Use Of Animal Models Research Articles

Discovery of 5-(Substituted Phenyl)-2-aryl Benzimidazole Derivatives as SIRT1 Activators: Their Design, in silico Studies, Synthesis, and in vitro Evaluation.

Silent information regulator two homologue one (SIRT1) is an emerging target for managing metabolic disorders. This study aimed to synthesize novel 5-(- substituted phenyl)-2-aryl benzimidazole derivatives and evaluate them for SIRT1 activation. The compounds were designed according to the findings of the QSAR models framed in our previous studies. Molecular docking and dynamics studies were also performed to explore the interactions of designed compounds with the active site of the SIRT1 enzyme using AutoDock Vina and Schrödinger Maestro version 11.8.012, respectively. Compounds with good binding affinity were synthesized by Suzuki-Miyaura cross-coupling and spectrally characterized. The molecules were evaluated for their in vitro SIRT1 activation properties using a fluorescent screening kit. Based on the results of in vitro assay, a structure-activity relationship was established. SwissADME was employed to calculate the pharmacokinetics characteristics of the synthesized molecules. The molecular docking studies revealed that all the activators were effectively docked in the catalytic active site. All compounds demonstrated interactions with important amino acids like Glu230 and Arg446. In molecular dynamics simulations, the root mean square deviation (RMSD) of compound 5m and protein SIRT1 remained stable, i.e., below 3mm. Compound 5m, 4-(2-(3,4-dihydroxy-5-nitrophenyl)-1H-benzo[d]imidazol- 5-yl)benzaldehyde, was the most potent compound with an EC50 value of 0.006 mM (±0.001) and maximum activation of 240.5%. All the synthesized compounds had acceptable theoretical ADME profiles, and drug-likeness properties complied with Lipinski's rule. According to the findings, synthesized compounds may be viable leads for SIRT1 activators and may be used to advance preclinical in vivo research utilizing animal models.

Bibliometric analysis of the interplay between epilepsy and microglia: trends, hotspots, and emerging research areas.

Epilepsy, a common neurological disorder, has been increasingly associated with neuroinflammation, especially microglia activation. To gain insights into the research trends and patterns in this intersection, we conducted a bibliometric analysis of studies published between 2005 and 2024. Using the Web of Science Core Collection, we identified 1,229 relevant articles and reviews, focusing on the relationship between epilepsy and microglia. We employed the Bibliometrix R package and VOSviewer to analyze the data. Our search strategy combined epilepsy-related terms with microglia and microglial cell keywords. The analysis encompassed publication trends, country and institutional contributions, journal sources, authors, keywords, and thematic evolution. The number of publications has steadily increased, particularly after 2019, indicating growing research interest. The United States, China, and Germany emerged as the most productive countries, with extensive collaboration between China and the United States. Epilepsia and Journal of Neuroinflammation were the most influential journals. Aronica E, Vezzani A, and Engel T were the most prolific authors. Thematic analysis revealed clusters focused on temporal lobe epilepsy, epilepsy-related disorders, and microglia activation. Over the past several years, research has shifted from fundamental brain function studies to in-vivo investigations of specific molecular mechanisms. The CSTB (-) mouse model and NF-κB signaling pathway both merit further in-depth investigation. In conclusion, this bibliometric study reveals a surge in epilepsy-microglia research, led by key countries, journals, and researchers. Temporal lobe epilepsy, epilepsy-related disorders, and microglia activation are focal themes. Future directions include exploring microglia activation mechanisms, utilizing animal models, and interdisciplinary approaches.

Establishing a rabbit model with massive supraspinatus tendon defect for investigating scaffold-assisted tendon repair

