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Flawed but still greatPros: Crystal clear screens Cons: Made by asus (see other thoughts for more[1]) Other Thoughts: [1]Took two RMAs for ASUS to fix the laptop correctly (2 weeks each time). The only parts not replaced were the keyboard and case so the QA over at ASUS is seriously lacking, and their RMA department is very lazy. I had to explicitly tell the techs what the issue with my laptop was for them to replace the parts, otherwise they would skim over problems. Did you find this review helpful? |
great ultrabookPros: you turn it on 1 sec later you can use it. its amazing. speed is great i play EVE. and i max it out and it runs great. love the dual screen its a first for me along with the touch screen great response time. amazing computer over all it can do anything you want it to do!! Cons: notice that the java with dual screen isnt good doesnt let you do some of the things you would like gets pretty toasty Did you find this review helpful? |
Dissatisfied CustomerPros: Notebook is great Cons: Just bought the Taichi 21 not even for two months yet and already the ac adapter is acting up. The led light doesn't light up when I plug it in nor does it even charge. I contacted ASUS service center and their representatives were horrible! Absolute worst. On top of that they wouldn't even give me free shipping for their defective product! I'm completely shocked at how their company handle this. I'd hope for better services since ASUS is so well known and a reputation to live up too. Manufacturer Response: 1 out of 2 people found this review helpful. Did you? |
Pros: Fast, very solid feeling in my hands, lots of storage. It runs all my games fine, and with 2 usb ports, it allows for a mouse, and something else to be plugged in. Cons: None that I can see, possibly battery life,but 3 and a half hours normal use is pretty solid as far as battery life goes. I do wish it had more RAM, 4GB is a little low for laptops these days. Other Thoughts: Internal Wireless card doesn't seem to work with my router after a while, but i had a USB wireless card and it works just fine. 3 out of 3 people found this review helpful. Did you? |
Beautiful Battery HogPros: Build Quality Cons: Battery Life Other Thoughts: At about six weeks in, I have mixed feelings about the Taichi. It is drop-dead gorgeous, slim and well put together. Both displays work well. It is light and well balanced enough to use as a tablet and is a wonderful travel companion -- better than a laptop or a tablet as it fuflfills both missions. 7 out of 7 people found this review helpful. Did you? |
Great machine, but lacks..Pros: Probably best in it's class when it comes to design. The keyboard is outstanding. It's the only ultrabook/convirtable that has two screens and a 256 Gb SSD - large SSDs adds to the price, but are finally coming down in price. 11.1" screen, 64-bit o.s., writing stylus - all make this a strong machine. Networking is dual band; has BT 4.0, 2 USB 3.0 ports, 3rd gen i7 processor, and comes with several nice accessories - stylus, USB Ethernet connector, USB VGA connector, and a soft cover. Cons: Asus missed the mark for a couple of reasons - both displays rate only 215 Nits in brightness - Asus has laptop displays that are very bright at 400 Nits and great for out door reading. The other downside is that it only comes with 4 Gb of RAM; they should have offered 8 Gb of RAM. One key thing to understand is that you cannot upgrade the RAM or SSD because all of the components are soldered directly onto the motherboard. There's no way to upgrade these devices. Also, Asus advertises a case for the Asus Taichi called the Taichi Suit, which looks like a definite accessory the you would want to purchase to protect the hefty cost of this machine - but, try to find one - you can't buy them. Even Asus cannot sell you one or tell you who actually has them. Another issue with the Asus Taichi is that you cannot find one to actually touch and feel to see if you would like or be able to tolerate the keyboard for your typing pleasure - which you might use a lot of the time if you are replacing your desktop or taptop with this device. The battery life is poor as it is with all the ultrabook laptops. Trying to get information from the Asus website or even trying to find out how to contact them is very difficult. Optional accessories are very difficut to locate and purchase right now. Asus also makes mention of a Asus Taichi machine with a 13" display, which is what I wanted, but there's no clue when or if this will ever be available. Other Thoughts: It's a nice machine, but better ones are coming out - larger SSDs, larger amount of RAM, brighter displays with higher NIT ratings, newer low voltage/wattage processors. 12 out of 12 people found this review helpful. Did you? |


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This very stylish unisex ring features a clear Baguette Shape CZ (Cubic Zirconia) mounted in a band of High Polish Stainless Steel with a Satin Finish center. Only the best quality stainless steel is used in the creation of our jewelry. Band width: 8mm
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Ephesians 5 September 26, 2011 BQ92611
Because so much of the church has long disregarded the full teaching of Scripture, many believers find some of its truths to be unfamiliar and even hard to accept. And because the church has been so engulfed in, identified with, and victimized by worldly standards, God's standards seem out–of–date, irrelevant, and offensive to modern mentalities. His way is so high and so contrary to the way of the world that it is incomprehensible to many in and out of the church.
Few areas of modern living have been so distorted and corrupted by the devil and the world and caused the church so much confusion as those of marriage and the family. It is these issues that Paul confronts in Ephesians 5:22—6:9. He expands and clarifies the general principle of mutual submission ("be subject to one another in the fear of Christ," v. 21) by giving several illustrations from the family, beginning with the relationship of husbands and wives. Scripture makes clear that there are no spiritual or moral distinctions among Christians. "There is neither Jew nor Greek, there is neither slave nor free man, there is neither male nor female; for you are all one in Christ Jesus" (Gal. 3:28). There are no classifications of Christians. Every believer in Jesus Christ has exactly the same salvation, the same standing before God, the same divine nature and resources, and the same divine promises and inheritance (cf. Acts 10:34; Rom. 2:11; James 1:1–9).
