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: Where is McPherson County located?

Read the following text and answer briefly.

Context 1: 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




ground_truth: McPherson County is located in the U.S. state of Kansas.

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: How are thalassemias classified?

Read the following text and answer briefly.

Context 2: Thalassaemia minor | definition of Thalassaemia minor by Medical dictionary
Thalassaemia minor | definition of Thalassaemia minor by Medical dictionary
https://medical-dictionary thefreedictionary com/Thalassaemia+minor
(redirected from Thalassaemia minor)
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 3: A special tribute to Del Bigtree (pictured) and his team at ICAN for his stunning 88 page letter to the HHS regarding vaccine safety  As Del reported - in the latest edition of Highwire - the letter, in response to an earlier reply from the then acting Director National Vaccine Program Office, Melinda Wharton, took virtually a year to compile, and is a meticulous piece of research  Most sensationally they researched the HHS claim through US government archives that at least some pediatric vaccines had been trialed against genuine placebo, and came to a negative conclusion  Not only that, they established that none of the vaccines those vaccines had been trialed against had ever been trialed against genuine placebo either  At the end of the line the toxic products were only being compared with other toxic products, rather than against saline 
Leave aside the sceptics, for any believer in the vaccine program as a necessary intervention in public health, this should be a devastating finding  Fundamentally, the research into the safety of any of the products before marketing was simply not there  The manufacturers apparently had no faith that their proto-products could withstand this scrutiny, and for the rest they just did not care: under the alleged imperative of protecting the population it seems anything went  So even before all the sham monitoring procedures and reviews which Del and his team dismantle in forensic detail we are left with the proposition that none of the present products being given to US children – and frequently other children across most of the developed world – have any meaningful pre-marketing safety data all  If you are believer in the program you have been let down: if you wanted a program with any pretensions to safety - supposing such a thing to be possible - it looks like you would have to start from scratch  The manufacturers did this: the governments, the politicians and the regulators (internationally) let it happen 
This damning document is published simultaneously with a demand in the UK from the Royal Society for Public Health (which I had never heard of) to shut down comment about vaccines on the web  It echoes calls from Seth Berkley of GAVI, Heidi Larson of the Vaccine Confidence Project and the European Parliament  The pamphlet airily dismisses concerns that vaccines have side effects or that you could possibly have too many  It is pure public relations, and if the RSPH claims to be "independent" it also admits that the publication was paid for by Merck, a detail which was reported by British Medical Journal and the Guardian, but not true to form by the BBC  We have, in truth, been building to this moment for two decades: as the evidence piles up that every single aspect of the program lacks integrity or is simply rotten to the core all the perpetrators can do is call for the silencing of their critics, and maintain the products are safe because they say so 
Please help give the ICAN letter the widest possible distribution, particularly to politicians 
"The outcome of disease always depends both on the virulence of the pathogen and the health of the individual immune system "
Nope  This makes no sense  Lots of people who seemed vibrant will get a very severe case of the same illness that a vulnerable baby overcomes in a day 
And under the germ theory it doesn't matter how strong your immune system *was*  Once it's been overcome by the pathogen it is every bit as weak as anybody else's with that pathogen 
What you say makes no sense  There's no reason for me to reply to you again 
"Why do you think that within a few years (not many) of the introduction of the vaccines for them, pertussis, measles, mumps, rubella, tetanus, diphtheria, Hib disease, and chickenpox (and others) almost entirely disappeared?"
Why do you keep asking this question when I've already provided the answer hundreds of times? Why are you so desperate to believe the people who you already recognize are harming our children?
Why would Walter Reed be any more trustworthy than Paul Offit or Senator Pan? Why would Jenner or Pasteur?
