Hemolysis
Anemia, Hemolytic
Erythrocytes
Hemoglobinuria
Osmotic Fragility
HELLP Syndrome
Glucosephosphate Dehydrogenase Deficiency
Erythrocyte Membrane
Anemia, Hemolytic, Autoimmune
Hemolysin Proteins
Hemoglobinuria, Paroxysmal
Hemoglobins
Haptoglobins
Coombs Test
Phenylhydrazines
Anemia, Sickle Cell
Hemolytic Plaque Technique
Blood Group Incompatibility
Favism
Methemoglobin
Sheep
Complement System Proteins
Reticulocyte Count
Heinz Bodies
Hemagglutination
Complement C8
Rho(D) Immune Globulin
Blood Specimen Collection
Jaundice, Neonatal
Erythrocyte Aging
Vitamin E Deficiency
Spherocytosis, Hereditary
Streptolysins
L-Lactate Dehydrogenase
Hemopexin
Erythrocytes, Abnormal
ABO Blood-Group System
Hyperbilirubinemia
Complement C5
Antigens, CD59
Erythrocyte Deformability
Hemagglutination Inhibition Tests
Rickettsia prowazekii
Chromium Isotopes
Complement C6
Amidines
Blood Preservation
Glucosephosphate Dehydrogenase
Brown Recluse Spider
Rabbits
Glycogen Storage Disease Type VII
Complement C7
Rubella virus
Hypotonic Solutions
Changes in haematological parameters and iron metabolism associated with a 1600 kilometre ultramarathon. (1/3524)
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)Improved methods using the reverse transcriptase polymerase chain reaction to detect tumour cells. (2/3524)
Reverse transcriptase polymerase chain reaction (RT-PCR) is increasingly used to detect small numbers of circulating tumour cells, though the clinical benefit remains controversial. The largest single contributing factor to the controversy of its value is the different approaches to sample processing. The aim of this study was to compare the sensitivity and reproducibility of RT-PCR for the detection of tumour cells after four commonly used different methods of sample processing. Using RT-PCR, one tumour cell spiked in 2 ml of whole blood was detected after analysis of separated mononuclear cell RNA, whole blood total or poly-A+ RNA. No false positives were identified with any method. However, the reproducibility of tumour cell detection was reduced after isolation of the mononuclear cell fraction. Only analysis of poly-A+ RNA had a sensitivity of 100% in all the cell spiking experiments. In patient blood samples, analysis of poly-A+ RNA increased the number of blood samples positive for tyrosine hydroxylase (TH) mRNA compared with those positive after analysis of total RNA. This may reflect high levels of cDNA reducing the efficiency of the PCR. Isolation of poly-A+ RNA increases the sensitivity and reproducibility of tumour cell detection in peripheral blood. (+info)Antioxidative activity of 4-oxy- and 4-hydroxy-nitroxides in tissues and erythrocytes from rats. (3/3524)
AIM: To compare the activities of antioxidation of 4-oxy- and 4-hydroxy-nitroxides in tissues and RBC from rats. METHODS: The homogenates of liver, heart, and kidneys of rats were used to determine malondialdehyde (MDA) formation using TBA colorimetric method. H2O2-caused hemolysis was measured spectrometrically. Superoxide anion from zymosan-stimulated neutrophils of rats was assayed by NBT reduction method. RESULTS: Nitroxide free radicals OTMPO and HTMPO inhibited MDA generation caused by .OH generation system (MIC 10.5 and 21 mumol.L-1, respectively), antagonized hemolysis induced by H2O2 (MIC: 338 and 168 mumol.L-1, respectively), but did not affect O2- formation from activated neutrophils. 1-Hydroxyl compounds OTMPOH and HTMPOH possessed similarly potent antilipoperoxidative activities. But nonfree radical OTMP and HTMP had no effect on peroxidation of tissues. CONCLUSION: Nitroxides exert their antilipoperoxidative effect by specifically scavenging .OH free radicals in biological system. Trapping of .OH free radicals by nitroxides is not by reduction of NO. group in nitroxides. Both NO. group and NOH group are essential active groups. (+info)Isolation and characterization of Vibrio parahaemolyticus causing infection in Iberian toothcarp Aphanius iberus. (4/3524)
High mortality among laboratory cultured Iberian toothcarp Aphanius iberus occurred in February 1997 in Valencia (Spain). The main signs of the disease were external haemorrhage and tail rot. Bacteria isolated from internal organs of infected fish were biochemically homogeneous and identified as Vibrio parahaemolyticus. The bacteria were haemolytic against erythrocytes from eel Anguilla anguilla, amberjack Seriola dumerili, toothcarp A. iberus and humans, and were Kanagawa-phenomenon-negative. Infectivity tests showed that the virulence for A. iberus was dependent on salinity. Finally, all strains were virulent for amberjack and eel. (+info)Hemolysis associated with 25% human albumin diluted with sterile water--United States, 1994-1998. (5/3524)
Since 1994, a shortage of 5% human albumin, a product used off-label during therapeutic plasma exchange (TPE), has existed in the United States. Because of this shortage, hospital pharmacists may prepare 5% solution of human albumin by diluting 25% human albumin with 0.9% NaCl or, when sodium load is a concern, 5% dextrose. However, if sterile water alone is used as the diluent, the osmolarity (tonicity) of the albumin solution is reduced and may cause hemolysis in recipients. This report describes two of 10 episodes of hemolysis (one fatal) among persons who received 25% human albumin diluted with sterile water and emphasizes that sterile water alone should not be used to dilute albumin. (+info)Novel techniques for in vivo hemolysis studies in guinea pigs. (6/3524)
The in vivo toxic-hemolytic studies using small experimental animals are complicated by difficulties in preventing hemolysis during repeated collection of blood specimens and in measuring hemoglobin concentration in small amounts of plasma sample. To solve these problems we tried to develope the new techniques for the in vivo hemolysis studies using guinea pigs. The hemolysis accident was minimized to 2.75 mg/dl by collecting the blood directly into heparinized microhematocrit tubes by small longitudinal incision in the auricular artery. The hemoglobin in a small amount of sample (10 microliters) was determined by the new analytical system using a microflow spectrophotometer with a modified cyanmethemoglobin method. The standard curve of the hemoglobin concentration in the system revealed a line of Y = 1.8X + 0.79 (r = 0.999), CV < 1% with a minimum detectable concentration of 1.25 mg/dl. By using the new techniques, it was found that the plasma hemoglobin concentration in normal animals were 7.27 +/- 0.44 mg/dl (mean +/- S.E.). The in vivo hemolytic activity of saponin was observed dose-dependently at doses of 30-50 mg/kg, i.v. in the guinea pigs. It is concluded that the present techniques are useful for in vivo hemolytic studies in small experimental animals such as guinea pigs. (+info)The hemolytic activity of bracken extracts in guinea pigs. (7/3524)
This study was conducted to elucidate the hemolytic activity of a new toxic substance in bracken fern. A crude extract (CE) was prepared from the methanol extracts of bracken by the column chromatography. When the CE was injected subcutaneously in guinea pigs, the hemoglobinuria and hemolysis were observed within 6 hr, and 3 days later edema and hemorrhages in the urinary bladder were observed. The CE was then fractionated by high performance liquid chromatography (HPLC), and three (HF, BF and CF) of the fractions showed the toxic activities in guinea pigs. The HF caused the hemolysis, whereas both the BF and the CF caused the hemorrhagic cystitis without any hemolytic activities. The HF was further fractionated by the HPLC, resulting of the 3 fractions (HF-I, II and III). The hemolysis was caused only with the HF-II, and HF-II as well as HF did not cause the hemorrhagic cystitis. HPLC analysis revealed that both BF and CF contains braxin B and braxin C, respectively, and both HF and HF-II do not contain braxin A, B or C. These facts suggest that bracken fern contains a new toxic substance (hemolysin) which induces the acute hemolysis in guinea pigs. (+info)The rgg gene of Streptococcus pyogenes NZ131 positively influences extracellular SPE B production. (8/3524)
Streptococcus pyogenes produces several extracellular proteins, including streptococcal erythrogenic toxin B (SPE B), also known as streptococcal pyrogenic exotoxin B and streptococcal proteinase. Several reports suggest that SPE B contributes to the virulence associated with S. pyogenes; however, little is known about its regulation. Nucleotide sequence data revealed the presence, upstream of the speB gene, of a gene, designated rgg, that was predicted to encode a polypeptide similar to previously described positive regulatory factors. The putative Rgg polypeptide of S. pyogenes NZ131 consisted of 280 amino acids and had a predicted molecular weight of 33,246. To assess the potential role of Rgg in the production of SPE B, the rgg gene was insertionally inactivated in S. pyogenes NZ131, which resulted in markedly decreased SPE B production, as determined both by immunoblotting and caseinolytic activity on agar plates. However, the production of other extracellular products, including streptolysin O, streptokinase, and DNase, was not affected. Complementation of the rgg mutant with an intact rgg gene copy in S. pyogenes NZ131 could restore SPE B production and confirmed that the rgg gene product is involved in the production of SPE B. (+info)Hemolysis is the destruction or breakdown of red blood cells, resulting in the release of hemoglobin into the surrounding fluid (plasma). This process can occur due to various reasons such as chemical agents, infections, autoimmune disorders, mechanical trauma, or genetic abnormalities. Hemolysis may lead to anemia and jaundice, among other complications. It is essential to monitor hemolysis levels in patients undergoing medical treatments that might cause this condition.
