Murine Coronavirus-Induced Subacute Fatal Peritonitis in C57BL/6 Mice Deficient in Gamma Interferon

Gamma interferon-deficient (IFN-γ−/−) mice with a C57BL/6 background were infected intraperitoneally with mouse hepatitis virus strain JHM (JHMV). In contrast to IFN-γ-+/− and IFN-γ+/+ mice, JHMV persisted in IFN-γ−/− mice and induced death during the subacute phase of the infection. Unexpectedly, infected IFN-γ−/− mice showed severe peritonitis accompanying the accumulation of a viscous fluid in the abdominal and thoracic cavities in the subacute phase. Destructive changes of hepatocytes were not observed. Administration of recombinant IFN-γ protracted the survival time of IFN-γ−/− mice after JHMV infection. These results demonstrate that IFN-γ plays a critical role in viral clearance in JHMV infection. They also show that a resultant persistent JHMV infection induces another form of disease in IFN-γ−/− mice, which bears a resemblance to feline infectious peritonitis in cats.     

不同方法建立C57BL/6J小鼠抑郁症模型的探讨

目的用不同方法建立C57BL/6J小鼠抑郁症模型,为探讨GalR蛋白对小鼠抑郁症的治疗作用打下基础。方法 C57BL/6J小鼠经体重、敞箱实验及反抗抓获实验初筛后,随机分为4组:Ⅰ.CUMS组,Ⅱ.CUMS+CORT组,Ⅲ.CORT组,Ⅳ.正常对照组。每天记录小鼠体重及摄食量。28d后进行液体消耗及强迫游泳实验测试。结果小鼠抑郁模型在第28d建立成功。Ⅱ组小鼠短期内体重迅速下降并死亡。与Ⅰ组小鼠相比,Ⅲ组小鼠液体消耗和强迫游泳实验指标改变更明显。结论成功建立C57BL/6J小鼠抑郁症模型。CUMS和CORT模型结合,小鼠不能耐受,短期内死亡。单独CORT模型造模效果要优于CUMS模型。在后续试验中,将用CORT法建立C57BL/6J小鼠抑郁症模型。     

Blueberry and Mulberry Juice Prevent Obesity Development in C57BL/6 Mice

Objectives

To establish whether blueberry (Vaccinium ashei) and mulberry (Morus australis Poir) juice, anthocyanin rich fruit juice, may help counteract obesity.

Design

And Methods: Four-week-old C57BL/6 mice were fed a high-fat diet (HFD) with or without blueberry and mulberry juice for 12 weeks. Body weight, serum and hepatic lipids, liver and adipose tissues morphology, insulin and leptin were assessed.

Results

Mice fed HFD exhibited increased body weight, insulin resistance, serum and hepatic lipids. In comparison, blueberry and mulberry juice inhibited body weight gain, decreased the serum cholesterol, reduced the resistance to insulin, attenuated lipid accumulation and decreased the leptin secretin.

Conclusion

These results indicate that blueberry and mulberry juice may help counteract obesity.     

Accelerated Progression of a Murine Retrovirus-Induced Immunodeficiency Syndrome In Fas Mutant C57BL/6/lpr/lpr Mice