But in matters of role and function God has made distinctions. Although there are no differences in intrinsic worth or basic spiritual privilege and rights among His people, the Lord has given rulers in government certain authority over the people they rule, to church leaders He has delegated authority over their congregations, to husbands He has given authority over their wives, to parents He has given authority over their children, and to employers He has given authority over employees.
In Ephesians 5:22–24 Paul begins this list by outlining the role, duties, and priorities of the wife in relation to her husband's authority First he deals with the basic matter of the submission.
Wives, be subject to your own husbands, (Ephesians 5:22a)
Wives is not qualified, and therefore applies to every Christian wife, regardless of her social standing, education, intelligence, spiritual maturity or giftedness, age, experience, or any other consideration. Nor is it qualified by her husband's intelligence, character, attitude, spiritual condition, or any other consideration. Paul says categorically to all believing wives: be subject to your own husbands.
As indicated by italics in most translations, be subject is not in the original text, but the meaning is carried over from verse 21. The idea is: "Be subject to one another in the fear of Christ [and, as a first example,] wives, … to your own husbands." Hupotasso means to relinquish one's rights, and the Greek middle voice (used in v. 21 and carried over by implication into v. 22) emphasizes the willing submitting of oneself God's command is to those who are to submit. That is, the submission is to be a voluntary response to God's will in giving up one's independent rights to other believers in general and to ordained authority in particular—in this case the wife's own husband.
The wife is not commanded to obey (hupakouo) her husband, as children are to obey their parents and slaves their masters (6:1, 5). A husband is not to treat his wife as a servant or as a child, but as an equal for whom God has given him care and responsibility for provision and protection, to be exercised in love. She is not his to order about, responding to his every wish and command. As Paul proceeds to explain in considerable detail (vv. 25–33), the husband's primary responsibility as head of the household is to love, provide, protect, and serve his wife and family—not to lord it over them according to his personal whims and desires.
Your own husband suggests the intimacy and mutuality of the wife's submission. She willingly makes herself subject to the one she possesses as her own husband (cf. 1 Cor. 7:3–4). Husbands and wives are to have a mutual possessiveness as well as a mutual submissiveness. They belong to each other in an absolute equality. The husband no more possesses his wife than she possesses him. He has no superiority and she no inferiority, any more than one who has the gift of teaching is superior to one with the gift of helps. A careful reading of 1 Corinthians 12:12–31 will show that God has designed every person for a unique role in the Body of Christ, and the pervasive attitude governing all those roles and blending them together is "the more excellent way" of love (ch. 13).
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County To Offer Free Emergency Preparedness Classes
(WMC-TV) – The Shelby County Office of Preparedness will be offering free classes to all county residents on the methods and procedures to survive common emergency situations.
Participants will take Community Emergency Response Team (CERT) classes. The classes consist of two-day sessions and will provide participants with life-saving information through hands-on exercises, lectures and videos. Every common emergency, from first-aid skills to how to spot terrorism will be discusses in the classes, and students will learn how to assist their families and neighbors in the event of a catastrophic natural or manmade disaster.
You must pre-register for the classes, which will be held at 1075 Mullins Station Road. The dates for future classes are:


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Taking steps to create a better world for our associates, ourselves and our communities
Corporate Social Responsibility (CSR) at Sitel is about demonstrating and sustaining our commitment to conducting business in a socially and environmentally responsible manner. It is a commitment that stems from our Vision. Passion. Purpose. culture and values of corporate citizenship.
Sitel Footprints is an encompassing CSR program that aspires to become an agent of societal change in all Sitel locations around the globe-more than 120 contact centers in total. Our goal is to primarily improve the quality of life of our associates, to provide value to the business and our clients, and to contribute to the communities where we operate and call home. This organization serves as the umbrella program for numerous CSR projects focused on (1) Education and Job Generation, (2) Health and Wellness, (3) Social Responsibility and (4) Environmental Conservation.


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Berita Indonesia
Environmental Certification for University of Canterbury
Wednesday, 15 February 2012
The University of Canterbury has become the first university outside the UK to be certified under the CEMARS scheme by carboNZero Holdings Limited.
CEMARS (Certified Emissions Management And Reduction Scheme) is the world's first internationally accredited greenhouse gas certification scheme to measure and reduce the emissions created by an organisation's operational activities. CEMARS is a certification option provided by carboNZero Holdings Limited, a wholly owned subsidiary of New Zealand Crown Research Institute - Landcare Research.
UC joins other large organisations, such as Meridian Energy, Wellington International Airport and the NZ Rugby Union in achieving CEMARS certification.
As part of its CEMARS certifcation the University proposes to reduce its emissions over the next five years in line with New Zealand's national targets under the Kyoto Protocol (i.e. 10-20 per cent by 2020 based on 1990 levels). Some of the projects that will be undertaken to help achieve this goal are to:
- Increase the combustion and operational efficiency of its coal boiler by upgrading its management control
- Reduce air travel through providing leading edge video conferencing facilities across campus
- Benchmark high energy use in buildings and apply remedial measures
"Becoming CEMARS certified is an important step for the University," said University of Canterbury Vice-Chancellor, Dr Rod Carr. "It has allowed us to comprehensively measure and verify our emissions and to set targets for the reduction of those emissions. On campus, CEMARS will support our efforts to become more energy conscious and efficient. Off campus and in the wider community, it will broaden and enhance our organisation's sustainability credentials and its reputation as a great place to study or work."
"CEMARS certification is another key step in our sustainability journey. The challenge now is to maintain our focus and deliver upon our commitment as one of the few universities in the world with this distinction."


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The Acura distributor rotor's main role is to guarantee that electricity from car ignition will be directed successfully to the plugs to start the automotive engine and keep the vehicle running. The Acura distributor rotor provides spark and ensures perfect timing to ignite spark plugs. With no fully functional rotor that maintains a constant supply of electric current, you'll have to be ready for bad car ignition efficiency that'll lead to lots of trouble on your vehicle.
