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动物模型与实验医学（英文）

动物模型与实验医学（英文）

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AMEM围绕实验动物科学基础和应用研究，聚焦实验动物物种资源、人类疾病动物模型资源、比较医学资源等，展示实验动物科学及实验医学的最新学术、理论、技术、应用成果，以及实验动物在生命科学、医学、生物学、药学、兽医学等交叉学科中的实验研究，拓展实验动物相关设备材料的研发、实验动物管理与法律标准、实验动物福利伦理等新思路，是一本注重学科交叉、注重成果转化、引领实验动物科学及实验医学发展的英文专业期刊。
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  • 国内刊号/CN：10-1546/R
    国际刊号/ISSN：2096-5451
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  • 主管单位：中国科学技术协会
    主办单位：中国实验动物学会;中国医学科学院医学实验动物研究所
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动物模型与实验医学（英文） >2023年第6期

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  • 摘要：Background:Multiple mitochondrial dysfunction syndromes(MMDS)presents as complex mitochondrial damage,thus impairing a variety of metabolic pathways.Heart dysplasia has been reported in MMDS patients;however,the specific clinical symptoms and pathogenesis remain unclear.More urgently,there is a lack of an animal model to aid research.Therefore,we selected a reported MMDS causal gene,Isca1,and established an animal model of MMDS complicated with cardiac dysplasia.Methods:The myocardium-specific Isca1 knockout heterozygote(Isca1 HET)rat was obtained by crossing the Isca1 conditional knockout(Isca1 cKO)rat with theαmyosin heavy chain Cre(α-MHC-Cre)rat.Cardiac development characteristics were determined by ECG,blood pressure measurement,echocardiography and histopatho-logical analysis.The responsiveness to pathological stimuli were observed through adriamycin treatment.Mitochondria and metabolism disorder were determined by activity analysis of mitochondrial respiratory chain complex and ATP production in myocardium.Results:ISCA1 expression in myocardium exhibited a semizygous effect.Isca1 HET rats exhibited dilated cardiomyopathy characteristics,including thin-walled ventri-cles,larger chambers,cardiac dysfunction and myocardium fibrosis.Downregulated ISCA1 led to deteriorating cardiac pathological processes at the global and organiza-tional levels.Meanwhile,HET rats exhibited typical MMDS characteristics,including damaged mitochondrial morphology and enzyme activity for mitochondrial respira-tory chain complexesⅠ,ⅡandⅣ,and impaired ATP production.Conclusion:We have established a rat model of MMDS complicated with cardiomyopathy,it can also be used as model of myocardial energy metabolism dysfunction and mitochondrial cardiomyopathy.This model can be applied to the study of the mechanism of energy metabolism in cardiovascular diseases,as well as research and development of drugs.
  • 摘要：The cornea is an avascular,transparent tissue that is essential for visual function.Any disturbance to the corneal transparency will result in a severe vision loss.Due to the avascular nature,the cornea acquires most of the oxygen supply directly or indirectly from the atmosphere.Corneal tissue hypoxia has been noticed to influence the structure and function of the cornea for decades.The etiology of hypoxia of the cornea is distinct from the rest of the body,mainly due to the separation of cornea from the atmosphere,such as prolonged contact lens wearing or closed eyes.Corneal hypoxia can also be found in corneal inflammation and injury when a higher oxygen requirement exceeds the oxygen supply.Systemic hypoxic state during lung diseases or high altitude also leads to corneal hypoxia when a second oxygen consumption route from aqueous humor gets blocked.Hypoxia affects the cornea in multiple aspects,including disturbance of the epithelium barrier function,corneal edema due to endothelial dysfunction and metabolism changes in the stroma,and thinning of corneal stroma.Cornea has also evolved mechanisms to adapt to the hypoxic state initiated by the activation of hypoxia inducible factor(HIF).The aim of this review is to introduce the pathology of cornea under hypoxia and the mechanism of hypoxia adaptation,to discuss the current animal models used in this field,and future research directions.
