Erythrocytes
Erythrocyte Membrane
Erythrocyte Aging
Erythrocyte Deformability
Anion Exchange Protein 1, Erythrocyte
Hemolysis
Erythrocyte Aggregation
Erythrocyte Volume
Glycophorin
Plasmodium falciparum
Osmotic Fragility
Hemagglutination
Spectrin
Blood Group Antigens
Anemia, Hemolytic
Hemagglutination Tests
Erythrocyte Indices
Hemoglobins
Rosette Formation
Receptors, Complement 3b
Erythrocyte Transfusion
Blood Proteins
Membrane Proteins
Anemia, Sickle Cell
Sheep
Turkeys
MNSs Blood-Group System
Duffy Blood-Group System
Receptors, Complement
Antigens, Protozoan
Ankyrins
Malaria, Falciparum
Membrane Lipids
Hematocrit
Rabbits
Chickens
Reticulocytes
Electrophoresis, Polyacrylamide Gel
Heinz Bodies
2,3-Diphosphoglycerate
Immune Adherence Reaction
Plasmodium
ABO Blood-Group System
Malaria
Rh-Hr Blood-Group System
Phosphatidylserines
Merozoites
Hemoglobin, Sickle
Phenylhydrazines
Spherocytosis, Hereditary
Neuraminidase
Glucosephosphate Dehydrogenase Deficiency
Cell Membrane
Trypsin
Biological Transport
Molecular Sequence Data
Blood Viscosity
Chromium Isotopes
Phospholipids
Complement System Proteins
Hydrogen-Ion Concentration
Hemoglobinuria, Paroxysmal
Erythropoiesis
Phagocytosis
Hemolytic Plaque Technique
Glutathione
Hemolysin Proteins
Spherocytes
Glutathione Reductase
I Blood-Group System
Coombs Test
Amino Acid Sequence
Immunoglobulin G
Cell Membrane Permeability
Microscopy, Electron
Elliptocytosis, Hereditary
Acetylcholinesterase
Antigens, CD55
Sialoglycoproteins
Antigens, CD59
Potassium
Immune Sera
Protein Binding
Temperature
Diamide
Agglutinins
Blood Preservation
Cytochrome-B(5) Reductase
Hemagglutinins
Lectins
Glutathione Peroxidase
Antigen-Antibody Complex
Sialic Acids
Adenosine Triphosphate
Erythroblasts
Host-Parasite Interactions
Carrier Proteins
Hemoglobins, Abnormal
Binding Sites
Horses
Antibody Formation
Cattle
Hemoglobin C
Hemoglobin A
Hemagglutination Inhibition Tests
Biological Transport, Active
Sodium
Protoporphyrins
Complement C3b
Trout
Catalase
Complement C3
N-Acetylneuraminic Acid
Anemia, Hemolytic, Autoimmune
Lipid Peroxidation
Microscopy, Electron, Scanning
Plasma
Species Specificity
Hemadsorption
Magnesium
Schizonts
Osmolar Concentration
Thiamine deficiency is prevalent in a selected group of urban Indonesian elderly people. (1/16882)
This cross-sectional study involved 204 elderly individuals (93 males and 111 females). Subjects were randomly recruited using a list on which all 60-75 y-old-people living in seven sub-villages in Jakarta were included. The usual food intake was estimated using semiquantitative food frequency questionnaires. Hemoglobin, plasma retinol, vitamin B-12, red blood cell folate and the percentage stimulation of erythrocyte transketolase (ETK), as an indicator of thiamine status, were analyzed. Median energy intake was below the assessed requirement. More than 75% of the subjects had iron and thiamine intakes of approximately 2/3 of the recommended daily intake, and 20.2% of the study population had folate intake of approximately 2/3 of the recommended daily intake. Intakes of vitamins A and B-12 were adequate. Biochemical assessments demonstrated that 36.6% of the subjects had low thiamine levels (ETK stimulation > 25%). The elderly men tended to have lower thiamine levels than the elderly women. The overall prevalence of anemia was 28.9%, and the elderly women were affected more than the elderly men. Low biochemical status of vitamins A, B-12 and RBC folate was found in 5.4%, 8.8 % and 2.9% of the subjects, respectively. Dietary intakes of thiamine and folate were associated with ETK stimulation and plasma vitamin B-12 concentration (r = 0.176, P = 0.012 and r = 0.77, P = 0.001), respectively. Results of this study suggest that anemia, thiamine and possibly vitamin B-12 deficiency are prevalent in the elderly living in Indonesia. Clearly, micronutrient supplementation may be beneficial for the Indonesian elderly population living in underprivileged areas. (+info)Regulation of AMP deaminase from chicken erythrocytes. A kinetic study of the allosteric interactions. (2/16882)
The allosteric properties of AMP deaminase [EC 3.5.4.6] from chicken erythrocytes have been qualitatively and quantitatively accounted for by the concerted transition theory of Monod et al., on the assumption that this enzyme has different numbers of binding sites for each ligand. Theoretical curves yield a satisfactory fit for all experimental saturation functions with respect to activation by alkali metals and inhibition by Pi, assuming that the numbers of binding sites for AMP, alkali metals, and Pi are 4, 2, and 4, respectively. The enzyme was inhibited by concentrations of ATP and GTP below 0.1 and 0.25 mM, respectively, whereas activation of the enzyme was observed at ATP and GTP concentrations above 0.4 and 1.5 mM, respectively. These unusual kinetics with respect to ATP and GTP could be also accounted for by assuming 2 inhibitory and 4 activating sites for each ligand. (+info)Regulation of chicken erythrocyte AMP deaminase by phytic acid. (3/16882)
