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"agglutinin" Definitions
  1. a substance (such as an antibody) producing agglutination

78 Sentences With "agglutinin"

How to use agglutinin in a sentence? Find typical usage patterns (collocations)/phrases/context for "agglutinin" and check conjugation/comparative form for "agglutinin". Mastering all the usages of "agglutinin" from sentence examples published by news publications.

Cooking it would result in "the inactivation of WGA," which is an acronym for wheat germ agglutinin, the lectin protein present in gluten.
Secondary cold agglutinin syndrome refers to cold agglutinin disease that is identified to be caused by viral infection, autoimmune disorder, lymphoid malignancy, or any other underlying disease.
Agglutinin might also be associated with diseases of which the most common is an autoimmune disease known as cold agglutinin disease. In cold agglutinin disease, the body produces agglutinins or antibodies that coagulate erythrocytes and lyse them at room temperature or lower. Under normal circumstances, the lifespan of erythrocytes is 120 days after which they are degraded by the spleen. In individuals that have cold agglutinin disease, the lifespan of erythrocytes is shortened.
Complement activation plays a definitive but limited role in warm-antibody AIHA (w-AIHA), whereas primary cold agglutinin disease (CAD), secondary cold agglutinin syndrome (CAS), and paroxysmal cold hemoglobinuria (PCH) are entirely complement-dependent disorders.
PDB entry 2dvd Peanut agglutinin (PNA) is plant lectin protein derived from the fruits of Arachis hypogaea. Peanut agglutinin may also be referred to as Arachis hypogaea lectin. Lectins recognise and bind particular sugar sequences in carbohydrates; peanut agglutinin binds the carbohydrate sequence Gal-β(1-3)-GalNAc. The name "peanut agglutinin" originates from its ability to stick together (agglutinate) cells, such as neuraminidase-treated erythrocytes, which have glycoproteins or glycolipids on their surface which include the Gal-β(1-3)-GalNAc carbohydrate sequence.
Its seeds contain high activity of soybean lectins (soybean agglutinin or SBA).
The extract of Clavulinopsis fusiformis contains anti-B red blood cell agglutinin.
Mononucleosis is sometimes accompanied by secondary cold agglutinin disease, an autoimmune disease in which abnormal circulating antibodies directed against red blood cells can lead to a form of autoimmune hemolytic anemia. The cold agglutinin detected is of anti-i specificity.
An agglutinin is a substance in the blood that causes particles to coagulate and aggregate; that is, to change from fluid-like state to a thickened-mass (solid) state. Agglutinins can be antibodies that cause antigens to aggregate by binding to the antigen-binding sites of antibodies. Agglutinins can also be any substance other than antibodies, such as sugar-binding protein lectins. When an agglutinin is added to a uniform suspension of particles, such as bacteria or blood, in a test tube (in vitro), agglutinin binds to the agglutinin-specific structure on the particle causing the particles to aggregate and fall to the bottom, leaving a clear suspension.
On excluding warm autoimmune hemolytic anemia (WAIHA), the cold agglutinin titer should be examined for cold agglutinin disease (CAD). The diagnosis of PCH is suspected when both WAIHA and CAD are excluded. The complement level is usually low. Donath- Landsteiner test is the confirmatory test for PCH.
This opsonization enhances the clearance of red blood cell by phagocytes in the liver, spleen, and lungs, a process termed extravascular hemolysis. Individuals with cold agglutinin disease present with signs and symptoms of hemolytic anemia. Those with secondary agglutinin disease may also present with an underlying disease, often autoimmune.
Cold agglutinin disease most commonly affects adults who are of middle age and older. Some studies also report a slight bias in favor of females in the incidence of cold agglutinin disease, particularly in older populations. People with infectious mononucleosis, lymphoproliferative diseases, or mycoplasma pneumonia are more susceptible to this condition. Cold agglutinin disease represents an estimated 16–32% of autoimmune hemolytic anemia, whose annual incidence is estimated to be between 1/35,000-1/80,000 in North America and Western Europe.
