Graft Rejection
Graft Survival
Skin Transplantation
Corneal Transplantation
Gait Ataxia
Rejection (Psychology)
Immunosuppressive Agents
Keratoplasty, Penetrating
Endophthalmitis
Transplantation Tolerance
Isoantigens
Cyclosporine
Liver Transplantation
Immunosuppression
Isoantibodies
Transplantation, Isogeneic
Bone Marrow Transplantation
Histocompatibility Testing
Graft Enhancement, Immunologic
Graft vs Host Disease
Transplantation, Heterotopic
Lung Transplantation
Islets of Langerhans Transplantation
T-Lymphocytes
Cyclosporins
Histocompatibility
Tissue Donors
Transplantation
Organ Transplantation
Graft vs Host Reaction
Lymphocyte Depletion
Transplantation Chimera
Antilymphocyte Serum
H-Y Antigen
Host vs Graft Reaction
Blood Vessel Prosthesis
Immune Tolerance
Treatment Outcome
Pimenta
CD8-Positive T-Lymphocytes
Corneal Opacity
Cornea
Biopsy
Postoperative Complications
Anemia, Aplastic
HLA Antigens
Catabolite Repression
Polytetrafluoroethylene
DNA Probes, HLA
Histocompatibility Antigens
Minor Histocompatibility Antigens
Lymphocyte Culture Test, Mixed
CD40 Ligand
T-Lymphocytes, Cytotoxic
Radiation Chimera
HLA-DR6 Antigen
Lymphocyte Activation
Corneal Edema
Cytotoxicity, Immunologic
Kidney
Mice, Inbred Strains
T-Lymphocyte Subsets
T-Lymphocytes, Regulatory
Complement C4b
Follow-Up Studies
Facial Bones
Corneal Neovascularization
CD4-Positive T-Lymphocytes
Adoptive Transfer
Transplantation Conditioning
Polyethylene Terephthalates
Whole-Body Irradiation
Mice, Knockout
Primary Graft Dysfunction
Mycoplasma hyorhinis
Azathioprine
Immunoconjugates
Histocompatibility Antigens Class I
Hematopoietic Stem Cell Transplantation
Cytokines
Blood Vessel Prosthesis Implantation
Transplants
Killer Cells, Natural
Interferon-gamma
Models, Animal
Bronchiolitis Obliterans
Hypersensitivity, Delayed
Carbonic Anhydrase V
Antigens, CD8
Mice, Transgenic
ABO Blood-Group System
Flow Cytometry
Leukocyte Transfusion
Sirolimus
Antigens, CD
Cytotoxicity Tests, Immunologic
Histocompatibility Antigens Class II
Projection
Risk Factors
Antigens, CD4
Lymphocytes
Bass
Anastomosis, Surgical
Drug Therapy, Combination
Antibodies, Blocking
CTLA-4 Antigen
Receptors, Interleukin-2
Cytomegalovirus Infections
Cells, Cultured
Fetal Tissue Transplantation
Immunization, Passive
Chimerism
Disease Models, Animal
Lymphocyte Transfusion
Propylene Glycols
Coronary Artery Bypass
Interleukin-10
Immunization
Prospective Studies
Biological Markers
Mice, SCID
Plasmapheresis
Antibodies
Antigens, CD28
Dendritic Cells
Fas Ligand Protein
Opportunistic Infections
Injections, Intraperitoneal
Survival Analysis
Administration, Topical
Immunologic Memory
Swine
Lymph Nodes
Blood Transfusion
Arteriovenous Shunt, Surgical
Forkhead Transcription Factors
Antibodies, Heterophile
Interleukin-2
Transplantation, Autologous
Complement System Proteins
Organ Preservation
Immunomodulation
Antibody Formation
Th2 Cells
Cell Movement
Interleukin-2 Receptor alpha Subunit
Antigens, Differentiation
Hematologic Neoplasms
Th1 Cells
Survival Rate
Jugular Veins
Allografts
Models, Immunological
Prednisolone
B-Lymphocytes
Chronic Disease
Antigen-Presenting Cells
Immune Sera
Skin
Tissue and Organ Harvesting
Rabbits
RNA, Messenger
Cyclophosphamide
Thymic selection by a single MHC/peptide ligand: autoreactive T cells are low-affinity cells. (1/6768)
In H2-M- mice, the presence of a single peptide, CLIP, bound to MHC class II molecules generates a diverse repertoire of CD4+ cells. In these mice, typical self-peptides are not bound to class II molecules, with the result that a very high proportion of H2-M- CD4+ cells are responsive to the various peptides displayed on normal MHC-compatible APC. We show here, however, that such "self" reactivity is controlled by low-affinity CD4+ cells. These cells give spectacularly high proliferative responses but are virtually unreactive in certain other assays, e.g., skin graft rejection; responses to MHC alloantigens, by contrast, are intense in all assays. Possible explanations for why thymic selection directed to a single peptide curtails self specificity without affecting alloreactivity are discussed. (+info)T lymphocyte adhesion mechanisms within inflamed human kidney: studies with a Stamper-Woodruff assay. (2/6768)
Renal inflammatory conditions are characterized by mononuclear cell recruitment to sites of inflammation. We have developed a modified Stamper-Woodruff assay system to analyze mechanisms of functional T cell adhesion to cryostat sections of renal biopsy material from patients with vasculitic glomerulonephritis (GN) and acute allograft rejection. Peripheral blood T cells adhered to intraglomerular, periglomerular, and tubulointerstitial regions of the cortex. Blocking monoclonal antibodies against tissue expressed ICAM-1, VCAM-1, and the CS-1 domain of fibronectin (CS-1Fn) differentially attenuated T cell adhesion. Glomerular adhesion in vasculitic GN and tubulointerstitial adhesion in acute rejection were particularly sensitive to both anti-ICAM-1 and anti-VCAM-1 antibodies, indicating a prominent role for ICAM-1 and VCAM-1 at glomerular sites in vasculitis and at tubulointerstitial sites in rejection. Furthermore, using KL/4 cells (LFA-1 expressing) and Jurkat cells (VLA-4 expressing), we demonstrated specific LFA-1/ICAM-1- and VLA-4/VCAM-1-mediated interactions within glomerular and tubulointerstitial compartments. Jurkat cells also adhered to VCAM-1-free sites, and binding was inhibitable by anti-CS-1Fn antibody, thereby demonstrating a role for VLA-4/fibronectin interactions especially at intraglomerular sites in acute rejection where VCAM-1 is notably absent. We therefore propose a prominent functional role for ICAM-1, VCAM-1, and CS-1 domain fibronectin in T cell recruitment to the inflamed kidney. (+info)Reduced kidney transplant rejection rate and pharmacoeconomic advantage of mycophenolate mofetil. (3/6768)
BACKGROUND: Several multinational controlled clinical trials have shown that triple therapy immunosuppressive regimens which include mycophenolate mofetil (MMF), cyclosporin A (CSA) and steroids (S) are superior compared with conventional regimens which include azathioprine (AZA), CSA and S, mainly because MMF reduces the rate of acute rejection episodes in the first 6 months after kidney transplantation. Post-marketing studies are useful to evaluate the general applicability and costs of MMF-based immunosuppressive regimens. METHODS: Based on the excellent results of the published controlled clinical trials, we have changed the standard triple therapy immunosuppressive protocol (AZA+CSA+S) to an MMF-based regimen (MMF+CSA+S) at our centre. To analyse the impact of this change in regimen, we have monitored 6-month patient and graft survival, rejection rate, serum creatinine and CSA levels, as well as the costs of the immunosuppressive and anti-rejection treatments, in 40 consecutive renal transplant recipients (MMF group) and have compared the data with 40 consecutive patients transplanted immediately prior to the change in regimen (AZA group). RESULTS: Recipient and donor characteristics were similar in the AZA and MMF groups. Patient survival (37/40; 92.5% in the AZA group vs 38/40; 95% in the MMF group), graft survival (36/40 vs 36/40; both 90%) and serum creatinine (137+/-56 vs 139+/-44 micromol/l) after 6 months were not significantly different. However, the rate of acute rejection episodes (defined as a rise in creatinine without other obvious cause and treated at least with pulse steroids) was significantly reduced with MMF from 60 to 20% (P=0.0005). The resulting cost for rejection treatment was lowered 8-fold (from sFr. 2113 to 259 averaged per patient) and the number of transplant biopsies was lowered > 3-fold in the MMF group. The cost for the immunosuppressive therapy was increased 1.5-fold with MMF (from sFr. 5906 to 9231 per patient for the first 6 months). CONCLUSIONS: The change from AZA to MMF resulted in a significant reduction in early rejection episodes, resulting in fewer diagnostic procedures and rehospitalizations. The optimal long-term regimen in terms of patient and pharmacoeconomic benefits remains to be defined. (+info)Primary adult liver transplantation under tacrolimus: more than 90 months actual follow-up survival and adverse events. (4/6768)