AMP deaminase [EC 3.5.6.4] purified from chicken erythrocytes was inhibited by phytic acid (inositol hexaphosphate), which is the principal organic phosphate in chicken red cells. Kinetic analysis has indicated that this inhibition is of an allosteric type. The estimated Ki value was within the normal range of phytic acid concentration, suggesting that this compound acts as a physiological effector. Divalent cations such as Ca2+ and Mg2+ were shown to affect AMP deaminase by potentiating inhibition by lower concentrations of phytic acid, and by relieving the inhibition at higher concentrations of phytic acid. These results suggests that Ca2+ and Mg2+ can modify the inhibition of AMP deaminase by phytic acid in chicken red cells. (+info)H5 Histone and DNA-relaxing enzyme of chicken erythrocytes. Interaction with superhelical DNA. (4/16882)
The interaction of closed circular duplex DNA with the lysine-rich H5 histone fraction of avian erythrocytes has been studied. H5, like H1 histone, interacts preferentially with superhelical DNA. The extent of interaction increases with increasing negative or positive superhelicity. Salt-extracted lysine-rich histones show the same specificity for interaction with superhelices as do acid-extracted preparations. Chicken erythrocyte nuclei contain DNA-relaxing enzyme. This enzyme is extracted from the nuclei at lower salt concentrations than those required to extract H1 and H5 histones and is, therefore, probably a function of a protein distinct from H1 and H5 histones. (+info)Changes in haematological parameters and iron metabolism associated with a 1600 kilometre ultramarathon. (5/16882)
OBJECTIVE: To investigate haematological variations and iron related changes in the serum of participants in a 1600 kilometre ultramarathon run. PARTICIPANTS: Seven male and two female participants in a 1600 km foot race. METHODS: Blood samples were obtained from the participants before, after four and 11 days of running, and at the end of the event. Samples were analysed by standard methods for haemoglobin, packed cell volume, total red cell count, mean red cell volume, mean red cell haemoglobin, total white cell count and differential, platelets, reticulocytes, iron, ferritin, total iron binding capacity, percentage transferrin saturation, haptoglobin, and bilirubin and corrected for changes in plasma volume. RESULTS: The following variables decreased during the event (p < 0.05): haemoglobin, packed cell volume, mean red cell volume, percentage lymphocytes, percentage monocytes, serum iron, total iron binding capacity, and percentage transferrin saturation. Increases (p < 0.05) were found in plasma volume, total red cell count (day 4 only), total white cell count, percentage and absolute numbers of neutrophils and reticulocytes, absolute numbers of lymphocytes and monocytes (day 4 only), absolute numbers of eosinophils (day 11 and race end), absolute numbers of basophils (race end only), platelets, ferritin, haptoglobin, and bilirubin (day 4 only). CONCLUSION: Ultramarathon running is associated with a wide range of changes in haematological parameters, many of which are related to the normal acute phase response to injury. These should not be confused with indicators of disease. (+info)Preparation of antibodies directed to the Babesia ovata- or Theileria sergenti-parasitized erythrocytes. (6/16882)
To investigate the surface antigens of the bovine red blood cells (RBCs) parasitized by Babesia ovata or Theileria sergenti, attempts were made to produce monoclonal antibodies (mAbs) with BALB/c mice. Comparable numbers of hybridomas producing anti-piroplasm mAbs, as well as anti-bovine RBC mAbs, were obtained from the mice immunized with B. ovata- or T. sergenti-PRBCs. However, mAbs directed to the surface of parasitized RBCs (PRBCs) were obtained only from the mice immunized with B. ovata-PRBCs, but not from those immunized with T. sergenti-PRBCs. When serum samples from the immunized mice and the infected cattle were examined, antibodies recognizing B. ovata-PRBC surface were detected in the sera against B. ovata, but analogous antibodies were undetectable in the sera against T. sergenti, despite that the sera showed substantial antibody titers to T. sergenti piroplasms. The results suggest that significant antigenic modifications occur on the surface of B. ovata-PRBCs, but not on the surface of T. sergenti-PRBCs. (+info)Evidence for a correlation between the number of marginal band microtubules and the size of vertebrate erthrocytes. (7/16882)
In 23 species of vertebrates the dimensions of erythrocytes and the number of their marginal band microtubules were examined. A positive correlation was found between the size of erythrocytes and the number of microtubules. The absence of microtubules in diskoid erythrocytes of mammals-Camelidae-is discussed. (+info)Methemoglobin formation by hydroxylamine metabolites of sulfamethoxazole and dapsone: implications for differences in adverse drug reactions. (8/16882)