Hemolytic anemia is a type of anemia that occurs when red blood cells are destroyed (hemolysis) faster than they can be produced. Red blood cells are essential for carrying oxygen throughout the body. When they are destroyed, hemoglobin and other cellular components are released into the bloodstream, which can lead to complications such as kidney damage and gallstones.
Hemolytic anemia can be inherited or acquired. Inherited forms of the condition may result from genetic defects that affect the structure or function of red blood cells. Acquired forms of hemolytic anemia can be caused by various factors, including infections, medications, autoimmune disorders, and certain medical conditions such as cancer or blood disorders.
Symptoms of hemolytic anemia may include fatigue, weakness, shortness of breath, pale skin, jaundice (yellowing of the skin and eyes), dark urine, and a rapid heartbeat. Treatment for hemolytic anemia depends on the underlying cause and may include medications, blood transfusions, or surgery.
Erythrocytes, also known as red blood cells (RBCs), are the most common type of blood cell in circulating blood in mammals. They are responsible for transporting oxygen from the lungs to the body's tissues and carbon dioxide from the tissues to the lungs.
Erythrocytes are formed in the bone marrow and have a biconcave shape, which allows them to fold and bend easily as they pass through narrow blood vessels. They do not have a nucleus or mitochondria, which makes them more flexible but also limits their ability to reproduce or repair themselves.
In humans, erythrocytes are typically disc-shaped and measure about 7 micrometers in diameter. They contain the protein hemoglobin, which binds to oxygen and gives blood its red color. The lifespan of an erythrocyte is approximately 120 days, after which it is broken down in the liver and spleen.
Abnormalities in erythrocyte count or function can lead to various medical conditions, such as anemia, polycythemia, and sickle cell disease.
Hemoglobinuria is a medical condition characterized by the presence of hemoglobin in the urine. Hemoglobin is a protein found in red blood cells that carries oxygen throughout the body. Normally, when red blood cells die, they are broken down and their hemoglobin is recycled. However, in certain conditions such as intravascular hemolysis (the destruction of red blood cells inside blood vessels), hemoglobin can be released into the bloodstream and then filtered by the kidneys into the urine.
Hemoglobinuria can be a symptom of various underlying medical conditions, including hemolytic anemias, disseminated intravascular coagulation (DIC), severe infections, snake bites, and exposure to certain toxins or medications. It is important to identify the underlying cause of hemoglobinuria, as treatment will depend on the specific condition.
In some cases, hemoglobinuria can lead to kidney damage due to the toxic effects of free hemoglobin on the renal tubules. This can result in acute or chronic kidney injury, and in severe cases, it may require dialysis or transplantation.
Osmotic fragility is a term used in medicine, specifically in the field of hematology. It refers to the susceptibility or tendency of red blood cells (RBCs) to undergo lysis (rupture or breaking open) when exposed to hypotonic solutions (solutions with lower osmotic pressure than the RBCs). This test is often used to diagnose and monitor hereditary spherocytosis, a genetic disorder that affects the structure and stability of red blood cells.
In this condition, the RBC membrane proteins are defective, leading to abnormally shaped and fragile cells. When these abnormal RBCs come into contact with hypotonic solutions, they rupture more easily than normal RBCs due to their decreased osmotic resistance. The degree of osmotic fragility can be measured through a laboratory test called the "osmotic fragility test," which evaluates the stability and structural integrity of RBCs in response to varying osmotic pressures.
In summary, osmotic fragility is a medical term that describes the increased susceptibility of red blood cells to lysis when exposed to hypotonic solutions, often associated with hereditary spherocytosis or other conditions affecting RBC membrane stability.
HELLP syndrome is a serious complication in pregnancy, characterized by Hemolysis (the breakdown of red blood cells), Elevated Liver enzymes, and Low Platelet count. It is often considered a variant of severe preeclampsia or eclampsia, although it can also occur without these conditions.
The symptoms of HELLP syndrome include headache, nausea and vomiting, upper right abdominal pain, and visual disturbances. It can lead to serious complications for both the mother and the baby, such as liver failure, placental abruption, disseminated intravascular coagulation (DIC), and even death if not promptly diagnosed and treated.
The exact cause of HELLP syndrome is not known, but it is thought to be related to problems with the blood vessels that supply the placenta. Treatment typically involves delivering the baby as soon as possible, even if the baby is premature. Women who have had HELLP syndrome are at increased risk for complications in future pregnancies.
Glucose-6-Phosphate Dehydrogenase (G6PD) deficiency is a genetic disorder that affects the normal functioning of an enzyme called G6PD. This enzyme is found in red blood cells and plays a crucial role in protecting them from damage.
In people with G6PD deficiency, the enzyme's activity is reduced or absent, making their red blood cells more susceptible to damage and destruction, particularly when they are exposed to certain triggers such as certain medications, infections, or foods. This can lead to a condition called hemolysis, where the red blood cells break down prematurely, leading to anemia, jaundice, and in severe cases, kidney failure.
G6PD deficiency is typically inherited from one's parents in an X-linked recessive pattern, meaning that males are more likely to be affected than females. While there is no cure for G6PD deficiency, avoiding triggers and managing symptoms can help prevent complications.
An erythrocyte, also known as a red blood cell, is a type of cell that circulates in the blood and is responsible for transporting oxygen throughout the body. The erythrocyte membrane refers to the thin, flexible barrier that surrounds the erythrocyte and helps to maintain its shape and stability.
The erythrocyte membrane is composed of a lipid bilayer, which contains various proteins and carbohydrates. These components help to regulate the movement of molecules into and out of the erythrocyte, as well as provide structural support and protection for the cell.
The main lipids found in the erythrocyte membrane are phospholipids and cholesterol, which are arranged in a bilayer structure with the hydrophilic (water-loving) heads facing outward and the hydrophobic (water-fearing) tails facing inward. This arrangement helps to maintain the integrity of the membrane and prevent the leakage of cellular components.
