Hallucinations represent a transdiagnostic phenomenon observed in multiple neuropsychiatric disorders, including schizophrenia, substance use disorder and substance-induced psychotic conditions. Despite their clinical prevalence, objective assessment remains challenging due to its subjective nature, underscoring the critical need for validated translational models. The present study explores the biological mechanisms underlying hallucinations, evaluates the animal models developed to date, and discusses methods for analyzing these models along specific pathways. Hallucinations are primarily mediated through glutamatergic and/or serotonergic pathways. Numerous animal models for assessing hallucinations have been extensively reported; however, these models have mainly been designed to investigate specific neurotransmitter mechanisms, rather than encompassing all relevant pathways. Therefore, this study systematically examines currently established animal models based on the aforementioned neurotransmitter mechanisms and proposes future directions for developing universal animal models capable of comprehensively evaluating hallucinatory phenomena. The present study aims to provide deeper insights for future research involving animal models of hallucination.

Oral squamous cell carcinoma (OSCC), which accounts for over 90% of malignancies in the oral cavity, is associated with a poor prognosis, with a 5-year mortality rate reaching of up to 44%. The incidence of OSCC continues to rise annually, and current treatment typically involves a combination of surgical resection, chemotherapy, and radiotherapy. In recent years, there has been growing interest in targeted therapies that exploit molecular markers involved in tumor growth and metastasis. Among these targets, immune checkpoint molecules such as programmed cell death 1 receptor (PD-1) and its ligand, programmed cell death-ligand 1 (PD-L1), have garnered significant attention. Therapies that inhibit these immune checkpoints have been approved for various malignancies, offering new avenues for treatment. Pembrolizumab (Keytruda), a PD-1 immune checkpoint inhibitor, has emerged as a promising therapuetic option for OSCC. However, its clinical response rate in OSCC patients remains below 20%, highlighting the need for combination strategies to enhance therapeutic efficacy. One such approach involves non-thermal plasma (NTP), a novel modality that selectively induces apoptosis in cancer cells. In this study, the authors evaluated the combined effect of Keytruda and NTP in an OSCC xenograft mouse model. The combination therapy demonstrated the tendency of suppressed tumor growth compared to Keytruda monotherapy. This effect was accompanied by increased apoptosis, as indicated by elevated cleaved caspase-3 expression, and reduced proliferation, as shown by decreased Ki-67 expression. Although preliminary, these findings may support the potential clinical application of Keytruda-NTP combined therapy as a novel treatment strategy for OSCC.

Periodontitis is a chronic inflammatory disease characterized by the progressive destruction of periodontal tissue and alveolar bone loss. To develop effective treatment strategies, a model that mimics this disease must be implemented. From this perspective, animal models can be used to investigate its mechanisms by reproducing disease progression and providing insights into host-microbe interactions, immune responses, and bone remodeling. In addition, periodontitis-associated bone loss fundamentally differs from systemic bone loss. Targeted treatments require distinguishing periodontitis-induced and systemic bone loss mechanisms. This review examines the rationale for using animal models in periodontal research and evaluates various experimental approaches, such as bacterial inoculation, ligature-induced periodontitis, and chemically induced inflammation. These models have advanced our understanding of periodontal disease but have limitations in replicating the chronic nature of periodontitis and human immune responses. However, current models cannot fully replicate chronic disease progression and human immune responses. Recent developments have focused on improving animal models to more accurately simulate disease progression and host responses, which has led to the elucidation of the immunomodulatory mechanisms of periodontitis and their relevance to the human dental environment. Moreover, new approaches, such as developing age-related periodontitis models and improving ligature techniques, could enhance experimental reproducibility and translational potential. Future studies are needed to reflect these improvements and enhance the clinical relevance of periodontitis models.

We previously reported that pyridoxine and its derivatives exert antidiabetic effects by alleviating postprandial hyperglycemia via inhibition of carbohydrate-hydrolyzing enzymes in normal sprague–dawley (SD) rats. In this study, we aimed to further evaluate whether long-term pyridoxal supplementation decreases the blood glucose levels using SD rats. SD rats were randomly assigned to groups fed a high-carbohydrate diet (66.1% cornstarch) with or without pyridoxal (4%) for 36 days. Changes in body weight, blood glucose levels, and food intake were measured daily for 36 days. Dietary supplementation with pyridoxal significantly decreased the blood glucose levels (P<0.001) and body weight (P<0.001) in mice. Glycated hemoglobin (HbA1c) levels, which are good indicators of plasma glucose concentrations over prolonged periods, were also significantly decreased over five weeks (P<0.001). Similarly, dietary treatment with Acarbose ® (0.04%), a positive control, also significantly decreased the blood glucose and HbA1c levels and body weight. Overall, our findings suggest that pyridoxal inhibits weight gain and alleviates postprandial hyperglycemia by decreasing glucose absorption and HbA1c levels.

