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Question: How are thalassemias classified?

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Context 1: Thalassaemia minor | definition of Thalassaemia minor by Medical dictionary
Thalassaemia minor | definition of Thalassaemia minor by Medical dictionary
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Related to Thalassaemia minor: thalassaemia major
Thalassemia describes a group of inherited disorders characterized by reduced or absent amounts of hemoglobin, the oxygen-carrying protein inside the red blood cells  There are two basic groups of thalassemia disorders: alpha thalassemia and beta thalassemia  These conditions cause varying degrees of anemia, which can range from insignificant to life threatening 
All types of thalassemias are considered quantitative diseases of hemoglobin, because the quantity of hemoglobin produced is reduced or absent  Usual adult hemoglobin is made up of three components: alpha globin, beta globin, and heme  Thalassemias are classified according to the globin that is affected, hence the names alpha and beta thalassemia  Although both classes of thalassemia affect the same protein, the alpha and beta thalassemias are distinct diseases that affect the body in different ways 
Beta thalassemia may be the most best-known type of thalassemia and is also called Cooley's anemia  It is caused by a change in the gene for the beta globin component of hemoglobin  Beta thalassemia causes variable anemia that can range from moderate to severe, depending in part on the exact genetic change underlying the disease  Beta thalassemia can be classified based on clinical symptoms  Beta thalassemia major usually causes severe anemia that can occur within months after birth  If left untreated, severe anemia can result in insufficient growth and development, as well as other common physical complications that can lead to a dramatically decreased life-expectancy  Fortunately, in developed countries beta thalassemia is usually identified by screening in the newborn period, before symptoms have developed  Children who are identified early can be started on ongoing blood transfusion therapy as needed  Although transfusion therapy prevents many of the complications of severe anemia, the body is unable to eliminate the excess iron contained in the transfused blood  Over time, the excess iron deposits in tissues and organs, resulting in damage and organ failure  Another medication must be administered to help the body eliminate the excess iron and prevent iron-over-load complications  Beta thalassemia intermedia describes the disease in individuals who have moderate anemia that only requires blood transfusions intermittently, if at all 
Alpha thalassemia is the result of changes in the genes for the alpha globin component of hemoglobin  There are two main types of alpha thalassemia disease: hemoglobin H disease and alpha thalassemia major  The two diseases are quite different from beta thalassemia as well as from one another  Individuals with hemoglobin H disease can experience events of hemolytic anemia—anemia caused by the rapid breakdown of the red blood cells  These events are thought to be triggered by various environmental causes, such as infection and/or exposure to certain chemicals  Hemoglobin H disease is in most cases milder than beta thalassemia  It does not generally require transfusion therapy  Alpha thalassemia major is a very serious disease that results in severe anemia that begins even before birth  Most affected babies do not survive to be born or die shortly after birth 
The thalassemias are among the most common genetic diseases worldwide  Both alpha and beta thalassemia have been described in individuals of almost every ancestry, but the conditions are more common among certain ethnic groups  Unaffected carriers of all types of thalassemia traits do not experience health problems  In fact, the thalassemia trait is protective against malaria, a disease caused by blood-borne parasites transmitted through mosquito bites  According to a widely accepted theory, most genetic changes—mutations—that cause thalassemia occurred multiple generations ago  Coincidentally, these mutations increased the likelihood that carriers would survive malaria infection  Survivors passed the mutation onto their offspring, and the trait became established throughout areas where malaria is common  As populations migrated, so did the thalassemia traits 
Beta thalassemia trait is seen most commonly in people with the following ancestry: Mediterranean (including North African, and particularly Italian and Greek), Middle Eastern, Indian, African, Chinese, and Southeast Asian (including Vietnamese, Laotian, Thai, Singaporean, Filipino, Cambodian, Malaysian, Burmese, and Indonesian)  Alpha-thalassemia trait is seen with increased frequency in the same ethnic groups  However, there are different types of alpha thalassemia traits within these populations  The frequency of hemoglobin H disease and alpha thalassemia major depends on the type of alpha thalassemia trait  The populations in which alpha thalassemia diseases are most common include Southeast Asians and Chinese (particularly Southern Chinese) 
It is difficult to obtain accurate prevalence figures for various types of thalassemia within different populations  This difficulty arises due to testing limitations in determining exact genetic diagnoses, as well as the fact that many studies have focused on small, biased hospital populations 
Two studies reflect prevalence figures that can be helpful counseling families and determining who to screen for beta thalassemia  Between the years of 1990 and 1996, the State of California screened more than 3 1 million infants born in the state for beta thalassemia  Approximately 1 in 114,000 infants had beta thalassemia major, with prevalence rates being highest among Asian Indians (about one in 4,000), Southeast Asians (about one in 10,000), and Middle Easterners (about one in 7,000)  Another type of beta thalassemia disease, E/beta thalassemia, was represented in approximately one in 110,000 births, all of which occurred in families of Southeast Asian ancestry  Among Southeast Asians, the prevalence of E/beta thalassemia was approximately one in 2,600 births  This is in keeping with the observation that hemoglobin E trait carrier rates are relatively high within the Southeast Asian population: 16% in a study of 768 immigrants to California, and up to 25% in some specific Southeast Asian populations such as Cambodians  While these California studies address some of the limitations of earlier population studies, the pattern observed in California is expected to be different in other areas of the United States and the world  For example, Italians are underrepresented in this population when compared to the population of the East Coast of the United States 
Determining prevalence figures for alpha thalassemia is even more difficult due to increased limitations in diagnostic testing  All types of alpha thalassemia disease are most common among people of Southeast Asian and Chinese descent, for reasons that become clearer with an understanding of the underlying genetics of alpha thalassemia  One study of 500 pregnant women in Northern Thailand estimated a frequency of one in 500 pregnancies affected by alpha thalassemia major, for example  Prevalence of alpha thalassemia disease is significantly lower in the United States primarily because of immigration patterns; although at least one state, California, has observed growing hemoglobin H disease incidence rates that are high enough to justify universal newborn screening for the condition 
Humans normally make several types of the oxygen-carrying protein hemoglobin  An individual's stage in development determines whether he or she makes primarily embryonic, fetal, or adult hemoglobins  All types of hemoglobin are made of three components: heme, alpha (or alpha-like) globin, and beta (or beta-like) globin  All types of thalassemia are caused by changes in either the alpha- or beta-globin gene  These changes cause little or no globin to be produced  The thalassemias are, therefore, considered quantitative hemoglobin diseases  All types of thalassemias are recessively inherited, meaning that a genetic change must be inherited from both the mother and the father  The severity of the disease is influenced by the exact thalassemia mutations inherited, as well as other genetic and environmental factors  There are rare exceptions, notably with beta thalassemia, where globin gene mutations exhibit a dominant pattern of inheritance in which only one gene needs to be altered in order to see disease expression  Scientists continue to study the causes  For instance, a new mutation for alpha-thalassemia was discovered for the first time among Iranian patients in 2004 