Differences in the incidence of adverse drug reactions to trimethoprim-sulfamethoxazole and dapsone may result from differences in the formation, disposition, toxicity, and/or detoxification of their hydroxylamine metabolites. In this study, we examine whether differences in the biochemical processing of sulfamethoxazole hydroxylamine (SMX-NOH) and dapsone hydroxylamine (DDS-NOH) by erythrocytes [red blood cells (RBCs)] contribute to this differential incidence. The methemoglobin (MetHgb)-forming capacity of both metabolites was compared after a 60-min incubation with washed RBCs from four healthy human volunteers. DDS-NOH was significantly more potent (P =.004) but equally efficacious with SMX-NOH in its ability to form MetHgb. The elimination of potential differences in disposition by lysing RBCs did not change the MetHgb-forming potency of either hydroxylamine. At pharmacologically relevant concentrations, greater reduction to the parent amine occurred with DDS-NOH. Maintenance of MetHgb-forming potency was dependent on recycling with glutathione, but no difference in cycling efficiency was observed between DDS-NOH and SMX-NOH. In contrast, the pharmacodynamics of hydroxylamine-induced MetHgb formation were not changed by pretreatment with the glucose 6-phosphate dehydrogenase inhibitor epiandrosterone or by compounds that alter normal antioxidant enzyme activity. Methylene blue, which stimulates NADPH-dependent MetHgb reductase activity, decreased MetHgb levels but did not alter the differential potency of these hydroxylamines. DDS-NOH was also significantly more potent when incubated with purified human hemoglobin A0. Collectively, these data suggest that the inherently greater reactivity of DDS-NOH with hemoglobin, the greater conversion of DDS-NOH to its parent amine, and potential differences in disposition of hydroxylamine metabolites may contribute to the preferential development of dapsone-induced hemotoxicity and sulfamethoxazole-induced hypersensitivity reactions. (+info)There are two main types of hemolysis:
1. Intravascular hemolysis: This type occurs within the blood vessels and is caused by factors such as mechanical injury, oxidative stress, and certain infections.
2. Extravascular hemolysis: This type occurs outside the blood vessels and is caused by factors such as bone marrow disorders, splenic rupture, and certain medications.
Hemolytic anemia is a condition that occurs when there is excessive hemolysis of RBCs, leading to a decrease in the number of healthy red blood cells in the body. This can cause symptoms such as fatigue, weakness, pale skin, and shortness of breath.
Some common causes of hemolysis include:
1. Genetic disorders such as sickle cell anemia and thalassemia.
2. Autoimmune disorders such as autoimmune hemolytic anemia (AIHA).
3. Infections such as malaria, babesiosis, and toxoplasmosis.
4. Medications such as antibiotics, nonsteroidal anti-inflammatory drugs (NSAIDs), and blood thinners.
5. Bone marrow disorders such as aplastic anemia and myelofibrosis.
6. Splenic rupture or surgical removal of the spleen.
7. Mechanical injury to the blood vessels.
Diagnosis of hemolysis is based on a combination of physical examination, medical history, and laboratory tests such as complete blood count (CBC), blood smear examination, and direct Coombs test. Treatment depends on the underlying cause and may include supportive care, blood transfusions, and medications to suppress the immune system or prevent infection.
Symptoms of hemolytic anemia may include fatigue, weakness, shortness of breath, dizziness, headaches, and pale or yellowish skin. Treatment options depend on the underlying cause but may include blood transfusions, medication to suppress the immune system, antibiotics for infections, and removal of the spleen (splenectomy) in severe cases.
Prevention strategies for hemolytic anemia include avoiding triggers such as certain medications or infections, maintaining good hygiene practices, and seeking early medical attention if symptoms persist or worsen over time.
It is important to note that while hemolytic anemia can be managed with proper treatment, it may not be curable in all cases, and ongoing monitoring and care are necessary to prevent complications and improve quality of life.
Sickle cell anemia is caused by mutations in the HBB gene that codes for hemoglobin. The most common mutation is a point mutation at position 6, which replaces the glutamic acid amino acid with a valine (Glu6Val). This substitution causes the hemoglobin molecule to be unstable and prone to forming sickle-shaped cells.
The hallmark symptom of sickle cell anemia is anemia, which is a low number of healthy red blood cells. People with the condition may also experience fatigue, weakness, jaundice (yellowing of the skin and eyes), infections, and episodes of severe pain. Sickle cell anemia can also increase the risk of stroke, heart disease, and other complications.
Sickle cell anemia is diagnosed through blood tests that measure hemoglobin levels and the presence of sickle cells. Treatment typically involves managing symptoms and preventing complications with medications, blood transfusions, and antibiotics. In some cases, bone marrow transplantation may be recommended.
Prevention of sickle cell anemia primarily involves avoiding the genetic mutations that cause the condition. This can be done through genetic counseling and testing for individuals who have a family history of the condition or are at risk of inheriting it. Prenatal testing is also available for pregnant women who may be carriers of the condition.
Overall, sickle cell anemia is a serious genetic disorder that can significantly impact quality of life and life expectancy if left untreated. However, with proper management and care, individuals with the condition can lead fulfilling lives and manage their symptoms effectively.
Falciparum malaria can cause a range of symptoms, including fever, chills, headache, muscle and joint pain, fatigue, nausea, and vomiting. In severe cases, the disease can lead to anemia, organ failure, and death.
