Uroxatral (Alfuzosin) is used for treating symptoms of benign prostatic hyperplasia (BPH) in men with an enlarged prostate.
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Uroxatral (Alfuzosin) is used for treating symptoms of benign prostatic hyperplasia (BPH) in men with an enlarged prostate.
Active Ingredient: Alfuzosin
Uroxatral (Urion) as known as: Alcinin, Alfetim, Alfu, Alfugen, Alfuhexal, Alfulek, Alfunar, Alfural, Alfusin, Alfusosin, Alfusozina, Alfuzin, Alfuzosini, Alfuzosinum, Alfuzostad, Alreos, Alugen, Benestan, Cezin, Dalfaz, Dazular xl, Flotral, Innosensitive, Lafunomyl, Mittoval, Ofuxal, Tevax, Unibenestan, Urion, Xantral, Xatger, Xatral, Zatral
In the face of “overwhelming” scientific evidence, they complained, A.D.H.D. was regularly portrayed in the media as “myth, fraud or benign condition” — an artifact of too-strict teachers, perhaps, or too much television.
In recent years, it has been rarer to hear serious doubt that the disorder really exists, and the evidence explaining its neurocircuitry and genetics has become more convincing and more complex.
Even so, I’ve lately read a number of articles and essays that use attention (or its lack) as a marker and a metaphor for something larger in society — for the multitasking, the electronic distractions, the sense that the nature of concentration may be changing, that people feel nibbled at, overscheduled, distracted, irritable.
But A.D.H.D. is not a metaphor. It is not the restlessness and rambunctiousness that happen when grade-schoolers are deprived of recess, or the distraction of socially minded teenagers in the smartphone era. Nor is it the reason your colleagues check their e-mail in meetings and even (spare me!) conversations.
“Attention is a really complex cognitive phenomenon that has a lot of pieces in it,” said Dr. David K. Urion of Harvard, who directs the learning disabilities and behavioral neurology program at Boston Children’s Hospital. “What we’re specifically talking about in kids with attention deficit is a problem compared to age- and gender-based peers in selective attention — what do you glom onto and what do you ignore?”
Moreover, the disorder occurs along a broad spectrum, from mild to extreme. Boys are more likely to be hyperactive and impulsive, girls to be inattentive. (One reason many girls don’t get an official diagnosis is that those with the inattentive form may be well behaved in school, but still unable to focus.)
“There’s a lot we still don’t know,” said Bruce F. Pennington, a professor of psychology at the University of Denver and an expert on the genetics and neuropsychology of attention disorders. “But we know enough to say it is a brain-based disorder, and we have some idea about which circuits are involved and which genes.”
Imaging studies of people with attention deficits have shown a consistent pattern of below-normal activity in the brain’s frontal lobes, where so-called executive function resides. And scientists are focusing on the pathways for dopamine and similar neurotransmitters active in the circuits that pass information to and from the frontal lobes.
Low levels of activity in specific circuits may help explain the seeming paradox of using stimulants like Ritalin to treat children who already seem overstimulated. In many children with A.D.H.D. these drugs can help the circuits function more normally.
“If you have a deficit in dopamine, it’s harder to concentrate on goal-oriented behavior,” Professor Pennington said. “The psychostimulants change the availability of dopamine in these same circuits.”
Although recent research has identified environmental factors that may increase the likelihood of developing the disorder, it is thought to have a stronger genetic component. Dr. Maximilian Muenke, chief of the medical genetics branch at the National Human Genome Research Institute. said that among identical twins. if one has A.D.H.D. the second has an 80 percent chance of having it as well. (Among fraternal twins, the comparable figure is 20 to 30 percent, the same as for any siblings.)
Dr. Muenke’s group published a paper last month identifying a gene, LPHN3, that is associated both with the disorder and with a favorable response to stimulants. But no one thinks that just one gene is responsible; just as attention is a complex phenomenon, so are the genetics of attention deficits.
When I asked Dr. Muenke whether genetic studies could someday play a role in treating the disorder, his reply was cautious. He spoke of eventually predicting which children will respond to specific medications, sparing families the frustration of switching from one medicine to another with no relief. He sounded more hopeful about the long-term prospects.