We reported previously that CD4⁺ T cells and B cells in mice with retrovirus-induced murine acquired immunodeficiency syndrome (MAIDS) caused by LP-BM5 murine leukemia virus (MuLV) mixtures increased the expression of Fas antigen (Fas) during progression of the disease. However, the contribution of the Fas/Fas ligand (Fas L) system to the pathogenesis of MAIDS remained unknown. Here, we examined the susceptibility of C57BL/6 (B6) lpr/lpr mice, which has been reported to be defective for the expression of Fas, to MAIDS. We found that the Thy 1.2^? CD4 T cells and IgK dull B220⁺ cells, which are characteristic of MAIDS, increased after the inoculation of LP-BM5 MuLV in B6 lpr/lpr mice. B22⁺ TCR αβ T cells, unique to lupus prone mice, also increased in the B6 lpr/lpr mice after infection. CD4⁺ B220⁺ TCR αβ T cells increased profoundly among the B220⁺ TCR αβ T cells from LP-BM5 MuLV-infected B6 lpr/lpr mice, while the B220⁺ TCR αβ T cells observed in non-infected B6 lpr/lpr mice were largely of the CD4^? CD8^? phenotype. A DNA PCR analysis of the LP-BM5 MuLV-infected B6 lpr/lpr mice revealed the genome integration of defective LP-BM5 virus, further confirming that MAIDS is inducible to B6 lpr/lpr mice. LP-BM5 MuLV-infected lpr/lpr mice died within 3 months, while MAIDS-infected B6 +/+ mice usually died within 5 to 6 months, and B6 lpr/lpr mice not infected with LP-BM5 MuLV lived more than 6 months. Taken together, these results suggest that MAIDS is inducible independently with functional Fas expression and the possibility of accelerated progression of murine AIDS and lpr-associated autoimmune disease in B6 lpr/lpr mice infected with LP-BM5 MuLV.     

C57BL/6J-HBV转基因小鼠的繁育与检测

目的　摸清C57BL 6J -HBV转基因小鼠的繁育规律 ,建立可靠的HBsAg表达检测方法。方法　对C57BL 6J-HBV转基因小鼠两种不同交配方式的繁殖性能和HBsAg的表达情况进行比较研究 ;应用免疫组化的方法证实血清学诊断HBsAg的准确性并用激光扫描共聚焦显微镜确定HBsAg在肝细胞中的表达部位。结果与结论　从繁殖性能来看 ,两种交配方式窝产仔数差异不显著 (P >0 .0 5 ) ,而离乳数差异具有显著性 ( 0 .0 1

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Perinatal Exposure to Low-Dose Methoxychlor Impairs Testicular Development in C57BL/6 Mice

Methoxychlor (MXC), an organochlorine pesticide, has adverse effects on male reproduction at toxicological doses. Humans and wild animals are exposed to MXC mostly through contaminated dietary intake. Higher concentrations of MXC have been found in human milk, raising the demand for the risk assessment of offspring after maternal exposure to low doses of MXC. In this study, pregnant mice (F0) were given intraperitoneal daily evening injections of 1 mg/kg/d MXC during their gestational (embryonic day 0.5, E0.5) and lactational periods (postnatal day 21.5, P21.5), and the F1 males were assessed. F1 testes were collected at P0.5, P21.5 and P45.5. Maternal exposure to MXC disturbed the testicular development. Serum testosterone levels decreased, whereas estradiol levels increased. To understand the molecular mechanisms of exposure to MXC in male reproduction, the F1 testes were examined for changes in the expression of steroidogenesis- and spermatogenesis- related genes. RT-PCR analysis demonstrated that MXC significantly decreased Cyp11a1 and increased Cyp19a1; furthermore, it downregulated certain spermatogenic genes (Dazl, Boll, Rarg, Stra8 and Cyclin-a1). In summary, perinatal exposure to low-dose MXC disturbs the testicular development in mice. This animal study of exposure to low-dose MXC in F1 males suggests similar dysfunctional effects on male reproduction in humans.     

