Chimerism
Transplantation Chimera
Transplantation Tolerance
Bone Marrow Transplantation
Transplantation, Homologous
Transplantation Conditioning
Graft Survival
Skin Transplantation
Hematopoietic Stem Cell Transplantation
Whole-Body Irradiation
Graft vs Host Disease
Host vs Graft Reaction
Radiation Chimera
Immune Tolerance
Lymphocyte Transfusion
Transplantation Immunology
Leukocyte Transfusion
Histocompatibility Testing
Tissue Donors
Graft Rejection
Lymphocyte Depletion
Busulfan
Hematologic Neoplasms
Vidarabine
Immunosuppressive Agents
Graft Enhancement, Immunologic
Cord Blood Stem Cell Transplantation
T-Lymphocytes
Lymphocyte Culture Test, Mixed
Myeloablative Agonists
Histocompatibility
Tandem Repeat Sequences
Y Chromosome
Hematopoiesis
CD40 Ligand
Freemartinism
Immunosuppression
Graft vs Tumor Effect
Hemibody Irradiation
Leukemia
Isoantigens
Blood Grouping and Crossmatching
Bone Marrow Cells
Polymerase Chain Reaction
Mosaicism
Organ Transplantation
Chromosomes, Human, Y
HLA Antigens
Models, Animal
Stem Cell Transplantation
Mice, Inbred NOD
Transplantation, Isogeneic
Allografts
Antilymphocyte Serum
Islets of Langerhans Transplantation
Fetal Therapies
Minisatellite Repeats
In Situ Hybridization, Fluorescence
Neoplasm, Residual
Lymphatic Irradiation
Saguinus
Bone Marrow
Leukemia, Myelogenous, Chronic, BCR-ABL Positive
Severe Combined Immunodeficiency
Peripheral Tolerance
Graft vs Host Reaction
beta-Thalassemia
Hydrozoa
Clonal Deletion
Major Histocompatibility Complex
Flow Cytometry
Twins, Dizygotic
Blood Transfusion, Intrauterine
Graft vs Leukemia Effect
Thymus Gland
Transplants
Amelogenin
Reticulocyte Count
ABO Blood-Group System
Cell Lineage
Anemia, Aplastic
Treatment Outcome
Peripheral Blood Stem Cell Transplantation
Mice, Inbred Strains
Callithrix
Mycophenolic Acid
Cyclosporine
Cyclophosphamide
Histocompatibility Antigens
Cell Transplantation
Blood Group Incompatibility
Cytogenetics
Genes, sry
Thalassemia
B-Lymphocytes
Antigens, CD8
Granulomatous Disease, Chronic
Antigens, CD34
Immunoconjugates
Vascularized Composite Allotransplantation
Fetal Diseases
Parabiosis
Revisiting liver transplant immunology: from the concept of immune engagement to the dualistic pathway paradigm. (1/276)
Ever since the demonstration that allografts are rejected through immune reactions of the host, clinical therapies for organ allografts have relied on immune suppression to prevent these destructive events. A growing body of clinical and experimental data suggests that allografts elicit multiple, interactive immune responses. The result is not inevitably graft rejection, and "spontaneous" acceptance of fully allogeneic liver grafts occurs in rodents without immunosuppression. A spectrum of results range from spontaneous acceptance without immunosuppression to rejection with immunosuppression. The "dualistic pathway paradigm" aims to reconcile apparently conflicting observations in liver transplantation and proposes that: (1) immune engagement between the host and the allograft is instrumental in both rejection and acceptance; (2) there exist in all mammalian species congruent interactive pathways of immune activation whereby the fate of the allograft is determined by the quantitative results of these interactions; (3) the dualistic effect of immunosuppressive drugs on pathways of immune activation, conferring the capacity for favorable or unfavorable graft outcome should be investigated in experimental models in which organ allografts are spontaneously accepted. In conclusion the design of clinical strategies based on this research may contribute to protocols resulting in allograft acceptance without chronic immunosuppression. (+info)Living donor liver transplant with clinical tolerance, laboratory evidence of chimerism, and spontaneous clearance of HBV. (2/276)
We present a case of functional and histopathologic tolerance, chimerism, and spontaneous clearance of HBV in a patient four years after living donor liver transplant (LDLT). A 19-year-old male patient underwent a LDLT for HBV cirrhosis. He voluntarily ceased immunosuppression and antiviral therapy after 6 months. He is now four years status post transplant without any episodes of rejection or clinical manifestation of liver disease. PCR and VNTR were used to show donor-recipient chimerism and a large degree of genetic similarity between the pair. MLC and cytokine elaboration were used to show recipient hyporeactivity towards donor antigen. He also has clinical evidence of clearing his HBV without continued use of HBIG. (+info)Maternal and sibling microchimerism in twins and triplets discordant for neonatal lupus syndrome-congenital heart block. (3/276)
