Canavan disease: noiembrie 2012

vineri, 30 noiembrie 2012

Sir Peter Alexander Ustinov ? Renaissance Funny Man

Sir Peter Ustinov was one of Britain's greatest icons and is recognised worldwide as one of the greatest comic actors, dramatist, director, writer of the 20th Century. I thought it would be interesting to write the story of this famous icon from his birth in London on April 26th 1921 to his present day status as a great British Icon.
He was born Peter Alexander Freiherr von Ustinov on April 16, 1921, in Swiss Cottage, London, England. Ustinov was of Russian, German, French, Italian and Ethiopian descent, with ancestral connections to Russian nobility as well as the Ethiopian Royal Family. His grandmother, Magdalena, was daughter of a Swiss military engineer and Ethiopian princess. His father, Iona von Ustinov, also known as "Klop" in Russian and Yiddish, was a pilot in Luftwaffe during the First World War. In 1919 he joined his mother and sister in St. Petersburg, Russia. There he met artist Nadia Benois who worked for the Imperial Mariinsky Ballet and Opera House in St. Petersburg. In 1920, in a modest and discrete ceremony at a Russian-German Church in St. Petersburg, Ustinov's father married Nadia Benois. Later, when she was 7 months pregnant with Peter Ustinov, the couple emigrated from Russia in 1921, in the aftermath of the Communist Revolution. Young Peter Ustinov was brought up in a
multi-lingual family, he was fluent in Russian, French, Italian, and German, and also was a native English speaker. He attended the Westminster College in 1934-37, took the drama and acting class under Michel St. Denis at the London Theatre Studio, 1937-39, and made his stage debut in 1938, in a theatre in Surrey. In 1939, he made his London stage debut in a revue sketch, then had regular performances with Aylesbury Repertory Company. In 1940 he made his film debut in Hullo Fame (1940). From 1942-46 Ustinov served as a private soldier with the British Army's Royal Sussex Regiment, during the Second World War. He was batman for David Niven and the two became life-long friends. Ustinov spent most of his service working with the Army Cinema Unit, where he was involved in making recruitment films, wrote plays, and appeared in three films as actor. At that time he wrote and directed his film, The Way Ahead (1944) (aka.. The Immortal Battalion). Eventually, U
stinov made a stellar film career as actor, director, and writer, appearing in more than 100 film and television productions. He was awarded two Oscars for Best Supporting Actor, one for his role in Spartacus (1960) and one for his role in Topkapi (1964); and received two more Oscar nominations as an actor and writer. During the 1970s he had a slowdown in his career, before making a comeback as Hercule Poirot in Death on The Nile (1978) by director John Guillermin. In the 1980s, Ustinov reprised the Poirot role in several subsequent television movies and theatrical films, such as Evil under the Sun (1982) and Appointment with Death (1988). Later he appeared as a sympathetic doctor in the disease thriller Lorenzo's Oil (1992). Ustinov's effortless style, his expertise in dialectal and physical comedy made him a regular guest of numerous talk shows and late night comedians. His witty and multi-dimensional humour was legendary, and he later published a collection of
his jokes and quotations, summarizing his wide popularity as a raconteur. He was also an internationally acclaimed TV journalist. For one of his projects Ustinov covered over one hundred thousand miles and visited more than 30 Russian cities during the making of his well-received BBC television series 'Peter Ustinov's Russia'. In his autobiographical books, such as 'Dear Me' (1977) and 'My Russia' (1996), Ustinov revealed a wealth of thoughtful and deep observations about how his life and career was formed by his rich multi-cultural and multi-ethnic background. Ustinov wrote and directed numerous stage plays, having success with presenting his plays in several countries, such as his 'Photofinish' had acclaimed staging in New York, London, and St. Petersburg, Russia, starring Elena Solovey and Petr Shelokhonov among other actors. Outside of his film and acting professions, Ustinov served as a roving ambassador for the United Nations Children's Fund. He w
as knighted Sir Peter Ustinov in 1990. From 1971 to his death in 2004, Ustinov lived in his own Chteau in the village of Bursins, Vaud, Switzerland, He died of a heart failure on March 28, 2004, in Genolier, Vaud, Switzerland. His funeral service was held at Geneva's historic cathedral of St. Pierre, and he was laid to rest in the village cemetery of Bursins, Switzerland. He was survived by three daughters, Tamara, Pavla, and Andrea, and son, Igor Ustinov.

"I am an international citizen conceived in Russia, born in England, working in Hollywood, living in Switzerland, and touring the World" said Peter Ustinov.
Please visit my Funny Animal Art Prints Collection @ 
My other website is called Directory of British Icons: 
The Chinese call Britain 'The Island of Hero's' which I think sums up what we British are all about. We British are inquisitive and competitive and are always looking over the horizon to the next adventure and discovery. 
Please feel free to vote for my article by scrolling down the page and clicking Stars.
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joi, 29 noiembrie 2012

Scoring System for Plain Chest Radiographs in Patients with Asbestos Related Disease

One interesting study is called, "Methods for the quantitative determination of asbestos and quartz in bulk samples using X-ray diffraction" by M. Taylor - Analyst, 1978, 103, 1009 � 1020. Here is an excerpt: "Procedures are described for the quantitative determination of the asbestos and -quartz contents of bulk samples by use of X-ray powder diffractometry. The method gives satisfactory results for several different types of asbestos and for mixtures of two or more different types. Problems with sample grinding and preferred-orientation effects have been largely overcome. An effective procedure has been developed for grinding samples to a suitable particle size for accurate quantitative work. This procedure works equally well for all the types of asbestos studied and the sample is intimately mixed with the internal standard, nickel (II) oxide, at the same time. A sample press has been designed that enables the same pressure to be applied to each sample when sample holder
s are filled for the diffractometer, giving the same degree of preferred orientation each time. Calibration lines have been calculated for chrysotile, amosite, crocidolite and anthophyllite, and results are given for mixtures containing two or more types of asbestos as well as other commonly occurring minerals.Similar techniques are used to grind samples containing quartz and to mix them with internal standard. Work on both synthetic and real samples is described and results are compared with those obtained by use of an infrared spectroscopic method."
Another interesting study is called, "A new high resolution computed tomography scoring system for pulmonary fibrosis, pleural disease, and emphysema in patients with asbestos related disease." By N A Jarad, P Wilkinson, M C Pearson, R M Rudd - Br J Ind Med 1992;49:73-84. Here is an excerpt: "Abstract - The aim of this study was to describe a scoring system for high resolution computed tomographic (HRCT) scans analogous to the International Labour Office (ILO) scoring system for plain chest radiographs in patients with asbestos related disease. Interstitial fibrosis, pleural disease, and emphysema were scored, the reproducibility and the interobserver agreement using this scoring system were examined, and the extent of the various types of disease was correlated with measurements of lung function. Sixty asbestos workers (five women and 55 men) mean age 59 (range 34-78) were studied. The lungs were divided into upper, middle, and lower thirds. An HRCT score for the extent o
f pleural disease and pulmonary disease in each third was recorded in a way analogous to the International Labour Office (ILO) method of scoring pleural and parenchymal disease on chest radiographs. A CT score for the extent of emphysema was also recorded. Pleural disease and interstitial fibrosis on the plain chest radiographs were assessed according to the ILO scoring system. A chest radiographic score for emphysema analogous to that used for HRCT was also recorded. Two independent readers assigned HRCT scores that differed by two categories or less in 96%, 92%, and 85% compared with 90%, 78%, and 79% of cases for chest radiographs for fibrosis, emphysema, and pleural disease respectively. There was better intraobserver repeatability for the HRCT scores than for the chest radiograph scores for all disorders. Multiple regression analysis showed that scores for interstitial fibrosis, emphysema, and pleural disease on chest radiographs and HRCT correlated to a similar degree
with impairment of lung function."

Another interesting study is called, "Declining Relative Risks for Lung Cancer After Cessation of Asbestos Exposure" by Walker, Alexander M. M.D., Dr. P.H. - June 1984 - Volume 26 - Issue 6. Here is an excerpt: "Abstract All studies that provide follow-up information for workers more than 35 years after initial exposure to asbestos show a declining ratio of observed to expected lung cancer deaths at the end of follow-up. The most parsimonious explanation of this finding is that relative risk for lung cancer begins to decline sometime after cessation of asbestos exposure."
Another interesting study is called, "Scavengers of active oxygen species prevent cigarette smoke-induced asbestos fiber penetration in rat tracheal explants." By A. Churg, J. Hobson, K. Berean, and J. Wright - Am J Pathol. 1989 October; 135(4): 599�603. Here is an excerpt: "Abstract - It was previously shown that rat tracheal explants first exposed to cigarette smoke and then to amosite asbestos take up more asbestos fibers than explants exposed to air and asbestos. To examine the mechanism of this process, the same experimental design was followed but test groups were added in which the asbestos was mixed with catalase or superoxide dismutase, scavengers of active oxygen species, or deferoxamine, an iron chelator that prevents formation of hydroxyl radical. All three agents protected against the cigarette smoke effect. Heat inactivated catalase or superoxide dismutase was not protective. These observations indicate that active oxygen species, probably derived from the ci
garette smoke, play a role in smoke-mediated fiber transport into tracheobronchial epithelia."
If you found any of these excerpts interesting, please read the studies in their entirety. We all owe a debt of gratitude to these researchers for their hard work. <a href="http://iautoblog.com">iAutoblog</a> the premier <a href="http://iautoblog.com">autoblogger</a> software

miercuri, 28 noiembrie 2012

Vinegar: condiment, cleaner - or essence of life?