Endpoint Refinement for Total Body Irradiation of C57BL/6 Mice

Acute radiation syndrome is a life-threatening condition that has the potential to affect large populations of humans. Although several animal models of this syndrome are available, the total-body–irradiated mouse has emerged as an important tool to evaluate the efficacy of prospective prophylaxis, mitigation, and treatment compounds. Despite the widespread use of this model, humane endpoints have not been clearly identified. To address this issue, we developed a cageside observation-based scoring system specifically for total-body–irradiated mice to assess the progression of clinical signs associated with acute radiation syndrome. Male C57BL/6 mice (n = 175; age, 8 to 9 wk) received an anticipated LD₅₀ dose of radiation and were observed for progression of clinical signs of acute radiation syndrome for 30 d. All mice were scored individually through cageside observation of their body posture (score, 0 to 3), eye appearance (0 to 3), and activity level (0 to 3). Retrospective analysis of the score data indicated that death could be predicted accurately by using increasing cumulative scores (0 to 9). Total scores of 6, 7, 8, and 9 were associated with mortality rates of 78.6%, 86.4%, 93.3%, and 100%, respectively. Furthermore, scores of 6, 7, and 8 predicted death within 3, 1.5, and 0.5 d, respectively. The use of this scoring system provides investigators and IACUCs with predictive humane, surrogate endpoints for total-body–irradiated mice. This system allows preemptive euthanasia of mice before they become moribund, thereby minimizing pain and distress associated with acute radiation syndrome and improving animal welfare.Abbreviations: ARS, acute radiation syndrome; LD_50/30, the dose of radiation that is lethal for 50% of the test subjects within 30 d; TBI, total body irradiationAcute radiation syndrome (ARS) due to either accidental radiation exposure or nuclear attack is a life-threatening condition that has the potential to affect a large population of people. The severity of ARS is dependent on the overall dose, dose rate, radiation quality, and proportion of the body that is irradiated. ARS typically progresses through 4 clinical phases: prodrome, latency, illness, and either recovery or death.^1,7 The prodromal period is characterized by nausea, vomiting, and fatigue and can include autonomic instability and loss of consciousness at high doses in humans.¹ After the latent phase, which can be absent with high doses of radiation, the illness phase manifests in various organ systems as particular syndromes of the hematopoietic, gastrointestinal, skin, and neurovascular systems.^1,8 The hematopoietic system is the most sensitive to radiation, and decreased blood cell counts can be detected even in asymptomatic patients.¹ Increasing radiation doses cause complete destruction of bone marrow, sloughing of the mucosal layer of the gastrointestinal system, skin burns, and breakdown of the neurologic and cardiovascular systems, ultimately resulting in death.^1,8Preparatory planning for the medical management of ARS is essential and requires the use of total body irradiation (TBI) models in animals to evaluate the efficacy of prospective prophylaxis, mitigation, and treatment compounds.^8,28 The 2 body systems most sensitive to TBI are the hematopoietic and gastrointestinal systems, and mice are an excellent model for both; the C57BL/6 and C3H/He strains are used most often.²⁸ To study the hematopoietic syndrome, the most widely used TBI condition for acute radiation damage is the LD₅₀, because of the temporal predictability of the development of subsequent clinical signs. The temporal sequence and outcome of the hematopoietic syndrome occur considerably more rapidly in mice than in humans, and the experimental outcome is defined as the LD_50/30 (50% population death within 30 d of irradiation) in mouse models.²⁸ In addition, because mice have been deemed an appropriate species for testing radioprotectors or mitigators, the clinical efficacy of various drugs can be evaluated easily in a mouse TBI model.²⁸Although mice are an exceedingly common model for ARS, there are currently no established humane endpoint criteria for these types of studies. Similar to sepsis models, TBI and ARS studies typically use LD_50/30 as the standard of comparison, and this practice has resulted in the frequent and widespread use of death or moribund state as the experimental endpoint.^5,7,18,26 The moribund condition, an unresponsive and immobile animal, is a commonly used endpoint for a variety of research protocols associated with high mortality or progressive and severe disease states.^23,24 Using this criterion requires the animal to progress through all potential phases of pain and distress associated with the chosen model to a near-death state before the animal is euthanized.¹⁷The ability to predict death with a high probability and high accuracy in TBI studies would allow for preemptive euthanasia, with the intent to (1) ameliorate terminal pain and distress associated with ARS and (2) improve animal welfare. To this end, the current study sought to establish an observation-based scoring system to assess the health status of irradiated mice. Specifically, mice that received a targeted LD_50/30 TBI dose were evaluated by using daily cageside observational scoring of body posture, eye appearance, and activity level. This observation-based study was performed in conjunction with an approved IACUC study of the effects of synthetic parathyroid hormone in irradiated mice. The results were analyzed to identify the predictive nature of these criteria of impending death, with the goal of establishing useful endpoint criteria for future TBI studies.     