BackgroundShoulder pain and disability from rotator cuff tears remain challenging clinical problem despite advancements in surgical techniques and materials. To advance our understanding of injury progression and develop effective therapeutics using tissue engineering and regenerative medicine approaches, it is crucial to develop and utilize animal models that closely resemble the anatomy and display the pathophysiology of the human rotator cuff. Among various animal models, the rabbit shoulder defect model is particularly favored due to its similarity to human rotator cuff pathology. However, a standardized protocol for creating a massive rotator cuff defect in the rabbits is not well defined. Therefore, the objective of our study was to establish a robust and reproducible model of a rotator cuff defect to evaluate the regenerative efficacy of scaffolds.ResultsIn our study, we successfully developed a rabbit model with a massive supraspinatus tendon defect that closely resembles the common rotator cuff injuries observed in humans. This defect involved a complete transection of the tendon, spanning 10 mm in length and encompassing its full thickness and width. To ensure stable scaffolding, we employed an innovative bridging suture technique that utilized a modified Mason-Allen suture as a structural support. Moreover, to assess the therapeutic effectiveness of the model, we utilized different scaffolds, including a bovine tendon extracellular matrix (ECM) scaffold and a commercial acellular dermal matrix (ADM) scaffold. Throughout the observation period, no scaffold damage was observed. Notably, comprehensive histological analysis demonstrated that the regenerative tissue in the tendon ECM scaffold group exhibited an organized and aligned fiber structure, indicating tendon-like tissue regeneration while the tissue in the ADM group showed comparatively less organization.ConclusionsThis study presents a comprehensive description of the implemented procedures for the development of a highly reproducible animal model that induces massive segmental defects in rotator cuff tendons. This protocol can be universally implemented with alternative scaffolds to investigate extensive tendon defects and evaluate the efficacy of regenerative treatments. The application of our animal model offers a standardized and reproducible platform, enabling researchers to systematically evaluate, compare, and optimize scaffold designs. This approach holds significant importance in advancing the development of tissue engineering strategies for effectively repairing extensive tendon defects.

Disease-Specific Alteration of Cardiac Lymphatics: A Review from Animal Disease Models to Clinics.

For many years, the significance of cardiac lymphatic vessels was largely overlooked in clinical practice, with little consideration given to their role in the pathophysiology or treatment of cardiac diseases. However, recent research has brought renewed attention to these vessels, progressively illuminating their function and importance within the realm of cardiovascular science. Experimental studies, particularly those utilizing animal models of cardiac disease, have demonstrated a clear relationship between cardiac lymphatic vessels and both the pathogenesis and progression of these conditions. These findings have prompted a growing interest in potential therapeutic applications that specifically target the cardiac lymphatic system. Conversely, while clinical investigations into cardiac lymphatics remain limited, recent studies have begun to explore their identification through specific surface markers, as well as the expression dynamics of lymphangiogenic factors. These studies have increasingly highlighted associations of lymphatic dysfunction with inflammation and fibrosis, both of which negatively impact cardiac function and remodeling across various pathological states. Despite these advances, comprehensive reviews of the current knowledge regarding the cardiac lymphatic vasculature, particularly within specific disease contexts, remain scarce. This review aims to address this gap by providing a detailed synthesis of existing reports, encompassing both animal model research and studies on human clinical specimens, with a special focus on the role of cardiac lymphatic vessels in different disease states.

Protective effect of hydroxysafflor yellow a on thioacetamide-induced liver injury and osteopenia in zebrafish

Hydroxysafflor yellow A (HSYA) is the main water-soluble compound of safflower. It is commonly used in liver disease treatment and has anti-osteoporotic activity. However, the specific mechanism of HSYA is not yet fully understood. Thioacetamide (TAA) has toxic effects on the liver and is widely used in establishing animal models of cirrhosis and liver fibrosis. In research of liver-related diseases and bone deformation in vivo, the zebrafish has become a frequently utilized animal model. In establishing a TAA-induced zebrafish liver injury model, we found that TAA-induced zebrafish also developed osteopenia. The aim of our study is to investigate the protective effect of HSYA on TAA-induced liver injury and osteopenia in zebrafish. The findings demonstrated that HSYA alleviated hepatic oxidative stress, inhibited the release of inflammatory factors, and promoted in vivo skeletal mineralization in zebrafish larvae. Further Real-time Polymerase Chain Reaction and Western blotting analyses showed that HSYA altered the expression levels of SIRT1, HMGB1, TLR4, MYD88 and NF-ΚB, ameliorated TAA-induced liver injury, reduced the release of inflammation-related factors IL-6, IL-1β, TNF-α, regulated the ratio of RANKL/OPG, ameliorated TAA-induced osteopenia. In conclusion, our study demonstrated that HSYA exhibited a noteworthy beneficial influence on TAA-induced liver injury and osteopenia in zebrafish, this finding provide a foundation for the application of HSYA in clinical research.

