PKU disease is recessive. A man and a woman are both carriers for PKU disease.?
348504
Genotype of the man-Pp\nGenotype of the woman-Pp\nPossible genotypes of children-PP, 2Pp, pp\nPossible phenotypes of children-2 carriers, one that has it, one that is completly free of it\nProbability of PKU disease in their children-25%
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genetics and hormones
510378
It is not given for a specific disease but rather to a condition that is deficient with potassium.
222852
a dominant genetic disorder only requires one copy of the causitive gene, so if one of your parents had one copy of the gene and the other none, you would have a 50% chance of getting it. if its recessive, it takes two copies of the gene to actually have the disease, so both parents would both have to have a causitive gene. so dominant usually affects every generation, while recessives usually skip and are less frequently manifested. thats if its autosomal (meaning not on a sex chromosome). if its X-linked, then it gets more complicated. see the link below (pages 4-9) for more help and examples of diseases.
715961
If this is a single-gene trait (which your problem assumes) for which the disease is the recessive trait, and everyone else is healthy, both parents must be Cc, since that is the only way they could possibly not have the trait but be able to pass it on.
722254
www.mda.org\nwww.mdausa.org\nwww.ninds.nih.gov\nwww.muscular-dystrophy\n\nWikipedia info \nGenetics\n\n\n\nDuchenne dystrophy is a type of dystrophinopathy which includes a spectrum of muscle disease caused by mutations in the DMD gene, which encodes the protein dystrophin. Becker's muscular dystrophy is a milder type of dystrophinopathy. Although it is caused by a defective gene, it often occurs in people from families without a known family history of the condition.\n\nDuchenne muscular dystrophy is inherited in an X-linked recessive pattern. Because of random X inactivation, some women carriers can actually be partially affected by this disease, despite its recessive nature. X inactivation leads to women being in a state of X0, not XX as is usually thought (see below). Women who carry the defective gene can pass an abnormal X on to their sons. Since boys have an X from their mother and a Y from father, there is no second X to make up for the defective gene from the carrier mother. The sons of carrier females each have a 50% chance of having the disease, and the daughters each have a 50% chance of being carriers. Daughters of men with Duchenne will always be carriers, since they will inherit an affected X chromosome from their father (note that the diagram only shows the results from an unnaffected father). Some females will also have very mild degrees of muscular dystrophy, and this is known as being a manifesting carrier.\n\nPrenatal testing, such as amniocentesis, for pregnancies at risk is possible if the DMD disease-causing mutation has been identified in a family member or if informative linked markers have been identified.\n\nIn 30% of the cases, the disease is a result of a spontaneous mutation.\n\nIn some female cases, DMD is caused by skewed x inactivation. In these cases, two copies of the x chromosome exist, but for reasons currently unknown, the flawed x chromosome manifests instead of the unflawed copy. In these cases, a mosaic form of DMD is seen, in which some muscle cells are completely normal while others exhibit classic DMD findings. The effects of a mosaic form of DMD on long-term outlook is not known.\n\n[edit]\nPatho-mechanism\nDuchenne muscular dystrophy is caused by a mutation of the dystrophin gene whose protein product is responsible for linking the actin filaments of muscle fibres to the extracellular matrix through a protein complex containing many subunits. As a result, the sarcolemma is damaged through shearing forces and muscle fibres undergo necrosis and are ultimately replaced with adipose and connective tissue.\n\n\n\n\n[edit]\nSymptoms\nMuscle weakness \nRapidly progressive \nFrequent falls \nDifficulty with motor skills (running, hopping, jumping) \nProgressive difficulty walking \nAbility to walk can be lost by age 11 \nFatigue \nIntellectual impairment (in approx. 30% of Duchenne's patients) \nSkeletal deformities \nChest and back (scoliosis) \nMuscle deformities \nContractures of heels, legs \nPseudohypertrophy of tongue and calf muscles \nMild mental retardation in some cases \nScoliosis in some cases \n\nSymptoms usually appear before age 6 and may appear as early as infancy. There is progressive muscle weakness of the legs and pelvis, which is associated with a loss of muscle mass (wasting). Muscle weakness also occurs in the arms, neck, and other areas, but not as severely or as early as in the lower half of the body. Calf muscles initially enlarge -- the enlarged muscle tissue is eventually replaced by fat and connective tissue (pseudohypertrophy). Muscle contractures occur in the legs, rendering the muscles unusable because the muscle fibers shorten and fibrosis occurs in connective tissue.\n\n[edit]\nSigns and tests\nThe pattern of symptom development resembles that of Duchenne's muscular dystrophy, but with a much slower rate of progression. Muscle wasting begins in the legs and pelvis, then progresses to the muscles of the shoulders and neck, followed by loss of arm
774901
Some diseases are carried on the x chromosome and others on the y.