BETA-THALASSEMIA  Most individuals have two normal copies of the beta globin gene, which is located on chromosome 11 and makes the beta globin component of normal adult hemoglobin, hemoglobin A  There are approximately 100 genetic mutations that have been described that cause beta thalassemia, designated as either beta0 or beta + mutations  No beta globin is produced with a beta0 mutation, and only a small fraction of the normal amount of beta globin is produced with a beta + mutation 
When an individual has one normal beta globin gene and one with a beta thalassemia mutation, he or she is said to carry the beta thalassemia trait  Beta thalassemia trait, like other hemoglobin traits, is protective against malaria infection  Trait status is generally thought not to cause health problems, although some women with beta thalassemia trait may have an increased tendency toward anemia during pregnancy 
When two members of a couple carry the beta thalassemia trait, there is a 25% chance that each of their children will inherit beta thalassemia disease by inheriting two beta thalassemia mutations, one from each parent  The clinical severity of the beta thalassemia disease—whether an individual has beta thalassemia intermedia or beta thalassemia major—will depend largely on whether the mutations inherited are beta0 thalassemia or beta + thalassemia mutations  Two beta0 mutations generally lead to beta thalassemia major, and two beta+ thalassemia mutations generally lead to beta thalassemia intermedia  Inheritance of one beta0 and one beta + thalassemia mutation tends to be less predictable 
Although relatively uncommon, there are other thalassemia-like mutations that can affect the beta globin gene  Hemoglobin E is the result of a substitution of a single nucleotide  This change results in a structurally altered hemoglobin that is produced in decreased amounts  Therefore, hemoglobin E is unique in that it is both a quantitative (i e  thalassemia-like) and qualitative trait  When co-inherited with a beta thalassemia trait, it causes a disease that is almost indistinguishable from beta thalassemia disease  Large deletions around and including the beta globin gene can lead to delta/beta thalassemia or hereditary persistence of fetal hemoglobin (HPFH)  Interestingly, delta/beta thalassemia trait behaves very similarly to beta thalassemia trait in its clinical manifestations  However, HPFH trait does not tend to cause hemoglobin disease when co-inherited with a second thalassemia or other beta globin mutation 
ALPHA-THALASSEMIA  Most individuals have four normal copies of the alpha globin gene, two copies on each chromosome 16  These genes make the alpha globin component of normal adult hemoglobin, which is called hemoglobin A  Alpha globin is also a component of fetal hemoglobin and the other major adult hemoglobin called hemoglobin A2  Mutations of the alpha globin genes are usually deletions of the gene, resulting in absent production of alpha globin  Since there are four genes (instead of the usual two) to consider when looking at alpha globin gene inheritance, there are several alpha globin types that are possible 
Absence of one alpha globin gene leads to a condition known as silent alpha thalassemia trait  This condition causes no health problems and can be detected only by special genetic testing  Alpha thalassemia trait occurs when two alpha globin genes are missing  This can occur in two ways  The genes may be deleted from the same chromosome, causing the 'cis' type of alpha thalassemia trait  Alternately, they may be deleted from different chromosomes, causing the 'trans' type of alpha thalassemia trait  In both instances, there are no associated health problems, although the trait status may be detected by more routine blood screening 
Hemoglobin H disease results from the deletion of three alpha globin genes, such that there is only one functioning gene  Typically, this can occur when one parent carries the silent alpha thalassemia trait, and the other parent carries the 'cis' type of the alpha thalassemia trait  In this situation, there is a 25% chance for hemoglobin H disease in each of such a couple's children 
Hemoglobin H disease-like symptoms can also be a part of a unique condition called alpha thalassemia mental retardation syndrome  Alpha thalassemia mental retardation syndrome can be caused by a deletion of a significant amount of chromosome 16, affecting the alpha globin genes  This is usually not inherited, but rather occurs sporadically in the affected individual  Affected individuals have mild hemoglobin H disease, mild-to-moderate mental retardation, and characteristic facial features  This syndrome can also occur as a sex-linked form in which a mutation is inherited in a particular gene on the X-chromosome  This gene influences alpha globin production, as well as various other developmental processes  Individuals affected with this form of the syndrome tend to have more severe mental retardation, delayed development, nearly absent speech, characteristic facial features, and genital-urinary abnormalities  The remaining discussion will focus only on aspects of hemoglobin H disease 
Alpha thalassemia major results from the deletion of all four alpha globin genes, such that there are no functioning alpha globin genes  This can occur when both parents carry the 'cis' type of the alpha thalassemia trait  In this situation, there is a 25% chance for alpha thalassemia major in each of such a couple's children 
Beta thalassemia major is characterized by severe anemia that can begin months after birth  In the United States and other developed countries beta thalassemia is identified and treated early and effectively  Therefore, the following discussion of symptoms applies primarily to affected individuals in the past and unfortunately in some underdeveloped countries now  If untreated, beta thalassemia major can lead to severe lethargy, paleness, and delays in growth and development  The body attempts to compensate by producing more blood, which is made inside the bones in the marrow  However, this is ineffective without the needed genetic instructions to make enough functioning hemoglobin  Instead, obvious bone expansion and changes occur that cause characteristic facial and other changes in appearance, as well as increased risk of fractures  Severe anemia taxes other organs in the body—such as the heart, spleen, and liver—which must work harder than usual  This can lead to heart failure, as well as enlargement and other problems of the liver and spleen  When untreated, beta thalassemia major generally results in childhood death, usually due to heart failure  In 2004, the first known heart attack associated with beta thalassemia major was reported  Fortunately, in developed countries diagnosis is usually made early, often before symptoms have begun  This allows for treatment with blood transfusion therapy, which can prevent most of the complications of the severe anemia caused by beta thalassemia major  Individuals with beta thalassemia intermedia have a more moderate anemia that may only require treatment with transfusion intermittently, such as when infections occur and stress the body  As a person with beta thalassemia intermedia gets older, however, the need for blood transfusions may increase to the point that they are required on a regular basis  When this occurs their disease becomes more similar to beta thalassemia major  Other genetic and environmental factors can influence the course of the disease as well  For example, co-inheritance of one or two alpha thalassemia mutations can tend to ameliorate some of the symptoms of beta thalassemia disease, which result in part from an imbalance in the amount of alpha- and beta-globin present in the red blood cells 
Hemoglobin h disease