Diagnosis of falciparum malaria typically involves a physical examination, medical history, and laboratory tests to detect the presence of parasites in the blood or other bodily fluids. Treatment usually involves the use of antimalarial drugs, such as artemisinin-based combination therapies (ACTs) or quinine, which can effectively cure the disease if administered promptly.
Prevention of falciparum malaria is critical to reducing the risk of infection, and this includes the use of insecticide-treated bed nets, indoor residual spraying (IRS), and preventive medications for travelers to high-risk areas. Eliminating standing water around homes and communities can also help reduce the number of mosquitoes and the spread of the disease.
In summary, falciparum malaria is a severe and life-threatening form of malaria caused by the Plasmodium falciparum parasite, which is responsible for the majority of malaria-related deaths worldwide. Prompt diagnosis and treatment are essential to prevent complications and death from this disease. Prevention measures include the use of bed nets, indoor spraying, and preventive medications, as well as reducing standing water around homes and communities.
There are several different types of malaria, including:
1. Plasmodium falciparum: This is the most severe form of malaria, and it can be fatal if left untreated. It is found in many parts of the world, including Africa, Asia, and Latin America.
2. Plasmodium vivax: This type of malaria is less severe than P. falciparum, but it can still cause serious complications if left untreated. It is found in many parts of the world, including Africa, Asia, and Latin America.
3. Plasmodium ovale: This type of malaria is similar to P. vivax, but it can cause more severe symptoms in some people. It is found primarily in West Africa.
4. Plasmodium malariae: This type of malaria is less common than the other three types, and it tends to cause milder symptoms. It is found primarily in parts of Africa and Asia.
The symptoms of malaria can vary depending on the type of parasite that is causing the infection, but they typically include:
1. Fever
2. Chills
3. Headache
4. Muscle and joint pain
5. Fatigue
6. Nausea and vomiting
7. Diarrhea
8. Anemia (low red blood cell count)
If malaria is not treated promptly, it can lead to more severe complications, such as:
1. Seizures
2. Coma
3. Respiratory failure
4. Kidney failure
5. Liver failure
6. Anemia (low red blood cell count)
Malaria is typically diagnosed through a combination of physical examination, medical history, and laboratory tests, such as blood smears or polymerase chain reaction (PCR) tests. Treatment for malaria typically involves the use of antimalarial drugs, such as chloroquine or artemisinin-based combination therapies. In severe cases, hospitalization may be necessary to manage complications and provide supportive care.
Prevention is an important aspect of managing malaria, and this can include:
1. Using insecticide-treated bed nets
2. Wearing protective clothing and applying insect repellent when outdoors
3. Eliminating standing water around homes and communities to reduce the number of mosquito breeding sites
4. Using indoor residual spraying (IRS) or insecticide-treated wall lining to kill mosquitoes
5. Implementing malaria control measures in areas where malaria is common, such as distribution of long-lasting insecticidal nets (LLINs) and indoor residual spraying (IRS)
6. Improving access to healthcare services, particularly in rural and remote areas
7. Providing education and awareness about malaria prevention and control
8. Encouraging the use of preventive medications, such as intermittent preventive treatment (IPT) for pregnant women and children under the age of five.
Early diagnosis and prompt treatment are critical in preventing the progression of malaria and reducing the risk of complications and death. In areas where malaria is common, it is essential to have access to reliable diagnostic tools and effective antimalarial drugs.
Also known as: Hereditary spherocytosis (HSS)
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The condition is inherited in an X-linked recessive pattern, meaning that the gene for G6PD deficiency is located on the X chromosome and affects males more frequently than females. Females may also be affected but typically have milder symptoms or may be carriers of the condition without experiencing any symptoms themselves.
G6PD deficiency can be caused by mutations in the G6PD gene, which can lead to a reduction in the amount of functional enzyme produced. The severity of the condition depends on the specific nature of the mutation and the degree to which it reduces the activity of the enzyme.
Symptoms of G6PD deficiency may include jaundice (yellowing of the skin and eyes), fatigue, weakness, and shortness of breath. In severe cases, the condition can lead to hemolytic anemia, which is characterized by the premature destruction of red blood cells. This can be triggered by certain drugs, infections, or foods that contain high levels of oxalic acid or other oxidizing agents.
Diagnosis of G6PD deficiency typically involves a combination of clinical evaluation, laboratory tests, and genetic analysis. Treatment is focused on managing symptoms and preventing complications through dietary modifications, medications, and avoidance of triggers such as certain drugs or infections.
Overall, G6PD deficiency is a relatively common genetic disorder that can have significant health implications if left untreated. Understanding the causes, symptoms, and treatment options for this condition is important for ensuring appropriate care and management for individuals affected by it.
The disorder is caused by mutations in the HBB gene that codes for the beta-globin subunit of hemoglobin. These mutations result in the production of abnormal hemoglobins that are unstable and prone to breakdown, leading to the release of free hemoglobin into the urine.
HP is classified into two types based on the severity of symptoms:
1. Type 1 HP: This is the most common form of the disorder and is characterized by mild to moderate anemia, occasional hemoglobinuria, and a normal life expectancy.