For most people, that bottle of vinegar sitting on the pantry shelf serves a multitude of purposes. Not only is it a condiment, food preservative, and a general household cleaner, but for many, it's a medicinal wonder. Most often, it's taken for granted, and people only see a bottle of vinegar. However, to scientists studying the origins of life on Earth, acetic acid/vinegar, is thought to have played the key role in biochemical development of the first primitive life forms, and without it, life, as we know it would not exist.
Historical documentation of vinegar's use for dye making, medicinal purposes, invigorating tonics, a condiment, and as a food preservative dates back to the earliest known records. Natural vinegar is produced by the secondary fermentation of the alcohol in wine and is a three to five percent solution of acetic acid in water. Acetic acid is what gives vinegar its distinctive biting taste and aroma. It was probably the first commercially produced acid in the world. Acetic acid in fundamental to our existence, not only from a essential biological standpoint, but also in the production of chemicals, light industry, textiles, pharmaceuticals, printing/dyeing, rubber, pesticides, plastics, photographic chemicals, electronics, and food processing to name a few. In nature, a family of bacteria called acetobacter converts alcohol into acetic acid, and they are the single largest producer of acetic acid to keep Earth's the life machine running. The micro
scopic, acid resistant critters are pervasive in the environment. They thrive in the alcoholic ecological niches of flowers, fruits, water, soil, and in a dormant stage, they're even floating around in the air we breathe. Acetobacter also thrive in the intestines of all living creatures where they are essential to the digestive process and most likely, the major suppliers of acetate to keep our system functioning. According to the widely accepted Wchtershuser's theory on how primitive life forms evolved from the primordial soup, the first organic molecule in the chain of events was acetic acid. He based his theory on the fact that the formation of acetic acid is a primary step in metabolism in most all living things that provides the energy cells use to manufacture all the biological ingredients an organism needs to exist. There is a metabolic activity essential to life called acetylation, and among many other roles the process has in the body, it also plays th
e key role in the repair of DNA. A study published in the 2000 Elsevier publication Cell about DNA repair states: "Data show that cells defective for DNA-break repair capability lack the histone acetylase [acetylation] activity leading to apoptotic machinery breakdown." Acetate hemodialysis is a common therapy for people suffering with kidney failure. In several studies, aside from acetate's buffering effect, it has shown to aid in dialysis by dilating veins, thus increasing the effectiveness of the treatment. One 1987 study on stated: "Acetate provoked vascular dilatation, which was compensated for by a heart rate-dependent increase in cardiac index." Acetic acid is fundamental to the biochemistry of almost all forms of life. It's the foundation for the acetyl/acetate group which is a plays the essential in the Krebs Cycle/Citric Acid cycle. The Krebs Cycle occurs in all plants and animals. The importance of the function lies in the
efficiency with which it captures energy released from nutrient molecules and stores it in a usable form.
In humans and animals, functioning of the Krebs cycle relies on a product produced in our system called Acetyl Coenzyme A created during the synthesis of fatty acids. Another acetate-based enzyme called Acetyl Cholinesterase/AchE is integral to the operation of brain functions and the central nervous system. In fact, there are a number of acetyl-based enzymes that are essential to human/animal life down to the chemical composition of genes. Curiously, when it comes to explaining where the acetate comes from to feed the processes, scientists' explanations seem to be somewhat vague, convoluted, and often, contradictory. However, aside from the metabolic production of acetate by organ functions, large amounts of acetic acid is produced by acetobacter in the intestines which is absorbed into the system; and it would logically appear that that process provides most of the acetate needed. In a 1985 study published in the Journal of Clinical Investiga
tion, Carbohydrate fermentation in the human colon and its relation to acetate concentrations in venous blood, the authors' state: "These studies show that the large intestine makes an important contribution to blood acetate levels in man and that fermentation may influence metabolic processes well beyond the wall of this organ." Several studies suggest that there may be such a thing as an acetate deficiency, and acetate supplementation may be useful in the treatment of Canavan disease, a hereditary, neurodegenerative disorder. In folk medicine, apple cider vinegar is touted as a cure for many health problems such as a host of allergies, sinus infections, acne, high cholesterol, flu, chronic fatigue, candida, acid reflux, sore throats, contact dermatitis, arthritis, and gout. While apple cider vinegar is the traditional choice, the only ingredient of any volume that may have an effect at the dosage recommended (one two tablespoons a day) is
acetic acid. As far as cider vinegar's effectiveness for alleviating gout and arthritis symptoms, the anecdotal (testimonial) evidence is overwhelming. And some studies give credence to the claim; however, they all point to the acetic acid content. The interesting aspect of the cider vinegar is that unlike the parent apple for which, possibly, is the most well researched fruit, there is no research to be about cider vinegar or even plain of vinegar as having any health benefits. To an investigative writer, in light of all the abundant health claims made for cider vinegar, the paucity of research, especially to disprove the claims, evokes a great deal of suspicion the unmistakable aroma of a rat rotting somewhere in the woodwork. It's most unusual not to see volumes of scientific studies into a product that is so entrenched in folk medicine. Both the parochial scientists and naturopaths fail to see the possibility of acetate deficiencies. Maybe, i
t's simply a question of not seeing the forest for the for the [apple] trees.' However, the role of acetate in animal health has been well researched in animal husbandry, and farm animal feedstock is routinely supplemented with either vinegar or acetic acid. However, when realizing that primordial formation of acetic acid is postulated to be responsible for the creation of the first life on earth, and the essential function acetate plays in biochemistry, there has to be something special about vinegar. ### <a href="http://iautoblog.com">iAutoblog</a> the premier <a href="http://iautoblog.com">autoblogger</a> software

marți, 27 noiembrie 2012

Vitamin B12 - Why do we need it?

"If it swims, flies or runs, it has vitamin B12" - Dr Victor Herbert
One of the major nutritional problems that people on a non-meat diet face is the inability to obtain suitable sources of bioavailable vitamin B12. This is particularly worse in those that also do not eat fish and even more pronounces in the strict vegan or lacto-ova group.
Plants do not produce vitamin B12 unless they are contaminated with a vitamin B12 producing microorganism and although the large intestine manufactures a large quantity of vitamin B12, it does not reach the small intestine where is is absorbed.
Therefore, animal protein in the only source of vitamin B12 because as Dr Herbert's quote states "If it swims, flies or runs, it has vitamin B12".
Why do we need vitamin B12?
Vitamin B12, working with folic acid, maintain the myelin sheath around the nerve structures. This insulating sheath stop the electrical impulses from "shorting out" across breaks in the insulation. Multiple sclerosis would have to be the most publicly known form of a disease with decreased myelin, others include; acquired toxic metabolic disorder, HIV Encephalitis, Progressive Multifocal Leukoencephalopathy and Canavan Disease.
Vitamin B12 is also responsible for the maintenance of bone marrow which is essential for the production of healthy red blood cells.

Most importantly, vitamin B12 maintains and supports the health of every cell in the body and is a major contributor to the production of DNA and RNA, both essential to cell replication and life itself.
Vitamin B12 is not very effective by itself. For best results, vitamin B6 and folic acid are required as they act synergistically. This is evident when vitamin B12 is involved in the conversion of amino acids into neurotransmitters as without the help of vitamin B6, this would not occur.
Elevated levels of homocysteine (a condition called hyperhomocysteinemia) is responsible for an increase risk of hardening of the arteries (atherosclerosis) which could eventually lead to a heart attack or stroke, and also an increased incidence of blood clots which could also lead to a stroke. A rare genetic condition with the acronym of MTHFR Inhibitor causes increased levels of homocysteine.
Vitamin B12 acts as a methyl donor in the metabolism of homocysteine to a less damaging component called methionine. Vitamins B12, B6 and Folic acid are all involved in the reduction of homocysteine.
Absorption of Vitamin B12
Vitamin B12 is only absorbed in the lower portion of the small bowel or from mucosal lining such as those found in the mouth.
Vitamin B12 is tolerant to high heat for short periods of time and there is very little loss so the best way to cook meat is to pan fry, BBQ or grill. Boiling meat at high temperatures for 45 minutes will result in a 30% loss of vitamin B12.
Unfortunately, taking tablets has little effect on the amount of vitamin B12 that is absorbed as the acids in the stomach and only about 1% of ingested vitamin B12 is actually absorbed. That means you are throwing away 99% of your vitamin B12 supplement which is generally excreted in the urine.
There are two effective methods of obtaining vitamin B12 from sources other than food. These are the painful and expensive injections from the doctor or a sublingual B12 supplement such as that offered by Trivita.
Taking sublingual B12 (with vitamin B6 and folic acid) is the most cost effective and painless way to get a daily dose of these essential vitamins.
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luni, 26 noiembrie 2012