Microglial senescence in neurodegeneration: Insights, implications, and therapeutic opportunities.

The existing literature on neurodegenerative diseases (NDDs) reveals a common pathological feature: the accumulation of misfolded proteins. However, the heterogeneity in disease onset mechanisms and the specific brain regions affected complicates the understanding of the diverse clinical manifestations of individual NDDs. Dementia, a hallmark symptom across various NDDs, serves as a multifaceted denominator, contributing to the clinical manifestations of these disorders. There is a compelling hypothesis that therapeutic strategies capable of mitigating misfolded protein accumulation and disrupting ongoing pathogenic processes may slow or even halt disease progression. Recent research has linked disease-associated microglia to their transition into a senescent state-characterized by irreversible cell cycle arrest-in aging populations and NDDs. Although senescent microglia are consistently observed in NDDs, few studies have utilized animal models to explore their role in disease pathology. Emerging evidence from experimental rat models suggests that disease-associated microglia exhibit characteristics of senescence, indicating that deeper exploration of microglial senescence could enhance our understanding of NDD pathogenesis and reveal novel therapeutic targets. This review underscores the importance of investigating microglial senescence and its potential contributions to the pathophysiology of NDDs, including Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis. Additionally, it highlights the potential of targeting microglial senescence through iron chelation and senolytic therapies as innovative approaches for treating age-related NDDs.

Circadian Regulatory Networks of Glucose Homeostasis and Its Disruption as a Potential Cause of Undernutrition.

The circadian clock system, an evolutionarily conserved mechanism, orchestrates diurnal rhythms in biological activities such as behavior and metabolism, aligning them with the earth's 24-hour light/dark cycle. This synchronization enables organisms to anticipate and adapt to predictable environmental changes, including nutrient availability. However, modern lifestyles characterized by irregular eating and sleeping habits disrupt this synchrony, leading to metabolic disorders such as obesity and metabolic syndrome, evidenced by higher obesity rates among shift workers. Conversely, circadian disturbances are also associated with reduced nutrient absorption and an increased risk of malnutrition in populations such as the critically ill or the elderly. The precise mechanisms of these disturbances in leading to either overnutrition or undernutrition is complex and not yet fully understood. Glucose, a crucial energy source, is closely linked to obesity when consumed excessively and to weight loss when intake is reduced, which suggests that circadian regulation of glucose metabolism is a key factor connecting circadian disturbances with nutritional outcomes. In this review, we describe how the biological clock in various tissues regulates glucose metabolism, with a primary focus on studies utilizing animal models. Additionally, we highlight current clinical evidence supporting the association between circadian disturbance and glucose metabolism, arguing that such disruption could predominantly contribute to undernutrition due to impaired efficient utilization of nutrients.

Targeting Rap1b signaling cascades with CDNF: Mitigating platelet activation, plasma oxylipins and reperfusion injury in stroke

Cerebral reperfusion injury in stroke, stemming from interconnected thrombotic and inflammatory signatures, often involves platelet activation, aggregation and its interaction with various immune cells, contributing to microvascular dysfunction. However, the regulatory mechanisms behind this platelet activation and the resulting inflammation are not well understood, complicating the development of effective stroke therapies. Utilizing animal models and platelets from hemorrhagic stroke patients, our research demonstrates that human cerebral dopamine neurotrophic factor (CDNF) acts as an endogenous antagonist, mitigating platelet aggregation and associated neuroinflammation. CDNF moderates mitochondrial membrane potential, reactive oxygen species production, and intracellular calcium in activated platelets by interfering with GTP binding to Rap1b, thereby reducing Rap1b activation and downregulating the Rap1b-MAPK-PLA2 signaling pathway, which decreases release of the pro-inflammatory mediator thromboxane A2. Additionally, CDNF reduces the inflammatory response in BV2 microglial cells co-cultured with activated platelets. Consistent with ex vivo findings, subcutaneous administration of CDNF in a rat model of ischemic stroke significantly reduces platelet activation, aggregation, lipid mediator production, infarct volume, and neurological deficits. In summary, our study highlights CDNF as a promising therapeutic target for mitigating platelet-induced inflammation and enhancing recovery in stroke. Harnessing the CDNF pathway may offer a novel therapeutic strategy for stroke intervention.