“I truly believe in the long run we will be able to develop personalized medicine for a child with A.D.H.D.,” he said, adding that when the specific underlying cause or causes are known, “this child will have a very specific treatment, whether this treatment is behavioral treatment alone or medication,” and the medication will be tailored to the child.
Perhaps eager to make clear that A.D.H.D. is far more than a metaphor for the distractions of modern life, scientists love to point out examples that date to well before the term was invented.
Dr. Urion invoked Sir George Frederick Still, the first British professor of pediatric medicine, who in 1902 described the syndrome precisely, speaking of a boy who was “unable to keep his attention even to a game for more than a very short time,” and as a result was “backward in school attainments, although in manner and ordinary conversation he appeared as bright and intelligent as any child could be.”
Dr. Muenke brought up “Der Struwwelpeter“ (“Slovenly Peter”), the 1845 children’s book by Heinrich Hoffmann, which contains the story of “Zappel-Philipp,” or “Fidgety Philip.” (One English translation was done by Mark Twain. that great chronicler of boys.)
The circumstances of modern life can give rise to the false belief that a culture full of electronics and multitasking imperatives creates the disorder. “People have this idea that we live in a world that gives people A.D.H.D.,” Dr. Urion said. Of course one shouldn’t drive and text at the same time, he continued, but for “a harbor pilot bringing a huge four-masted sailing vessel into Boston Harbor, paying attention was a good idea then, too.”
The Hypogonadism Knowledge Centre provides healthcare professionals with free access to disease awareness sections such as epidemiology, pathophysiology, signs and symptoms, treatment options to assist the process of diagnosis, treatment and monitoring of patients with the condition. The regularly updated publications digest area contains analysis and comment on recent scientific articles related to male hypogonadism.
The Prostate Cancer Learning Hub has been designed with the busy healthcare professional in mind. The resource conveniently organises a range of up-to-date education content, reference materials and decision support tools, all focussing on prostate cancer. The disease awareness section provides you with access to a Prostate Cancer Knowledge Centre, which has been developed to provide you with easy to digest best practice guidance for the treatment and management of patients with prostate cancer.Urion®; -S Dosage Urion®; -S Adult Dosage
Lactose, mikrokristalline Cellulose, Povidon, Poly(O-carboxymethyl)stärke, Natriumsalz, Magnesiumstearat, Hypromellose, Titandioxid (E 171), Macrogol 400. Propylenglycol, Eisen(III)-oxid (E 172).Urion®; -S Child Dosage
Urion®; -S Precautions, Reactions and Contraindications
Urion®; -S Special Precautions
Urion®; -S Special Precautions
Urion® S Retardtabletten
Zus.: 1 Retardtbl. enth. Alfuzosin-HCl 5 mg (entspr. 4,58 mg Alfuzosin).
Weit. Bestandteile: Calciumhydrogenphosphat, Mikrokristalline Cellulose, Povidon, Magnesiumstearat, raffiniertes Rizinusöl, Hypromellose, Titandioxid (E 171),
Bekannte orthostatische Hypotonie, gleichz. Anw. mit anderen Alpha1-Rezeptoren-Antagonisten. Bek. Überempfindlichk. gegen and. Alpharezeptoren- Blocker. Schwere Leberinsuffizienz.Related Drugs - Urological and Kidney Diseases
Uroxatral is used for treating symptoms of benign prostatic hyperplasia (BPH) in men with an enlarged prostate. It may also be used for certain conditions as determined by your doctor.
Uroxatral (alfuzosin) belongs to a group of drugs called alpha-adrenergic blockers. Uroxatral relaxes the muscles in the prostate and bladder neck, making it easier to urinate.
Uroxatral may also be used for other purposes not listed in this medication guide.
Take Uroxatral exactly as prescribed by your doctor. Do not take in larger or smaller amounts or for longer than recommended. Follow the directions on your prescription label.
Your doctor may occasionally change your dose to make sure you get the best results.
Uroxatral is usually taken once a day, just after a meal. Try to take this medication at the same time each day. Do not take it on an empty stomach. Do not crush, chew, or break an extended-release tablet. Swallow it whole. Breaking the pill may cause too much of the drug to be released at one time. Uroxatral lowers blood pressure and may cause dizziness or fainting, especially when you first start taking it, or when you start taking it again. Call your doctor if you have severe dizziness or feel like you might pass out.