Hereditary Endowments

Hereditary endowments are one of the events that take place during fertilization. The chromosomes in mature male cell contain nearly 40,000 to 60,000 genes and the equal number in a mature ovum, i.e., female cell. Thus the newly produced baby's hereditary endowment contains 80,000 to 1,20,000 genes, each carrying potentials for physical and mental traits. The inherited characteristics of a baby is determined the possible combinations of chromosomes passed from different ancestors on the maternal or paternal side. Thus the union of sperm and ovum means the blending of two distinct hereditary lines will result into newly conceived individual. This baby form its own distinct personality by inheriting characters from parents, grandparents and other more remote ancestors. Though most of the inherited characteristics are influenced by environment, other characteristics like eye color and skin texture are not influenced by environmental conditions. Favorable environ
mental conditions, stimulates genetic prospective while unfavorable environmental conditions throttle this development. Laws of heredity determine what we are to be and what we will do in this world by third or fourth week of our prenatal existence. The genes thus transferred may also carry diseases to progeny also along with them. These disorders may develop either due to suffering of mother from some infection or due to side effect of certain drugs or chemicals or exposure to radiation during pregnancy. Rubella can result in the baby born with a heart defect, mental retardation etc. Other innate problems involve Down's syndrome, hemophilia, sickle cell anemia, Color blindness, Neurofibromatosis, Cystic fibrosis, Celiac disease, Canavan disease to name a few. About an average of 2% babies are born with serious diseases.
The amount of estrogen gradually increases, the lining of the uterus thickens and ovarian follicles devlops in the follicular phase. The egg is released from the potential follicle when Luteinizing Hormone acts on ovary and this is better known as ovulation. Ovulation typically occurs mid-cycle, usually 14th day. Factors Affecting Physical Development The physical development of an individual in their life is greatly affected by hereditary endowments which took place at the time of conception. Hereditary endowments place limits beyond which an individual cannot go. The hereditary endowment is purely a matter of chance; it cannot be controlled by any means. Both environmental and hereditary factors combined together to have a significant effects on physical development of a child. Below are some of the heredity characters that affects physical traits and growth of child: Genes In Heredity Genes are
passed from both the parents to an individual. These Genes carry information about height, weight, skin color, eye color, hair color, cognitive and mental processes through generations. Dominant and Recessive There are always a recessive gene and a dominant gene. The characteristic that will appear physically in front of all is according to the information carried by dominant genes. For instance, if one parent has dark hair and the other has light, the dominant gene will determine the color of the resulting child's hair. Milestones The physical development in children is measured in milestones at specific ages. Physicians use these developmental milestones to gauge the growth of the child. He can monitor if the child is making adequate physical progress or not. Disorders Sometimes an abnormality occurs in the DNA of parents which is carried to offsprings. This abnorma
lity results in physical disorders in a child. The Genetic disorders cause cerebral palsy, spina bifida, and cystic fibrosis, like physical disabilities.
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duminică, 25 noiembrie 2012

Vinegar: condiment, cleaner - or essence of life?

For most people, that bottle of vinegar sitting on the pantry shelf serves a multitude of purposes. Not only is it a condiment, food preservative, and a general household cleaner, but for many, it's a medicinal wonder. Most often, it's taken for granted, and people only see a bottle of vinegar. However, to scientists studying the origins of life on Earth, acetic acid/vinegar, is thought to have played the key role in biochemical development of the first primitive life forms, and without it, life, as we know it would not exist.
Historical documentation of vinegar's use for dye making, medicinal purposes, invigorating tonics, a condiment, and as a food preservative dates back to the earliest known records. Natural vinegar is produced by the secondary fermentation of the alcohol in wine and is a three to five percent solution of acetic acid in water. Acetic acid is what gives vinegar its distinctive biting taste and aroma. It was probably the first commercially produced acid in the world. Acetic acid in fundamental to our existence, not only from a essential biological standpoint, but also in the production of chemicals, light industry, textiles, pharmaceuticals, printing/dyeing, rubber, pesticides, plastics, photographic chemicals, electronics, and food processing to name a few. In nature, a family of bacteria called acetobacter converts alcohol into acetic acid, and they are the single largest producer of acetic acid to keep Earth's the life machine running. The micro
scopic, acid resistant critters are pervasive in the environment. They thrive in the alcoholic ecological niches of flowers, fruits, water, soil, and in a dormant stage, they're even floating around in the air we breathe. Acetobacter also thrive in the intestines of all living creatures where they are essential to the digestive process and most likely, the major suppliers of acetate to keep our system functioning. According to the widely accepted Wchtershuser's theory on how primitive life forms evolved from the primordial soup, the first organic molecule in the chain of events was acetic acid. He based his theory on the fact that the formation of acetic acid is a primary step in metabolism in most all living things that provides the energy cells use to manufacture all the biological ingredients an organism needs to exist. There is a metabolic activity essential to life called acetylation, and among many other roles the process has in the body, it also plays th
e key role in the repair of DNA. A study published in the 2000 Elsevier publication Cell about DNA repair states: "Data show that cells defective for DNA-break repair capability lack the histone acetylase [acetylation] activity leading to apoptotic machinery breakdown." Acetate hemodialysis is a common therapy for people suffering with kidney failure. In several studies, aside from acetate's buffering effect, it has shown to aid in dialysis by dilating veins, thus increasing the effectiveness of the treatment. One 1987 study on stated: "Acetate provoked vascular dilatation, which was compensated for by a heart rate-dependent increase in cardiac index." Acetic acid is fundamental to the biochemistry of almost all forms of life. It's the foundation for the acetyl/acetate group which is a plays the essential in the Krebs Cycle/Citric Acid cycle. The Krebs Cycle occurs in all plants and animals. The importance of the function lies in the efficiency with which it ca
ptures energy released from nutrient molecules and stores it in a usable form.
In humans and animals, functioning of the Krebs cycle relies on a product produced in our system called Acetyl Coenzyme A created during the synthesis of fatty acids. Another acetate-based enzyme called Acetyl Cholinesterase/AchE is integral to the operation of brain functions and the central nervous system. In fact, there are a number of acetyl-based enzymes that are essential to human/animal life down to the chemical composition of genes. Curiously, when it comes to explaining where the acetate comes from to feed the processes, scientists' explanations seem to be somewhat vague, convoluted, and often, contradictory. However, aside from the metabolic production of acetate by organ functions, large amounts of acetic acid is produced by acetobacter in the intestines which is absorbed into the system; and it would logically appear that that process provides most of the acetate needed. In a 1985 study published in the Journal of Clinical Investiga
tion, Carbohydrate fermentation in the human colon and its relation to acetate concentrations in venous blood, the authors' state: "These studies show that the large intestine makes an important contribution to blood acetate levels in man and that fermentation may influence metabolic processes well beyond the wall of this organ." Several studies suggest that there may be such a thing as an acetate deficiency, and acetate supplementation may be useful in the treatment of Canavan disease, a hereditary, neurodegenerative disorder. In folk medicine, apple cider vinegar is touted as a cure for many health problems such as a host of allergies, sinus infections, acne, high cholesterol, flu, chronic fatigue, candida, acid reflux, sore throats, contact dermatitis, arthritis, and gout. While apple cider vinegar is the traditional choice, the only ingredient of any volume that may have an effect at the dosage recommended (one two tablespoons a day) is acetic acid. As far as cider vinegar's effectiveness for alleviating gout and arthritis symptoms, the anecdotal (testimonial) evidence is overwhelming. And some studies give credence to the claim; however, they all point to the acetic acid content. The interesting aspect of the cider vinegar is that unlike the parent apple for which, possibly, is the most well researched fruit, there is no research to be about cider vinegar or even plain of vinegar as having any health benefits. To an investigative writer, in light of all the abundant health claims made for cider vinegar, the paucity of research, especially to disprove the claims, evokes a great deal of suspicion the unmistakable aroma of a rat rotting somewhere in the woodwork. It's most unusual not to see volumes of scientific studies into a product that is so entrenched in folk medicine. Both the parochial scientists and naturopaths fail to see the possibility of acetate deficiencies. Maybe, it's simply a quest
ion of not seeing the forest for the for the [apple] trees.' However, the role of acetate in animal health has been well researched in animal husbandry, and farm animal feedstock is routinely supplemented with either vinegar or acetic acid. However, when realizing that primordial formation of acetic acid is postulated to be responsible for the creation of the first life on earth, and the essential function acetate plays in biochemistry, there has to be something special about vinegar. ### <a href="http://iautoblog.com">iAutoblog</a> the premier <a href="http://iautoblog.com">autoblogger</a> software

sâmbătă, 24 noiembrie 2012

Vitamin B12 - Why do we need it?

"If it swims, flies or runs, it has vitamin B12" - Dr Victor Herbert
One of the major nutritional problems that people on a non-meat diet face is the inability to obtain suitable sources of bioavailable vitamin B12. This is particularly worse in those that also do not eat fish and even more pronounces in the strict vegan or lacto-ova group.
Plants do not produce vitamin B12 unless they are contaminated with a vitamin B12 producing microorganism and although the large intestine manufactures a large quantity of vitamin B12, it does not reach the small intestine where is is absorbed.
Therefore, animal protein in the only source of vitamin B12 because as Dr Herbert's quote states "If it swims, flies or runs, it has vitamin B12".
Why do we need vitamin B12?
Vitamin B12, working with folic acid, maintain the myelin sheath around the nerve structures. This insulating sheath stop the electrical impulses from "shorting out" across breaks in the insulation. Multiple sclerosis would have to be the most publicly known form of a disease with decreased myelin, others include; acquired toxic metabolic disorder, HIV Encephalitis, Progressive Multifocal Leukoencephalopathy and Canavan Disease.
Vitamin B12 is also responsible for the maintenance of bone marrow which is essential for the production of healthy red blood cells.