The introduction of tacrolimus has shown decreased rates of acute and steroid-resistant rejection after liver transplantation (LTx). The aim of the present study is to examine the long-term efficacy and safety of tacrolimus in primary liver transplant recipients. The first 121 consecutive adults (aged >16 years) who underwent primary LTx at a single center from August 1989 to February 1990 were followed up until August 1997. The mean follow-up was 93.2 +/- 1.2 months (range, 90.5 to 96.5 months). Patient survival, graft survival, rate of rejection, and adverse events were examined. The actual 7-year patient survival rate was 67.8%, and the graft survival rate was 63.6%. Infections, recurrence of disease, de novo malignancies, and cardiovascular events constituted the main causes of graft loss and death in the long term. Graft loss related to acute or chronic rejection was rare. The rate of acute rejection beyond 2 years was approximately 3% per year, and most rejections were steroid responsive. Approximately 70% of the patients received only tacrolimus after 1 year. Four patients developed end-stage renal disease, and 2 patients underwent kidney transplantation. Hyperkalemia and hypertension were observed in one third of the patients. New-onset insulin-dependent diabetes mellitus was observed in 9% and 13% of the patients at the 1-year and 7-year follow-up, respectively. Seven patients developed de novo malignancies, including two skin malignancies. Six patients developed posttransplantation lymphoproliferative disorder during the entire follow-up period. Actual patient and graft survival at 7 years was excellent, and few adverse events developed after the first year. Graft loss from acute or chronic rejection was rare under tacrolimus, and approximately 70% of the patients were steroid free on tacrolimus monotherapy after the first year after LTx. (+info)Xenotransplantation. (5/6768)
As transplantation waiting lists lengthen because of the shortage of donor organs, the death rates of patients continue to rise. Xenotransplantation offers the potential to solve the problem of organ shortage br providing an unlimited supply of healthy donor organs. However, there are several barriers to xenotransplantation, including graft rejection, potential xenozoonosis, physiologic incompatibilities and ethical concerns. Experimental xenotransplantation studies continue in several areas, ranging from tissue to whole- organ grafting. Clinical studies continue in the area of tissue xenotransplantation. Trials with extracorporeal xenografts in an acute setting to support fulminant organ failure are likely to begin in the near future. The reintroduction of whole-organ xenotransplantation must be based on sound scientific analysis with broad societal input so as to offer the maximal benefit to transplant recipients and their families. (+info)Long-term results of pancreas transplantation under tacrolius immunosuppression. (6/6768)
BACKGROUND: The long-term safety and efficacy of tacrolimus in pancreas transplantation has not yet been demonstrated. The observation of prolonged pancreatic graft function under tacrolimus would indicate that any potential islet toxicity is short-lived and clinically insignificant. We report herein the results of pancreas transplantation in patients receiving primary tacrolimus immunosuppression for a minimum of 2 years. METHODS: From July 4, 1994 until April 18, 1996, 60 patients received either simultaneous pancreas-kidney transplant (n=55), pancreas transplant only (n=4), or pancreas after kidney transplantation (n=1). Baseline immunosuppression consisted of tacrolimus and steroids without antilymphocyte induction. Azathioprine was used as a third agent in 51 patients and mycophenolate mofetil in 9. Rejection episodes within the first 6 months occurred in 48 (80%) patients and were treated with high-dose corticosteroids. Antilymphocyte antibody was required in eight (13%) patients with steroid-resistant rejection. RESULTS: With a mean follow-up of 35.1+/-5.9 months (range: 24.3-45.7 months), 6-month and 1-, 2-, and 33-year graft survival is 88%, 82%, 80%, and 80% (pancreas) and 98%, 96%, 93%, and 91% (kidney), respectively. Six-month and 1-, 2-, and 3-year patient survival is 100%, 98%, 98%, and 96.5%. Mean fasting glucose is 91.6+/-13.8 mg/dl, and mean glycosylated hemoglobin is 5.1+/-0.7% (normal range: 4.3-6.1%). Mean tacrolimus dose is 6.5+/-2.6 mg/day and mean prednisone dose 2.0+/-2.9 mg/day at follow-up. Complete steroid withdrawal was possible in 31 (65%) of the 48 patients with functioning pancreases. CONCLUSIONS: These data show for the first time that tacrolimus is a safe and effective long-term primary agent in pancreas transplantation and provides excellent long-term islet function without evidence of toxicity while permitting steroid withdrawal in the majority of patients. (+info)Pediatric renal transplantation under tacrolimus-based immunosuppression. (7/6768)
BACKGROUND: Tacrolimus has been used as a primary immunosuppressive agent in adult and pediatric renal transplant recipients, with reasonable outcomes. Methods. Between December 14, 1989 and December 31, 1996, 82 pediatric renal transplantations alone were performed under tacrolimus-based immunosuppression without induction anti-lymphocyte antibody therapy. Patients undergoing concomitant or prior liver and/or intestinal transplantation were not included in the analysis. The mean recipient age was 10.6+/-5.2 years (range: 0.7-17.9). Eighteen (22%) cases were repeat transplantations, and 6 (7%) were in patients with panel-reactive antibody levels over 40%. Thirty-four (41%) cases were with living donors, and 48 (59%) were with cadaveric donors. The mean donor age was 27.3+/-14.6 years (range: 0.7-50), and the mean cold ischemia time in the cadaveric cases was 26.5+/-8.8 hr. The mean number of HLA matches and mismatches was 2.8+/-1.2 and 2.9+/-1.3; there were five (6%) O-Ag mismatches. The mean follow-up was 4.0+/-0.2 years. RESULTS: The 1- and 4-year actuarial patient survival was 99% and 94%. The 1- and 4-year actuarial graft survival was 98% and 84%. The mean serum creatinine was 1.1+/-0.5 mg/dl, and the corresponding calculated creatinine clearance was 88+/-25 ml/min/1.73 m2. A total of 66% of successfully transplanted patients were withdrawn from prednisone. In children who were withdrawn from steroids, the mean standard deviation height scores (Z-score) at the time of transplantation and at 1 and 4 years were -2.3+/-2.0, -1.7+/-1.0, and +0.36+/-1.5. Eighty-six percent of successfully transplanted patients were not taking anti-hypertensive medications. The incidence of acute rejection was 44%; between December 1989 and December 1993, it was 63%, and between January 1994 and December 1996, it was 23% (P=0.0003). The incidence of steroid-resistant rejection was 5%. The incidence of delayed graft function was 5%, and 2% of patients required dialysis within 1 week of transplantation. The incidence of cytomegalovirus was 13%; between December 1989 and December 1992, it was 17%, and between January 1993 and December 1996, it was 12%. The incidence of early Epstein-Barr virus-related posttransplant lymphoproliferative disorder (PTLD) was 9%; between December 1989 and December 1992, it was 17%, and between January 1993 and December 1996, it was 4%. All of the early PTLD cases were treated successfully with temporary cessation of immunosuppression and institution of antiviral therapy, without patient or graft loss. CONCLUSIONS: These data demonstrate the short- and medium-term efficacy of tacrolimus-based immunosuppression in pediatric renal transplant recipients, with reasonable patient and graft survival, routine achievement of steroid and anti-hypertensive medication withdrawal, gratifying increases in growth, and, with further experience, a decreasing incidence of both rejection and PTLD. (+info)Dual roles of sialyl Lewis X oligosaccharides in tumor metastasis and rejection by natural killer cells. (8/6768)