High-Efficient FLPo Deleter Mice in C57BL/6J Background

Conditional gene manipulation in mice becomes a routine for genetic studies of mammalian gene functions. Additional site-specific recombinases such as FLP or φ31 provide one more level of gene manipulation flexibility. The recombination activity of the currently available FLP deleter mice remains low. We generated a new FLP deleter mouse line with the mouse codon-optimized FLPo gene in C57BJ/6 background, which showed superior recombination efficacy in comparison to FLPe deleter mice. 100% complete removal of FRT-flanked Neo cassette was observed in all F1 progeny mice carrying both FLPo and Neo cassette, which can be transmitted to F2 generation independent of FLPo activity. Our new FLPo transgenic mice (on pure C57BJ/6 background) will largely facilitate the gene targeting process and is valuable for conditional gene manipulation.     

乙酰基亚硝基脲(ENU)对C57BL/6J雄鼠睾丸组织的影响

目的 观察乙酰基亚硝基脲(ENU)对雄鼠睾丸及其他组织器官的影响,分析引起小鼠死亡的原因,探索ENU处理雄鼠后的最佳配种时间.方法 将8～10周龄的C57BL/6J雄鼠分为实验组和对照组.实验组腹腔注射ENU 100 mg/kg,每周1次,共3次,对照组以同样方法注射生理盐水.首次注射ENU后的第1周至12周,每周分别取4只实验组小鼠和对照组小鼠剖检及组织病理学观察;取其睾丸附睾称重及精子计数.记录死亡小鼠数量,并对其剖检及组织病理学观察.结果 对死亡小鼠剖检发现胸腔纵隔内有巨大肿块,明显压迫心脏;组织切片观察发现睾丸和肝脏有明显病变.实验组小鼠睾丸从ENU处理的第2周起开始萎缩,第9周开始恢复;精子数量第4周至第9周稀少.结论 ENU为小鼠的一种强诱变剂,纵隔肿瘤是导致雄鼠死亡的主要原因,雄鼠注射ENU后最佳配种时间应在首次注射后的第9周.     

Pectin- Derived Acidic Oligosaccharides Improve the Outcome of Pseudomonas aeruginosa Lung Infection in C57BL/6 Mice

The administration of prebiotics as oligosaccharides (OS), by acting on intestinal microbiota, could modulate the immune and inflammatory response and represent a new strategy to improve the outcome of bacterial infection. The aim of this study was to determine whether pectin-derived acidic oligosaccharides (pAOS) could modulate the outcome of pulmonary P. aeruginosa (PA) infection in C57BL/6 mice, which develop a Th1 response to PA lung infection. Mice were randomized for 5 weeks to consume a control or a 5% pAOS diet and chronically infected by PA. Resistance to a second PA infection was also analyzed by reinfecting the surviving mice 2 weeks after the first infection. Compared with control mice, mice fed pAOS had reduced mortality (P<0.05). This improvement correlated with a better control of the inflammatory response with a lower neutrophil count on day 1 (P<0.05), a sustained neutrophil and macrophage recruitment on days 2 and 3 (P<0.01) a greater and sustained IL-10 release in lung (P<0.05) and a reduction of the Th1 response and M1 activation with a lower IFN-γ/IL-4 (P<0.01) and nos2/arg1 (P<0.05) ratios. These results coincided with a modulation of the intestinal microbiota as shown by an increased butyric acid concentration in feces (P<0.05). Moreover, pAOS decreased the bacterial load (P<0.01) in mice reinfected 2 weeks after the first infection, suggesting that pAOS could reduce pulmonary exacerbations. In conclusion, pAOS improved the outcome of PA infection in C57BL/6 mice by modulating the intestinal microbiota and the inflammatory and immune responses.     