  • 摘要：Background:Liqoseal consists of a watertight layer of poly(ester)ether urethane and an adhesive layer containing polyethylene glycol-N-hydroxysuccinimide(PEG-NHS).It is designed to prevent cerebrospinal fluid(CSF)leakage after intradural surgery.This study assessed the safety and biodegradability of Liqoseal in a porcine craniotomy model.Methods:In 32 pigs a craniotomy plus durotomy was performed.In 15 pigs Liqoseal was implanted,in 11 control pigs no sealant was implanted and in 6 control pigs a control dural sealant(Duraseal or Tachosil)was implanted.The safety of Liqoseal was evaluated by clinical,MRI and histological assessment.The degradation of Liqoseal was histologically estimated.Results:Liqoseal,2 mm thick before application,did not swell and significantly was at maximum mean thickness of 2.14(±0.37)mm at one month.The foreign body reaction induced by Liqoseal,Duraseal and Tachosil were comparable.Liqoseal showed no adherence to the arachnoid layer and was completely resorbed between 6 and 12 months postoperatively.In one animal with Liqoseal,an epidural fluid collection containing CSF could not be excluded.Conclusion:Liqoseal seems to be safe for intracranial use and is biodegradable.The safety and performance in humans needs to be further assessed in clinical trials.
  • 摘要：Background:Wound healing can result in various outcomes,including hypertrophic scar(HTS).Pigs serve as models to study wound healing as their skin shares physi-ologic similarity with humans.Yorkshire(Yk)and Duroc(Dc)pigs have been used to mimic normal and abnormal wound healing,respectively.The reason behind this differential healing phenotype was explored here.Methods:Excisional wounds were made on Dc and Yk pigs and were sampled and imaged for 98 days.PCR arrays were used to determine differential gene expression.Vancouver Scar Scale(VSS)scores were given.Re-epithelialization was analyzed.H&E,Mason's trichrome,and immunostains were used to determine cellularity,col-lagen content,and blood vessel density,respectively.Results:Yk wounds heal to a“port wine”HTS,resembling scarring in Fitzpatrick skin types(FST)I-III.Dc wounds heal to a dyspigmented,non-pliable HTS,resembling scarring in FST IV-VI.Gene expression during wound healing was differentially regulated versus uninjured skin in 40/80 genes,15 of which differed between breeds.Yk scars had a higher VSS score at all time points.Yk and Dc wounds had equivalent re-epithelialization,collagen disorganization,and blood vessel density.Conclusions:Our findings demonstrate that Dc and Yk pigs can produce HTS.Wound creation and healing were consistent among breeds,and differences in gene expression were not sufficient to explain differences in resulting scar phenotype.Both pig breeds should be used in animal models to investigate novel therapeutics to provide insight into a treatment's effectiveness on various skin types.
  • 摘要：Background:Elevated intracranial pressure(ICP)occurs in several physiological and pathological conditions,yet long-term sequellae are not common,which implies that blood flow is preserved above ischemic thresholds.Methods:This pilot study sought to confirm this hypothesis using a closed cranial window model in a rat in which ICP was elevated to 120 mmHg for 12 min,and superficial cortical perfusion was measured by laser Doppler flowmetry and laser speckle flowmetry.Results:Following a transient increase,cortical blood flow decreased to between 25%and 75%of baseline.These levels correspond to disrupted metabolism and decreased protein synthesis but did not exceed thresholds for electrical signaling or membrane integrity.This may partially explain how some episodes of elevated ICP remain benign.Conclusion:The closed cranial window model provides a platform for prospective study of physiologic responses to artificially elevated ICP during neurosurgery to promote hemostasis.
  • 摘要：The kidneys are a vital organ that is vulnerable to both acute kidney injury(AKI)and chronic kidney disease(CKD)which can be caused by numerous risk factors such as ischemia,sepsis,drug toxicity and drug overdose,exposure to heavy metals,and diabetes.In spite of the advances in our understanding of the pathogenesis of AKI and CKD as well AKI transition to CKD,there is still no available therapeutics that can be used to combat kidney disease effectively,highlighting an urgent need to further study the pathological mechanisms underlying AKI,CKD,and AKI progression to CKD.In this regard,animal models of kidney disease are indispensable.This article reviews a widely used animal model of kidney disease,which is induced by folic acid(FA).While a low dose of FA is nutritionally beneficial,a high dose of FA is very toxic to the kidneys.Following a brief description of the procedure for disease induction by FA,major mechanisms of FA-induced kidney injury are then reviewed,including oxidative stress,mitochondrial abnormalities such as impaired bioenergetics and mitophagy,ferroptosis,pyroptosis,and increased expression of fibroblast growth factor 23(FGF23).Finally,application of this FA-induced kidney disease model as a platform for testing the efficacy of a variety of therapeutic approaches is also discussed.Given that this animal model is simple to create and is reproducible,it should remain useful for both studying the pathological mechanisms of kidney disease and identifying therapeutic targets to fight kidney disease.