Most importantly, vitamin B12 maintains and supports the health of every cell in the body and is a major contributor to the production of DNA and RNA, both essential to cell replication and life itself.
Vitamin B12 is not very effective by itself. For best results, vitamin B6 and folic acid are required as they act synergistically. This is evident when vitamin B12 is involved in the conversion of amino acids into neurotransmitters as without the help of vitamin B6, this would not occur.
Elevated levels of homocysteine (a condition called hyperhomocysteinemia) is responsible for an increase risk of hardening of the arteries (atherosclerosis) which could eventually lead to a heart attack or stroke, and also an increased incidence of blood clots which could also lead to a stroke. A rare genetic condition with the acronym of MTHFR Inhibitor causes increased levels of homocysteine.
Vitamin B12 acts as a methyl donor in the metabolism of homocysteine to a less damaging component called methionine. Vitamins B12, B6 and Folic acid are all involved in the reduction of homocysteine.
Absorption of Vitamin B12
Vitamin B12 is only absorbed in the lower portion of the small bowel or from mucosal lining such as those found in the mouth.
Vitamin B12 is tolerant to high heat for short periods of time and there is very little loss so the best way to cook meat is to pan fry, BBQ or grill. Boiling meat at high temperatures for 45 minutes will result in a 30% loss of vitamin B12.
Unfortunately, taking tablets has little effect on the amount of vitamin B12 that is absorbed as the acids in the stomach and only about 1% of ingested vitamin B12 is actually absorbed. That means you are throwing away 99% of your vitamin B12 supplement which is generally excreted in the urine.
There are two effective methods of obtaining vitamin B12 from sources other than food. These are the painful and expensive injections from the doctor or a sublingual B12 supplement such as that offered by Trivita.
Taking sublingual B12 (with vitamin B6 and folic acid) is the most cost effective and painless way to get a daily dose of these essential vitamins.
For more information, please visit <a rel="nofollow" onclick="javascript:_gaq.push(['_trackPageview', '/outgoing/article_exit_link/5191439']);" href=""></a> <a href="http://iautoblog.com">iAutoblog</a> the premier <a href="http://iautoblog.com">autoblogger</a> software

vineri, 23 noiembrie 2012

Hereditary Endowments

<a rel="nofollow" onclick="javascript:_gaq.push(['_trackPageview', '/outgoing/article_exit_link/3942897']);" href="/ArticleHereditaryendowments.aspx" target="_self" title="Article on Hereditary endowments">Hereditary endowments</a> are one of the events that take place during fertilization. The chromosomes in mature male cell contain nearly 40,000 to 60,000 genes and the equal number in a mature ovum, i.e., female cell. Thus the newly produced baby's hereditary endowment contains 80,000 to 1,20,000 genes, each carrying potentials for physical and mental traits. The inherited characteristics of a baby is determined the possible combinations of chromosomes passed from different ancestors on the maternal or paternal side. Thus the union of sperm and ovum means the blending of two distinct hereditary lines will result into newly conceived individual. This baby form its own distinct personality by inheriting characters from parents, grandparents and other more remote anc
estors. Though most of the inherited characteristics are influenced by environment, other characteristics like eye color and skin texture are not influenced by environmental conditions. Favorable environmental conditions, stimulates genetic prospective while unfavorable environmental conditions throttle this development. Laws of heredity determine what we are to be and what we will do in this world by third or fourth week of our prenatal existence. The genes thus transferred may also carry diseases to progeny also along with them. These disorders may develop either due to suffering of mother from some infection or due to side effect of certain drugs or chemicals or exposure to radiation during <a rel="nofollow" onclick="javascript:_gaq.push(['_trackPageview', '/outgoing/article_exit_link/3942897']);" href="" target="_self" title="Pregnancy tips">pregnancy</a>. Rubella can result in the baby born with a heart defect, mental retardation etc. Other innate problems
involve Down's syndrome, hemophilia, sickle cell anemia, Color blindness, Neurofibromatosis, Cystic fibrosis, Celiac disease, Canavan disease to name a few. About an average of 2% babies are born with serious diseases.
The amount of estrogen gradually increases, the lining of the uterus thickens and ovarian follicles devlops in the follicular phase. The egg is released from the potential follicle when Luteinizing Hormone acts on ovary and this is better known as ovulation. Ovulation typically occurs mid-cycle, usually 14th day. Factors Affecting Physical Development The physical development of an individual in their life is greatly affected by hereditary endowments which took place at the time of conception. Hereditary endowments place limits beyond which an individual cannot go. The hereditary endowment is purely a matter of chance; it cannot be controlled by any means. Both environmental and hereditary factors combined together to have a significant effects on physical development of a child. Below are some of the heredity characters that affects physical traits and growth of child: Genes In Heredity Genes are
passed from both the parents to an individual. These Genes carry information about height, weight, skin color, eye color, hair color, cognitive and mental processes through generations. Dominant and Recessive There are always a recessive gene and a dominant gene. The characteristic that will appear physically in front of all is according to the information carried by dominant genes. For instance, if one parent has dark hair and the other has light, the dominant gene will determine the color of the resulting child's hair. Milestones The physical development in children is measured in milestones at specific ages. Physicians use these developmental milestones to gauge the growth of the child. He can monitor if the child is making adequate physical progress or not. Disorders Sometimes an abnormality occurs in the DNA of parents which is carried to offsprings. This abnorma
lity results in physical disorders in a child. The Genetic disorders cause cerebral palsy, spina bifida, and cystic fibrosis, like physical disabilities.
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joi, 22 noiembrie 2012

Symptoms of Canavan Disease

Symptoms of Canavan disease, which appear in early infancy and progress rapidly, may include mental retardation, loss of previously acquired motor skills, feeding difficulties, abnormal muscle tone (floppiness or stiffness), and an abnormally large, poorly controlled head. Paralysis, blindness, or hearing loss may also occur.

 Children are characteristically quiet and apathetic. Although Canavan disease may occur in any ethnic group, it is more frequent among Ashkenazi Jews from eastern Poland, Lithuania, and western Russia, and among Saudi Arabians. The signs of Canavan disease usually appear when the children are between 3 and 6 months of age. They include developmental delay (significant motor slowness), enlargement of the head (macrocephaly), loss of muscle tone (hypotonia), poor head control, and severe feeding problems. As the disease progresses, convulsions (seizures), shrinkage of the nerve to the eye (optic atrophy) and often blondness, heartburn (gastrointestinal reflux) and deterioration of swallowing develop. Symptoms of Canavan disease appear in early infancy and progress rapidly, but generally include rapidly increasing head circumference, lack of head control, reduced visual responsiveness and abnormal muscle tone such as stiffness or fl
oppiness. Canavan disease can be identified by a simple prenatal blood test that screens for the missing enzyme or for mutations in the gene that controls aspartoacylase. The signs of Canavan disease usually appear between 3 to 6 months of age. The signs include developmental delay (significant motor slowness), enlargement of the head (macrocephaly), loss of muscle tone (hypotonia), poor head control, and severe feeding problems. Symptoms of Canavan disease, which appear in early infancy and progress rapidly, may include mental retardation, loss of previously acquired motor skills, feeding difficulties, abnormal muscle tone (i.e., floppiness or stiffness), poor head control, and megalocephaly (abnormally enlarged head). Paralysis, blindness, or seizures may also occur.
 Affected children may also have mental retardation, feeding difficulties and loss of previously acquired motor skills. Paralysis, blindness, or hearing loss may also occur. Children with CD are characteristically quiet and apathetic. As the child grows, motor skills and mental functioning deteriorate. The child eventually becomes blind, but hearing remains sharp. Affected children continue to recognize and respond to the voices of their primary caregivers. Difficulties which arise as the child grows include stiffness, weakness of the muscles, seizures, and feeding problems. May include mental retardation, loss of previously acquired motor skills, feeding difficulties, abnormal muscle tone (i.e., floppiness or stiffness), poor head control, and megalocephaly (abnormally enlarged head). Paralysis, blindness, or seizures may also occur. Typically, symptoms begin in the first year of life. Parents tend to notice when a child is not
reaching particular developmental milestones, including lack of head control. The child will also have poor muscle tone. Eventually, the child can develop feeding problems, seizures, and loss of vision. Although death often occurs before 18 months of age, some patients live until they are teenagers or, rarely, young adults. Thalassemia - Individuals of Mediterranean, Southeast Asian and African ancestry have the greatest chance 1 in 3 and 1 in 30, respectively of being carriers for thalassemia. In general, this group of blood disorders affects a person's ability to produce hemoglobins, the protein in our blood that carries oxygen and nutrients to all parts of the body. In severe cases, children with thalassemia may not survive. Others have anemia, bone growth problems and liver and spleen involvement. Blood transfusions may be needed for treatment. <a href="http://iautoblog.com">iAutoblog</a> the premier <a href="http://iautoblog.com">autoblog
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miercuri, 21 noiembrie 2012