The distributor rotor of your Acura can get ruined after some time because it can eventually get scorched due to the electrical power it delivers. A defective Acura distributor rotor may the effect of this component's exposure to intense temperatures and driving conditions that put stress on the engine. It's certainly advised that you examine the distributor rotor whenever you're performing scheduled checkup or after every two years of use to see if the rotor is in good form. Never make it possible for a rusty distributor rotor to bring about difficult ignition system failure—look for a durable rotor to suit your Acura .
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Topics & Tools
Health Topics
- Healthline →
- Symptoms and Conditions →
- Muscular dystrophy
Muscular dystrophy
Muscular dystrophy is the name for a group of inherited disorders in which strength and muscle bulk gradually decline. Nine types of muscular dystrophies are generally recognized.
The muscular dystrophies include:
- Duchenne muscular dystrophy (DMD): DMD affects young boys, causing progressive muscle weakness, usually beginning in the legs. It is a severe form of muscular dystrophy. DMD occurs in about one in 3,500 male births, and affects approximately 8,000 boys and young men in the United States. A milder form occurs in a very small number of female carriers.
- Becker muscular dystrophy (BMD): BMD affects older boys and young men, following a milder course than DMD. It occurs in about one in 30,000 male births.
- Emery-Dreifuss muscular dystrophy (EDMD): EDMD affects both males and females because it can be inherited as an autosomal dominant or recessive disorder. Symptoms include contractures and weakness in the calves, weakness in the shoulders and upper arms, and problems in the way electrical impulses travel through the heart to make it beat (heart conduction defects). Fewer than 300 cases of EDMD have been reported in the medical literature.
- Limb-girdle muscular dystrophy (LGMD): LGMD begins in late childhood to early adulthood and affects both men and women, causing weakness in the muscles around the hips and shoulders, and weakness in the limbs. It is the most variable of the muscular dystrophies, and there are several different forms of the condition now recognized. Many people with suspected LGMD have probably been misdiagnosed in the past, and therefore, the prevalence of the condition is difficult to estimate. The highest prevalence of LGMD is in a small mountainous Basque province in northern Spain, where the condition affects 69 persons per million.
- Facioscapulohumeral muscular dystrophy (FSH): FSH, also known as Landouzy-Dejerine condition, begins in late childhood to early adulthood and affects both men and women, causing weakness in the muscles of the face, shoulders, and upper arms. The hips and legs may also be affected. FSH occurs in about one out of every 20,000 people, and affects approximately 13,000 people in the United States.
- Myotonic dystrophy: Also known as Steinert's disease, it affects both men and women, causing generalized weakness first seen in the face, feet, and hands. It is accompanied by the inability to relax the affected muscles (myotonia). Symptoms may begin from birth through adulthood. It is the most common form of muscular dystrophy, affecting more than 30,000 people in the United States.
- Oculopharyngeal muscular dystrophy (OPMD): OPMD affects adults of both sexes, causing weakness in the eye muscles and throat. It is most common among French Canadian families in Quebec, and in Spanish-American families in the southwestern United States.
- Distal muscular dystrophy (DD): DD is a group of rare muscle diseases that have weakness and wasting of the distal (farthest from the center) muscles of the forearms, hands, lower legs, and feet in common. In general, the DDs are less severe, progress more slowly, and involve fewer muscles than the other dystrophies. DD usually begins in middle age or later, causing weakness in the muscles of the feet and hands. It is most common in Sweden, and rare in other parts of the world.
- Congenital muscular dystrophy (CMD): CMD is a rare group of muscular dystrophies that have in common the presence of muscle weakness at birth (congenital), and abnormal muscle biopsies. CMD results in generalized weakness, and usually progresses slowly. A subtype, called Fukuyama CMD, also involves mental retardation and is more common in Japan.
Genetic profile
The muscular dystrophies are genetic conditions, meaning they are caused by alterations in genes. Genes, which are linked together on chromosomes, have two functions; they code for the production of proteins, and they are the material of inheritance. Parents pass along genes to their children, providing them with a complete set of instructions for making their own proteins.
Because both parents contribute genetic material to their offspring, each child carries two copies of almost every gene, one from each parent. For some conditions to occur, both copies must be altered. Such conditions are called autosomal recessive conditions. Some forms of LGMD and DD exhibit this pattern of inheritance, as does CMD. A person with only one altered copy, called a carrier, will not have the condition, but may pass the altered gene on to his children. When two carriers have children, the chances of having a child with the condition is one in four for each pregnancy.
Other conditions occur when only one altered gene copy is present. Such conditions are called autosomal dominant conditions. DM, FSH, and OPMD, exhibit this pattern of inheritance, as do some forms of DD and LGMD. When a person affected by the condition has a child with someone not affected, the chances of having an affected child is one in two.
Because of chromosomal differences between the sexes, some genes are not present in two copies. The chromosomes that determine whether a person is male or female are called the X and Y chromosomes. A person with two X chromosomes is female, while a person with one X and one Y is male. While the X chromosome carries many genes, the Y chromosome carries almost none. Therefore, a male has only one copy of each gene on the X chromosome, and if it is altered, he will have the condition that alteration causes. Such conditions are said to be X-linked. X-linked conditions include DMD, BMD, and EDMD. Women are not usually affected by X-linked conditions, since they will likely have one unaltered copy between the two chromosomes. Some female carriers of DMD have a mild form of the condition, probably because their one unaltered gene copy is shut down in some of their cells.
Women carriers of X-linked conditions have a one in two chance of passing the altered gene on to each child born. Daughters who inherit the altered gene will be carriers. A son born without the altered gene will be free of the condition and cannot pass it on to his children. A son born with the altered gene will have the condition. He will pass the altered gene on to each of his daughters, who will then be carriers, but to none of his sons (because they inherit his Y chromosome).