OBJECTIVE: Neonatal lupus syndrome-congenital heart block (NLS-CHB) is an acquired autoimmune disease in which maternal autoantibodies are necessary but not sufficient for disease. Maternal myocardial cells have been found in the hearts of patients with NLS-CHB, suggesting that maternal microchimerism may also play a role. In this study we asked whether levels of microchimerism in the blood are associated with NLS-CHB in discordant twins and triplets. METHODS: Human leucocyte antigen (HLA)-specific and Y-chromosome-specific real-time quantitative polymerase chain reaction (PCR) was used to quantitatively assay maternal and sibling microchimerism in peripheral blood. Because of HLA allele sharing in families, it was not always possible to distinguish between multiple sources of microchimerism. RESULTS: In one family, maternal and/or sibling microchimerism was detected in two triplets who had CHB, but not in the triplet with transient hepatitis. Levels ranged from 4 to 948 genome-equivalents of foreign deoxyribonucleic acid per million host genome-equivalents (gEq/million). Over the first year levels of sibling microchimerism decreased in the triplet with complete CHB and increased in the triplet who progressed from first- to second-degree CHB. In a second family, maternal and/or sibling microchimerism was detected in the healthy twin (1223 gEq/million) but not in the twin with CHB. CONCLUSIONS: Maternal and/or sibling microchimerism was detectable in the blood of infant twins and triplets discordant for NLS. Microchimerism in the blood was not specific for NLS-CHB, although in one family levels correlated with disease. Thus, microchimerism in the blood and/or tissues may be involved in the pathogenesis or progression of NLS-CHB, but additional factors must also contribute. Further investigation is warranted. (+info)Male microchimerism in women with systemic sclerosis and healthy women who have never given birth to a son. (4/276)
BACKGROUND: Male DNA or cells are often used to measure microchimerism in a woman. In studies of autoimmune diseases male microchimerism is most often attributed to the previous birth of a son. OBJECTIVE: To determine the frequency of male microchimerism in healthy women or women with systemic sclerosis who had never given birth to a son. METHODS: Real time quantitative polymerase chain reaction targeting the Y chromosome specific sequence DYS14 was employed to test DNA extracted from peripheral blood mononuclear cells of 26 women with systemic sclerosis and 23 healthy women who had never given birth to a son. RESULTS: are expressed as the genome equivalent number of male cells per million host cells (gEq/mil).Results: Male DNA was found in 15% of women with systemic sclerosis (range 0 to 23.7 gEq/mil) and in 13% of healthy women (range 0 to 5.1 gEq/mil). Although two women with male DNA had an induced abortion, most had no history of spontaneous or induced abortion (either systemic sclerosis or healthy). CONCLUSIONS: Microchimerism with male DNA can be found in the circulation of women who have never given birth to a son. Thus sources other than a male birth must be considered when male DNA is used to measure microchimerism. Although other studies are needed, there was no apparent difference in women with systemic sclerosis and healthy women. Possible sources of male DNA include unrecognised male pregnancy or unrecognised male twin, an older male sibling with transfer through the maternal circulation, or sexual intercourse alone. (+info)Emergent autoimmunity in graft-versus-host disease. (5/276)
Donor T-cell recognition of host alloantigens presented by host antigen-presenting cells (APCs) is necessary for the induction of graft-versus-host disease (GVHD), but whether direct alloreactivity is sufficient for the propagation of GVHD is unknown. In this study, we demonstrate that GVHD cannot be effectively propagated through the direct pathway of allorecognition. Rather, donor T-cell recognition of antigens through the indirect pathway is necessary for the perpetuation of GVHD. Furthermore, GVHD results in the breaking of self tolerance, resulting in the emergence of donor T cells that can cause autoimmune disease in syngeneic recipients. Notably, GVHD-induced autoreactivity is donor APC dependent, transferable into secondary hosts, and involves cells of the innate immune system. These results indicate that donor T-cell--mediated pathologic damage during GVHD becomes donor APC dependent and provide a mechanistic explanation for the long-standing observation that GVHD is associated with autoimmune clinical manifestations. (+info)Pkd1 regulates immortalized proliferation of renal tubular epithelial cells through p53 induction and JNK activation. (6/276)
Autosomal dominant polycystic kidney disease (ADPKD) is the most common human monogenic genetic disorder and is characterized by progressive bilateral renal cysts and the development of renal insufficiency. The cystogenesis of ADPKD is believed to be a monoclonal proliferation of PKD-deficient (PKD(-/-)) renal tubular epithelial cells. To define the function of Pkd1, we generated chimeric mice by aggregation of Pkd1(-/-) ES cells and Pkd1(+/+) morulae from ROSA26 mice. As occurs in humans with ADPKD, these mice developed cysts in the kidney, liver, and pancreas. Surprisingly, the cyst epithelia of the kidney were composed of both Pkd1(-/-) and Pkd1(+/+) renal tubular epithelial cells in the early stages of cystogenesis. Pkd1(-/-) cyst epithelial cells changed in shape from cuboidal to flat and replaced Pkd1(+/+) cyst epithelial cells lost by JNK-mediated apoptosis in intermediate stages. In late-stage cysts, Pkd1(-/-) cells continued immortalized proliferation with downregulation of p53. These results provide a novel understanding of the cystogenesis of ADPKD patients. Furthermore, immortalized proliferation without induction of p53 was frequently observed in 3T3-type culture of mouse embryonic fibroblasts from Pkd1(-/-) mice. Thus, Pkd1 plays a role in preventing immortalized proliferation of renal tubular epithelial cells through the induction of p53 and activation of JNK. (+info)Multi-lineage potential of fetal cells in maternal tissue: a legacy in reverse. (7/276)