Absence of three alpha globin genes causes an imbalance of alpha and beta globin proteins in the red blood cells  The excess beta globin proteins tend to come together to form hemoglobin H, which is unable to release oxygen to the tissues  In addition, hemoglobin H tends to precipitate out in the cells, causing damage to the red blood cell membrane  When affected individuals are exposed to certain drugs and chemicals known to make the membrane more fragile, the cells are thought to become vulnerable to breakdown in large numbers, a complication called hemolytic anemia  Fever and infection are also considered to be triggers of hemolytic anemia in hemoglobin H disease  This can result in fatigue, paleness, and a yellow discoloration of the skin and whites of eyes called jaundice  Usually, the anemia is mild enough not to require treatment  Severe anemia events may require blood transfusion, however, and are usually accompanied by such other symptoms as dark feces or urine and abdominal or back pain  These events are uncommon in hemoglobin H disease, although they occur more frequently in a more serious type of hemoglobin H disease called hemoglobin H/Constant Spring disease  Individuals effected with this type of hemoglobin H disease are also more likely to have enlargement of and other problems with the spleen 
Alpha thalassemia major
Because alpha globin is a necessary component of all major hemoglobins and some minor hemoglobins, absence of all functioning alpha globin genes leads to serious medical consequences that begin even before birth  Affected fetuses develop severe anemia as early as the first trimester of pregnancy  The placenta, heart, liver, spleen, and adrenal glands may all become enlarged  Fluid can begin collecting throughout the body as early as the start of the second trimester, causing damage to developing tissues and organs  Growth retardation is also common  Affected fetuses usually miscarry or die shortly after birth  In addition, women carrying affected fetuses are at increased risk of developing complications of pregnancy and delivery  Up to 80% of such women develop toxemia, a disturbance of metabolism that can potentially lead to convulsions and coma  Other maternal complications include premature delivery and increased rates of delivery by cesarean section, as well as hemorrhage after delivery 
Thalassemia may be suspected if an individual shows signs that are suggestive of the disease  In all cases, however, laboratory diagnosis is essential to confirm the exact diagnosis and to allow for the provision of accurate genetic counseling about recurrence risks and testing options for parents and affected individuals  Screening is likewise recommended to determine trait status for individuals of high-risk ethnic groups 
The following tests are used to screen for thalassemia disease and/or trait:
hemoglobin electrophoresis with quantitative hemoglobin A2 and hemoglobin F
free erythrocyte-protoporphyrin (or ferritin or other studies of serum iron levels)
A complete blood count will identify low levels of hemoglobin, small red blood cells, and other red blood cell abnormalities that are characteristic of a thalassemia diagnosis  Since thalassemia trait can sometimes be difficult to distinguish from iron deficiency, tests to evaluate iron levels are important  A hemoglobin electrophoresis is a test that can help identify the types and quantities of hemoglobin made by an individual  This test uses an electric field applied across a slab of gel-like material  Hemoglobins migrate through this gel at various rates and to specific locations, depending on their size, shape, and electrical charge  Isoelectric focusing and high-performance liquid chromatography (HPLC) use similar principles to separate hemoglobins and can be used instead of or in various combinations with hemoglobin electrophoresis to determine the types and quantities of hemoglobin present  Hemoglobin electrophoresis results are usually within the normal range for all types of alpha thalassemia  However, hemoglobin A2 levels and sometimes hemoglobin F levels are elevated when beta thalassemia disease or trait is present  Hemoglobin electrophoresis can also detect structurally abnormal hemoglobins that may be co-inherited with a thalassemia trait to cause thalassemia disease (i e , hemoglobin E) or other types of hemoglobin disease (i e , sickle hemoglobin)  Sometimes DNA testing is needed in addition to the above screening tests  This can be performed to help confirm the diagnosis and establish the exact genetic type of thalassemia 
Diagnosis of thalassemia can occur under various circumstances and at various ages  Several states offer thalassemia screening as part of the usual battery of blood tests done for newborns  This allows for early identification and treatment  Thalassemia can be identified before birth through the use of prenatal diagnosis  Chorionic villus sampling (CVS) can be offered as early as 10 weeks of pregnancy and involves removing a sample of the placenta made by the baby and testing the cells  CVS carries a risk of causing a miscarriage that is between 0 5%-1%  Amniocentesis is generally offered between 15 and 22 weeks of pregnancy, but can sometimes be offered earlier  Two to three tablespoons of the fluid surrounding the baby is removed  This fluid contains fetal cells that can be tested  The risk of miscarriage associated with amniocentesis ranges from 0 33-0 5%  Pregnant woman and couples may choose prenatal testing in order to prepare for the birth of a baby that may have thalassemia  Alternately, knowing the diagnosis during pregnancy allows for the option of pregnancy termination  Preimplantation genetic diagnosis (PGD) is a relatively new technique that involves in-vitro fertilization followed by genetic testing of one cell from each developing embryo  Only the embryos unaffected by sickle cell disease are transferred back into the uterus  PGD is currently available on a research basis only and is relatively expensive 
Individuals with beta thalassemia major receive regular blood transfusions, usually on a monthly basis  This helps prevent severe anemia and allows for more normal growth and development  Transfusion therapy does have limitations, however  Individuals can develop reactions to certain proteins in the blood—called a transfusion reaction  This can make locating appropriately matched donor blood more difficult  Although blood supplies in the United States are very safe, particularly relative to the past and to other areas of the world, there remains an increased risk of exposure to such blood-borne infections as hepatitis  Additionally, the body is not able to get rid of the excess iron that accompanies each transfusion  An additional medication called desferoxamine is administered, usually five nights per week over a period of several hours, using an automatic pump that can be used during sleep or taken anywhere the person goes  This medication is able to bind to the excess iron, which can then be eliminated through urine  If desferoxamine is not used regularly or is unavailable, iron overload can develop and cause tissue damage and organ damage and failure  The heart, liver, and endocrine organs are particularly vulnerable  Desferoxamine itself may rarely produce allergic or toxic side effects, including hearing damage  Signs of desferoxamine toxicity are screened for and generally develop in individuals who overuse the medication when body iron levels are sufficiently low  Overall, however, transfusion and desferoxamine therapy have increased the life expectancy of individuals with the most severe types of beta thalassemia major to the 4th or 5th decade  This can be expected to improve with time and increased developments in treatment, as well as for those with more mild forms of the disease 
New treatments offer additional options for some individuals with beta thalassemia major  There are various medications that target the production of red blood cells (i e  erythropoeitin) or fetal hemoglobin (i e  hydroxyurea and butyrate)  Their effectiveness in ameliorating the severity of beta thalassemia is currently being investigated  Another promising new treatment is bone marrow transplantation, in which the bone marrow of an affected individual is replaced with the bone marrow of an unaffected donor  If successful, this treatment can provide a cure  However, there is an approximately 10-15% chance the procedure could be unsuccessful (i e  the thalassemia returns); result in complications (i e  graft-versus-host disease); or result in death  The risk for specific individuals depends on current health status, age, and other factors  Because of the risks involved and the fact that beta thalassemia is a treatable condition, transplant physicians require a brother or sister donor who has an identically matched tissue type, called HLA type  HLA type refers to the unique set of proteins present on each individual's cells, which allows the immune system to recognize "self" from "foreign " HLA type is genetically determined, so there is a 25% chance for two siblings to be a match  Transplant physicians and researchers are also investigating ways to improve the safety and effectiveness of bone marrow transplantation  Using newborn sibling umbilical cord blood—the blood from the placenta that is otherwise discarded after birth but contains cells that can go on to make bone marrow—seems to provide a safer and perhaps more effective source of donor cells  Donors and recipients may not have to be perfect HLA matches for a successful transplant using cord blood cells  Trials are also underway to determine the effectiveness of "partial transplants," in which a safer transplant procedure is used to replace only a percentage of the affected individual's bone marrow  Other possible treatments on the horizon may include gene therapy techniques aimed at increasing the amount of normal hemoglobin the body is able to make 