Aberrant expression of cell surface carbohydrates such as sialyl Lewis X is associated with tumor formation and metastasis. In order to determine the roles of sialyl Lewis X in tumor metastasis, mouse melanoma B16-F1 cells were stably transfected with alpha1, 3-fucosyltransferase III to express sialyl Lewis X structures. The transfected B16-F1 cells, B16-FTIII, were separated by cell sorting into three different groups based on the expression levels of sialyl Lewis X. When these transfected cells were injected into tail veins of C57BL/6 mice, B16-FTIII.M cells expressing moderate amounts of sialyl Lewis X in poly-N-acetyllactosamines produced large numbers of lung tumor nodules. Surprisingly, B16-FTIII.H cells expressing the highest amount of sialyl Lewis X in shorter N-glycans died in lung blood vessels, producing as few lung nodules as B16-FTIII.N cells which lack sialyl Lewis X. In contrast, B16-FIII.H cells formed more tumors in beige mice and NK cell-depleted C57BL/6 mice than did B16-FTIII.M cells. B16-FTIII.H cells bound to E-selectin better than did B16-FTIII.M cells, but both cells grew at the same rate. These results indicate that excessive expression of sialyl Lewis X in tumor cells leads to rejection by NK cells rather than tumor formation facilitated by attachment to endothelial cells. (+info)The main symptoms of gait ataxia include:
* Unsteadiness
* Lack of coordination
* Wobbling or staggering while walking
* Increased risk of falling
* Difficulty with balance and equilibrium
* Slow and deliberate movements
Gait ataxia can be assessed using various clinical tests such as the Clinical Test of Sensory Integration and Balance, the Berg Balance Scale, and the Timed Up and Go test. Treatment options for gait ataxia depend on the underlying cause of the condition and may include physical therapy, occupational therapy, speech therapy, medications, and in some cases, surgery.
In summary, gait ataxia is a term used to describe an abnormal gait pattern due to dysfunction in the nervous system. It can be caused by various factors and can affect individuals of all ages. The symptoms include unsteadiness, lack of coordination, and increased risk of falling, among others. Treatment options depend on the underlying cause of the condition and may include physical therapy, medications, and in some cases, surgery.
Endophthalmitis can be classified into several types based on its causes, such as:
1. Postoperative endophthalmitis: This type of endophthalmitis occurs after cataract surgery or other intraocular surgeries. It is caused by bacterial infection that enters the eye through the surgical incision.
2. Endogenous endophthalmitis: This type of endophthalmitis is caused by an infection that originates within the eye, such as from a retinal detachment or uveitis.
3. Exogenous endophthalmitis: This type of endophthalmitis is caused by an infection that enters the eye from outside, such as from a penetrating injury or a foreign object in the eye.
The symptoms of endophthalmitis can include:
1. Severe pain in the eye
2. Redness and swelling of the conjunctiva
3. Difficulty seeing or blind spots in the visual field
4. Sensitivity to light
5. Increased sensitivity to touch or pressure on the eye
6. Fever and chills
7. Swollen lymph nodes
8. Enlarged pupil
9. Clouding of the vitreous humor
If you suspect that you or someone else has endophthalmitis, it is important to seek medical attention immediately. Early diagnosis and treatment can help prevent vision loss. Treatment options for endophthalmitis may include antibiotics, vitrectomy (removal of the vitreous humor), and in some cases, removal of the affected eye.
Graft occlusion can occur due to a variety of factors, including:
1. Blood clots forming within the graft
2. Inflammation or infection within the graft
3. Narrowing or stenosis of the graft
4. Disruption of the graft material
5. Poor blood flow through the graft
The signs and symptoms of vascular graft occlusion can vary depending on the location and severity of the blockage. They may include:
1. Pain or tenderness in the affected limb
2. Swelling or redness in the affected limb
3. Weakness or numbness in the affected limb
4. Difficulty walking or moving the affected limb
5. Coolness or discoloration of the skin in the affected limb
If you experience any of these symptoms, it is important to seek medical attention as soon as possible. A healthcare professional can diagnose vascular graft occlusion using imaging tests such as ultrasound, angiography, or MRI. Treatment options for vascular graft occlusion may include:
1. Medications to dissolve blood clots or reduce inflammation
2. Surgical intervention to repair or replace the graft
3. Balloon angioplasty or stenting to open up the blocked graft
4. Hyperbaric oxygen therapy to improve blood flow and promote healing.
Preventive measures to reduce the risk of vascular graft occlusion include:
1. Proper wound care and infection prevention after surgery
2. Regular follow-up appointments with your healthcare provider
3. Avoiding smoking and other cardiovascular risk factors
4. Taking medications as directed by your healthcare provider to prevent blood clots and inflammation.
It is important to note that vascular graft occlusion can be a serious complication after surgery, but with prompt medical attention and appropriate treatment, the outcome can be improved.
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.
Examples of acute diseases include:
1. Common cold and flu
2. Pneumonia and bronchitis
3. Appendicitis and other abdominal emergencies
4. Heart attacks and strokes
5. Asthma attacks and allergic reactions
6. Skin infections and cellulitis
7. Urinary tract infections
8. Sinusitis and meningitis
9. Gastroenteritis and food poisoning
10. Sprains, strains, and fractures.
Acute diseases can be treated effectively with antibiotics, medications, or other therapies. However, if left untreated, they can lead to chronic conditions or complications that may require long-term care. Therefore, it is important to seek medical attention promptly if symptoms persist or worsen over time.
1. Infection: Bacterial or viral infections can develop after surgery, potentially leading to sepsis or organ failure.
2. Adhesions: Scar tissue can form during the healing process, which can cause bowel obstruction, chronic pain, or other complications.
3. Wound complications: Incisional hernias, wound dehiscence (separation of the wound edges), and wound infections can occur.
4. Respiratory problems: Pneumonia, respiratory failure, and atelectasis (collapsed lung) can develop after surgery, particularly in older adults or those with pre-existing respiratory conditions.
5. Cardiovascular complications: Myocardial infarction (heart attack), cardiac arrhythmias, and cardiac failure can occur after surgery, especially in high-risk patients.