Fetal cells circulate in pregnant women and persist in blood and tissue for decades post-partum. The mother thus becomes chimeric. Factors that may influence such fetal cell microchimerism include histocompatibility, fetal or placental abnormalities, or a reproductive history that includes miscarriage or elective termination. Fetal cell microchimerism is associated with some maternal autoimmune diseases, such as systemic sclerosis. Moreover, a novel population of fetal cells, the pregnancy-associated progenitor cells (PAPCs), appears to differentiate in diseased or injured maternal tissue. The cellular origin of these cells is at present unknown but could be a hematopoietic stem cell, a mesenchymal stem cell, or a novel cell type. Pregnancy therefore results in the acquisition of cells with stem-cell-like properties that may influence maternal health post-partum. Rather than triggering disease, these cells may instead combat it. (+info)Chimerism in kidneys, livers and hearts of normal women: implications for transplantation studies. (8/276)
Tissue chimerism was recently described in transplanted organs from female donors into male recipients, by demonstration of the Y-chromosome in tissue-derived cells. It was claimed that these Y-chromosome positive cells were recipient derived. To find out whether the chimeric cells, derived from pregnancies of sons or blood transfusions, could have been present in the solid organs before transplantation, we performed the following study. In situ hybridization for the Y-chromosome was performed on the normal organs (51 kidneys, 51 livers, 69 hearts) from 75 women of the normal population, whose child and blood transfusion status were known. Chimeric cells were found in 13 kidneys, 10 livers and 4 hearts, of 23 women. There was no relation between the child status or the blood transfusion history with the presence of Y-chromosome positive cells. We have for the first time demonstrated that male cells are present in normal kidneys, livers and hearts. Theoretically, these organs could have been used for the transplantation. Therefore, our findings demonstrate that the chimeric cells thus far described in transplantation studies, are not necessarily donor derived, and could have been present in the organs before the transplantation. (+info)The diagnosis of GVHD is based on a combination of clinical findings, laboratory tests, and biopsies. Treatment options include immunosuppressive drugs, corticosteroids, and in severe cases, stem cell transplantation reversal or donor lymphocyte infusion.
Prevention of GVHD includes selecting the right donor, using conditioning regimens that minimize damage to the recipient's bone marrow, and providing appropriate immunosuppression after transplantation. Early detection and management of GVHD are critical to prevent long-term complications and improve survival rates.
Hematologic neoplasms refer to abnormal growths or tumors that affect the blood, bone marrow, or lymphatic system. These types of cancer can originate from various cell types, including red blood cells, white blood cells, platelets, and lymphoid cells.
There are several subtypes of hematologic neoplasms, including:
1. Leukemias: Cancers of the blood-forming cells in the bone marrow, which can lead to an overproduction of immature or abnormal white blood cells, red blood cells, or platelets. Examples include acute myeloid leukemia (AML) and chronic lymphocytic leukemia (CLL).
2. Lymphomas: Cancers of the immune system, which can affect the lymph nodes, spleen, liver, or other organs. Examples include Hodgkin lymphoma and non-Hodgkin lymphoma.
3. Multiple myeloma: A cancer of the plasma cells in the bone marrow that can lead to an overproduction of abnormal plasma cells.
4. Myeloproliferative neoplasms: Cancers that affect the blood-forming cells in the bone marrow, leading to an overproduction of red blood cells, white blood cells, or platelets. Examples include polycythemia vera and essential thrombocythemia.
5. Myelodysplastic syndromes: Cancers that affect the blood-forming cells in the bone marrow, leading to an underproduction of normal blood cells.
The diagnosis of hematologic neoplasms typically involves a combination of physical examination, medical history, laboratory tests (such as complete blood counts and bone marrow biopsies), and imaging studies (such as CT scans or PET scans). Treatment options for hematologic neoplasms depend on the specific type of cancer, the severity of the disease, and the overall health of the patient. These may include chemotherapy, radiation therapy, stem cell transplantation, or targeted therapy with drugs that specifically target cancer cells.
Freemartinism is caused by the abnormal development of the reproductive system of the calves. During fetal development, the two female calves may fail to fully separate from each other, leading to a shared uterus and vagina. This can result in a range of physical and reproductive abnormalities, including:
* Unusual genitalia: The shared uterus and vagina can cause the genitalia to appear abnormal or incomplete.
* Reproductive difficulties: Freemartinism can make it difficult or impossible for the calves to breed or conceive.
