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Pediatric Disease Annotations & Medicines




Disease severe combined immunodeficiency
Phenotype |severe combined immunodefic
Sentences 174
PubMedID- 20020426 Adult male severe combined immunodeficient (scid) mice (c.b-17/icrhsd-scid) were purchased (harlan, indianapolis, in, http://www.harlan.com).
PubMedID- 25605016 Male severe combined immunodeficient (scid) mice, age-matched and 6~8 weeks old, were used in assays for tumor growth and lung metastasis in an orthotopic graft model.
PubMedID- 26301084 The study was conducted on male severe combined immunodeficient (scid) mice, 6 weeks old with an average body weight of ~20 g. all animals were maintained in pathogen-free sterile isolators and in a controlled atmosphere with a 12 h light to 12 h dark cycle according to institutional guidelines.
PubMedID- 24595136 Four-week-old female non-obese diabetic-severe combined immunodeficient (nod-scid) mice were purchased from the institute of zoology, chinese academy of sciences, and subcutaneously inoculated in the flank region with a suspension of h1975 cells (5.0×106 cells).
PubMedID- 26329825 Female balb/c severe combined immunodeficient (scid) mice (charles river, margate, uk) were housed in individually ventilated cages at a 12 hour light/dark cycle, with ad libitum access to food and water.
PubMedID- 23542179 Four-week male athymic nod cb17-prkdc/scid (severe combined immunodeficiency) mice were purchased from jackson laboratory and maintained in the animal facilities according to the protocol approved by the american association for accreditation of laboratory animal care.
PubMedID- 23056487 The severe combined immunodeficiency (scid) mice (6–8 weeks old, 18–20 g body weight), bred in-house, were maintained throughout in specific pathogen-free (spf) environment.
PubMedID- 23764770 Female cb17 mice at 6–8 weeks of age with severe combined immunodeficiency (scid) were used for in vivo tumor modeling studies (charles river laboratories inc., holister, ca) and were housed in polycarbonate cages using a hepa-filtered, ventilated rack system (allentown inc., allentown, nj).
PubMedID- 21931671 severe combined immunodeficient (scid)-beige mice were purchased from taconic (germantown, ny) and housed in a pathogen-free environment.
PubMedID- 24772353 severe combined immunodeficient (scid) mice lacking either t and b lymphocytes or nude mice lacking only t cells have impaired proliferation and neurogenesis in normal and ee housing compared to wild-type mice [155], as well as impaired performance in the water maze [156].
PubMedID- 26270350 severe combined immunodeficiencies are inherited disorders characterized by a block in the differentiation of the t lymphoid lineage and defects in other hematopoietic lineages.1, 2 the autosomal recessive severe combined immunodeficiency known as reticular dysgenesis (rd) is characterized by the absence of neutrophils, t and natural killer (nk) lymphocytes and by bilateral sensorineural deafness.
PubMedID- 25387827 severe combined immunodeficiency (scid) mice were subcutaneously injected with 6 × 106 m+g or m−g cells in 200 μl of dmem.
PubMedID- 26420058 Nonobese diabetic/severe combined immunodeficient (nod/scid) mice and cd-1 nude female mice were purchased from charles river laboratories (calco, italy) and maintained in hyperventilated cages.
PubMedID- 22469436 A 12-year-old girl with severe combined immunodeficiency was admitted to the freiburg university medical center, germany, in november 2009 for treatment of progressive respiratory problems and cytomegalovirus (cmv) disease.
PubMedID- 24497838 severe combined immunodeficiency (scid) beige mice were maintained in a pathogen–free environment under controlled conditions of light and humidity.
PubMedID- 25961067 Therefore, experiment 1 compared the water-maze performance of il-2 congenic mice on the severe combined immunodeficient (scid) background that we have bred in our colony, and have used in previous studies to disentangle the effects of the loss of brain-derived il-2 from peripheral il-2 on nerve injury and sensorimotor function [15,23].
PubMedID- 24083030 severe combined immunodeficiency (scid) or nude mice (charles river laboratories, wilmington, ma), approximately 4–6 weeks of age and weighing approximately 30 g received subcutaneous (sc) tumor implants performed using various ratios of gfp expressing sk-n-sh wild type cells (sk-n-sh gfp-wt) and sk-n-sh doxorubicin drug-resistant cells (sk-n-sh doxr) or sk-n-sh hmk (sk-n-sh hmk) cells with a total of 106 cells in 100 μl per implant.
