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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 and main results}


In this note we are interested in the existence versus non-existence of stable sub- and super-solutions of equations of the form
\begin{equation} \label{eq1}
-div( \omega_1(x) \nabla u ) = \omega_2(x) f(u) \qquad \mbox{in $ {\mathbb{R}}^N$,}
\end{equation} where $f(u)$ is one of the following non-linearities: $e^u$,  $ u^p$ where $ p>1$ and $ -u^{-p}$ where $ p>0$   We assume that $ \omega_1(x)$ and $ \omega_2(x)$, which we call \emph{weights},  are smooth positive functions (we allow $ \omega_2$ to be zero at say a point) and which satisfy various growth conditions at $ \infty$     Recall that we say that a solution $ u $ of $ -\Delta u = f(u)$ in $ {\mathbb{R}}^N$ is stable provided
\[ \int f'(u) \psi^2 \le \int | \nabla \psi|^2, \qquad \forall \psi \in C_c^2,\] where $ C_c^2$ is the set of $ C^2$ functions defined on $ {\mathbb{R}}^N$ with compact support   Note that the stability of $u$ is just saying that the second variation at $u$ of the energy associated with the equation is non-negative      In our setting this becomes:  We say a $C^2$ sub/super-solution $u$ of (\ref{eq1}) is \emph{stable} provided
\begin{equation} \label{stable}
\int \omega_2 f'(u) \psi^2 \le \int \omega_1 | \nabla \psi|^2 \qquad \forall \psi \in C_c^2 
\end{equation}
One should note that (\ref{eq1}) can be re-written as
\begin{equation*}
- \Delta u  + \nabla \gamma(x) \cdot \nabla u ={ \omega_2}/{\omega_1}\ f(u) \qquad \text{ in $ \mathbb{R}^N$},
\end{equation*}
where
$\gamma = - \log( \omega_1)$ and on occasion we shall take this point of view 


\begin{remark} \label{triv} Note that  if $ \omega_1$ has enough integrability then it is immediate that if $u$ is a stable solution  of (\ref{eq1}) we have $ \int \omega_2 f'(u) =0 $  (provided $f$ is increasing)    To see this let $ 0 \le \psi \le 1$ be supported in a ball of radius $2R$ centered at the origin ($B_{2R}$) with $ \psi =1$ on $ B_R$ and such that $  | \nabla \psi | \le \frac{C}{R}$ where $ C>0$ is independent of $ R$    Putting this $ \psi$ into $ (\ref{stable})$ one obtains
\[ \int_{B_R} \omega_2 f'(u) \le \frac{C}{R^2} \int_{R < |x| <2R} \omega_1,\] and so if the right hand side goes to zero as $ R \rightarrow \infty$ we have the desired result 

\end{remark}





The existence versus non-existence of stable solutions of  $ -\Delta u =  f(u)$ in $ {\mathbb{R}}^N$ or $ -\Delta u = g(x) f(u)$ in $ {\mathbb{R}}^N$ is now quite well understood, see  \cite{dancer1, farina1, egg, zz, f2, f3, wei, ces, e1, e2}   We remark that some of these results are examining the case where $ \Delta $ is replaced with $ \Delta_p$ (the $p$-Laplacian) and also in many cases the authors are interested in finite Morse index solutions or solutions which are stable outside a compact set 
  Much of the interest in these Liouville type theorems  stems from the fact that the non-existence of a stable solution is related to the existence of a priori estimates for stable solutions of a related equation on a bounded domain 




       In \cite{Ni}  equations similar to  $ -\Delta u = |x|^\alpha u^p$  where examined on the unit ball in $ {\mathbb{R}}^N$ with zero Dirichlet boundary conditions   There it was shown that for $ \alpha >0$ that  one can obtain positive solutions for $ p $ supercritical with respect to Sobolev embedding and so one can view that the term $ |x|^\alpha$ is restoring some compactness       A similar feature happens for equations of the form
\[ -\Delta u = |x|^\alpha f(u) \qquad \mbox{in $ {\mathbb{R}}^N$};\]    the value of $ \alpha$ can vastly alter the existence versus non-existence of a stable solution,  see \cite{e1, ces, e2, zz, egg} 

We now come to our main results and for this we need to define a few quantities:

\begin{eqnarray*}
I_G&:=& R^{-4t-2} \int_{ R < |x|<2R} \frac{ \omega_1^{2t+1}}{\omega_2^{2t}}dx , \\
 J_G&:=& R^{-2t-1} \int_{R < |x| <2R} \frac{| \nabla \omega_1|^{2t+1} }{\omega_2^{2t}} dx  ,\\I_L&:=& R^\frac{-2(2t+p-1)}{p-1}  \int_{R<|x|<2R }{ \left(   \frac{w_1^{p+2t-1}}{w_2^{2t}}    \right)^{\frac{1}{p-1} }  }  dx,\\ J_L&:= &R^{-\frac{p+2t-1}{p-1} }  \int_{R<|x|<2R }{ \left(   \frac{|\nabla w_1|^{p+2t-1}}{w_2^{2t}}     \right)^{\frac{1}{p-1} }  }  dx,\\
I_M  &:=&   R^{-2\frac{p+2t+1}{p+1} }  \int_{R<|x|<2R }{ \left(   \frac{w_1^{p+2t+1}}{w_2^{2t}}    \right)^{\frac{1}{p+1} }  } \ dx, \\
J_M  &:= &  R^{-\frac{p+2t+1}{p+1} }  \int_{R<|x|<2R }{ \left(   \frac{|\nabla w_1|^{p+2t+1}}{w_2^{2t}}     \right)^{\frac{1}{p+1} }  }  dx 
\end{eqnarray*}