If you missed a dose take it as soon as you remember. Skip the missed dose if it is almost time for your next scheduled dose. Do not take extra medicine to make up the missed dose.
Use the medicine as prescribed by your doctor.
Store Uroxatral at room temperature, between 68 and 77 degrees F (20 and 25 degrees C). Store away from heat, moisture, and light. Keep Uroxatral out of the reach of children and away from pets.
Active Ingredient: Alfuzosin
You should not use Uroxatral if you are allergic to alfuzosin, if you have severe liver disease, or if you are also using ketoconazole (Nizoral), itraconazole (Sporanox), or ritonavir (Norvir). Do not take Uroxatral with other similar medicines such as doxazosin (Cardura), prazosin (Minipress), silodosin (Rapaflo), tamsulosin (Flomax), or terazosin (Hytrin).
Uroxatral may cause dizziness or fainting. Be careful if you drive or do anything that requires you to be alert. Avoid standing for long periods of time or becoming overheated during exercise and in hot weather. Avoid getting up too fast from a sitting or lying position, or you may feel dizzy.
Uroxatral can affect your pupils during cataract surgery. Tell your eye surgeon ahead of time that you are using this medication. Do not stop using Uroxatral before surgery unless your surgeon tells you to.
There are many other drugs that can interact with Uroxatral. Tell your doctor about all medications you use.
Before taking Uroxatral
Do not use Uroxatral if you are allergic to alfuzosin, or if you have:
severe liver disease;
if you are also taking similar medicines such as doxazosin (Cardura), prazosin (Minipress), silodosin (Rapaflo), tamsulosin (Flomax), or terazosin (Hytrin); or
if you are also using ketoconazole (Nizoral), itraconazole (Sporanox), or ritonavir (Norvir).
If you have any of these other conditions, you may need an Uroxatral dose adjustment or special tests:
a personal or family history of Long QT syndrome;
angina (chest pain);
coronary artery disease (hardened arteries);
a history of low blood pressure (even when caused by taking medications); or
if you are taking certain medicines to treat HIV or AIDS.
Uroxatral can affect your pupils during cataract surgery. Tell your eye surgeon ahead of time that you are using this medication. Do not stop using Uroxatral before surgery unless your surgeon tells you to.
Although this medication is not for use in women, Uroxatral is not expected to harm an unborn baby. If you are a woman using this medication, tell your doctor if you are pregnant or breast-feeding. Uroxatral is not for use in children.
Important safety information:
Uroxatral may impair your thinking or reactions. Be careful if you drive or do anything that requires you to be alert.
To prevent dizziness, avoid standing for long periods of time or becoming overheated during exercise and in hot weather.
Avoid getting up too fast from a sitting or lying position, or you may feel dizzy. Get up slowly and steady yourself to prevent a fall. Drinking alcohol can increase certain side effects of Uroxatral.
Many drugs can interact with Uroxatral. Below is just a partial list. Tell your doctor if you are using:
arsenic trioxide (Trisenox);
diltiazem (Cardizem CD, Cartia XT, Tiazac);
isoniazid (for treating tuberculosis);
an antibiotic such as clarithromycin (Biaxin), dalfopristin/quinupristin (Synercid), erythromycin (E.E.S. EryPed, Ery-Tab, Erythrocin), levofloxacin (Levaquin), moxifloxacin (Avelox), pentamidine (NebuPent, Pentam); or telithromycin (Ketek);
an antidepressant such as amitriptylline (Elavil, Vanatrip), clomipramine (Anafranil), desipramine (Norpramin), or nefazodone;
an antifungal medication such as clotrimazole (Mycelex Troche) o voriconazole (Vfend);
anti-malaria medications such as chloroquine (Arelan) or mefloquine (Lariam);
a nitrate heart medication, such as nitroglycerin (Nitrostat, Nitrolingual, Nitro-Dur, Nitro-Bid, and others), isosorbide dinitrate (Dilatrate-SR, Isordil, Sorbitrate), or isosorbide mononitrate (Imdur, ISMO, Monoket);
heart or blood pressure medication such as diltiazem (Cartia, Cardizem), felodipine (Plendil), nifedipine (Nifedical, Procardia), verapamil (Calan, Covera, Isoptin, Verelan), and others;
heart rhythm medicine such as amiodarone (Cordarone, Pacerone), dofetilide (Tikosyn), disopyramide (Norpace), ibutilide (Corvert), procainamide (Pronestyl), propafenone (Rythmol), quinidine (Quin-G), or sotalol (Betapace);
HIV/AIDS medicine such as atazanavir (Reyataz), delavirdine (Rescriptor), fosamprenavir (Lexiva), indinavir (Crixivan), nelfinavir (Viracept), saquinavir (Invirase), or ritonavir (Norvir);
medicine to prevent or treat nausea and vomiting, such as dolasetron (Anzemet) or ondansetron (Zofran);
medicines to treat psychiatric disorders, such as chlorpromazine (Thorazine), clozapine (FazaClo, Clozaril), haloperidol (Haldol), pimozide (Orap), thioridazine (Mellaril), or ziprasidone (Geodon);
migraine headache medicine such as sumatriptan (Imitrex) or zolmitriptan (Zomig); or
narcotic medication such as methadone (Dolophine, Methadose).