610918
Here the woman is a carrier of both haemophilia and colorblindness, but she is normal.So her possibilities of children with the colorblind man will be a normal daughter, a colorblind daughter, a haemophiliac son and a color blind son. So the statment as i worked it out maybe correct and not wrong.
802960
The women and the man would have a heterozygous geneotype\n\nThe woman's genotype would consist of a gene for B blood and for O blood.\nThe man's genotypes would consist of a gene for A blood and B blood.  \n\nSince O is a ressisve gene, A and B would dominiant the blood type for their children who could have an A, B or AB blood type.  \n\nFollowing a basic 2 x 2 Punnett square, the statistics of a child getting a homozygous B blood type would be 1/4; a AB blood type would be 1/4; for getting a heterzygous A or B blood type with a ressive O gene would be 2/4 or 1/2.
185809
Phenylketonuria (PKU) diet\n\nA low-protein diet is the main treatment for phenylketonuria (PKU). This is because people with PKU lack an enzyme to properly process the amino acid phenylalanine, a component of protein. PKU diets generally do not contain high-protein foods such meat, eggs, and nuts, or bread and wheat products.\n\nThe PKU diet may result in certain nutritional deficiencies. It is important that everyone with PKU see a specialist for nutritional counseling. This is especially important for those considering pregnancy.\n\nRead food labels carefully. Phenylalanine is present in all protein foods and in some nonprotein foods, such as soda pop and artificial sweeteners (for example, aspartame [such as Nutrasweet]). All foods that contain phenylalanine should have "contains phenylalanine" on the label. http://health.yahoo.com/ency/healthwise/ug1465\n\n What is Included in a Low Phenylalanine Food Pattern?\nThe diet for PKU consists of a phenylalanine-free medical formula and carefully measured amounts of fruits, vegetables, bread, pasta, and cereals. Many people who follow a low phenylalanine (phe) food pattern eat special low protein breads and pastas. They are nearly free of phe, allow greater freedom in food choices, and provide energy and variety in the food pattern. \n\nWhat is Not Included in a Low Phenylalanine Food Pattern?\nFoods that contain large amounts of phe must be eliminated from a low phe diet. These foods are high protein foods, such as milk, dairy products, meat, fish, chicken, eggs, beans, and nuts. These foods cause high blood phe levels for people with PKU.  \n \nA low phe diet helps most young adults with PKU to feel better and improves attention span, concentration, and memory. In general, young adults who have made these changes report that they think and feel better. The effort that it takes to bring down blood phe levels is well worth it for everyone, no matter how long they have been "off diet." \nhttp://depts.washington.edu/pku/diet.html
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None, really, unless the man or woman is malnourished.\n\nFor information on the subject, try reading _Fertility, Cycles, and Nutrition_ by Marilyn Shannon.  I haven't read the book, but I have seen it recommended.