Hemoglobin H disease is a relatively mild form of thalassemia that may go unrecognized  It is not generally considered a condition that will reduce one's life expectancy  Education is an important part of managing the health of an individual with hemoglobin H disease  It is important to be able to recognize the signs of severe anemia that require medical attention  It is also important to be aware of the medications, chemicals, and other exposures to avoid due to the theoretical risk they pose of causing a severe anemia event  When severe anemia occurs, it is treated with blood transfusion therapy  For individuals with hemoglobin H disease, this is rarely required  For those with the hemoglobin H/Constant Spring form of the disease, the need for transfusions may be intermittent or ongoing, perhaps on a monthly basis and requiring desferoxamine treatment  Individuals with this more severe form of the disease may also have an increased chance of requiring removal of an enlarged and/or overactive spleen 
Anemia — A blood condition in which the level of hemoglobin or the number of red blood cells falls below normal values  Common symptoms include paleness, fatigue, and shortness of breath 
Bilirubin — A yellow pigment that is the end result of hemoglobin breakdown  This pigment is metabolized in the liver and excreted from the body through the bile  Bloodstream levels are normally low; however, extensive red cell destruction leads to excessive bilirubin formation and jaundice 
Bone marrow — A spongy tissue located in the hollow centers of certain bones, such as the skull and hip bones  Bone marrow is the site of blood cell generation 
Bone marrow transplantation — A medical procedure used to treat some diseases that arise from defective blood cell formation in the bone marrow  Healthy bone marrow is extracted from a donor to replace the marrow in an ailing individual  Proteins on the surface of bone marrow cells must be identical or very closely matched between a donor and the recipient 
Desferoxamine — The primary drug used in iron chelation therapy  It aids in counteracting the life-threatening buildup of iron in the body associated with long-term blood transfusions 
Globin — One of the component protein molecules found in hemoglobin  Normal adult hemoglobin has a pair each of alpha-globin and beta-globin molecules 
Heme — The iron-containing molecule in hemoglobin that serves as the site for oxygen binding 
Hemoglobin — Protein-iron compound in the blood that carries oxygen to the cells and carries carbon dioxide away from the cells 
Hemoglobin A — Normal adult hemoglobin that contains a heme molecule, two alpha-globin molecules, and two beta-globin molecules 
Hemoglobin electrophoresis — A laboratory test that separates molecules based on their size, shape, or electrical charge 
Hepatomegaly — An abnormally large liver 
HLA type — Refers to the unique set of proteins called human leukocyte antigens  These proteins are present on each individual's cell and allow the immune system to recognize 'self' from 'foreign'  HLA type is particularly important in organ and tissue transplantation 
Hydroxyurea — A drug that has been shown to induce production of fetal hemoglobin  Fetal hemoglobin has a pair of gamma-globin molecules in place of the typical beta-globins of adult hemoglobin  Higher-than-normal levels of fetal hemoglobin can ameliorate some of the symptoms of thalassemia 
Iron overload — A side effect of frequent blood transfusions in which the body accumulates abnormally high levels of iron  Iron deposits can form in organs, particularly the heart, and cause life-threatening damage 
Jaundice — Yellowing of the skin or eyes due to excess of bilirubin in the blood 
Mutation — A permanent change in the genetic material that may alter a trait or characteristic of an individual, or manifest as disease, and can be transmitted to offspring 
Placenta — The organ responsible for oxygen and nutrition exchange between a pregnant mother and her developing baby 
Red blood cell — Hemoglobin-containing blood cells that transport oxygen from the lungs to tissues  In the tissues, the red blood cells exchange their oxygen for carbon dioxide, which is brought back to the lungs to be exhaled 
Screening — Process through which carriers of a trait may be identified within a population 
Splenomegaly — Enlargement of the spleen 
Because alpha thalassemia major is most often a condition that is fatal in the prenatal or newborn period, treatment has previously been focused on identifying affected pregnancies in order to provide appropriate management to reduce potential maternal complications  Pregnancy termination provides one form of management  Increased prenatal surveillance and early treatment of maternal complications is an approach that is appropriate for mothers who wish to continue their pregnancy with the knowledge that the baby will most likely not survive  In recent years, there have been a handful of infants with this condition who have survived long-term  Most of these infants received experimental treatment including transfusions before birth, early delivery, and even bone marrow transplantation before birth, although the latter procedure has not yet been successful  For those infants that survive to delivery, there seems to be an increased risk of developmental problems and physical effects, particularly heart and genital malformations  Otherwise, their medical outlook is similar to a child with beta thalassemia major, with the important exception that ongoing, life-long blood transfusions begin right at birth 
As discussed above, the prognosis for individuals with the most serious types of thalassemia has improved drastically in the last several years following recent medical advances in transfusion, chemo-, and transplantation therapy  Advances continue and promise to improve the life expectancy and quality of life further for affected individuals 
"First Known Heart Attack Associated With Beta-thalassemia Major Reported " Heart Disease Weekly February 22, 2004: 10 
"Novel Alpha-thalassemia Mutations Identified " Hematology Week January 26, 2004: 19 
Children's Blood Foundation  333 East 38th St , Room 830, New York, NY 10016-2745  (212) 297-4336  cfg@nyh med cornell edu 
Cooley's Anemia Foundation, Inc  129-09 26th Ave  #203, Flushing, NY 11354  (800) 522-7222 or (718) 321-2873  http://www thalassemia org 
March of Dimes Birth Defects Foundation  1275 Mamaroneck Ave , White Plains, NY 10605  (888) 663-4637  resourcecenter@modimes org  http://www modimes org 
National Heart, Lung, and Blood Institute  PO Box 30105, Bethseda, MD 20824-0105  (301) 592-8573  nhlbiinfo@rover nhlbi nih gov  http://www nhlbi nih gov 
National Organization for Rare Disorders (NORD)  PO Box 8923, New Fairfield, CT 06812-8923  (203) 746-6518 or (800) 999-6673  Fax: (203) 746-6481  http://www rarediseases org 
Bojanowski J  "Alpha Thalassemia Major: The Possibility of Long-Term Survival " Pamphlet from the Northern California Comprehensive Thalassemia Center  (1999) 
Children's Hospital Oakland, Northern California Comprehensive Thalassemia Center website  http://www thalassemia com 
Cooley's Anemia Foundation, Inc  website  http://www thalassemia org/gohome html 
Joint Center for Sickle Cell and Thalassemic Disorders website  http://cancer mgh harvard edu/medOnc/sickle htm 
[thal″ah-se´me-ah]
a heterogeneous group of hereditary hemolytic anemias marked by a decreased rate of synthesis of one or more hemoglobin polypeptide chains, classified according to the chain involved (α, β, δ); the two major categories are α- and β-thalassemia 
α-thalassemia (alpha-thalassemia) that caused by diminished synthesis of alpha chains of hemoglobin  The homozygous form is incompatible with life, the stillborn infant displaying severe hydrops fetalis  The heterozygous form may be asymptomatic or marked by mild anemia 
β-thalassemia (beta-thalassemia) that caused by diminished synthesis of beta chains of hemoglobin  The homozygous form is called t  major and the heterozygous form is called t  minor 