This list is not complete and there are many other drugs that can interact with Uroxatral. Tell your doctor about all medications you use. This includes prescription, over-the-counter, vitamin, and herbal products. Do not start a new medication without telling your doctor. Keep a list of all your medicines and show it to any healthcare provider who treats you.
Get emergency medical help if you have any of these signs of an allergic reaction to Uroxatral: hives; difficulty breathing; swelling of your face, lips, tongue, or throat. Stop using Uroxatral and call your doctor at once if you have a serious side effect such as:
new or worsening chest pain;
nausea, stomach pain, low fever, loss of appetite, dark urine, clay-colored stools, jaundice (yellowing of the skin or eyes);
feeling like you might pass out; or
penis erection that is painful or lasts 4 hours or longer.
Less serious Uroxatral side effects may include:
tired feeling; or
cold symptoms such as stuffy nose, sneezing, sore throat.
This is not a complete list of side effects and others may occur. Call your doctor for medical advice about side effects.
Epizootic Hemorrhagic Disease is not a public health issue, according to the New Jersey Division of Fish and Wildlife. Infected deer cannot transmit the disease to people, other deer or any other animals, and humans are not at risk by handling infected deer.
However, state officials caution against eating meat of sickened deer because it may contain secondary infections that could be harmful to humans.
In 2011, there were no reported cases of EHD in Salem County. but the number of cases elsewhere throughout New Jersey were higher by this time last year, Stansley said.
EHD is a common viral disease in deer that is contracted from a species of small biting flies called midges. Outbreaks generally begin in August and end with the first frost, which kills the midges.
While EHD is closely related to Bluetongue virus and cross-reacts with it on many blood tests although they are different diseases, officials said.
Death happens swiftly for the deer after symptoms appear, which may include lethargy, disorientation and difficulty breathing. They suffer high fevers, and are commonly found near bodies of water in an attempt to cool off. They stop eating and drinking and may have bloody discharge coming from the nose or mouth. They also may lose their fear of people.
There is no vaccine or treatment.
EHD outbreaks have occurred in various parts of New Jersey since 1955, Stansley said.
Outbreaks in 1955, 1975 and 1999 were caused by the EHD serotype 1 virus, while outbreaks in 2007, 2010, 2011 and 2012 were caused by the EHD serotype 2 virus. The serotype 2 virus occurs every year in parts of the southern U.S.
Eileen Urion, who lives on a six and a half acre tract in Pilesgrove Township that includes part of Oldmans Creek, has noticed several deer on her property who appear to be infected.
Those who find dead deer are asked to call the Division of Fish and Wildlife at 908-236-2118 so officials can take tissue samples.
Becker muscular dystrophy is in the category of inherited muscle wasting diseases caused by a gene abnormality (mutation) that results in deficient or abnormal production of the dystrophin protein (dystrophinopathies). The abnormal gene is called DMD and is located on the X chromosome. Becker muscular dystrophy follows x-linked recessive inheritance so it mostly affects males, but some females are affected. Becker muscular dystrophy usually begins in the teens or early twenties and symptoms vary greatly between affected individuals. Muscle deterioration progresses slowly but usually results in the need for a wheel chair. Muscles of the heart deteriorate (cardiomyopathy) in some affected individuals, and this process can become life-threatening. Learning disabilities involving visual abilities may be present.Signs & Symptoms
Symptoms of Becker muscular dystrophy usually begin in the teens or late twenties. Initial symptoms may include cramping during exercise and reduced stamina during exercise. Muscle gradually deteriorates in the hips, pelvis, thighs and shoulders that can lead to walking on toes with the stomach forward. Shortening of muscle fibers can result in the inability to move certain muscles (contractures). The progression of BMD is slower and more variable than Duchenne muscular dystrophy but usually results in the need for a wheel chair. The heart muscle is also affected and can result in feeling breathless, fluid accumulation in the lungs and swelling in the feet and lower legs. Dilated cardiomyopathy is the most common cause of death in individuals with BMD, and most affected individuals die in their mid 40’s.