And you went no way to explaining my arguments against germ theory  If we are attacked by billions of viruses every day then if even a tiny fraction of them are pathogenic then we couldn't possibly survive  And even if we could, we would already be immune rendering every vaccine pointless  Once we had survived our first few days on earth, then we could never get sick again 
If that's wrong then we must conclude that precisely 0% of germs are pathogenic 
Plus your comment about the immune system completely misunderstood my point  The immune system does not allow us to overcome our math problem  In fact, it makes it worse 
You did provide one solitary example of a patient with what are presumably yellow fever symptoms but you didn't say whether they had been given any toxic medical treatments 
And like I said before, the whole "incubation period" is more than a little suspicious  Clearly they never found what they thought they would and just rigged the results to tell them what they want to hear 
Like every other germ theorist/vaccine promoter in history 
Many kinds of bacteria are constantly evolving and changing, like flu viruses  Others are more stable over time, like the yellow fever virus  Those that change develop new ways of infiltrating the cells of the organism being attacked (from our point of view, from its unconscious point of view, it's just carrying out its need to replicate, which it can only do inside the cells of its host)  The changes which allow it to better infiltrate are more successful and result in more viruses with those traits 
Our immune system is designed to detect and destroy potentially dangerous invading pathogens  Many bacteria are usually harmless and absolutely necessary  The minority are dangerous, and most people's immune systems do a good job of analyzing them and killing them, often with no signs of disease  Others experience a clinical infection, and the immune system usually mounts a successful attack on them 
The outcome of disease always depends both on the virulence of the pathogen and the health of the individual immune system  Vaccines are usually effective in giving immunity to the targeted diseases  They also have many dangers which everyone should be aware of, and vaccines should be avoided whenever possible  But in the case of the most dangerous diseases, everyone should learn about them and think about what he wants to do to protect himself and his children from them, considering all the factors involved  And no one can have 100% certainty that he has made the right decision, but that's life  But if you live in the Congo and many people around you are currently dying of yellow fever, then that means that you yourself are at risk of being bitten by a loaded mosquito and getting, often dying, of yellow fever  The yellow fever vaccine is very effective at preventing yellow fever  From there, each person must make a choice 
At the end of this stage there is a remission of two or three days  About 80% of those with clinical disease recover at this point, with permanent immunity  The other 20% enter the toxic stage, with a return of the fever, black vomit (coffee-ground emesis), diarrhea, a slowing of the pulse (Faget's sign), jaundice, yellow eyes, yellow skin, and failure of the kidneys, liver, and heart  The patient gets a strange hiccup (like with Ebola, a related disease), falls into a coma, and dies  About half of those patients who enter the toxic stage dies, even now, even with the best of hospital care  The Faget's sign can also occur at the end of the first stage 
You asked specifically about the symptoms of the Americans on Dr  Reed's team who got yellow fever in Cuba in 1900  I'll give the passage from The American Plague (162-5), which describes the course of Jesse Lazear's illness  "In his logbook, Lazear wrote an unusual entry on September 13  In all cases before those, page after page of records, Lazear had used the soldier's name and simply the date he was bitten, with no other attention to the mosquito  A one-line entry with a name and a date  On that day, however, in his elegant hand, Lazear did not write the soldier's name, but instead wrote 'Guinea Pig No  1 ' He went on to write that this guinea pig had been bitten by a mosquito that developed from an egg laid by a mosquito that developed from an egg laid by a mosquito that fed on a number of yellow fever cases: Suarez, Hernández, De Long, Ferández  It was a precise, detailed history that proved beyond doubt that the mosquito was loaded with the virus when it bit a healthy soldier   (If he had entered his name, then his death would have been considered medical suicide by the insurance company, and his wife and two children would not have gotten any payment ) For the next few days, Lazear's life continued much as it had over the last few months in Cuba  He fed and cared for the mosquitoes in the lab    Then he began to lose his appetite  He skipped a few meals in the mess hall  He didn't mention it to anyone, nor did he ask to see one of the yellow fever doctors; instead, he worked hard in the lab trying to ignore the oncoming headache 