thalassemia ma´jor the homozygous form of β-thalassemia, in which hemoglobin A is completely absent; it appears in the newborn period and is marked by hemolytic, hypochromic, microcytic anemia; hepatosplenomegaly; skeletal deformation; mongoloid facies; and cardiac enlargement 
thalassemia mi´nor the heterozygous form of β-thalassemia; it is usually asymptomatic, but there may be mild anemia 
sickle cell–thalassemia a hereditary anemia involving simultaneous heterozygosity for hemoglobin S and thalassemia 
thal·as·se·mi·a
, thalassanemia (thal'ă-sē'mē-ă, thă-las-ă-nē'mē-ă),
Any of a group of inherited disorders of hemoglobin metabolism in which there is impaired synthesis of one or more of the polypeptide chains of globin; several genetic types exist, and the corresponding clinical picture may vary from barely detectable hematologic abnormality to severe and fatal anemia 
[G  thalassa, the sea, + haima, blood]
/thal·as·se·mia/ (thal″ah-se´me-ah) a heterogeneous group of hereditary hemolytic anemias marked by a decreased rate of synthesis of one or more hemoglobin polypeptide chains, classified according to the chain involved (α, β, δ); the two major categories are α- and β-thalassemia 
α-thalassemia that caused by diminished synthesis of alpha chains of hemoglobin  The homozygous form is incompatible with life, the stillborn infant displaying severe hydrops fetalis  The heterozygous form may be asymptomatic or marked by mild anemia 
β-thalassemia that caused by diminished synthesis of beta chains of hemoglobin  The homozygous form is called t  major and the heterozygous form is called t  minor 
thalassemia ma´jor the homozygous form of &#x03B2;, in which hemoglobin A is completely absent; it appears in the newborn period and is marked by hemolytic, hypochromic, microcytic anemia, hepatosplenomegaly, skeletal deformation, mongoloid facies, and cardiac enlargement 
thalassemia mi´nor the heterozygous form of &#x03B2;, usually asymptomatic, although there is sometimes mild anemia 
(thăl′ə-sē′mē-ə)
An inherited form of anemia occurring chiefly among people of Mediterranean descent, caused by faulty synthesis of part of the hemoglobin molecule  Also called Mediterranean anemia 
thal′as·se′mic adj 
[thal′əsē′mē·ə]
Etymology: Gk, thalassa, sea, a + haima, without blood
production and hemolytic anemia characterized by microcytic, hypochromic red blood cells  Thalassemia is caused by inherited deficiency of alpha- or beta-globin synthesis  See also hemochromatosis, hemosiderosis 
Beta thalassemia, clinical thalassemia, Cooley's anemia, Mediterranean anemia, thalassemia major Hematology A group of genetic diseases by underproduction of hemoglobin due to mutations in the beta globin gene, which is more common in Mediterraneans Heredity Parents are carriers–heterozygotes; one in 4 children is homozygous for the mutation and thus has full-blown disease Clinical See Anemia  Cf Sickle cell anemia 
α-thalassemia
Hemoglobin Barts Hematology An inherited condition caused by a defect in the synthesis of the Hb α chain; Hb Barts hemoglobinopathy is characterized by the presence of 4 gamma chains; it is more common in southeast Asians; the most severe form of alpha thalassemia causes stillbirth due to hydrops fetalis Heredity Parents are carriers–heterozygotes; one in 4 children is homozygous for the mutation and thus has full-blown disease Clinical Pallor, fatiguability, FTT, fever, infections, diarrhea Management Transfusions
Thalassemia major Hematology A hemoglobinopathy caused by a defect in the synthesis of Hb β chain Clinical Pallor, fatigability, FTT, fever due to infections, diarrhea, bone deformities, hepatosplenomegaly Management Transfusions, but iron overload can damage the heart, liver, and endocrine systems, ergo iron chelation–early use of deferiprone, deferoxamine ↓ transfusion-related iron overload and may protect against DM, cardiac disease, early death
δ-thalassemia
Hematology A condition characterized by a defect of Hb A2–α2δ2; because Hb A2 comprises only 3% of the circulating Hb, even its complete absence; δ-thalassemia has little clinical or hematologic impact
γ-thalassemia
Hematology A condition characterized by a defect of gamma–γ Hb chains found in Hb F–α2γ2; because Hb F is present primarily in the fetus and newborns, it is rarely seen outside of the neonatal period, but may cause transient neonatal hemolytic anemia 
, thalassanemia (thal'ă-sē'mē-ă, -ă-să-nē'mē-ă)
Any of a group of inherited disorders of hemoglobin metabolism in which there is impaired synthesis of one or more of the polypeptide chains of globin; several genetic types exist, and the corresponding clinical picture may vary from barely detectable hematologic abnormality to severe and fatal anemia  People of Mediterranean, extraction are more often affected than others by this type of anemia 
Synonym(s): thalassaemia, thalassanaemia 
Any of a group of inherited disorders of hemoglobin metabolism with impaired synthesis of one or more polypeptide chains of globin; several genetic types exist 
<a href="https://medical-dictionary thefreedictionary com/Thalassaemia+minor">thalassemia</a>
Barts hemoglobin
beta hemoglobinopathy
beta-delta thalassemia
beta-thalassaemia
Bite Cell
black gallstone
I know of a couple, totally unrelated and unbeknownst to them, who are silent carriers of Thalassaemia minor 
Pakistan: Genetic factor: All in the genes
But, unfortunately, when one person with thalassaemia minor carrier happens to marry another with the same diagnosis, there is a strong possibility that their child would be thalassaemia major, as happened in the case of Taneja 
' My life depends upon a monthly blood transfusion '
0] thalassaemia demonstrates variable severity, ranging from a condition similar to [beta] thalassaemia minor to something approaching thalassaemia major 
A retrospective review of homozygous haemoglobin E patients
Thal, Alan P 
thalame
thalamencephalic
thalamencephalon
thalamic
thalamic fasciculus
thalamic nucleus
thalamic pain syndrome
thalamic peduncle
thalamic radiation
thalamo-
thalamocoele
thalamocortical
thalamocortical fibers
thalamogeniculate artery
thalamolenticular
thalamoperforating artery
thalamostriate radiation
thalamotuberal artery
Thalassaemia minor
thalassaemiaor Cooley's disease
thalassemic facies
thalasso-
Thalassobacter
Thalassobacter utilis
thalassoplankton
thalassoposia
thalidomide neuropathy
Thalidomider
thallium poisoning
Thalarctos
THALAS
Thalasaemia
Thalassaemia Association of Malaysia
thalassaemia major
Thalassaemias
thalassaemic
thalassanaemia
Thalassemia Action Group
Thalassemia Clinical Research Network
thalassemia syndrome
Context 2: \section{Introduction}\label{S1}

The multiple access interferences (MAI) is the root of user
limitation in CDMA systems \cite{R1,R3}  The parallel least mean
square-partial parallel interference cancelation (PLMS-PPIC) method
is a multiuser detector for code division multiple access (CDMA)
receivers which reduces the effect of MAI in bit detection  In this
method and similar to its former versions like LMS-PPIC \cite{R5}
(see also \cite{RR5}), a weighted value of the MAI of other users is
subtracted before making the decision for a specific user in
different stages \cite{cohpaper}  In both of these methods, the
normalized least mean square (NLMS) algorithm is engaged
\cite{Haykin96}  The $m^{\rm th}$ element of the weight vector in
each stage is the true transmitted binary value of the $m^{\rm th}$
user divided by its hard estimate value from the previous stage  The
magnitude of all weight elements in all stages are equal to unity 
Unlike the LMS-PPIC, the PLMS-PPIC method tries to keep this
property in each iteration by using a set of NLMS algorithms with
different step-sizes instead of one NLMS algorithm used in LMS-PPIC 
In each iteration, the parameter estimate of the NLMS algorithm is
chosen whose element magnitudes of cancelation weight estimate have
the best match with unity  In PLMS-PPIC implementation it is assumed
that the receiver knows the phases of all user channels  However in
practice, these phases are not known and should be estimated  In
this paper we improve the PLMS-PPIC procedure \cite{cohpaper} in
such a way that when there is only a partial information of the
channel phases, this modified version simultaneously estimates the
phases and the cancelation weights  The partial information is the
quarter of each channel phase in $(0,2\pi)$ 

The rest of the paper is organized as follows: In section \ref{S4}
the modified version of PLMS-PPIC with capability of channel phase
estimation is introduced  In section \ref{S5} some simulation