PubMedID- 24487407 Five- to six-week-old cb-17 severe combined immunodeficiency (scid) male mice (charles river laboratories international, wilmington, ma, usa) had xenograft tumors induced by injecting 1×106 pc3 cells suspended in 50 μl of pbs subcutaneously in the upper hind legs of the animals.
PubMedID- 20668627 Ada deficiency is the major metabolic cause of severe combined immunodeficiency disease.31,32 ada is important for the development of the immune system in humans.
PubMedID- 23396406 severe combined immunodeficiency (scid) is a fatal syndrome characterized by the absence of t cells and, in some molecular types, also of b or nk cells.1,2 without immune reconstitution by hematopoietic stem cell transplantation or gene therapy, infants with scid will die in the first two years of life.
PubMedID- 24224014 6- to 8- week-old female cb-17 severe combined immunodeficient (scid) mice were obtained from the national cancer institute frederick animal production program and maintained in a pathogen-free facility prior to experiments according to guidelines of the animal research advisory committee of national institutes of health.
PubMedID- 21547019 When severe combined immunodeficient (scid) mice that lack b- and t-lymphocytes are challenged with p. gingivalis, there is considerably less bone resorption than in wild-type normal mice (114).
PubMedID- 26097871 Six to eight week-old female severe combined immunodeficiency (scid) and balb/c mice were purchased from charles river laboratories (calco, italy), and housed in our specific pathogen free (spf) animal facility.
PubMedID- 23502467 Six-week old female severe combined immunodeficient (scid)/beige mice were purchased from charles river laboratories (wilmington, ma, usa) and housed in the institutional animal facilities.
PubMedID- 26151747 Immunodeficient nonobese diabetous/shi-severe combined immunodeficiency/interleukin-2rgammanull (nsg) mice under 2.5% isoflurane anesthesia (belamont, piramal healthcare, northumberland, uk) were injected subcutaneously into the right flank with 105 ags reporter cells, gc10 or gc06 gastric tumor cells resuspended in 100 μl of 7 mg/ml matrigel (bd biosciences, le pont de claix, france) in ice cold pbs.
PubMedID- 24799913 Hypomorphic variants of rag genes with null mutations cause severe combined immunodeficiency (scid) as was found in an increasing number of patients with combined immunodeficiency [20].
PubMedID- 24533454 severe combined immunodeficient (scid) mice (5-7-week-old male cb.17.scid; charles river, wilmington, ma) were anesthetized with ketamine and xylazine, and 2 scaffolds were implanted in the subcutaneous space of the dorsal region of each mouse, i.e.
PubMedID- 24776983 severe combined immunodeficiency (scid) mice, which are deficient in t and b cells, appear to be resistant to the enteropathic effects of seb.
PubMedID- 24587182 Male cb-17 severe combined immunodeficient (scid) mice (6- to 8-weeks old; harlan laboratories, inc., indianapolis) were housed and monitored in our animal research facility.
PubMedID- 22174689 The absence of cd45 leads to a severe combined immunodeficiency (scid) phenotype in humans [31]–[33] and mice [34]–[36].
PubMedID- 22111002 severe combined immunodeficiency (scid) is a rare disease in which the affected organism is unable to mount an immune response due to loss of b and t lymphocytes.
PubMedID- 24454751 Nonobese diabetic/severe combined immunodeficiency (nod/scid) mice (sankyo-lab service, tsukuba, japan) were bred and maintained in accordance with our institutional guidelines for the use of laboratory animals.
PubMedID- 23226053 This is true of patients with ataxia telangiectasia (at), ataxia telangiectasia-like disorder, severe combined immunodeficiency, ligase iv syndrome, rothmund–thompson syndrome, seckel syndrome, werner syndrome, nijmegen breakage syndrome, all due to defective repair of double-strand breaks (dsbs)5 or stalled replication forks.6 it is also true of patients with fanconi anemia caused by defective repair of dna interstrand crosslinks (icls) and patients with xeroderma pigmentosum due to a defect in nucleotide excision repair (ner) of helix-distorting dna adducts.7,8 since nsclc and hnscc are treated with cisplatin and radiation therapy, it is logical to predict that patients with reduced dsb repair, single-strand break (ssb) repair, icl repair, or ner due to polymorphisms affecting the expression or function of dna repair proteins might be most responsive to dna damaging agents.
PubMedID- 20226009 Scid (severe combined immunodeficiency) mice were maintained in a specific pathogen-free environment in compliance with institutional policy and all animal procedures were previously approved by the iacuc (institutional animal care and use committee) at taipei medical university.
