Cereals that Contain 100% of the Daily Value of Folic Acid

Cereals that Contain 100% of the Daily Value of Folic Acid

A single serving of many breakfast cereals has the amount of folic acid that a woman needs each day. The following cereals contain 100% of the DV of folic acid per serving size. Please look at nutrition label on the side of the cereal box for the serving size.

General Mills

Multibran Chex®
Wheat Chex®
Multi-Grain Cheerios®
Raisin Bran®

General Mills Total®

Raisin Bran
Whole Grain
Cranberry Crunch
Honey Clusters
Cinnamon Crunch

Kashi® Heart to Heart

Kellogg’s®

All-Bran® Bran Buds®
All-Bran® Complete® Wheat Flakes
All-Bran® Extra Fiber
All-Bran® Original
All-Bran® Yogurt Bites
All-Bran® Strawberry Medley
Low-Fat Granola with Raisins
Low-Fat Granola without Raisins
Product 19®
Mueslix
Smart Start®
Special K®

Malt-O-Meal® Crispy Rice
Malt-O-Meal® Spooners

Quaker® Oats

Cap'n Crunch Original ®
Cap'n Crunch’s Crunch Berries®
Cap'n Crunch's Choco Crunch™
Cap'n Crunch's Peanut Butter Crunch®
Honey Graham OH!s®
King Vitamin®
Cinnamon Life®
Squares Brown Sugar
Squares Cinnamon
Squares Golden Maple
Quisp®

Quaker® Toasted Oatmeal Cereal Brown Sugar Bliss
Quaker® Toasted Oatmeal Cereal Honey Nut Heaven

cdc

What other names do people use for cystic fibrosis?

What other names do people use for cystic fibrosis?

CF

Cystic fibrosis of pancreas

Fibrocystic Disease of Pancreas

Mucoviscidosis

cdc

Folic Acid can help prevent major birth defects

Folic acid is very important because it can help prevent major birth defects of the baby’s brain and spine (anencephaly and spina bifida) by 50% to 70%.

How much folic acid a woman needs

400 micrograms (mcg) every day.

When to start taking folic acid

For folic acid to help prevent major birth defects, a woman needs to start taking it at least one month before she becomes pregnant and while she is pregnant.

However, every woman needs folic acid every day, whether she’s planning to get pregnant or not, for the healthy new cells the body makes daily. Think about the skin, hair, and nails. These – and other parts of the body – make new cells each day.

How a woman can get enough folic acid

There are two easy ways to be sure to get enough folic acid each day:

1.Take a vitamin that has folic acid in it every day.

Most multivitamins sold in the United States have the amount of folic acid women need each day. Women can also choose to take a small pill (supplement) that has only folic acid in it each day.

Check the label on your vitamins to be sure it contains 100% of the daily value (DV) of folic acid, which is 400 micrograms (mcg).

Eat a bowl of breakfast cereal that has 100% of the daily value of folic acid every day.

Not every cereal has this amount. Check the label on the side of the box, and look for one that has “100%” next to folic acid.

cdc

Norovirus

Noroviruses (genus Norovirus, family Caliciviridae) are a group of related, single-stranded RNA, nonenveloped viruses that cause acute gastroenteritis in humans. Norovirus was recently approved as the official genus name for the group of viruses provisionally described as “Norwalk-like viruses” (NLV).
CDC

How do people inherit Huntington disease?

This condition is inherited in an autosomal dominant pattern, which means one copy of the altered gene in each cell is sufficient to cause the disorder. An affected person usually inherits the altered gene from one affected parent. In rare cases, an individual with Huntington disease does not have a parent with the disorder.

As the altered HTT gene is passed from one generation to the next, the size of the CAG trinucleotide repeat often increases in size. A larger number of repeats is usually associated with an earlier onset of signs and symptoms. This phenomenon is called anticipation. People with the adult-onset form of Huntington disease typically have 40 to 50 CAG repeats in the HTT gene, while people with the early-onset form of the disorder tend to have more than 60 CAG repeats.

Individuals who have 27 to 35 CAG repeats in the HTT gene do not develop Huntington disease, but they are at risk of having children who will develop the disorder. As the gene is passed from parent to child, the size of the CAG trinucleotide repeat may lengthen into the range associated with Huntington disease (36 repeats or more).
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Blood coagulation factor

Synonym(s): blood clotting factor, clotting factor, coagulation factors

Definition(s): Endogenous substances, usually proteins, that are involved in the blood coagulation process.

Factors in the blood that are essential for blood coagulation. The absence or mutation of these factors can lead to hemophilia and blood clotting disorders.

MeSH, National Library of Medicine

What is hemophilia?