Approximately 5-10% of female DMD gene carriers have some symptoms of muscle weakness that progress slowly or not at all. Muscle weakness is frequently more severe on one side of the body (asymmetric).Causes
Becker muscular dystrophy is caused by abnormalities (mutations) in the DMD gene that is responsible for the production of the dystrophin protein. Dystrophin is necessary for the stability and protection of muscle. The gene mutation causes the dystrophin protein to be shorter than normal and not function normally.
The DMD gene is located on the X chromosome and Becker muscular dystrophy follows x-linked recessive inheritance. Females have two X chromosomes but one of the X chromosomes is “turned off” and all of the genes on that chromosome are inactivated. Females who have a disease gene present on one of their X chromosomes are carriers for that disorder. Carrier females usually do not display symptoms of the disorder because it is usually the X chromosome with the abnormal gene that is “turned off”. A male has one X chromosome and if he inherits an X chromosome that contains a disease gene, he will develop the disease. Males with X-linked disorders pass the disease gene to all of their daughters, who will be carriers. A male cannot pass an X-linked gene to his sons because males always pass their Y chromosome instead of their X chromosome to male offspring. Female carriers of an X-linked disorder have a 25% chance with each pregnancy to have a carrier daughter like themselves, a 25% chance to have a non-carrier daughter, a 25% chance to have a son affected with the disease, and a 25% chance to have an unaffected son.Affected Populations
Becker muscular dystrophy occurs in approximately 1 in 30,000 male births.Related Disorders
Symptoms of the following disorders can be similar to those of Becker muscular dystrophy (BMD). Comparisons may be useful for a differential diagnosis:
Duchenne muscular dystrophy is an x-linked recessive genetic disease that is also caused by mutations in the DMD gene. The DMD gene mutations that cause Duchenne muscular dystrophy result in little or no dystrophin protein to be made. Symptoms usually begin in early childhood and progress rapidly. The disease is initially characterized by delays in sitting and standing and difficulty climbing. Children often need a wheel chair by the age of twelve. A disease affecting the heart muscle (cardiomyopathy) occurs in the teenage years and can be life threatening. (For more information about this condition, choose “Duchenne” as your search term in the Rare Disease Database.)
Limb-girdle muscular dystrophy is a group of inherited, progressive disorders that are characterized by weakness and of muscles of the hip and shoulder areas. Several different forms of the disorder have been identified that are caused by mutations in certain genes. Some of these disease subtypes follow autosomal recessive inheritance and some follow autosomal dominant inheritance. In most individuals with limb-girdle muscular dystrophy, symptoms begin during childhood, but they may also begin during adolescence or adulthood. Muscle weakness may spread from the lower limbs to the upper limbs or vice versa. Although the disorder typically progresses slowly, some affected individuals experience rapid disease progression. (For more information about this condition, choose “limb girdle” as your search term in the Rare Disease Database.)
Emery-Dreifuss muscular dystrophy is a rare, often slowly progressive form of muscular dystrophy affecting the muscles of the arms, legs, face, neck, spine and heart. The disorder consists of weakness and degeneration of certain muscles, joints that are fixed in a flexed or extended position (contractures), and abnormalities affecting the heart (cardiomyopathy). Major symptoms may include muscle wasting and weakness particularly in the upper legs and arms and contractures of the elbows, Achilles tendons, and upper back muscles. In some cases, additional abnormalities may be present. Emery-Dreifuss muscular dystrophy is inherited as an x-linked, autosomal dominant or autosomal recessive trait. (For more information about this condition, choose “Emery Dreifuss” as your search term in the Rare Disease Database.)