* Health problems: Freemartinism can increase the risk of health problems, such as urinary tract infections and reproductive tract infections.
Freemartinism is typically diagnosed through ultrasound examination during pregnancy or after birth. Treatment options for freemartinism are limited, and may include surgery to correct physical abnormalities and hormone therapy to stimulate reproductive function. In some cases, euthanasia may be necessary due to the severity of the condition.
Prevention of freemartinism is not possible, as it is a congenital condition that occurs during fetal development. However, careful breeding practices and proper veterinary care can help reduce the risk of complications associated with this condition.
There are several different types of leukemia, including:
1. Acute Lymphoblastic Leukemia (ALL): This is the most common type of leukemia in children, but it can also occur in adults. It is characterized by an overproduction of immature white blood cells called lymphoblasts.
2. Acute Myeloid Leukemia (AML): This type of leukemia affects the bone marrow's ability to produce red blood cells, platelets, and other white blood cells. It can occur at any age but is most common in adults.
3. Chronic Lymphocytic Leukemia (CLL): This type of leukemia affects older adults and is characterized by the slow growth of abnormal white blood cells called lymphocytes.
4. Chronic Myeloid Leukemia (CML): This type of leukemia is caused by a genetic mutation in a gene called BCR-ABL. It can occur at any age but is most common in adults.
5. Hairy Cell Leukemia: This is a rare type of leukemia that affects older adults and is characterized by the presence of abnormal white blood cells called hairy cells.
6. Myelodysplastic Syndrome (MDS): This is a group of disorders that occur when the bone marrow is unable to produce healthy blood cells. It can lead to leukemia if left untreated.
Treatment for leukemia depends on the type and severity of the disease, but may include chemotherapy, radiation therapy, targeted therapy, or stem cell transplantation.
A residual neoplasm is a remaining portion of a tumor that may persist after primary treatment. This can occur when the treatment does not completely remove all of the cancer cells or if some cancer cells are resistant to the treatment. Residual neoplasms can be benign (non-cancerous) or malignant (cancerous).
It is important to note that a residual neoplasm does not necessarily mean that the cancer has come back. In some cases, a residual neoplasm may be present from the start and may not grow or change over time.
Residual neoplasms can be managed with additional treatment, such as surgery, chemotherapy, or radiation therapy. The choice of treatment depends on the type of cancer, the size and location of the residual neoplasm, and other factors.
It is important to follow up with your healthcare provider regularly to monitor the residual neoplasm and ensure that it is not growing or causing any symptoms.
Recurrence can also refer to the re-emergence of symptoms in a previously treated condition, such as a chronic pain condition that returns after a period of remission.
In medical research, recurrence is often studied to understand the underlying causes of disease progression and to develop new treatments and interventions to prevent or delay its return.
The BCR-ABL gene is a fusion gene that is present in the majority of cases of CML. It is created by the translocation of two genes, called BCR and ABL, which leads to the production of a constitutively active tyrosine kinase protein that promotes the growth and proliferation of abnormal white blood cells.
There are three main phases of CML, each with distinct clinical and laboratory features:
1. Chronic phase: This is the earliest phase of CML, where patients may be asymptomatic or have mild symptoms such as fatigue, night sweats, and splenomegaly (enlargement of the spleen). The peripheral blood count typically shows a high number of blasts in the blood, but the bone marrow is still functional.
2. Accelerated phase: In this phase, the disease progresses to a higher number of blasts in the blood and bone marrow, with evidence of more aggressive disease. Patients may experience symptoms such as fever, weight loss, and pain in the joints or abdomen.
3. Blast phase: This is the most advanced phase of CML, where there is a high number of blasts in the blood and bone marrow, with significant loss of function of the bone marrow. Patients are often symptomatic and may have evidence of spread of the disease to other organs, such as the liver or spleen.
Treatment for CML typically involves targeted therapy with drugs that inhibit the activity of the BCR-ABL protein, such as imatinib (Gleevec), dasatinib (Sprycel), or nilotinib (Tasigna). These drugs can slow or stop the progression of the disease, and may also produce a complete cytogenetic response, which is defined as the absence of all Ph+ metaphases in the bone marrow. However, these drugs are not curative and may have significant side effects. Allogenic hematopoietic stem cell transplantation (HSCT) is also a potential treatment option for CML, but it carries significant risks and is usually reserved for patients who are in the blast phase of the disease or have failed other treatments.
In summary, the clinical course of CML can be divided into three phases based on the number of blasts in the blood and bone marrow, and treatment options vary depending on the phase of the disease. It is important for patients with CML to receive regular monitoring and follow-up care to assess their response to treatment and detect any signs of disease progression.
People with SCID are extremely susceptible to infections, particularly those caused by viruses, and often develop symptoms shortly after birth. These may include diarrhea, vomiting, fever, and failure to gain weight or grow at the expected rate. Without treatment, SCID can lead to life-threatening infections and can be fatal within the first year of life.