The three equations we examine are
\[ -div( \omega_1 \nabla u ) = \omega_2 e^u \qquad \mbox{ in $ {\mathbb{R}}^N$ } \quad  (G), \]
\[  -div( \omega_1 \nabla u ) = \omega_2 u^p \qquad \mbox{ in $ {\mathbb{R}}^N$ } \quad  (L), \]
\[ -div( \omega_1 \nabla u ) = - \omega_2 u^{-p} \qquad \mbox{ in $ {\mathbb{R}}^N$ } \quad  (M),\]  and where we restrict $(L)$ to the case $ p>1$ and $(M)$ to $ p>0$     By solution we always mean a $C^2$ solution    We now come to our main results in terms of abstract $ \omega_1 $ and $ \omega_2$     We remark that our approach to non-existence of stable solutions is the approach due to Farina, see \cite{f2,f3,farina1} 

\begin{thm} \label{main_non_exist} \begin{enumerate}


\item   There is no  stable sub-solution of $(G)$ if $ I_G, J_G \rightarrow 0$ as $ R \rightarrow \infty$   for some   $0<t<2$ 
 \item    There is no positive   stable sub-solution (super-solution) of $(L)$  if  $ I_L,J_L \rightarrow 0$ as $ R \rightarrow \infty$   for some   $p- \sqrt{p(p-1)}   < t<p+\sqrt{p(p-1)} $  ($0<t<\frac{1}{2}$) 
\item   There is no positive   stable super-solution of (M) if  $ I_M,J_M \rightarrow 0$ as $ R \rightarrow \infty$  for some $0<t<p+\sqrt{p(p+1)}$ 

\end{enumerate}

\end{thm}     If we assume that $ \omega_1$ has some monotonicity we can do  better    We will assume that the monotonicity conditions is satisfied for big $x$  but really all ones needs is for it to be satisfied on a suitable sequence of annuli 

\begin{thm} \label{mono}  \begin{enumerate} \item There is no  stable sub-solution of $(G)$ with $  \nabla \omega_1(x) \cdot  x \le 0$ for big $x$ if  $ I_G \rightarrow 0$ as $ R \rightarrow \infty$   for some   $0<t<2$ 

\item There is no positive  stable sub-solution of  $(L)$ provided  $  I_L \rightarrow 0$ as $ R \rightarrow \infty$ for either:
\begin{itemize}
\item  some $  1 \le t < p + \sqrt{p(p-1)}$ and $  \nabla \omega_1(x) \cdot x \le 0$ for big $x$,  or  \\

\item some $ p - \sqrt{p(p-1)} < t \le 1$ and $ \nabla \omega_1(x) \cdot x \ge 0$ for big $ x$ 
\end{itemize}
 There is no positive super-solution of $(L)$ provided $ I_L \rightarrow 0$ as $ R \rightarrow \infty$ for some $ 0 < t < \frac{1}{2}$ and $ \nabla \omega_1(x) \cdot x \le 0$ for big $x$ 



\item  There is no positive stable super-solution of $(M)$ provided  $ I_M \rightarrow 0$ as $ R \rightarrow \infty$  for some  $0<t<p+\sqrt{p(p+1)}$ 

\end{enumerate}

\end{thm}


\begin{cor}  \label{thing}  Suppose $ \omega_1 \le C  \omega_2$  for big $ x$, $ \omega_2 \in L^\infty$,  $ \nabla \omega_1(x) \cdot  x \le 0$ for big $ x$ 
\begin{enumerate} \item There is no stable sub-solution of $(G)$ if $ N \le 9$ 

\item  There is no positive stable sub-solution of $(L)$ if  $$N<2+\frac{4}{p-1} \left( p+\sqrt{p(p-1)}  \right) $$

\item  There is no positive stable super-solution of $(M)$ if $$N<2+\frac{4}{p+1} \left( p+\sqrt{p(p+1)}  \right) $$

\end{enumerate}

\end{cor}


If one takes $ \omega_1=\omega_2=1$ in the above corollary, the results obtained for $(G)$ and  $(L)$,  and for some values of $p$ in $(M)$, are optimal, see \cite{f2,f3,zz} 





We now drop all monotonicity conditions on $ \omega_1$ 

\begin{cor} \label{po} Suppose  $ \omega_1 \le C \omega_2$ for big $x$, $ \omega_2 \in L^\infty$, $ | \nabla \omega_1| \le C \omega_2$ for big $x$ 
\begin{enumerate} \item  There is no stable sub-solution of $(G)$ if $ N \le 4$ 

\item  There is no positive stable sub-solution of $(L)$ if $$N<1+\frac{2}{p-1} \left( p+\sqrt{p(p-1)}  \right) $$

\item There is no positive super-solution of $(M)$ if $$N<1+\frac{2}{p+1} \left( p+\sqrt{p(p+1)}  \right) $$

\end{enumerate}

\end{cor}

Some of the conditions on $ \omega_i$ in Corollary \ref{po} seem somewhat artificial   If we shift over to the advection equation (and we take $ \omega_1=\omega_2$  for simplicity)
\[ -\Delta u + \nabla \gamma \cdot \nabla u = f(u), \] the conditions on $ \gamma$ become: $ \gamma$ is bounded from below and has a bounded gradient 



In what follows we examine the case where $ \omega_1(x) = (|x|^2 +1)^\frac{\alpha}{2}$ and $ \omega_2(x)= g(x) (|x|^2 +1)^\frac{\beta}{2}$,  where $ g(x) $ is positive except at say a point, smooth and where $ \lim_{|x| \rightarrow \infty} g(x) = C \in (0,\infty)$      For this class of weights we can essentially obtain optimal results 


\begin{thm} \label{alpha_beta}   Take $ \omega_1 $ and $ \omega_2$ as above 
\begin{enumerate}