Cold agglutinins are antibodies, typically immunoglobulin M (IgM), that are acquainted with and then binding the antigens on red blood cells, typically antigens "I" or "i" on the RBC surface, in the environment in which the temperatures are lower than normal core body temperature and, thus, ends up leading to agglutinations of the red blood cells and hemolysis reaction occurring outside the vessels (extra-vessels), resulting in anemia without hemoglobinuria in ordinary cases. Cold agglutinins can cause two pathological conditions, that are, primary cold agglutinin disease (CAD) and secondary cold agglutinin syndrome (CAS), both of which are sole two subtypes of cold agglutinin disease. Primary cold agglutinin disease is idiopathic, meaning the phenomenons of agglutinations of the red blood cells and hemolysis reaction occurring outside the vessels are absent from any underlying cause. Nevertheless, what is known is, those with idiopathic cold agglutinin disease are susceptible to having or developing mild clonal bone marrow disorder.
The long-term outlook (prognosis) for people with cold agglutinin disease varies based on many factors including the severity of the condition, the signs and symptoms present in each person and the underlying cause. For example, people with cold agglutinin disease caused by bacterial or viral infections tend to have an excellent prognosis; in these cases, the symptoms typically disappear within 6 months after the infection has resolved. Mild to moderate primary (unknown cause) cold agglutinin disease can also be associated with a good prognosis if excessive exposure to the cold is avoided. Those with cold agglutinin disease caused by HIV infection or certain types of cancer generally have a poor prognosis due to the nature of the underlying condition.
Cold agglutinin disease can be either primary (unknown cause) or secondary (a result of another pathology/ caused by an underlying condition).
Cold agglutinin disease can be primary (unknown cause) or secondary, due to an underlying condition such as an infection, another autoimmune disease, or certain cancers. Treatment depends on many factors including the severity of the condition, the signs and symptoms present in each person, and the underlying cause. Cold agglutinin disease was first described in 1957.
Steroids and splenectomy are less efficacious in cold agglutinin disease. Paroxysmal cold hemoglobinuria is treated by removing the underlying cause, such as infection.
Hemolysis induced by cold agglutinin disease taking place outside the vessels while which of Donath-Landsteiner antibodies is taking place inside the vessels.
AFP-L3, an isoform of AFP which binds Lens culinaris agglutinin, can be particularly useful in early identification of aggressive tumors associated with HCC.
Yamashiki, N., et al., Oncology Reports, 6, 1229-1232, 1999. # Relationship between lens culinaris agglutinin reactive alpha-fetoprotein and biological features of hepatocellular carcinoma.
Eventually, those gametangia merge and zygosporangia form. As these two different mating types meet each other, each mating type transfers the sex-specific precursor of the trisporoid TSA, and acts as a signal for the synthesis of the surface protein agglutinin. Agglutinin allows the two TSAs to recognize each other. It then causes rapid contact and efficient interactions between those two different mating types.
Although there is some overlap of symptoms, cryoglobulinemia and cold agglutinin disease differ in the process by which blood vessels become blocked. In cryoglobulinemia, antibodies accumulate and block blood vessels. In cold agglutinin disease, antibodies (different from those in cryoglobulinemia) attack and kill red blood cells, which then accumulate and block blood vessels. Three types of pathological cold sensitive antibodies can all trigger Raynaud's phenomenon.
Snowdrops contain an active lectin or agglutinin named GNA for Galanthus nivalis agglutinin. In 1995, Árpád Pusztai genetically modified potatoes to express the GNA gene, which he discussed on a radio interview in 1998, and published in the Lancet in 1999. These remarks started the so-called Pusztai affair. This early research caused the GNA to be found in the edible part of the plant, i.e.
Wheat germ agglutinin (WGA) is a lectin that protects wheat (Triticum) from insects, yeast and bacteria. An agglutinin protein, it binds to N-acetyl-D- glucosamine and Sialic acid. Succinylated WGA is selective for β-GlcNAc, making it a useful tool for detecting O-GlcNAc. N-acetyl-D-glucosamine in the natural environment of wheat is found in the chitin of insects, and the cell membrane of yeast & bacteria.
Cold agglutinin disease is not an inherited condition. It is designated as either primary (unknown cause) or secondary (associated with or caused by another condition). In some cases, cold agglutinin may be multifactorial which means that multiple environmental factors and genes likely interact to predispose a person to developing the condition. However, to our knowledge, no disease-causing genes have been identified and no familial cases have been reported.