examples illustrate the results of the proposed method  Finally the
paper is concluded in section \ref{S6} 

\section{Multistage Parallel Interference Cancelation: Modified PLMS-PPIC Method}\label{S4}

We assume $M$ users synchronously send their symbols
$\alpha_1,\alpha_2,\cdots,\alpha_M$ via a base-band CDMA
transmission system where $\alpha_m\in\{-1,1\}$  The $m^{th}$ user
has its own code $p_m( )$ of length $N$, where $p_m(n)\in \{-1,1\}$,
for all $n$  It means that for each symbol $N$ bits are transmitted
by each user and the processing gain is equal to $N$  At the
receiver we assume that perfect power control scheme is applied 
Without loss of generality, we also assume that the power gains of
all channels are equal to unity and users' channels do not change
during each symbol transmission (it can change from one symbol
transmission to the next one) and the channel phase $\phi_m$ of
$m^{th}$ user is unknown for all $m=1,2,\cdots,M$ (see
\cite{cohpaper} for coherent transmission)  According to the above
assumptions the received signal is
\begin{equation}
\label{e1} r(n)=\sum\limits_{m=1}^{M}\alpha_m
e^{j\phi_m}p_m(n)+v(n),~~~~n=1,2,\cdots,N,
\end{equation}
where $v(n)$ is the additive white Gaussian noise with zero mean and
variance $\sigma^2$  Multistage parallel interference cancelation
method uses $\alpha^{s-1}_1,\alpha^{s-1}_2,\cdots,\alpha^{s-1}_M$,
the bit estimates outputs of the previous stage, $s-1$, to estimate
the related MAI of each user  It then subtracts it from the received
signal $r(n)$ and makes a new decision on each user variable
individually to make a new variable set
$\alpha^{s}_1,\alpha^{s}_2,\cdots,\alpha^{s}_M$ for the current
stage $s$  Usually the variable set of the first stage (stage $0$)
is the output of a conventional detector  The output of the last
stage is considered as the final estimate of transmitted bits  In
the following we explain the structure of a modified version of the
PLMS-PIC method \cite{cohpaper} with simultaneous capability of
estimating the cancelation weights and the channel phases 

Assume $\alpha_m^{(s-1)}\in\{-1,1\}$ is a given estimate of
$\alpha_m$ from stage $s-1$  Define
\begin{equation}
\label{e6} w^s_{m}=\frac{\alpha_m}{\alpha_m^{(s-1)}}e^{j\phi_m} 
\end{equation}
From (\ref{e1}) and (\ref{e6}) we have
\begin{equation}
\label{e7} r(n)=\sum\limits_{m=1}^{M}w^s_m\alpha^{(s-1)}_m
p_m(n)+v(n) 
\end{equation}
Define
\begin{subequations}
\begin{eqnarray}
\label{e8} W^s&=&[w^s_{1},w^s_{2},\cdots,w^s_{M}]^T,\\
\label{e9}
\!\!\!\!\!\!\!\!\!\!\!\!\!\!\!\!\!\!\!\!X^{s}(n)\!\!\!&=&\!\!\![\alpha^{(s-1)}_1p_1(n),\alpha^{(s-1)}_2p_2(n),\cdots,\alpha^{(s-1)}_Mp_M(n)]^T 
\end{eqnarray}
\end{subequations}
where $T$ stands for transposition  From equations (\ref{e7}),
(\ref{e8}) and (\ref{e9}), we have
\begin{equation}
\label{e10} r(n)=W^{s^T}X^{s}(n)+v(n) 
\end{equation}
Given the observations $\{r(n),X^{s}(n)\}^{N}_{n=1}$, in modified
PLMS-PPIC, like the PLMS-PPIC \cite{cohpaper}, a set of NLMS
adaptive algorithm are used to compute
\begin{equation}
\label{te1} W^{s}(N)=[w^{s}_1(N),w^{s}_2(N),\cdots,w^{s}_M(N)]^T,
\end{equation}
which is an estimate of $W^s$ after iteration $N$  To do so, from
(\ref{e6}), we have
\begin{equation}
\label{e13} |w^s_{m}|=1 ~~~m=1,2,\cdots,M,
\end{equation}
which is equivalent to
\begin{equation}
\label{e14} \sum\limits_{m=1}^{M}||w^s_{m}|-1|=0 
\end{equation}
We divide $\Psi=\left(0,1-\sqrt{\frac{M-1}{M}}\right]$, a sharp
range for $\mu$ (the step-size of the NLMS algorithm) given in
\cite{sg2005}, into $L$ subintervals and consider $L$ individual
step-sizes $\Theta=\{\mu_1,\mu_2,\cdots,\mu_L\}$, where
$\mu_1=\frac{1-\sqrt{\frac{M-1}{M}}}{L}, \mu_2=2\mu_1,\cdots$, and
$\mu_L=L\mu_1$  In each stage, $L$ individual NLMS algorithms are
executed ($\mu_l$ is the step-size of the $l^{th}$ algorithm)  In
stage $s$ and at iteration $n$, if
$W^{s}_k(n)=[w^s_{1,k},\cdots,w^s_{M,k}]^T$, the parameter estimate
of the $k^{\rm th}$ algorithm, minimizes our criteria, then it is
considered as the parameter estimate at time iteration $n$  In other
words if the next equation holds
\begin{equation}
\label{e17} W^s_k(n)=\arg\min\limits_{W^s_l(n)\in I_{W^s}
}\left\{\sum\limits_{m=1}^{M}||w^s_{m,l}(n)|-1|\right\},
\end{equation}
where $W^{s}_l(n)=W^{s}(n-1)+\mu_l \frac{X^s(n)}{\|X^s(n)\|^2}e(n),
~~~ l=1,2,\cdots,k,\cdots,L-1,L$ and
$I_{W^s}=\{W^s_1(n),\cdots,W^s_L(n)\}$, then we have
$W^s(n)=W^s_k(n)$, and therefore all other algorithms replace their
weight estimate by $W^{s}_k(n)$  At time instant $n=N$, this
procedure gives $W^s(N)$, the final estimate of $W^s$, as the true
parameter of stage $s$ 

Now consider $R=(0,2\pi)$ and divide it into four equal parts
$R_1=(0,\frac{\pi}{2})$, $R_2=(\frac{\pi}{2},\pi)$,
$R_3=(\pi,\frac{3\pi}{2})$ and $R_4=(\frac{3\pi}{2},2\pi)$  The
partial information of channel phases (given by the receiver) is in
a way that it shows each $\phi_m$ ($m=1,2,\cdots,M$) belongs to
which one of the four quarters $R_i,~i=1,2,3,4$  Assume
$W^{s}(N)=[w^{s}_1(N),w^{s}_2(N),\cdots,w^{s}_M(N)]^T$ is the weight
estimate of the modified algorithm PLMS-PPIC at time instant $N$ of
the stage $s$  From equation (\ref{e6}) we have
\begin{equation}
\label{tt3}
\phi_m=\angle({\frac{\alpha^{(s-1)}_m}{\alpha_m}w^s_m}) 
\end{equation}
We estimate $\phi_m$ by $\hat{\phi}^s_m$, where
\begin{equation}
\label{ee3}
\hat{\phi}^s_m=\angle{(\frac{\alpha^{(s-1)}_m}{\alpha_m}w^s_m(N))} 
\end{equation}
Because $\frac{\alpha^{(s-1)}_m}{\alpha_m}=1$ or $-1$, we have
\begin{eqnarray}
\hat{\phi}^s_m=\left\{\begin{array}{ll} \angle{w^s_m(N)} &
\mbox{if}~
\frac{\alpha^{(s-1)}_m}{\alpha_m}=1\\
\pm\pi+\angle{w^s_m(N)} & \mbox{if}~
\frac{\alpha^{(s-1)}_m}{\alpha_m}=-1\end{array}\right 
\end{eqnarray}
Hence $\hat{\phi}^s_m\in P^s=\{\angle{w^s_m(N)},
\angle{w^s_m(N)+\pi, \angle{w^s_m(N)}-\pi}\}$  If $w^s_m(N)$
sufficiently converges to its true value $w^s_m$, the same region
for $\hat{\phi}^s_m$ and $\phi_m$ is expected  In this case only one
of the three members of $P^s$ has the same region as $\phi_m$  For
example if $\phi_m \in (0,\frac{\pi}{2})$, then $\hat{\phi}^s_m \in
(0,\frac{\pi}{2})$ and therefore only $\angle{w^s_m(N)}$ or
$\angle{w^s_m(N)}+\pi$ or $\angle{w^s_m(N)}-\pi$ belongs to
$(0,\frac{\pi}{2})$  If, for example, $\angle{w^s_m(N)}+\pi$ is such
a member between all three members of $P^s$, it is the best
candidate for phase estimation  In other words,
\[\phi_m\approx\hat{\phi}^s_m=\angle{w^s_m(N)}+\pi \]
We admit that when there is a member of $P^s$ in the quarter of
$\phi_m$, then $w^s_m(N)$ converges  What would happen when non of
the members of $P^s$ has the same quarter as $\phi_m$? This
situation will happen when the absolute difference between $\angle
w^s_m(N)$ and $\phi_m$ is greater than $\pi$  It means that
$w^s_m(N)$ has not converged yet  In this case where we can not
count on $w^s_m(N)$, the expected value is the optimum choice for
the channel phase estimation, e g  if $\phi_m \in (0,\frac{\pi}{2})$
then $\frac{\pi}{4}$ is the estimation of the channel phase
$\phi_m$, or if $\phi_m \in (\frac{\pi}{2},\pi)$ then
$\frac{3\pi}{4}$ is the estimation of the channel phase $\phi_m$ 
The results of the above discussion are summarized in the next
equation
\begin{eqnarray}
\nonumber \hat{\phi}^s_m = \left\{\begin{array}{llll} \angle
{w^s_m(N)} & \mbox{if}~
\angle{w^s_m(N)}, \phi_m\in R_i,~~i=1,2,3,4\\
\angle{w^s_m(N)}+\pi & \mbox{if}~ \angle{w^s_m(N)}+\pi, \phi_m\in
R_i,~~i=1,2,3,4\\
\angle{w^n_m(N)}-\pi & \mbox{if}~ \angle{w^s_m(N)}-\pi, \phi_m\in
R_i,~~i=1,2,3,4\\
\frac{(i-1)\pi+i\pi}{4} & \mbox{if}~ \phi_m\in
R_i,~~\angle{w^s_m(N)},\angle
{w^s_m(N)}\pm\pi\notin R_i,~~i=1,2,3,4 \\
\end{array}\right 
\end{eqnarray}
Having an estimation of the channel phases, the rest of the proposed
method is given by estimating $\alpha^{s}_m$ as follows:
\begin{equation}
\label{tt4}
\alpha^{s}_m=\mbox{sign}\left\{\mbox{real}\left\{\sum\limits_{n=1}^{N}
q^s_m(n)e^{-j\hat{\phi}^s_m}p_m(n)\right\}\right\},
\end{equation}
where
\begin{equation} \label{tt5}
q^{s}_{m}(n)=r(n)-\sum\limits_{m^{'}=1,m^{'}\ne
m}^{M}w^{s}_{m^{'}}(N)\alpha^{(s-1)}_{m^{'}} p_{m^{'}}(n) 
\end{equation}
The inputs of the first stage $\{\alpha^{0}_m\}_{m=1}^M$ (needed for
computing $X^1(n)$) are given by
\begin{equation}
\label{qte5}
\alpha^{0}_m=\mbox{sign}\left\{\mbox{real}\left\{\sum\limits_{n=1}^{N}
r(n)e^{-j\hat{\phi}^0_m}p_m(n)\right\}\right\}



ground_truth: According to the globin that is affected (alpha or beta).

prompt_front: Now, answer the following question based on the text below, only give me the answer and do not output any other words.

Question: What algorithm is engaged in the PLMS-PPIC method?

Read the following text and answer briefly.