\item If $ N+ \alpha - 2 <0$ then there is no stable sub-solution for $(G)$, $(L)$ (here we require it to be positive) and in the case of $(M)$ there is no positive  stable  super-solution  This case is the trivial case, see Remark \ref{triv}   \\



\textbf{Assumption:} For the remaining cases we assume that $ N + \alpha -2 > 0$ 

  \item If  $N+\alpha-2<4(\beta-\alpha+2)$ then there is no  stable sub-solution for $ (G)$ 

\item If $N+\alpha-2<\frac{ 2(\beta-\alpha+2)   }{p-1} \left( p+\sqrt{p(p-1)}  \right)$ then there is  no positive stable sub-solution of $(L)$ 

\item If $N+\alpha-2<\frac{2(\beta-\alpha+2)   }{p+1} \left( p+\sqrt{p(p+1)}  \right)$ then there is no positive stable super-solution of $(M)$ 

\item Further more 2,3,4 are optimal in the sense if $ N + \alpha -2 > 0$ and the remaining inequality is not satisfied (and in addition we assume we don't have equality in the inequality) then we can find a suitable function $ g(x)$ which satisfies the above properties and a stable sub/super-solution $u$ for the appropriate equation 

\end{enumerate}

\end{thm}

\begin{remark}  Many of the above results can be extended to the case of equality in either the $ N + \alpha - 2 \ge 0$ and also the other inequality which depends on the equation we are  examining   We omit the details because one cannot prove the results in a unified way 

\end{remark}






















In showing that an explicit solution is stable we will need the   weighted Hardy inequality given in \cite{craig} 
\begin{lemma} \label{Har}
Suppose $ E>0$ is a smooth function   Then one has
\[ (\tau-\frac{1}{2})^2 \int E^{2\tau-2} | \nabla E|^2 \phi^2 + (\frac{1}{2}-\tau) \int (-\Delta E) E^{2\tau-1} \phi^2 \le \int E^{2\tau} | \nabla \phi|^2,\] for all $ \phi \in C_c^\infty({\mathbb{R}}^N)$ and $ \tau \in {\mathbb{R}}$ 
\end{lemma}  By picking an appropriate function $E$ this gives,

\begin{cor} \label{Hardy}
For all $ \phi \in C_c^\infty$ and $ t , \alpha \in {\mathbb{R}}$  We have
  \begin{eqnarray*}
\int (1+|x|^2)^\frac{\alpha}{2} |\nabla\phi|^2 &\ge& (t+\frac{\alpha}{2})^2 \int |x|^2 (1+|x|^2)^{-2+\frac{\alpha}{2}}\phi^2\\
&&+(t+\frac{\alpha}{2})\int  (N-2(t+1)   \frac{|x|^2}{1+|x|^2}) (1+|x|^2)^{-1+\frac{\alpha} {2}} \phi^2 
\end{eqnarray*}
 \end{cor}























\section{Proof of main results}

\textbf{ Proof of Theorem \ref{main_non_exist} }   (1)  Suppose $ u$ is a stable sub-solution of $(G)$ with $ I_G,J_G \rightarrow 0$ as $ R \rightarrow \infty$ and  let $ 0 \le \phi \le 1$ denote a smooth compactly supported function   Put $ \psi:= e^{tu} \phi$ into (\ref{stable}), where $ 0 <t<2$, to arrive at
\begin{eqnarray*}
\int \omega_2 e^{(2t+1)u} \phi^2 &\le & t^2 \int \omega_1 e^{2tu} | \nabla u|^2 \phi^2 \\
&& +\int \omega_1 e^{2tu}|\nabla \phi|^2 + 2 t \int \omega_1 e^{2tu} \phi \nabla u \cdot \nabla \phi 
\end{eqnarray*}  Now multiply $(G)$ by $ e^{2tu} \phi^2$ and integrate by parts to arrive at
\[ 2t \int \omega_1 e^{2tu} | \nabla u|^2 \phi^2 \le \int \omega_2 e^{(2t+1) u} \phi^2 - 2 \int \omega_1 e^{2tu} \phi \nabla u \cdot \nabla \phi,\]
and now if one equates like terms they arrive at
\begin{eqnarray} \label{start}
\frac{(2-t)}{2} \int \omega_2 e^{(2t+1) u} \phi^2  & \le & \int \omega_1 e^{2tu} \left( | \nabla \phi |^2 - \frac{ \Delta \phi}{2} \right) dx \nonumber \\
&& - \frac{1}{2} \int e^{2tu} \phi \nabla \omega_1 \cdot \nabla \phi 
\end{eqnarray}   Now substitute $ \phi^m$ into this inequality for $ \phi$ where $ m $ is a big integer to obtain
\begin{eqnarray} \label{start_1}
\frac{(2-t)}{2} \int \omega_2 e^{(2t+1) u} \phi^{2m}  & \le & C_m \int \omega_1 e^{2tu} \phi^{2m-2}  \left( | \nabla \phi |^2 + \phi |\Delta \phi|  \right) dx \nonumber \\
&& - D_m \int e^{2tu} \phi^{2m-1} \nabla \omega_1 \cdot \nabla \phi
\end{eqnarray} where $ C_m$ and $ D_m$ are positive constants just depending on $m$    We now estimate the  terms on the right but we mention that when ones assume the appropriate monotonicity on $ \omega_1$ it is the last integral on the right which one is able to drop 

