Mice, Inbred DBA
Anemia, Diamond-Blackfan
Mice, Inbred Strains
Species Specificity
Mice, Inbred C57BL
Crosses, Genetic
Mice, Inbred BALB C
Glaucoma
Mice, Inbred C3H
Disease Models, Animal
Leukemia, Experimental
Complement C5
Collagen Type II
Blood thymidine level and iododeoxyuridine incorporation and reutilization in DNA in mice given long-acting thymidine pellets. (1/5198)
A long-acting thymidine pellet consisting of 190 mg of cholesterol and 60 mg of thymidine has been developed for the study of thymidine metabolism and reutilization in vivo. Implantation of such a pellet s.c. in adult mice will maintain the blood plasma concentration of thymidine at levels between 40 and 8 X 10(-6) M, which are from 36 to 7 times those of normal mice, for periods up to 48 hr. During this period, in vivo uptake and reutilization of [125I]iododeoxyuridine, a thymidine analog, into intestinal and tumor DNA were almost completely suppressed. While iododeoxyuridine reutilization is not large in normal proliferative tissue even in the absence of pellet implants, reutilization of over 30% was measured in large, rapidly growing ascites tumors. The inhibition of iododeoxyuridine incorporation by elevated thymidine blood levels is directly proportional to serum concentration. This appears to be due to a thymidine pool in rapid equilibrium with blood thymidine. This pool is at least 10 times larger than the 4-nmole pool of extracellular thymidine. (+info)Tissue pharmacokinetics, inhibition of DNA synthesis and tumor cell kill after high-dose methotrexate in murine tumor models. (2/5198)
In Sarcoma 180 and L1210 ascites tumor models, the initial rate of methotrexate accumulation in tumor cells in the peritoneal cavity and in small intestine (intracellularly) after s.c. doses up to 800 mg/kg, showed saturation kinetics. These results and the fact that initial uptake in these tissues within this dosage range was inhibited to the expected relative extent by the simultaneous administration of leucovorin suggest that carrier mediation and not passive diffusion is the major route of drug entry at these extremely high doses. Maximum accumulation of intracellular drug occurred within 2 hr and reached much higher levels in small intestine than in tumor cells at the higher dosages. At a 3-mg/kg dose of methotrexate s.c., intracellular exchangeable drug levels persisted more than four times longer in L1210 cells than in small intestine, but differences in persistence (L1210 cell versus gut) diminished markedly with increasing dosage. At 96 mg/kg, the difference in persistence was less than 2-fold. In small intestine and L1210 cells, theduration of inhibition of DNA synthesis at different dosages correlated with the extent to which exchangeable drug was retained. Toxic deaths occurred when inhibition in small intestine lasted longer than 25 to 30 hr. Recovery of synthesis in small intestine and L1210 cells occurred synchronously and only below dosages of 400 mg/kg. Within 24 hr after dosages of greater than 24 mg/kg, the rate of tumor cell loss increased to a point characterized by a single exponential (t1/2=8.5 hr). The total cell loss, but not the rate of cell loss, was dose dependent. (+info)Lung weight parallels disease severity in experimental coccidioidomycosis. (3/5198)
Evidence provided by histopathological study of lesions is a valuable adjunct for evaluating chemotherapeutic efficacy in experimental animal models, In addition, this should be correlated with a measure of disease severity in the same animal. The latter could be obtained by homogenization of infected organs and quantitative enumeration of viable cells of the etiological agent, but this would preclude histopathological studies in the same animal. Progression of disease in pulmonary infection is associated with replacement of air space by fluid, cells, and cellular debris. Therefore, an increase in lung weight should reflect severity of disease. Results with the murine model of coccidioidomycosis demonstrate that increasing lung weight parallels the increasing census of fungus cells in the lungs of both treated and nontreated infected mice. This was supported with evidence obtained from microscopic studies of lesions indicating that specific chemotherapy limited spread of the infection and inhibited multiplication of the fungus in the lung. Therefore, lung weight can be used as a measure of disease severity in the murine model of coccidioidomycosis. (+info)Prevention of collagen-induced arthritis by gene delivery of soluble p75 tumour necrosis factor receptor. (4/5198)