Not all genetic alterations are inherited. As many as one third of the cases of DMD are due to new mutations that arise during egg formation in the mother. New mutations are less common in other forms of muscular dystrophy.
Several of the muscular dystrophies, including DMD, BMD, CMD, and most forms of LGMD, are due to alterations in the genes for a complex of muscle proteins. This complex spans the muscle cell membrane (a thin sheath that surrounds each muscle cell) to unite a fibrous network on the interior of the cell with a fibrous network on the outside. Theory holds that by linking these two networks, the complex acts as a "shock absorber," redistributing and evening out the forces generated by contraction of the muscle, thereby preventing rupture of the muscle membrane. Alterations in the proteins of the complex lead to deterioration of the muscle during normal contraction and relaxation cycles. Symptoms of these conditions set in as the muscle gradually exhausts its ability to repair itself.
Both DMD and BMD are caused by alterations in the gene for the protein called dystrophin. The alteration leading to DMD prevents the formation of any dystrophin, while that of BMD allows some protein to be made, accounting for the differences in severity and age of onset between the two conditions. Differences among the other muscular dystrophies in terms of the muscles involved and the ages of onset are less easily explained.
A number of genes have been found to cause LGMD. A majority of the more severe autosomal recessive types of LGMD with childhood-onset are caused by alterations in the genes responsible for making proteins called sarcoglycans. The sarcoglycans are a complex of proteins that are normally located in the muscle cell membrane along with dystrophin. Loss of these proteins causes the muscle cell membrane to lose some of its shock absorber qualities. The genes responsible include LGMD2D on chromosome 17, which codes for the alpha-sarcoglycan protein; LGMD2E on chromosome 4, which codes for the beta-sarcoglycan protein; LGMD2C on chromosome 13, which codes for the gamma-sarcoglycan protein; and LGMD2F on chromosome 5, which codes for the delta-sarcoglycan protein. Some cases of autosomal recessive LGMD are caused by an alteration in a gene, LGMD2A, on chromosome 15, which codes for a muscle enzyme, calpain 3. The relationship between this alteration and the symptoms of the condition is unclear. Alterations in a gene called LGMD2B on chromosome 2 that codes for the dysferlin protein, is also responsible for a minority of autosomal recessive LGMD
The genes causing these types of LGMD, their chromosomal location, and the proteins they code for (when known) are listed below:
- LGMD1A (chromosome 5): myotilin
- LGMD1B (chromosome 1): laminin
- LGMD1C (chromosome 3): caveolin
- LGMD1D (chromosome 6)
- LGMD1E (chromosome 7)
- COL6A1 (chromosome 21): collagen VI alpha 1
- COL6A2 (chromosome 21): collagen VI alpha 2
- COL6A3 (chromosome 2): collagen VI alpha 3
The causes of the other muscular dystrophies are not as well understood:
- EDMD is due to a alteration in the gene for a protein called emerin, which is found in the membrane of a cell's nucleus, but whose exact function is unknown.
- Myotonic dystrophy is caused by alterations in a gene on chromosome 19 for an enzyme called myotonin protein kinase that may control the flow of charged particles within muscle cells. This gene alteration is called a triple repeat, meaning it contains extra triplets of DNA code. It is possible that this alteration affects nearby genes as well, and that the widespread symptoms of myotonic dystrophy are due to a range of genetic disruptions.
- The gene for OPMD appears to also be altered with a triple repeat. The function of the affected protein may involve translation of genetic messages in a cell's nucleus.
- The gene(s) for FSH is located on the long arm of chromosome 4 at gene location 4q35. Nearly all cases of FSH are associated with a deletion (missing piece) of genetic material in this region. Researchers are investigating the molecular connection of this deletion and FSH. It is not yet certain whether the deleted material contains an active gene or changes the regulation or activity of a nearby FSH gene. A small number of FSH cases are not linked to chromosome 4. Their linkage to any other chromosome or genetic feature is under investigation.
- The gene(s) responsible for DD have not yet been found.
- •About 50% of individuals with CMD have their condition as a result of deficiency in a protein called merosin, which is made by a gene called laminin. The merosin protein usually lies outside muscle cells and links them to the surrounding tissue. When merosin is not produced, the muscle fibers degenerate soon after birth. A second gene called integrin is responsible for CMD in a few individuals but alterations in this gene are a rare cause of CMD. The gene responsible for Fukuyama CMD is FCMD and it is responsible for making a protein called fukutin whose function is not clear.
Signs and symptoms
All of the muscular dystrophies are marked by muscle weakness as the major symptom. The distribution of symptoms, age of onset, and progression differ significantly. Pain is sometimes a symptom of each, usually due to the effects of weakness on joint position.
DUCHENNE MUSCULAR DYSTROPHY (DMD) A boy with Duchenne muscular dystrophy usually begins to show symptoms as a pre-schooler. The legs are affected first, making walking difficult and causing balance problems. Most patients walk three to six months later than expected and have difficulty running. Later on, a boy with DMD will push his hands against his knees to rise to a standing position, to compensate for leg weakness. About the same time, his calves will begin to enlarge, though with fibrous tissue rather than with muscle, and feel firm and rubbery; this condition gives DMD one of its alternate names, pseudohypertrophic muscular dystrophy. He will widen his stance to maintain balance, and walk with a waddling gait to advance his weakened legs. Contractures (permanent muscle tightening) usually begin by age five or six, most severely in the calf muscles. This pulls the foot down and back, forcing the boy to walk on tip-toes, and further decreases balance. Climbing stairs and rising unaided may become impossible by age nine or ten, and most boys use a wheelchair for mobility by the age of 12. Weakening of the trunk muscles around this age often leads to scoliosis (a side-to-side spine curvature) and kyphosis (a front-to-back curvature).