PubMedID- 24728301 The 6- to 8-week old male nod-scid mice (non-obese diabetes severe combined immunodeficiency mice) were used to evaluate the in vivo meta-static behavior of tumor cells.
PubMedID- 24564963 The 21- to 23-week-old female severe combined immunodeficient (scid/beige) or dba/1 mice (five per group) were grown in our animal facilities.
PubMedID- 21544519 severe combined immunodeficiency (scid) is part of the differential diagnosis of cd40l deficiency (van der burg m, gennery a, the expanding spectrum of severe combined immunodeficiency, ejp in press), but in contrast to most cases of scid, analysis of lymphocyte subpopulation in pad patients will show normal t cell counts.
PubMedID- 21573181 Immunodeficient non obese diabetous/shi-severe combined immunodeficiency/interleukin-2rγnull (nog) mice were injected with pm7 and ags mixed at a ratio of 8∶1 (2 250 000 and 375 000 cells, respectively) resuspended in 200 µl of 7 mg/ml matrigel (bd biosciences) in ice cold pbs.
PubMedID- 23879992 Three-week old female non-obese/severe combined immunodeficiency (nod/scid) mice were obtained from jackson labs (bar harbor, me, usa) and maintained in a pathogen-free animal facility.
PubMedID- 24141776 Six to eight-week old female non-obese diabetic/severe combined immunodeficient (nod/scid) mice were obtained from the fhcrc core center of excellence in hematology (dk-56465) and housed under pathogen-free conditions at the fhcrc comparative medicine shared resource.
PubMedID- 25942583 Sixteen severe combined immunodeficiency (cb17/scid) mice obtained from charles river (wilmington, ma) were housed in an animal care facility and held for 10 days to acclimatize.
PubMedID- 24318653 Next, we utilized the severe combined immunodeficiency (nod-scid) mouse model and injected lymphoma cells with or without stromal cells and observed a more robust growth of tumor in mice receiving hk and lymphoma cells[7].
PubMedID- 24447304 Eight week old female nonobese diabetic/severe combined immunodeficiency mice (nod/scid; harlan, in) were used as hosts for tumor xenografts.
PubMedID- 24587095 severe combined immunodeficient (scid) mice (male, 5-week-old) were purchased from jackson laboratory and maintained in m. d. anderson’s animal facilities.
PubMedID- 24839982 Male cb-17 non-obese diabetic/severe combined immunodeficient (nod.scid) mice (6- to 8-weeks old; harlan laboratories, inc., indianapolis, in, us) were housed and monitored in our animal research facility.
PubMedID- 24039951 Six-week-old female nonobese diabetic/severe combined immunodeficient (nod/scid) mice (jackson laboratory) were implanted with 5.0×103 sorted aldh-positive sum-149 cells in a 30 µl 50% matrigel (bd biosciences, cb-40230a) solution (1∶1 dilution of matrigel with ham’s f-12 medium) in the fourth inguinal mammary fat pad.
PubMedID- 20427943 severe combined immunodeficiency (scid) is a primary immunodeficiency disorder with heterogeneous genetic etiologies, characterized by a profound defect in both t and b lymphocytes.12 affected individuals usually present in early infancy with severe and persistent infections.3 without hematopoietic stem cell transplantation (hsct) or gene therapy, most patients die in early childhood.45 transplacentally derived maternal t lymphocytes are frequently detected in healthy newborns; however, they are rapidly eliminated by immune competent t lymphocytes.67 on the contrary, scid infants do not usually reject maternally engrafted cells; therefore maternal t cells were detected in 24% to 40% of patients undergoing hematopoietic stem cell transplantation.89 since these t cells are usually non-functional, they do not alter the course of the disease and patients present typically in early infancy with severe infection.9 we present a typical case of scid masked by a clinically functional maternal t-cell engraftment leading to late presentation of the disease at the age of 9 years with pneumocystis jiroveci pneumonia (pjp) and cytomegalovirus (cmv) infections, probably following exhaustion of maternally engrafted t lymphocytes.
PubMedID- 19834493 Adult male severe combined immunodeficient (scid) mice [c.b.17/icrhsd-scid] were purchased (harlan, indianapolis, in).
PubMedID- 26086199 This mutation is also responsible for the severe combined immunodeficiency (scid) phenotype in mice and rats [59].
PubMedID- 23226020 About 2 weeks before the experiment, female beige severe combined immunodeficiency mice were injected subcutaneously into the left flank with 2.5 × 106 u-87 mg cells and tumors were left to grow until they reached a size of about 1 cm in diameter.

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