\begin{eqnarray*}
\int \omega_1 e^{2tu} \phi^{2m-2} | \nabla \phi|^2 & = & \int \omega_2^\frac{2t}{2t+1} e^{2tu} \phi^{2m-2}  \frac{ \omega_1 }{\omega_2^\frac{2t}{2t+1}} | \nabla \phi|^2  \\
& \le &  \left( \int \omega_2 e^{(2t+1) u} \phi^{(2m-2) \frac{(2t+1)}{2t}} dx \right)^\frac{2t}{2t+1}\\ &&\left( \int \frac{ \omega_1 ^{2t+1}}{\omega_2^{2t}} | \nabla \phi |^{2(2t+1)} \right)^\frac{1}{2t+1} 
\end{eqnarray*}
Now, for fixed $ 0 <t<2$ we can take $ m $ big enough so $ (2m-2) \frac{(2t+1)}{2t} \ge 2m $ and since $ 0 \le \phi \le 1$ this allows us to replace the power on $ \phi$ in the first term on the right with $2m$   and hence we obtain
 \begin{equation} \label{three}
 \int \omega_1 e^{2tu} \phi^{2m-2} | \nabla \phi|^2  \le \left( \int \omega_2 e^{(2t+1) u} \phi^{2m} dx \right)^\frac{2t}{2t+1} \left( \int \frac{ \omega_1 ^{2t+1}}{\omega_2^{2t}} | \nabla \phi |^{2(2t+1)} \right)^\frac{1}{2t+1} 
 \end{equation}    We now take the test functions $ \phi$ to be such that $ 0 \le  \phi \le 1$ with $ \phi $ supported in the ball $ B_{2R}$ with $ \phi = 1 $ on $ B_R$ and $ | \nabla \phi | \le \frac{C}{R}$ where $ C>0$ is independent of $ R$    Putting this choice of $ \phi$ we obtain
 \begin{equation} \label{four}
 \int \omega_1 e^{2tu} \phi^{2m-2} | \nabla \phi |^2 \le \left( \int \omega_2 e^{(2t+1)u} \phi^{2m} \right)^\frac{2t}{2t+1} I_G^\frac{1}{2t+1} 
 \end{equation}  One similarly shows that
 \[ \int \omega_1 e^{2tu} \phi^{2m-1} | \Delta \phi| \le \left( \int \omega_2 e^{(2t+1)u} \phi^{2m} \right)^\frac{2t}{2t+1} I_G^\frac{1}{2t+1}
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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 are the stability conditions for a solution of $-\Delta u = f(u)$?

Read the following text and answer briefly.

Context 2: \]
 So, combining the results we obtain

 \begin{eqnarray} \label{last} \nonumber \frac{(2-t)}{2} \int \omega_2 e^{(2t+1) u} \phi^{2m} &\le& C_m \left( \int \omega_2 e^{(2t+1) u} \phi^{2m} dx \right)^\frac{2t}{2t+1} I_G^\frac{1}{2t+1}\\
 &&- D_m \int e^{2tu} \phi^{2m-1}  \nabla \omega_1 \cdot \nabla \phi 
 \end{eqnarray}
 We now estimate this last term   A similar argument using H\"{o}lder's inequality shows that
 \[ \int e^{2tu} \phi^{2m-1} | \nabla \omega_1| | \nabla \phi| \le \left(  \int \omega_2 \phi^{2m} e^{(2t+1) u} dx \right)^\frac{2t}{2t+1} J_G^\frac{1}{2t+1}  \] Combining the results gives that
\begin{equation} \label{last}
(2-t) \left( \int \omega_2 e^{(2t+1) u} \phi^{2m} dx \right)^\frac{1}{2t+1} \le I_G^\frac{1}{2t+1} + J_G^\frac{1}{2t+1},
\end{equation} and now we send $ R \rightarrow \infty$ and use the fact that $ I_G, J_G \rightarrow 0$ as $ R \rightarrow \infty$ to see that
\[ \int \omega_2 e^{(2t+1) u} =0, \] which is clearly a contradiction    Hence there is no stable sub-solution of $(G)$ 

(2)    Suppose that $u >0$ is a stable sub-solution (super-solution) of $(L)$   Then a similar calculation as in (1) shows that for  $ p - \sqrt{p(p-1)} <t < p + \sqrt{p(p-1)}$,  $( 0 <t<\frac{1}{2})$ one has

\begin{eqnarray}   \label{shit}
(p  -\frac{t^2}{2t-1}   )\int \omega_2 u^{2t+p-1} \phi^{2m} & \le & D_m \int \omega_1 u^{2t} \phi^{2(m-1)} (|\nabla\phi|^2  +\phi |\Delta \phi |) \nonumber \\
&& +C_m \frac{(1-t)}{2(2t-1)} \int u^{2t} \phi^{2m-1}\nabla \omega_1 \cdot  \nabla \phi 
 \end{eqnarray}    One now applies H\"{o}lder's argument as in (1) but the terms $ I_L$ and $J_L$ will appear on the right hand side of the resulting
 equation       This shift from a sub-solution to a super-solution depending on whether $ t >\frac{1}{2}$ or $ t < \frac{1}{2}$ is a result from the sign change of $ 2t-1$ at $ t = \frac{1}{2}$    We leave the details for the reader 


(3)   This case is also similar to (1) and (2) 