6. Renal (kidney) problems: Acute kidney injury or chronic kidney disease can develop postoperatively, particularly in patients with pre-existing renal impairment.
7. Neurological complications: Stroke, seizures, and neuropraxia (nerve damage) can occur after surgery, especially in patients with pre-existing neurological conditions.
8. Pulmonary embolism: Blood clots can form in the legs or lungs after surgery, potentially causing pulmonary embolism.
9. Anesthesia-related complications: Respiratory and cardiac complications can occur during anesthesia, including respiratory and cardiac arrest.
10. delayed healing: Wound healing may be delayed or impaired after surgery, particularly in patients with pre-existing medical conditions.
It is important for patients to be aware of these potential complications and to discuss any concerns with their surgeon and healthcare team before undergoing surgery.
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.
In medicine, cadavers are used for a variety of purposes, such as:
1. Anatomy education: Medical students and residents learn about the human body by studying and dissecting cadavers. This helps them develop a deeper understanding of human anatomy and improves their surgical skills.
2. Research: Cadavers are used in scientific research to study the effects of diseases, injuries, and treatments on the human body. This helps scientists develop new medical techniques and therapies.
3. Forensic analysis: Cadavers can be used to aid in the investigation of crimes and accidents. By examining the body and its injuries, forensic experts can determine cause of death, identify suspects, and reconstruct events.
4. Organ donation: After death, cadavers can be used to harvest organs and tissues for transplantation into living patients. This can improve the quality of life for those with organ failure or other medical conditions.
5. Medical training simulations: Cadavers can be used to simulate real-life medical scenarios, allowing healthcare professionals to practice their skills in a controlled environment.
In summary, the term "cadaver" refers to the body of a deceased person and is used in the medical field for various purposes, including anatomy education, research, forensic analysis, organ donation, and medical training simulations.
Some common symptoms of corneal edema include:
* Blurred vision
* Haziness or clouding of the cornea
* Increased sensitivity to light
* Redness or discharge in the eye
* Pain or discomfort in the eye
Corneal edema can be diagnosed through a comprehensive eye exam, which may include a visual acuity test, dilated eye exam, and imaging tests such as cornea scans or ultrasound. Treatment for corneal edema depends on the underlying cause and may involve antibiotics, anti-inflammatory medications, or other therapies to reduce swelling and promote healing. In some cases, surgery may be necessary to remove scar tissue or improve drainage of fluid from the eye.
If left untreated, corneal edema can lead to more serious complications such as corneal ulcers or vision loss. Therefore, it is important to seek medical attention if you experience any symptoms of corneal edema to prevent any further damage and ensure proper treatment.
1. Keratoconus: This is a progressive thinning of the cornea that can cause it to bulge into a cone-like shape, leading to blurred vision and sensitivity to light.
2. Fuchs' dystrophy: This is a condition in which the cells in the innermost layer of the cornea become damaged, leading to clouding and blurred vision.
3. Bullous keratopathy: This is a condition in which there is a large, fluid-filled bubble on the surface of the cornea, which can cause blurred vision and discomfort.
4. Corneal ulcers: These are open sores on the surface of the cornea that can be caused by infection or other conditions.
5. Dry eye syndrome: This is a condition in which the eyes do not produce enough tears, leading to dryness, irritation, and blurred vision.
6. Corneal abrasions: These are scratches on the surface of the cornea that can be caused by injury or other conditions.
7. Trachoma: This is an infectious eye disease that can cause scarring and blindness if left untreated.
8. Ocular herpes: This is a viral infection that can cause blisters on the surface of the cornea and lead to scarring and vision loss if left untreated.
9. Endophthalmitis: This is an inflammation of the inner layer of the eye that can be caused by bacterial or fungal infections, and can lead to severe vision loss if left untreated.
10. Corneal neovascularization: This is the growth of new blood vessels into the cornea, which can be a complication of other conditions such as dry eye syndrome or ocular trauma.
These are just a few examples of the many different types of corneal diseases that can affect the eyes. It's important to seek medical attention if you experience any symptoms such as pain, redness, or blurred vision in one or both eyes. Early diagnosis and treatment can help prevent complications and preserve vision.
CNV can cause vision loss and blindness if left untreated. It can also increase the risk of complications such as cataracts, glaucoma, and corneal ulcers.
There are several treatment options for CNV, including:
1. Anti-vascular endothelial growth factor (VEGF) injections: These medications can help reduce the growth of new blood vessels and preserve vision.
2. Photodynamic therapy: This involves the use of a light-sensitive medication and low-intensity laser to damage and shrink the new blood vessels.
3. Corneal transplantation: In severe cases, a corneal transplant may be necessary to replace the damaged or diseased cornea with a healthy one.
4. Surgical removal of the neovascularized tissue: This can be done through a surgical procedure called vitrectomy, where the new blood vessels are removed and the eye is filled with a gas or oil bubble.
Early detection and treatment of CNV are crucial to prevent vision loss and improve outcomes. Ophthalmologists use a range of diagnostic tests such as imaging studies and visual acuity assessments to diagnose and monitor the progression of the condition.
The primary graft dysfunction syndrome is a complex clinical entity characterized by severe respiratory and cardiovascular dysfunction, which develops within the first week after transplantation. PGD is associated with high morbidity and mortality rates, and it is one of the leading causes of graft failure after solid organ transplantation.
There are several risk factors for primary graft dysfunction, including:
1. Recipient age and comorbidities
2. Donor age and comorbidities
3. Cold ischemic time (CIT)
4. Hypoxic injury during procurement
5. Delayed recipient surgery
6. Inadequate immunosuppression
7. Sepsis
8. Pulmonary infection
9. Hemodynamic instability
10. Pulmonary edema
The diagnosis of primary graft dysfunction is based on a combination of clinical, radiologic, and pathologic findings. The condition can be classified into three categories:
1. Mild PGD: characterized by mild respiratory and cardiovascular dysfunction, with no evidence of severe inflammation or fibrosis.
2. Moderate PGD: characterized by moderate respiratory and cardiovascular dysfunction, with evidence of severe inflammation and/or fibrosis.
3. Severe PGD: characterized by severe respiratory and cardiovascular dysfunction, with extensive inflammation and/or fibrosis.
The treatment of primary graft dysfunction is aimed at addressing the underlying cause of the condition. This may include administration of immunosuppressive drugs, management of infections, and correction of any anatomical or functional abnormalities. In severe cases, lung transplantation may be necessary.
Prevention of primary graft dysfunction is crucial to minimize the risk of complications after lung transplantation. This can be achieved by careful donor selection, optimization of recipient condition before transplantation, and meticulous surgical technique during the procedure. Additionally, prompt recognition and management of early signs of PGD are essential to prevent progression to more severe forms of the condition.
In conclusion, primary graft dysfunction is a complex and multifactorial complication after lung transplantation that can lead to significant morbidity and mortality. Understanding the causes, clinical presentation, diagnosis, and treatment of PGD is essential for optimal management of patients undergoing lung transplantation.
The exact cause of Bronchiolitis Obliterans is not fully understood, but it is believed to be due to a combination of genetic and environmental factors. The condition is often associated with allergies and asthma, and viral infections such as respiratory syncytial virus (RSV) can trigger the onset of symptoms.