Spinal muscular atrophy is an inherited progressive neuromuscular disorder characterized by degeneration of groups of nerve cells (motor nuclei) within the lowest region of the brain (lower brainstem) and certain motor neurons in the spinal cord (anterior horn cells). Motor neurons are nerve cells that transmit nerve impulses from the spinal cord or brain (central nervous system) to muscle or glandular tissue. Typical symptoms are a slowly progressive muscle weakness and muscle wasting. Affected individuals have poor muscle tone, muscle weakness on both sides of the body without, or with minimal, involvement of the face muscles, twitching tongue and a lack of deep tendon reflexes. SMA is divided into subtypes based on age of onset of symptoms and maximum function achieved. Spinal muscular atrophy is inherited as an autosomal recessive trait and is caused by mutations in the SMN (survival motor neuron) gene. (For more information about this condition, choose “spinal muscular atrophy” as your search term in the Rare Disease Database.)Diagnosis
The diagnosis of Becker muscular dystrophy is based on physical symptoms, family history, an elevated concentration of creatine kinase (CK) in the blood indicating destruction of muscle, and molecular genetic testing. DMD is the only gene that has been associated with Becker muscular dystrophy and many different types of DMD gene mutations have been identified in individuals with this condition. Identification of a DMD gene mutation from molecular genetic testing confirms the diagnosis. If molecular genetic testing is performed and a DMD gene mutation is not found, a skeletal muscle biopsy is recommended to examine the appearance of the dystrophin protein.Standard Therapies
No specific treatment is available for Becker muscular dystrophy but quality of life and lifespan can be improved with appropriate care. Physical and occupational therapy can reduce or delay joint contractures. Surgery is sometimes recommended to treat contractures or scoliosis. Weight control can help to reduce stress on the heart and muscles. Corticosteroids are often prescribed to help slow down the loss of muscle function. Routine monitoring by a cardiologist is recommended.Investigational Therapies
Information on current clinical trials is posted on the Internet at www.clinicaltrials.gov. All studies receiving U.S. government funding, and some supported by private industry, are posted on this government web site.
For information about clinical trials being conducted at the National Institutes of Health (NIH) in Bethesda, MD, contact the NIH Patient Recruitment Office:
Tollfree: (800) 411-1222
TTY: (866) 411-1010
For information about clinical trials sponsored by private sources, contact:
In April of 2008, PTC Therapeutics, Inc. (PTC), announced the initiation of an international pivotal trial of PTC124 in patients with Duchenne/Becker muscular dystrophy (DMD/BMD) due to a nonsense mutation. The primary objective of this registration-directed Phase 2b trial is to demonstrate the efficacy of PTC124 as measured by improvements in the walking ability of patients with this progressive genetic disease.
PTC124 is a novel, orally delivered drug in development for the treatment of patients with genetic disorders due to a nonsense mutation, a type of mutation found in approximately 13% of patients with DMD. In this double-blind study, patients will be randomized to receive placebo, or one of two dose levels of PTC124, three times per day. Eligible patients will be boys with nonsense-mutation-mediated DMD/BMD who are at least 5 years of age and are able to walk at least 75 meters or approximately 80 yards in six minutes. PTC expects to enroll a total of 165 patients at approximately 35 investigational sites; all study subjects will undergo 48 weeks of blinded treatment. Thereafter, all participants, including those who have been receiving placebo, will be eligible to enroll in an open-label PTC124 extension study.
For more information please contact:
or more information:
PTC Therapeutics, Inc.NORD Member Organizations Other Organizations References
Ascadi G. Becker Muscular Dystrophy. In: The NORD Guide to Rare Disorders, Philadelphia: Lippincott, Williams and Wilkins, 2003:622.
Bushby KM and Gardner-Medwin D. The clinical, gentic and dystrophin characteristics of Becker muscular dystophy. I. Natural history [published erratum appears in J Neurol 1993 Jul;240 (7):453]j Neurol 240:98-104.
Hoffman EP, Fischbeck KH, Brown, et al. Characterization of dystrophin in muscle-biopsy specimens from patients with Duchenne’s or Becker’s muscle dystrophy. N Engl J Med 1998;318:1363-8.
Nolan MA Jones OD, Pederson RL, et al. Cardiac assessment in childhood carriers of Duchenne and Becker muscle dystrophies. Neuromuscul Disord 2003;13:129-32.