"On September 18, he complained of feeling 'out of sorts,' and stayed in his officer's quarters  His head pounded and L  decided to write a letter    (he wrote to his mother, and referred to his one-year old son Houston and the baby his wife Mabel was about to have: they were staying with his mother in the US)    That night, L  started to feel chilled as the fever came on  He never went to sleep but worked at his desk all through the night, trying to get all the information about the mosquitoes organized  By morning, he showed all the signs of a severe attack of yellow fever  The camp doctors made the diagnosis, and L  agreed to go to the yellow fever ward    L  was carried by litter out of the two-room, white pine board house in which he had lived since he and Mabel first arrived in Cuba    (In the yellow fever ward, in a separate one-room building), Lena Warner (the immune nurse who had survived the yellow fever in 1878, when she was nine, and was found in her boarded-up house by a former slave who first thought she was dead, and carried her to safety) nursed J L , recording his vitals  (I put up a link to his case record and vital signs last week  The surgeon general required that this record be made for every yellow fever patient )    (On September 25,) Lena Warner braced L's arms with all of her weight, shouting for help  Still he bolted from the bed, darting around the small frame-wood room as wildly as a trapped insect beating against glass  Two soldiers ran into the ward, pinning L to his bed, tying restraints around his wrists and elbows    Warner sponged his body with iced whiskey and water  She recorded his temperature, which had held at 104 degrees for days, on the chart beside his bed    (Warner watched him sleep ) But the quiet did not last  L's body began to lurch, and black vomit rolled from his mouth; through the bar hanging above his hospital cot  He writhed in the bed, and his skin grew deep yellow  His 104 temperature slowly fell, leveling out 99 degrees, and JL died at 8:45 p m  at the age of thirty-four "
As is obvious, there are many problems with vaccines  But, that being said, most of them usually work for a period of time to prevent the targeted diseases  The basic science behind vaccines is correct  Why do you think that within a few years (not many) of the introduction of the vaccines for them, pertussis, measles, mumps, rubella, tetanus, diphtheria, Hib disease, and chickenpox (and others) almost entirely disappeared? In the case of the routine childhood diseases, this was a bad thing, but it is a true thing 
Vaccines usually don't cause any obvious reactions  While they usually prevent the diseases, and that's why people continue to get them  With the increasing vaccination schedule, more and more are severely and permanently damaged, and it is immoral to mandate any vaccine for anyone for this reason  But it would also be immoral to prohibit vaccines for those who want them enough to take the risk 
Your article said as though it had any probative value that 90% of those who get pertussis had been vaxxed  The old DPT vaccine was MUCH more effective at preventing pertussis, but it was so dangerous (again, not to most, but to many), that developed countries replaced it with the acellular version, DTaP  From the beginning about twenty years ago, it was clear that it was not very effective and that huge numbers of vaxxed people got pertussis anyway, including my daughter who got pertussis at eight month old after having gotten three DTaPs  The pertussis vaccine continues to be very dangerous, and I do not recommend that anyone get it  It used to be a killer disease, but evolved to become much milder, to the extent that the disease is very rarely dangerous (usually only to newborns under three months old), while the vaccine is very dangerous  And they're trying to see how they can go back to the old DPT  This does not show that vaccine science has collapsed, but rather that the vaccine they developed to replace the DPT turned out to be much less effective than they first thought, while continuing to be much more dangerous than they first thought 
Your article extrapolated from that that modern medical science in general has collapsed, but that, again, is going too far  A older woman in Mexico City who is like my mother to me had a pacemaker inserted about two months ago to aid her failing heart, and it has restored her to optimism and energy, when she was despondent, weak, and close to death  I took my daughter to the dentist yesterday, who said she has three wisdom teeth coming in and that she said that the lower right one was sore  So, although I am cautious about X-rays, I made an appointment for a panoramic X-ray in a month to assess the wisdom teeth, and, if it seems appropriate, I'll take her to an oral surgeon to have one or more extracted under IV sedation, in his office, if possible (the dentist thought that it would be)  And I am confident that there will be no serious problems, but this is thanks to technology and training in modern medicine that haven't been available for that long 
I think that everyone should inform himself on all medical procedures before agreeing to anything, but I also think that he should have access to any medical procedure which is reasonable (and opinions can differ as to that) 
One problem is that you have not said how you think people should protect themselves against tetanus, bacterial meningitis, and yellow fever in the relevant cases, for example  These are diseases which healthy, well-nourished people used to die from very readily 
If most people stopped vaxxing and the mortality from these diseases rose to something like pre-vaccine levels, do you think they should just accept dying from them?