Symptoms of Bronchiolitis Obliterans include:
* Persistent coughing, which may be worse at night
* Shortness of breath or wheezing
* Chest tightness or discomfort
* Fatigue and poor appetite
* Recurrent respiratory infections
BO is typically diagnosed through a combination of physical examination, medical history, and diagnostic tests such as chest X-rays or pulmonary function tests. There is no cure for Bronchiolitis Obliterans, but treatment options are available to manage symptoms and slow the progression of the disease. These may include:
* Medications such as bronchodilators and corticosteroids to reduce inflammation and improve lung function
* Pulmonary rehabilitation programs to improve breathing and overall health
* Oxygen therapy to help increase oxygen levels in the blood
* In severe cases, lung transplantation may be considered.
While Bronchiolitis Obliterans can significantly impact quality of life, with proper management and care, many individuals with the condition are able to lead active and productive lives.
Examples of delayed hypersensitivity reactions include contact dermatitis (a skin reaction to an allergic substance), tuberculin reactivity (a reaction to the bacteria that cause tuberculosis), and sarcoidosis (a condition characterized by inflammation in various organs, including the lungs and lymph nodes).
Delayed hypersensitivity reactions are important in the diagnosis and management of allergic disorders and other immune-related conditions. They can be detected through a variety of tests, including skin prick testing, patch testing, and blood tests. Treatment for delayed hypersensitivity reactions depends on the underlying cause and may involve medications such as antihistamines, corticosteroids, or immunosuppressants.
CMV infections are more common in people with weakened immune systems, such as those with HIV/AIDS, cancer, or taking immunosuppressive drugs after an organ transplant. In these individuals, CMV can cause severe and life-threatening complications, such as pneumonia, retinitis (inflammation of the retina), and gastrointestinal disease.
In healthy individuals, CMV infections are usually mild and may not cause any symptoms at all. However, in some cases, CMV can cause a mononucleosis-like illness with fever, fatigue, and swollen lymph nodes.
CMV infections are diagnosed through a combination of physical examination, blood tests, and imaging studies such as CT scans or MRI. Treatment is generally not necessary for mild cases, but may include antiviral medications for more severe infections. Prevention strategies include avoiding close contact with individuals who have CMV, practicing good hygiene, and considering immunoprophylaxis (prevention of infection through the use of immune globulin) for high-risk individuals.
Overall, while CMV infections can be serious and life-threatening, they are relatively rare in healthy individuals and can often be treated effectively with supportive care and antiviral medications.
1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.
2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.
3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.
4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.
5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.
6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.
7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.
8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.
9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.
10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.
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.
Examples of OIs include:
1. Pneumocystis pneumonia (PCP): A type of pneumonia caused by the fungus Pneumocystis jirovecii, which is commonly found in the lungs of individuals with HIV/AIDS.
2. Cryptococcosis: A fungal infection caused by Cryptococcus neoformans, which can affect various parts of the body, including the lungs, central nervous system, and skin.
3. Aspergillosis: A fungal infection caused by Aspergillus fungi, which can affect various parts of the body, including the lungs, sinuses, and brain.
4. Histoplasmosis: A fungal infection caused by Histoplasma capsulatum, which is commonly found in the soil and can cause respiratory and digestive problems.
5. Candidiasis: A fungal infection caused by Candida albicans, which can affect various parts of the body, including the skin, mouth, throat, and vagina.
6. Toxoplasmosis: A parasitic infection caused by Toxoplasma gondii, which can affect various parts of the body, including the brain, eyes, and lymph nodes.
7. Tuberculosis (TB): A bacterial infection caused by Mycobacterium tuberculosis, which primarily affects the lungs but can also affect other parts of the body.
8. Kaposi's sarcoma-associated herpesvirus (KSHV): A viral infection that can cause various types of cancer, including Kaposi's sarcoma, which is more common in individuals with compromised immunity.
The diagnosis and treatment of OIs depend on the specific type of infection and its severity. Treatment may involve antibiotics, antifungals, or other medications, as well as supportive care to manage symptoms and prevent complications. It is important for individuals with HIV/AIDS to receive prompt and appropriate treatment for OIs to help prevent the progression of their disease and improve their quality of life.
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.
The burden of chronic diseases is significant, with over 70% of deaths worldwide attributed to them, according to the World Health Organization (WHO). In addition to the physical and emotional toll they take on individuals and their families, chronic diseases also pose a significant economic burden, accounting for a large proportion of healthcare expenditure.
In this article, we will explore the definition and impact of chronic diseases, as well as strategies for managing and living with them. We will also discuss the importance of early detection and prevention, as well as the role of healthcare providers in addressing the needs of individuals with chronic diseases.
What is a Chronic Disease?
A chronic disease is a condition that lasts for an extended period of time, often affecting daily life and activities. Unlike acute diseases, which have a specific beginning and end, chronic diseases are long-term and persistent. Examples of chronic diseases include:
1. Diabetes
2. Heart disease
3. Arthritis
4. Asthma
5. Cancer
6. Chronic obstructive pulmonary disease (COPD)
7. Chronic kidney disease (CKD)
8. Hypertension
9. Osteoporosis
10. Stroke
Impact of Chronic Diseases
The burden of chronic diseases is significant, with over 70% of deaths worldwide attributed to them, according to the WHO. In addition to the physical and emotional toll they take on individuals and their families, chronic diseases also pose a significant economic burden, accounting for a large proportion of healthcare expenditure.
Chronic diseases can also have a significant impact on an individual's quality of life, limiting their ability to participate in activities they enjoy and affecting their relationships with family and friends. Moreover, the financial burden of chronic diseases can lead to poverty and reduce economic productivity, thus having a broader societal impact.
Addressing Chronic Diseases
Given the significant burden of chronic diseases, it is essential that we address them effectively. This requires a multi-faceted approach that includes:
1. Lifestyle modifications: Encouraging healthy behaviors such as regular physical activity, a balanced diet, and smoking cessation can help prevent and manage chronic diseases.
2. Early detection and diagnosis: Identifying risk factors and detecting diseases early can help prevent or delay their progression.
3. Medication management: Effective medication management is crucial for controlling symptoms and slowing disease progression.
4. Multi-disciplinary care: Collaboration between healthcare providers, patients, and families is essential for managing chronic diseases.
5. Health promotion and disease prevention: Educating individuals about the risks of chronic diseases and promoting healthy behaviors can help prevent their onset.
6. Addressing social determinants of health: Social determinants such as poverty, education, and employment can have a significant impact on health outcomes. Addressing these factors is essential for reducing health disparities and improving overall health.
7. Investing in healthcare infrastructure: Investing in healthcare infrastructure, technology, and research is necessary to improve disease detection, diagnosis, and treatment.
8. Encouraging policy change: Policy changes can help create supportive environments for healthy behaviors and reduce the burden of chronic diseases.
9. Increasing public awareness: Raising public awareness about the risks and consequences of chronic diseases can help individuals make informed decisions about their health.
10. Providing support for caregivers: Chronic diseases can have a significant impact on family members and caregivers, so providing them with support is essential for improving overall health outcomes.
Conclusion
Chronic diseases are a major public health burden that affect millions of people worldwide. Addressing these diseases requires a multi-faceted approach that includes lifestyle changes, addressing social determinants of health, investing in healthcare infrastructure, encouraging policy change, increasing public awareness, and providing support for caregivers. By taking a comprehensive approach to chronic disease prevention and management, we can improve the health and well-being of individuals and communities worldwide.
The term "acute-phase" describes the rapid onset and short duration of this reaction, which typically lasts for hours to days before resolving as the body's inflammatory response subsides. APR is characterized by a series of molecular events that result in altered expression of genes involved in inflammation, immune response, and tissue repair.
Some key components of an acute-phase reaction include:
1. Cytokine production: Cytokines are signaling molecules released by immune cells, such as white blood cells, that coordinate the immune response. During an APR, cytokine levels increase, triggering a cascade of downstream effects.