2. Type 2 HP: This is a more severe form of the disorder and is characterized by severe anemia, recurrent hemoglobinuria, and a shorter life expectancy.
There is no cure for HP, but treatment options are available to manage symptoms and prevent complications. These may include blood transfusions, folic acid supplements, and medications to reduce the frequency and severity of hemoglobinuria episodes.
The main symptoms of hereditary elliptocytosis are mild anemia, fatigue, jaundice, and splenomegaly (enlargement of the spleen). The disorder can also cause recurrent infections, including bacterial infections such as pneumonia and urinary tract infections. In severe cases, hereditary elliptocytosis can lead to a condition called hemolytic anemia, which is characterized by the premature destruction of RBCs.
Hereditary elliptocytosis is diagnosed through a combination of physical examination, medical history, and laboratory tests, including blood smears and genetic analysis. Treatment for the disorder is generally focused on managing symptoms and preventing complications. This may include blood transfusions, antibiotics to treat infections, and splenectomy (removal of the spleen) in severe cases.
The prognosis for hereditary elliptocytosis is generally good, with most individuals leading normal lives with proper management and care. However, the disorder can be inherited by children of affected parents, and genetic counseling may be helpful for families who have a history of the condition.
There are many different types of anemia, each with its own set of causes and symptoms. Some common types of anemia include:
1. Iron-deficiency anemia: This is the most common type of anemia and is caused by a lack of iron in the diet or a problem with the body's ability to absorb iron. Iron is essential for making hemoglobin.
2. Vitamin deficiency anemia: This type of anemia is caused by a lack of vitamins, such as vitamin B12 or folate, that are necessary for red blood cell production.
3. Anemia of chronic disease: This type of anemia is seen in people with chronic diseases, such as kidney disease, rheumatoid arthritis, and cancer.
4. Sickle cell anemia: This is a genetic disorder that affects the structure of hemoglobin and causes red blood cells to be shaped like crescents or sickles.
5. Thalassemia: This is a genetic disorder that affects the production of hemoglobin and can cause anemia, fatigue, and other health problems.
The symptoms of anemia can vary depending on the type and severity of the condition. Common symptoms include fatigue, weakness, pale skin, shortness of breath, and dizziness or lightheadedness. Anemia can be diagnosed with a blood test that measures the number and size of red blood cells, as well as the levels of hemoglobin and other nutrients.
Treatment for anemia depends on the underlying cause of the condition. In some cases, dietary changes or supplements may be sufficient to treat anemia. For example, people with iron-deficiency anemia may need to increase their intake of iron-rich foods or take iron supplements. In other cases, medical treatment may be necessary to address underlying conditions such as kidney disease or cancer.
Preventing anemia is important for maintaining good health and preventing complications. To prevent anemia, it is important to eat a balanced diet that includes plenty of iron-rich foods, vitamin C-rich foods, and other essential nutrients. It is also important to avoid certain substances that can interfere with the absorption of nutrients, such as alcohol and caffeine. Additionally, it is important to manage any underlying medical conditions and seek medical attention if symptoms of anemia persist or worsen over time.
In conclusion, anemia is a common blood disorder that can have significant health implications if left untreated. It is important to be aware of the different types of anemia, their causes, and symptoms in order to seek medical attention if necessary. With proper diagnosis and treatment, many cases of anemia can be successfully managed and prevented.
Autoimmune hemolytic anemia (AIHA) is a specific type of hemolytic anemia that occurs when the immune system mistakenly attacks and destroys red blood cells. This can happen due to various underlying causes such as infections, certain medications, and some types of cancer.
In autoimmune hemolytic anemia, the immune system produces antibodies that coat the surface of red blood cells and mark them for destruction by other immune cells called complement proteins. This leads to the premature destruction of red blood cells in the spleen, liver, and other organs.
Symptoms of autoimmune hemolytic anemia can include fatigue, weakness, shortness of breath, jaundice (yellowing of the skin and eyes), dark urine, and a pale or yellowish complexion. Treatment options for AIHA depend on the underlying cause of the disorder, but may include medications to suppress the immune system, plasmapheresis to remove antibodies from the blood, and in severe cases, splenectomy (removal of the spleen) or bone marrow transplantation.
In summary, autoimmune hemolytic anemia is a type of hemolytic anemia that occurs when the immune system mistakenly attacks and destroys red blood cells, leading to premature destruction of red blood cells and various symptoms such as fatigue, weakness, and jaundice. Treatment options depend on the underlying cause of the disorder and may include medications, plasmapheresis, and in severe cases, splenectomy or bone marrow transplantation.
Erythrocyte rosetting
Erythrocyte deformability
Erythrocyte aggregation
Erythrocyte fragility
Erythrocyte sedimentation rate
Plasmodium falciparum erythrocyte membrane protein 1
Glycophorin A
Babesia motasi
Anthemosoma
Plasmodium ashfordi
Inner nuclear membrane protein
Microbotics
Gheorghe Benga
Bartonella henselae
Dactylosoma
Glutathione reductase
Virginia Minnich
Plasmodium cephalophi
Hedera nepalensis
Nobel Prize controversies
Phosphoglycolate phosphatase
Biohybrid microswimmer
NPU terminology
John Tileston Edsall
Complement receptor
NME1
Chionodraco rastrospinosus
List of OMIM disorder codes
Coombs test
Human genetic resistance to malaria
Intrahepatocyte Erythrocytes and Pigment - The Digitized Atlas of Mouse Liver Lesions
JCI -
Developmental changes in glucose transport of guinea pig erythrocytes.