  • 摘要：Oxygen is one of the important substances for the survival of most life systems on the earth,and plateau and underground burrow systems are two typical hypoxic environments.Small mammals living in hypoxic environments have evolved different adaptation strategies,which include increased oxygen delivery,metabolic regulation of physiological responses and other physiological responses that change tissue oxygen utilization.Multiomics predictions have also shown that these animals have evolved different adaptations to extreme environments.In particular,vascular endothelial growth factor(VEGF)and erythropoietin(EPO),which have specific functions in the control of O_(2) delivery,have evolved adaptively in small mammals in hypoxic environments.Naked mole-rats and blind mole-rats are typical hypoxic model animals as they have some resistance to cancer.This review primarily summarizes the main living environment of hypoxia tolerant small mammals,as well as the changes of phenotype,physiochemical characteristics and gene expression mode of their long-term living in hypoxia environment.
  • 摘要：Background : Hematopoietic stem cells (HSC) maintain the hematopoietic system homeostasis through self- renewal and multilineage differentiation potential. HSC are regulated by the microenvironment, cytokine signaling, and transcription factors. Recent results have shown that lipid pathways play a key role in the regulation of HSC quiescence, proliferation, and division. However, the mechanism by which lipid metabolism regulates HSC proliferation and differentiation remains to be clarified. Lipoprotein lipase (LPL) is an essential enzyme in the anabolism and catabolism of very low- density lipoprotein, chylomicrons, and triglyceride- rich lipoproteins. Methods : The percentage of hematopoietic stem/progenitor cells and immune cells were determined by fluorescence- activated cell sorting (FACS). The function and the mechanism of HSCs were analyzed by cell colony forming assay and qPCR analysis. The changes in LPL^(+/−) HSC microenvironment were detected by transplantation as- says using red fluorescent protein (RFP) transgenic mice. Results : To explore the function of LPL in HSC regulation, heterozygous LPL- knockout mice (LPL^(+/−)) were established and analyzed by FACS. LPL^(+/−) mice displayed decreased hematopoietic stem/progenitor cell compartments. In vitro single- cell clono- genic assays and cell-cycle assays using FACS promoted the cell cycle and increased proliferation ability. qPCR analysis showed the expression of p57^(KIP2) and p21^(WAF1)/ ^(CIP1) in LPL^(+/−) mice was upregulated. Conclusions : LPL^(+/−) mice exhibited HSC compartment impairment due to promotion of HSC proliferation, without any effects on the bone marrow (BM) microenvironment.
  • 摘要：Background:Chronic kidney disease(CKD)has a high global prevalence and large unmet need.Central to developing new CKD therapies are in vivo models in CKD.However,next-generation antibody,protein,and gene therapies are highly specific,meaning some do not cross-react with rodent targets.This complicates preclinical development,as established in vivo rodent models cannot be utilized unless tool therapeutics are also developed.Tool compounds can be difficult to develop and,if available,typically have different epitopes,sequences,and/or altered affinity,making it unclear how efficacious the lead therapeutic may be,or what dosing regimen to investigate.To address this,we aimed to develop a nonhuman primate model of CKD.Methods:In vivo rodent unilateral ureteral obstruction(UUO)models kidney fibrosis and is commonly used due to its rapidity,consistency,and ease.We describe translation of this model to the cynomolgus monkey,specifically optimizing the model duration to allow adequate time for assessment of novel therapeutics prior to the fibrotic plateau.Results:We demonstrated that disease developed more slowly in cynomolgus monkeys than in rodents post-UUO,with advanced fibrosis developing by 6 weeks.The tubulointerstitial fibrosis in cynomolgus monkeys was more consistent with human obstructive disease than in rodents,having a more aggressive tubular basement expansion and a higher fibroblast infiltration.The fibrosis was also associated with increased transglutaminase activity,consistent with that seen in patients with CKD.Conclusion:This cynomolgus monkey UUO model can be used to test potential human-specific therapeutics in kidney fibrosis.
  • 摘要：Oxygen plays a pivotal role in the metabolism and activities of mammals.However,oxygen is restricted in some environments-subterranean burrow systems or habitats at high altitude or deep in the ocean-and this could exert hypoxic stresses such as oxidative damage on organisms living in these environments.In order to cope with these stresses,organisms have evolved specific strategies to adapt to hypoxia,including changes in physiology,gene expression regulation,and genetic mutations.Here,we review how mammals have adapted to the three high-altitude plateaus of the world,the limited oxygen dissolved in deep water habitats,and underground tunnels,with the aim of better understanding the adaptation of mammals to hypoxia.