Treatment for SCID typically involves bone marrow transplantation or enzyme replacement therapy. Bone marrow transplantation involves replacing the patient's faulty immune system with healthy cells from a donor, while enzyme replacement therapy involves replacing the missing or dysfunctional enzymes that cause the immune deficiency. Both of these treatments can help restore the patient's immune system and improve their quality of life.
In summary, severe combined immunodeficiency (SCID) is a rare genetic disorder that impairs the body's ability to fight infections and can be fatal without treatment. Treatment options include bone marrow transplantation and enzyme replacement therapy.
There are two main types of beta-thalassemia:
1. Beta-thalassemia major (also known as Cooley's anemia): This is the most severe form of the condition, and it can cause serious health problems and a shortened lifespan if left untreated. Children with this condition are typically diagnosed at birth or in early childhood, and they may require regular blood transfusions and other medical interventions to manage their symptoms and prevent complications.
2. Beta-thalassemia minor (also known as thalassemia trait): This is a milder form of the condition, and it may not cause any noticeable symptoms. People with beta-thalassemia minor have one mutated copy of the HBB gene and one healthy copy, which allows them to produce some normal hemoglobin. However, they may still be at risk for complications such as anemia, fatigue, and a higher risk of infections.
The symptoms of beta-thalassemia can vary depending on the severity of the condition and the age of onset. Common symptoms include:
* Fatigue
* Weakness
* Pale skin
* Shortness of breath
* Frequent infections
* Yellowing of the skin and eyes (jaundice)
* Enlarged spleen
Beta-thalassemia is most commonly found in people of Mediterranean, African, and Southeast Asian ancestry. It is caused by mutations in the HBB gene, which is inherited from one's parents. There is no cure for beta-thalassemia, but it can be managed with blood transfusions, chelation therapy, and other medical interventions. Bone marrow transplantation may also be a viable option for some patients.
In conclusion, beta-thalassemia is a genetic disorder that affects the production of hemoglobin, leading to anemia, fatigue, and other complications. While there is no cure for the condition, it can be managed with medical interventions and bone marrow transplantation may be a viable option for some patients. Early diagnosis and management are crucial in preventing or minimizing the complications of beta-thalassemia.
Symptoms of aplastic anemia may include fatigue, weakness, shortness of breath, pale skin, and increased risk of bleeding or infection. Treatment options for aplastic anemia typically involve blood transfusions and immunosuppressive drugs to stimulate the bone marrow to produce new blood cells. In severe cases, a bone marrow transplant may be necessary.
Overall, aplastic anemia is a rare and serious condition that requires careful management by a healthcare provider to prevent complications and improve quality of life.
Examples of hematologic diseases include:
1. Anemia - a condition where there are not enough red blood cells or hemoglobin in the body.
2. Leukemia - a type of cancer that affects the bone marrow and blood, causing an overproduction of immature white blood cells.
3. Lymphoma - a type of cancer that affects the lymphatic system, including the bone marrow, spleen, and lymph nodes.
4. Thalassemia - a genetic disorder that affects the production of hemoglobin, leading to anemia and other complications.
5. Sickle cell disease - a genetic disorder that affects the production of hemoglobin, causing red blood cells to become sickle-shaped and prone to breaking down.
6. Polycythemia vera - a rare disorder where there is an overproduction of red blood cells.
7. Myelodysplastic syndrome - a condition where the bone marrow produces abnormal blood cells that do not mature properly.
8. Myeloproliferative neoplasms - a group of conditions where the bone marrow produces excessive amounts of blood cells, including polycythemia vera, essential thrombocythemia, and primary myelofibrosis.
9. Deep vein thrombosis - a condition where a blood clot forms in a deep vein, often in the leg or arm.
10. Pulmonary embolism - a condition where a blood clot travels to the lungs and blocks a blood vessel, causing shortness of breath, chest pain, and other symptoms.
These are just a few examples of hematologic diseases, but there are many others that can affect the blood and bone marrow. Treatment options for these diseases can range from watchful waiting and medication to surgery, chemotherapy, and stem cell transplantation. It is important to seek medical attention if you experience any symptoms of hematologic disease, as early diagnosis and treatment can improve outcomes.
Blood group incompatibility can occur in various ways, including:
1. ABO incompatibility: This is the most common type of blood group incompatibility and occurs when the patient's blood type (A or B) is different from the donor's blood type.
2. Rh incompatibility: This occurs when the patient's Rh factor is different from the donor's Rh factor.
3. Other antigens: In addition to ABO and Rh, there are other antigens on red blood cells that can cause incompatibility, such as Kell, Duffy, and Xg.
Blood group incompatibility can be diagnosed through blood typing and cross-matching tests. These tests determine the patient's and donor's blood types and identify any incompatible antigens that may cause an immune response.
Treatment of blood group incompatibility usually involves finding a compatible donor or using specialized medications to reduce the risk of a negative reaction. In some cases, plasmapheresis, also known as plasma exchange, may be used to remove the incompatible antibodies from the patient's blood.