\hfill $ \Box$

 \textbf{Proof of Theorem \ref{mono} }   (1)   Again we suppose there is a stable sub-solution $u$ of $(G)$   Our starting point  is (\ref{start_1}) and we wish to be able to drop the term
 \[ - D_m \int e^{2tu} \phi^{2m-1} \nabla \omega_1 \cdot \nabla \phi, \] from (\ref{start_1})     We can choose $ \phi$ as in the proof of Theorem \ref{main_non_exist} but also such that $ \nabla \phi(x) = - C(x) x$ where $ C(x) \ge 0$      So if we assume that $ \nabla \omega_1 \cdot x \le 0$ for big $x$ then we see that this last term is non-positive and hence we can drop the term   The the proof is as before but now we only require that $ \lim_{R \rightarrow \infty} I_G=0$ 

 (2)      Suppose that $ u >0$ is a stable sub-solution of $(L)$  and so (\ref{shit}) holds for all $  p - \sqrt{p(p-1)} <t< p + \sqrt{p(p-1)}$    Now we wish to use monotonicity to drop the term from (\ref{shit}) involving the term $ \nabla \omega_1 \cdot \nabla \phi$       $ \phi$ is chosen the same as in (1)  but here one notes that the co-efficient for this term changes sign at $ t=1$ and hence by restriction $t$ to the appropriate side of 1 (along with the above condition on $t$ and $\omega_1$) we can drop the last term depending on which monotonicity we have and hence to obtain a contraction we only require that $ \lim_{R \rightarrow \infty} I_L =0$    The result for the non-existence of a stable super-solution is similar be here one restricts $ 0 < t < \frac{1}{2}$ 


(3)   The proof here is similar to (1) and (2) and we omit the details 




 \hfill $\Box$













\textbf{Proof of Corollary \ref{thing} }   We suppose  that $ \omega_1 \le C  \omega_2$  for big $ x$, $ \omega_2 \in L^\infty$,  $ \nabla \omega_1(x) \cdot  x \le 0$ for big $ x$      \\
(1)     Since $ \nabla \omega_1 \cdot x \le 0$ for big $x$ we can apply Theorem \ref{mono} to show the non-existence of a stable solution to $(G)$    Note that  with the above assumptions on $ \omega_i$ we have that
\[ I_G \le \frac{C R^N}{R^{4t+2}} \]  For $ N \le 9$  we can take $ 0 <t<2$  but close enough to $2$ so the right hand side goes to zero as $ R \rightarrow \infty$ 

Both (2) and (3) also follow directly from applying Theorem \ref{mono}    Note that one can say more about (2) by taking the multiple cases as listed in Theorem \ref{mono} but we have choice to leave this to the reader 


\hfill $ \Box$


\textbf{Proof of Corollary \ref{po} }   Since we have no monotonicity conditions now we will need both $I$ and $J$ to go to zero to show the non-existence of a stable solution    Again the results are obtained immediately by applying Theorem \ref{main_non_exist}  and we prefer to omit the details 


\hfill $\Box$
















\textbf{Proof of Theorem \ref{alpha_beta} }  (1)   If $ N + \alpha -2 <0$ then using Remark \ref{triv}  one easily sees there is no stable sub-solution of $(G)$ and $(L)$ (positive for $(L)$) or a positive stable super-solution of $(M)$    So we now assume that $ N + \alpha -2 > 0$      Note that the monotonicity of $ \omega_1$ changes when $ \alpha $ changes sign and hence one would think that we need to consider separate cases if we hope to utilize the monotonicity results    But a computation shows that in fact $ I$ and $J$ are just multiples of each other in all three cases so it suffices to show, say, that $ \lim_{R \rightarrow \infty} I =0$  \\
(2)    Note that for $ R >1$ one has
\begin{eqnarray*}
I_G & \le  & \frac{C}{R^{4t+2}} \int_{R <|x| < 2R} |x|^{ \alpha (2t+1) - 2t \beta} \\
& \le  &  \frac{C}{R^{4t+2}}  R^{N + \alpha (2t+1) - 2t \beta},
\end{eqnarray*} and so to show the non-existence we want to find some $ 0 <t<2$ such that
$  4t+2 > N  + \alpha(2t+1) - 2 t \beta$,   which is equivalent to  $ 2t ( \beta - \alpha +2) > (N + \alpha -2)$     Now recall that we are assuming that $ 0 < N + \alpha -2 < 4 ( \beta - \alpha +2) $ and hence we have the desired result by taking $  t <2$ but sufficiently close 
The proof of the non-existence results for
(3) and (4) are similar and we omit the details    \\
(5)   We now assume that $N+\alpha-2>0$   In showing the existence of stable sub/super-solutions we need to consider  $ \beta - \alpha + 2 <0$ and $ \beta - \alpha +2 >0$ separately 

\begin{itemize} \item $(\beta - \alpha + 2 <0)$  Here we take $ u(x)=0$ in the case of $(G)$ and $ u=1$ in the case of $(L)$ and $(M)$  In addition we take $ g(x)=\E$   It is clear that in all cases $u$ is the appropriate sub or super-solution   The only thing one needs to check is the stability     In all cases this reduces to trying to show that we have
\[ \sigma \int       (1+|x|^2)^{\frac{\alpha}{2}  -1}    \phi^2 \le \int      (1+|x|^2)^{\frac{\alpha}{2}}   | \nabla\phi  |^2,\]  for all $ \phi \in C_c^\infty$ where  $ \sigma $ is some small positive constant; its either $ \E$ or $ p \E$ depending on which equation were are examining 
To show this we use the result from Corollary \ref{Hardy} and we drop a few positive terms to arrive at
\begin{equation*}
\int (1+|x|^2)^\frac{\alpha}{2} |\nabla\phi|^2\ge (t+\frac{\alpha}{2})\int \left (N-2(t+1)   \frac{|x|^2}{1+|x|^2}\right) (1+|x|^2)^{-1+\frac{\alpha} {2}}
\end{equation*} which holds for all $ \phi \in C_c^\infty$ and $ t,\alpha \in {\mathbb{R}}$ 
  Now, since $N+\alpha-2>0$, we can choose $t$ such that $-\frac{\alpha}{2}<t<\frac{n-2}{2}$   So, the integrand function in the right hand side is positive and since for small enough $\sigma$ we have
  \begin{equation*}
\sigma \le  (t+\frac{\alpha}{2})(N-2(t+1)   \frac{|x|^2}{1+|x|^2})  \ \ \ \text {for all} \ \ x\in \mathbb{R}^N
\end{equation*}
 we get stability 