782924
genetic predisposition
399075
Yes.\n\nBoth colour blindness and hemophilia are X-linked, and recessive. This means that if you are male, you will have the trait (because you only have 1 X chromosome), but if you are female, you have to have the disease on both your X chromosomes.\n\nThe 'normal healthy woman' had to get a hemophilia-X from her father (since he only has 1 X) - call it X(h) - and he was *not* colourblind so the X(h) doesn't carry the colourblindness mutation.\n\nShe also *had* to get a colour-blind-X from her mother, since her mother has to have 2 copies in order to *be* colourblind - call it X(b). So, she is X(h) X(b).\n\nShe marries a colourblind but not hemophiliac man: he must be X(b)Y. No other option.\n\nThere are thus four different possible outcomes for their children:\n\nX(b) X(h) mates with X(b)Y:\n\nX(b) X(b) - colour blind daughter\nX(b) Y - colour blind son\nX(h) X(b) - normal daughter (but carries both recessive traits)\nX(h) Y - hemophiliac son\n\nHope that was clear enough! :)
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Genotypes of man and woman : DdPp x DdPp\nPossible gametes of man and woman: DP Dp dP dp X DP Dp dP dp\nChildren: I guess its a dihybrid cross with 9:3:3:1 ratio of phenotypes since you have not mentioned the kind of inheritance.
54056
Phenylketonuria is not deabilitating.  Get a job and eat right.
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The most common form is Duchenne muscular dystrophy. This form is caused by mutations of the gene for the dystrophin protein. The dystrophin is the second largest gene in mammals.\n\nThe dystrophin gene is located on the X chromosome, thus making it a 'sex-linked' disorder. Accordingly, muscular dystrophies are much more common in males, as females have two copies of the X chromosome while males have only one.\n\nDuchenne muscular dystrophy is caused by an X-linked gene. This means that only boys are affected but that their mothers may be carriers. In almost half of all affected boys, the faulty gene has arisen by mutation in the boy himself and no other family member carries it. However, this may be difficult to prove and can be decided only after careful and expert assessment of the family.\n\nIn the remaining cases (somewhat over half of all cases), the mother carries the gene but is usually not herself affected by it. Such women are known as ‘carriers’. Each subsequent son of a carrier has a 50:50 chance of being affected and each daughter has a 50:50 chance of being a carrier herself. A small number of female carriers of the gene have a mild degree of muscle weakness themselves and are then known as ‘manifesting carriers’.\n\nOne of the most important things that needs to be done soon after the diagnosis of a boy with Duchenne muscular dystrophy is to seek genetic advice and appropriate tests for those family members who are at risk of being carriers.\n\nFemale carriers of muscular dystrophy who are considering having children should be aware that prenatal diagnosis is available. Tests can be carried out during pregnancy, to try to find out if the fetus (unborn child) is affected.\n\nA couple may want to consider whether or not to continue the pregnancy if the fetus is affected. Alternatively, they may wish to know if the fetus is affected so that they can carry on with the pregnancy armed with knowledge that will help them to prepare and plan for the future.\n\nDifferent types of prenatal tests can be carried out after about 10 weeks of pregnancy. Chorionic villus sampling (CVS) can be done at 10-12 weeks, and amniocentesis at about 14-16 weeks, while placental biopsy and fetal blood sampling can be done at about 18 weeks. \n\nAbout 100 boys with Duchenne muscular dystrophy are born in the UK each year. There are about 1,500 known boys with the disorder living in the UK at any one time. For the general population the risk of having an affected child is about one in every 3,500 male births.\n\nThe most frequent symptoms are muscle weakness (frequent falls, walking problems, drooping eyelid) and skeletal and muscle deformities. Neurologic examination often reveals loss of muscle tissue (wasting), muscle contracture, pseudohypertrophy, and weakness. Diagnosis is usually established by muscle biopsy, elevated serum creatine kinase levels and electromyography, which is consistent with myogenic involvement. Some types of muscular dystrophies may result with additional cardiac diseases, intellectual deterioration and infertility.
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Not that I'm aware of. This genetic condition involves the X and Y chromosomes, and not anything else.