I put that in a separate paragraph because it is the crucial issue 
balinaheuchter Air Traffic Control You Tube - Colin Campbell example of - How to "Fudge a Nudge" -"Deal" or "No Deal" "Not in a month of Sundays" "No exceptions/no compromise?" -make a trade off -do an exception- everyone get's a good deal /good outcome!
Hans, you are right that we are looking at one of the biggest crimes in all history  When I read the story of that poor girl who was so healthy and is now confined to a wheelchair after getting her third Gardasil shot I could not believe that Merck could produce such a toxic vaccine and give it out to girls like it was something they absolutely had to have only to be mislead and made into cripples  Merck should be prosecuted for the damage they have done to so many girls who got the Gardasil vaccine and were physically debilitated for life  There is a place for the people who perpetrated this crime on young girls and women and it is called hell  They have destroyed people's lives and gotten away with it  My heart goes out to those who have suffered this damage for no damn good reason except to help make huge profits for Merck!
Here is the reason that the germ theory is nonsense 
1) Everyday we are bombarded with billions of germs  Presumably at least some of them are of the kind that germ theorists believe are dangerous (otherwise we would have to conclude that none of them are dangerous)  So how do we survive?
2) Let's just say that we ignore 1 and imagine that, by way of magic, none of the billions of viruses we get bombarded with are pathogenic but all those that are are tucked away somewhere  Ok  But presumably they reside in sick people right? So where are there lots of sick people? Doctor offices and hospitals! So everybody must be dying the moment they enter these places right?
3) I love this one because I have never seen anybody else ever raise it  Under the germ theory there are no negative feedbacks  This makes a stable biological system by definition impossible  The immune system is *not* a negative feedback it is the opposite  It actually reinforces our math problem because the immune system will weaken as the number of pathogens increase 
There is no way of resolving this problem without a discontinuity  A Deus ex Machina as The Almighty Pill so beautifully put it  So the germ theory is quite literally, mathematically impossible 
There is as much chance of it being true as 2+2 = 5 
There are plenty of other massive problems with germ theory such as why did things like SARS and bird flu magically disappear? Why do we have the symptoms that we do? Is our body controlling the symptoms to help fight the germs and if so, why would suppressing the symptoms with antibiotics or Tamiflu be considered a good idea? If the virus is causing the symptoms then why would it cause these kinds of things?



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 were the vaccines trialed against?

Read the following text and answer briefly.