  • 摘要：Objective/Background:Proliferation is a widely recognized trigger for pulmonary hypertension(PH),a life-threatening,progressive disorder of pulmonary blood vessels.This study was aimed to identify some proliferation associated genes/targets for better comprehension of PH pathogenesis.Methods:Human pulmonary arterial smooth muscle cells(hPASMCs)were cultured in the presence or absence of human recombinant platelet derived growth factor(rhPDGF)-BB.Cells were collected for metabolomics or transcriptomics study.Gene profiling of lungs of PH rats after hypoxia exposure or of PH patients were retrieved from GEO database.Results:90 metabolites(VIP score>1,fold change>2 or2 or<0.5 and p<.05).152 differentially expressed MAGs were then determined,out of which 9 hub genes(IL6,CXCL8,CCL2,CXCR4,CCND1,PLAUR,PLAU,HBEGF and F3)were defined as core proliferation associated hub genes in protein proten interaction analysis.In addition,the hub gene-based LASSO model can predict the occurrence of PH(AUC=0.88).The expression of CXCR4,as one of the hub genes,was positively correlated to immune cell infiltrates.Conclusion:Our findings revealed some key proliferation associated genes in PH,which provide the crucial information concerning complex metabolic reprogramming and inflammatory modulation in response to proliferation signals and might offer therapeutic gains for PH.
  • 摘要：Background:This study aims to assess the safety and efficacy of direct hemoperfu-sion using a new polymyxin B-immobilized resin column(disposable endotoxin ad-sorber,KCEA)in an endotoxin/lipopolysaccharide(LPS)-induced sepsis model.Methods:Eighteen beagles were randomized into 1 intervention group(KCEA group,n=6)and 2 control groups(sham group and model group,n=6 each).Sepsis was in-duced by continuous intravenous application of 0.5 mg/kg body weight of endotoxin for 60 min.An extracorporeal hemoperfusion device made with KCEA for endotoxin adsorption was used.Model group beagles received standard treatment with fluids and vasoactive drugs,KCEA group beagles received standard treatment and direct hemoperfusion of KCEA for 2 h,and sham group beagles were treated with standard treatment and direct hemoperfusion of a sham column for 2 h.Results:Good blood compatibility of KCEA was confirmed by assessing clinical pa-rameters.Blood endotoxin peak levels in the KCEA group were significantly lower,resulting in a significant suppression of IL-6,TNF-αand procalcitonin,which improved mean arterial pressure and significantly lowered vasopressor demand,thereby pro-tecting organ function and improving survival time and rate.In the KCEA group,MAP was significantly higher over 6 h than those recorded both in the sham group and model group.The 7-day survival rates of the KCEA,sham and model groups were 50%,0%and 0%,respectively.Conclusion:KCEA hemoadsorption was effective at detoxifying circulatory endotoxin and inflammatory mediators and contributed to the decreased mortality rate in the sepsis beagles.
  • 摘要：Autoimmune hepatitis(AIH)is a chronic inflammatory liver disease occurring in indi-viduals of all ages with a higher incidence in females and characterized by hypergam-maglobulinemia,elevated serum autoantibodies and histological features of interface hepatitis.AIH pathogenesis remains obscure and still needs in-depth study,which is likely associated with genetic susceptibility and the loss of immune homeostasis.Steroids alone and in combination with other immunosuppressant agents are the pri-mary choices of AIH treatment in the clinic,whereas,in some cases,severe adverse effects and disease relapse may occur.Chinese medicine used for the treatment of AIH has proven its merits over many years and is well tolerated.To better under-stand the pathogenesis of AIH and to evaluate the efficacy of novel therapies,several animal models have been generated to recapitulate the immune microenvironment of patients with AIH.In the current review,we summarize recent advances in the study of animal models for AIH and their application in pharmacological research of Chinese medicine-based therapies and also discuss current limitations.This review aims to provide novel insights into the discovery of Chinese medicine-originated therapies for AIH using cutting-edge animal models.
  • 摘要：Inflammation is a common disease involved in the pathogenesis,complications,and sequelae of a large number of related diseases,and therefore considerable research has been directed toward developing anti-inflammatory drugs for the prevention and treatment of these diseases.Traditional Chinese medicine(TCM)has been used to treat inflammatory and related diseases since ancient times.According to the re-view of abundant modern scientific researches,it is suggested that TCM exhibit anti-inflammatory effects at different levels,and via multiple pathways with various targets,and recently a series of in vitro and in vivo anti-inflammatory models have been developed for anti-inflammation research in TCM.Currently,the reported classic mechanisms of TCM and experimental models of its anti-inflammatory effects pro-vide reference points and guidance for further research and development of TCM.Importantly,the research clearly confirms that TCM is now and will continue to be an effective form of treatment for many types of inflammation and inflammation-related diseases.