The proteins found in the erythrocyte membrane include integral proteins, which span the entire width of the membrane, and peripheral proteins, which are attached to the inner or outer surface of the membrane. These proteins play a variety of roles, such as transporting molecules across the membrane, maintaining the shape of the erythrocyte, and interacting with other cells and proteins in the body.
The carbohydrates found in the erythrocyte membrane are attached to the outer surface of the membrane and help to identify the cell as part of the body's own immune system. They also play a role in cell-cell recognition and adhesion.
Overall, the erythrocyte membrane is a complex and dynamic structure that plays a critical role in maintaining the function and integrity of red blood cells.
Hemolytic anemia, autoimmune is a type of anemia characterized by the premature destruction of red blood cells (RBCs) in which the immune system mistakenly attacks and destroys its own RBCs. This occurs when the body produces autoantibodies that bind to the surface of RBCs, leading to their rupture (hemolysis). The symptoms may include fatigue, weakness, shortness of breath, and dark colored urine. The diagnosis is made through blood tests that measure the number and size of RBCs, reticulocyte count, and the presence of autoantibodies. Treatment typically involves suppressing the immune system with medications such as corticosteroids or immunosuppressive drugs, and sometimes removal of the spleen (splenectomy) may be necessary.
Hemolysins are a type of protein toxin produced by certain bacteria, fungi, and plants that have the ability to damage and destroy red blood cells (erythrocytes), leading to their lysis or hemolysis. This results in the release of hemoglobin into the surrounding environment. Hemolysins can be classified into two main categories:
1. Exotoxins: These are secreted by bacteria and directly damage host cells. They can be further divided into two types:
* Membrane attack complex/perforin-like proteins (MACPF): These hemolysins create pores in the membrane of red blood cells, disrupting their integrity and causing lysis. Examples include alpha-hemolysin from Staphylococcus aureus and streptolysin O from Streptococcus pyogenes.
* Enzymatic hemolysins: These hemolysins are enzymes that degrade specific components of the red blood cell membrane, ultimately leading to lysis. An example is streptolysin S from Streptococcus pyogenes, which is a thiol-activated, oxygen-labile hemolysin.
2. Endotoxins: These are part of the outer membrane of Gram-negative bacteria and can cause indirect hemolysis by activating the complement system or by stimulating the release of inflammatory mediators from host cells.
Hemolysins play a significant role in bacterial pathogenesis, contributing to tissue damage, impaired immune responses, and disease progression.
Paroxysmal nocturnal hemoglobinuria (PNH) is a rare, acquired disorder of the blood characterized by the destruction of red blood cells (hemolysis), which can cause symptoms such as fatigue, dark colored urine (especially in the morning), chest pain, shortness of breath, and an increased risk of blood clots. The hemoglobin from the lysed red blood cells appears in the urine, hence the term "hemoglobinuria."
The paroxysmal nature of the disorder refers to the sudden and recurring episodes of hemolysis that can occur at any time, although they may be more frequent at night. The condition is caused by mutations in a gene called PIG-A, which leads to the production of defective red blood cell membranes that are sensitive to destruction by complement, a component of the immune system.
PNH is a serious and potentially life-threatening condition that can lead to complications such as kidney damage, pulmonary hypertension, and thrombosis. Treatment typically involves supportive care, such as blood transfusions, and medications to manage symptoms and prevent complications. In some cases, stem cell transplantation may be considered as a curative treatment option.
Hemoglobin (Hb or Hgb) is the main oxygen-carrying protein in the red blood cells, which are responsible for delivering oxygen throughout the body. It is a complex molecule made up of four globin proteins and four heme groups. Each heme group contains an iron atom that binds to one molecule of oxygen. Hemoglobin plays a crucial role in the transport of oxygen from the lungs to the body's tissues, and also helps to carry carbon dioxide back to the lungs for exhalation.
There are several types of hemoglobin present in the human body, including:
* Hemoglobin A (HbA): This is the most common type of hemoglobin, making up about 95-98% of total hemoglobin in adults. It consists of two alpha and two beta globin chains.
* Hemoglobin A2 (HbA2): This makes up about 1.5-3.5% of total hemoglobin in adults. It consists of two alpha and two delta globin chains.
* Hemoglobin F (HbF): This is the main type of hemoglobin present in fetal life, but it persists at low levels in adults. It consists of two alpha and two gamma globin chains.
* Hemoglobin S (HbS): This is an abnormal form of hemoglobin that can cause sickle cell disease when it occurs in the homozygous state (i.e., both copies of the gene are affected). It results from a single amino acid substitution in the beta globin chain.
* Hemoglobin C (HbC): This is another abnormal form of hemoglobin that can cause mild to moderate hemolytic anemia when it occurs in the homozygous state. It results from a different single amino acid substitution in the beta globin chain than HbS.
Abnormal forms of hemoglobin, such as HbS and HbC, can lead to various clinical disorders, including sickle cell disease, thalassemia, and other hemoglobinopathies.
Haptoglobins are proteins found in the blood that bind to free hemoglobin, which is released when red blood cells break down. The resulting complex is then removed from the bloodstream by the liver, preventing the loss of iron and potential kidney damage caused by the breakdown products of hemoglobin. Haptoglobins are produced in the liver and their levels can be measured to help diagnose various medical conditions such as hemolytic anemia, liver disease, and inflammation.
The Coombs test is a laboratory procedure used to detect the presence of antibodies on the surface of red blood cells (RBCs). It is named after the scientist, Robin Coombs, who developed the test. There are two types of Coombs tests: direct and indirect.
1. Direct Coombs Test (DCT): This test is used to detect the presence of antibodies directly attached to the surface of RBCs. It is often used to diagnose hemolytic anemia, a condition in which RBCs are destroyed prematurely, leading to anemia. A positive DCT indicates that the patient's RBCs have been coated with antibodies, which can occur due to various reasons such as autoimmune disorders, blood transfusion reactions, or drug-induced immune hemolysis.
2. Indirect Coombs Test (ICT): This test is used to detect the presence of antibodies in the patient's serum that can agglutinate (clump) foreign RBCs. It is commonly used before blood transfusions or during pregnancy to determine if the patient has antibodies against the RBCs of a potential donor or fetus, respectively. A positive ICT indicates that the patient's serum contains antibodies capable of binding to and agglutinating foreign RBCs.
In summary, the Coombs test is a crucial diagnostic tool in identifying various hemolytic disorders and ensuring safe blood transfusions by detecting the presence of harmful antibodies against RBCs.
Phenylhydrazines are organic compounds that contain a phenyl group (a benzene ring with a hydrogen atom substituted by a hydroxy group) and a hydrazine group (-NH-NH2). They are aromatic amines that have been used in various chemical reactions, including the formation of azos and hydrazones. In medicine, phenylhydrazines were once used as vasodilators to treat angina pectoris, but their use has largely been discontinued due to their toxicity and potential carcinogenicity.
Sickle cell anemia is a genetic disorder that affects the hemoglobin in red blood cells. Hemoglobin is responsible for carrying oxygen throughout the body. In sickle cell anemia, the hemoglobin is abnormal and causes the red blood cells to take on a sickle shape, rather than the normal disc shape. These sickled cells are stiff and sticky, and they can block blood vessels, causing tissue damage and pain. They also die more quickly than normal red blood cells, leading to anemia.
People with sickle cell anemia often experience fatigue, chronic pain, and jaundice. They may also have a higher risk of infections and complications such as stroke, acute chest syndrome, and priapism. The disease is inherited from both parents, who must both be carriers of the sickle cell gene. It primarily affects people of African descent, but it can also affect people from other ethnic backgrounds.
