Introduction
Miroslav Holub in Immunology of Nude Mice, 2020
The nude mutant may have been here since 1962, or indeed since 1850, when two hairless mice died in a zoologist’s grape vase and the third one escaped. Even since 1962 or 1968, the year the immunological career of the nude mutant started, when it occurred to one of the nude mice pioneers to check what the nude mouse had inside, the nude mouse may have changed considerably due to nu gene transfer to different background strains and for different levels of backcrossing, and as a result of progressively improving housing conditions, breeding and husbandry, with consequent elimination of some known or unknown natural pathogens. It cannot be claimed that an SPF BALB/c(10th backcross)nu/nu mouse of 1987 is exactly the same as such a mouse from 1972. This is very good for the mouse which nowadays has litters from homozygous (nu/nu x nu/nu) matings in almost every breeding center — a rarity 15 years ago; but this is not good for the results or the comparability of immunological and physiological studies (Figure 1).
The Nude (nu) and Streaker (nustr) Mutations, Chromosome 11
John P. Sundberg in Handbook of Mouse Mutations with Skin and Hair Abnormalities, 2020
The nude mouse has been used in large numbers of studies, unrelated to skin research, in which immunodeficiency is useful. One of the more common uses is for tumor transplantation studies, which include skin tumors.40–42 Cutaneous xenographs from a variety of species have been successfully maintained on nu/nu mice.43,44 Grafts of human skin with a variety of diseases have been used to study normal skin,44–50 sebaceous glands,51 lamellar ichthyosis,47,52 alopecia areata,53,54 balding,55 psoriasis,56–59 and other diseases. Nude mice are also useful for studying the skin of new mouse mutations that exist in very few numbers or exist on hybrid backgrounds for which syngeneic grafts cannot be done (Figure 7).60
Immunopathogenesis and Therapy of Gonadal Disorders and Infertility
George S. Eisenbarth in Immunotherapy of Diabetes and Selected Autoimmune Diseases, 2019
Afollicular premature ovarian failure may result from a variety of causes. Infections have the most impact at periods of high follicle turnover such as at birth, puberty, and peripartum. Viral oophoritis associated with mumps is a common cause.5 Mycobacterial infections, toxins, radiation therapy, chemotherapy (e.g., cyclophosphamide), and surgery exert physical or environmental insult to the ovary.6,7 Congenital disorders may be associated with accelerated follicular atresia. Turner’s syndrome (monosomy X) is associated with a normal number of follicles at 20 weeks gestation and normal histology until the fourth intrauterine month. This is followed by accelerated follicular loss.8-11 Sex chromosome mosaicism 45, XO/46, XX improves ovarian function when compared with Turner’s syndrome, and menstruation may occur in up to 30%.12 Accelerated atresia may also occur in the presence of thymic aplasia.13 An example of this is the athymie nude mouse model. Thymic peptides may stimulate GnRH. Ataxia telangiectasia, myotonia dystrophica, and galactosemia (possible failure of germ cell migration) have all been associated with premature menopause.14 Familial afollicular premature menopause has been reported and may be X-linked dominant or possibly autosomal dominant. Autoimmune disease may also cause an afollicular (or decreased follicular number) form of premature ovarian failure.
The latest animal models of ovarian cancer for novel drug discovery
Published in Expert Opinion on Drug Discovery, 2018
Elizabeth Magnotti, Wayne A. Marasco
The most common strains of mice that have been utilized for in vivo ovarian cancer mouse models are the Nude mouse and the SCID mouse. The Nude mouse contains the autosomal recessive nu mutation, which causes thymic dysgenesis [53]. Consequently, Nude mice lack T cells and suffer from a lack of cell-mediated immunity. While Nude mice offer the advantage in that tumor growth can be easily observed due to their absence of hair, tumor xenografts in Nude mice are constrained by poor tumor growth, host-versus-graft reactivity, and an altered tumor microenvironment, due to the presence of functional humoral immunity and NK cells in these mice [54]. The SCID mouse contains a scid mutation which causes defective rearrangement of genes that code for antigen-specific receptors on B cells and T cells and consequently deficiencies in mature B and T cells [40]. Although the SCID mouse supports local and metastatic growth of tumor cells, SCID mice are prone to the development of thymic lymphoma and leakiness in which T cells and B cells develop in aged mice [39].
Qici Sanling decoction suppresses bladder cancer growth by inhibiting the Wnt/Β-catenin pathway
Published in Pharmaceutical Biology, 2019
Hua Gong, Weihua Chen, Lanhua Mi, Dan Wang, Youkang Zhao, Chao Yu, Aiguang Zhao
BALB/c-nu nude mice were purchased from the Shanghai Laboratory Animal Research Centre (Shanghai, China). All mice were 4–6 weeks old and housed at 20–23 °C in a 12 h light/dark cycle with food and tap water supplied ad libitum. Nude mouse xenograft models were established as previously described (Zhao P et al. 2016). T24 cells were collected and washed twice in PBS, then the cells were resuspended in PBS to a concentration of 2 × 107 cells/mL. Each mouse was subcutaneously injected with 0.2 mL of cell suspension under the right armpit. Tumour growth was monitored by measuring tumour diameters every 3 days. Tumour volume (mm3) was calculated using the equation, V = 0.5 (LW2), where L and W are the length and width of the tumour. After almost 2 weeks, 30 mice were randomly divided into five groups (control; 20 mg/kg XAV-939; 100, 200, and 400 mg/kg QCSL) and each group was given different treatments by gavage once a day. XAV-939 treatment was used as positive control and PBS treatment was used as a negative control. After 7 weeks, the mice were anaesthetised by isoflurane and xenografts were excised. Part of xenografts was fixed in 10% (v/v) formalin for pathological and immunohistochemical examination. Part of the xenografts was frozen for real-time PCR and western blot.
Ultrasound-mediated nanobubble destruction (UMND) facilitates the delivery of A10-3.2 aptamer targeted and siRNA-loaded cationic nanobubbles for therapy of prostate cancer
Published in Drug Delivery, 2018
Meng Wu, Hongyun Zhao, Liang Guo, Yiru Wang, Jiao Song, Xueli Zhao, Chongyan Li, Lan Hao, Dong Wang, Jie Tang
LNCaP cells (human prostate cancer cells line) were from American Type Culture Collection (ATCC, Manassas, VA) and PC3 cells (human prostate cancer cells line) were obtained from Department of Urology, The First Affiliated Hospital of Chongqing Medical University (Chongqing, China). Cells were cultured using DMEM F12 culture medium containing 10% heat-inactivated fetal bovine serum at a 37 °C and 5% CO2 incubator. BALB/c nude mice (male, four to six weeks aged, ∼20 g) were provided from the Laboratory Animal Centre of Chongqing Medical University. Tumor cells were implanted into BALB/c nude mice for the growth into tumor xenografts. Resuspension of the cells (1 × 107/mL) in 0.2 mL of PBS was done, followed by subcutaneous injection into the right hip. Twenty-one days after inoculation with the tumor cells, xenograft growth was successful (150 mm3), and experiments were performed according to the International Guiding Principles. Approval for all of the experimental and nude mouse treatments was received from the Animal Ethics Committee of Chongqing Medical University.
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