Palmucci L, Mongini T, Chido-Piat L, et al. Dystrophinopathy expressing as either cardiomyopathy or Becker dystrophy in the same family. Neurology 2000; 54:529-30.
Quinlivan R, Ball J, Dunckley M, et al. Becker muscle dystrophy presenting with complete heart block in the sixth decade. Neurology 1995;242:398-400.
FROM THE INTERNET
Kork BR, Darras BT, and Urion DK (Updated 10/4/04) Dystrophinopathies In: GeneReviews at GeneTests: Medical Genetics Information Resource (database online). Copyright, University of Washington, Seattle. 1997-2005. Available at http://genetests.org. Accessed 6/05.
McKusick VA ed. Online Inheritance in Man (OMIM). Baltimore, MD: The Johns Hopkins University: Entry No. 300376, Last Update: 4/2/02.Years Published
1989, 1997, 1998, 2005, 2007
The information in NORD’s Rare Disease Database is for educational purposes only and is not intended to replace the advice of a physician or other qualified medical professional.
The content of the website and databases of the National Organization for Rare Disorders (NORD) is copyrighted and may not be reproduced, copied, downloaded or disseminated, in any way, for any commercial or public purpose, without prior written authorization and approval from NORD. Individuals may print one hard copy of an individual disease for personal use, provided that content is unmodified and includes NORD’s copyright.
National Organization for Rare Disorders (NORD)
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The FAA hopes new pilot training standards will enhance airline safety
The Federal Aviation Administration (FAA) is recognizing James Lyman Urion with inclusion in the prestigious FAA Airmen Certification Database.
The database, which appears on the agency's website at www.faa.gov, names Urion and other certified pilots who have met or exceeded the high educational, licensing and medical standards established by the FAA.
Pilot certification standards have evolved over time in an attempt to reduce pilot errors that lead to fatal crashes. FAA standards, which are set in consultation with the aviation industry and the public, are among the highest in the world.
Transportation safety experts strongly recommend against flying with an uncertified pilot. FAA pilot certification can be the difference between a safe flight and one that ends in tragedy.
The FAA recently announced that is it increasing the qualification requirements for co-pilots who fly for U.S. passenger and cargo airlines. These requirements mandate additional minimum flight time and training, as well as aircraft specific training.
"Safety will be my overriding priority as Secretary, so I am especially pleased to mark my first week by announcing a rule that will help us maintain our unparalleled safety record," said Transportation Secretary Anthony Foxx in a press release. "We owe it to the traveling public to have only the most qualified and best trained pilots."
According to the FAA, the new regulations stem in part from the crash of Colgan Air 3407 in February 2009. An investigation of the crash revealed that pilot Renslow, had failed three "check rides" (the flying equivalent of driver proficiency tests) and may not have had adequate training to respond to the emergency leading up to the crash.
The FAA offers a variety of pilots licenses and certificates, each with a different set of privileges. These levels include Student, Recreational, Sport, Private, Commercial And Airline Transport Pilot.
Pilots with a student pilot certification are not permitted to fly solo and are barred from carrying passengers. Sport pilot certificate holders can not carry more than one passenger and are permitted to only fly light-sport aircraft during the daytime.
The highest level of certification is the Airline Transport Pilot Certificate (ATP), which is required to fly a commercial airliner.
To obtain Airline Transport Pilot Certificate, pilots must possess a commercial pilot license, have more than 1500 hours of experience in aircraft and be at least 21 years old. However, pilots with an aviation degree can qualify for the certificate with just 1,000 hours.
Pilots obtaining an Airline Transport Pilot Certificate must also pass an exam covering air law, general aircraft knowledge, flight planning, meteorology, navigation, instrumentation and other important topics.
Pilots are required to pass a physical examination administered by a FAA-authorized medical examiner.
There are a number of medical conditions that the FAA considers disqualifying, such as Bipolar disease, cardiac valve replacement, coronary heart disease, diabetes mellitus requiring hypoglycemic medications, disturbance of consciousness without satisfactory explanation of cause, epilepsy, heart replacement, Myocardial infarction, permanent cardiac pacemaker, personality disorder that is severe enough to have repeatedly manifested itself by overt acts, psychosis, substance abuse, substance dependence, transient loss of control of nervous system function(s) without satisfactory explanation of cause.