\item ($\beta-\alpha+2>0$) In the case of $(G)$ we take   $u(x)=-\frac{\beta-\alpha+2}{2} \ln(1+|x|^2)$ and $g(x):= (\beta-\alpha+2)(N+(\alpha-2)\frac{|x|^2}{1+|x|^2})$  By a computation one sees that $u$ is a sub-solution of $(G)$ and hence we need now to only show the stability, which amounts to showing that
\begin{equation*}
\int \frac{g(x)\psi^2}{(1+|x|^{2   })^{-\frac{\alpha}{2}+1}}\le \int\frac{|\nabla\psi|^2}{    (1+|x|^2)^{-\frac{\alpha}{2}}     },
\end{equation*} for all $ \psi \in C_c^\infty$   To show this we use  Corollary \ref{Hardy}   So  we  need to choose an appropriate $t$ in   $-\frac{\alpha}{2}\le t\le\frac{N-2}{2}$  such that for all $x\in {\mathbb{R}}^N$ we have
 \begin{eqnarray*}
 (\beta-\alpha+2)\left(    N+  (\alpha-2)\frac{|x|^2}{1+|x|^2}\right)         &\le& (t+\frac{\alpha}{2})^2 \frac{ |x|^2 }{(1+|x|^2}\\
&&+(t+\frac{\alpha}{2}) \left(N-2(t+1)   \frac{|x|^2}{1+|x|^2}\right) 
\end{eqnarray*}
With a  simple calculation one sees we need just to have
   \begin{eqnarray*}
 (\beta-\alpha+2)&\le& (t+\frac{\alpha}{2}) \\
  (\beta-\alpha+2)     \left(    N+  \alpha-2\right)      &   \le&  (t+\frac{\alpha}{2}) \left(N-t-2+\frac{\alpha}{2}) \right) 
 \end{eqnarray*}     If one takes $ t= \frac{N-2}{2}$ in the case where $ N \neq 2$ and $ t $ close to zero in the case for $ N=2$ one easily sees the above inequalities both hold, after considering all the constraints on $ \alpha,\beta$ and $N$ 

 We now consider the case of $(L)$   Here one takes $g(x):=\frac {\beta-\alpha+2}{p-1}(    N+  (\alpha-2-\frac{\beta-\alpha+2}{p-1})
\frac{|x|^2}{1+|x|^2})$ and $ u(x)=(1+|x|^2)^{ -\frac  {\beta-\alpha+2}{2(p-1)} }$    Using essentially the same approach as in $(G)$ one shows that $u$ is a stable sub-solution of $(L)$ with this choice of $g$    \\
For the case of $(M)$ we take   $u(x)=(1+|x|^2)^{ \frac  {\beta-\alpha+2}{2(p+1)}   }$ and $g(x):=\frac {\beta-\alpha+2}{p+1}(    N+  (\alpha-2+\frac{\beta-\alpha+2}{p+1})
\frac{|x|^2}{1+|x|^2})$ 



\end{itemize}


\hfill  $  \Box$












ground_truth: $\int f'(u) \psi^2 \le \int | \nabla \psi|^2, \forall \psi \in C_c^2$.

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: Can someone sell or modify the Agency Spotter Content?

Read the following text and answer briefly.