Complete Information on Canavan Disease

The Canavan disease is the aspartic acid metabolism the confusion which inherits. It for degeneration (dispersing) brain white question description. This kind of disease the group gene chaotic is called leukodystrophies one by one. The Canavan disease is inherited the autosomal recessive fashion. The Canavan disease creates by a slight defect ASPA gene. This enzyme division by centralized brain member N acetazolamide aspartate. The aspartoacylase activity which reduces is prevented N the acetazolamide aspartate normal breakdown, and lacks the breakdown by some method interference nerve fiber myelin sheath growth in the brain.
The myelin sheath is surrounds the nerve cell and the motion takes the insulator, considered the nerve impulse the high efficiency the transmission fatty cover. The Canavan disease symptom, appears in the early initial period and rapidly progresses, perhaps included previously the movement skillful intelligence flaw, the loss which gained, fed, the unusual muscle difficultly anxious, was unusual big with, badly is controlled the head. Perhaps the paralysis, blindness, or hearing loss and occurs. The child typically peaceful and is aloof. The Canavan disease possibly identifies that screen by the simple pre-natal blood test for to lack the enzyme. Canavan disease causes progressive brain atrophy. Treatment is symptomatic and supportive. There is no cure or effective treatment for Canavan disease but several approaches are currently being explored. The first is gene therapy whereby functional aspartoacylase genes are introduced into an affected child's brain to increa
se the levels of aspartoacylase. The second is the introduction of functional neuronal stem cells into an affected child's brain to increase the number of neurons that make aspartoacylase. Physical therapy minimizes contractures and maximizes motor abilities and seating posture. Seizures are treated with anti-epileptic drugs. <a href="http://iautoblog.com">iAutoblog</a> the premier <a href="http://iautoblog.com">autoblogger</a> software

marți, 20 noiembrie 2012

Canavan Disease ? Causes and Symptoms of Canavan Disease

Canavan disease is characterized by macrocephaly, lack of head control, and developmental delays by the age of three to five months, severe hypotonia, and failure to achieve independent sitting, ambulation, or speech. Hypotonia eventually changes to spasticity. Assistance with feeding becomes necessary. Life expectancy is usually into the teens. Canavan Disease can be found in people of all ethnicities. However, it has especially high prevalence among Ashkenazi Jewish people; the frequency of carriers is thought to be approximately 1 in every 40 within this population.

 Canavan disease is a rare, but always fatal, inherited , degenerative brain disorders that primarily affects children of eastern and central European Jewish descent. This includes about 90 percent of the Jews in America. It is estimated that one in 40 Ashkenazi Jews is a carrier of the Canavan gene. Is most common in people of Ashkenazi Jewish ancestry, with a carrier incidence of 1 in 40. Canavan disease is a central nervous system disease that is usually fatal in childhood, with a few people surviving to adulthood. This disease is the result of a substance that destroys the central nervous system over time. There is presently no effective treatment for Canavan disease. Causes of Canavan disease Canavan disease belongs to a group of conditions known as leukodystrophies, which result from defects in myelin. Myelin, a substance made up of proteins and lipids, is an integral component of the nervous system. It is commonly known as the "wh
ite matter" in the brain; its function is to protect nerves and allow messages to be sent to and from the brain. In Canavan disease the white matter deteriorates because affected children have a deficiency of the enzyme aspartoacylase, which leads to the accumulation of a chemical, called N-acetyl-aspartic acid (NAA), in the brain.
 A demyelination of nerve cells within the white matter of the brain (the area of the brain in which signals are sent to the other parts of brain and spinal cord). Myelin protects nerve cells, and without it, the proper messages are not able to be sent from the brain to the body. Babies with Canavan disease are missing an essential enzyme called aspartocyclase. Canavan disease is caused by the deficiency of an enzyme, called aspartoacylase. Without this necessary enzyme, a substance (called N-acetylaspartic acid) builds up and damages the brain, resulting in the features of Canavan disease. It is caused by a deficiency of an enzyme called aspartoacylase. Canavan disease is one of a group of genetic disorders called the leukodystrophies that affect growth of the myelin sheath of the nerve fibers in the brain. The myelin sheath is the fatty covering surrounding nerve cells that acts as an insulator. Symptoms of Canavan disease 
 Typically, symptoms begin in the first year of life. Parents tend to notice when a child is not reaching particular developmental milestones, including lack of head control. The child will also have poor muscle tone. Eventually, the child can develop feeding problems, seizures, and loss of vision. The signs of Canavan disease usually appear when the children are between 3 and 6 months of age. They include developmental delay (significant motor slowness), enlargement of the head (macrocephaly), loss of muscle tone (hypotonia), poor head control, and severe feeding problems. As the disease progresses, convulsions (seizures), shrinkage of the nerve to the eye (optic atrophy) and often blondness, heartburn (gastrointestinal reflux) and deterioration of swallowing develop. <a href="http://iautoblog.com">iAutoblog</a> the premier <a href="http://iautoblog.com">autoblogger</a> software

luni, 19 noiembrie 2012

Information on Canavan Disease ?

Canavan disease, one of the most common cerebral degenerative diseases of infancy, is a gene-linked, neurological birth disorder in which the white matter of the brain degenerates into spongy tissue riddled with microscopic fluid-filled spaces. Canavan disease is one of a group of genetic disorders known as the leukodystrophies.

 These diseases cause imperfect growth or development of the myelin sheath, the fatty covering that acts as an insulator around nerve fibers in the brain. Myelin, which lends its color to the "white matter" of the brain, is a complex substance made up of at least ten different chemicals. Each of the leukodystrophies affects one (and only one) of these substances. Canavan disease is caused by mutations in the gene for an enzyme called aspartoacylase. Canavan disease (CD) belongs to a group of conditions known as leukodystrophies, which result from defects in myelin. Myelin, a substance made up of proteins and lipids, is an integral component of the nervous system. It is commonly known as the "white matter" in the brain; its function is to protect nerves and allow messages to be sent to and from the brain. Children with Canavan disease cannot crawl, walk, sit or talk. Over time they may suffer seizures, become paralyzed, mentally retarded or blind and
have trouble swallowing. Although hearing usually remains a functioning sense, deafness may also result. Most children do not live past age 10. Canavan disease is inherited in an autosomal recessive manner. At conception, the sibs of an affected individual have a 25% chance of being affected, a 50% chance of being an asymptomatic carrier, and a 25% chance of being unaffected and not a carrier. Each pregnancy of a couple in which both partners are heterozygous for a disease-causing mutation in the ASPA gene has a 25% chance of resulting in a child with Canavan disease. Prenatal testing for pregnancies at 25% risk is possible when molecular genetic testing has determined the specific ASPA disease-causing allele in both parents.
 The fight to give Max and other children battling Canavan disease, access to the most ambitious research and treatments that can be found, has given way to breakthroughs in gene therapy, which can potentially help millions suffering from neurodegenerative diseases. Canavan disease demonstrates bilateral symmetric T2 white matter hyperintensity, including involvement of the subcortical arcuate fibers. This disease appears diffusely throughout the cerebral white matter, does not enhance at computed tomography (CT) or MR imaging, and demonstrates variable involvement of the basal ganglia and cerebellar white matter . Patients with Alexander disease present with clinical and imaging findings similar to those of patients with Canavan disease; this condition often results in a clinical conundrum. The gene for Canavan disease has been located. Research supported by the NINDS includes studies to understand how the brain and nervous system normally d
evelop and function and how they are affected by genetic mutations. These studies contribute to a greater understanding of gene-linked disorders such as Canavan disease, and have the potential to open promising new avenues of treatment. Genetic screening of Ashkenazi Jewish individuals for Canavan disease carriers can be done by checking for these two mutations. Screening for Canavan disease carriers requires molecular diagnostic methods. Simple enzyme tests, as commonly used in Tay-Sachs screening, cannot be used for Canavan disease because the activity of the deficient enzyme, aspartoacylase, is not detectable in blood. Testing for the most common Canavan disease mutations -- there are actually three of them -- will identify about 97% of Ashkenazi Jewish carriers (and 40-50% of the non-Jewish carriers). <a href="http://iautoblog.com">iAutoblog</a> the premier <a href="http://iautoblog.com">autoblogger</a> software

duminică, 18 noiembrie 2012

Stories of Lives Saved by Cord Blood

The advancements of medicine and technology are saving lives each year that would otherwise be lost to disease or medical disorder. Each year, more and more children are living through potentially terminal diseases and battling their way back to health with help of cord blood. Cord blood is found within the umbilical cord and preserved upon the birth of the child. Since the blood contains stem cells, numerous diseases and disorders are successfully treated and even cured through transplants. Parents today are choosing to either bank cord blood for future use or donate their newborn's cord blood so that ill children can take advantage of this life-saving blood.