Collagen type II-induced arthritis (CIA) in DBA/1 mice can be passively transferred to SCID mice with spleen B- and T-lymphocytes. In the present study, we show that infection ex vivo of splenocytes from arthritic DBA/1 mice with a retroviral vector, containing cDNA for the soluble form of human p75 receptor of tumour necrosis factor (TNF-R) before transfer, prevents the development of arthritis, bone erosion and joint inflammation in the SCID recipients. Assessment of IgG subclass levels and studies of synovial histology suggest that down-regulating the effector functions of T helper-type 1 (Th1) cells may, at least in part, explain the inhibition of arthritis in the SCID recipients. In contrast, the transfer of splenocytes infected with mouse TNF-alpha gene construct resulted in exacerbated arthritis and enhancement of IgG2a antibody levels. Intriguingly, infection of splenocytes from arthritic DBA/1 mice with a construct for mouse IL-10 had no modulating effect on the transfer of arthritis. The data suggest that manipulation of the immune system with cytokines, or cytokine inhibitors using gene transfer protocols can be an effective approach to ameliorate arthritis. (+info)Tissue-specific knockout of the insulin receptor in pancreatic beta cells creates an insulin secretory defect similar to that in type 2 diabetes. (5/5198)
Dysfunction of the pancreatic beta cell is an important defect in the pathogenesis of type 2 diabetes, although its exact relationship to the insulin resistance is unclear. To determine whether insulin signaling has a functional role in the beta cell we have used the Cre-loxP system to specifically inactivate the insulin receptor gene in the beta cells. The resultant mice exhibit a selective loss of insulin secretion in response to glucose and a progressive impairment of glucose tolerance. These data indicate an important functional role for the insulin receptor in glucose sensing by the pancreatic beta cell and suggest that defects in insulin signaling at the level of the beta cell may contribute to the observed alterations in insulin secretion in type 2 diabetes. (+info)The cerebral metabolic consequences of nitric oxide synthase deficiency: glucose utilization in endothelial and neuronal nitric oxide synthase null mice. (6/5198)
Nitric oxide has multiple physiologic roles in the CNS. Inhibiting nitric oxide synthesis might therefore alter functional activity within the brain. We used [14C]-2-deoxyglucose in vivo autoradiography to measure local CMRglc in "knockout" mice lacking the genes for either the endothelial (eNOS) or neuronal (nNOS) isoforms of nitric oxide synthase, and in the progenitor strains (SV129, C57B1/6). Glucose utilization levels did not significantly differ between nNOS and eNOS knockout mice and C57B1/6 mice in any of the 48 brain regions examined, but were relatively lower in some subcortical regions in SV129 mice. (+info)T cell subsets in experimental lupus nephritis: modulation by bacterial superantigen. (7/5198)
Chronic graft-vs-host disease (GvH), induced by injection of DBA/2 lymphocytes into (C57BL/6 x DBA/2)F1 hybrids, is a murine model for lupus nephritis, associated with a Th2-dependent polyclonal B cell activation. The development of glomerulosclerosis in this model is preceded by a glomerular influx of LFA-1+ T cells. We investigated whether exposure to bacterial superantigen would modulate the course of this autoimmune syndrome. Injection of the bacterial superantigen staphylococcal enterotoxin B (SEB) in mice has been shown to induce the activation of TcRVbeta8+ T cells. Within 2 weeks after GvH induction, mice were injected twice with 20 microg of SEB and the following parameters were examined: cytokine and Ig profile, proteinuria and renal pathology. The second SEB injection induced in GvH mice an increased release of both interferon-gamma (IFN-gamma) and interleukin-10 (IL-10) as compared with control F1 mice. No differences were observed in IL-2 production. SEB-treated GvH mice demonstrated a delayed onset of proteinuria. Histological analysis of the kidney showed that SEB-challenged GvH mice displayed significantly more interstitial inflammation and mesangial proliferation together with more IgG2a deposits in glomeruli than non-injected GvH mice. From these results, we conclude that GvH mice are more responsive to SEB in terms of cytokine production and that bacterial infection can modulate the course of this renal disease from a membranous to a more proliferative type of nephropathy. (+info)Development and function of autospecific dual TCR+ T lymphocytes. (8/5198)
Recent studies have challenged the long held concept that each T lymphocyte expresses on its surface only a single, unique alphabetaTCR. Dual TCR+ T cells have been recognized, however, their origin and potential to escape screening for self-reactivity remain obscure. We now report the thymic generation of dual alphabetaTCR+ T cells in the H-2Db/H-Y-specific TCR transgenic (Tg) mouse. Dual TCR+ thymocytes were positively selected less efficiently than single TCR+ thymocytes, although a subset attained maturity. Importantly, when TCR Tg mice were bred onto a negatively selecting background, auto-specific cells survived central deletion and matured as CD4+ dual TCR+ cells. These cells were autoreactive when CD8 expression was restored. The existence of autospecific, dual TCR+ T cells may have implications for the maintenance of self tolerance. (+info)'DBA' is an abbreviation for 'Database of Genotypes and Phenotypes,' but in the context of "Inbred DBA mice," it refers to a specific strain of laboratory mice that have been inbred for many generations. The DBA strain is one of the oldest inbred strains, and it was established in 1909 by C.C. Little at the Bussey Institute of Harvard University.