Context 3: 
(b) Agency Spotter may also offer the Services through applications built using Agency Spotter’s platform (“Agency Spotter Applications”), including smart phone applications, “Share” and other similar buttons and other interactive plugins distributed on websites across the Internet  Agency Spotter Applications are distinct from Third-Party Materials and applications address in Section 14(a), above  If you use an Agency Spotter application or interact with a website that has deployed a plugin, you agree that information about you and your use of the Services, including, but not limited to, your device, your mobile carrier, your internet access provider, your physical location, and/or web pages containing Agency Spotter plugins that load in your browser may be communicated to us  You acknowledge that you are responsible for all charges and necessary permissions related to accessing Agency Spotter through your mobile access provider  You should therefore check with your provider to find out if the Services are available and the terms for these services for your specific mobile devices  Finally, by using any downloadable application to enable your use of the Services, you are explicitly confirming your acceptance of the terms of the End User License Agreement associated with the application provided at download or installation, or as may be updated from time to time 
16  International Use  Agency Spotter makes no representation that materials on this site are appropriate or available for use in locations outside the United States, and accessing them from territories where their contents are illegal is prohibited  Those who choose to access this site from other locations do so on their own initiative and are responsible for compliance with local laws 
17  Dispute Resolution  These Terms and any claim, cause of action or dispute (“claim”) arising out of or related to these Terms shall be governed by the laws of the State of Georgia, regardless of your country of origin or where you access Agency Spotter, and notwithstanding any conflicts of law principles and the United Nations Convention for the International Sale of Goods  You and Agency Spotter agree that all claims arising out of or related to these Terms must be resolved exclusively by a state or federal court located in Fulton County, Georgia, except as otherwise mutually agreed in writing by the parties or as described in the Arbitration option in Section 16(b), below  You and Agency Spotter agree to submit to the personal jurisdiction of the courts located within Fulton County, Georgia, for the purpose of litigating all such claims  Notwithstanding the foregoing, you agree that Agency Spotter shall still be allowed to seek injunctive remedies (or an equivalent type of urgent legal relief) in any jurisdiction 
18  Arbitration  You agree that any dispute, claim or controversy arising hereunder or relating in any way to the Terms, shall be settled by binding arbitration in Fulton County, Georgia, in accordance with the commercial arbitration rules of Judicial Arbitration and Mediation Services (“JAMS”)  The arbitrator shall issue a written decision specifying the basis for the award made  The party filing a claim or counterclaim in the arbitration proceeding shall pay the deposit(s) determined by JAMS with respect to such claim or counterclaim  All other costs associated with the arbitration and imposed by JAMS shall be paid as determined by the arbitrator(s) and, in absence of such determination, equally by each party to the arbitration  In addition, unless the arbitrator awards payment of reasonable attorney and other fees to a party, each party to the arbitration shall be responsible for its own attorneys’ fees and other professional fees incurred in connection with the arbitration  Determinations of the arbitrator will be final and binding upon the parties to the arbitration, and judgment upon the award rendered by the arbitrator may be entered in any court having jurisdiction, or application may be made to such court for a judicial acceptance of the award and an order of enforcement, as the case may be  The arbitrator shall apply the substantive law of the State of Georgia, without giving effect to its conflict of laws rules 
19  Export Control  You agree to comply with all relevant export laws and regulations, including, but not limited to, the U S  Export Administration Regulations and Executive Orders (“Export Controls”)  You warrant that you are not a person, company or destination restricted or prohibited by Export Controls (“Restricted Person”)  You will not, directly or indirectly, export, re-export, divert, or transfer the Site or Service or any related software, any portion thereof or any materials, items or technology relating to Agency Spotter’s business or related technical data or any direct product thereof to any Restricted Person, or otherwise to any end user and without obtaining the required authorizations from the appropriate governmental entities 
(a) These Terms will continue until terminated in accordance with this Section 
(b) You may cancel your legal agreement with Agency Spotter at any time by (i) notifying Agency Spotter in writing, (ii) ceasing to use the Services, and (iii) closing your accounts for all of the Services which you use, if we have made this option available to you  Your cancellation of the Services will not alter your obligation to pay all charges incurred prior to your effective date of termination 
Agency Spotter may terminate its legal agreement with you if, (i) you have breached any provision of the Terms (or have acted in manner which clearly shows that you do not intend to, or are unable to comply with the provisions of the Terms), or (ii) Agency Spotter is required to do so by law (for example, where the provision of the Services to you is, or becomes, unlawful), or (iii) Agency Spotter is transitioning to no longer providing the Services to users in the country in which you are resident or from which you use the service, or (iv) the provision of the Services to you by Agency Spotter is, in Agency Spotters’ opinion, no longer commercially viable 
(c) The terms provided in Sections 2, 3, 6, 11, 12, 13, 14, 17, 19, 20, 21 and 22 of these Terms shall survive any termination of these Terms 
21  Independent Contractors  The parties are and intend to be independent contractors with respect to the Services contemplated hereunder  You agree that neither you nor any of your employees or contractors shall be considered as having an employee status with Agency Spotter  No form of joint employer, joint venture, partnership, or similar relationship between the parties is intended or hereby created 
22  Assignment and Delegation  You may not assign or delegate any rights or obligations under these Terms  Any purported assignment or delegation shall be ineffective  We may freely assign or delegate all rights and obligations under these Terms, fully or partially, without notice to you  We may also substitute, by way of unilateral novation, effective upon notice to you, Agency Spotter Inc  for any third party that assumes our rights and obligations under these Terms 
The personally identifiable information we collect from you allows us to provide you with the Services and to enable users to navigate and enjoy using the Site  We will also use your personally identifiable information to develop, improve and advertise the Site and Services  We may also use your personally identifiable information for internal purposes such as auditing, data analysis and research to improve our Services and customer communications  We do not rent, sell or otherwise provide your personally identifiable information to third parties without your consent, except as described in this policy or as required by law 
When you register with us through the Site or Services and become a Registered User, or when you wish to contact another Registered User, we will ask you for personally identifiable information  This refers to information about you that can be used to contact or identify you (“Personally Identifiable Information“)  Personally Identifiable Information includes, but is not limited to, your name, phone numbers, email address, home postal address, business address, social media user names, employer/affiliated organization, reasons for accessing the Site, and intended usage of requested information, but does not include your credit card number or billing information  We may also use your email address or phone number (if provided by you) to contact you regarding changes to the Services; system maintenance and outage issues; account issues; or otherwise to troubleshoot problems  In order to process some of your transactions through the Site and Services, we may also ask for your credit card number and other billing information (“Billing Information“; and, together with Personally Identifiable Information, “Personal Information“) 