Context 2: 
\end{equation}
Assuming $\phi_m\in R_i$, then
\begin{equation}
\label{qqpp} \hat{\phi}^0_m =\frac{(i-1)\pi+i\pi}{4} 
\end{equation}
Table \ref{tab4} shows the structure of the modified PLMS-PPIC
method  It is to be notified that
\begin{itemize}
\item Equation (\ref{qte5}) shows the conventional bit detection
method when the receiver only knows the quarter of channel phase in
$(0,2\pi)$  \item With $L=1$ (i e  only one NLMS algorithm), the
modified PLMS-PPIC can be thought as a modified version of the
LMS-PPIC method 
\end{itemize}

In the following section some examples are given to illustrate the
effectiveness of the proposed method 

\section{Simulations}\label{S5}

In this section we have considered some simulation examples 
Examples \ref{ex2}-\ref{ex4} compare the conventional, the modified
LMS-PPIC and the modified PLMS-PPIC methods in three cases: balanced
channels, unbalanced channels and time varying channels  In all
examples, the receivers have only the quarter of each channel phase 
Example \ref{ex2} is given to compare the modified LMS-PPIC and the
PLMS-PPIC in the case of balanced channels 

\begin{example}{\it Balanced channels}:
\label{ex2}
\begin{table}
\caption{Channel phase estimate of the first user (example
\ref{ex2})} \label{tabex5} \centerline{{
\begin{tabular}{|c|c|c|c|c|}
\hline
\multirow{6}{*}{\rotatebox{90}{$\phi_m=\frac{3\pi}{8},M=15~~$}} & N(Iteration) & Stage Number& NLMS & PNLMS  \\
&&&&\\
\cline{2-5} & \multirow{2}{*}{64}& s = 2 &  $\hat{\phi}^s_m=\frac{3 24\pi}{8}$ & $\hat{\phi}^s_m=\frac{3 18\pi}{8}$ \\
\cline{3-5} & & s = 3 & $\hat{\phi}^s_m=\frac{3 24\pi}{8}$ & $\hat{\phi}^s_m=\frac{3 18\pi}{8}$ \\
\cline{2-5} & \multirow{2}{*}{256}& s = 2 &  $\hat{\phi}^s_m=\frac{2 85\pi}{8}$ & $\hat{\phi}^s_m=\frac{2 88\pi}{8}$ \\
\cline{3-5} & & s = 3 & $\hat{\phi}^s_m=\frac{2 85\pi}{8}$ & $\hat{\phi}^s_m=\frac{2 88\pi}{8}$ \\
\cline{2-5} \hline
\end{tabular} }}
\end{table}
Consider the system model (\ref{e7}) in which $M$ users
synchronously send their bits to the receiver through their
channels  It is assumed that each user's information consists of
codes of length $N$  It is also assumd that the signal to noise
ratio (SNR) is 0dB  In this example there is no power-unbalanced or
channel loss is assumed  The step-size of the NLMS algorithm in
modified LMS-PPIC method is $\mu=0 1(1-\sqrt{\frac{M-1}{M}})$ and
the set of step-sizes of the parallel NLMS algorithms in modified
PLMS-PPIC method are
$\Theta=\{0 01,0 05,0 1,0 2,\cdots,1\}(1-\sqrt{\frac{M-1}{M}})$,
i e  $\mu_1=0 01(1-\sqrt{\frac{M-1}{M}}),\cdots,
\mu_4=0 2(1-\sqrt{\frac{M-1}{M}}),\cdots,
\mu_{12}=(1-\sqrt{\frac{M-1}{M}})$  Figure~\ref{Figexp1NonCoh}
illustrates the bit error rate (BER) for the case of two stages and
for $N=64$ and $N=256$  Simulations also show that there is no
remarkable difference between results in two stage and three stage
scenarios  Table~\ref{tabex5} compares the average channel phase
estimate of the first user in each stage and over $10$ runs of
modified LMS-PPIC and PLMS-PPIC, when the the number of users is
$M=15$ 
\end{example}

Although LMS-PPIC and PLMS-PPIC, as well as their modified versions,
are structured based on the assumption of no near-far problem
(examples \ref{ex3} and \ref{ex4}), these methods and especially the
second one have remarkable performance in the cases of unbalanced
and/or time varying channels 

\begin{example}{\it Unbalanced channels}:
\label{ex3}
\begin{table}
\caption{Channel phase estimate of the first user (example
\ref{ex3})} \label{tabex6} \centerline{{
\begin{tabular}{|c|c|c|c|c|}
\hline
\multirow{6}{*}{\rotatebox{90}{$\phi_m=\frac{3\pi}{8},M=15~~$}} & N(Iteration) & Stage Number& NLMS & PNLMS  \\
&&&&\\
\cline{2-5} & \multirow{2}{*}{64}& s=2 &  $\hat{\phi}^s_m=\frac{2 45\pi}{8}$ & $\hat{\phi}^s_m=\frac{2 36\pi}{8}$ \\
\cline{3-5} & & s=3 & $\hat{\phi}^s_m=\frac{2 71\pi}{8}$ & $\hat{\phi}^s_m=\frac{2 80\pi}{8}$ \\
\cline{2-5} & \multirow{2}{*}{256}& s=2 &  $\hat{\phi}^s_m=\frac{3 09\pi}{8}$ & $\hat{\phi}^s_m=\frac{2 86\pi}{8}$ \\
\cline{3-5} & & s=3 & $\hat{\phi}^s_m=\frac{2 93\pi}{8}$ & $\hat{\phi}^s_m=\frac{3 01\pi}{8}$ \\
\cline{2-5} \hline
\end{tabular} }}
\end{table}
Consider example \ref{ex2} with power unbalanced and/or channel loss
in transmission system, i e  the true model at stage $s$ is
\begin{equation}
\label{ve7} r(n)=\sum\limits_{m=1}^{M}\beta_m
w^s_m\alpha^{(s-1)}_m c_m(n)+v(n),
\end{equation}
where $0<\beta_m\leq 1$ for all $1\leq m \leq M$  Both the LMS-PPIC
and the PLMS-PPIC methods assume the model (\ref{e7}), and their
estimations are based on observations $\{r(n),X^s(n)\}$, instead of
$\{r(n),\mathbf{G}X^s(n)\}$, where the channel gain matrix is
$\mathbf{G}=\mbox{diag}(\beta_1,\beta_2,\cdots,\beta_m)$  In this
case we repeat example \ref{ex2}  We randomly get each element of
$G$ from $[0,0 3]$  Figure~\ref{Figexp2NonCoh} illustrates the BER
versus the number of users  Table~\ref{tabex6} compares the channel
phase estimate of the first user in each stage and over $10$ runs of
modified LMS-PPIC and modified PLMS-PPIC for $M=15$ 
\end{example}

\begin{example}
\label{ex4} {\it Time varying channels}: Consider example \ref{ex2}
with time varying Rayleigh fading channels  In this case we assume
the maximum Doppler shift of $40$HZ, the three-tap
frequency-selective channel with delay vector of $\{2\times
10^{-6},2 5\times 10^{-6},3\times 10^{-6}\}$sec and gain vector of
$\{-5,-3,-10\}$dB  Figure~\ref{Figexp3NonCoh} shows the average BER
over all users versus $M$ and using two stages 
\end{example}


\section{Conclusion}\label{S6}

In this paper, parallel interference cancelation using adaptive
multistage structure and employing a set of NLMS algorithms with
different step-sizes is proposed, when just the quarter of the
channel phase of each user is known  In fact, the algorithm has been
proposed for coherent transmission with full information on channel
phases in \cite{cohpaper}  This paper is a modification on the
previously proposed algorithm  Simulation results show that the new
method has a remarkable performance for different scenarios
including Rayleigh fading channels even if the channel is
unbalanced 





ground_truth: The normalized least mean square (NLMS) algorithm.

prompt_front: Now, answer the following question based on the text below, only give me the answer and do not output any other words.

Question: When was McPherson County established as a county?

Read the following text and answer briefly.

Context 3: McPherson County (standard abbreviation: MP) is a county located in the U S  state of Kansas   As of the 2020 census, the county population was 30,223  The largest city and county seat is McPherson  The county is named for Civil War General James B  McPherson 

History

Early history

For many millennia, the Great Plains of North America was inhabited by nomadic Native Americans  From the 16th century to 18th century, the Kingdom of France claimed ownership of large parts of North America  In 1762, after the French and Indian War, France secretly ceded New France to Spain, per the Treaty of Fontainebleau  In 1802, Spain returned most of the land to France, but keeping title to about 7,500 square miles 

In 1803, most of the land for modern day Kansas was acquired by the United States from France as part of the 828,000 square mile Louisiana Purchase for 2 83 cents per acre  In 1848, after the Mexican–American War, the Treaty of Guadalupe Hidalgo with Spain brought into the United States all or part of land for ten future states, including southwest Kansas  In 1854, the Kansas Territory was organized, then in 1861 Kansas became the 34th U S  state 

19th century

From the 1820s to 1870s, the Santa Fe Trail passed through, what is now McPherson County  The trail entered the county, east of Canton, then south of Galva, then north of Inman, and west towards Lyons  In 1855, Charles O  Fuller established a ranch adjacent to the Running Turkey Creek Crossing about two miles south and one mile east of Galva  Fuller's Ranch provided accommodations for travelers on the Santa Fe Trail and was probably the first white settlement in McPherson County 

Peketon County was established in 1860, by the passage of a bill by S  N  Wood:  An act to establish Peketon County  Section 1  - That all that territory west of the sixth principal meridian and south of Township 16, in Kansas Territory, be and the same is hereby erected into a county, to be known by the name of Peketon County  On February 17, 1865, Peketon County was abolished, and McPherson County was made a part of Marion County, which extended from the west line of Chase County to the present western boundary of Kansas 

In 1868, Solomon Stephens and L  N  Holmberg were appointed Justices of the Peace—the first officers in what is now McPherson County  The next year (1869) occurred the first election for the township, now the county of McPherson  McPherson was regularly organized as a county in the spring of 1870, a mass meeting being held at Sweadal  Sweadal, the county seat thus selected, was located about one mile and a half southwest of the present site of Lindsborg  In September, however, the County Commissioners resolved to meet at the latter place, McPherson which had already been located some two years 