2. Leukocyte trafficking: White blood cells migrate towards sites of inflammation or infection, where they phagocytose (engulf and digest) pathogens and cellular debris. This process helps to limit the spread of infection and initiate tissue repair.
3. Coagulation cascade: The APR triggers a complex series of events involving blood coagulation factors, leading to the formation of blood clots and preventing excessive bleeding.
4. Anti-inflammatory response: As the APR progresses, anti-inflammatory cytokines, such as interleukin-10 (IL-10), are produced to dampen the inflammatory response and promote tissue repair.
5. Cellular proliferation: To replace damaged cells and tissues, the APR stimulates cellular proliferation and tissue regeneration.
6. Nutrient mobilization: The APR enhances nutrient uptake and utilization by immune cells, allowing them to mount an effective response to the stress.
7. Hormonal changes: The APR is accompanied by changes in hormone levels, such as the increase in corticotropin-releasing factor (CRF) and cortisol, which help to mobilize energy resources and regulate metabolism.
8. Immune tolerance: The APR helps to establish immune tolerance, preventing excessive or inappropriate immune responses that can lead to autoimmune diseases or allergies.
9. Tissue remodeling: The APR stimulates the remodeling of damaged tissues, allowing for the restoration of normal tissue function.
10. Memory formation: The APR sets the stage for the formation of immunological memory, which enables the immune system to mount a more effective response to future infections or stressors.
There are several types of ischemia, including:
1. Myocardial ischemia: Reduced blood flow to the heart muscle, which can lead to chest pain or a heart attack.
2. Cerebral ischemia: Reduced blood flow to the brain, which can lead to stroke or cognitive impairment.
3. Peripheral arterial ischemia: Reduced blood flow to the legs and arms.
4. Renal ischemia: Reduced blood flow to the kidneys.
5. Hepatic ischemia: Reduced blood flow to the liver.
Ischemia can be diagnosed through a variety of tests, including electrocardiograms (ECGs), stress tests, and imaging studies such as CT or MRI scans. Treatment for ischemia depends on the underlying cause and may include medications, lifestyle changes, or surgical interventions.
There are several types of prosthesis-related infections, including:
1. Bacterial infections: These are the most common type of prosthesis-related infection and can occur around any type of implanted device. They are caused by bacteria that enter the body through a surgical incision or other opening.
2. Fungal infections: These types of infections are less common and typically occur in individuals who have a weakened immune system or who have been taking antibiotics for another infection.
3. Viral infections: These infections can occur around implanted devices, such as pacemakers, and are caused by viruses that enter the body through a surgical incision or other opening.
4. Parasitic infections: These types of infections are rare and occur when parasites, such as tapeworms, infect the implanted device or the surrounding tissue.
Prosthesis-related infections can cause a range of symptoms, including pain, swelling, redness, warmth, and fever. In severe cases, these infections can lead to sepsis, a potentially life-threatening condition that occurs when bacteria or other microorganisms enter the bloodstream.
Prosthesis-related infections are typically diagnosed through a combination of physical examination, imaging tests such as X-rays or CT scans, and laboratory tests to identify the type of microorganism causing the infection. Treatment typically involves antibiotics or other antimicrobial agents to eliminate the infection, and may also involve surgical removal of the infected implant.
Prevention is key in avoiding prosthesis-related infections. This includes proper wound care after surgery, keeping the surgical site clean and dry, and taking antibiotics as directed by your healthcare provider to prevent infection. Additionally, it is important to follow your healthcare provider's instructions for caring for your prosthesis, such as regularly cleaning and disinfecting the device and avoiding certain activities that may put excessive stress on the implant.
Overall, while prosthesis-related infections can be serious, prompt diagnosis and appropriate treatment can help to effectively manage these complications and prevent long-term damage or loss of function. It is important to work closely with your healthcare provider to monitor for signs of infection and take steps to prevent and manage any potential complications associated with your prosthesis.
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History and naming of human leukocyte antigens
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List of people who adopted matrilineal surnames
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NIH Guide: IMMUNOPATHOGENESIS OF CHRONIC GRAFT REJECTION
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Allograft rejection10
- In 1944, Medawar showed that skin allograft rejection is a host versus graft response. (medscape.com)
- Histocompatibility antigens are encoded on more than 40 loci, but the loci responsible for the most vigorous allograft rejection reactions are on the major histocompatibility complex (MHC). (medscape.com)
- 11. B cells in cluster or in a scattered pattern do not correlate with clinical outcome of renal allograft rejection. (nih.gov)
- 16. Pretransplant low CD3+CD25high cell counts or a low CD3+CD25high/CD3+HLA-DR+ ratio are associated with an increased risk to acute renal allograft rejection. (nih.gov)
- Suppression of allograft rejection by regulatory B cells induced via TLR signaling. (harvard.edu)
- Late severe acute intestinal allograft rejection is associated with increased risk of morbidity and mortality and, in the majority of cases, ends with total enterectomy. (stanfordchildrens.org)
- The rIL-12p70 alloactivated Ts1 cells markedly delayed PVG, but not third party Lewis, cardiac allograft rejection in normal DA recipients. (frontiersin.org)
- These Th1-like Treg delayed specific donor allograft rejection demonstrating therapeutic potential. (frontiersin.org)
- 1:1 of nTreg:effector CD4 + T cells to inhibit organ allograft rejection ( 2 , 8 ) or graft versus host disease (GVHD) ( 11 ). (frontiersin.org)
- Thus, extremely large numbers of nTreg are required in vivo to prevent allograft rejection and GVHD in unmodified recipients ( 13 ). (frontiersin.org)
Survival15
- Knowledge of these mechanisms is also critical in developing strategies to minimize rejection and in developing new drugs and treatments that blunt the effects of the immune system on transplanted organs, thereby ensuring longer survival of these organs. (medscape.com)
- In follow-up, in a period of three years there was no statistically significant difference in blood creatinine level, glomerular filtration rate, number of clinical rejections during the monitoring period, and three-year survival of the transplanted kidney in patients, regardless of where the treatment of subclinical rejection was applied. (rsu.lv)
- This study evaluated the prevalence and graft survival of herpes simplex virus type 1 (HSV-1) and varicella zoster virus (VZV) DNA in recipient corneas during PK. (mdpi.com)
- 9. CD20+ lymphocytes in renal allografts are associated with poor graft survival in pediatric patients. (nih.gov)
- 10. The Effect of Histological CD20-Positive B Cell Infiltration in Acute Cellular Rejection on Kidney Transplant Allograft Survival. (nih.gov)
- While the differences in one-year and five-year graft survival between children and adults are less pronounced than when the Cooperative Clinical Trial in Pediatric Transplantation (CCTPT) was established in 1994, children still do not achieve the long-term graft survival rates of adults who receive cadaveric renal transplants. (nih.gov)
- Although many factors have been implicated in the difference in graft survival between pediatric and adult kidney transplant recipients, the most important appears to be the pediatric immune system. (nih.gov)
- Therefore, changes in standard immunosuppression or the use of new treatment regimens that reduce or abolish the need for global immunosuppression hold the promise of improving graft survival and reducing adverse side effects. (nih.gov)