Yamashita, F., Eur. J. Gastroenterol. Hepatol., 7, 627-633, 1995. # Evaluation of curability and prediction of prognosis after surgical for hepatocellular carcinoma by lens culinaris agglutinin-reactive alpha- fetoprotein.
Red cell agglutination in a patient with cold agglutinin disease. In hematology, red cell agglutination or autoagglutination is a phenomenon in which red blood cells clump together, forming aggregates. It is caused by the surface of the red cells being coated with antibodies. This often occurs in cold agglutinin disease, a type of autoimmune hemolytic anemia in which people produce antibodies (termed cold agglutinins) that bind to their red blood cells at cold temperatures and destroy them.
Donath-Landsteiner antibodies share similarities with cold agglutinin disease in recognition and connection of the antigens on the red blood cells' surface in the presence of relatively lower temperatures compared to core body temperature. Yet, the place where the hemolysis taking place differentiates between antibodies and cold agglutinin. D-L antibodies rather fix complement system which result in hemolysis in vessels (intra-vessels). Blood vessels are pathways carrying living-required elements to reach everywhere inside the body through circulation.
Reaction of particles with agglutinin is used to indicate present or past host contact with a pathogen . A host infected with a pathogen produces antibodies to neutralize the pathogen. As a result, the blood of a host applied to a diagnostic kit causes the aggregation of the pathogenic particles due to the antigen-agglutinin interaction. Conversely, agglutination can also be used to identify new bacteria or cells with a specific antigen by exposing them to serum containing known agglutinins.
For example, there was a case study reporting that autoimmune hemolytic anemia where an IgA Donath-Landsteiner denoted as [D-L] antibody appeared to cause Donath-Landsteiner cold hemoglobinuria. The most notable difference between DLHA and CAD (cold agglutinin disease) is the causative agent. For cold agglutinin disease, the causative agent is constantly owing to a cold-active IgM antibody. In 1865, it was widely accepted as a common sense that cold exposure may result in hemoglobinuria paroxysms.
Okuda, K., et al., Inter. J. Oncol., 14, 265-271, 1999. # Usefulness of lens culinaris agglutinin A-reactive fraction of alpha- fetoprotein (AFP-L3) as a marker of distant metastasis from hepatocellular carcinoma.
J., 45, 187-193, 1998. # Clinical utility of lens culinaris agglutinin-reactive alpha-fetoprotein in small hepatocellular carcinoma: Special reference to imaging diagnosis. Kumada, T., et al., J. Hepatol., 30, 125-130, 1999.
Snowdrops contain an active substance called galantamine (or galanthamine) which can be helpful in the treatment of Alzheimer's disease, though it is not a cure. Snowdrops contain also an active lectin or agglutinin named GNA for Galanthus nivalis agglutinin. Potatoes have been genetically modified with the GNA gene. In 1998 Árpád Pusztai said in an interview on a World in Action programme that his group had observed damage to the intestines and immune systems of rats fed the genetically modified potatoes.
Soybean agglutinin, Glycine max. Soybean agglutinins (SBA) also known as soy bean lectins (SBL) are lectins found in soybeans. It is a family of similar legume lectins. As a lectin, it is an antinutrient that chelates minerals.
The primary form is caused by excessive cell proliferation of B lymphocytes, characterized by clonal lymphoproliferative disorder. Primary cold agglutinin disease occurs after the fifth decade of life and peaks prevalence in a person's 70s and 80s.
While motility measurements are critical for identifying the presence of hyperactive motility, additional methods have been developed to identify the occurrence of the acrosome reaction. A simple method uses Coomassie brilliant blue G250 to stain cells, providing visual evidence of intact or reacted acrosomes. More advanced techniques employ fluorescent or electron microscopy methods. Fluorescein-conjugated Peanut agglutinin (FITC-PNA) or Pisum sativum agglutinin (FITC-PSA) can be used to fluorescently tag the acrosome of sperm cells, which can be then used to assess the status of the acrosome using a fluorescent microscope.
Kusaba, T., Kurume Med. J., 45, 113-120, 1998. # Tumor vascularity and lens culinaris agglutinin reactive alpha-fetoprotein are predictors of long-term prognosis in patients with hepatocellular carcinoma after percutaneous ethanol injection therapy. Fukuda, H., Kurume Med.
