how much the frequency of lysosomal storage desease?
971122
Please see the webpages for more details on Lysosomal storage disease.
644504
It is somewhat common for this disease to recur in a patient, but as long as they have good access to a good doctor, it is not cause for undue concern.\n\nYou should read the wiki on it, and not worry so much:\n\nhttp://en.wikipedia.org/wiki/Scrofula\n\nhope it works out.
500214
Yes, as long as its done correctly.  There are many genetic diseases that could be erradicated by this process.
875126
Here's 100\n\nhttp://www.answersingenesis.org/docs/3880.asp
882815
Once a day at least.  Less means you're probably chronically constipated.\n\nTwo or three times is good.\nOne per meal-sized meal or snack is ideal.\n\nMuch more than that, though, and you may have diarrhea!
885433
it depends on the illness. can you give mor detail please
237262
VERY rarely.  Like 2 times a month if that.  You dont want them to get used to sweet stuff early because they wont want to eat anything nutritious.  Not to mention, they will develop cavities at a young age.
542747
It depends on how long the lysate was thawed...anything over 5-10 minutes and I would throw it out.  Also, if it's thawed/frozen again more than once, I would throw it out.  If you were going to extract DNA it wouldn't be so critical, but with RNA...well, you know how fragile it is!!
887569
I have vitilago since I was 7 I am now 41. So no it's not deadly. But it is often a symptom of an autoimmune disorder such as lupus etc. I would not worry to much about it and have your father discuss w/ his doctor the cause and request blood test to rule out any underlying problem.
32805
Normally 86,400 to 115,200 times per day.  But it is variable due to various factors like age, sex stature , activity, emotions etc. etc.
353515
http://www.cyberlipid.org/fa/acid0001.htm#3
53611
An estimated 34,810 new cases of leukemia will be diagnosed in the United States in 2005. Acute leukemias account for nearly 11 percent more of the cases than chronic leukemias. Most cases occur in older adults; more than half of all cases occur after age 67. Leukemia is expected to strike 9 times as many adults as children in 2004. (About 31,289 adults compared with 3,521 children, ages 0-19). About 30 percent of cancers in children ages 0-14 years are leukemia. The most common form of leukemia among children under 19 years of age is Acute Lymphocytic Leukemia (ALL).\n\nDuring 1995- 2001 relative survival rates overall were: \n\nAcute lymphocytic leukemia (ALL): 64.6 percent overall; 88.4 percent for children under 5 \nChronic lymphocytic leukemia (CLL): 74.2  percent \nAcute myelogenous leukemia (AML): 19.8 percent overall; 52 percent for children under 15 \nChronic myelogenous leukemia (CML): 39.3 percent\nAt the present time there are approximately 198,257 people living with leukemia in the United States. \n\nIt is anticipated that approximately 22,570 deaths in the United States will be attributed to leukemia in 2005 (12,540 males and 10,030 females). There will be an estimated 4,600 deaths from chronic lymphocytic leukemia and 1,490 deaths from acute lymphocytic leukemia. There will be an estimated 9,000 deaths from acute myelogenous leukemia and 850 deaths from chronic myelogenous leukemia. Unclassified forms of leukemia will account for 6,630 additional deaths. \n\nThe estimated numbers of deaths attributed to leukemia in the United States are about 25 percent higher for males than females.\nThe leukemia death rate for children 0-14 years of age in the United States has declined 60 percent over the past three decades. Despite this decline, leukemia causes more deaths than any other cancer among children under age 20. Approximately 413 children from 0-14 years of age are expected to die from leukemia in 2005.
832349
actually, the one out of every 500,000 is just short hand for we don't have enough cases to figure out what the real statistics is for this disease. This fact was actually brought up in an class on evolution I had the other week, but yeah, don't rely on the one out 500,000 or 1 out 200,000 statistics, it's just some guestimate that sounds better then we don't know.