There is no cure for sickle cell anemia, but treatments such as blood transfusions, medications to manage pain and prevent complications, and bone marrow transplantation can help improve quality of life for affected individuals. Regular medical care and monitoring are essential for managing the disease effectively.
I'm sorry for any confusion, but "Hemolytic Plaque Technique" is not a widely recognized or established medical term. It seems like it might be a combination of two different concepts in medical and scientific research: the Hemolytic Assay and the Plaque Assay technique.
A Hemolytic Assay is a method used to measure the amount of hemolysis, or the rupturing of red blood cells, caused by a substance such as a toxin or an antibody. This assay can help determine the concentration of the hemolysin in a sample.
On the other hand, the Plaque Assay Technique is a method used to measure the number of infectious virus particles in a sample. It involves adding a layer of cells (like bacteria) that the virus can infect and then covering it with a nutrient agar overlay. After a period of incubation, clear areas or "plaques" appear in the agar where the viruses have infected and lysed the cells. By counting these plaques, researchers can estimate the number of infectious virus particles present in the original sample.
Therefore, if you're looking for a definition of a Hemolytic Plaque Technique, it might refer to a research method that combines both concepts, possibly measuring the amount of a substance (like an antibody) that causes hemolysis in red blood cells and correlating it with the number of infectious virus particles present. However, I would recommend consulting the original source or author for clarification on their intended meaning.
Hemagglutination is a process where red blood cells (RBCs) agglutinate or clump together. Viral hemagglutination refers to the ability of certain viruses to bind to and agglutinate RBCs. This is often due to viral surface proteins known as hemagglutinins, which can recognize and attach to specific receptors on the surface of RBCs.
In virology, viral hemagglutination assays are commonly used for virus identification and quantification. For example, the influenza virus is known to hemagglutinate chicken RBCs, and this property can be used to identify and titrate the virus in a sample. The hemagglutination titer is the highest dilution of a virus that still causes visible agglutination of RBCs. This information can be useful in understanding the viral load in a patient or during vaccine production.
Blood group incompatibility refers to a situation where the blood type of a donor and a recipient are not compatible, leading to an immune response and destruction of the donated red blood cells. This is because the recipient's immune system recognizes the donor's red blood cells as foreign due to the presence of incompatible antigens on their surface.
The most common type of blood group incompatibility occurs between individuals with different ABO blood types, such as when a person with type O blood receives type A, B, or AB blood. This can lead to agglutination and hemolysis of the donated red blood cells, causing potentially life-threatening complications such as hemolytic transfusion reaction.
Another type of blood group incompatibility occurs between Rh-negative mothers and their Rh-positive fetuses. If a mother's immune system is exposed to her fetus's Rh-positive red blood cells during pregnancy or childbirth, she may develop antibodies against them. This can lead to hemolytic disease of the newborn if the mother becomes pregnant with another Rh-positive fetus in the future.
To prevent these complications, it is essential to ensure that donated blood is compatible with the recipient's blood type before transfusion and that appropriate measures are taken during pregnancy and childbirth to prevent sensitization of Rh-negative mothers to Rh-positive red blood cells.
Favism is a genetic disorder that results in a sensitivity to broad beans (Vicia faba) and related plants. It is most commonly found in populations from the Mediterranean, Middle East, and Asia. The disorder is caused by a deficiency of the enzyme glucose-6-phosphate dehydrogenase (G6PD), which is necessary for protecting red blood cells from damage.
When individuals with favism eat broad beans or inhale their pollen, the beans' metabolites can cause the release of harmful oxidative agents that destroy red blood cells, leading to hemolytic anemia. Symptoms of favism can include weakness, fatigue, abdominal pain, dark urine, and jaundice. In severe cases, it can lead to kidney failure, seizures, or even death.
Avoiding broad beans and related plants is the primary treatment for favism. In some cases, blood transfusions or medications that boost red blood cell production may be necessary to manage symptoms. It's important to note that not all people with G6PD deficiency will develop favism, and not all people with favism have G6PD deficiency.
Methemoglobin is a form of hemoglobin in which the iron within the heme group is in the ferric (Fe3+) state instead of the ferrous (Fe2+) state. This oxidation reduces its ability to bind and transport oxygen effectively, leading to methemoglobinemia when methemoglobin levels become too high. Methemoglobin has a limited capacity to release oxygen to tissues, which can result in hypoxia (reduced oxygen supply) and cyanosis (bluish discoloration of the skin and mucous membranes).
Methemoglobin is normally present in small amounts in the blood, but certain factors such as exposure to oxidizing agents, genetic predisposition, or certain medications can increase its levels. Elevated methemoglobin levels can be treated with methylene blue, which helps restore the iron within hemoglobin back to its ferrous state and improves oxygen transport capacity.
I apologize, but "sheep" is not a term that has a medical definition. It is a common animal with the scientific name Ovis aries. If you have any medical or health-related questions, I would be happy to try and help answer those for you.
The complement system is a group of proteins found in the blood and on the surface of cells that when activated, work together to help eliminate pathogens such as bacteria, viruses, and fungi from the body. The proteins are normally inactive in the bloodstream. When they encounter an invading microorganism or foreign substance, a series of reactions take place leading to the activation of the complement system. Activation results in the production of effector molecules that can punch holes in the cell membranes of pathogens, recruit and activate immune cells, and help remove debris and dead cells from the body.
There are three main pathways that can lead to complement activation: the classical pathway, the lectin pathway, and the alternative pathway. Each pathway involves a series of proteins that work together in a cascade-like manner to amplify the response and generate effector molecules. The three main effector molecules produced by the complement system are C3b, C4b, and C5b. These molecules can bind to the surface of pathogens, marking them for destruction by other immune cells.
Complement proteins also play a role in the regulation of the immune response. They help to prevent excessive activation of the complement system, which could damage host tissues. Dysregulation of the complement system has been implicated in a number of diseases, including autoimmune disorders and inflammatory conditions.
In summary, Complement System Proteins are a group of proteins that play a crucial role in the immune response by helping to eliminate pathogens and regulate the immune response. They can be activated through three different pathways, leading to the production of effector molecules that mark pathogens for destruction. Dysregulation of the complement system has been linked to various diseases.
A reticulocyte count is a laboratory test that measures the percentage of reticulocytes in the peripheral blood. Reticulocytes are immature red blood cells produced in the bone marrow and released into the bloodstream. They contain residual ribosomal RNA, which gives them a reticular or net-like appearance under a microscope when stained with certain dyes.
The reticulocyte count is often used as an indicator of the rate of red blood cell production in the bone marrow. A higher than normal reticulocyte count may indicate an increased production of red blood cells, which can be seen in conditions such as hemolysis, blood loss, or response to treatment of anemia. A lower than normal reticulocyte count may suggest a decreased production of red blood cells, which can be seen in conditions such as bone marrow suppression, aplastic anemia, or vitamin deficiencies.
The reticulocyte count is usually expressed as a percentage of the total number of red blood cells, but it can also be reported as an absolute reticulocyte count (the actual number of reticulocytes per microliter of blood). The normal range for the reticulocyte count varies depending on the laboratory and the population studied.
Heinz bodies are small, irregularly shaped inclusions found in the red blood cells (RBCs). They are aggregates of denatured hemoglobin and are typically seen in RBCs that have been exposed to oxidative stress. This can occur due to various factors such as exposure to certain chemicals, drugs, or diseases.