The most serious weakness of DMD is weakness of the diaphragm, the sheet of muscles at the top of the abdomen that perform the main work of breathing and coughing. Diaphragm weakness leads to reduced energy
Among males with DMD, the incidence of cardiomyopathy (weakness of the heart muscle), increases steadily in teenage years. Almost all patients have cardiomyopathy after 18 years of age. It has also been shown that carrier females are at increased risk for cardiomyopathy and should also be screened.
About one third of males with DMD experience specific learning disabilities, including difficulty learning by ear rather than by sight and difficulty paying attention to long lists of instructions. Individualized educational programs usually compensate well for these disabilities.
BECKER MUSCULAR DYSTROPHY (BMD) The symptoms of BMD usually appear in late childhood to early adulthood. Though the progression of symptoms may parallel that of DMD, the symptoms are usually milder and the course more variable. The same pattern of leg weakness, unsteadiness, and contractures occur later for the young man with BMD, often allowing independent walking into the twenties or early thirties. Scoliosis may occur, but is usually milder and progresses more slowly. Cardiomyopathy occurs more commonly in BMD. Problems may include irregular heartbeats (arrhythmias) and congestive heart failure. Symptoms may include fatigue, shortness of breath, chest pain, and dizziness. Respiratory weakness also occurs, and may lead to the need for mechanical ventilation.
EMERY-DREIFUSS MUSCULAR DYSTROPHY (EDMD) This type of muscular dystrophy usually begins in early childhood, often with contractures preceding muscle weakness. Weakness affects the shoulder and upper arm initially, along with the calf muscles, leading to foot-drop. Most men with EDMD survive into middle age, although an abnormality in the heart's rhythm (heart block) may be fatal if not treated with a pacemaker.
LIMB-GIRDLE MUSCULAR DYSTROPHY (LGMD) While there are several genes that cause the various types of LGMD, two major clinical forms of LGMD are usually recognized. A severe childhood form is similar in appearance to DMD, but is inherited as an autosomal recessive trait. Symptoms of adult-onset LGMD usually appear in a person's teens or twenties, and are marked by progressive weakness and wasting of the muscles closest to the trunk. Contractures may occur, and the ability to walk is usually lost about 20 years after onset. Some people with LGMD develop respiratory weakness that requires use of a ventilator. Life-span may be somewhat shortened. Autosomal dominant forms usually occur later in life and progress relatively slowly.
FACIOSCAPULOHUMERAL MUSCULAR DYSTROPHY (FSH) FSH varies in its severity and age of onset, even among members of the same family. Symptoms most commonly begin in the teens or early twenties, though infant or childhood onset is possible. Symptoms tend to be more severe in those with earlier onset. The condition is named for the regions of the body most severely affected by the condition: muscles of the face (facio-), shoulders (scapulo-), and upper arms (humeral). Hips and legs may be affected as well. Children with FSH may develop partial or complete deafness.
The first symptom noticed is often difficulty lifting objects above the shoulders. The weakness may be greater on one side than the other. Shoulder weakness also causes the shoulder blades to jut backward, called scapular winging. Muscles in the upper arm often lose bulk sooner than those of the forearm, giving a "Popeye" appearance to the arms. Facial weakness may lead to loss of facial expression, difficulty closing the eyes completely, and inability to drink through a straw, blow up a balloon, or whistle. A person with FSH may not be able to wrinkle thier forehead. Contracture of the calf muscles may cause foot-drop, leading to frequent tripping over curbs or rough spots. People with earlier onset often require a wheelchair for mobility, while those with later onset rarely do.
MYOTONIC DYSTROPHY Symptoms of myotonic dystrophy include facial weakness and a slack jaw, drooping eyelids (ptosis), and muscle wasting in the forearms and calves. A person with myotonic dystrophy has difficulty relaxing his grasp, especially if the object is cold. Myotonic dystrophy affects heart muscle, causing arrhythmias and heart block, and the muscles of the digestive system, leading to motility disorders and constipation. Other body systems are affected as well; myotonic dystrophy may cause cataracts, retinal degeneration, mental deficiency, frontal balding, skin disorders, testicular atrophy, sleep apnea, and insulin resistance. An increased need or desire for sleep is common, as is diminished motivation. The condition is extremely variable; some individuals show profound weakness as a newborn (congenital myotonic dystrophy), others show mental retardation in childhood, many show characteristic facial features and muscle wasting in adulthood, while the most mildly affected individuals show only cataracts in middle age with no other symptoms. Individuals with a severe form of mytonic dystropy typically have severe disabilites within 20 years of onset, although most do not require a wheelchair even late in life.
OCULOPHARYNGEAL MUSCULAR DYSTROPHY (OPMD) OPMD usually begins in a person's thirties or
DISTAL MUSCULAR DYSTROPHY (DD) DD usually begins in the twenties or thirties, with weakness in the hands, forearms, and lower legs. Difficulty with fine movements such as typing or fastening buttons may be the first symptoms. Symptoms progress slowly, and the condition usually does not affect life span.
CONGENITAL MUSCULAR DYSTROPHY (CMD) CMD is marked by severe muscle weakness from birth, with infants displaying "floppiness," very poor muscle tone, and they often have trouble moving their limbs or head against gravity. Mental function is normal but some are never able to walk. They may live into young adulthood or beyond. In contrast, children with Fukuyama CMD are rarely able to walk, and have severe mental retardation. Most children with this type of CMD die in childhood.
The diagnosis of muscular dystrophy involves a careful medical history and a thorough physical exam to determine the distribution of symptoms and to rule out other causes. Family history may give important clues, since all the muscular dystrophies are genetic conditions (though no family history will be evident in the event of new mutations; in autosomal recessive inheritance, the family history may also be negative).