Context 4: 
An electric circuit is an interconnection of electric components such that electric charge is made to flow along a closed path (a circuit), usually to perform some useful task 
Electric power is the rate at which electric energy is transferred by an electric circuit  The SI unit of power is the watt, one joule per second 
Electricity generation is often done with electric generators, but can also be supplied by chemical sources such as electric batteries or by other means from a wide variety of sources of energy  Electric power is generally supplied to businesses and homes by the electric power industry  Electricity is usually sold by the kilowatt hour (3 6 MJ) which is the product of power in kilowatts multiplied by running time in hours  Electric utilities measure power using electricity meters, which keep a running total of the electric energy delivered to a customer  Unlike fossil fuels, electricity is a low entropy form of energy and can be converted into motion or many other forms of energy with high efficiency 
Electronics deals with electrical circuits that involve active electrical components such as vacuum tubes, transistors, diodes, optoelectronics, sensors and integrated circuits, and associated passive interconnection technologies  The nonlinear behaviour of active components and their ability to control electron flows makes amplification of weak signals possible and electronics is widely used in information processing, telecommunications, and signal processing  The ability of electronic devices to act as switches makes digital information processing possible  Interconnection technologies such as circuit boards, electronics packaging technology, and other varied forms of communication infrastructure complete circuit functionality and transform the mixed components into a regular working system 
Today, most electronic devices use semiconductor components to perform electron control  The study of semiconductor devices and related technology is considered a branch of solid state physics, whereas the design and construction of electronic circuits to solve practical problems come under electronics engineering 
Thus, the work of many researchers enabled the use of electronics to convert signals into high frequency oscillating currents, and via suitably shaped conductors, electricity permits the transmission and reception of these signals via radio waves over very long distances 
Early 20th-century alternator made in Budapest, Hungary, in the power generating hall of a hydroelectric station (photograph by Prokudin-Gorsky, 1905–1915) 
In the 6th century BC, the Greek philosopher Thales of Miletus experimented with amber rods and these experiments were the first studies into the production of electrical energy  While this method, now known as the triboelectric effect, can lift light objects and generate sparks, it is extremely inefficient  It was not until the invention of the voltaic pile in the eighteenth century that a viable source of electricity became available  The voltaic pile, and its modern descendant, the electrical battery, store energy chemically and make it available on demand in the form of electrical energy  The battery is a versatile and very common power source which is ideally suited to many applications, but its energy storage is finite, and once discharged it must be disposed of or recharged  For large electrical demands electrical energy must be generated and transmitted continuously over conductive transmission lines 
Electrical power is usually generated by electro-mechanical generators driven by steam produced from fossil fuel combustion, or the heat released from nuclear reactions; or from other sources such as kinetic energy extracted from wind or flowing water  The modern steam turbine invented by Sir Charles Parsons in 1884 today generates about 80 percent of the electric power in the world using a variety of heat sources  Such generators bear no resemblance to Faraday's homopolar disc generator of 1831, but they still rely on his electromagnetic principle that a conductor linking a changing magnetic field induces a potential difference across its ends  The invention in the late nineteenth century of the transformer meant that electrical power could be transmitted more efficiently at a higher voltage but lower current  Efficient electrical transmission meant in turn that electricity could be generated at centralised power stations, where it benefited from economies of scale, and then be despatched relatively long distances to where it was needed 
Since electrical energy cannot easily be stored in quantities large enough to meet demands on a national scale, at all times exactly as much must be produced as is required  This requires electricity utilities to make careful predictions of their electrical loads, and maintain constant co-ordination with their power stations  A certain amount of generation must always be held in reserve to cushion an electrical grid against inevitable disturbances and losses 