An inspiring case is that of siblings Ashley and Kelvin J. of Maryland. These two children were both born with severe combined immunodeficiency syndrome that is usually terminal, since the body's immune system cannot fend off the germs that would otherwise be harmless to a healthy body. Projected life span for children diagnosed with severe combined immunodeficiency syndrome (SCIDS) is approximately six months; however, both Ashley and Kelvin received a transplant of cord blood from anonymous donors whose cord blood was donated to public blood banks. Another story that shows the success of using cord blood to treat potentially deadly diseases and disorders is that of brothers Blayke and Garrett L. of Los Angeles. Born three years apart, both boys developed a rare disorder known as lymphoproliferative disease. Blayke and Garrett's immune systems were unable to successfully fight off germs commonly found in the world around them. Generally, at a very early age childre
n diagnosed with lymphoproliferative disease develop mononucleosis, a potentially fatal disease that individuals with a working immune system commonly recover from. Again, thanks to the donation of cord blood from an anonymous donor, both boys are now living happy and healthy lives due to a blood transplant. If this option was not available, the young brothers' only hope would be a painful and complicated bone marrow transplant that would not have had the same success rate as the cord blood transplant.
In addition to children using donated cord blood to survive the odds, more and more children are using their own cord blood to treat or cure diseases or medical disorders. These diseases are disorders may be present before birth or be developed after birth, but regardless the case, cord blood is an excellent tool in the fight to preserve life. A recent study at Duke University involved children diagnosed with Krabbe's diseasea rare genetic disorder that affects the brain and attacks cognitive and motor functions. Twenty-five children diagnosed with Krabbe's disease were followed and studied regarding their treatments. For those children treated with a cord blood transplant immediately after birth, 100 percent showed positive development and survival, whereas 43 percent of children treated with cord blood transplant after development of symptoms saw success. These children are testament to the vitality of umbilical cord blood and should inspire parents to not let thi
s life-saving blood go to waste. According to the informative Web site <a rel="nofollow" onclick="javascript:_gaq.push(['_trackPageview', '/outgoing/article_exit_link/14872']);" href="">Should You Bank Cord Blood</a>,upon delivery of the child, technicians must work quickly to ensure they preserve the cord blood before it begins to clot and becomes useless. Whether you choose to store your child's cord blood in a private blood bank or donate your child's cord blood to a public blood bank so that it can potentially save the life of an Ashley, Kelvin, Blayke, or Garrett in the country, ensure that your child's cord blood is used in the best possible manner. More and more, hospitals around the country are developing a system to ensure that all cord blood is either stored or donatedbut not wasted. <a href="http://iautoblog.com">iAutoblog</a> the premier <a href="http://iautoblog.com">autoblogger</a> software

sâmbătă, 17 noiembrie 2012

Bluetick Coonhound Dog Breed

Description: The Bluetick Coonhound breed has a broad head with a domed skull. Here we see the muzzle that is square long, deep, broad and has a predominant stop. This breed has round eyes, which are dark brown and widely set.This breed has low ears, and these are thin. The tail is high, tapering to a beautiful point. The legs are straight, from the elbow; we see feet that are compact, with well arched toes. The hind legs are long and muscular. Their coats are glossy and smooth, dense and short, feeling slightly coarse to the touch.The colours of this breed are dark blue, with thick mottled body, spotted with shapes of black spots on the back, we see this on the back, sides, and ears. The tricolour coat as a speckled blue to look at, its heavy ticking is in point of fact made up of black coloured hairs on a white background, which creates a blueing effect. Ears and head are principally black.This breed can come with tan or without tan markings. If they
appear, they should be on the chest, cheeks, and eyes and below the tail. If your dog has tan markings then you should see red ticking on feet and lower legs. Some standards prefer a more blue and black on the dog's body, at all times there needs to be more blue ticking than white.
History: Here we have the state dog of Tennessee. It is said to have come from selective breeding, in Louisiana of the foxhounds, English Coonhound and curs. This breed has a very strong instinct to tree animals, this means scenting out the animal and chasing them literally at the tree. Raccoons live in all states of America, and have been pursued by hunters with the help of the Bluetick Coonhound.The dog is expected to find, trail and tree the raccoons. Due to the fact that each dog has its own unique bark, which sounds more like a bay cry, night hunting with these dogs' is often used, as the hunter can follow the sound made by each individual dog.Temperament: This breed is very intelligent and is exceptionally devoted to his family. It does well living outdoors, and is a good guardian to the family and home. This dog needs strong leadership, with firm handling, showing the owner as pack leader. Socialising this dog, whilst young, will avoid lots of problems
with strangers and other dogs.This dog is a hunter and is fervent about it; there should be no trust in this dog with other non-canine pets. Here we see an extremely alert and active dog, able to work over difficult terrain, and in any weather. This is not a dog to take off the lead, as his natural instincts will take over, and he will be off on the hunt. These dogs are usually best with older children.Health issues: This breed is prone to hit dyspepsia, Krabbe disease, and cataracts.Grooming: This dog is low maintenance only needing an occasional brushing. Regular attention to the ears is a must, to prevent infection.Living conditions: This is not an apartment dog. They will do best in a large garden that is secure and well fenced, this is due to the fact that they catch in the Wind scents and may wish to follow. <a href="http://iautoblog.com">iAutoblog</a> the premier <a href="http://iautoblog.com">autoblogger</a> software

vineri, 16 noiembrie 2012

Fatty acid metabolism and its pathways and disorders

What is Fatty acid metabolism: Fatty acids metabolism is a process of yielding energy from the fatty acids to the living organisms by carrying a set of biochemical reactions. Fatty acids are mostly used for the protein modification process in converting energy from one form to another form. In our body, if the glucose presence is in excess rate then it is stored as fat content in the cells. Each cell membrane consists two fatty acids which are useful for the occurrence of metabolism in the living organisms. Triglyceride is one of the chemical compounds of fatty acids which produce more energy than proteins and carbohydrates. Fatty acid metabolism is carried in two metabolic pathways they are: Fatty acid catabolism: fatty acid metabolism involves the break down of large fat molecules into smaller units for energy production and for the formation of primary metabolites. Fatty acid anabolism: fatty acids me
tabolism involves in grouping the dietary products and biologically molecules into building blocks of cells and tissues.
Fatty acids are commonly referred to carboxylic acid .Fatty acids are comprised by the group of carbons which can be found in saturated or unsaturated mode. Derivation of fatty acids can be carried by hydrolysis process of ester products like animal fat, vegetable fat and wax.Fatty acids are very useful for the body cells and tissues as a source of energy. All the cells and tissues in the body require large quantities of energy packets (ATP) for performing specific functions and this energy packets are produced by the fatty acids by metabolic pathways. Fatty acids are directly utilized by the skeletal muscle and heart where as brain cannot use fatty acids for fuel, it depends on glucose or ketones. Fatty acid metabolism produces ketones in the liver during low calcium intake or prolonged starvation. Liver is the main site for occurrence of metabolic pathways as it supports many biochemical reactions which are necessary for metabolism.For the fatty acid metabolism pr
ocess liver play a major role in carrying many functions in the body, like decomposition of fatty acids in red blood cells, glycogen storage, ketones production, plasma protein synthesis and detoxification of drugs. Liver adds an alkaline compound for easy digestion process and also releases bile with the support of fatty acids, which we intake through food.Fatty acids easily undergoes acid-base reactions and esterification process for production of energy packets as a fuel source for cells and tissues. Fatty alcohols are produced by the reduction of fatty acid content .These two reactions are common in both types of fatty acids. An additional process is included for unsaturated fatty acids, called as hydrogenation, which is useful in producing margarine from vegetable oil. Fatty acid metabolism disorders: If there is any defect in the enzymes of the fatty acids then fatty acid metabolism disorder occurs.Cardiovascular disease, genetic disorders, lipi
d storage disorders, inborn disorders, acid lipase disease, krabbe disease and fabry disease arises due to the disorder in fatty acids metabolism. <a href="http://iautoblog.com">iAutoblog</a> the premier <a href="http://iautoblog.com">autoblogger</a> software

joi, 15 noiembrie 2012

How to Get Tax Credits for Hypotonia Disability in Canada?