The "Inbred DBA" mice are genetically identical mice that have been produced by brother-sister matings for more than 20 generations. This extensive inbreeding results in a homozygous population, where all members of the strain have the same genetic makeup. The DBA strain is further divided into several sub-strains, including DBA/1, DBA/2, and DBA/J, among others.
DBA mice are known for their black coat color, which can fade to gray with age, and they exhibit a range of phenotypic traits that make them useful for research purposes. For example, DBA mice have a high incidence of retinal degeneration, making them a valuable model for studying eye diseases. They also show differences in behavior, immune response, and susceptibility to various diseases compared to other inbred strains.
In summary, "Inbred DBA" mice are a specific strain of laboratory mice that have been inbred for many generations, resulting in a genetically identical population with distinct phenotypic traits. They are widely used in biomedical research to study various diseases and biological processes.
Diamond-Blackfan anemia is a rare, congenital bone marrow failure disorder characterized by a decreased production of red blood cells (erythroblasts) in the bone marrow. This results in a reduced number of circulating red blood cells, leading to anemia and related symptoms such as fatigue, weakness, and pallor. The disorder is typically diagnosed in infancy or early childhood and can also be associated with physical abnormalities.
The exact cause of Diamond-Blackfan anemia is not fully understood, but it is believed to involve genetic mutations that affect the development and function of the bone marrow. In many cases, the disorder is inherited in an autosomal dominant manner, meaning that a child has a 50% chance of inheriting the mutated gene from an affected parent. However, some cases may arise spontaneously due to new genetic mutations.
Treatment for Diamond-Blackfan anemia typically involves regular blood transfusions to maintain adequate red blood cell levels and alleviate symptoms. Corticosteroid therapy may also be used to stimulate red blood cell production in some cases. In severe or refractory cases, stem cell transplantation may be considered as a curative treatment option.
Inbred strains of mice are defined as lines of mice that have been brother-sister mated for at least 20 consecutive generations. This results in a high degree of homozygosity, where the mice of an inbred strain are genetically identical to one another, with the exception of spontaneous mutations.
Inbred strains of mice are widely used in biomedical research due to their genetic uniformity and stability, which makes them useful for studying the genetic basis of various traits, diseases, and biological processes. They also provide a consistent and reproducible experimental system, as compared to outbred or genetically heterogeneous populations.
Some commonly used inbred strains of mice include C57BL/6J, BALB/cByJ, DBA/2J, and 129SvEv. Each strain has its own unique genetic background and phenotypic characteristics, which can influence the results of experiments. Therefore, it is important to choose the appropriate inbred strain for a given research question.
Species specificity is a term used in the field of biology, including medicine, to refer to the characteristic of a biological entity (such as a virus, bacterium, or other microorganism) that allows it to interact exclusively or preferentially with a particular species. This means that the biological entity has a strong affinity for, or is only able to infect, a specific host species.
For example, HIV is specifically adapted to infect human cells and does not typically infect other animal species. Similarly, some bacterial toxins are species-specific and can only affect certain types of animals or humans. This concept is important in understanding the transmission dynamics and host range of various pathogens, as well as in developing targeted therapies and vaccines.
C57BL/6 (C57 Black 6) is an inbred strain of laboratory mouse that is widely used in biomedical research. The term "inbred" refers to a strain of animals where matings have been carried out between siblings or other closely related individuals for many generations, resulting in a population that is highly homozygous at most genetic loci.
The C57BL/6 strain was established in 1920 by crossing a female mouse from the dilute brown (DBA) strain with a male mouse from the black strain. The resulting offspring were then interbred for many generations to create the inbred C57BL/6 strain.
C57BL/6 mice are known for their robust health, longevity, and ease of handling, making them a popular choice for researchers. They have been used in a wide range of biomedical research areas, including studies of cancer, immunology, neuroscience, cardiovascular disease, and metabolism.
One of the most notable features of the C57BL/6 strain is its sensitivity to certain genetic modifications, such as the introduction of mutations that lead to obesity or impaired glucose tolerance. This has made it a valuable tool for studying the genetic basis of complex diseases and traits.
Overall, the C57BL/6 inbred mouse strain is an important model organism in biomedical research, providing a valuable resource for understanding the genetic and molecular mechanisms underlying human health and disease.