- Research Objectives and Scope The purpose of this RFA is to support a program of multi-site, cooperative clinical trials in pediatric kidney transplantation to improve graft and patient survival. (nih.gov)
- When compared to patients up to age 12 yr with FSGS, graft survival in both LD and CD transplants was worse in adolescents with FSGS (LD p = 0.035, CD p (emmes.com)
- In conclusion, FSGS has a negative impact on graft survival in adolescents. (emmes.com)
- Recurrence of FSGS results in a loss of the expected LD graft survival advantage in adolescents. (emmes.com)
- Furthermore, adolescents with FSGS have decreased graft survival compared to younger children with FSGS. (emmes.com)
- These data suggest that the rationale for LD transplantation in adolescents with FSGS should be based on factors other than the increased graft survival typically seen with LD transplantation. (emmes.com)
- The authors concluded that the tagging of islet cells could be useful in clinical practice to help evaluate graft survival and, during graft rejection, to monitor the response to therapies. (cmaj.ca)
Transplantation10
- Torque-teno virus for the prediction of graft rejection and infection disease after kidney transplantation: A systematic review and meta-analysis. (bvsalud.org)
- Torque teno virus (TTV) is a promising novel marker for quantifying the immune function in solid organ recipients, whose diagnostic accuracy of acute rejection (AR) and infection after kidney transplantation (KT) has not been evaluated. (bvsalud.org)
- In this prospective study, 3 months after transplantation 30 patients who received renal transplants from unrelated living donors were enrolled and divided into two groups, 20 patients with stable graft function and 10 patients with biopsy proven acute rejection. (ac.ir)
- The higher percentage of CD4+ IFN-γ+Th1 subset and number of IFN-γ secreting cells and also the lower expression of Foxp3 could prone the patients to acute rejection episode post transplantation. (ac.ir)
- We report biological demonstration of alloimmunisation without signs of rejection in four grafted patients out of 13 studied during the course of a clinical trial involving fetal neural transplantation in patients with Huntington's Disease. (urc-mondor.fr)
- All the macaques that received the grafts showed transient arrhythmias-problems with the rate or rhythm of the heartbeat-that subsided by 4 weeks post-transplantation. (nih.gov)
- Immunomodulatory agents to prevent graft rejection and biomarkers to predict transplantation outcomes. (nih.gov)
- Our goal is to identify lung graft injury and dysfunction after transplantation in the early stages, so we can perform the proper interventions. (upmc.com)
- To reduce the risk of graft rejection when used in conjunction with high-dose busulfan and cyclophosphamide as a preparative regimen for allogeneic hematopoietic progenitor (stem) cell transplantation (HSCT) for pediatric patients with class 3 beta-thalassemia. (nih.gov)
- Images of cells in islet grafts have successfully been made in the laboratory, for example by rendering the cells bioluminescent ( Transplantation 2005;79:768-76). (cmaj.ca)
Immunosuppressive8
- Although the actual extent of this privilege is controversial, there is general consensus about the limited need in intracerebral neural grafts for immunosuppressive regimens comparable to those used in other cases of allotransplantation. (urc-mondor.fr)
- The rejection process was, however, fully reversible under immunosuppressive treatment and graft activity recovered within six months. (urc-mondor.fr)
- Treating COVID-19 in solid organ transplant, hematopoietic cell transplant (HCT), and cellular immunotherapy recipients can be challenging due to the presence of coexisting medical conditions, the potential for transplant-related cytopenias, and the need for chronic immunosuppressive therapy to prevent graft rejection and graft-versus-host disease. (nih.gov)
- In contrast to adults, children require higher doses of immunosuppressive therapy to prevent rejection. (nih.gov)
- 2. Clinical trials to evaluate the safety and efficacy of new, less toxic immunosuppressive agents or regimens to prevent rejection or new approaches to reduce the number of immunosuppressive agents required to prevent rejection. (nih.gov)
- The main problem focuses on preventing the graft from rejection with the use of immunosuppressive agents. (nel.edu)
- With the help of immunosuppressive drugs, such as tacrolimus, sirolimis, mycophenolic acid, and everolimus, rejection rates of transplanted human organs can be reduced. (rgare.com)
- Severe Late-Onset Acute Cellular Rejection in a Pediatric Patient With Isolated Small Intestinal Transplant Rescued With Aggressive Immunosuppressive Approach: A Case Report. (stanfordchildrens.org)
Islet grafts1
- Both were previously at the University of Louisville, where they generated the SA-PD-L1, a novel form of the molecule that can be positionally displayed on the surface of islet grafts or microgels for delivery to the graft site. (news-medical.net)
Transplant22
- Transplant rejection is a process in which a transplant recipient's immune system attacks the transplanted organ or tissue. (medlineplus.gov)
- Mismatched organs, or organs that are not matched closely enough, can trigger a blood transfusion reaction or transplant rejection. (medlineplus.gov)
- Hyperacute rejection occurs a few minutes after the transplant when the antigens are completely unmatched. (medlineplus.gov)
- Acute rejection may occur any time from the first week after the transplant to 3 months afterward. (medlineplus.gov)
- Suppressing the immune response may prevent transplant rejection. (medlineplus.gov)
- Chronic rejection is the leading cause of organ transplant failure. (medlineplus.gov)
- Use in liver transplant patients is not recommended due to an increased risk of graft loss and death. (nih.gov)
- NULOJIX is a selective T cell costimulation blocker indicated for prophylaxis of organ rejection in adult patients receiving a kidney transplant. (nih.gov)
- One of the 3 patients engrafted but lost the graft at 7 months post-transplant. (nih.gov)
- Based on the three patients losing their grafts, stopping rules were met and the study moved to the 2nd cohort where 1 dose of Cy was given at 50mg/kg on day 3 post-transplant. (nih.gov)
- 1. CD20+ B-cell infiltration is related to the time after transplant and poor prognosis of acute cellular rejection in renal transplant. (nih.gov)
- 2. Expression patterns of B cells in acute kidney transplant rejection. (nih.gov)
- 3. Pathologic characteristics of early or late acute cellular rejection and outcome after kidney transplant. (nih.gov)
- 19. Refractory acute kidney transplant rejection with CD20 graft infiltrates and successful therapy with rituximab. (nih.gov)
- graft loss requires that the patient be returned to the transplant waiting list and dialysis with its attendant morbidity and side effects. (nih.gov)
- The UPMC Division of Lung Transplant/Lung Failure conducts research to identify and quantify biological markers of graft rejection. (upmc.com)
- Nowadays, the main cause for early graft loss is renal graft thrombosis because kidney transplant outcomes have improved drastically owing to advances in immunological techniques and immunosuppression. (lww.com)
- It was not until 1954 that the first successful human kidney transplant was completed between identical twins, with the recipient surviving eight years with normal graft function. (rgare.com)
- Perturbations of the T-cell immune repertoire in kidney transplant rejection. (ucsf.edu)
- The work we are doing is taking a page from that discovery and using immunotherapy in the opposite sense used by cancer treatments to control and 'turn off' an immune response to transplant a graft," Coronel said. (news-medical.net)
- When you get a transplant, like an islet transplant or organ transplant, even if it's matched, you will have an immune response to that graft, and your immune system will recognize it as non-self and will try to reject and attack the site of the graft. (news-medical.net)
- The microgels, which resemble clusters of micro-sized fish eggs, held and delivered a protein (SA-PD-L1) to a specific transplant area that successfully signaled the immune system to hold back an immune response, protecting a transplanted islet graft from being rejected. (news-medical.net)
