were published in the last 20 years.
Results. The review of available experimental options of spinal cord injury in laboratory animals revealed that a generally accepted universal model is not yet established. The experimental animal models had characteristics that do not correspond to the same parameters in an actual clinical situation. Besides, some difficulties were encountered in the estimation of pathological processes of experimental animals, translations with clinical changes, and interpretations of achieved functional results in experimental animals, which complicated the application in clinical practice.
Conclusion. Development of experimental models of spinal cord injury that can consider multifactorial aspects of the trauma process, including its biomechanics and time factor, is necessary.
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Vissarionov, Sergey V., Timofey S. Rybinskikh, Marat S. Asadulaev, and Nikita O. Khusainov. "Modeling spinal cord injuries: advantages and disadvantages." Pediatric Traumatology, Orthopaedics and Reconstructive Surgery 8, no. 4 (January 9, 2021): 485–94. http://dx.doi.org/10.17816/ptors34638.
Анотація:
Background. Spinal cord injuries have diverse characteristics and associated traumatic changes; they are known as the most severe injuries of locomotorium. The creation of an optimal experimental model of spinal cord injuries using experimental animals, which would have similar changes in humans, is important to assess and analyze the pathological processes, as well as to develop complex treatment methods.
Aim. This study aimed to analyze various experimental models of spinal cord injury using laboratory animals by assessing its advantages and disadvantages for further research and implementation in clinical practice.
Materials and methods. A literature review was performed on the capabilities of experimental models of traumatic spinal cord injury in laboratory animals. A literature search was carried out using databases of PubMed, Science Direct, E-library, and Google Scholar for the period from 1981 to 2019; the keywords are shown below. In total, 105 foreign and 37 domestic articles were identified, 59 articles were analyzed after exclusion, and 75% of studies were published in the last 20 years.
Results. The review of available experimental options of spinal cord injury in laboratory animals revealed that a generally accepted universal model is not yet established. The experimental animal models had characteristics that do not correspond to the same parameters in an actual clinical situation. Besides, some difficulties were encountered in the estimation of pathological processes of experimental animals, translations with clinical changes, and interpretations of achieved functional results in experimental animals, which complicated the application in clinical practice.
Conclusion. Development of experimental models of spinal cord injury that can consider multifactorial aspects of the trauma process, including its biomechanics and time factor, is necessary.
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Cartoni Mancinelli, Alice, Simona Mattioli, Laura Menchetti, Alessandro Dal Bosco, Claudia Ciarelli, Monica Guarino Amato, and Cesare Castellini. "The Assessment of a Multifactorial Score for the Adaptability Evaluation of Six Poultry Genotypes to the Organic System." Animals 11, no. 10 (October 18, 2021): 2992. http://dx.doi.org/10.3390/ani11102992.
Анотація:
This study aimed to develop an adaptability score (AS) for chicken strains, which includes behavioral, plumage conditions, and body lesion indicators through a multifactorial approach. A total of 600 male chickens from 6 poultry genotypes—Ranger Classic (R1), Ranger Gold (R2), Rowan Ranger (R3), Hubbard Red JA (A), CY Gen 5 × JA87 (CY), and M22 × JA87 (M)—were reared under organic conditions, fed ad libitum, and individually weighed weekly to calculate the daily weight gain (DWG). The behavioral observations consisted of the explorative attitude (EA), recorded at 21 days, and the behavioral patterns (BPs) recorded the week before the slaughter. The AS was established by a principal component analysis, and the AS of these genotypes was compared. Moreover, the effect of DWG and genotype on the AS was evaluated by univariable and multivariable regression models. Although the DWG and genotype were strictly dependent, genotype was the most important factor affecting the AS. In fact, its effect was significant both in univariable (p < 0.001) and multivariable models (p < 0.001). Conversely, the DWG was significant only in the univariable and lost significance when the effect of genotype was introduced in the model.
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Kamei, Akinobu, Yamara S. Coutinho-Sledge, Joanna B. Goldberg, Gregory P. Priebe, and Gerald B. Pier. "Mucosal Vaccination with a Multivalent, Live-Attenuated Vaccine Induces Multifactorial Immunity againstPseudomonas aeruginosaAcute Lung Infection." Infection and Immunity 79, no. 3 (December 13, 2010): 1289–99. http://dx.doi.org/10.1128/iai.01139-10.
Анотація:
ABSTRACTMany animal studies investigating adaptive immune effectors important for protection againstPseudomonas aeruginosahave implicated opsonic antibody to the antigenically variable lipopolysaccharide (LPS) O antigens as a primary effector. However, active and passive vaccination of humans against these antigens has not shown clinical efficacy. We hypothesized that optimal immunity would require inducing multiple immune effectors targeting multiple bacterial antigens. Therefore, we evaluated a multivalent live-attenuated mucosal vaccination strategy in a murine model of acuteP. aeruginosapneumonia to assess the contributions to protective efficacy of various bacterial antigens and host immune effectors. Vaccines combining 3 or 4 attenuated strains having different LPS serogroups were associated with the highest protective efficacy compared to vaccines with fewer components. Levels of opsonophagocytic antibodies, which were directed not only to the LPS O antigens but also to the LPS core and surface proteins, correlated with protective immunity. The multivalent live-attenuated vaccines overcame prior problems involving immunologic interference in the development of O-antigen-specific antibody responses when closely related O antigens were combined in multivalent vaccines. Antibodies to the LPS core were associated within vitrokilling andin vivoprotection against strains with O antigens not expressed by the vaccine strains, whereas antibodies to the LPS core and surface proteins augmented the contribution of O-antigen-specific antibodies elicited by vaccine strains containing a homologous O antigen. Local CD4 T cells in the lung also contributed to vaccine-based protection when opsonophagocytic antibodies to the challenge strain were absent. Thus, multivalent live-attenuated vaccines elicit multifactorial protective immunity toP. aeruginosalung infections.
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Balmus, Ioana-Miruna, and Alin Ciobica. "Main Plant Extracts’ Active Properties Effective on Scopolamine-Induced Memory Loss." American Journal of Alzheimer's Disease & Other Dementiasr 32, no. 7 (June 23, 2017): 418–28. http://dx.doi.org/10.1177/1533317517715906.
Анотація:
Alzheimer’s disease leads to progressive cognitive function loss, which may impair both intellectual capacities and psychosocial aspects. Although the current knowledge points to a multifactorial character of Alzheimer’s disease, the most issued pathological hypothesis remains the cholinergic theory. The main animal model used in cholinergic theory research is the scopolamine-induced memory loss model. Although, in some cases, a temporary symptomatic relief can be obtained through targeting the cholinergic or glutamatergic neurotransmitter systems, no current treatment is able to stop or slow cognitive impairment. Many potentially successful therapies are often blocked by the blood–brain barrier since it exhibits permeability only for several classes of active molecules. However, the plant extracts’ active molecules are extremely diverse and heterogeneous regarding the biochemical structure. In this way, many active compounds constituting the recently tested plant extracts may exhibit the same general effect on acetylcholine pathway, but on different molecular ground, which can be successfully used in Alzheimer’s disease adjuvant therapy.