The presence of Heinz bodies can lead to the premature destruction of RBCs, a condition known as hemolysis. This can result in anemia and related symptoms such as fatigue, weakness, and shortness of breath. It's important to note that while Heinz bodies are often associated with certain diseases, they can also be present in otherwise healthy individuals who have been exposed to oxidative stress.
It's worth mentioning that the term "Heinz bodies" comes from the name of the scientist Robert Heinz, who first described them in 1890.
Bilirubin is a yellowish pigment that is produced by the liver when it breaks down old red blood cells. It is a normal byproduct of hemoglobin metabolism and is usually conjugated (made water-soluble) in the liver before being excreted through the bile into the digestive system. Elevated levels of bilirubin can cause jaundice, a yellowing of the skin and eyes. Increased bilirubin levels may indicate liver disease or other medical conditions such as gallstones or hemolysis. It is also measured to assess liver function and to help diagnose various liver disorders.
Hemagglutination is a medical term that refers to the agglutination or clumping together of red blood cells (RBCs) in the presence of an agglutinin, which is typically a protein or a polysaccharide found on the surface of certain viruses, bacteria, or incompatible blood types.
In simpler terms, hemagglutination occurs when the agglutinin binds to specific antigens on the surface of RBCs, causing them to clump together and form visible clumps or aggregates. This reaction is often used in diagnostic tests to identify the presence of certain viruses or bacteria, such as influenza or HIV, by mixing a sample of blood or other bodily fluid with a known agglutinin and observing whether hemagglutination occurs.
Hemagglutination inhibition (HI) assays are also commonly used to measure the titer or concentration of antibodies in a serum sample, by adding serial dilutions of the serum to a fixed amount of agglutinin and observing the highest dilution that still prevents hemagglutination. This can help determine whether a person has been previously exposed to a particular pathogen and has developed immunity to it.
Complement C8 is a protein component of the complement system, which is a part of the immune system that helps to eliminate pathogens and damaged cells from the body. Specifically, C8 is a part of the membrane attack complex (MAC), which forms a pore in the membrane of target cells, leading to their lysis or destruction.
C8 is composed of three subunits: alpha, beta, and gamma. It is activated when it binds to the complement component C5b67 complex on the surface of a target cell. Once activated, C8 undergoes a conformational change that allows it to insert into the target cell membrane and form a pore, which disrupts the cell's membrane integrity and can lead to its death.
Deficiencies in complement components, including C8, can make individuals more susceptible to certain infections and autoimmune diseases. Additionally, mutations in the genes encoding complement proteins have been associated with various inherited disorders, such as atypical hemolytic uremic syndrome (aHUS), which is characterized by thrombotic microangiopathy and kidney failure.
Blood specimen collection is the process of obtaining a sample of blood from a patient for laboratory testing and analysis. This procedure is performed by trained healthcare professionals, such as nurses or phlebotomists, using sterile equipment to minimize the risk of infection and ensure accurate test results. The collected blood sample may be used to diagnose and monitor various medical conditions, assess overall health and organ function, and check for the presence of drugs, alcohol, or other substances. Proper handling, storage, and transportation of the specimen are crucial to maintain its integrity and prevent contamination.
Neonatal jaundice is a medical condition characterized by the yellowing of a newborn baby's skin and eyes due to an excess of bilirubin in the blood. Bilirubin is a yellowish substance produced by the normal breakdown of red blood cells, which are then processed by the liver and excreted through the bile. In neonatal jaundice, the liver is not yet fully developed and cannot process bilirubin quickly enough, leading to its accumulation in the body.
Neonatal jaundice typically appears within the first 2-4 days of life and can range from mild to severe. Mild cases may resolve on their own without treatment, while more severe cases may require medical intervention such as phototherapy or a blood transfusion. Risk factors for neonatal jaundice include prematurity, bruising during birth, blood type incompatibility between mother and baby, and certain genetic disorders.
It is important to monitor newborns closely for signs of jaundice and seek medical attention if concerned, as untreated neonatal jaundice can lead to serious complications such as brain damage or hearing loss.
Erythrocyte aging, also known as red cell aging, is the natural process of changes and senescence that occur in red blood cells (erythrocytes) over time. In humans, mature erythrocytes are devoid of nuclei and organelles, and have a lifespan of approximately 120 days.
During aging, several biochemical and structural modifications take place in the erythrocyte, including:
1. Loss of membrane phospholipids and proteins, leading to increased rigidity and decreased deformability.
2. Oxidative damage to hemoglobin, resulting in the formation of methemoglobin and heinz bodies.
3. Accumulation of denatured proteins and aggregates, which can impair cellular functions.
4. Changes in the cytoskeleton, affecting the shape and stability of the erythrocyte.
5. Increased expression of surface markers, such as Band 3 and CD47, that signal the spleen to remove aged erythrocytes from circulation.
The spleen plays a crucial role in removing senescent erythrocytes by recognizing and phagocytosing those with altered membrane composition or increased expression of surface markers. This process helps maintain the overall health and functionality of the circulatory system.
Vitamin E deficiency is a condition that occurs when there is a lack of sufficient vitamin E in the body. Vitamin E is a fat-soluble antioxidant that plays an essential role in maintaining the health of cell membranes, protecting them from damage caused by free radicals. It also helps to support the immune system and promotes healthy blood vessels and nerves.
Vitamin E deficiency can occur due to several reasons, including malnutrition, malabsorption disorders such as cystic fibrosis or celiac disease, premature birth, or genetic defects affecting the alpha-tocopherol transfer protein (alpha-TTP), which is responsible for transporting vitamin E from the liver to other tissues.
Symptoms of vitamin E deficiency may include:
* Neurological problems such as peripheral neuropathy, ataxia (loss of coordination), and muscle weakness
* Retinopathy (damage to the retina) leading to vision loss
* Increased susceptibility to oxidative stress and inflammation
* Impaired immune function
Vitamin E deficiency is rare in healthy individuals who consume a balanced diet, but it can occur in people with certain medical conditions or those who have undergone bariatric surgery. In these cases, supplementation may be necessary to prevent or treat vitamin E deficiency.
Hereditary Spherocytosis is a genetic disorder that affects the red blood cells (RBCs) causing them to take on a spherical shape instead of their normal biconcave disc shape. This occurs due to mutations in the genes responsible for the proteins that maintain the structure and flexibility of RBCs, such as ankyrin, band 3, spectrin, and protein 4.2.
The abnormally shaped RBCs are fragile and prone to hemolysis (premature destruction), which can lead to anemia, jaundice, and gallstones. Symptoms can vary from mild to severe and may include fatigue, weakness, shortness of breath, and a yellowing of the skin and eyes (jaundice). Diagnosis is typically made through a combination of family history, physical examination, complete blood count (CBC), and specialized tests such as osmotic fragility test, eosin-5'-maleimide binding test, or direct antiglobulin test. Treatment may include monitoring, supplementation with folic acid, and in severe cases, splenectomy (surgical removal of the spleen) to reduce RBC destruction.
Streptolysins are exotoxins produced by certain strains of Streptococcus bacteria, primarily Group A Streptococcus (GAS). These toxins are classified into two types: streptolysin O (SLO) and streptolysin S (SLS).
1. Streptolysin O (SLO): It is a protein exotoxin that exhibits oxygen-labile hemolytic activity, meaning it can lyse or destroy red blood cells in the presence of oxygen. SLO is capable of entering host cells and causing various cellular damages, including inhibition of phagocytosis, modulation of immune responses, and induction of apoptosis (programmed cell death).
2. Streptolysin S (SLS): It is a non-protein, oxygen-stable hemolysin that can also lyse red blood cells but does so independently of oxygen presence. SLS is more heat-resistant than SLO and has a stronger ability to penetrate host cell membranes.