小鼠动物实验方法系列专题(三) 三硝基苯磺酸诱导的C57/BL6小鼠结肠炎模型的建立方法

2,4,6-三硝基苯磺酸(TNBS)诱导的小鼠结肠炎模型是研究人类炎性肠病(inflammatory bowl disease,IBD)的主要手段之一,但在实际应用中,常用的C57/BL品系小鼠却对TNBS有较高耐受性,不易建模。本文主要介绍一种可以有效诱导C57/BL6小鼠TNBS结肠炎的方法,并对疾病评价指标进行了具体的描述。对基因工程小鼠IBD模型的研究具有重要意义。     

链脲佐菌素诱导C57BL/6J小鼠2型糖尿病模型研究

目的建立与2型糖尿病(非胰岛素依赖型糠尿病、NIDDM)病人临床特征和发病过程相似的NIDDM动物模型.方法用高脂肪饲料喂养C57BL/6J雄性断乳小鼠3周,腹腔注射链脲佐菌素(STZ),继续喂养4周,测定给药前和给药后1、3、4周非空腹血糖、实验结束时非空腹胰岛素水平,观察胰腺形态学变化.结果喂养3周后(给药前)高脂饲料-STZ组及高脂饲料-柠檬酸组血糖浓度(7.0±0.39)mmol/L、( 6.8±0.45)mmol/L高于普通饲料-STZ组及普通饲料-柠檬酸组(5.3±0.40)mmol/L、(5. 4±0.39)mmol/L,P＜0.05;实验结束时,高脂饲料-STZ组血糖浓度(13 .1±2.01)mmo/L高于高脂饲料-柠檬酸(6.9±0.46)mmol/L、普通饲料-柠檬酸组(6.0± 0.46)mmol/L和普通饲料-STZ组(7.1±0.62)mmol/L(P＜0.05),各组间血浆胰岛素浓度、体重及饮水量差异无显著性,P＞0.05;实验过程中高脂饲料STZ组和柠檬酸组小鼠每天进食热量(64.49±9.2)kJ/只,(70.7±9.6)kJ/只, 显著高于普通饲料STZ组和柠檬酸组(52.7±7.9)kJ/只,(57.3±11.7)kJ/只;各组小鼠胰腺和胰岛细胞形态正常.结论高脂肪饲料和STZ是用C57BL/6J断乳幼鼠建立NIDDM模型所必须的,100mg/kg体重STZ对普通饲料小鼠血糖无影响;用高脂饲料和STZ 处理的小鼠血糖升高、胰岛素浓度正常,与NIDM病人临床特征和发病过程相似;C57BL/6J小鼠易得,建模方法简便,费用低,是在NIDDM实验研究中能广泛使用的较理想的非遗传性NID DM动物模型.     

Long-Term Artificial Sweetener Acesulfame Potassium Treatment Alters Neurometabolic Functions in C57BL/6J Mice

With the prevalence of obesity, artificial, non-nutritive sweeteners have been widely used as dietary supplements that provide sweet taste without excessive caloric load. In order to better understand the overall actions of artificial sweeteners, especially when they are chronically used, we investigated the peripheral and central nervous system effects of protracted exposure to a widely used artificial sweetener, acesulfame K (ACK). We found that extended ACK exposure (40 weeks) in normal C57BL/6J mice demonstrated a moderate and limited influence on metabolic homeostasis, including altering fasting insulin and leptin levels, pancreatic islet size and lipid levels, without affecting insulin sensitivity and bodyweight. Interestingly, impaired cognitive memory functions (evaluated by Morris Water Maze and Novel Objective Preference tests) were found in ACK-treated C57BL/6J mice, while no differences in motor function and anxiety levels were detected. The generation of an ACK-induced neurological phenotype was associated with metabolic dysregulation (glycolysis inhibition and functional ATP depletion) and neurosynaptic abnormalities (dysregulation of TrkB-mediated BDNF and Akt/Erk-mediated cell growth/survival pathway) in hippocampal neurons. Our data suggest that chronic use of ACK could affect cognitive functions, potentially via altering neuro-metabolic functions in male C57BL/6J mice.     