Information you provide to us also includes your account profile and your contributions to discussion groups and community features Agency Spotter may offer  Do not upload or insert any information to or into the Site or Services that you do not want to be shared or used in the manner described in this section 
In addition, when you use the Site, our servers automatically record certain information that your web browser sends whenever you visit any website  These server logs may include information such as your web request, Internet Protocol address, browser type, browser language, referring/exit pages and URLs, platform type, number of clicks, domain names, landing pages, pages viewed and the order of those pages, the amount of time spent on particular pages, the date and time of your request, and one or more cookies that may uniquely identify your browser 
Information from third party services and other websites 
Do not upload or insert any information to or into the Site or Services that you do not want to be shared or used in the manner described in this section 
Advertisements  Advertisers who present ads on the Site may use technological methods to measure the effectiveness of their ads and to personalize advertising content  You may use your browser cookie settings to limit or prevent the placement of cookies by advertising networks  Agency Spotter does not share personally identifiable information with advertisers unless we get your permission 
Links  When you click on links on Agency Spotter you may leave our site  We are not responsible for the privacy practices of other sites, and we encourage you to read their privacy statements 
If we are requested to disclose your information to a government agency or official, we will do so if we believe in good faith, after considering your privacy interests and other relevant factors, that such disclosure is necessary to: (i) conform to legal requirements or comply with a legal process with which we are involved; (ii) protect our rights or property or the rights or property of our affiliated companies; (iii) prevent a crime or protect national security; or (iv) protect the personal safety of Site users or the public  Because Agency Spotter is a United States limited liability company and information collected on our Site is stored in whole or in part in the United States, your information may be subject to U S  law 
We also reserve the right to disclose Personally Identifiable Information and/or other information about users that Agency Spotter believes, in good faith, is appropriate or necessary to enforce our agreements, take precautions against liability, investigate and defend itself against ay third-party claims or allegations, assist government enforcement agencies, protect the security or integrity of our Site or Services, and protect the rights, property or personal safety of Agency Spotter, our users and others 
Cookies allow us to (i) manage, present and keep track of temporary information, such as data you upload onto the Site for use with the Services; (ii) register you as a Registered User on the Site or in other various programs associated with the Site; (iii) remember you when you log in to the places on the Site that require you to be a Registered User of the Site; (iv) help us understand the size of our audience and traffic patterns; (v) collect and record information about what you viewed on the Site; and (vi) deliver specific information to you based on your interests 
When you access the Site, the Site automatically collects certain non-personally identifiable information through the use of electronic images known as web beacons (sometimes called single-pixel gifs) and log files  Such information may include your IP address, browser type, the date, time and duration of your access and usage of the Site and whether you opened emails You received from us 
This information is collected for all visits to the Site and then analyzed in the aggregate  This information is useful for, among other things, tracking the performance of our online advertising, such as online banner ads, and determining where to place future advertising on other websites 
Editing your profile  You may review and change or remove your personal information or the settings for your Agency Spotter account at any time by going to your account profile  You can edit your name, email address, password and other account information here  Please be aware that even after your request for a change is processed, Agency Spotter may, for a time, retain residual information about you in its backup and/or archival copies of its database 
Deactivating or deleting your account  If you want to stop using your account you may deactivate it or delete it  When you deactivate an account, no user will be able to see it, but it will not be deleted  We save your profile information in case you later decide to reactivate your account  Many users deactivate their accounts for temporary reasons and in doing so are asking us to maintain their information until they return to Agency Spotter  You will still have the ability to reactivate your account and restore your profile in its entirety  When you delete an account, it is permanently deleted from Agency Spotter  You should only delete your account if you are certain you never want to reactivate it  You may deactivate your account or delete your account within your account profile 
Limitations on removal  Even after you remove information from your profile or delete your account, copies of that information may remain viewable elsewhere to the extent it has been shared with others, it was otherwise distributed pursuant to your privacy settings, or it was copied or stored by other users  However, your name will no longer be associated with that information on Agency Spotter  (For example, if you post something to another user’s or Agency’s profile or Agency’s portfolio and then you delete your account, that post may remain, but be attributed to an “Anonymous Agency Spotter User ”) Additionally, we may retain certain information to prevent identity theft and other misconduct even if deletion has been requested  If you have given third party applications or websites access to your information, they may retain your information to the extent permitted under their terms of service or privacy policies  But they will no longer be able to access the information through our platform after you disconnect from them 
Default Settings  Because the mission of Agency Spotter is to connect businesses and agencies, enabling them to save time, be more productive and successful, we have established what we believe are reasonable default settings that we have found most agencies and professionals desire  Because Registered Users may use and interact with Agency Spotter in a variety of ways, and because those uses may change over time, we designed our settings to provide our users control over the information they share  We encourage our Registered Users to review their account settings and adjust them in accordance with their preferences 
Risks inherent in sharing information  Please be aware that no security measures are perfect or impenetrable, and no method of transmission over the Internet, or method of electronic storage, is 100% secure  We cannot control the actions of other users with whom you share your information  We cannot guarantee that only authorized persons will view your information  We cannot ensure that information you share on the Site or through the Services will not become publicly available  We are not responsible for third party circumvention of any privacy or security measures on Agency Spotter  You can reduce these risks by using common sense security practices such as choosing a strong password, using different passwords for different services, and using up to date antivirus software 
If you receive an unsolicited email that appears to be from us or one of our members that requests personal information (such as your credit card, login, or password), or that asks you to verify or confirm your account or other personal information by clicking on a link, that email was likely to have been sent by someone trying to unlawfully obtain your information, sometimes referred to as a “phisher” or “spoofer ” We do not ask for this type of information in an email  Do not provide the information or click on the link  Please contact us at [email protected] if you get an email like this  Notwithstanding the foregoing, after your initial account setup, we may send an email to your registered account address solely to confirm that we have the correct, valid email address for your account 
If You have concerns about your privacy in connection with your use of the Site or any general questions related thereto, please tell us by emailing us at [email protected] We will make every reasonable effort to address your concerns 
Thank You for supporting websites, such as ours  We take your privacy seriously by implementing written privacy policies, such as this one 



ground_truth: No.