For instance, Ulex europaeus agglutinin-1 (UEA-1), a plant-extracted lectin capable of binding to human blood type O antigen, can also bind to unrelated glycans such as 2'-fucosyllactose, GalNAcα1-4(Fucα1-2)Galβ1-4GlcNAc, and Lewis-Y antigen.
J. Gastroenterol. Hepatol. 11, 1387-1392, 1999. # A simultaneous monitoring of lens culinaris agglutinin A-reactive alpha-fetoprotein and des-gamma-carboxy prothrombin as an early diagnosis of hepatocellular carcinoma in the follow-up of cirrhotic patients. Shimauchi, Y., et al.
The conjugation was confirmed by liquid chromatography- electrospray ionisation-mass spectrometry (LC-ESI-MS) and lectin blot with the GlcNAc-binding wheat germ agglutinin attached to AlexaFluor 647. Having successfully introduced GlcNAc, the monomer was extended with a glycan structure containing GlcNAc, mannose (Man) and galactose (Gal) (Fig. 3C). A mutant endoglycosidase EndoS (EndoS-D233Q) was utilised as it is highly specific for IgG Fc N-linked GlcNAc residues and does not elongate Asn-GlcNAc sites on other proteins or on denatured IgGs. Product formation was again monitored by LC-ESI-MS and lectin blot probing with the sialic acid-binding sambucus nigra agglutinin attached to fluorescein isothiocyanate.
Creatinine is occasionally elevated and electrolytes are occasionally abnormal. A high blood calcium level is noted in approximately 4% of patients. The LDH level is frequently elevated, indicating the extent of Waldenström macroglobulinemia–related tissue involvement. Rheumatoid factor, cryoglobulins, direct antiglobulin test and cold agglutinin titre results can be positive.
For those who fail to respond or have recurrent disease, splenectomy may be considered. Other options for recurrent or relapsed disease include immunosuppressants such as rituximab, danazol, cyclophosphamide, azathioprine, or cyclosporine. Cold agglutinin disease is treated with avoidance of cold exposure. Patients with more severe disease (symptomatic anemia, transfusion dependence) may be treated with rituximab.
Cold hemagglutination was first reported by Landsteiner in 1903Landsteiner K. Über Beziehungen zwischen dem Blutserum und den Körperzellen. Münchener medizinische Wochenschrift. 1903;50:1812–1814. and found to occur in human beings in 1918.Clough MC, Richter IM. A study of an auto-agglutinin occurring in human serum. Johns Hopkins Hosp Bull. 1918;29:86–93.
Cold sensitive antibodies (CSA) are antibodies sensitive to cold temperature. Some cold sensitive antibodies are pathological and can lead to blood disorder. These pathological cold sensitive antibodies include cold agglutinins, Donath-Landsteniner antibodies, and cryoglobulins which are the culprits of cold agglutinin disease, paroxysmal cold hemoglobinuria in the process of Donath-Landsteiner hemolytic anemia, and vasculitis, respectively.
"Pyrosequencing Reveals a Highly Diverse and Cultivar-Specific Bacterial Endophyte Community in Potato Roots." Microbial Ecology 60(1): 157-166Zhang, J., et al. (2012). "Isolation and characterization of plant growth-promoting rhizobacteria from wheat roots by wheat germ agglutinin labeled with fluorescein isothiocyanate." The Journal of Microbiology 50(2): 191-198Haichar, F. e. Z., et al. (2008).
When mycoparasites get attachment of mycohost, they will recognize each other. It is indicated that the recognition between mycoparasites and their host fungi is related to the agglutinin on the cell surface of the mycohost. The carbohydrate residues on the cell wall of mycoparasites could specifically bind to the lectins on the surface of the host fungi to achieve mutual recognition.
Antibodies to cysticerci can be demonstrated in serum by enzyme linked immunoelectrotransfer blot (EITB) assay and in CSF by ELISA. An immunoblot assay using lentil-lectin (agglutinin from Lens culinaris) is highly sensitive and specific. However, individuals with intracranial lesions and calcifications may be seronegative. In the CDC's immunoblot assay, cysticercosis-specific antibodies can react with structural glycoprotein antigens from the larval cysts of Taenia solium.