Treatment with Extracellular Vesicles from Giardia lamblia Alleviates Dextran Sulfate Sodium-Induced Colitis in C57BL/6 Mice

Inflammatory bowel disease (IBD) is a chronic and recurrent illness of the gastrointestinal tract. Treatment of IBD traditionally involves the use of aminosalicylic acid and steroids, while these drugs has been associated with untoward effects and refractoriness. The absence of effective treatment regimen against IBD has led to the exploration of new targets. Parasites are promising as an alternative therapy for IBD. Recent studies have highlighted the use of parasite-derived substances, such as excretory secretory products, extracellular vesicles (EVs), and exosomes, for the treatment of IBD. In this report, we examined whether EVs secreted by Giardia lamblia could prevent colitis in a mouse model. G. lamblia EVs (GlEVs) were prepared from in vitro cultures of Giardia trophozoites. Clinical signs, microscopic colon tissue inflammation, and cytokine expression levels were detected to assess the effect of GlEV treatment on dextran sulfate sodium (DSS)-induced experimental murine colitis. The administration of GlEVs prior to DSS challenge reduced the expression levels of pro-inflammatory cytokines, including tumor necrosis factor alpha, interleukin 1 beta, and interferon gamma. Our results indicate that GlEV can exert preventive effects and possess therapeutic properties against DSS-induced colitis.     

Diet-Induced Obesity in Male C57BL/6 Mice Decreases Fertility as a Consequence of Disrupted Blood-Testis Barrier

Obesity is a complex metabolic disease that is a serious detriment to both children and adult health, which induces a variety of diseases, such as cardiovascular disease, type II diabetes, hypertension and cancer. Although adverse effects of obesity on female reproduction or oocyte development have been well recognized, its harmfulness to male fertility is still unclear because of reported conflicting results. The aim of this study was to determine whether diet-induced obesity impairs male fertility and furthermore to uncover its underlying mechanisms. Thus, male C57BL/6 mice fed a high-fat diet (HFD) for 10 weeks served as a model of diet-induced obesity. The results clearly show that the percentage of sperm motility and progressive motility significantly decreased, whereas the proportion of teratozoospermia dramatically increased in HFD mice compared to those in normal diet fed controls. Besides, the sperm acrosome reaction fell accompanied by a decline in testosterone level and an increase in estradiol level in the HFD group. This alteration of sperm function parameters strongly indicated that the fertility of HFD mice was indeed impaired, which was also validated by a low pregnancy rate in their mated normal female. Moreover, testicular morphological analyses revealed that seminiferous epithelia were severely atrophic, and cell adhesions between spermatogenic cells and Sertoli cells were loosely arranged in HFD mice. Meanwhile, the integrity of the blood-testis barrier was severely interrupted consistent with declines in the tight junction related proteins, occludin, ZO-1 and androgen receptor, but instead endocytic vesicle-associated protein, clathrin rose. Taken together, obesity can impair male fertility through declines in the sperm function parameters, sex hormone level, whereas during spermatogenesis damage to the blood-testis barrier (BTB) integrity may be one of the crucial underlying factors accounting for this change.     

Comparison of 3 Topical Treatments against Ulcerative Dermatitis in Mice with a C57BL/6 Background