Both streptolysins contribute to the virulence of Streptococcus pyogenes, which can cause various clinical infections such as pharyngitis (strep throat), impetigo, scarlet fever, and invasive diseases like necrotizing fasciitis and toxic shock syndrome.
The detection of streptolysin O antibodies (ASO titer) is often used as a diagnostic marker for past or recent GAS infections, particularly in cases of rheumatic fever, where elevated ASO titers indicate ongoing or previous streptococcal infection.
L-Lactate Dehydrogenase (LDH) is an enzyme found in various tissues within the body, including the heart, liver, kidneys, muscles, and brain. It plays a crucial role in the process of energy production, particularly during anaerobic conditions when oxygen levels are low.
In the presence of the coenzyme NADH, LDH catalyzes the conversion of pyruvate to lactate, generating NAD+ as a byproduct. Conversely, in the presence of NAD+, LDH can convert lactate back to pyruvate using NADH. This reversible reaction is essential for maintaining the balance between lactate and pyruvate levels within cells.
Elevated blood levels of LDH may indicate tissue damage or injury, as this enzyme can be released into the circulation following cellular breakdown. As a result, LDH is often used as a nonspecific biomarker for various medical conditions, such as myocardial infarction (heart attack), liver disease, muscle damage, and certain types of cancer. However, it's important to note that an isolated increase in LDH does not necessarily pinpoint the exact location or cause of tissue damage, and further diagnostic tests are usually required for confirmation.
Hemopexin is a protein found in blood plasma. It's primary function is to bind and transport heme, a potentially toxic molecule that is released when hemoglobin from red blood cells is broken down. Hemopexin helps to prevent damage to tissues and organs by keeping free heme levels low in the bloodstream. It also plays a role in the immune response and has antioxidant properties. A deficiency in hemopexin can lead to increased risk of tissue damage and inflammation.
Erythrocyte count, also known as red blood cell (RBC) count, is a laboratory test that measures the number of red blood cells in a sample of blood. Red blood cells are important because they carry oxygen from the lungs to the rest of the body. A low erythrocyte count may indicate anemia, while a high count may be a sign of certain medical conditions such as polycythemia. The normal range for erythrocyte count varies depending on a person's age, sex, and other factors.
Abnormal erythrocytes refer to red blood cells that have an abnormal shape, size, or other characteristics. This can include various types of abnormalities such as:
1. Anisocytosis: Variation in the size of erythrocytes.
2. Poikilocytosis: Variation in the shape of erythrocytes, including but not limited to teardrop-shaped cells (dacrocytes), crescent-shaped cells (sickle cells), and spherical cells (spherocytes).
3. Anemia: A decrease in the total number of erythrocytes or a reduction in hemoglobin concentration, which can result from various underlying conditions such as iron deficiency, chronic disease, or blood loss.
4. Hemoglobinopathies: Abnormalities in the structure or function of hemoglobin, the protein responsible for carrying oxygen in erythrocytes, such as sickle cell anemia and thalassemia.
5. Inclusion bodies: Abnormal structures within erythrocytes, such as Heinz bodies (denatured hemoglobin) or Howell-Jolly bodies (nuclear remnants).
These abnormalities can be detected through a complete blood count (CBC) and peripheral blood smear examination. The presence of abnormal erythrocytes may indicate an underlying medical condition, and further evaluation is often necessary to determine the cause and appropriate treatment.
A spider bite is not a medical condition in and of itself, but rather an injury caused by the puncture of the skin by the fangs of a spider. Not all spiders are capable of penetrating human skin, and only a small number of species found in certain parts of the world have venom that can cause harmful reactions in humans.
The symptoms of a spider bite can vary widely depending on the species of spider, the amount of venom injected, the sensitivity of the person bitten, and the location of the bite. Some common symptoms include redness, swelling, pain, itching, and formation of a blister at the site of the bite. In more severe cases, symptoms such as muscle cramps, nausea, vomiting, fever, chills, and difficulty breathing can occur.
It is important to note that many skin reactions that are attributed to spider bites may actually be caused by other factors such as bacterial infections or allergic reactions. Accurate identification of the spider responsible for a bite is often difficult, and in most cases, treatment is directed at relieving symptoms and preventing complications.
The ABO blood-group system is a classification system used in blood transfusion medicine to determine the compatibility of donated blood with a recipient's blood. It is based on the presence or absence of two antigens, A and B, on the surface of red blood cells (RBCs), as well as the corresponding antibodies present in the plasma.
There are four main blood types in the ABO system:
1. Type A: These individuals have A antigens on their RBCs and anti-B antibodies in their plasma.
2. Type B: They have B antigens on their RBCs and anti-A antibodies in their plasma.
3. Type AB: They have both A and B antigens on their RBCs but no natural antibodies against either A or B antigens.
4. Type O: They do not have any A or B antigens on their RBCs, but they have both anti-A and anti-B antibodies in their plasma.
Transfusing blood from a donor with incompatible ABO antigens can lead to an immune response, causing the destruction of donated RBCs and potentially life-threatening complications such as acute hemolytic transfusion reaction. Therefore, it is crucial to match the ABO blood type between donors and recipients before performing a blood transfusion.
Hyperbilirubinemia is a medical condition characterized by an excessively high level of bilirubin in the bloodstream. Bilirubin is a yellowish pigment produced by the liver when it breaks down old red blood cells. Normally, bilirubin is conjugated (made water-soluble) in the liver and then excreted through the bile into the digestive system. However, if there is a problem with the liver's ability to process or excrete bilirubin, it can build up in the blood, leading to hyperbilirubinemia.
Hyperbilirubinemia can be classified as either unconjugated or conjugated, depending on whether the bilirubin is in its direct (conjugated) or indirect (unconjugated) form. Unconjugated hyperbilirubinemia can occur due to increased production of bilirubin (such as in hemolytic anemia), decreased uptake of bilirubin by the liver, or impaired conjugation of bilirubin in the liver. Conjugated hyperbilirubinemia, on the other hand, is usually caused by a problem with the excretion of conjugated bilirubin into the bile, such as in cholestatic liver diseases like hepatitis or cirrhosis.
Symptoms of hyperbilirubinemia can include jaundice (yellowing of the skin and eyes), dark urine, light-colored stools, itching, and fatigue. Treatment depends on the underlying cause of the condition and may involve medications, dietary changes, or surgery.
Complement C5 is a protein that plays a crucial role in the complement system, which is a part of the immune system that helps to eliminate pathogens and damaged cells from the body. The complement system is a complex series of biochemical reactions that help to identify and destroy foreign substances, such as bacteria and viruses.
Complement C5 is one of several proteins in the complement system that are activated in a cascading manner in response to an activating event, such as the binding of an antibody to a pathogen. Once activated, Complement C5 can be cleaved into two smaller proteins, C5a and C5b.
C5a is a powerful anaphylatoxin, which means it can cause the release of histamine from mast cells and basophils, leading to inflammation and increased vascular permeability. It also acts as a chemoattractant, drawing immune cells to the site of infection or injury.
C5b, on the other hand, plays a role in the formation of the membrane attack complex (MAC), which is a protein structure that can punch holes in the membranes of pathogens, leading to their lysis and destruction.
Overall, Complement C5 is an important component of the immune system's response to infection and injury, helping to eliminate pathogens and damaged cells from the body.
CD59 is a type of protein found on the surface of many cells in the human body, including red and white blood cells, that functions as an inhibitor of the complement system. The complement system is a part of the immune system that helps to eliminate pathogens such as bacteria and viruses from the body.
CD59 specifically inhibits the formation of the membrane attack complex (MAC), which is a protein structure that forms pores in the cell membrane and can lead to cell lysis or death. By preventing the formation of the MAC, CD59 helps to protect cells from complement-mediated damage.