Specifically, he acts like Wilson. Wilson later notes that mirror patients always mirror the most dominant person in the room, which means that Wilson was more dominant than House. House explains that as a consequence of the fact that Wilson was in charge of the surgery. House notices that the patient's blood thickens dangerously when his body temperature drops (cold agglutinin disease), something that cannot be faked.
Also, Foreman is troubled by his discovery that Thirteen is on a placebo, and consults with Chase about surreptitiously switching her to the real thing. Chase tells him that this is unwise. Tests revealed no structural heart defects, and after some deliberations the possibility of cold agglutinin disease is raised. House wants to give the patient an ice bath to confirm, and goes to Cameron again.
Warm antibody autoimmune hemolytic anemia (WAIHA) is the most common form of autoimmune haemolytic anemia. About half of the cases are of unknown cause, with the other half attributable to a predisposing condition or medications being taken. Contrary to cold autoimmune hemolytic anemia (e.g., cold agglutinin disease and paroxysmal cold hemoglobinuria) which happens in cold temperature (28–31 °C), WAIHA happens at body temperature.
The experimental potatoes had been transformed with the Galanthus nivalis agglutinin (GNA) gene from the Galanthus (snowdrop) plant, allowing the GNA lectin protein to be synthesised. This lectin is toxic to some insects. Rats were fed raw and cooked genetically modified potatoes, using unmodified Desiree Red potatoes as controls. One control group ate an unmodified Desiree Red potato spiked with the GNA snowdrop lectin.
In most cases, the diagnosis is based on evidence of hemolytic anemia (from symptoms and/or blood tests). A person may also be physically examined for spleen or liver enlargement. An antiglobulin test (called the Coombs test) may be performed to determine the presence of a specific type of antibody. In people with cold agglutinin disease, the Coomb's test is almost always positive for immunoglobulin M (IgM).
Cases may also arise with complement alone or with IgA, IgM or a combination of these three antibody classes and complement. Cold-type AIHA usually reacts with antisera to complement and occasionally to the above antibodies. This is the case in both cold agglutinin disease and cold paroxysmal hematuria. In general, mixed warm and cold AIHA shows a positive reaction to IgG and complement, sometimes IgG alone, and sometimes complement alone.
Two bacteriologists, Herbert Edward Durham (-1945) and Max von Gruber (1853–1927), discovered specific agglutination in 1896. The clumping became known as Gruber-Durham reaction. Gruber introduced the term agglutinin (from the Latin) for any substance that caused agglutination of cells. French physician Fernand Widal (1862–1929) put Gruber and Durham's discovery to practical use later in 1896, using the reaction as the basis for a test for typhoid fever.
Lectin affinity chromatography is a form of affinity chromatography where lectins are used to separate components within the sample. Lectins, such as concanavalin A are proteins which can bind specific alpha-D-mannose and alpha- D-glucose carbohydrate molecules. Some common carbohydrate molecules that is used in lectin affinity chromatography are Con A-Sepharose and WGA-agarose. Another example of a lectin is wheat germ agglutinin which binds D-N-acetyl- glucosamine.
Mycoplasma pneumoniae is a very small bacterium in the class Mollicutes. It is a human pathogen that causes the disease mycoplasma pneumonia, a form of atypical bacterial pneumonia related to cold agglutinin disease. M. pneumoniae is characterized by the absence of a peptidoglycan cell wall and resulting resistance to many antibacterial agents. The persistence of M. pneumoniae infections even after treatment is associated with its ability to mimic host cell surface composition.
The rate of erythrocyte production by the bone marrow is lower than the rate of destruction, thus, individuals with cold agglutinin disease develop a form of anemia. A body might produce agglutinins to attack the erythrocytes due to allergies to foods, inhalants, chemicals and infections. A person suffering from this condition will likely have cooler body parts such as fingers, nose, and ears attacked more often than warmer areas such as armpits .
In cross-matching, donor red blood cells and the recipient's serum or plasma are incubated together. If agglutination occurs, this indicates that the donor and recipient blood types are incompatible. When a person produces antibodies against their own red blood cells, as in cold agglutinin disease and other autoimmune conditions, the cells may agglutinate spontaneously. This is called autoagglutination and it can interfere with laboratory tests such as blood typing and the complete blood count.