Lab tests may include:
- Blood level of the muscle enzyme creatine kinase (CK). CK levels rise in the blood due to muscle damage, and may be seen in some conditions even before symptoms appear.
- Muscle biopsy, in which a small piece of muscle tissue is removed for microscopic examination. Changes in the structure of muscle cells and presence of fibrous tissue or other aberrant structures are characteristic of different forms of muscular dystrophy. The muscle tissue can also be stained to detect the presence or absence of particular proteins, including dystrophin.
- Electromyogram (EMG). This electrical test is used to examine the response of the muscles to stimulation. Decreased response is seen in muscular dystrophy. Other characteristic changes are seen in DM.
- Genetic tests. Several of the muscular dystrophies can be positively identified by testing for the presence of the altered gene involved. Accurate genetic tests are available for DMD, BMD, DM, several forms of LGMD, and EDMD. Genetic testing for some of these conditions in future pregnancies of an affected individual or parents of an affected individual can be done before birth through amniocentesis or chorionic villus sampling. Prenatal testing can only be undertaken after the diagnosis in the affected individual has been genetically confirmed and the couple has been counseled regarding the risks of recurrence.
- Other specific tests as necessary. For EDMD, DMD and BMD, for example, an electrocardiogram may be needed to test heart function, and hearing tests are performed for children with FSH.
For most forms of muscular dystrophy, accurate diagnosis is not difficult when done by someone familiar with the range of conditions. There are exceptions, however. Even with a muscle biopsy, it may be difficult to distinguish between FSH and another muscle condition, polymyositis. Childhood-onset LGMD is often mistaken for the much more common DMD, especially when it occurs in boys. BMD with an early onset appears very similar to DMD, and a genetic test may be needed to accurately distinguish them. The muscular dystrophies may be confused with conditions involving the motor neurons, such as spinal muscular atrophy; conditions of the neuromuscular junction, such as myasthenia gravis; and other muscle conditions, as all involve generalized weakness of varying distribution.
Prenatal diagnosis (testing of the baby while in the womb) can be done for those types of muscular dystrophy where the specific disease-causing gene alteration has been identified in a previously affected family member. Prenatal diagnosis can be done utilizing DNA extracted from tissue obtained by chorionic villus sampling or amniocentesis.
There are no cures for any of the muscular dystrophies. Prednisone, a corticosteroid, has been shown to delay the progression of DMD somewhat, for reasons that are still unclear. Some have reported improvement in strength and function in patients treated with a single dose. Improvement begins within ten days and plateaus after three months. Long-term benefit has not been demonstrated. Prednisone is also prescribed for BMD, though no controlled studies have tested its benefit. A study is under way in the use of gentamicin, an antibiotic that may slow down the symptoms of DMD in a small number of cases. No other drugs are currently known to have an effect on the course of any other muscular dystrophy.
Treatment of muscular dystrophy is mainly directed at preventing the complications of weakness, including decreased mobility and dexterity, contractures, scoliosis, heart alterations, and respiratory insufficiency.
Physical therapy
Physical therapy, regular stretching in particular, is used to maintain the range of motion of affected muscles and to prevent or delay contractures. Braces are used as well, especially on the ankles and feet to prevent tip-toeing. Full-leg braces may be used in children with DMD to prolong the period of independent walking. Strengthening other muscle groups to compensate for weakness may be possible if the affected muscles are few and isolated, as in the earlier stages of the milder muscular dystrophies. Regular, nonstrenuous exercise helps maintain general good health. Strenuous exercise is usually not recommended, since it may damage muscles further.
When contractures become more pronounced, tenotomy surgery may be performed. In this operation, the tendon of the contractured muscle is cut, and the limb is braced in its normal resting position while the tendon regrows. In FSH, surgical fixation of the scapula can help compensate for shoulder weakness. For a person with OPMD, surgical lifting of the eyelids may help compensate for weakened muscular control. For a person with DM, sleep apnea may be treated surgically to maintain an open airway. Scoliosis surgery is often needed in boys with DMD, but much less often in other muscular dystrophies. Surgery is recommended at a much lower degree of curvature for DMD than for scoliosis due to other conditions, since the decline in respiratory function in DMD makes surgery at a later time dangerous. In this surgery, the vertebrae are fused together to maintain the spine in the upright position. Steel rods are inserted at the time of operation to keep the spine rigid while the bones grow together.
When any type of surgery is performed in patients with muscular dystrophy, anesthesia must be carefully selected. People with MD are susceptible to a severe reaction, known as malignant hyperthermia, when given halothane anesthetic.
Occupational therapy
The occupational therapist suggests techniques and tools to compensate for the loss of strength and dexterity. Strategies may include modifications in the home, adaptive utensils and dressing aids, compensatory movements and positioning, wheelchair accessories, or communication aids.
Good nutrition helps to promote general health in all the muscular dystrophies. No special diet or supplement has been shown to be of use in any of the conditions. The weakness in the throat muscles seen especially in OPMD and later DMD may necessitate the use of a gastrostomy tube, inserted in the stomach to provide nutrition directly.
Cardiac care
The arrhythmias of EDMD and BMD may be treatable with antiarrhythmia drugs. A pacemaker may be implanted if these do not provide adequate control. Heart transplants are increasingly common for men with BMD. A complete cardiac evaluation is recommended at least once in all carrier females of DMD and EDMD.