Obesity is the cause of many diseases, and its severity continues to increase. Promoting non-shivering thermogenesis is attracting attention as a new treatment strategy for obesity. This study summarized the studies that evaluated the effect of Panax ginseng on promoting non-shivering thermogenesis in animal models. A total of 7 studies were included according to the selection criteria, of which five were judged to have a high risk of bias. Indicators of UCP1 mRNA, UCP1 protein, and PGC- 1a were used in the meta-analysis, and the certainty of evidence progressed for each indicator, with UCP1 protein showing the highest certainty of evidence. Meta-analysis was conducted on 5 works of literature with standard indicators. As a result of meta-analysis, UCP1 protein level and PGC-1a mRNA level were significantly increased statistically. In addition, the protein levels of PRDM16 and TFAM increased in several studies (not a meta-analysis). These findings suggest that Panax ginseng could be a potential therapeutic agent for obesity. However, further research is needed to understand its mechanisms and possible side effects fully. Thus, it is concluded that Panax ginseng in animal models can promote non-shivering thermogenesis and improve mitochondria function in animal models, opening up new avenues for research and potential clinical applications.

본 연구는 CIA에 의해 유발된 DBA/1 마우스를 통해 류마티스관절염 바이오마커에 대한 두 충 추출물의 효과를 평가하였다. 평가를 위해 류마티스관절염 동물모델 제작 후 100 ㎎/㎏/day로 4주간 경구 투여하고 혈청 바이오마커, 방사선, 구조적 매개변수 분석을 통해 치료 효과를 확인하였다. 음성대 조군과 비교하여, 두충 추출물은 염증 및 면역글로불린 마커(TNF-α, IgG 및 hs-CRP)의 생성을 유의 하게 감소시켰고, 백혈구의 단핵구 수를 유의적으로 감소시켰다. 또한, 두충 추출물은 관절 파괴를 효과 적으로 보존하고 관절 변형을 줄였으며, 골 밀도의 증가와 유의적으로 골 염증을 감소시켰다. 이러한 결 과는 두충 추출물이 류마티스관절염 증상을 개선하는 것을 나타낸다. 따라서, 두충 추출물은 류마티스관 절염 관리를 위한 새로운 치료 옵션이 될 수 있음을 보여준다.

Gilles de la Tourette Syndrome (GTS) is a neuropsychiatric disorder defined by the motor and phonic tics affecting approximately 1% of the children worldwide. The symptoms of GTS typically arise at the age of 5 to 7 and generally improve with increasing age. Affected individuals can have a social stigma and poor quality of life, especially when tics are severe or accompanied by other neuropsychiatric disorders. Abnormalities in neurotransmitter signaling affecting basal ganglia circuits have been suggested as representatives of neurobiological mechanisms underlying GTS. While several evidences suggest GTS as an inherited disorder, the detailed genetic abnormalities responsible for the pathophysiology of GTS remain poorly understood. Currently, there is no satisfactory treatment option for moderate-to-severe GTS due to the limited efficacy, often complicated with side effects of available pharmacological drugs. Therefore, a number of animal models have been established to explore potential pathophysiological targets in GTS and to further screen candidate drugs. In this review, we revisit the experimental findings that describe the genetic and immunologic abnormalities in GTS as well as animal models established for studying GTS.

In the last several decades, cell therapy research has increased worldwide. Many studies have been conducted on cell therapy, and have revealed that transplanted cells did not survive for long, and implanted cells remained inactive causing immune rejection depending on the patient’s condition. Therefore, studies on cell-free therapy need to be conducted. To overcome these limitations, an alternative is the use of supernatant from cells, called “conditioned media (CM).” During in vitro cell culture, culture media supply nutrients to maintain cell characteristics and viability. In the culture, cells not only consume nutrients but also release beneficial proteins and substances, which are called “secretome.” CM from cells can be stored for a long time and is easy to handle. Moreover, secretome in CM can also be measured; exact amount of secretome is important to set the standard value for disease treatment. Here, we reviewed studies on CM and confirmed that various secretomes from CM were identified in these studies. Moreover, these findings could benefit cell and animal studies in future. In conclusion, CM could be a potential candidate for an alternative to cell therapy.