Prevention of blood group incompatibility is important, and this can be achieved by ensuring that patients receive only compatible blood products during transfusions. Blood banks maintain a database of donor blood types and perform thorough testing before releasing blood for transfusion to ensure compatibility. Additionally, healthcare providers should carefully review the patient's medical history and current medications to identify any potential allergies or sensitivities that may affect blood compatibility.
There are two main types of thalassemia: alpha-thalassemia and beta-thalassemia. Alpha-thalassemia is caused by abnormalities in the production of the alpha-globin chain, which is one of the two chains that make up hemoglobin. Beta-thalassemia is caused by abnormalities in the production of the beta-globin chain.
Thalassemia can cause a range of symptoms, including anemia, fatigue, pale skin, and shortness of breath. In severe cases, it can lead to life-threatening complications such as heart failure, liver failure, and bone deformities. Thalassemia is usually diagnosed through blood tests that measure the levels of hemoglobin and other proteins in the blood.
There is no cure for thalassemia, but treatment can help manage the symptoms and prevent complications. Treatment may include blood transfusions, folic acid supplements, and medications to reduce the severity of anemia. In some cases, bone marrow transplantation may be recommended.
Preventive measures for thalassemia include genetic counseling and testing for individuals who are at risk of inheriting the disorder. Prenatal testing is also available for pregnant women who are carriers of the disorder. In addition, individuals with thalassemia should avoid marriage within their own family or community to reduce the risk of passing on the disorder to their children.
Overall, thalassemia is a serious and inherited blood disorder that can have significant health implications if left untreated. However, with proper treatment and management, individuals with thalassemia can lead fulfilling lives and minimize the risk of complications.
Also known as: chronic granulomatous disease, CGD.
Examples of fetal diseases include:
1. Down syndrome: A genetic disorder caused by an extra copy of chromosome 21, which can cause delays in physical and intellectual development, as well as increased risk of heart defects and other health problems.
2. Spina bifida: A birth defect that affects the development of the spine and brain, resulting in a range of symptoms from mild to severe.
3. Cystic fibrosis: A genetic disorder that affects the respiratory and digestive systems, causing thick mucus buildup and recurring lung infections.
4. Anencephaly: A condition where a portion of the brain and skull are missing, which is usually fatal within a few days or weeks of birth.
5. Clubfoot: A deformity of the foot and ankle that can be treated with casts or surgery.
6. Hirschsprung's disease: A condition where the nerve cells that control bowel movements are missing, leading to constipation and other symptoms.
7. Diaphragmatic hernia: A birth defect that occurs when there is a hole in the diaphragm, allowing organs from the abdomen to move into the chest cavity.
8. Gastroschisis: A birth defect where the intestines protrude through a opening in the abdominal wall.
9. Congenital heart disease: Heart defects that are present at birth, such as holes in the heart or narrowed blood vessels.
10. Neural tube defects: Defects that affect the brain and spine, such as spina bifida and anencephaly.
Early detection and diagnosis of fetal diseases can be crucial for ensuring proper medical care and improving outcomes for affected babies. Prenatal testing, such as ultrasound and blood tests, can help identify fetal anomalies and genetic disorders during pregnancy.
Genetic chimerism in fiction
Microchimerism
Wied's marmoset
Thomas Starzl
Horse markings
Human-animal hybrid
Mixed-field agglutination
Genetically modified animal
True hermaphroditism
Genetically modified organism
Calico cat
Glossary of genetics
Lydia Fairchild
Glossary of genetics (M−Z)
Twist-necked turtle
Chimera (genetics)
STR analysis
Xenotransplantation
Microsatellite
DNA profiling
Sheep-goat hybrid
Marmoset
Yeast artificial chromosome
Freemartin
T-cell depletion
Veto cells
Mosaic (genetics)
BRT Laboratories
Bizzaria
Lindsay Seers
Browsing by Subject "Chimerism"
NOT-MH-20-048: Notice of Special Interest (NOSI): Chimerism in Marmosets and other New World Primates
The minimum required level of donor chimerism in hereditary hemophagocytic lymphohistiocytosis - PubMed
Combining sperm plug genotyping and coat color chimerism predicts germline transmission - PubMed
Does HLA-dependent chimerism underlie the pathogenesis of juvenile dermatomyositis? | Scholars@Duke
Chimera (genetics) - Wikipedia
Follow-up of post-transplant minimal residual disease and chimerism in childhood lymphoblastic leukaemia: 90 d to react. | Br...
Further Development 12.11: Chimerism - Developmental Biology 12e Student Resources - Learning Link
Impact of T Cell Chimerism on Clinical Outcome in 117 Patients Who Underwent Allogeneic Stem Cell Transplantation with a...
Non-myeloablative stem cell gene delivery effectively establishes long-term gene expression and mixed chimerism in...
Pervasive Chimerism in the Replication-Associated Proteins of Uncultured Single-Stranded DNA Viruses - Institut Pasteur
Early Sickle Mortality Prevention | NHLBI, NIH
etymologia: Chimera (ki-mir′ə) - Volume 14, Number 11-November 2008 - Emerging Infectious Diseases journal - CDC
"Single-cell DNA-methylation analysis reveals epigenetic chimerism in p" by Chanchao Lorthongpanich, Lih Feng Cheow et al.