Hypotonia disability is caused due to many types of diseases. It is a condition that causes low muscle tone making the movement difficult inside a muscle. It generally affects the muscle strength. It also affects the nerve control. Identifying the reasons responsible for hypotonia is quite difficult, but diagnosing hypotonia is quite straightforward. The people suffering from hypotonia are likely to have effect on development. At a later stage, such persons may suffer from muscle weakness. Physical therapy is the best solution for neurologic hypotonia. Hypotonia can be present either from birth or later due to damage to the nervous system in the brain. The main reasons for hypotonia include genetic disorders, achondroplasia, Down's syndrome, Krabbe disease, Menkes syndrome, Riley-Day syndrome, Canavan disease, Werdnig-Hoffman disease, Aicardi syndrome, Centronuclear myopathy, Tay-Sachs disease, developmental disability, Trisomy, Prader Willi syndrome, Methylmalonic
academia, 22q 13 deletion syndrome, Nonketotic Hyperglycinemia, hypotonic cerebral palsy, dyspraxia, cerebellar ataxia, teratogenesis and dysfunction in sensory integration. Genetic reasons for hypotonia include infections, Encephalitis, Guillian Barre syndrome, sepsis, muscular dystrophy, poliomyelitis, meningitis, metachromatic leukodytrophy, infant barre syndrome, abnormal vaccine reaction, metabolic disorders, autoimmunity disorders, rickets, kernicterus, myasthenia gravis and cerebellar lesions.
Symptoms of hypotonia include decreased muscle tone, speech difficulties, decreased strength, poor reflexes, rounded shoulder posture, poor attention, leaning on supports, hyperflexible joints and lack of motivation. The hypotonia severity may depend on age factor and the severity of affected muscles. Some people may feel constipated whereas others don't have such problems. The hypotonia identified during infant stage is called infantile hypotonia or floppy infant syndrome. Infants suffering hypotonia are generally called sack of jello or rag dolls. Such children are slipped through hands quite often. It will be difficult for them to maintain ligaments. They can't control movement of head. It is called chronic ataxia. It will be difficult to feed such infants. Low tone disability affects motor skills. Children suffering from hypotonia can have developmental delays. All of their movements are delayed. For example, infants may take more time to lift their head from th
e stomach. They may also face difficulty in crawling, walking, balancing and sitting. They may face difficulty in speaking. It is due to difficulty in adjusting the muscles in the mouth. Persons suffering from hypotonia disability can approach Canadian Disability Corporation (CDC) and file for disability tax credits. They can seek the help of CDC staff in completing the application form. The professionals at CDC examine your eligibility for tax credits and recommend for disability tax credits based on your disability condition. Summary
Disability tax credits offered through CDC helps the patients to pay for at least part of the treatment expenses. <a href="http://iautoblog.com">iAutoblog</a> the premier <a href="http://iautoblog.com">autoblogger</a> software

miercuri, 14 noiembrie 2012

Stem Cell Transplant - How It Can Save Your Life

Stem cell transplant is the new buzzword in medical technology. More and more parents are investing in cord blood stem cell banking as means of securing their kid's future. But do you really need to bank your kid's stem cells? Read on, while we tell you whether it is a good idea or not!The main reason why people go for stem cell transplants is because these cells are capable of growing into other types of cell or tissues. This opens up a whole new world of treatments for diseases like Alzheimer's, diabetes and Parkinson's, apart from debilitating blood diseases. So, should you invest in it?- Yes, if your family has a history of genetic disease that can be cured. Though your child will benefit the most from it, should he need it, you as a parent can also benefit from it. Research shows that a patient has more chances of success by transplants of stem cells than he does with a bone marrow. You should consider this more seriously under the following conditions:1. Susceptibility to leukemia- umbilical cord blood cells have been used to treat childhood leukemia for a time now. Fortunately, the treatment of leukemia, even in adults, has drastically improved with stem cell therapy. Stem cell have been revolutionary in the treatment of conditions like thalassemia and Parkinson's disease.2. Spinal injuries-Stem cell have also had miraculous results in treating spinal cord injuries. Umbilical stem cell has also been promising in case of a rare genetic disorder called Krabbe disease.3. Lymphoproliferative diseases - Cord blood stem cells have been widely acclaimed to be highly effective in treating such diseases.- If you are part of a specific community, then yes. Research shows that it is difficult to find cell matches for African Americans, Native Americans or Hispanics. If you need a stem cell match for treatment, you stand more of a chance with your own cells or that of a close relative's. The best part of s
tem cell transplant? You don't even need an exact biological match.- Stem cell transplant is also a good idea if you are adopting a baby at birth or do not know a lot about the genetic background of the baby. Since you will not be able to provide genetic support for such a kid, it is better to secure her future by banking the cells.- Treatmentsare also no longer confined to your dream. Cell banking facilities across the world have made it possible for you to preserve these precious cells, with the minimum of discomfort and expense.- Treatment may begin anytime. You do not have to look for matching donors. Also, you are less susceptible to viral infections.With the onslaught of new disease every few days, stem cell banking can be the best gift you provide your child- the gift of life! <a href="http://iautoblog.com">iAutoblog</a> the premier <a href="http://iautoblog.com">autoblogger</a> software

marți, 13 noiembrie 2012

Stem Cells Extraction from deciduous(baby) teeth

This type of stem cell can be extracted and deposited in stem cell banks. They can be used for: infarctionmyocardial tissue replacement
treatment of neurodegenerative diseases
treatment of various dental diseases
bone regeneration after fractures and osteoporosis
tooth pulp regeneration and vitalization
Tooth pulp stem cells are frequently used in therapies, for transplantation only to the person who did the harvesting. In the future these stem cells will be used for other people in the same family too. Relatives until grade 4 will benefit.
What are the dental pulp STEM CELLS?
These are cell that can transform and replace other cell types in your body.
Baby teeth pulp contains: mesenchymal cells
- These stem cells can be directly implanted in any organ and/or bone to help improving immunity or strength.
odontoblaste cells
- These stem cells forms odonto substance(the component of tooth) The stem cell from dental pulp are non-hematopoietic cells. Using these stem cells with hematopoietic cells the hematopoietic trasnpants are transformed in best results transplants.
Treatable diseases:
Bone Marrow Failure Disorders Amegakaryocytosis Aplastic Anemia (Severe) Blackfan-Diamond Anemia Congenital Cytopenia*
Pure Red Cell Aplasia Congenital Dyserythropoietic Anemia Dyskeratosis Congenita Fanconi Anemia Paroxysmal Nocturnal Hemoglobinuria (PNH) Sickle Cell Disease Histiocytic Disorders Familial Erythrophagocytic Lymphohistiocytosis Langerhans' Cell Histiocytosis (Histiocytosis X)

Hemophagocytosis Inherited Immune System Disorders Chronic Granulomatous Disease Congenital Neutropenia Leukocyte Adhesion Deficiency Severe Combined Immunodeficiencies (SCID) including: Adenosine Deaminase Deficiency*
Reticular Dysgenesis Kostmann Syndrome Omenn Syndrome Purine Nucleoside Phosphorylase Deficiency Wiskott-Aldrich Syndrome X-Linked Lymphoproliferative Disorder Inherited Metabolic Disorders Adrenoleukodystrophy Fucosidosis Gaucher Disease* Hunter Syndrome (MPS-II) Hurler Syndrome (MPS-IH) Krabbe Disease Lesch-Nyhan Syndrome Mannosidosis* Maroteaux-Lamy Syndrome (MPS-VI) Metachromatic Leukodystrophy Mucolipidosis II (I-cell Disease)* Neuronal Ceroid Lipofuscinosis (Batten Disease)* Niemann-Pick Disease* Sandhoff Disease* Sanfilippo Syndrome (MPS-III) Scheie Syndrome (MPS-IS) Sly Syndrome Tay Sachs* Wolman Disease Leukemias and Lymphomas 
Acute Biphenotypic Leukemia* Acute Lymphocytic Leukemia (ALL) Acute Myelogenous Leukemia (AML) Acute Undifferentiated Leukemia* Adult T Cell Leukemia/Lymphoma Chronic Lymphocytic Leukemia (CLL) Chronic Myelogenous Leukemia (CML) Hodgkin's Lymphoma Juvenile Chronic Myelogenous Leukemia (JCML) Juvenile Myelomonocytic Leukemia (JMML) Myeloid/Natural Killer (NK) Cell Precursor Acute Leukemia Non-Hodgkin's Lymphoma Polymphocytic Leukemia Myelodysplastic/Myeloproliferative Disorders Acute Myelofibrosis* Agnogenic Myeloid Metaplasia (Myelofibrosis)* Amyloidosis Chronic Myelomonocytic Leukemia (CMML) Essential Thrombocythemia* Polycythemia Vera* Refractory Anemias (RA) including: Refractory Anemia with Excess Blasts (RAEB) Refra
ctory Anemia with Excess Blasts in Transformation (RAEB-T) Refractory Anemia with Ringed Sideroblasts (RARS) Plasma Cell Disorders Multiple Myeloma Plasma Cell Leukemia Waldenstrom's Macroglobulinemia Other Inherited Disorders Cartilage-Hair Hypoplasia Congenital Erythropoietic Porphyria (Gunther Disease) DiGeorge Syndrome Osteopetrosis Other Malignancies Brain Tumors** Ewing Sarcoma* Neuroblastoma Ovarian Cancer* Renal Cell Carcinoma* Rhabdomyosarcoma Small Cell Lung Cancer* Testicular Cancer* Thymoma (Thymic Carcinoma) Other Chronic Active Epstein Barr Evans Syndrome Multiple Sclerosis* Rheumatoid Arthritis* Systemic Lupus Erythematosus* Thymic Dysplasia * in clinical trials, Emerging Stem Cell Applications Diabetes Heart Disease Liver Disease Muscular Dystrophy Parkinson's Disease Spinal cord injury Stroke <a href="http://iautoblog.com">iAutoblog</a> the premier <a href="http://iautoblog.com">autoblogger</a> software

luni, 12 noiembrie 2012

Viability of Cord Blood in Treating Malignant Diseases

Having the capability of creating life-forming cells, cord blood has emerged as one of the most extraordinary discoveries in the past 2 decades. The process of cord blood banking is a highly specialized procedure that is taken up after the delivery of the placenta. Numerous positive outcomes have emerged in multiple cord blood cell transplants over the years and this is why medical practitioners are prioritizing the collection of these stem cells. Patients who are suffering from leukemia, liver disorders, heart attacks, some types of blindness, immune system disorders, diabetes, spinal cord damages etc, get relief from their severe conditions after cord blood cells are transplanted to them.