In the current study, we investigated the inhibitory activity of water soluble β-glucan from oat (Avena sativa) against various digestive enzymes such as α-glucosidase, sucrase, maltase and glucoamylase. Inhibition of these enzymes involved in the absorption of disaccharide can significantly decrease the post-prandial increase of blood glucose level after a mixed carbohydrate diet. The β-glucan had the highest documented rate of small intestinal sucrase inhibitory activity (2.83 mg/mL, IC50) relevant for potentially managing post-prandial hyperglycemia. Furthermore, we evaluated the effects of β-glucan on the level of post-prandial blood glucose in animal model. The post-prandial blood glucose levels were tested two hours after sucrose/starch administration, with and without β- glucan (100, and 500 mg/kg-body weight). The maximum blood glucose levels (Cmax) of β-glucan administration group were decreased by about 23% (from 219.06±27.82 to 190.44±13.18, p<0.05) and 10% (from 182.44±13.77 to 165.64±10.59, p<0.01) in starch and sucrose loading test, respectively, when compared to control in pharmacodynamics study. The β -Glucan administration significantly lowered the mean, maximum, and minimum level of post-prandial blood glucose at 30 min after meal. In view of the foregoing, it is felt that our findings suggest that β-glucan from oat serves to reduce post-prandial blood glucose rise secondary to slower absorption of glucose in the small intestine, via carbohydrate hydrolyzing enzymes inhibition.

Over the past decade, the magnitude and variety of modelling work in the realm of veterinary services has shown a significant increase. Accordingly, the need for enhancement of communication and cooperation among modellers (those who develop models), users (those who run models), policy makers (those who use model outputs in decision making on control policy) and coordinators (those who connect modellers with policy makers) has also shown a notable increase. In this paper, terms used in epidemiological models are listed alphabetically and explained. It is expected that development of this lexicon will help to boost communication and collaboration among those concerned with modelling work and its utilization.

Epidemic models on disease spread attempt to simulate disease transmission and associated control processes. This study reviewed published papers on epidemiological models for the management of foot-and-mouth disease in the world. In addition, an individual animal-based, spatially-explicit, stochastic disease transmission model, the Davis Animal Disease Simulation (DADS) model, was described in the frame of an international collaborative research project participating three countries: Republic of Korea, USA, and New Zealand. In this project, the Korean team is aiming at developing the most appropriate parameters for livestock and epidemiology of foot-and-mouth disease outbreaks. On the other hand, the purpose of foreign counterparts is validating their models: DADS (USA) and InterSpread Plus (New Zealand). Classification of farm types and preliminary estimations on the frequency of intra-herd contacts were also presented. This research project is expected to provide precious information to plan a strategy that will facilitate the eradication of foot-and-mouth disease from Korea.

The vast majority of embryo generated by Assisted Reproductive Technologies (ART) do not result in a live offspring and a multiple birth is the single biggest health risk associated with human fertility treatment, and the used of frozen embryos increased for medical or personal reasons. However, practical and ethical reasons might hamper study of human embryos. Therefore, animal models are necessary to elucidate the molecular and morphological changes during development. In the serial experiments, we employed mouse embryos and a Cdx-inducible ES cell system that transdifferentiates into TS cells. We found aberrant gene expression profiles including apoptosis associated (Bcl2), lineage formation related genes (Cdx-2, Tcfap2c, Oct4, and Nanog), and/or mitochondrial DNA replication related genes (mt-cox-1, mt-cox-2, Polg, Polg2, Tfam) in mouse embryos that showed developmentally retardation between morula to blastocyst transition or post implantation development after embryo transfer to surrogate mothers, compared to control embryos. To determine direct interaction between knockdown genes via siRNA approach and putative down-stream genes involved in blastocyst formation and further development, we carried out qPCR and Chip assay in either mouse embryos or the ES cells. qPCR and Chip assay results showed target gene directly bound to promoter regions of down-regulated genes in TS cells. In conclusion, we suggested that an increased understanding of epigenetic regulation of early embryonic development through animal models may ultimately lead to better methodologies for selecting more competent embryos and and/or protocols for augmenting embryos viability.