Electricity is a very convenient way to transfer energy, and it has been adapted to a huge, and growing, number of uses  The invention of a practical incandescent light bulb in the 1870s led to lighting becoming one of the first publicly available applications of electrical power  Although electrification brought with it its own dangers, replacing the naked flames of gas lighting greatly reduced fire hazards within homes and factories  Public utilities were set up in many cities targeting the burgeoning market for electrical lighting  In the late 20th century and in modern times, the trend has started to flow in the direction of deregulation in the electrical power sector 
The resistive Joule heating effect employed in filament light bulbs also sees more direct use in electric heating  While this is versatile and controllable, it can be seen as wasteful, since most electrical generation has already required the production of heat at a power station  A number of countries, such as Denmark, have issued legislation restricting or banning the use of resistive electric heating in new buildings  Electricity is however still a highly practical energy source for heating and refrigeration, with air conditioning/heat pumps representing a growing sector for electricity demand for heating and cooling, the effects of which electricity utilities are increasingly obliged to accommodate 
Electricity is used within telecommunications, and indeed the electrical telegraph, demonstrated commercially in 1837 by Cooke and Wheatstone, was one of its earliest applications  With the construction of first intercontinental, and then transatlantic, telegraph systems in the 1860s, electricity had enabled communications in minutes across the globe  Optical fibre and satellite communication have taken a share of the market for communications systems, but electricity can be expected to remain an essential part of the process 
The effects of electromagnetism are most visibly employed in the electric motor, which provides a clean and efficient means of motive power  A stationary motor such as a winch is easily provided with a supply of power, but a motor that moves with its application, such as an electric vehicle, is obliged to either carry along a power source such as a battery, or to collect current from a sliding contact such as a pantograph  Electrically powered vehicles are used in public transportation, such as electric buses and trains, and an increasing number of battery-powered electric cars in private ownership 
Electronic devices make use of the transistor, perhaps one of the most important inventions of the twentieth century, and a fundamental building block of all modern circuitry  A modern integrated circuit may contain several billion miniaturised transistors in a region only a few centimetres square 
A voltage applied to a human body causes an electric current through the tissues, and although the relationship is non-linear, the greater the voltage, the greater the current  The threshold for perception varies with the supply frequency and with the path of the current, but is about 0 1 mA to 1 mA for mains-frequency electricity, though a current as low as a microamp can be detected as an electrovibration effect under certain conditions  If the current is sufficiently high, it will cause muscle contraction, fibrillation of the heart, and tissue burns  The lack of any visible sign that a conductor is electrified makes electricity a particular hazard  The pain caused by an electric shock can be intense, leading electricity at times to be employed as a method of torture  Death caused by an electric shock is referred to as electrocution  Electrocution is still the means of judicial execution in some jurisdictions, though its use has become rarer in recent times 
Electricity is not a human invention, and may be observed in several forms in nature, a prominent manifestation of which is lightning  Many interactions familiar at the macroscopic level, such as touch, friction or chemical bonding, are due to interactions between electric fields on the atomic scale  The Earth's magnetic field is thought to arise from a natural dynamo of circulating currents in the planet's core  Certain crystals, such as quartz, or even sugar, generate a potential difference across their faces when subjected to external pressure  This phenomenon is known as piezoelectricity, from the Greek piezein (πιέζειν), meaning to press, and was discovered in 1880 by Pierre and Jacques Curie  The effect is reciprocal, and when a piezoelectric material is subjected to an electric field, a small change in physical dimensions takes place 
§Bioelectrogenesis in microbial life is a prominent phenomenon in soils and sediment ecology resulting from anaerobic respiration  The microbial fuel cell mimics this ubiquitous natural phenomenon 
Some organisms, such as sharks, are able to detect and respond to changes in electric fields, an ability known as electroreception, while others, termed electrogenic, are able to generate voltages themselves to serve as a predatory or defensive weapon  The order Gymnotiformes, of which the best known example is the electric eel, detect or stun their prey via high voltages generated from modified muscle cells called electrocytes  All animals transmit information along their cell membranes with voltage pulses called action potentials, whose functions include communication by the nervous system between neurons and muscles  An electric shock stimulates this system, and causes muscles to contract  Action potentials are also responsible for coordinating activities in certain plants 