 Cord Blood Vs Bone Marrow Practitioners have made use of the umbilical cord blood collected in several life threatening diseases that had earlier treatment options like drugs and radiation treatments, often a combination of both. Later, bone marrow transplants came as another alternative treatment to medicines, radiation and chemotherapy, though the later are still used in several cases. Painful extraction and application of bone marrow stem cells is one of the major disadvantages of bone marrow transplants. Moreover, the availability of the right donor is an issue most patients and their doctors struggle with. With cord blood in the picture, patients can be their own donors! The nature of the stem cells extracted from cord blood makes it even more valuable. Stem cells drained from the umbilical cords of babies can develop any type of cells required to cure certain types of diseases and decrease the incidence of graft versus host disea
se in transplants. One disadvantage, however, is the cord blood quantity, which is undoubtedly less than what patients can get in bone marrow. Success Stories Following are some of the case histories of cord blood cell treatments, that reinforce the importance of cord blood collection
 Adult Leukemia Benefits of cord blood preservation in treating childhood leukemia have been evident in the primitive period of its uses. Now treatments of adult leukemia with these cells have shown success as well. A patient, Stephan Sprague was diagnosed with Chronic Myelogenous Leukemia in 1995 and had been treated with chemotherapy for about seventeen years. Later, in April 1997, when he reached the final stage, he considered a clinical trial of cord blood cell treatment. After starting a cord blood cell transplant in November 1997, he went to become cancer free within 9 years. Spinal Cord Injuries A team of cord blood cell researchers transplanted stem cells to a thirty seven year old woman who was undergoing a spinal cord injury. Even after being paralyzed for about 19 years, she showed fast recovery. She was injected cord blood cells right at the particular area of injury in her spine. Within three weeks of transplantation
, progress was noteworthy. She started walking with a little support and today she claims to walk without any assistance. Krabbe Disease Researchers of Duke University and University of North Carolina from Chapel Hill claimed to show outstanding progress in treating this disease with cord blood cells. Researchers state that newborn cord blood cell recipients, with no symptoms of Krabbe disease, have greater possibility of recovery than older babies. Instances abound of the success of cord blood stem cells in treating various disorders. Cord blood preservation may sound expensive initially, but one cannot deny the potential a single unit of cord blood possesses. There will soon be a day when diseases such as Lymphoproliferative disease, Thalassemia and Fanconi Anemia will no longer be difficult to cure. <a href="http://iautoblog.com">iAutoblog</a> the premier <a href="http://iautoblog.com">autoblogger</a> soft
ware

duminică, 11 noiembrie 2012

Krabbe Disease ? Causes, Symptoms and Treatment

Krabbe disease is inherited in an autosomal recessive manner. If both parents are carriers, each child has a 25% chance of being affected, a 50% chance of being an asymptomatic carrier, and a 25% chance of being unaffected and not a carrier. Each healthy sib of a proband has a 2/3 chance of being a carrier. For genetic counseling purposes, a carrier frequency of one in 150 may be used for the general population. Prenatal diagnosis is possible either by measurement of GALC enzyme activity or by molecular genetic testing if both disease-causing alleles in an affected family member are known. Causes Krabbe disease is caused by mutations in the GALC gene, which causes a deficiency of an enzyme called galactosylceramidase. The buildup of unmetabolized lipids affects the growth of the nerve's protective myelin sheath (the covering that insulates many nerves) and causes severe degeneration of mental and motor skills. As part of a group of disorders known as leukodystrophies, Krab
be disease results from the imperfect growth and development of myelin. Persons with this gene defect do not make enough of a substance called galactocerebroside beta-galactosidase (galactosylceramidase). The body needs this substance to make myelin, the material that surrounds and protects nerve fibers. Without it, myelin breaks down, brain cells die, and nerves in the brain and other body areas do not work properly. The cause of Krabbe disease is a deficiency in an enzyme called galactocerebrosidase (GALC), which is essential for the maintenance of myelin a fatty substance that insulates your nerve fibers. A child needs to inherit an abnormal gene from each parent to trigger the disorder. Passing on the genes occurs in an inheritance pattern called autosomal recessive. A defect in the GALC gene causes Krabbe disease. Persons with this gene defect do not make enough of a substance called galactocerebroside beta-galactosidase (galactosylceramidase). The body needs this subs
tance to make myelin, the material that surrounds and protects nerve fibers. Without it, myelin breaks down, brain cells die, and nerves in the brain and other body areas do not work properly. Symptoms The symptoms of Krabbe disease usually begin before the age of 1 year (the infantile form). Initial signs and symptoms typically include irritability, muscle weakness, feeding difficulties, episodes of fever without any sign of infection, stiff posture, and slowed mental and physical development. As the disease progresses, muscles continue to weaken, affecting the infant's ability to move, chew, swallow, and breathe. Affected infants also experience vision loss and seizures. The cause of Krabbe disease is a deficiency in an enzyme called galactocerebrosidase (GALC), which is essential for the maintenance of myelin a fatty substance that insulates your nerve fibers. A child needs to inherit an abnormal gene from each parent to trigger the disorder. Passing on the genes occurs
in an inheritance pattern called autosomal recessive. Specifically, Krabbe disease has been linked to a defect in chromosome 14. Treatment There is no cure for Krabb disease. Results of a very small clinical trial of patients with infantile Krabb disease found that children who received umbilical cord blood stem cells from unrelated donors prior to symptom onset developed with little neurological impairment. Results also showed that disease progression stabilized faster in patients who receive cord blood compared to those who receive adult bone marrow. Bone marrow transplantation has been shown to benefit mild cases early in the course of the disease. Generally, treatment for the disorder is symptomatic and supportive. <a href="http://iautoblog.com">iAutoblog</a> the premier <a href="http://iautoblog.com">autoblogger</a> software

sâmbătă, 10 noiembrie 2012

What is Krabbe Disease?

Krabb disease is a rare, inherited degenerative disorder of the central and peripheral nervous systems. It is characterized by the presence of globoid cells (cells that have more than one nucleus), the breakdown of the nerve's protective myelin coating, and destruction of brain cells. Krabb disease is one of a group of genetic disorders called the leukodystrophies. These disorders impair the growth or development of the myelin sheath, the fatty covering that acts as an insulator around nerve fibers, and cause severe degeneration of mental and motor skills. Krabbe disease is part of a group of disorders known as leukodystrophies, which result from the loss of myelin (demyelination). This disorder is also characterized by the abnormal presence of globoid cells, which are globe-shaped cells that usually have more than one nucleus. Krabbe Disease patients show symptoms within the first year of life, there have been cases diagnosed at all ages, through late adulthood. In genera
l, the earlier the diagnosis, the more rapid the progression of the disease. Those who first show symptoms at ages 2-14 will regress and become severely incapacitated, and generally die 2-7 years following diagnosis. Some patients who have been diagnosed in the adolescent and adult years have symptoms that remain confined to weakness without any intellectual deterioration, while others may become bedridden and deteriorate both mentally and physically. In all individuals with Krabbe disease, galactocerebrosidase (GALC) enzyme activity is deficient in leukocytes isolated from whole heparinized blood or in cultured skin fibroblasts. Carrier testing by measurement of GALC enzyme activity in leukocytes or in cultured skin fibroblasts is unreliable because of the wide range of enzymatic activities observed in carriers and non-carriers. Molecular genetic testing of GALC, the only gene known to be associated with Krabbe disease, may be used for carrier detection in at-risk relatives
if the disease-causing alleles have been identified in an affected family member. In most cases, Krabbe disease develops in babies before six months of age, although it can occur in older children and in adults. Krabbe disease may be best known in the United States for the media attention it received when former professional football quarterback Jim Kelly raised awareness and research funds for the disorder, which had been diagnosed in his son, Hunter. Krabbe disease is one of a group of genetic conditions called leukodystrophies. Doctors sometimes refer to Krabbe disease as globoid cell leukodystrophy the globoid cells are storage cells that play a role in the disorder. The disease is named after the Danish neurologist who first reported infants with the condition in 1916. If the symptoms suggest Krabbe disease, a blood test can be done to see if the child or adult has GALC deficiency, which would confirm the diagnosis. A lumbar puncture can be done to sample the cerebros
pinal fluid, which in Krabbe disease has abnormally high levels of protein. The test for GALC deficiency can also be done on an unborn child if the parents carry the defective gene (on chromosome 14). Infants with Krabbe disease are normal at birth. Symptoms begin between the ages of 3 and 6 months with irritability, fevers, limb stiffness, and seizures, feeding difficulties, vomiting, and slowing of mental and motor development. In the first stages of the disease, doctors often mistake the symptoms for those of cerebral palsy. Other symptoms include muscle weakness, spasticity, deafness, optic atrophy and blindness, paralysis, and difficulty when swallowing. Prolonged weight loss may also occur. There are also juvenile- and adult-onset cases of Krabbe disease, which have similar symptoms but slower progression. <a href="http://iautoblog.com">iAutoblog</a> the premier <a href="http://iautoblog.com">autoblogger</a> software