Active calcium transport is carried out by calcium channel proteins, cytosolic buffering or transfer proteins, and pump proteins. Several components of this transport system have recently been determined using gene knockout (KO) models. The calbindin‐ D9k/28k and calbindin‐D9k/TRPV6 double KO mice were generated and reported that induction of expression of some duodenal calcium transport proteins can compensate for the CaBP‐9k gene deficiency. In CaBP‐9k KO mice, the levels of these hormones differ between the KO and wild‐type (WT) mice. The induction of TRPV6 in the duodenum was observed in adult KO male mice but induction was not modified by physiologic doses of 1,25(OH)2D3 and compensatory gene induction was not affected by PTH. Duodenal TRPV6 transcription in WT and female KO mice were modulated by 1,25(OH)2D3 in a dose‐dependent manner. Under calcium‐deficient dietary conditions, in DKO mice, serum calcium levels and bone length were decreased. The intestinal and renal expression of TRPV6 mRNA was significantly decreased in DKO mice fed a calcium‐deficient diet as compared to CaBP‐28k KO or WT mice, and DKO mice died after 4 weeks on a calcium‐deficient diet. Body weight, bone mineral density (BMD) and bone length were significantly reduced in all mice fed a calcium and 1,25‐(OH) D3‐ eficient diet, as compared to a normal diet, and none of the mice survived more than 4 weeks. Using microarray analysis, NCKX3 was identified as a gene that was differentially expressed in the kidneys of female and male mice. Although any hormones did not alter NCKX3 expression, however, aldosterone and hydrocortisone did down‐regulate renal NCKX3 expression in female mice. Taken together, these results indicate that deletions of CaBP‐9k and 28k has a significant effect on calcium processing under calcium‐deficient conditions, confirming the importance of dietary calcium and 1,25‐(OH)2D3 during growth and development

Dysplasia-associated seizure disorders are markedly resistant to pharmacological intervention. Relatively little research has been conducted studying the effects of antiepileptic drugs(AEDs)on seizure activity in a rat model of dysplasia. We have used rats exposed to methylazoxymethanol acetate(MAM) in utero, an animal model featuring nodular heterotopia, to investigate the effects of AEDs in the dysplastic brain. Pilocarpine was used to induce acute seizure in MAM-exposed and age-matched vehicle-injected control animals. Field potential recordings were used to monitor amplitude and numbers of population spikes, and paired pulse inhibition in response to stimulation of commissural pathway. Two commonly used AEDs were tested: diazepam 5, 2.5 mg/kg; phenytoin 40, 60 mg/kg. Diazepam(DZP) and phenytoin(PHT) reduced the amplitude of population spike in control and MAM-exposed rats. However, the amplitude of population spike was nearly eliminated in control rats as compared to the MAM-exposed rats. Pharmaco-resistance was tested by measuring seizure latencies in awake rats after pilocarpine administration(320 mg/kg, i.p.) with and without pretreatment with AEDs. Pre-treatment with PHT 60 mg prolonged seizure latency in control rats, but not in MAM-exposed animals. The main findings of this study are that acute seizures initiated in MAM-exposed rats are relatively resistant to standard AEDs assessed in vivo. These data suggest that animal model with cortical dysplasia can be used to screen the effects of potential AEDs.

Background: Taraxacum platycarpum has been used in traditional medicine in Korea to treat intoxication and edema and as a diuretic. According to previous reports, it has anti-cancer, anti-gastritis, and anti-inflammation effects. However, the improvement effect of T. platycarpum on rheumatoid arthritis has not been investigated. The anti-oxidative and anti-inflammation effects of the aerial parts of T. platycarpum are different from those of its subterranean parts. Thus, we evaluated the effect of the water extracts of Taraxaci radix (WTR) on type II collagen-induced rheumatoid arthritis (CIA) in animal models. Methods and Results: Rheumatoid arthritis was induced by type II collagen. WTR (100㎎/㎏ and 500㎎/㎏) was administered to the animal models. Methotrexate was used as the positive control. The levels of interleukin-6, TNF-alpha, and type II collagen IgG in the animals were measured by using enzyme-linked immunosorbent assay. Treatment with 500㎎/㎏ WTR decreased the serum levels of interleukin-6, TNF-alpha, and collagen IgG in the CIA models. Moreover, treatment with WTR diminished the arthritisinduced swelling of the hind legs and monocyte infiltration in the bloodvessels of the animal models. Conclusions: These results indicate that WTR has the potential to improve rheumatoid arthritis by reducing the levels of inflammatory cytokines such as interleukin-6 and TNF-alpha. However, further experiments are required to elucidate the influence of WTR on signal transduction in vitro and in vivo.