Respiratory care
People who develop weakness of the diaphragm or other ventilatory muscles may require a mechanical ventilator to continue breathing deeply enough. Air may be administered through a nasal mask or mouthpiece, or through a tracheostomy tube, which is inserted through a surgical incision through the neck and into the windpipe. Most people with muscular dystrophy do not need a tracheostomy, although some may prefer it to continual use of a mask or mouthpiece. Supplemental oxygen is not needed. Good hygiene of the lungs is critical for health and long-term survival of a person with weakened ventilatory muscles. Assisted cough techniques provide the strength needed to clear the airways of secretions; an assisted cough machine is also available and provides excellent results.
Experimental treatments
Two experimental procedures aiming to cure DMD have attracted a great deal of attention in the past decade. In myoblast transfer, millions of immature muscle cells are injected into an affected muscle. The goal of the treatment is to promote the growth of the injected cells, replacing the abnormal host cells with healthy new ones. Myoblast transfer is under investigation but remains experimental.
Gene therapy introduces unaltered copies of the altered gene into muscle cells. The goal is to allow the existing muscle cells to use the new gene to produce the protein it cannot make with its abnormal gene. Problems with gene therapy research have included immune rejection of the virus used to introduce the gene, loss of gene function after several weeks, and an inability to get the gene to enough cells to make a functional difference in the affected muscle. Researchers are preparing for the first gene therapy trial for LGMD in the United States. The goal will be to replace the missing sarcoglycan gene(s).
Genetic counseling
Individuals with muscular dystrophy and their families may benefit from genetic counseling for information on the condition and recurrence risks for future pregnancies.
The expected lifespan for a male with DMD has increased significantly in the past two decades. Most young men will live into their early or mid-twenties. Respiratory infections become an increasing problem as their breathing becomes weaker, and these infections are usually the cause of death.
The course of the other muscular dystrophies is more variable; expected life spans and degrees of disability are hard to predict, but may be related to age of onset and initial symptoms. Prediction is made more difficult because, as new genes are discovered, it is becoming clear that several of the dystrophies are not uniform disorders, but rather symptom groups caused by different genes.
People with dystrophies with significant heart involvement (BMD, EDMD, myotonic dystrophy) may nonetheless have almost normal life spans, provided that cardiac complications are monitored and treated aggressively. The respiratory involvement of BMD and LGMD similarly require careful and prompt treatment.
There is no way to prevent any of the muscular dystrophies in a person who has the genes responsible for these disorders. Accurate genetic tests, including prenatal tests, are available for some of the muscular dystrophies. Results of these tests may be useful for purposes of family planning.
Emery, Alan. Muscular Dystrophy: The Facts. Oxford Medical Publications, 1994.
Swash, Michael, and Martin Schwartz. Neuromuscular Conditions: A Practical Approach to Diagnosis and Management, 3rd edition. Springer, 1997.
Muscular Dystrophy Association. 3300 East Sunrise Dr., Tucson, AZ 85718. (520) 529-2000 or (800) 572-1717. <http://www.mdausa.org>.
Online Myotonic & Congenital Dystrophies Support Group International. 185 Unionville Road, Freedom, PA 15042. (724)775-9448 or (724)774-0261. <http://www.angelfire.com/pa2/MyotonicDystrophy/index.html>.
Nada Quercia, Msc, CCGC


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Jane Goodall Reveals Her Lifelong Fascination With…Plants?
After studying chimpanzees for decades, the celebrated scientist turns her penetrating gaze on another life-form
- By Jane Goodall
- Smithsonian magazine, March 2013, Subscribe
Editor's Note: There have been allegations of plagiarism in the book Seeds of Hope, from which this excerpt was drawn. Smithsonian has checked this material independently and ascertained to the best of our ability that everything published in the magazine and in this post is original.
From my window, as I write in my house in Bournemouth, England, I can see the trees I used to climb as a child. Up in the branches of one of them, a beech tree, I would read about Doctor Dolittle and Tarzan, and dream about the time when I, too, would live in the forest. I spent hours in that tree, perched in my special place. I had a little basket on the end of a long piece of string that was tied to my branch: I would load it before I climbed, then haul up the contents—a book, a saved piece of cake, sometimes my homework. I talked to "Beech," telling him my secrets. I often placed my hands or my cheek against the slightly rough texture of his bark. And how I loved the sound of his leaves in summertime: the gentle whispering as the breeze played with them, the joyous abandoned dancing and rustling as the breeze quickened, and the wild tossing and swishing sounds, for which I have no words, when the wind was strong and the branches swayed. And I was part of it all.
Growing up in this idyllic home and landscape of England was the foundation of my lifelong love of the plant kingdom and the natural world. The other day, when I was looking through a box of childhood treasures that had been lovingly preserved by my mother, I came across a "Nature Notebook," in which the 12-year-old Jane, with great attention to detail, had sketched and painted a number of local plants and flowers. Beside each drawing or watercolor I had handwritten a detailed description of the plant, based on my careful observations and probably a bit of book research. This was not a schoolbook. This wasn't done for an assignment. I just loved to draw and paint and write about the plant world.
I used to read, curled up in front of the fire, on winter evenings. Then I traveled in my imagination to The Secret Garden with Mary and Colin and Dickon. I was entranced by C.S. Lewis' Voyage to Venus, in which he describes, so brilliantly, flowers and fruits, tastes and colors and scents unknown on planet Earth. I raced through the skies with little Diamond, who was curled up in the flowing hair of the Lady North Wind, as she showed him what was going on in the world, the beauty and the sadness and the joy (At the Back of the North Wind). And, of course, I was utterly in love with Mole and Ratty and Mr. Badger in The Wind in the Willows. If The Lord of the Rings had been written when I was a child, there is no doubt I would have been entranced by Treebeard and the ancient forest of Fangorn, and Lothlórien, the enchanted forest of the elves.
And so I write now to acknowledge the enormous debt we owe to the plants and to celebrate the beauty, mystery and complexity of their world. That we may save this world before it is too late.