Differential promotion of hematopoietic chimerism and inhibition of alloreactive T cell proliferation by combinations of anti...
This Woman Is Her Own Twin, But How? | What Is Chimerism? | Your Twin Might Already Be Inside You ~ Amazing World Reality |...
Biomarkers Search
Clinical NEC prevention practices drive different microbiome profiles and functional responses in the preterm intestine |...
NIH Clinical Center Search the Studies: Study Number, Study Title
Current version of study NCT00408447 on ClinicalTrials.gov
JCI -
MLL-AF9- and HOXA9-mediated acute myeloid leukemia stem cell self-renewal requires JMJD1C
Results and long-term outcome in 39 patients with Wiskott-Aldrich syndrome transplanted from HLA-matched and -mismatched donors...
NIH Director's New Innovator Award Program - 2008 Award Recipients | NIH Common Fund
EasySepâ„¢ Direct Human NK Cell Isolation Kit | STEMCELL Technologies
Selected Publications
Rodgers, Griffin 2019 - Office of NIH History and Stetten Museum
Search | Page 4 | The Embryo Project Encyclopedia
Non-Myeloablative Conditioning for Unrelated Donor Umbilical Cord Blood Transplant - Full Text View - ClinicalTrials.gov
Hematopoietic chimerism5
- The evolutionary and functional consequences of hematopoietic chimerism, which is unique to marmosets and other callitrichid primates, are currently unknown. (nih.gov)
- Differential promotion of hematopoietic chimerism and inhibition of alloreactive T cell proliferation by combinations of anti-CD40Ligand, anti-LFA-1, everolimus, and deoxyspergualin. (novartis.com)
- However, DSG and everolimus were similarly synergistic with costimulation blockade for stable hematopoietic chimerism. (novartis.com)
- Thus, despite their strong inhibition of alloreactive T cell proliferation, combinations of anti-LFA-1 with everolimus or DSG did not reach the unique potency of anti-CD40L-based combinations to support stable hematopoietic chimerism in this system. (novartis.com)
- Solid organ allograft tolerance can be achieved by establishing mixed hematopoietic chimerism in recipients through transplantation of bone marrow (BM) from donors. (nih.gov)
Genetic2
- In fact, it is a genetic condition called chimerism , in which a human contains the cells of two or more individuals, containing two different sets of DNA. (amazingworldreality.com)
- Researchers later determined that the genetic mismatch was due to chimerism, a condition in which two genetically distinct cell lines are present in one body. (asu.edu)
Donor4
- This relatively low toxicity regimen allowed patients to become tolerant to the donor immune cells and to achieve stable mixed donor chimerism. (nih.gov)
- We hypothesized that AMD3100 may enhance mixed chimerism with less conditioning by providing a competitive advantage to reoccupy BM niches for infused donor BM cells over released recipient BM cells. (nih.gov)
- Mice receiving 50 million allogeneic donor BM cells attained 1.28% chimerism 1 month post-transplant, whereas mice receiving 10-25 million donor cells attained (nih.gov)
- In mice, ~1% chimerism is the threshold required for donor-specific tolerance. (nih.gov)
Post-transplant1
- Follow-up of post-transplant minimal residual disease and chimerism in childhood lymphoblastic leukaemia: 90 d to react. (bvsalud.org)
Bone2
- Allogeneic bone marrow (BM) engraftment for chimerism and transplantation tolerance may be promoted by combinations of costimulation blocking biologics and small molecular weight inhibitors. (novartis.com)
- We will generate through bone marrow chimerism mice that are predisposed to polyposis and also express a dominant negative Clock mutant in the immune compartment. (nih.gov)
Transplantation1
- The kinetics of chimerism were not useful for predicting relapse , whereas MRD monitoring up to 90 d post- transplantation was a valuable prognostic tool to guide therapeutic intervention. (bvsalud.org)
Chimeric2
- However, recent quantitative studies indicate that chimerism is limited to cells of the hematopoietic lineage, and that previous observation of widespread tissue chimerism was likely due to blood or lymphocyte infiltration of those tissues, as fibroblast cell lines from chimeric individuals were not chimeric. (nih.gov)
- By contrast, among the unclassified CRESS DNA viruses, 71% appear to have chimeric Reps. Such massive chimerism suggests that unclassified CRESS DNA viruses represent a dynamic population in which exchange of gene fragments encoding the nuclease and helicase domains is extremely common. (archives-ouvertes.fr)
Recipients1
- We showed previously in a mouse model that anti-CD40Ligand (anti-CD40L, CD154) combined with anti-LFA-1 or everolimus (40-O-(2-hydroxyethyl)-rapamycin) resulted in stable chimerism in almost all BM recipients, whereas anti-LFA-1 plus everolimus conferred approximately 50% chimerism stability. (novartis.com)
Mice2
Tissue1
- The immunogenetic adaptation in these species enables males to permanently fuse with their much larger female partners, a form of tissue chimaerism that is otherwise unknown in nature. (mpg.de)
Cells3