As an antigen, CD59 is a molecule that can be recognized by the immune system and stimulate an immune response. However, because it is a self-protein found on normal human cells, CD59 is not typically targeted by the immune system unless there is some kind of dysregulation or abnormality.
In certain medical conditions, such as autoimmune disorders or transplant rejection, the immune system may mistakenly target CD59 or other self-proteins, leading to damage to healthy cells and tissues. In these cases, treatments may be necessary to modulate or suppress the immune response and prevent further harm.
Erythrocyte deformability refers to the ability of red blood cells (erythrocytes) to change shape and bend without rupturing, which is crucial for their efficient movement through narrow blood vessels. This deformability is influenced by several factors including the cell membrane structure, hemoglobin concentration, and intracellular viscosity. A decrease in erythrocyte deformability can negatively impact blood flow and oxygen delivery to tissues, potentially contributing to various pathological conditions such as sickle cell disease, diabetes, and cardiovascular diseases.
Hemagglutination inhibition (HI) tests are a type of serological assay used in medical laboratories to detect and measure the amount of antibodies present in a patient's serum. These tests are commonly used to diagnose viral infections, such as influenza or HIV, by identifying the presence of antibodies that bind to specific viral antigens and prevent hemagglutination (the agglutination or clumping together of red blood cells).
In an HI test, a small amount of the patient's serum is mixed with a known quantity of the viral antigen, which has been treated to attach to red blood cells. If the patient's serum contains antibodies that bind to the viral antigen, they will prevent the antigen from attaching to the red blood cells and inhibit hemagglutination. The degree of hemagglutination inhibition can be measured and used to estimate the amount of antibody present in the patient's serum.
HI tests are relatively simple and inexpensive to perform, but they have some limitations. For example, they may not detect early-stage infections before the body has had a chance to produce antibodies, and they may not be able to distinguish between different strains of the same virus. Nonetheless, HI tests remain an important tool for diagnosing viral infections and monitoring immune responses to vaccination or infection.
"Rickettsia prowazekii" is a type of bacteria that causes typhus fever in humans. It's a gram-negative, obligate intracellular bacterium that is transmitted to humans through the bite of infected lice or through contact with their feces. The bacteria infect endothelial cells and cause systemic illness characterized by high fever, headache, muscle pain, and rash.
Typhus fever is a severe and potentially life-threatening disease, particularly in individuals with weakened immune systems. Early diagnosis and treatment with antibiotics are essential to prevent complications and reduce the risk of death.
"Rickettsia prowazekii" is named after Henry Ricketts and Stanislaus von Prowazek, two early researchers who studied typhus fever and made significant contributions to our understanding of the disease.
Chromium isotopes are different forms of the chemical element Chromium (Cr), which have different numbers of neutrons in their atomic nuclei. This results in each isotope having a different atomic mass, although they all have the same number of protons (24) and therefore share the same chemical properties.
The most common and stable chromium isotopes are Chromium-52 (Cr-52), Chromium-53 (Cr-53), Chromium-54 (Cr-54), and Chromium-56 (Cr-56). The other less abundant isotopes of Chromium, such as Chromium-50 (Cr-50) and Chromium-51 (Cr-51), are radioactive and undergo decay to become stable isotopes.
Chromium is an essential trace element for human health, playing a role in the metabolism of carbohydrates, lipids, and proteins. It is also used in various industrial applications, such as in the production of stainless steel and other alloys.
Complement C6 is a protein that plays a crucial role in the complement system, which is a part of the immune system that helps to eliminate pathogens and damaged cells from the body. Specifically, C6 is a component of the membrane attack complex (MAC), which is a group of proteins that work together to form a pore in the membrane of target cells, leading to their lysis or destruction.
The complement system is activated through several different pathways, including the classical pathway, the lectin pathway, and the alternative pathway. Once activated, these pathways converge at the level of C3, which is cleaved into C3a and C3b fragments. C3b can then bind to the surface of target cells and initiate the formation of the MAC.
C6 is one of several proteins that are required for the formation of the MAC. When C6 binds to C7, it undergoes a conformational change that allows it to interact with C8 and form a stable complex. This complex then recruits additional C9 molecules, which polymerize to form the pore in the target cell membrane.
Deficiencies in complement components, including C6, can lead to increased susceptibility to certain types of infections, as well as autoimmune disorders and other medical conditions.
Amidines are organic compounds that contain a functional group with the structure R-C=N-R, where R can be an alkyl or aromatic group. This functional group consists of a carbonyl (C=O) group and a nitrogen atom (N) connected to two organic groups (R).
In medical terminology, amidines are not commonly used. However, some amidine derivatives have been investigated for their potential therapeutic properties. For example, certain amidine compounds have shown antimicrobial, anti-inflammatory, and antiviral activities. Some of these compounds have also been studied as potential drugs for the treatment of various diseases, including cancer, cardiovascular disease, and neurological disorders.
It is important to note that while some amidines may have therapeutic potential, they can also be toxic at high concentrations and should be handled with care.
Blood preservation refers to the process of keeping blood viable and functional outside of the body for transfusion purposes. This is typically achieved through the addition of various chemical additives, such as anticoagulants and nutrients, to a storage solution in which the blood is contained. The preserved blood is then refrigerated or frozen until it is needed for transfusion.
The goal of blood preservation is to maintain the structural integrity and functional capacity of the red blood cells, white blood cells, and platelets, as well as the coagulation factors, in order to ensure that the transfused blood is safe and effective. Different storage conditions and additives are used for the preservation of different components of blood, depending on their specific requirements.
It's important to note that while blood preservation extends the shelf life of donated blood, it does not last indefinitely. The length of time that blood can be stored depends on several factors, including the type of blood component and the storage conditions. Regular testing is performed to ensure that the preserved blood remains safe and effective for transfusion.
Glyceraldehyde-3-phosphate dehydrogenase (GAPDH), also known as Glucosephosphate Dehydrogenase, is an enzyme that plays a crucial role in cellular metabolism, particularly in the glycolytic pathway. It catalyzes the conversion of glyceraldehyde 3-phosphate (G3P) to 1,3-bisphosphoglycerate (1,3-BPG), while also converting nicotinamide adenine dinucleotide (NAD+) to its reduced form NADH. This reaction is essential for the production of energy in the form of adenosine triphosphate (ATP) during cellular respiration. GAPDH has been widely used as a housekeeping gene in molecular biology research due to its consistent expression across various tissues and cells, although recent studies have shown that its expression can vary under certain conditions.
The brown recluse spider (Loxosceles reclusa) is a species of venomous spider that is native to North America. It is also known as the fiddleback spider or violin spider due to the distinctive violin-shaped marking on its cephalothorax. The brown recluse spider is a medium-sized spider, with adults ranging in size from 6 to 20 millimeters in body length. It is characterized by its light to dark brown coloration and lack of conspicuous markings on the abdomen.
The brown recluse spider is known for its necrotic bite, which can cause significant tissue damage and scarring. The venom of the brown recluse spider contains a number of different proteins, including sphingomyelinase D, which is thought to be responsible for the necrotic effects of the bite. The severity of the reaction to a brown recluse spider bite can vary widely, ranging from mild localized reactions to severe systemic reactions that can be life-threatening.
Brown recluse spiders are typically found in the central and southern United States, particularly in the states of Texas, Oklahoma, Kansas, Arkansas, Missouri, Mississippi, Louisiana, Alabama, Georgia, Florida, Tennessee, Kentucky, Ohio, and Indiana. They prefer to live in warm, dry environments and are often found in woodpiles, sheds, barns, and other outbuildings. Inside homes, they can be found in closets, attics, crawl spaces, and underneath furniture.