At this time though the chemical nature of what exactly in the blood conferred this protection was not known. In a few decades to follow, it was shown that the protective serum could neutralize and precipitate toxins, and clump bacteria. All these functions were attributed to different substances in the serum, and named accordingly as antitoxin, precipitin and agglutinin. That all the three substances were one entity (gamma globulins) was demonstrated by Elvin A. Kabat in 1939.
In research, calcofluor-white is also used to stain bud scars of yeast cells because the bud scars have a higher content of chitin, which stains them more than the rest of the cell membrane. Due to this stain it is possible to count the bud scars which is an indication for the age of the cell. It shows similar staining patterns as Wheat Germ Agglutinin (WGA). It is especially useful for the identification of Mucor and the causative agents of zygomycosis.
Modern wheat cultivation, by breeding for high ATI content, may play a role in the onset and course of disorders such as celiac disease and gluten sensitivity. However, it has been questioned whether there is sufficient empirical evidence to support this claim, because as of 2018 we lack studies that directly compare modern wheat versus ancient cultivars with low ATI content (such as einkorn wheat) in people with NCGS. Wheat germ agglutinin is also considered to be a possible trigger of NCGS-like symptoms.
However, studies revealed the existence of a few cases of WAIHA that may also carry cold agglutinin antibodies that are active at the environment where the temperatures is generally equal to or warmer than 30 °C (86 °F). Such coexistence suggests a diagnosis of the mixed (warm- and cold-antibody) autoimmune hemolytic anemia abbreviated as MAIHA. Mixed warm and cold AIHA runs a chronic course with severe intermittent exacerbations, such as serious anemia, and is treated by blood transfusion. Successful therapeutic options for the treatment of hemolysis associated with mixed AIHA are limited but increasing.
Because of the way automated analysers count blood cells, a very high MCHC (greater than about 370 g/L) may indicate the blood is from someone with a cold agglutinin, or there may be some other problem resulting in one or more artifactual results affecting the MCHC. For example, for some patients with cold agglutinins, when their blood gets colder than 37 °C, the red cells will clump together. As a result, the analyzer may incorrectly report a low number of very dense red blood cells. This will result in an impossibly high number when the analyzer calculates the MCHC.
The study began in April 2016 and is estimated to conclude in September 2017. The study is currently recruiting participants from U.S. states including Arizona, California, D.C., Massachusetts, New York, North Carolina, and Texas. Subjects must have had a diagnosis of primary or secondary warm antibody AIHA, and must have failed at least 1 prior treatment regimen for AIHA. Subjects cannot have a platelet count less than 30,000/μL, have AIHA secondary to autoimmune disease, have uncontrolled or poorly controlled hypertension, or have cold antibody AIHA, cold agglutinin syndrome, mixed type AIHA, or paroxysmal cold hemoglobinuria.
There is also a group of tracers that consist of protein products that can be taken up by the cell and transported across the synapse into the next cell. Wheat-germ agglutinin (WGA) and Phaseolus vulgaris leucoagglutinin are the most well known tracers, however they are not strict anterograde tracers: especially WGA is known to be transported anterogradely as well as retrogradely. WGA enters the cell by binding to Oligosaccharides, and is then taken up via endocytosis via a caveolae-dependent pathway. Other anterograde tracers widely used in neuroanatomy are the biotinylated dextran amines (BDA), also used in retrograde tracing.
Detection of antibodies (cold or warm) and /or complement system on RBC from the patient is a direct Coombs antiglobulin test. Detection of antibodies in serum of the patient (still circulating in the blood, that have not yet formed any complexes with RBC) is an indirect Coombs antiglobulin test. A diagnosis of cold agglutinin disease may be made after several types of tests are performed by a health care provider. In some cases, the diagnosis is first suspected by chance if a routine complete blood count (CBC) detects abnormal clumping (agglutination) of the red blood cells.