Liver - Intrahepatocellular Erythrocytes - Nonneoplastic Lesion Atlas
NHANES 2001-2002:
Erythrocyte Protoporphyrin Data Documentation, Codebook, and Frequencies
Erythrocyte Sedimentation Rate (ESR): MedlinePlus Medical Test
The fluid membrane determines mechanics of erythrocyte extracellular vesicles and is softened in hereditary spherocytosis |...
Effect of Lysolecithin on Bovine Erythrocyte Osmotic Fragility | Acta Haematologica | Karger Publishers
Deutsch
Adhesion of Plasmodium falciparum-infected erythrocytes to hyaluronic acid in placental malaria. | Burnet Institute
Estimation of Cholinesterase Activity (EC 3.1.1.7; 3.1.1.8) in Undiluted Plasma and Erythrocytes as a Tool for Measuring In...
Modulation of spectrin-actin assembly by erythrocyte adducin. | Scholars@Duke
Acute consumption of organic and conventional tropical grape juices (Vitis labrusca L.) increases antioxidants in plasma and...
RePub, Erasmus University Repository:
Erythrocyte sedimentation rate as an independent prognostic marker for mortality: a...
WHO EMRO | Comparison of erythrocyte indices to differentiate between iron deficiency and alpha-thalassaemias in children with...
JCI Insight -
Classical and intermediate monocytes scavenge non-transferrin-bound iron and damaged erythrocytes
Erythrocyte survival in severe falciparum malaria - MORU Tropical Health Network
Two Plasmodium knowlesi-specific antigens on the surface of schizont-infected Rhesus monkey erythrocytes induce antibody...
Characterization of β-Adrenoreceptors of Rainbow Trout (Oncorhynchus Mykiss) Erythrocytes | Journal of Experimental Biology |...
Subjects: Erythrocytes - Digital Collections - National Library of Medicine Search Results
Triggering of Suicidal Erythrocyte Death Following Boswellic Acid Exposure
Increased adhesion of Plasmodium falciparum infected erythrocytes to ICAM-1 in children with acute intestinal injury | Malaria...
Human Erythrocytes -biotin-ProtTech Inc.
Resealed erythrocytes: A novel carrier
Liver - Intrahepatocellular Erythrocytes - Nonneoplastic Lesion Atlas
IMSEAR at SEARO: Linoleic acid hemolysis of erythrocytes.
In silico modeling and metabolome analysis of long-stored erythrocytes to improve blood storage methods<...
Detection of Hypertension-Induced Changes in Erythrocytes by SERS Nanosensors. | Biosensors (Basel);12(1)2022 Jan 08. |...
Results of search for 'su:{Erythrocytes.}'
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WHO HQ Library catalog
Sedimentation3
- What is an Erythrocyte Sedimentation Rate (ESR)? (medlineplus.gov)
- An erythrocyte sedimentation rate (ESR) is a blood test that that can show if you have inflammation in your body. (medlineplus.gov)
- Background: A very high erythrocyte sedimentation rate (ESR) is usually an indication of underlying pathology. (eur.nl)
Membranes6
- The developmental changes in the capacity for D-glucose transport of guinea pig erythrocyte membranes were compared to alterations in the electrophoretic pattern of erythrocyte membrane components. (jci.org)
- This suggests that the decrease of D-glucose transport capacity during development is caused by the loss of one or more protein components from the erythrocyte membranes. (jci.org)
- Purified schizonts (6--10 nuclei) and membranes of schizont-infected erythrocytes from the Malaysian and Philippine strain of Plasmodium knowlesi are analyzed immunochemically using immunoglobulin of rhesus monkey hyperimmune sera against schizonts and of sera from naturally immune monkeys. (rupress.org)
- Analyses of schizonts and membranes of parasitized erythrocytes of the two different strains of P. knowlesi yields only some minor quantitative, but no qualitative differences when analyzed with both types of antisera. (rupress.org)
- The study aimed to detect the total cholesterol Content of Erythrocyte Membranes (CEM) and plasma Cholesterol Efflux Capacity (CEC), and to analyse its correlations with Acute Coronary Syndrome (ACS), in attempt to explore the possible causes of increasing CEM in patients. (biomedres.info)
- Incubation of blood with citrated and phosphate buffered saline caused a time dependent decrease of the number of intact erythrocytes in samples that was ascribed to a disintegration of erythrocyte membranes. (bionanoteam.com)
Aggregation3
- In rats of the older group, erythrocyte aggregation was increased, as indicated by an increase in the numberof erythrocytes that entered the aggregates in the blood and an increase in the number of most erythrocyte aggregates with a decrease in the level of free erythrocytes. (jbiochemtech.com)
- For two-year-old rats, low content of erythrocytes-disconcytes in the blood and an excess number of erythrocytes with a modified shape, as well as an increase in their aggregation, are characteristics. (jbiochemtech.com)
- PA-treated erythrocytes showed strong thrombogenic activities, as demonstrated by increased thrombin generation, endothelial cell adhesion, and erythrocyte aggregation. (ewha.ac.kr)
Plasmodium4
- Adhesion of Plasmodium falciparum-infected erythrocytes to hyaluronic acid in placental malaria. (edu.au)