"Genetic crosses" refer to the breeding of individuals with different genetic characteristics to produce offspring with specific combinations of traits. This process is commonly used in genetics research to study the inheritance patterns and function of specific genes.
There are several types of genetic crosses, including:
1. Monohybrid cross: A cross between two individuals that differ in the expression of a single gene or trait.
2. Dihybrid cross: A cross between two individuals that differ in the expression of two genes or traits.
3. Backcross: A cross between an individual from a hybrid population and one of its parental lines.
4. Testcross: A cross between an individual with unknown genotype and a homozygous recessive individual.
5. Reciprocal cross: A cross in which the male and female parents are reversed to determine if there is any effect of sex on the expression of the trait.
These genetic crosses help researchers to understand the mode of inheritance, linkage, recombination, and other genetic phenomena.
Occupational noise is defined as exposure to excessive or harmful levels of sound in the workplace that has the potential to cause adverse health effects such as hearing loss, tinnitus, and stress-related symptoms. The measurement of occupational noise is typically expressed in units of decibels (dB), and the permissible exposure limits are regulated by organizations such as the Occupational Safety and Health Administration (OSHA) in the United States.
Exposure to high levels of occupational noise can lead to permanent hearing loss, which is often irreversible. It can also interfere with communication and concentration, leading to decreased productivity and increased risk of accidents. Therefore, it is essential to implement appropriate measures to control and reduce occupational noise exposure in the workplace.
BALB/c is an inbred strain of laboratory mouse that is widely used in biomedical research. The strain was developed at the Institute of Cancer Research in London by Henry Baldwin and his colleagues in the 1920s, and it has since become one of the most commonly used inbred strains in the world.
BALB/c mice are characterized by their black coat color, which is determined by a recessive allele at the tyrosinase locus. They are also known for their docile and friendly temperament, making them easy to handle and work with in the laboratory.
One of the key features of BALB/c mice that makes them useful for research is their susceptibility to certain types of tumors and immune responses. For example, they are highly susceptible to developing mammary tumors, which can be induced by chemical carcinogens or viral infection. They also have a strong Th2-biased immune response, which makes them useful models for studying allergic diseases and asthma.
BALB/c mice are also commonly used in studies of genetics, neuroscience, behavior, and infectious diseases. Because they are an inbred strain, they have a uniform genetic background, which makes it easier to control for genetic factors in experiments. Additionally, because they have been bred in the laboratory for many generations, they are highly standardized and reproducible, making them ideal subjects for scientific research.
Glaucoma is a group of eye conditions that damage the optic nerve, often caused by an abnormally high pressure in the eye (intraocular pressure). This damage can lead to permanent vision loss or even blindness if left untreated. The most common type is open-angle glaucoma, which has no warning signs and progresses slowly. Angle-closure glaucoma, on the other hand, can cause sudden eye pain, redness, nausea, and vomiting, as well as rapid vision loss. Other less common types of glaucoma also exist. While there is no cure for glaucoma, early detection and treatment can help slow or prevent further vision loss.
'C3H' is the name of an inbred strain of laboratory mice that was developed at the Jackson Laboratory in Bar Harbor, Maine. The mice are characterized by their uniform genetic background and have been widely used in biomedical research for many decades.
The C3H strain is particularly notable for its susceptibility to certain types of cancer, including mammary tumors and lymphomas. It also has a high incidence of age-related macular degeneration and other eye diseases. The strain is often used in studies of immunology, genetics, and carcinogenesis.
Like all inbred strains, the C3H mice are the result of many generations of brother-sister matings, which leads to a high degree of genetic uniformity within the strain. This makes them useful for studying the effects of specific genes or environmental factors on disease susceptibility and other traits. However, it also means that they may not always be representative of the genetic diversity found in outbred populations, including humans.
Animal disease models are specialized animals, typically rodents such as mice or rats, that have been genetically engineered or exposed to certain conditions to develop symptoms and physiological changes similar to those seen in human diseases. These models are used in medical research to study the pathophysiology of diseases, identify potential therapeutic targets, test drug efficacy and safety, and understand disease mechanisms.
The genetic modifications can include knockout or knock-in mutations, transgenic expression of specific genes, or RNA interference techniques. The animals may also be exposed to environmental factors such as chemicals, radiation, or infectious agents to induce the disease state.
Examples of animal disease models include:
1. Mouse models of cancer: Genetically engineered mice that develop various types of tumors, allowing researchers to study cancer initiation, progression, and metastasis.