  • 摘要：Background:Inflammation is a complex physiological and pathological process.Although many types of inflammation are well characterized,their physiological func-tions are largely unknown.tRNA aspartic acid methyltransferase 1(TRDMT1)has been implicated as a stress-related protein,but its intrinsic biological role is unclear.Methods:We constructed a Trdmt1 knockout rat and adopted the LPS-induced sepsis model.Survival curve,histopathological examination,expression of inflammatory fac-tors,and protein level of TLR4 pathway were analyzed.Results:Trdmt1 deletion had no obvious impact on development and growth.Trdmt1 de-letion slightly increased the mortality during aging.Our data showed that Trdmt1 strongly responded in LPS-treated rats,and Trdmt1 knockout rats were vulnerable to LPS treat-ment with declined survival rate.We also observed more aggravated tissue damage and more cumulative functional cell degeneration in LPS-treated knockout rats compared with control rats.Further studies showed upregulated TNF-αlevel in liver,spleen,lung,and serum tissues,which may be explained by enhanced p65 and p38 phosphorylation.Conclusions:Our data demonstrated that Trdmt1 plays a protective role in inflamma-tion by regulating the TLR4-NF-κB/MAPK-TNF-αpathway.This work provides useful information to understand the TRDMT1 function in inflammation.
  • 摘要：Animal models of human diseases play a critical role in medical research.Pigs are anatomically and physiologically more like humans than are small rodents such as mice,making pigs an attractive option for modeling human diseases.Advances in recent years in genetic engineering have facilitated the rapid rise of pig models for use in studies of human disease.In the present review,we summarize the current status of pig models for human cardiovascular,metabolic,neurodegenerative,and various genetic diseases.We also discuss areas that need to be improved.Animal models of human diseases play a critical role in medical research.Advances in recent years in genetic engineering have facilitated the rapid rise of pig models for use in studies of human disease.In the present review,we summarize the current status of pig models for human cardiovascular,metabolic,neurodegenerative,various genetic diseases and xenotransplantation.
  • 摘要：Background:Nicotine administration can generate severe oxidative stress and lipid peroxidation.Royal jelly,with its antioxidant properties,acts as a scavenger of reactive oxygen species.This study describes the apitherapy effects of royal jelly on testicular damage following nicotine administration.Methods:Forty-eight male BALB/c mice were divided into 8 groups(n=6):saline,3 different doses of royal jelly(100,150,and 200 mg/kg body weight(BW)per day),nicotine(1.5 mg/kg),and 3 different groups of Nic+Roy(1.5 mg/kg of Nic+100,150,and 200 mg/kg BW per day of royal jelly).Nicotine was administrated intraperitoneally,and royal jelly was prescribed orally for 10 consecutive days.Serum levels of hormones(testosterone,luteinizing hormone,and follicle-stimulating hormone),total antioxidant capacity,nitric oxide(NO)status,malondialdehyde levels,sperm DNA fragmentation,sperm parameters,histopathological changes(H&E staining),immunohistochemistry against apoptotic proteins,and gene expression of Bcl-2,p53,Caspase-3,and Nrf2(real-time PCR)were assessed to evaluate the molecular and histological changes.Results:Hormone levels,sperm parameters,and status of antioxidants were decreased significantly(p<.05)following nicotine administration.Moreover,royal jelly treatment normalized hormonal and antioxidant characteristics,decreased apoptotic gene expression,increased Nfr2 gene expression,and restored histopathological alteration to the physiological status significantly(p<.05).Conclusion:Royal jelly upregulates the antioxidant status,inhibits the mitochondrialdependent apoptosis pathway,and increases the rate of proliferation.This therapeutic agent effectively protected the testis against nicotine-associated damages by antioxidant and anti-apoptotic effects.