691873
lysosomes, they are responsible for the release of corroding enzymes. The bacteria or invading pathogens are killed in the lysosomes. likewise the cells may induce destruction or apoptosis which would activate the lysosomes to pour in its corrosive enzymes and detroy the cell
190080
Treatment    Return to top \n\nTreatment for this disease concentrates on avoiding low blood sugar. Frequent feedings are needed during the day, especially foods that contain carbohydrates (starches). Neither fruit nor milk sugar can be adequately broken down in this disease, and are best avoided.\n\nOvernight fasting is avoided by continuous feedings (through a tube that goes through the nose into the stomach) of sugars or uncooked cornstarch. The tube can be put in at bedtime and taken out each morning. A medication called allopurinol, which can lower blood uric acid and decrease the risk for gout, is often used.\n\nSynonyms:\nvon Gierkes disease\nGlucose-6-Phosphatase Deficiency Glycogen Storage Disease\nType I Glycogenosis\nHepatorenal Glycogenosis\n\nIn Type I Glycogen Storage Disease, the enzyme glucose-6-phosphatase is defective in the liver, kidney, and small intestine, where it normally functions. However, the metabolic problem is centered in the liver.\n\nPatients with Type I GSD are unable to release glucose from glycogen. They cannot maintain their blood glucose levels and within a few hours after eating develop hypoglycemia (low blood sugar). The low levels of glucose in the blood of these patients often result in chronic hunger, fatigue, and irritability that is especially noticeable in infants. Symptoms of hypoglycemia only begin to appear when the interval between feedings increases and the infant sleeps through the night or when an illness prevents normal feeding routine. If the blood sugar falls to a low enough point, some patients may experience seizures. \n\nSince Type I patients are able to store glucose as glycogen but not release it normally, with time the stored glycogen builds up in the liver. Hormones, lactic acid, triglycerides, and other products are increased in the blood as the body attempts to raise blood sugar. Fats are stored in the liver along with the glycogen, which leads to enlargement of the liver. The liver does its many other functions normally, and there is not usually any evidence of liver failure. The kidneys are also enlarged due to glycogen accumulation. \n\nThe continued presence of low blood sugar eventually leads the body to experience severe biochemical abnormalities and delayed growth and development. Untreated patients may have muscle wasting and a buildup of body fat.\n\nWhen blood studies are done, it is discovered that there is usually a low blood sugar, elevated blood lactic acid, elevated cholesterol and other fats, and elevated uric acid concentration. High blood pressure has also been seen in a number of patients and when this occurs, appropriate treatment must be given.\n\nIn addition to the problems described above, patients with Glycogen Storage Disease Type Ib can develop frequent bacterial and fungal infections, due to abnormal functioning of the white blood cells. They may also develop chronic pancreatitis, chronic inflammatory bowel disease, and Crohn's disease. \n\nThe diagnosis of Type I GSD will always include blood studies, x-rays (including some of the kidneys), measurements, and ultrasound of the liver. Gene-based mutation analysis can be used to diagnose the majority of Type I patients, while liver biopsy analysis may be needed in some cases. \n\nThe treatments of Type I Glycogen Storage Disease are aimed at correcting the biochemical abnormalities and promoting growth and development. Current treatments consist of providing a continuous source of glucose by giving the patient glucose drinks frequently during the day and, in most cases, continuously overnight. Many medical centers have replaced these glucose feedings with uncooked cornstarch doses, mixed in water, Kool-Aid, or formula. \n\nLinks:\nvon Gierke Disease info from National Organization for Rare Disorders            [NORD]\nOMIM GSD Type I on Online Mendelian Inheritance in Man\n     searchable database\nGSD Type I from emedicine\nAmerican Liver Foundation information on Type I\nvon Gierke D
479864
I think it depends on what stage it is at.  You should check with a doctor though.  Also, it depends a lot on diet and current health of the individual...as well as personal internal attitude.  I knew someone who had multiple myaloma (cancer of the bone marrow) and the normal term for that is supposed to be six months....she lived for three years beyond that!  She was always positive about life though and went about it with lots of energy until her last days.  And she was older than 35 -- she was 57 when she died.
456832
http://www.webmd.com/content/article/7/1680_53609.htm