Hemophilia is a bleeding disorder that slows the blood clotting process. People with this condition often experience prolonged bleeding or oozing following an injury, surgery, or having a tooth pulled. In severe cases of hemophilia, heavy bleeding occurs after minor trauma or even in the absence of injury (spontaneous bleeding). Serious complications can result from bleeding into the joints, muscles, brain, or other internal organs. Milder forms of hemophilia do not involve spontaneous bleeding, and the condition may only become apparent when abnormal bleeding occurs following surgery or a serious injury.

The major types of this condition are hemophilia A (also known as classic hemophilia) and hemophilia B (also known as Christmas disease). Although the two types have very similar signs and symptoms, they are caused by mutations in different genes. People with an unusual form of hemophilia B, known as hemophilia B Leyden, experience episodes of excessive bleeding in childhood, but have few bleeding problems after puberty. Another form of the disorder, acquired hemophilia, is not caused by inherited gene mutations. This rare condition is characterized by abnormal bleeding into the skin, muscles, or other soft tissues, usually beginning in adulthood.

How common is hemophilia?
The two major forms of hemophilia occur much more commonly in males than in females. Hemophilia A is the most common type of the condition; about 1 in 4,000 males worldwide are born with this disorder. Hemophilia B occurs in approximately 1 in 20,000 newborn males worldwide.

What genes are related to hemophilia?
Mutations in the F8 and F9 genes cause hemophilia.

Changes in the F8 gene are responsible for hemophilia A, while mutations in the F9 gene cause hemophilia B. The F8 gene provides instructions for making a protein called coagulation factor VIII. A related protein, coagulation factor IX, is produced from the F9 gene. Coagulation factors are proteins that work together in the clotting process. After an injury, blood clots protect the body by sealing off damaged blood vessels and preventing further blood loss.

Mutations in the F8 or F9 gene lead to the production of an abnormal version of coagulation factor VIII or coagulation factor IX. The altered protein cannot participate effectively in the blood clotting process and, in some cases, the protein does not work at all. A shortage of either protein prevents clots from forming properly in response to injury. These problems with blood clotting lead to excessive bleeding that can be difficult to control. Some mutations almost completely eliminate the activity of coagulation factor VIII or coagulation factor IX, resulting in severe hemophilia. Other mutations reduce but do not eliminate the activity of one of these proteins, which usually causes mild or moderate hemophilia.

The other, rare form of this condition, acquired hemophilia, results when the body makes specialized proteins called autoantibodies that attack and disable coagulation factor VIII. The production of autoantibodies is sometimes associated with pregnancy, immune system disorders, cancer, or allergic reactions to certain drugs. In about half of cases, the cause of acquired hemophilia is unknown.

How do people inherit hemophilia?
Hemophilia A and hemophilia B are inherited in an X-linked recessive pattern. A condition is considered X-linked if the mutated gene that causes the disorder is located on the X chromosome, one of the two sex chromosomes. In males (who have only one X chromosome), one altered copy of the gene in each cell is sufficient to cause the condition. In females (who have two X chromosomes), a mutation must be present in both copies of the gene to cause the disorder. Males are affected by X-linked recessive disorders much more frequently than females. A striking characteristic of X-linked inheritance is that fathers cannot pass X-linked traits to their sons.

In X-linked recessive inheritance, a female with one altered copy of the gene in each cell is called a carrier. She can pass on the altered gene to her children, but usually does not experience signs and symptoms of the disorder. In about 10 percent of cases, however, females who carry one altered copy of the F8 or F9 gene will experience mild problems with bleeding.

 nih

What is neurofibromatosis type 1?

What id neurofibromatosis type 1?

Neurofibromatosis type 1 is a condition characterized by changes in skin coloring (pigmentation) and the growth of tumors along nerves in the skin, brain, and other parts of the body. The signs and symptoms of this condition vary widely among affected people.

Beginning in early childhood, almost all people with neurofibromatosis type 1 have multiple café-au-lait spots, which are flat patches on the skin that are darker than the surrounding area. These spots increase in size and number as the individual grows older. Freckles in the underarms and groin typically develop later in childhood.

Most adults with neurofibromatosis type 1 develop neurofibromas, which are noncancerous (benign) tumors that are usually located on or just under the skin. These tumors may also occur in nerves near the spinal cord or along nerves elsewhere in the body. Some people with neurofibromatosis type 1 develop cancerous tumors that grow along nerves. These tumors, which usually develop in adolescence or adulthood, are called malignant peripheral nerve sheath tumors. People with neurofibromatosis type 1 also have an increased risk of developing other cancers, including brain tumors and cancer of blood-forming tissue (leukemia).