  • 摘要：Background:We aimed to reveal the mechanism of functional constipation in the treatment of Atractylodes macrocephala Koidz.(AMK)and Paeonia lactiflora Pall.(PLP).Methods:The main active ingredients of AMK and PLP were screened by the Traditional Chinese Medicine Systems Pharmacology(TCMSP)platform.A database of functional constipation targets was established by GeneCard and OMIM.An“ingredient-target”network map was constructed with Cytoscape software(version 3.7.1),and molecular docking analysis was performed on the components and genes with the highest scores.The rats in the normal group were given saline,and those in the other groups were given 10 mg/kg diphenoxylate once a day for 14 days.The serum and intestinal tissue levels of adenosine monophosphate(cAMP),protein kinase A(PKA),and adenylyl cyclase(AC)of the rats and aquaporin(AQP)1,AQP3,and AQP8 were measured.Results:AMK and PLP had a significant role in the regulation of targets in the treatment of functional constipation.After treatment with AMK,PLP,or mosapride,the serum and intestinal tissue levels of AC,cAMP,and PKA were significantly downregulated.Groups receiving AMK and PLP or mosapride exhibited a reduction in the level of AQP1,AQP3,and AQP8 to varying degrees.Conclusion:Molecular docking analysis revealed that AMK and PLP had a significant role in the regulation of targets in the treatment of functional constipation.Studies have confirmed that AMK and PLP can also affect AC,cAMP,and PKA.AC,cAMP,and PKA in model rats were significantly downregulated.AQP expression is closely related to AC,cAMP,and PKA.AMK and PLP can reduce the expression of AQP1,AQP3,and AQP9 in the colon of constipated rats.
  • 摘要：Background:A safe,effective,and ethically sound animal model is essential for preclinical research to investigate spinal medical devices.We report the initial failure of a porcine spinal survival model and a potential solution by fixating the spine.Methods:Eleven female Dutch Landrace pigs underwent a spinal lumbar interlaminar decompression with durotomy and were randomized for implantation of a medical device or control group.Magnetic resonance imaging(MRI)was performed before termination.Results:Neurological deficits were observed in 6 out of the first 8 animals.Three of these animals were terminated prematurely because they reached the predefined humane endpoint.Spinal cord compression and myelopathy was observed on postoperative MRI imaging.We hypothesized postoperative spinal instability with epidural hematoma,inherent to the biology of the model,and subsequent spinal cord injury as a potential cause.In the subsequent 3 animals,we fixated the spine with Lubra plates.All these animals recovered without neurological deficits.The extent of spinal cord compression on MRI was variable across animals and did not seem to correspond well with neurological outcome.Conclusion:This study shows that in a porcine in vivo model of interlaminar decompression and durotomy,fixation of the spine after lumbar interlaminar decompression is feasible and may improve neurological outcomes.Additional research is necessary to evaluate this hypothesis.
  • 摘要：Chuan Qin,MD,PhD,is the President of the Chinese Association for Laboratory Animal Sciences(CALAS),and the Director of the Institute of Laboratory Animal Sciences(ILAS),Chinese Academy of Medical Sciences&Peking Union Medical College.She is also the Vice-President of the Asian Federation of Laboratory Animal Science Associations(AFLAS),a board member of the International Council for Laboratory Animal Science(ICLAS),and Chairman of the National Standardization Technical Committee of Laboratory Animals.In addition to Animal Models and Experimental Medicine,Prof.Qin is also the Editor-in-Chief of Acta Laboratorium Animalis Scientia Sinica and Chinese Journal of Comparative Medicine.
  • 摘要：Accurate and reproducible analysis of murine small and large intestinal tissue is key for preclinical models involving intestinal pathology.Currently,there is no easily ac-cessible,standardized method that allows researchers of different skill levels to con-sistently dissect intestines in a time-efficient manner.Here,we describe the design and use of the 3D-printed“Mouse Intestinal Slicing Tool”(MIST),which can be used to longitudinally dissect murine intestines for further analysis.We benchmarked the MIST against a commonly used procedure involving scissors to make a longitudinal cut along the intestines.Use of the MIST halved the time per mouse to prepare the intestines and outperformed alternative methods in smoothness of the cutting edge and overall reproducibility.By sharing the plans for printing the MIST,we hope to contribute a uniformly applicable method for saving time and increasing consistency in studies of the mouse gastrointestinal tract.
  • 摘要：Alzheimer's disease(AD)is a neurodegenerative disorder.The pathology of AD is characterized by extracellular amyloid beta(Aβ)plaques,neurofibrillary tangles com-posed of hyperphosphorylated tau,neuronal death,synapse loss,and brain atrophy.Many therapies have been tested to improve or at least effectively modify the course of AD.Meaningful data indicate that the transplantation of stem cells can alleviate neuropathology and significantly ameliorate cognitive deficits in animal models with Alzheimer's disease.Transplanted stem cells have shown their inherent advantages in improving cognitive impairment and memory dysfunction,although certain weak-nesses or limitations need to be overcome.This review recapitulates rodent models for AD,the therapeutic efficacy of stem cells,influencing factors,and the underlying mechanisms behind these changes.Stem cell therapy provides perspective and chal-lenges for its clinical application in the future.