In the 19th and early 20th century, electricity was not part of the everyday life of many people, even in the industrialised Western world  The popular culture of the time accordingly often depicted it as a mysterious, quasi-magical force that can slay the living, revive the dead or otherwise bend the laws of nature  This attitude began with the 1771 experiments of Luigi Galvani in which the legs of dead frogs were shown to twitch on application of animal electricity  "Revitalization" or resuscitation of apparently dead or drowned persons was reported in the medical literature shortly after Galvani's work  These results were known to Mary Shelley when she authored Frankenstein (1819), although she does not name the method of revitalization of the monster  The revitalization of monsters with electricity later became a stock theme in horror films 
As the public familiarity with electricity as the lifeblood of the Second Industrial Revolution grew, its wielders were more often cast in a positive light, such as the workers who "finger death at their gloves' end as they piece and repiece the living wires" in Rudyard Kipling's 1907 poem Sons of Martha  Electrically powered vehicles of every sort featured large in adventure stories such as those of Jules Verne and the Tom Swift books  The masters of electricity, whether fictional or real—including scientists such as Thomas Edison, Charles Steinmetz or Nikola Tesla—were popularly conceived of as having wizard-like powers 
With electricity ceasing to be a novelty and becoming a necessity of everyday life in the later half of the 20th century, it required particular attention by popular culture only when it stops flowing, an event that usually signals disaster  The people who keep it flowing, such as the nameless hero of Jimmy Webb’s song "Wichita Lineman" (1968), are still often cast as heroic, wizard-like figures 
Ampère's circuital law, connects the direction of an electric current and its associated magnetic currents 
^ Diogenes Laertius  R D  Hicks (ed )  "Lives of Eminent Philosophers, Book 1 Chapter 1 "  Perseus Digital Library  Tufts University  Retrieved 5 February 2017  Aristotle and Hippias affirm that, arguing from the magnet and from amber, he attributed a soul or life even to inanimate objects 
^ Aristotle  Daniel C  Stevenson (ed )  "De Animus (On the Soul) Book 1 Part 2 (B4 verso)"  The Internet Classics Archive  Translated by J A  Smith  Retrieved 5 February 2017  Thales, too, to judge from what is recorded about him, seems to have held soul to be a motive force, since he said that the magnet has a soul in it because it moves the iron 
^ a b c Guarnieri, M  (2014)  "Electricity in the age of Enlightenment"  IEEE Industrial Electronics Magazine  8 (3): 60–63  doi:10 1109/MIE 2014 2335431 
^ Srodes, James (2002), Franklin: The Essential Founding Father, Regnery Publishing, pp  92–94, ISBN 0-89526-163-4 It is uncertain if Franklin personally carried out this experiment, but it is popularly attributed to him 
^ a b Guarnieri, M  (2014)  "The Big Jump from the Legs of a Frog"  IEEE Industrial Electronics Magazine  8 (4): 59–61, 69  doi:10 1109/MIE 2014 2361237 
^ Hertz, Heinrich (1887)  "Ueber den Einfluss des ultravioletten Lichtes auf die electrische Entladung"  Annalen der Physik  267 (8): S  983–1000  Bibcode:1887AnP   267  983H  doi:10 1002/andp 18872670827 
^ "The Nobel Prize in Physics 1921"  Nobel Foundation  Retrieved 2013-03-16 
^ John Sydney Blakemore, Solid state physics, pp  1–3, Cambridge University Press, 1985 ISBN 0-521-31391-0 
^ Richard C  Jaeger, Travis N  Blalock, Microelectronic circuit design, pp  46–47, McGraw-Hill Professional, 2003 ISBN 0-07-250503-6 
^ "The repulsive force between two small spheres charged with the same type of electricity is inversely proportional to the square of the distance between the centres of the two spheres " Charles-Augustin de Coulomb, Histoire de l'Academie Royal des Sciences, Paris 1785 
^ Sewell, Tyson (1902), The Elements of Electrical Engineering, Lockwood, p  18   The Q originally stood for 'quantity of electricity', the term 'electricity' now more commonly expressed as 'charge' 
^ a b Berkson, William (1974), Fields of Force: The Development of a World View from Faraday to Einstein, Routledge, p  370, ISBN 0-7100-7626-6 Accounts differ as to whether this was before, during, or after a lecture 
^ "Lab Note #105 EMI Reduction – Unsuppressed vs  Suppressed"  Arc Suppression Technologies  April 2011  Retrieved March 7, 2012 
^ Almost all electric fields vary in space  An exception is the electric field surrounding a planar conductor of infinite extent, the field of which is uniform 
^ Paul J  Nahin (9 October 2002)  Oliver Heaviside: The Life, Work, and Times of an Electrical Genius of the Victorian Age  JHU Press  ISBN 978-0-8018-6909-9 
^ "The Bumpy Road to Energy Deregulation"  EnPowered  2016-03-28 
^ a b c d e f g h Van Riper, op cit , p  71 
Look up electricity in Wiktionary, the free dictionary 
Basic Concepts of Electricity chapter from Lessons In Electric Circuits Vol 1 DC book and series 



ground_truth: Other toxic products.