- Infection with Plasmodium falciparum during pregnancy leads to the accumulation of parasite-infected erythrocytes in the placenta, and is associated with excess perinatal mortality, premature delivery and intrauterine growth retardation in the infant, as well as increased maternal mortality and morbidity. (edu.au)
- Two Plasmodium knowlesi-specific antigens on the surface of schizont-infected Rhesus monkey erythrocytes induce antibody production in immune hosts. (rupress.org)
- Two plasmodium-specific antigens (1 and 13) on the surface of infected erythrocytes are recognized by sera of rhesus monkeys rendered naturally immune against P. knowlesi infections and, therefore, represent antigens in vivo. (rupress.org)
Protoporphyrin4
- Also, see the documentation for the primary exam data for Laboratory 39 (Erythrocyte Protoporphyrin). (cdc.gov)
- Note: Erythrocyte Protoporphyrin was performed at Centers for Disease Control and Prevention in 2001 and the State of New York Department of Health in 2002. (cdc.gov)
- Free erythrocyte protoporphyrin (FEP) is measured by a modification of the method of Sassa et al. (cdc.gov)
- Free erythrocyte protoporphyrin was markedly elevated in all cases. (cdc.gov)
Iron deficiency1
- ABSTRACT Erythrocyte indices used to differentiate between iron deficiency anaemia (IDA) and thalassaemias have been studied mainly in countries with a high prevalence of IDA or beta-thalassaemias. (who.int)
RBCs1
- EVs from red blood cells (erythrocytes, RBCs) are released both in vivo as well as under blood bank storage conditions 7 . (nature.com)
Abstract1
- abstract = "There is currently no effective method for preventing ATP and 2,3-bisphosphoglycerate (2,3-BPG) depletion during long-term erythrocyte storage in the cold, although these metabolites are strongly associated with cell viability and oxygen delivery after transfusion. (elsevier.com)
Mathematical model2
- Here, we developed a mathematical model to predict metabolism in erythrocytes preserved with a mannitol-adenine-phosphate solution (MAP) at 4 °C, by modifying a published model of large-scale erythrocyte metabolism. (elsevier.com)
- A two dimensional mathematical model of the erythrocyte shape was constructed to illustrate and explain erythrocyte swelling of intially discocytic/echinocytic shape to the final spherical shape, which preceeds membrane rupture. (bionanoteam.com)
Electrophoretic1
- published an important study that identified differences in the electrophoretic mobilities of normal and sickled erythrocytes ( 3 ). (cdc.gov)
Induce1
- In conclusion, these results suggest that PA can induce thrombogenic activities in erythrocytes through PS exposure, which can increase thrombus formation and ultimately contribute to the development of cardiovascular diseases. (ewha.ac.kr)
Membrane properties1
- Relationship of phosphorylation of membrane proteins with membrane properties of malaria-infected erythrocytes / by Temduang Limpaiboon. (who.int)
Vitro1
- The same subset and, to a lesser extent, the intermediate population, efficiently cleared damaged erythrocytes in vitro and mediated erythrophagocytosis in vivo in healthy volunteers and patients having received blood transfusions. (jci.org)
Receptors1
- These included the iron exporter ferroportin (FPN1), ferritin, transferrin receptor, putative transporters of non-transferrin-bound iron (NTBI), and receptors for damaged erythrocytes. (jci.org)
Humans1
- Carrier erythrocytes have been evaluated in thousands of drug administration in humans proving safety and efficacy of the treatments. (thepharmajournal.com)
Decrease2
- We found that spontaneous hypertension in rats leads (i) to a decrease in the erythrocyte plasma membrane fluidity and (ii) to a decrease in the mobility of the heme of the membrane -bound hemoglobin . (bvsalud.org)
- In the blood of two-year-old rats, there was a decrease in the level of erythrocyte-discocytes. (jbiochemtech.com)
Characterization1
- Here, we use atomic force microscopy for mechanical characterization of erythrocyte, or red blood cell (RBC), EVs from healthy individuals and from patients with hereditary spherocytosis (HS) due to ankyrin deficiency. (nature.com)
Adhesion1
- In laboratory isolates selected for specific high-level adhesion, binding to hyaluronic acid could be inhibited by dodecamer or larger oligosaccharide fragments or polysaccharides, treatment of immobilized receptor with hyaluronidase, or treatment of infected erythrocytes with trypsin. (edu.au)
Metabolism1
- We also performed metabolome analysis of laboratory-made MAP-stored erythrocytes using capillary electrophoresis time-of-flight mass spectrometry (CE-TOFMS), which provided a comprehensive view of the metabolism dynamics. (elsevier.com)
Species4
- Erythrocytes are a critical part of oxygen transport and both their size and shape can change in relation to species-specific life-history, behavioural or ecological conditions. (lincoln.ac.uk)
- We collected data on erythrocyte size (area) and shape (L/W: elongation ratio) from Lepidosauria across the globe (N = 235 species). (lincoln.ac.uk)
- Smaller erythrocytes were associated with the need for faster delivery (active foragers, high-altitude species, warmer body temperatures), whereas species with greater oxygen demands (diving species, viviparous species) had larger erythrocytes. (lincoln.ac.uk)