  • 摘要：Background:Anoxic brain injuries represent the main determinant of poor outcome after cardiac arrest(CA).Large animal models have been described to investigate new treatments during CA and post-resuscitation phase,but a detailed model that includes extensive neuromonitoring is lacking.Method:Before an electrically-induced 10-minute CA and resuscitation,46 adult pigs underwent neurosurgery for placement of a multifunctional probe(intracranial pressure or ICP,tissue oxygen tension or PbtO_(2) and cerebral temperature)and a bolt-based technique for the placement and securing of a regional blood flow probe and two sEEG electrodes;two modified cerebral microdialysis(CMD)probes were also inserted in the frontal lobes and accidental misplacement was prevented using a perforated head support.Result:42 animals underwent the CA procedure and 41 achieved the return of spontaneous circulation(ROSC).In 4 cases(8.6%)an adverse event took place during preparation,but only in two cases(4.3%)this was related to the neurosurgery.In 6 animals(13.3%)the minor complications that occurred resolved after probe repositioning.Conclusion:Herein we provide a detailed comprehensive neuromonitoring approach in a large animal model of CA that might help future research.
  • 摘要：Circular RNAs(circRNAs)are endogenous RNAs with a covalently closed single-stranded transcript.They are a novel class of genomic regulators that are linked to many important development and disease processes and are being pursued as clinical and therapeutic targets.Using the most powerful RNA sequencing and bioinformatics techniques,a large number of circRNAs have been identified and further functional studies have been performed.It is known that circRNAs act as potential biomarkers,sponges for microRNAs(miRNAs)and RNA-binding proteins(RBPs),and regulators of mRNA transcription.They also participate in the translation of peptides or proteins.Many types of circRNAs are dysregulated in plasma or lung tissues,and they may be involved in regulating the proliferation and apoptosis of pulmonary artery endothelial cells(PAECs)and pulmonary artery smooth muscle cells(PASMCs),leading to pulmonary vascular remodeling in pulmonary hypertension(PH).One possible mechanism is that circRNAs can regulate the function of PAECs and PASMCs by acting as miRNA sponge.However,other potential mechanisms of action of circRNAs are still being actively explored in PH.This paper presents a systematic review of the biogenesis,biological characterization,relevant underlying functions,and future perspectives for studies of circRNAs in the pathogenesis of PH.
  • 摘要：Background:Porcine pancreatic elastase(PPE)is successfully used to induce abdominal aortic aneurysm(AAA)in mice.However,differences between mouse strains in susceptibility to PPE induction have been reported.Kunming mouse is one of the most frequently used strains in China but whether it is suitable for induction of AAA by PPE application remains unclear.Methods:PPE infusion(1.5 units/ml)in temporary controlled aorta was performed to induce AAAs in both C57BL/6J and Kunming mice.Phosphatebuffered saline(PBS)application was used as vehicle control.The aorta diameters of all mice were measured at days 0 and 14 after surgery to evaluate the AAA formation.Results:After 14 days of PPE or PBS infusion,all mice were sacrificed and aorta tissues were collected for histological staining analysis.At the 14th day after infusion,PPE successfully induced aortic dilation in Kunming mice and typical AAA in C57BL/6J mice.The aorta diameter increased by 0.23 mm in Kunming mice after PPE infusion,while it was 0.72 mm in the C57BL/6J strain.PPE induced mild elastin degradation,smooth muscle cell(SMC)depletion and mural leucocyte infiltration in Kunming mice,but in PPE-sensitive C57BL/6J mice,it induced total loss of SMCs,elastin disappearance and diffused infiltrated leucocytes in aortic aneurysmal segments.The effects of PPE in inducing angiogenesis and upregulating matrix metalloproteinase 2 and 9 expression in Kunming mice were also weaker than that in C57BL/6J mice.Conclusion:At the reported dose of PPE,Kunming mouse is not as susceptible to AAA formation as C57BL/6J mice.The failure of PPE to induce AAA formation in Kunming mice may be associated to its inability to boost a strong inflammatory response.