In 1939, Phillip Levine and Rufus Stetson published in a first case report the clinical consequences of non-recognized Rh factor, hemolytic transfusion reaction, and hemolytic disease of the newborn in its most severe form. It was recognized that the serum of the reported woman agglutinated with red blood cells of about 80% of the people although the then known blood groups, in particular ABO were matched. No name was given to this agglutinin when described. In 1940, Karl Landsteiner and Alexander S. Wiener made the connection to their earlier discovery, reporting a serum that also reacted with about 85% of different human red blood cells.
In oncology, AFP-L3 is an isoform of Alpha-fetoprotein (AFP), a substance typically used in the triple test during pregnancy and for screening chronic liver disease patients for hepatocellular carcinoma (HCC). AFP can be fractionated by affinity electrophoresis into 3 glycoforms: L1, L2, and L3 based on the reactivity with the lectin Lens culinaris agglutinin (LCA). AFP-L3 binds strongly to LCA via an additional α 1-6 fucose residue attached at the reducing terminus of N-acetylglucosamine; this is in contrast to the L1 isoform. It is the L1 isoform which is typically associated with non-HCC inflammation of liver disease condition.
Treatment varies based on the severity of the condition, the symptoms present in each person and the underlying cause. At least 90% of cases having cryoglobulins in body, hepatitis C is to blame, reflecting the importance of preclusion of hepatitis C. The presence of cryoglubulins in body satisfies the criterion of the diagnosis of cryoglobulinemia, a disease that inflame the blood vessels and organs like kidney, nerves, joints, lungs and skin. Normally, there are no cryoglobulins should be found in the body. Cryoglobulins more than often do not interact with red blood cells, unless it combines the features of cold agglutinin with cryoglobulins, although the chance is deemed rare.
All individuals have circulating antibodies directed against red blood cells, but their concentrations are often too low to trigger disease (titers under 64 at 4 °C). In individuals with cold agglutinin disease, these antibodies are in much higher concentrations (titers over 1000 at 4 °C). At body temperatures of 28–31 °C, such as those encountered during winter months, and occasionally at body temperatures of 37 °C, antibodies (generally IgM) bind to the polysaccharide region of glycoproteins on the surface of red blood cells (typically the I antigen, i antigen, and Pr antigens). Binding of antibodies to red blood cells activates the classical pathway of the complement system.
It is clear that each cell type contributes to different features of IgM malignancies but not clear that clonal plasma cells are critical to the development or progression of IgM MGUS. In all events, IgM MGUS is diagnosed in individuals who have serum IgM levels less than 30 gram/liter; have less than 10% of nucleated bone marrow cells with the lymphoplasmacytic morphology, and have no symptoms or findings of end organ dysfunction attributed to Waldenström's macroglobulinemia such as anemia, decreases in any white blood cell count, cold agglutinin disease, hyperviscosity of blood, lymphadenopathy, hepatomegaly, splenomegaly, peripheral neuropathy, cryoglobulinemia, or constitutional symptoms. There may be a modest increase in the incidence of IgM MGUS in people of African descent.
This problem is usually picked up by the laboratory before the result is reported. The blood can be warmed until the cells separate from each other, and quickly put through the machine while still warm. There are four steps to perform when a suspect increased MCHC (>370 g/L or >37.0 g/dL) is received from the analyzer: # Remix the EDTA tube—if the MCHC corrects, report corrected results # Incubation at 37 °C—if the MCHC corrects, report corrected results and comment on possible cold agglutinin # Saline replacement: Replace plasma with same amount of saline to exclude interference e.g. Lipemia and Auto-immune antibodies—if the MCHC corrects, report corrected results and comment on Lipemia # Check the slide for spherocytosis (e.g.
Some of the red blood cells are agglutinated, while others are not, making it difficult to interpret the result. This is called a mixed field reaction, and it can occur if someone has recently received a blood transfusion with a different blood type (as in a type A patient receiving type O blood), if they have received a bone marrow or stem cell transplant from someone with a different blood type, or in patients with certain ABO subgroups, such as A3. Investigation of the person's medical history can clarify the cause of the mixed field reaction. People with cold agglutinin disease produce antibodies against their own red blood cells that cause them to spontaneously agglutinate at room temperature, leading to false positive reactions in forward grouping.