In April, 1873, a petition was filed for the county seat re-location  It was signed by 483 voters, and a special election was accordingly ordered for June 10  Upon that day, McPherson received 605 votes, New Gottland 325, King City 3 and Lindsborg 1; McPherson's majority over all, 276  In May the McPherson Town Company had offered, as an inducement for the location of the county seat at this point, the free use of rooms for ten years, and the donation of two squares of land on the town site  The offer was accepted the next month, the County Commissioners selecting blocks 56 and 65  Thus the county seat was established at McPherson and has remained since 

As early as 1875, city leaders of Marion held a meeting to consider a branch railroad from Florence  In 1878, Atchison, Topeka and Santa Fe Railway and parties from Marion County and McPherson County chartered the Marion and McPherson Railway Company   In 1879, a branch line was built from Florence to McPherson, in 1880 it was extended to Lyons, in 1881 it was extended to Ellinwood  The line was leased and operated by the Atchison, Topeka and Santa Fe Railway  The line from Florence to Marion, was abandoned in 1968  In 1992, the line from Marion to McPherson was sold to Central Kansas Railway  In 1993, after heavy flood damage, the line from Marion to McPherson was abandoned  The original branch line connected Florence, Marion, Canada, Hillsboro, Lehigh, Canton, Galva, McPherson, Conway, Windom, Little River, Mitchell, Lyons, Chase, then connected with the original AT&SF main line at Ellinwood 

In 1887, the Chicago, Kansas and Nebraska Railway extended its main line from Herington to Pratt   This main line connected Herington, Ramona, Tampa, Durham, Waldeck, Canton, Galva, McPherson, Groveland, Inman, Medora, Hutchinson, Whiteside, Partridge, Arlington,  Langdon, Turon, Preston, Natrona, Pratt   In 1888, this main line was extended to Liberal   Later, this line was extended to Tucumcari, New Mexico and Santa Rosa, New Mexico, where it made a connection with the Southern Pacific from El Paso, Texas   The Chicago, Kansas and Nebraska Railway was absorbed by the Chicago, Rock Island and Pacific Railway  This line is also called the "Golden State Route" 

20th century
The National Old Trails Road, also known as the Ocean-to-Ocean Highway, was established in 1912, and was routed through Windom, Conway, McPherson 

Geography

According to the U S  Census Bureau, the county has a total area of , of which  is land and  (0 3%) is water 

Adjacent counties
 Saline County (north)
 Dickinson County (northeast)
 Marion County (east)
 Harvey County (southeast)
 Reno County (southwest)
 Rice County (west)
 Ellsworth County (northwest)

Major highways
  Interstate 135
  U S  Route 56
  U S  Route 81
  K-4
  K-61
  K-153

Demographics

The McPherson Micropolitan Statistical Area includes all of McPherson County 

2000 census
As of the census of 2000, there were 29,554 people, 11,205 households, and 7,966 families residing in the county   The population density was 33 people per square mile (13/km2)   There were 11,830 housing units at an average density of 13 per square mile (5/km2)   The racial makeup of the county was 96 53% White, 0 81% Black or African American, 0 34% Native American, 0 32% Asian, 0 06% Pacific Islander, 0 79% from other races, and 1 16% from two or more races   1 94% of the population were Hispanic or Latino of any race  37 1% were of German, 12 9% Swedish, 12 1% American, 6 7% English and 6 3% Irish ancestry according to Census 2000 

There were 11,205 households, out of which 33 00% had children under the age of 18 living with them, 62 50% were married couples living together, 6 00% had a female householder with no husband present, and 28 90% were non-families  25 50% of all households were made up of individuals, and 11 80% had someone living alone who was 65 years of age or older   The average household size was 2 49 and the average family size was 2 99 

In the county, the population was spread out, with 25 40% under the age of 18, 10 30% from 18 to 24, 25 20% from 25 to 44, 21 80% from 45 to 64, and 17 30% who were 65 years of age or older   The median age was 38 years  For every 100 females there were 95 90 males   For every 100 females age 18 and over, there were 92 90 males 

The median income for a household in the county was $41,138, and the median income for a family was $48,243  Males had a median income of $33,530 versus $21,175 for females  The per capita income for the county was $18,921   About 4 20% of families and 6 60% of the population were below the poverty line, including 5 20% of those under age 18 and 8 10% of those age 65 or over 

Government

Presidential elections
McPherson county is often carried by Republican candidates  The last time a Democratic candidate has carried this county was in 1964 by Lyndon B  Johnson 

Laws
Following amendment to the Kansas Constitution in 1986, the county remained a prohibition, or "dry", county until 1996, when voters approved the sale of alcoholic liquor by the individual drink with a 30 percent food sales requirement 

Education

Colleges
 McPherson College in McPherson
 Bethany College in Lindsborg
 Central Christian College in McPherson

Unified school districts
 Smoky Valley USD 400
 McPherson USD 418
 Canton-Galva USD 419
 Moundridge USD 423
 Inman USD 448

School district office in neighboring county
 Goessel USD 411
 Little River-Windom USD 444

Museums
 Birger Sandzén Memorial Gallery in Lindsborg
 McCormick-Deering Days Museum in Inman
 McPherson Museum in McPherson
 Lindsborg Old Mill & Swedish Heritage Museum in Lindsborg
 Kansas Motorcycle Museum in Marquette

Communities

Cities

 Canton
 Galva
 Inman
 Lindsborg
 Marquette
 McPherson (county seat) 
 Moundridge
 Windom

Unincorporated communities
† means a Census-Designated Place (CDP) by the United States Census Bureau 
 Conway
 Elyria†
 Groveland
 Johnstown
 New Gottland
 Roxbury†

Ghost towns
 Alta Mills
 Battle Hill
 Christian
 Doles Park
 Elivon
 King City
 Sweadal

Townships
McPherson County is divided into twenty-five townships   The cities of Lindsborg and McPherson are considered governmentally independent and are excluded from the census figures for the townships   In the following table, the population center is the largest city (or cities) included in that township's population total, if it is of a significant size 

See also
 List of people from McPherson County, Kansas
 National Register of Historic Places listings in McPherson County, Kansas
 McPherson Valley Wetlands
 Maxwell Wildlife Refuge

References

Notes

Further reading

 Wheeler, Wayne Leland  "An Analysis of Social Change in a Swedish-Immigrant Community: The Case of Lindsborg, Kansas " (PhD dissertation, University of Missouri-Columbia; ProQuest Dissertations Publishing, 1959  5905657) 

County
 Through the Years: A Pictorial History of McPherson County; McPherson Sentinel' Heritage House Publishing Co; 1992 
 McPherson County First Courthouse Built About 1869 or 1870; Lindsborg News-Record; March 30, 1959 
 Pioneer Life and Lore of McPherson County, Kansas; Edna Nyquist; Democratic-Opinion Press; 1932 
 A History of the Church of the Brethren in Kansas (includes McPherson College history); Elmer LeRoy Craik; McPherson Daily; Republican Press; 397 pages; 1922 
 Portrait and Biographical Record of Dickinson, Saline, McPherson, and Marion Counties, Kansas; Chapman Bros; 614 pages; 1893 
 Standard Atlas of McPherson County, Kansas; Geo  A  Ogle & Co; 82 pages; 1921 
 Plat Book of McPherson County, Kansas; North West Publishing Co; 50 pages; 1903 
 Edwards' Atlas of McPherson County, Kansas; John P  Edwards; 51 pages; 1884 

Trails
 The Story of the Marking of the Santa Fe Trail by the Daughters of the American Revolution in Kansas and the State of Kansas; Almira Cordry; Crane Co; 164 pages; 1915  (Download 4MB PDF eBook)
 The National Old Trails Road To Southern California, Part 1 (LA to KC); Automobile Club Of Southern California; 64 pages; 1916  (Download 6 8MB PDF eBook)

Mennonite Settlements
 Impact of Mennonite settlement on the cultural landscape of Kansas; Brenda Martin; Kansas State University; 1985/1988  
 Mennonite settlement : the relationship between the physical and cultural environment; Susan Movle; University of Utah; 1975/1886 
 Status of Mennonite women in Kansas in their church and home relationships; Eva Harshbarger; Bluffton College; 1925/1945 

External links

County
 
 McPherson County - Directory of Public Officials
Historical
 , from Hatteberg's People'' on KAKE TV news
Maps
 McPherson County Maps: Current, Historic, KDOT
 Kansas Highway Maps: Current, Historic, KDOT
 Kansas Railroad Maps: Current, 1996, 1915, KDOT and Kansas Historical Society

 
Kansas counties
1867 establishments in Kansas
Populated places established in 1867



ground_truth: McPherson County was established as a county in 1867.