Effects of insect consumption on exercise performance, body composition and metabolism: a review

Abstract Insects contain a number of beneficial macronutrients, micronutrients, and bioactive compounds that play crucial roles for optimal bodily functions and exercise. This review aims to consolidate information from studies involving humans and animals that investigated the effect of insect consumption, either alone or in combination with exercise, on exercise performance, body composition, and metabolism. In humans, insect supplementation with exercise could improve strength. Insect supplementation, with or without exercise, could also improve body composition. However, the lack of dietary and physical activity control may have influenced these findings. Insect consumption alone caused increased blood amino acids, followed by activation of the mammalian target of rapamycin complex-1 (mTORC1) signalling and increased muscle protein synthesis, which is further elevated when combined with resistance exercise. In animals, insect consumption alone could improve endurance and fatigue biomarkers. It could also reduce fat mass and increase muscle mass. The reduction in fat mass was attributed to improvements in blood lipid profiles, while the increase in muscle mass is attributed to elevated blood amino acids and mTORC1. Interestingly, in combination with exercise, greater changes in these variables were observed, including increases in energy metabolism. Findings from animal studies, such as changes in muscle mass and protein metabolism, have been validated in humans, while outcomes regarding endurance, fat mass, and blood lipids have not been validated in humans. This encourages future research to focus on these parameters. Due to ethical constraints and impracticality, there has been a reliance on animal studies to elucidate certain mechanisms and parameters in humans. Overall, insect consumption, with or without exercise, in both humans and animals showed promising results in improving exercise performance, body composition, and metabolism and thus, could function as an alternative exercise supplement. Additionally, utilizing animal models has allowed researchers to better understand the key mechanisms behind these improvements.

Reproductive Health in Trans and Gender Diverse Patients: Effects of transmasculine gender-affirming hormone therapy on future reproductive capacity: clinical data, animal models, and gaps in knowledge.

Animal studies are needed to inform clinical guidance on the effects of testosterone gender-affirming hormone therapy (T-GAHT) on fertility. This review summarizes current animal models of T-GAHT and identifies gaps in knowledge for future study. Testosterone gender affirming hormone therapy (T-GAHT) is frequently used by transgender and gender-diverse individuals assigned female at birth to establish masculinizing characteristics. Although many seek parenthood, particularly as a gestational parent or through surrogacy, the current standard guidance of fertility counseling for individuals on testosterone (T) lacks clarity. At this time, individuals are typically recommended to undergo fertility preservation or stop treatment, associating T-therapy with a loss of fertility; however, there is an absence of consistent information regarding the true fertility potential for transgender and gender-diverse adults and adolescents. This review evaluates recent studies that utilize animal models of T-GAHT to relate to findings from clinical studies, with a more specific focus on fertility. Relevant literature based on murine models in post- and pre-pubertal populations has suggested reversibility of the impacts of T-GAHT, alone or following gonadotropin-releasing hormone agonist (GnRHa), on reproduction. These studies reported changes in clitoral area and ovarian morphology, including corpora lutea, follicle counts, and ovarian weights from T-treated mice. Future studies should aim to determine the impact of the duration of T-treatment and cessation on fertility outcomes, as well as establish animal models that are clinically representative of these outcomes with respect to gender diverse populations.

Expression and pathogenesis of insulin-like growth factor-1 and insulin-like growth factor binding protein 3 in a mouse model of ulcerative colitis

Background and aimInsulin-like growth factor-1 may be involved in the epithelial-to-mesenchymal transition process. It can mitigate adverse effects when interacting with insulin-like growth factor binding protein 3. This study aimed to explore alterations in the expression of these two factors in the colonic tissue of mice with ulcerative colitis. MethodThis study utilized animal models. Mice were randomly allocated into three distinct groups. Disease activity index assessment was performed first, followed by histological grading of colitis. Protein and mRNA expression levels were determined using Western blotting and RT-qPCR. Immunohistochemical detection was used to determine histochemistry scores. Pearson correlation and SPSS 25.0 software were used for data analysis. ResultsThe findings indicated a reduction in the expression of the two investigated factors as well as in epithelial-to-mesenchymal transition epithelial markers during inflammation, while the expression of noninflammatory factors increased. These effects were notably amplified following treatment. Interestingly, the changes in epithelial-to-mesenchymal transition-inducing factors and mesenchymal markers contradicted this trend. Pearson correlation analysis revealed a correlation between molecular indicators of change and epithelial-to-mesenchymal transition. ConclusionInsulin-like growth factor-1 and insulin-like growth factor binding protein 3 may play a protective role in the development and progression of ulcerative colitis, potentially through their inhibition of the epithelial-to-mesenchymal transition. These factors hold promise as targets for the clinical diagnosis and treatment of ulcerative colitis.