Cold agglutinin disease (CAD) is a rare autoimmune disease characterized by the presence of high concentrations of circulating cold sensitive antibodies, usually IgM and autoantibodies that are also active at temperatures below , directed against red blood cells, causing them to agglutinate and undergo lysis. It is a form of autoimmune hemolytic anemia, specifically one in which antibodies bind red blood cells only at low body temperatures, typically 28–31 °C. When affected people's blood is exposed to cold temperatures ( to ), certain proteins that normally attack bacteria (IgM antibodies) attach themselves to red blood cells and bind them together into clumps (agglutination). This eventually causes red blood cells to be prematurely destroyed (hemolysis) leading to anemia and other associated signs and symptoms.
Smoldering Waldenström's macroglobulinemia is diagnosed in asymptomatic individuals that have a serum IgM level 30 gram/liter and/or a bone marrow lymphoplasmacytoid cell infilatrate >10% of total nucleated cells. These cases should have no symptoms or findings of end organ dysfunction attributed to Waldenström's macroglobulinemia such as anemia, decreases in any white blood cell count, cold agglutinin disease, hyperviscosity of blood, lymphadenopathy, hepatomegaly, splenomegaly, peripheral neuropathy, cryoglobulinemia, or constitutional symptoms. As determined by a Mayo Clinic study of 48 individuals, smoldering Waldenström's macroglobulinemia's risk of progression to Waldenström's macroglobulinemia is estimated to be ~12% per year and then falling of sharply for at least the next 5 years to 2% per year. In this study the only factor predictive of a more rapid progress was a finding of anemia (hemoglobin level <115 grams/liter).
Scytovirin is a 95-amino acid antiviral protein isolated from the cyanobacteria Scytonema varium. It has been cultured in E. coli and its structure investigated in detail. Scytovirin is thought to be produced by the bacteria to protect itself from viruses that might otherwise attack it, but as it has broad-spectrum antiviral activity against a range of enveloped viruses, scytovirin has also been found to be useful against a range of major human pathogens, most notably HIV / AIDS but also including SARS coronavirus and filoviruses such as Ebola virus and Marburg virus. While some lectins such as cyanovirin and Urtica dioica agglutinin are thought likely to be too allergenic to be used internally in humans, studies so far on scytovirin and griffithsin have not shown a similar level of immunogenicity.
A modified Désirée potato was developed in the 1990s by biochemist John Gatehouse at Cambridge Agricultural Genetics (later renamed Axis Genetics) and had gone through two years of field trials at Rothamsted Experimental Station.Arpad Pusztai GM Food Safety: Scientific and Institutional Issues Science as Culture, Volume 11 Number 1 March 2002 The potatoes were modified to express the Galanthus nivalis agglutinin (GNA) gene from the Galanthus (snowdrop) plant, which caused them to produce GNA lectin protein that is toxic to some insects. This variety of potatoes is the one which was involved in the Pusztai affair. In 2014, a team of British scientists published a paper about three- year field trial showing that another genetically modified version of the Désirée cultivar can resist infection after exposure to late blight, one of the most serious diseases of potatoes.
The rostral cingulate gyrus (Brodmanns's area 32) projects to the rostral superior temporal gyrus, midorbitofrontal cortex and lateral prefrontal cortex. The ventral anterior cingulate (Brodmann's area 24) sends projections to the anterior insular cortex, premotor cortex (Brodmann's area 6), Brodmann's area 8, the perirhinal area, the orbitofrontal cortex (Brodmann's area 12), the laterobasal nucleus of amygdala, and the rostral part of the inferior parietal lobule. Injecting wheat germ agglutinin and horseradish peroxidase conjugate into the anterior cingulate gyrus of cats, revealed that the anterior cingulate gyrus has reciprocal connections with the rostral part of the thalamic posterior lateral nucleus and rostral end of the pulvinar. The postsubiculum receives projections from the retrospleinal dysgranular cortex and the retrosplenial granular cortex A and B. The parasubiculum receives projections from the retrosplenial dysgranular cortex and retrosplenial granular cortex A. Caudal and lateral parts of the entorhinal cortex get projections from the retrosplenial dysgranular cortex, while the caudal medial entorhinal cortex receives projections from the retrosplenial granular cortex A. The retrosplenial dysgranular cortex sends projections to the perirhinal cortex.

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