It is important to note that brown recluse spiders are not aggressive and will only bite if they feel threatened or cornered. If you think you may have been bitten by a brown recluse spider, it is important to seek medical attention as soon as possible. Treatment for a brown recluse spider bite typically involves wound care, pain management, and in some cases, the use of antibiotics to prevent infection.
I believe there may be some confusion in your question. "Rabbits" is a common name used to refer to the Lagomorpha species, particularly members of the family Leporidae. They are small mammals known for their long ears, strong legs, and quick reproduction.
However, if you're referring to "rabbits" in a medical context, there is a term called "rabbit syndrome," which is a rare movement disorder characterized by repetitive, involuntary movements of the fingers, resembling those of a rabbit chewing. It is also known as "finger-chewing chorea." This condition is usually associated with certain medications, particularly antipsychotics, and typically resolves when the medication is stopped or adjusted.
"Hemolysin factors" is not a standard medical term, and it seems there might be some confusion in the question. However, I can provide information on hemolysins, which are substances that cause lysis (rupture) of red blood cells, resulting in the release of their contents into the surrounding fluid.
Hemolysins can be produced by various sources, such as:
1. Bacterial hemolysins: Some bacteria produce hemolysins as a virulence factor to aid in infecting the host. These hemolysins can be classified into two main types: exotoxins (secreted by the bacterium) and endotoxins (integral components of the bacterial cell membrane). Examples include streptolysin O and streptolysin S from Streptococcus pyogenes, hemolysin from Escherichia coli, and α-toxin from Staphylococcus aureus.
2. Complement system: The complement system is a part of the immune response that can cause hemolysis through the membrane attack complex (MAC). This complex forms pores in the red blood cell membrane, leading to lysis.
3. Autoimmune disorders: In some autoimmune diseases, such as autoimmune hemolytic anemia, the body produces antibodies against its own red blood cells, causing complement-mediated hemolysis.
4. Medicines and chemicals: Certain medications or chemicals can cause hemolysis as a side effect. These include some antibiotics (e.g., cephalosporins), chemotherapeutic agents, and snake venoms.
If you meant to ask about something else related to "hemolysin factors," please provide more context so I can give a more accurate answer.
Blood chemical analysis, also known as clinical chemistry or chemistry panel, is a series of tests that measure the levels of various chemicals in the blood. These tests can help evaluate the function of organs such as the kidneys and liver, and can also detect conditions such as diabetes and heart disease.
The tests typically include:
* Glucose: to check for diabetes
* Electrolytes (such as sodium, potassium, chloride, and bicarbonate): to check the body's fluid and electrolyte balance
* Calcium: to check for problems with bones, nerves, or kidneys
* Creatinine: to check for kidney function
* Urea Nitrogen (BUN): to check for kidney function
* Albumin: to check for liver function and nutrition status
* ALT (Alanine Transaminase) and AST (Aspartate Transaminase): to check for liver function
* Alkaline Phosphatase: to check for liver or bone disease
* Total Bilirubin: to check for liver function and gallbladder function
* Cholesterol: to check for heart disease risk
* Triglycerides: to check for heart disease risk
These tests are usually ordered by a doctor as part of a routine check-up, or to help diagnose and monitor specific medical conditions. The results of the blood chemical analysis are compared to reference ranges provided by the laboratory performing the test, which take into account factors such as age, sex, and race.
Glycogen Storage Disease Type VII, also known as Tarui's disease, is a rare inherited metabolic disorder caused by a deficiency of the enzyme phosphofructokinase (PFK), which is required for glycogenolysis – the breakdown of glycogen to glucose-1-phosphate and ultimately into glucose. This enzyme deficiency results in the accumulation of glycogen, particularly in muscle and red blood cells, leading to symptoms such as exercise-induced muscle cramps, myoglobinuria (the presence of myoglobin in the urine), and hemolytic anemia. The disease can also cause muscle weakness, fatigue, and dark-colored urine after strenuous exercise. It is inherited in an autosomal recessive manner, meaning that an individual must inherit two copies of the mutated gene (one from each parent) to develop the condition.
Complement C7 is a protein that plays a role in the complement system, which is a part of the immune system that helps to clear pathogens and damaged cells from the body. Specifically, C7 is a component of the membrane attack complex (MAC), which is a group of proteins that forms a pore in the membrane of target cells, leading to their lysis or destruction.
C7 is activated when it binds to the C5b-7 complex, which is formed by the cleavage of C5 and C6 by the C5 convertase. Once bound to the C5b-7 complex, C7 undergoes a conformational change that allows it to insert into the target cell membrane. This forms the basis for the formation of the MAC and subsequent lysis of the target cell.
Deficiencies in complement components, including C7, can lead to increased susceptibility to certain infections and autoimmune disorders. Additionally, abnormal regulation of the complement system has been implicated in a variety of diseases, including inflammatory and degenerative conditions.
Rubella virus is the sole member of the genus Rubivirus, within the family Togaviridae. It is a positive-sense single-stranded RNA virus that causes the disease rubella (German measles) in humans. The virus is typically transmitted through respiratory droplets and has an incubation period of 12-23 days.
Rubella virus infection during pregnancy, particularly during the first trimester, can lead to serious birth defects known as congenital rubella syndrome (CRS) in the developing fetus. The symptoms of CRS may include hearing impairment, eye abnormalities, heart defects, and developmental delays.
The virus was eradicated from the Americas in 2015 due to widespread vaccination programs. However, it still circulates in other parts of the world, and travelers can bring the virus back to regions where it has been eliminated. Therefore, maintaining high vaccination rates is crucial for preventing the spread of rubella and protecting vulnerable populations from CRS.
A hypotonic solution is a type of fluid that has a lower osmotic pressure than another fluid. In the context of medical and physiological terms, it typically refers to a solution that has a lower solute concentration (and therefore lower osmolarity) than the fluids found in the body's cells.
When a hypotonic solution is introduced into the body or comes into contact with body tissues, water molecules tend to move from the area of lower solute concentration (the hypotonic solution) to the area of higher solute concentration (the body's fluids), in an attempt to equalize the osmotic pressure. This movement of water can cause cells to swell and potentially burst if the difference in osmolarity is significant or if the exposure is prolonged.
Hypotonic solutions are sometimes used medically for specific purposes, such as in irrigation solutions or in certain types of intravenous fluids, where careful control of osmotic pressure is required. However, it's important to use them appropriately and under medical supervision to avoid potential adverse effects.
'Clostridium perfringens' is a type of Gram-positive, rod-shaped, spore-forming bacterium that is commonly found in the environment, including in soil, decaying vegetation, and the intestines of humans and animals. It is a major cause of foodborne illness worldwide, producing several toxins that can lead to symptoms such as diarrhea, abdominal cramps, nausea, and vomiting.
The bacterium can contaminate food during preparation or storage, particularly meat and poultry products. When ingested, the spores of C. perfringens can germinate and produce large numbers of toxin-producing cells in the intestines, leading to food poisoning. The most common form of C. perfringens food poisoning is characterized by symptoms that appear within 6 to 24 hours after ingestion and last for less than 24 hours.
In addition to foodborne illness, C. perfringens can also cause other types of infections, such as gas gangrene, a serious condition that can occur when the bacterium infects a wound and produces toxins that damage surrounding tissues. Gas gangrene is a medical emergency that requires prompt treatment with antibiotics and surgical debridement or amputation of affected tissue.
Prevention measures for C. perfringens food poisoning include proper cooking, handling, and storage of food, as well as rapid cooling of cooked foods to prevent the growth of the bacterium.