Enterovirus-A71 preferentially infects and replicates in human motor neurons, inducing neurodegeneration by ferroptosis

ABSTRACT Enterovirus A71 (EV-A71) causes Hand, Foot, and Mouth Disease and has been clinically associated with neurological complications. However, there is a lack of relevant models to elucidate the neuropathology of EV-A71 and its mechanism, as the current models mainly utilize animal models or immortalized cell lines. In this study, we established a human motor neuron model for EV-A71 infection. Single cell transcriptomics of a mixed neuronal population reveal higher viral RNA load in motor neurons, suggesting higher infectivity and replication of EV-A71 in motor neurons. The elevated RNA load in motor neurons correlates with the downregulation of ferritin-encoding genes. Subsequent analysis confirms that neurons infected with EV-A71 undergo ferroptosis, as evidenced by increased levels of labile Fe2+ and peroxidated lipids. Notably, the Fe2+ chelator Deferoxamine improves mitochondrial function and promotes survival of motor neurons by 40% after EV-A71 infection. These findings deepen understanding of the molecular pathogenesis of EV-A71 infection, providing insights which suggest that improving mitochondrial respiration and inhibition of ferroptosis can mitigate the impact of EV-A71 infection in the central nervous system.

Detection of the selective androgen receptor modulator S-23 and its metabolites in equine urine and plasma following oral administration.

S-23 is an arylpropionamide selective androgen receptor modulator that has been investigated in animal models for use as a male hormonal contraceptive but is not yet available therapeutically. S-23 is available alongside other selective androgen receptor modulators (SARMs) to purchase online via uncontrolled sites, sold as supplement products. It has been detected in several human doping cases, highlighting the importance of identifying the best analytical targets for equine doping control. The purpose of this study was to investigate the detection of S-23 and its phase I metabolites in equine urine and plasma following a multiple dose oral administration to two Thoroughbred racehorses. Liquid chromatography-high resolution mass spectrometry was used for metabolite identification, and liquid chromatography-tandem mass spectrometry was used for full sample analysis and generation of urine and plasma profiles. S-23 and seven phase I metabolites were observed in urine following enzyme hydrolysis and solvolysis. The most abundant analyte detected was the hydroxylated 4-amino-2-(trifluoromethyl)benzonitrile metabolite, which also allowed the longest duration of detection in urine from both horses, for up to 360 h following administration. The data suggest that this metabolite was likely to be highly conjugated with both sulphate and glucuronide moieties. In plasma, S-23 and two phase I metabolites were observed. S-23 was the most abundant analyte detected for both horses, allowing detection for up to 143 h post-administration. To the best of the authors' knowledge, this is the first report of S-23 and metabolites in equine urine and plasma samples.

From Agriculture to Clinics: Unlocking the Potential of Magnetized Water for Planetary and Human Health.

Magnetized water (MW) is a form of liquid water that has been exposed to a magnetic field to alter its hydrogen bonding structure, resulting in the formation of water molecule clusters of various sizes and configurations connected by hydrogen bonds. This magnetization process induces several changes in the physicochemical properties of water, such as increased pH, electrical conductivity, and dissolved oxygen content, as well as decreased surface tension, density, and evaporation temperature compared to untreated water. In this narrative review, we explore the effective utilization of MW in agriculture, where it has a well-established history of applications, and its potential for direct applications in the medical field, which are currently at the forefront of research. MW is one of the most promising innovations for facilitating the transition from unsustainable to sustainable agriculture, which is expected to yield positive human health outcomes by promoting the consumption of less processed foods and reducing resource consumption. In addition to these indirect effects on human health, preclinical research utilizing animal models has demonstrated that water magnetization exerts beneficial effects on diabetes, renal function, bone health, and fertility. These health benefits appear to stem from the ability of MW to increase the activity of antioxidant enzymes while decreasing lipid peroxidation and inflammatory markers. In terms of direct human applications, MW has been primarily studied in the fields of dentistry and dermatology. MW mouthrinse has consistently shown efficacy against Streptococcus mutans, with studies reporting comparable effects to chlorhexidine. In dermatology, the topical application of MW has demonstrated improvements in skin biophysical parameters, increased hair count and hair mass index, and promoted the healing of challenging wounds. Intriguingly, these effects on human skin seem to be mediated by local activation of autophagy, potentially through mild alkaline stress. In conclusion, this review underscores the promising role of MW in promoting a holistic approach to planetary and human health. Future studies should focus on standardizing the magnetization process, exploring the molecular mechanisms underlying MW-induced autophagy, and investigating the potential of MW as a complementary strategy for treating human diseases characterized by impaired autophagy.