- Erythrocyte size shows considerable cross-species variation, with a range of factors linked to the oxygen delivery requirements being major drivers of these differences. (lincoln.ac.uk)
Invasion1
- Studies on the inhibitory effects of erythrocyte band 3 protein on malarial (merozoite invasion of human erythrocytes / by Vincent C. N. Okoye. (who.int)
Excess1
- This was accompanied in them by an excess content of erythrocytes in the blood, which had a changed shape to varying degrees. (jbiochemtech.com)
Human4
- Human Erythrocytes -biotin-ProtTech Inc. (prottech.com.cn)
- In the present study, we demonstrated that PA can enhance thrombogenic activities in human erythrocytes through phosphatidylserine (PS) exposure in a Ca 2+ -dependent manner. (ewha.ac.kr)
- In freshly isolated human erythrocytes, treatment of PA or PLD induced PS exposure. (ewha.ac.kr)
- Human erythrocyte spectrin dimers associate at the N-terminal region of α-spectrin (αN) and the C-terminal region of β-spectrin (βC) to form tetramers. (lsu.edu)
Search1
- Results of search for 'su:{Erythrocytes. (who.int)
Activation1
- An important reason for these changes is the weakening of the antioxidant protection of erythrocytes, leading to a pronounced activation of lipid peroxidation in them. (jbiochemtech.com)
Intact2
- Reconstitution of membrane preparations in liposomes resulted in a parallel change in the D-glucose uptake and D-glucose penetration of intact erythrocytes. (jci.org)
- Only three parasite-specific components (1, 13, and 19) are exposed on the surface of parasitized erythrocytes as revealed by both lactoperoxidase-catalyzed radioiodination and extensive absorption of anti-schizont Ig using intact infected erythrocytes. (rupress.org)
Pregnancy1
- A key future aspect for study would include within-individual plasticity and how changing states, for example, pregnancy, perhaps alter the size and shape of erythrocytes in Lepidosaurs. (lincoln.ac.uk)
Blood cells1
- Erythrocytes are red blood cells. (medlineplus.gov)
Properties1
- We applied plasmonic SERS nanosensors to assess changes in the properties of erythrocytes under normotensive and hypertensive conditions in the animal model . (bvsalud.org)
Shape2
- The relative abundance of different erythrocyte shape types (discocytes, echinocytes, spherically shaped erythrocytes) was determined on populations of cells, in suspensions with added carbon black nanomaterial and in control suspensions. (bionanoteam.com)
- Micrometre-sized agglomerates were formed in the blood and interacted with erythrocyte membrane without evidently disturbing local membrane curvature or global cell shape. (bionanoteam.com)
Total1
- Serum and erythrocyte (RBC) total folate are indicators of folate status. (nih.gov)
Studies1
- Studies of the erythrocyte spectrin tetramerization region" by Sunghyouk Park, Shahila Mehboob et al. (lsu.edu)
Plasma2
- Furthermore, we assessed the influence of erythrocyte handling, suspension medium and endogenous catechol amines on B max and K D . Maximal binding was obtained when erythrocytes were handled minimally and maintained suspended in plasma rather than physiological saline. (biologists.com)
- We identified SERS parameters that can be used to detect pathological changes in the plasma membrane and submembrane region of erythrocytes . (bvsalud.org)
Normal3
- Endogenous catecholamines, at levels considered normal for non-stressed animals, did not interfere with the radioligand binding assays, and thus eliminated the need to wash and resuspend erythrocytes. (biologists.com)
- These channels in normal erythrocytes could then be compared to erythrocytes of an individual with PKD. (murraystate.edu)
- The project presents results of immunohistochemical analysis of normal erythrocyte expression. (murraystate.edu)
Treatment1
- Erythrocytes mediated drug delivery has been reported with therapeutic enzymes and antiviral agents to maximize therapeutic performance, reduce the side effects, as circulating depots for controlled drug release, drug targeting, treatment of parasitic diseases, hepatic tumors, removal of toxic agents etc. (thepharmajournal.com)
Components2
- Each of these components must be considered when performing radioreceptor assays using these radioligands and this has significant implications for the interpretation of erythrocyte β -adrenoreceptor localization and mobilization. (biologists.com)
- Here, we test whether components of the environment (altitude), life history (reproductive mode, body temperature) and behaviour (diving, foraging mode) drive erythrocyte size variation in the Lepidosauria (lizards, snakes and rhynchocephalians). (lincoln.ac.uk)
Comparison1
- A comparison of the structures of erythrocyte spectrin with other published structures of Drosophila and chicken brain spectrin is discussed. (lsu.edu)
Study1
- Polycystin 1 and Polycystin 2, if located on or in the erythrocyte, could serve as a model for the study of calcium channels. (murraystate.edu)
Increase1
- In their erythrocytes, there was an increase in lipid peroxidation caused by a weakening of the activity of their antioxidant defense. (jbiochemtech.com)