Pilots are required to report to the FAA's Security and Investigations Division any alcohol-related vehicle actions, such as an arrest, administrative action, driver license suspension.
The FAA has reason to be concerned in general about alcohol use by pilots. Recently, a 48 year-old American Eagle pilot was forced from the aircraft cockpit after airline employees smells alcohol on him. The pilot, Kolbjorn Jarle Kristiansen. subsequently failed a breathalyzer test and was arrested.
The Federal Aviation Administration's Airmen Certification Database contains the following listing:
FirstName: James Lyman
Street1: 181 Cedar Creek Rd
AMD Technology Company is one of the top microprocessor producing company nowadays. Two of which are their Athlon and Turion microprocessors. Each of them are continually enhanced and developed. But how do they differ from each other? And which one is more superior?
Athlon is the first PC processor to run on AMD’s 64 bit platform. This technology enables a simultaneous 32 bit and 64 bit computing while maintaining compatibility with the existing software and operating systems. Later on, Turion was also designed for the 64 bit platform. Although these two processors have the same performance, the underlying technology used is different. Turion chips are built from low-voltage transistors that have less electrical leakage, and the layout of the chip has been designed for less power consumption. And Turion has a thermal control feature that prevents the processor from creating too much heat.
Although Turion chips consume less electrical power, it does not mean that they would also be much slower in speed. The chipÃs design is to reduce the maximum clock speed that the Turion can support. The effect of the slower transistors can be seen in the range of clock speeds for each processor: 1.6 – 2.4 GHz for Turion chips and 1.8 – 2.8 GHz for Athlon chips. So it is assumed that Athlon chips should be better overclockers than Turion. However Turion seems to be more advantage when it comes to their Hyper Transport technology (technology for high-speed I/O communication on system bus) feature. Turion can go up to 14.4 GB Hyper Transport I/O bandwidth while Athlon can go up to 8 GB Hyper Transport I/O bandwidth.
Another major factor for which we can compare these two processors is their cache capacity differences. Turion has its own L2 cache memory for each core. A total of 2MB capacity for L2 cache of Turion x2 ultra dual Ã± core mobile processor, and a total of 1MB capacity for L2 cache of Turion x2 dual Ã± core mobile processor. This enables a simultaneous independent core access to cache. While Athlon has a 64KB L1 instruction cache per core and 64KB L1 data cache per core, plus up to 1MB (socket 939) or 512KB (socket AM2) L2 cache per core.
As both processors are made by the same company, both have a lot similar architectural features. Only that one of them is more improved in one feature and the other on another feature. However, the AMD Company has done a good job selling Turion for notebooks or laptops. So people probably assume that it is less powerful than Athlon. That’s why more people still turn to Athlon. But whatever differences these two have, you should only choose whatever that best fit’s your needs.
1. Turion is more energy-saving because its chip is designed for less power consumption.
2. Turion has thermal control for a cooler PC.
3. Athlon has a faster clock speed but slower in Hyper Transport I/O bandwidth technology feature.
4. Turion has its own two L2 cache memory for each core with 2MB for Turion x2 ultra dual-core mobile processor and 1MB for Turion x2 dual-core mobile processor while Athlon has two types of L1 cache per core with 64KB each, and one 1MB or 512KB L2 cache per core.
5. Turion is widely used for notebooks while Athlon is widely used for desktops.Share this:
I had a amd athlon 1.6ghz single core and i put a amd turion 2.0ghz dual core. Seems to run alot faster and cooler one dumb thing i did is i reused the artic silver lol i should of just waited for the stuff i order to come in the mail it came the next day, but i dont see any heat problems so im not really worried about it. So anyways this computer has 4 gigs of ram and tl-60 prossessor so it should last a few years what you think
I think it is misunderstanding of civil engineers, Architecture is a professional degree and civil engr is general study of engineering, so after specializing CEs called designer. otherwise CEs do practical work in projects, Under the direction of Project Manager, Architecture, Structural Designer, Electrical and Mechanical Designer. If Architect can’t do any thing, After some year engineering projects should be typical and the skill labor also should call himself Engineer.Trackbacks Leave a Response
Written by. Ian F. and updated on May 19, 2011
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Ian F. "Diffference Between AMD Athlon and AMD Turion." DifferenceBetween.net. May 19, 2011.