Experimental models for peri-implant diseases: a narrative review.

Peri-implant diseases, being the most common implant-related complications, significantly impact the normal functioning and longevity of implants. Experimental models play a crucial role in discovering potential therapeutic approaches and elucidating the mechanisms of disease progression in peri-implant diseases. This narrative review comprehensively examines animal models and common modeling methods employed in peri-implant disease research and innovatively summarizes the in vitro models of peri-implant diseases. Articles published between 2015 and 2023 were retrieved from PubMed/Medline, Web of Science, and Embase. All studies focusing on experimental models of peri-implant diseases were included and carefully evaluated. Various experimental models of peri-implantitis have different applications and advantages. The dog model is currently the most widely utilized animal model in peri-implant disease research, while rodent models have unique advantages in gene knockout and systemic disease induction. In vitro models of peri-implant diseases are also continuously evolving to meet different experimental purposes. The utilization of experimental models helps simplify experiments, save time and resources, and promote advances in peri-implant disease research. Animal models have been proven valuable in the early stages of drug development, while technological advancements have brought about more predictive and relevant in vitro models. This review provides clear and comprehensive model selection strategies for researchers in the field of peri-implant diseases, thereby enhancing understanding of disease pathogenesis and providing possibilities for developing new treatment strategies.

A gene edited pig model for studying LGR5+ stem cells: implications for future applications in tissue regeneration and biomedical research.

Recent advancements in genome editing techniques, notably CRISPR-Cas9 and TALENs, have marked a transformative era in biomedical research, significantly enhancing our understanding of disease mechanisms and helping develop novel therapies. These technologies have been instrumental in creating precise animal models for use in stem cell research and regenerative medicine. For instance, we have developed a transgenic pig model to enable the investigation of LGR5-expressing cells. The model was designed to induce the expression of H2B-GFP under the regulatory control of the LGR5 promoter via CRISPR/Cas9-mediated gene knock-in. Notably, advancements in stem cell research have identified distinct subpopulations of LGR5-expressing cells within adult human, mouse, and pig tissues. LGR5, a leucine-rich repeat-containing G protein-coupled receptor, enhances WNT signaling and these LGR5+ subpopulations demonstrate varied roles and anatomical distributions, underscoring the necessity for suitable translational models. This transgenic pig model facilitates the tracking of LGR5-expressing cells and has provided valuable insights into the roles of these cells across different tissues and species. For instance, in pulmonary tissue, Lgr5+ cells in mice are predominantly located in alveolar compartments, driving alveolar differentiation of epithelial progenitors via Wnt pathway activation. In contrast, in pigs and humans, these cells are situated in a unique sub-basal position adjacent to the airway epithelium. In fetal stages a pattern of LGR5 expression during lung bud tip formation is evident in humans and pigs but is lacking in mice. Species differences with respect to LGR5 expression have also been observed in the skin, intestines, and cochlea further reinforcing the need for careful selection of appropriate translational animal models. This paper discusses the potential utility of the LGR5+ pig model in exploring the role of LGR5+ cells in tissue development and regeneration with the goal of translating these findings into human and animal clinical applications.