- Marmosets are obligate litter bearers with most pregnancies resulting in dizygotic twins that show chimerism in the blood and other cells from the hematopoietic lineage, as a result of in utero exchange of stem cells through placental anastomoses during early development, a process that leads to lifelong chimerism. (nih.gov)
- In simple words, Chimerism occurs when one of the twin in the womb dies and some of the cells of its deceased twin becomes absorbed by the surviving twin, resulting in the surviving twin having two sets of cells: its own, and some of its twin's. (amazingworldreality.com)
- Chimerism is a condition in which an individual has two genetically distinct types of cells in the blood. (nih.gov)
Study1
- This study investigated two patients with Rh chimerism: patient A, a healthy individual, and patient B with myelofibrosis. (who.int)
Cell2
Patients1
- Determine the presence of chimerism in patients treated with this regimen at days 21, 60, 100, 180, and 365. (clinicaltrials.gov)
Animals1
- It is also not known if chimerism limits or enhances the use of these animals as models for human physiology, health and disorders. (nih.gov)
Basis1
- The purpose of this Notice is to inform potential applicants to the National Institutes of Health (NIH) about a special interest in research project applications focusing on understanding the biological basis and functional implications of chimerism in the common marmoset ( Callithrix jacchus ) and other callitrichid primates. (nih.gov)
Achieve1
- Therefore, for this model to reach its full translational utility in furthering our understanding of human health and diseases, it is imperative that we achieve a better understanding of the functional consequences of chimerism and its contributions to health, behavior and diseases in New World primates. (nih.gov)
Marmosets and other callitrichid primates1
- The NOSI encourages applications focused on the biological and physiological significance and mechanisms that are responsible for chimerism in marmosets and other callitrichid primates. (nih.gov)
Donor chimerism1
- This relatively low toxicity regimen allowed patients to become tolerant to the donor immune cells and to achieve stable mixed donor chimerism. (nih.gov)
Tolerance12
- Study of the relatively few patients who have developed tolerance reveals that a state of chimerism may develop following transplantation. (medscape.com)
- Molecular and cellular effects of chimerism on immunological suppression/tolerance and reactivity including studies comparing immune responses elicited by a sibling twin to those of a third-party donor organ (e.g., kidney, heart, lung) or cellular (e.g., bone marrow or islet) transplant and mechanisms associated with transplant tolerance or rejection. (nih.gov)
- and the effects of chimerism on allograft transplant tolerance or rejection. (nih.gov)
- 1. Establishment of Chimerism and Organ Transplant Tolerance in Laboratory Animals: Safety and Efficacy of Adaptation to Humans. (nih.gov)
- 2. The importance of MHC class II in allogeneic bone marrow transplantation and chimerism-based solid organ tolerance in a rat model. (nih.gov)
- 3. Facilitating cells as a venue to establish mixed chimerism and tolerance. (nih.gov)
- 5. Methyl-Guanine-Methyl-Transferase Transgenic Bone Marrow Transplantation Allows N,N-bis(2-chloroethyl)-Nitrosourea Driven Donor Mixed-Chimerism Without Graft-Versus-Host Disease, and With Donor-Specific Allograft Tolerance. (nih.gov)
- 10. MHC-mismatched chimerism is required for induction of transplantation tolerance in autoimmune nonobese diabetic recipients. (nih.gov)
- 13. Chimerism-based tolerance in organ transplantation: preclinical and clinical studies. (nih.gov)
- 15. Mesenchymal stem cells enhance the induction of mixed chimerism and tolerance to rat hind-limb allografts after bone marrow transplantation. (nih.gov)
- 19. A nonlethal conditioning approach to achieve durable multilineage mixed chimerism and tolerance across major, minor, and hematopoietic histocompatibility barriers. (nih.gov)
- In mice, ~1% chimerism is the threshold required for donor-specific tolerance. (nih.gov)
Allogeneic bone marrow tra1
- 16. Apoptotic donor leukocytes limit mixed-chimerism induced by CD40-CD154 blockade in allogeneic bone marrow transplantation. (nih.gov)
Physiological significance1
- Applications in response to this NOSI should be aligned with the overall purpose, which is to improve our understanding of the biological and physiological significance of chimerism in this NHP model. (nih.gov)
Organ transplantation1
- 11. Mixed chimerism through donor bone marrow transplantation: a tolerogenic cell therapy for application in organ transplantation. (nih.gov)
Individual1
- This study investigated two patients with Rh chimerism: patient A, a healthy individual, and patient B with myelofibrosis. (who.int)
Enhance1
- We conclude that AMD3100 may enhance mixed chimerism in non-irradiated mice receiving allogeneic BM transplants. (nih.gov)
Health1
- It is also not known if chimerism limits or enhances the use of these animals as models for human physiology, health and disorders. (nih.gov)