2. Alzheimer's disease models: Transgenic mice expressing mutant human genes associated with Alzheimer's disease, which exhibit amyloid plaque formation and cognitive decline.
3. Diabetes models: Obese and diabetic mouse strains like the NOD (non-obese diabetic) or db/db mice, used to study the development of type 1 and type 2 diabetes, respectively.
4. Cardiovascular disease models: Atherosclerosis-prone mice, such as ApoE-deficient or LDLR-deficient mice, that develop plaque buildup in their arteries when fed a high-fat diet.
5. Inflammatory bowel disease models: Mice with genetic mutations affecting intestinal barrier function and immune response, such as IL-10 knockout or SAMP1/YitFc mice, which develop colitis.
Animal disease models are essential tools in preclinical research, but it is important to recognize their limitations. Differences between species can affect the translatability of results from animal studies to human patients. Therefore, researchers must carefully consider the choice of model and interpret findings cautiously when applying them to human diseases.
Experimental leukemia refers to the stage of research or clinical trials where new therapies, treatments, or diagnostic methods are being studied for leukemia. Leukemia is a type of cancer that affects the blood and bone marrow, leading to an overproduction of abnormal white blood cells.
In the experimental stage, researchers investigate various aspects of leukemia, such as its causes, progression, and potential treatments. They may conduct laboratory studies using cell cultures or animal models to understand the disease better and test new therapeutic approaches. Additionally, clinical trials may be conducted to evaluate the safety and efficacy of novel treatments in human patients with leukemia.
Experimental research in leukemia is crucial for advancing our understanding of the disease and developing more effective treatment strategies. It involves a rigorous and systematic process that adheres to ethical guidelines and scientific standards to ensure the validity and reliability of the findings.
Complement C5 is a protein that plays a crucial role in the complement system, which is a part of the immune system that helps to eliminate pathogens and damaged cells from the body. The complement system is a complex series of biochemical reactions that help to identify and destroy foreign substances, such as bacteria and viruses.
Complement C5 is one of several proteins in the complement system that are activated in a cascading manner in response to an activating event, such as the binding of an antibody to a pathogen. Once activated, Complement C5 can be cleaved into two smaller proteins, C5a and C5b.
C5a is a powerful anaphylatoxin, which means it can cause the release of histamine from mast cells and basophils, leading to inflammation and increased vascular permeability. It also acts as a chemoattractant, drawing immune cells to the site of infection or injury.
C5b, on the other hand, plays a role in the formation of the membrane attack complex (MAC), which is a protein structure that can punch holes in the membranes of pathogens, leading to their lysis and destruction.
Overall, Complement C5 is an important component of the immune system's response to infection and injury, helping to eliminate pathogens and damaged cells from the body.
The spleen is an organ in the upper left side of the abdomen, next to the stomach and behind the ribs. It plays multiple supporting roles in the body:
1. It fights infection by acting as a filter for the blood. Old red blood cells are recycled in the spleen, and platelets and white blood cells are stored there.
2. The spleen also helps to control the amount of blood in the body by removing excess red blood cells and storing platelets.
3. It has an important role in immune function, producing antibodies and removing microorganisms and damaged red blood cells from the bloodstream.
The spleen can be removed without causing any significant problems, as other organs take over its functions. This is known as a splenectomy and may be necessary if the spleen is damaged or diseased.
Collagen Type II is a specific type of collagen that is a major component of the extracellular matrix in articular cartilage, which is the connective tissue that covers and protects the ends of bones in joints. It is also found in other tissues such as the vitreous humor of the eye and the inner ear.
Collagen Type II is a triple helix molecule composed of three polypeptide chains that contain a high proportion of the amino acids proline and hydroxyproline. This type of collagen provides structural support and elasticity to tissues, and it also plays a role in the regulation of cell behavior and signaling.
Collagen Type II is a target for autoimmune responses in conditions such as rheumatoid arthritis, where the immune system mistakenly attacks the body's own collagen, leading to joint inflammation and damage. It is also a common component of various dietary supplements and therapies used to support joint health and treat osteoarthritis.
I'm sorry for any confusion, but "Leukemia L5178" is not a recognized medical term or classification for leukemia. The World Health Organization (WHO) and other organizations have established specific classifications for different types of leukemias based on factors such as cell type, genetic mutations, and other characteristics. However, "L5178" does not appear in these classifications.
It's possible that "L5178" might refer to a specific research cell line used in scientific studies, but without more context, it's difficult to provide a precise definition. If you have more information about where you encountered this term, I may be able to provide a more accurate response.
Mouse Models of Human Cancer database