  • 摘要：Background:Currently,increasing attention is being paid to the important role of intestinal microbiome in diabetes.However,few studies have evaluated the characteristics of gut microbiome in diabetic miniature pigs,despite it being a good model animal for assessing diabetes.Methods:In this study,a mini-pig diabetes model(DM)was established by 9-month high-fat diet(HFD)combined with lowdose streptozotocin,while the animals fed standard chow diet constituted the control group.16S ribosomal RNA(rRNA)gene sequencing was performed to assess the characteristics of the intestinal microbiome in diabetic mini-pigs.Results:The results showed that microbial structure in diabetic mini-pigs was altered,reflected by increases in levels of Coprococcus_3 and Clostridium_sensu_stricto_1,which were positively correlated with diabetes,and decreases in levels of the bac-teria Rikenellaceae,Clostridiales_vadinBB60_group,and Bacteroidales_RF16_group,which were inversely correlated with blood glucose and insulin resistance.Moreover,PICRUSt-predicted pathways related to the glycolysis and Entner-Doudoroff superpathway,enterobactin biosynthesis,and the L-tryptophan biosynthesis were significantly elevated in the DM group.Conclusion:These results reveal the composition and predictive functions of the intestinal microbiome in the mini-pig diabetes model,further verifying the relationship between HFD,gut microbiome,and diabetes,and providing novel insights into the application of the mini-pig diabetes model in gut microbiome research.
  • 摘要：Since the beginning of the 21st century,with the wide application of molecular biology and genetic engineering technology,the more holistic discipline of laboratory animal sciences has also developed rapidly and many excellent innovations based on laboratory animals,animal models and experimental medicine have continued to emerge.Animal Models and Experimental Medicine(AMEM)was launched in 2018,which was timely and attracted the attention of the industry.Four years have passed and AMEM has achieved fruitful results.
  • 摘要：The year 2022 marks the fifth year of the publication of Animal Models and Experimental Medicine( AMEM). We are intensely proud of the publication of each paper, because we recognize that all our efforts are worthwhile to provide a platform for communication and sharing of outstanding scientific results and reinforce the discipline position of animal models and experimental medicine.
  • 摘要：Background:Largely due to incidental detection,asymptomatic pancreatic cystic le-sions(PCLs)have become prevalent in recent years.Among them,intraductal papillary mucinous neoplasm(IPMN)infrequently advances to pancreatic ductal adenocarcinoma(PDAC).Conservative surveillance versus surgical intervention is a difficult clinical decision for both caregivers and PCL patients.Because RNF43 loss-of-function mutations and KRAS gain-of-function mutations concur in a subset of IPMN and PDAC,their biological significance and therapeutic potential should be elucidated.Methods:Pancreatic Rnf43 knockout and Kras activated mice(Rnf43^(−/−);Kras^(G12D))were generated to evaluate their clinical significance in pancreatic pre-neoplastic initiation and malignant transformation.Results:Loss of Rnf43 potentiated the occurrence and severity of IPMN and PDAC in oncogenic Kras mice.The Wnt/β-catenin signaling pathway was activated in pan-creatic Kras^(G12D)and Rnf43 knockout mice and the PORCN inhibitor LGK974 blocked pancreatic IPMN initiation and progression to PDAC accordingly.Conclusions:Rnf43 is a tumor suppressor in the prevention of pancreatic malignant transformation.This genetically reconstituted autochthonous pancreatic Rnf43^(−/−);Kras^(G12D)preclinical cancer model recapitulates the pathological process from pancreatic cyst to cancer in humans and can be treated with inhibitors of Wnt/β-catenin signaling.Since the presence of RNF43 and KRAS mutations in IPMNs predicts future development of advanced neoplasia from PCLs,patients with these genetic anomalies warrant surveillance,surgery,and/or targeted therapeutics such as Wnt/β-catenin inhibitors.
  • 摘要：Background:The Omicron(B.1.1.529)SARS-COV-2 variant has raised serious concerns because of its unprecedented rapid rate of spreading and the fact that there are 36 mutations in the spike protein.Since the vaccine-induced neutralizing antibody targets are the spike protein,this may lead to the possibility of vaccine-induced hu-moral immunity escape.Methods:We measured the neutralizing activity in vitro for Omicron and compared this with wild type(WH-09)and Delta variants in human and monkey sera from different types of immunity.The monkey sera samples were collected at 1 and 3 months post three-dose inactivated(PiCoVacc)and recombinant protein(ZF2001)vaccination.Human sera were collected from 1 month post three-dose inactivated vaccination.Results:In inactivated vaccine sera,at 1/3 months post three-dose,geometric mean titers(GMTs)of neutralization antibody(NAb)against the Omicron variant were 4.9/5.2-fold lower than those of the wild type.In recombinant protein vaccine sera,GMTs of NAb against Omicron were 15.7/8.9-fold lower than those of the wild type.In human sera,at 1 month post three-dose inactivated vaccination,GMTs of NAb against Omicron were 3.1-fold lower than those of the wild type.Conclusion:This study demonstrated that despite a reduction in neutralization titers,cross-neutralizing activity against Omicron and Delta variants was still observed after three doses of inactivated and recombinant protein vaccination.

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