Sacrifices on the Altar of Science: The Case of Model Organisms

This research traces and examines specific examples of the application of model organisms during the experimentation of biomedical sciences and psychology. The main purpose of the study is to compare how scientists utilize animal models for experiments with specific cases of humans who were used as test subjects, focusing on methodologies and main motivations. A core question that motivated this work is: Can we use the term ‘‘model organisms’’ to refer to human beings? In other words, can human beings be considered analogue models, specifically model organisms? This study will try to respond to the above question, by drawing upon theoretical frameworks and definitions from the field of philosophy of science, particularly focusing on the concepts of the analogue model, model organisms, and animal model. It will also analyze specific examples of experimental utilization of animal models, such as Hippocratic physicians’ experiments involving goat brains, Galen's experiments on a pig during the Greco-Roman period, and the utilization of guinea pigs in modern scientific research. Finally, the study will examine historical examples where humans were used as test subjects including the Nazi medical experiments during World War II and the Stanford prison experiment conducted by psychology professor Philip G. Zimbardo.

Experimental Animal Models in Heart Disease

Heart diseases constitute a significant global burden of mortality and morbidity. This encompassing word refers to a variety of illnesses, including coronary artery disease, heart failure, myocardial infarction, and valvular heart disease. Given the imperative need to comprehend and address these ailments, experimental studies are indispensable. Experimental animal models serve as indispensable tools in elucidating the mechanisms of heart disease. They are pivotal for developing novel treatments and assessing the efficacy of existing therapies. Among the commonly utilized animal models in heart disease research are mice, rats, rabbits, dogs, and pigs. Each model offers distinct advantages and limitations, allowing researchers to probe specific facets of cardiac pathology and unravel the intricate mechanisms involved in heart disease. In this comprehensive review, it was aimed to provide a succinct overview of the various animal models employed in heart disease research. The advantages and drawbacks of each model were delineated, the aspects of human heart disease they emulate were elucidated, and pivotal research findings facilitated by their utilization were highlighted. By synthesizing this information, it was the endeavor to provide researchers and clinicians with valuable insights into the diverse array of animal models available for investigating heart diseases, ultimately paving the way for enhanced understanding and treatment of these debilitating conditions.

Exploring the Genetic Landscape of Childhood Glaucoma.

Childhood glaucoma, a significant cause of global blindness, represents a heterogeneous group of disorders categorized into primary or secondary forms. Primary childhood glaucoma stands as the most prevalent subtype, comprising primary congenital glaucoma (PCG) and juvenile open-angle glaucoma (JOAG). Presently, multiple genes are implicated in inherited forms of primary childhood glaucoma. This comprehensive review delves into genetic investigations into primary childhood glaucoma, with a focus on identifying causative genes, understanding their inheritance patterns, exploring essential biological pathways in disease pathogenesis, and utilizing animal models to study these mechanisms. Specifically, attention is directed towards genes such as CYP1B1 (cytochrome P450 family 1 subfamily B member 1), LTBP2 (latent transforming growth factor beta binding protein 2), TEK (TEK receptor tyrosine kinase), ANGPT1 (angiopoietin 1), and FOXC1 (forkhead box C1), all associated with PCG; and MYOC (myocilin), associated with JOAG. Through exploring these genetic factors, this review aims to deepen our understanding of the intricate pathogenesis of primary childhood glaucoma, thereby facilitating the development of enhanced diagnostic and therapeutic strategies.

The role of Cannabinoid receptors in visceral pain sensation of rat: an interventional study

Visceral pain, originating from internal organs, represents a challenging aspect of pain management due to its intricate mechanisms and often debilitating nature. Understanding the underlying pathways involved in visceral pain perception is crucial for developing effective therapeutic strategies. The current study aimed to delve into recent advancements in the understanding of cannabinergic modulation of visceral pain perception, focusing on findings from interventional studies utilizing animal models, particularly rats. A total of 30 male rats aged 3 months, with an average weight of 220 g were randomly divided into 3 groups. The groups contained the control group which received intraperitoneal injection of normal saline, the second group received an intraperitoneal injection of anandamide (2 mg/kg), and the third group received an intraperitoneal injection of tramadol (20 mg/kg). The pain in all groups assessed by acetic acid test. The data obtained from the intraperitoneal injection of anandamide to the rats of the experimental group showed a significant decrease in the amount of perceived visceral pain compared to control group. In addition, the results showed that tramadol injection significantly decreased visceral pain in experimental group 2 compared to the control group. In conclusion, the current study provides an evidence for the involvement of cannabinoid receptors in the modulation of visceral pain sensation in rats.