Versus Host Disease1
- The pre-specified harms included serious adverse events (SAEs) (critical), immune-mediated disease (important), graft-versus-host-disease (important), graft rejection (important), and reactogenicity grade ≥3 (important). (cdc.gov)
Allografts4
- Allografts are grafts between members of the same species that differ genetically. (medscape.com)
- The degree to which allografts undergo rejection depends partly on the degree of similarity or histocompatibility between the donor and the recipient. (medscape.com)
- The aim of our study was to compare the percentage of CD4+ IFN-γ+ cells, the number of IFN-γ secreting cells and the amount of FoxP3 expression in patients with or without stable graft function, to determine the roles of these immunological factors in stable and rejected renal allografts. (ac.ir)
- 13. Lymphoid-Like Structures with Distinct B Cell Areas in Kidney Allografts are not Predictive for Graft Rejection. (nih.gov)
Recipients3
- All recipients have some amount of acute rejection. (medlineplus.gov)
- In nine patients with subclinical rejection, treatment with steroids was applied, while eight recipients did not receive any additional therapy. (rsu.lv)
- Higher rate of endometrial hyperplasia (without atypia) is reported in renal graft recipients. (nel.edu)
Chronic4
- This RFA, Immunopathogenesis of Chronic Graft Rejection, is related to the priority area of clinical prevention services. (nih.gov)
- Chronic rejection can take place over many years. (medlineplus.gov)
- and (4) develop surrogate biomarkers for acute and chronic rejection. (nih.gov)
- It carries notable risks, including, but not limited to, acute and chronic cellular rejection and graft malfunction. (stanfordchildrens.org)
Antigens2
- Other antigens cause only weaker reactions, but combinations of several minor antigens can elicit strong rejection responses. (medscape.com)
- Alloimmunisation to donor antigens and immune rejection following foetal neural grafts to the brain in patients with Huntington's disease. (urc-mondor.fr)
Signs of rejection1
- After you no longer have signs of rejection, the dosage will likely be lowered. (medlineplus.gov)
Immunosuppression2
Biopsy1
- A routine biopsy is often performed periodically to detect rejection early, before symptoms develop. (medlineplus.gov)
Acute cellular rejection2
- 12. Clinical impacts of CD38+ B cells on acute cellular rejection with CD20+ B cells in renal allograft. (nih.gov)
- Due to medication nonadherence, she developed severe late-onset acute cellular rejection manifested by high, bloody ostomy output and weight loss. (stanfordchildrens.org)
Evaluate1
- Evaluate for evidence of infection or rejection in patients who present with compatible symptoms. (medscape.com)
Prevention2
- However, data regarding the efficacy of antithrombotic therapy in the prevention of renal graft thrombosis are scarce. (lww.com)
- We wanted to use PD-L1 for the prevention of allogeneic islet graft rejection by simulating the way tumor cells use this molecule to evade the immune system, but without resorting to gene therapy. (news-medical.net)
Biopsies2
- Therefore, more attention is being paid to the so-called subclinical rejections of renal grafts, detected by protocol biopsies, as a possible factor affecting renal function in late period. (rsu.lv)
- Within the frame of the study 40 protocol biopsies were performed in 26 patients with immediate and stable renal graft function. (rsu.lv)
Donor1
- By 14 days, graft volume had retracted and GFP immunoreactivity was absent, indicating complete donor rejection. (nih.gov)
Cell-mediated1
- 7. C4d deposits in acute "cell-mediated" rejection: a marker for renal prognosis? (nih.gov)
Disease3
- Recurrent primary disease accounted for 15.2% of all graft failures in adolescents transplanted for FSGS with no difference between LD (17%) or CD (13.8%) grafts. (emmes.com)
- Recurrent disease accounted for 3.2% of graft failures in adolescents without FSGS. (emmes.com)
- Recurrent disease was the only cause of graft failure that differed between groups (p (emmes.com)
Tissue4
- Autografts, which are grafts from one part of the body to another (eg, skin grafts), are not foreign tissue and, therefore, do not elicit rejection. (medscape.com)
- On average, the grafts replaced 40% of damaged tissue. (nih.gov)
- We use blood, fluid, and tissue samples to detect biological signals that may reflect the body's rejection of the transplanted lung. (upmc.com)
- Transplanting less tissue helps preserve the integrity of the eye, lowers the risk of failure or rejection of the graft (the living tissue that is implanted), and speeds up the recovery period. (yalemedicine.org)
Vigorous1
- These measures are associated with more frequent and vigorous episodes of graft rejection that are not as responsive to therapy as in adults, resulting in a higher rate of graft loss. (nih.gov)
Recipient3
- This type of rejection is seen when a recipient is given the wrong type of blood. (medlineplus.gov)
- Most common abnormal uterine bleeding in graft recipient are: prolonged and profuse menstruation and inter-menstrual bleeding or spotting. (nel.edu)
- Over ten-year experiences of HRT administration in graft recipient have proved the benefits of the therapy. (nel.edu)
Immune system3
- These mechanisms are also involved in the rejection of transplanted organs, which are recognized as foreign by the recipient's immune system. (medscape.com)
- Some sites, such as the eye and the brain, are immunologically privileged (ie, they have minimal or no immune system cells and can tolerate even mismatched grafts). (medscape.com)
- Medicines that suppress the immune system may stop the rejection. (medlineplus.gov)
Cardiac1
- Ts1 cells re-cultured with rIL-2 and alloantigen remained of the Ts1 phenotype and did not suppress cardiac graft rejection in normal DA rats. (frontiersin.org)
Disparity2
- The degree of immune response to a graft depends partly on the degree of genetic disparity between the grafted organ and the host. (medscape.com)
- Xenografts, which are grafts between members of different species, have the most disparity and elicit the maximal immune response, undergoing rapid rejection. (medscape.com)
Patients3
- Our results underline the need for a reconsideration of the extent of the so-called immune privilege of the brain and of the follow-up protocols of patients with intracerebral grafts. (urc-mondor.fr)
- Stopping rules were built into the study so that if too many patients either rejected their grafts or developed moderate to severe GVHD, the study would move to the 2nd cohort. (nih.gov)
- 18. The extent of HLA-DR expression on HLA-DR(+) Tregs allows the identification of patients with clinically relevant borderline rejection. (nih.gov)
Vivo1
- It may also occur in vivo as in GRAFT REJECTION. (harvard.edu)
Dysfunction1
- Dysfunction of the implanted lung due to rejection gets worse over time and cannot be reversed. (upmc.com)
Prevent1
- Advances in genetic engineering, such as clustered regularly interspaced short palindromic repeats (CRISPR), have enabled gene editing to take place in vitro to prevent organ rejection. (rgare.com)
Clinical Trials1
- The CCTPT provides the infrastructure to conduct these clinical trials, perform studies of underlying mechanisms, and develop immune and surrogate markers of graft acceptance, rejection and function. (nih.gov)
Episodes1
- Single episodes of acute rejection rarely lead to organ failure. (medlineplus.gov)
Function2
Stable1
- In addition, the level of FoxP3 gene expression was higher in the group with stable graft compared to the acute rejection group. (ac.ir)
Cells2
- Over a 3-month period, the grafted cells infiltrated damaged heart muscle, matured, and organized into muscle fibers in all the monkeys who received the treatment. (nih.gov)
- But we don't replace the patient's own inner layer, the endothelial cells, so there is less chance of endothelial graft rejection. (yalemedicine.org)
Therapy1
- Standard therapy to control graft rejection generally involves a combination of corticosteroids, a calcineurin inhibitor (cyclosporine or tacrolimus), and an antiproliferative agent. (medscape.com)
Host2
Loss1
- Nowadays, the most prominent cause of early graft loss is renal graft thrombosis (RGT). (lww.com)