During childhood, benign growths called Lisch nodules often appear in the colored part of the eye (the iris). Lisch nodules do not interfere with vision. Some affected individuals also develop tumors that grow along the nerve leading from the eye to the brain (the optic nerve). These tumors, which are called optic gliomas, may lead to reduced vision or total vision loss. In some cases, optic gliomas have no effect on vision.

Additional signs and symptoms of neurofibromatosis type 1 include high blood pressure (hypertension), short stature, an unusually large head (macrocephaly), and skeletal abnormalities such as an abnormal curvature of the spine (scoliosis). Although most people with neurofibromatosis type 1 have normal intelligence, learning disabilities and attention deficit hyperactivity disorder (ADHD) occur frequently in affected individuals.

How common is neurofibromatosis type 1?

Neurofibromatosis type 1 occurs in 1 in 3,000 to 4,000 people worldwide.

What genes are related to neurofibromatosis type 1?

Mutations in the NF1 gene cause neurofibromatosis type 1.

The NF1 gene provides instructions for making a protein called neurofibromin. This protein is produced in many cells, including nerve cells and specialized cells surrounding nerves (oligodendrocytes and Schwann cells). Neurofibromin acts as a tumor suppressor, which means that it keeps cells from growing and dividing too rapidly or in an uncontrolled way. Mutations in the NF1 gene lead to the production of a nonfunctional version of neurofibromin that cannot regulate cell growth and division. As a result, tumors such as neurofibromas can form along nerves throughout the body. It is unclear how mutations in the NF1 gene lead to the other features of neurofibromatosis type 1, such as café-au-lait spots and learning disabilities.

How do people inherit neurofibromatosis type 1?

Neurofibromatosis type 1 is considered to have an autosomal dominant pattern of inheritance. People with this condition are born with one mutated copy of the NF1 gene in each cell. In about half of cases, the altered gene is inherited from an affected parent. The remaining cases result from new mutations in the NF1 gene and occur in people with no history of the disorder in their family.

Unlike most other autosomal dominant conditions, in which one altered copy of a gene in each cell is sufficient to cause the disorder, two copies of the NF1 gene must be altered to trigger tumor formation in neurofibromatosis type 1. A mutation in the second copy of the NF1 gene occurs during a person's lifetime in specialized cells surrounding nerves. Almost everyone who is born with one NF1 mutation acquires a second mutation in many cells and develops the tumors characteristic of neurofibromatosis type 1.

NIH

Rett Syndrome (RS)

Rett syndrome (RS) first appears in infancy or, more typically, early childhood and has no racial or ethnic predilection. It is a clinical neurodevelopmental syndrome seen primarily in females. Features include:
•normal development until approximately 1 to 1.5 years, followed by developmental regression
•loss of purposeful hand movements and onset of characteristic hand wringing
•growth retardation, particularly in head circumference, which is normal at birth but becomes microcephalic
•breathing difficulties, including hyperventilation, apnea, and air swallowing
•seizures in approximately 90% of individuals
•autistic behaviors, including mouthing, hand movements, sighing, and decreased verbalization
•teeth grinding, difficulty chewing, swallowing problems
•severe to profound mental retardation (see the Intellectual disability/mental retardation module)
•truncal ataxia and ataxic gait
•dystonia and spasticity
•in older girls, scoliosis, osteoporosis, and hand and foot deformities

Platelet storage pool deficiency

Platelet storage pool deficiencies are rare, platelet abnormalities that cause a mild to moderate bleeding disorder.  Platelet storage pool deficiencies comprise a number of disorders with variable degrees of reductions in the numbers and contents of dense granules (delta granules), alpha granules or both. The dense granules in platelets serve as a "storage pool" for ATP, ADP, serotonin, calcium, and pyrophosphate, which are secreted when the platelets are activated.  It is thought that the reduced release of ADP may result in the prolonged bleeding times.

Classically, the clinical manifestations of storage pool disorders include nosebleeds (epistaxis), abnormally heavy or prolonged menstruation (menorrhagia), easy bruising, recurrent anemia and obstetric or surgical bleeding.  Four major types of congenital platelet storage pool disease have been described – dense body deficiency, gray platelet syndrome, Factor V Quebec, and mixed alpha-granule/dense body deficiency.  The inheritance of an isolated platelet storage pool deficiency is thought to be autosomal dominate, but the penetrance of the gene vary from person to person.

Platelet storage pool deficiencies can all be part of other inherited conditions including Hermansky-Pudlak syndrome, Chediak-Higashi syndrome  which are autosomal recessive conditions, Wiskott-Aldrich syndrome, an X-linked recessive condition, and thrombocytopenia-absent radius (TAR) syndrome.

The inheritance pattern of TAR syndrome is unclear.

NIH

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