Ulcerative dermatitis (UD) is a common condition in C57BL/6 mice and strains with this background. The etiology of UD is unclear but appears to have a genetic component associated with the C57BL/6 strain and has been reported as secondary to a variety of conditions. Treatment is unrewarding, resulting in euthanasia in many cases. In the present study we compared 3 topical treatments against spontaneous UD in mice with a C57BL/6 background. In total, 301 mice of both sexes were included in this study, and the tested treatments comprised bacitracin–neomycin sulfate–polymixin B sulfate ointment twice daily, 10% povidone–iodine ointment plus 1% silver sulfadiazine cream once daily, and 0.005% sodium hypochlorite once daily. Lesion healing was defined as complete skin reepithelialization with or without hair regrowth. Sex, age, lesion location, and type and length of treatment were analyzed by using univariate and multivariate logistic regression. Of the 79 mice treated with triple-antibiotic ointment, 27 (34%) healed, compared with 43 of the 125 (34%) treated with povidone–iodine and sulfadiazine and 69 of the 97 (71%) treated with hypochlorite. Lesion size and treatment with 0.005% sodium hypochlorite were the only significant predictors of healing; all other variables were not statistically significant in multivariate analysis. We conclude that 0.005% sodium hypochlorite is an effective topical treatment alternative for UD in C57BL/6 mice and strains on this background, and a favorable prognosis depends on the early identification and treatment of those lesions.Abbreviations: B6, C57BL/6; UD, ulcerative dermatitisUlcerative dermatitis (UD) is a common condition in C57BL/6 (B6) mice and strains with a B6 background.^1,21 Early lesions are characterized by small skin erosions that can affect any part of the body but are typically found between the scapulae. Usually these lesions rapidly progress to form large, irregular areas of ulcerated skin.¹ The condition can be very pruritic, resulting in self-mutilation, skin degloving, and exposure of the subcutaneous tissues and, in some cases, musculature.¹ Common sequelae in mice that recover from this disease are marked lymphadenopathy and splenomegaly due to reactive immune modulation or activation, which can confound research results.^21,31 When UD affects extensive areas and then heals, contracture and scarring of the skin cause tension that alters normal posture and ambulation.¹Primary (idiopathic) UD is diagnosed by ruling out other conditions that cause dermatitis (secondary) in laboratory mice, such as allergy to fur mites,^8,18 fight wounds, staphylococcal skin infections,^20,32 phenotype,^19,21,31 and experimental manipulation.^13,22,33 The exact etiology of UD remains undetermined but seems to be multifactorial.⁹ Proposed etiologies include behavioral,^10,11,34,35 immune-complex–induced vasculitis,¹ cellular oxidative injury,²¹ and vitamin A toxicity.³¹ Calorie-restricted diets, providing 60% of the average calorie intake of the respective unrestricted group, seem to reduce ulcerative dermatitis,²⁸ whereas high-fat diets (35% crude fat) appear to exacerbate the condition.²⁷ UD has been reported to affect more female than male mice, with the highest incidence in mice older than 1 y, but UD can also occur in young mice.^1,19,31 Although UD occurs throughout the year, some authors report a peak incidence during spring and fall, whereas others note increased case numbers during the summer months.^19,31Attempts to find a cure for UD have not found a treatment that is completely effective. Treatment typically is unrewarding, resulting in euthanasia in many cases.²¹ Dietary supplementation with vitamin E reportedly has some efficacy favoring skin reepithelization in mice with UD.²¹ However, a recent study using vitamin E as a diet supplement to prevent the occurrence of UD yielded contradictory results.²⁴ In that study, mice fed a vitamin-E–fortified diet since weaning were more likely to develop UD than were mice fed a regular diet. However, to achieve the desire amount of vitamin E, the fat content of the diet had to be increased; high dietary fat is known to exacerbate UD.^24,27 Other studies have shown systemic administration of maropitant citrate reduces the size of UD lesions in mice by decreasing scratching,³⁵ and the oral administration of ibuprofen appears to help speed the healing of skin lesions by reducing inflammation and pain.¹¹ Topical and systemic antibiotics, corticosteroids, antihistamines, and lidocaine are poorly effective in the treatment of UD.^1,19,21,31 Among topical treatments, caladryl lotion, chlorhexidine, and cyclosporine appear to be the most effective in treating UD.^7,12,23 Toenail trimming has been reported as effective at reducing self-trauma due to scratching in UD, thus helping to speed healing.^26,29In the present study, we compared 3 topical treatments against spontaneous UD in mice with a B6 background.     

Differences in anxiety-related behavior between apolipoprotein E-deficient C57BL/6 and wild type C57BL/6 mice

The influence of ApoE gene deletion on the anxiety state has not been previously investigated. The elevated plus maze was used in this study to determine differences in anxiety-related behavior between apoE-deficient and wild type C57BL/6 mice. The apoE-deficient mice demonstrated less anxiety on the elevated plus maze by spending more time in the open arms of the elevated plus maze compared to wild type mice (p<0.001). Additionally, female apoE-deficient mice visited the open arm of the maze more often than their apoE-deficient male counterpart (p<0.05). The anxiety state and/or sex are possible variables to be considered when designing physiological and/or behavioral studies involving mice that are apoE-deficient.