Wouldn't it be fantastic if we had eyes that could see underground? So that we could observe everything down there in the same way we can look up through the skies to the stars. When I look at a giant tree I marvel at the gnarled trunk, the spreading branches, the multitude of leaves. Yet that is only half of the tree being—the rest is far, far down, penetrating deep beneath the ground.
There are so many kinds of roots. Aerial roots grow above the ground, such as those on epiphytes—which are plants growing on trees or sometimes buildings, taking water and nutrients from the air and rain—including many orchids, ferns, mosses and so on. Aerial roots are almost always adventitious, roots that can grow from branches, especially where they have been wounded, or from the tips of stems. Taproots, like those of carrots, act as storage organs. The small, tough adventitious roots of some climbing plants, such as ivy and Virginia creeper, enable the stems to cling to tree trunks—or the walls of our houses—with a viselike grip.
In the coastal mangrove swamps in Africa and Asia, I have seen how the trees live with their roots totally submerged in water. Because these roots are able to exclude salt, they can survive in brackish water, even that which is twice as saline as the ocean. Some mangrove trees send down "stilt roots" from their lowest branches; others have roots that send tubelike structures upward through the mud and water and into the air, for breathing.
Then there are those plants, such as the well-known mistletoe, beloved by young lovers at Christmastime but hated by foresters, that are parasitic, sending roots deep into the host tree to steal its sap. The most advanced of the parasitic plants have long ago given up any attempt at working for their own food—their leaves have become like scales, or are missing altogether.
The strangler fig is even more sinister. Its seeds germinate in the branches of other trees and send out roots that slowly grow down toward the ground. Once the end touches the soil it takes root. The roots hanging down all around the support tree grow into saplings that will eventually strangle the host. I was awestruck when I saw the famed temple at Angkor Wat in Cambodia, utterly embraced by the gnarled roots of a giant and ancient strangler fig. Tree and building are now so entwined that each would collapse without the support of the other.
The so-called clonal trees have remarkable root systems that seem capable of growing over hundreds of thousands of years. The most famous of them—Pando, or the Trembling Giant—has a root system that spreads out beneath more than 100 acres in Utah and has been there, we are told, for 80,000 to one million years! The multiple stems of this colony (meaning the tree trunks) age and die but new ones keep coming up. It is the roots that are so ancient.
The variety of leaves seems almost infinite. They are typically green from the chlorophyll that captures sunlight, and many are large and flat so as to catch the maximum amount. Indeed, some tropical leaves are so huge that people use them for umbrellas—and they are very effective, as I discovered during an aboriginal ceremony in Taiwan, when we were caught in a tropical downpour.
Orangutans have also learned to use large leaves during heavy rain. My favorite story concerns an infant, who was rescued from a poacher and was being looked after in a sanctuary. During one rainstorm she was sitting under the shelter provided but, after staring out, rushed into the rain, picked a huge leaf, and ran back to hold it over herself as she sat in the dry shelter.
Some leaves are delicate, some are tough and armed with prickles, yet others are long and stiff like needles. The often-vicious spines of the cactus are actually modified leaves—in these plants it is the stems that capture the energy from the sun. I used to think that the brilliant red of the poinsettia and the varied colors of bougainvillea were flowers, but, of course, they are leaves adapted to attract pollinating insects to the very small, insignificant-looking flowers in the center.
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The Teaching Academy at Purdue University
The Teaching Academy at Purdue strives to bring together the best teaching faculty across campus to create a collective voice for teaching and learning on campus. Faculty are nominated and selected by their peers to join this eclectic group of faculty. Faculty in the Teaching Academy contribute in a variety of ways, but even with the myriad activities their primary focus is to increase the effectiveness of all of the faculty at Purdue University.
Mission Statement
The mission of the Teaching Academy is to provide leadership and serve as a catalyst to enhance and strengthen the quality of undergraduate, graduate, and outreach teaching and learning.
Bringing together outstanding scholar-teachers from across the curriculum, the Teaching Academy provides all interested faculty, staff, and students the opportunity to talk, learn, and work together on important and meaningful educational initiatives. The Teaching Academy sponsors programs and activities fostering educational creativity, innovation, and effectiveness both in and outside the classroom.
The Academy is comprised of a dedicated and dynamic network of scholar-teachers committed to the continual improvement of teaching and learning at Purdue University. Under the auspices of the Office of the Executive Vice President for Academic Affairs, the Teaching Academy works with the academic schools, the Center for Instructional Excellence, and others to enrich the educational experiences of the entire Purdue University community.
Teaching Academy Charter
Nominating Members to the Teaching Academy
Each year the Teaching Academy accepts nominations for individuals who should be considered for membership in the Academy. The Academy has well defined requirements and procedures. Upon receiving nominations, the Executive Council of the Teaching Academy reviews and accepts a limited number of new fellows and associate fellows.
Timeline for 2013-2014 Nominations:
- Nominations due to Shelly Dunk in the Provost's Office on Friday, March 30, 2013.
- Nominees notified prior to the end of the spring 2013 semester.
- Induction Ceremony will take place in the fall of 2013 (date to be determined).
The links below provide access to relevant procedures documents as well as a template for nominees to structure their documentation for consideration.


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SPIE Photonics West 2014—Attend the largest and most influential event for the laser and photonics community in North America: 20,000 attendees, two exhibitions, 1,300 exhibiting companies, a wide range of papers on biomedical optics, biophotonics, translational research, industrial lasers, optoelectronics, microfabrication, optical MEMS, and more.
View the conference and course advance program (14 MB PDF)
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A variety of events, all in one week 4,600 papers * 17 plenary and hot topic presentations * 40 special events * 70 courses * BiOS Expo * Photonics West * industry events * prism awards
Exhibit space is filling up fast. Contact SPIE Sales today.
BiOS Expo, 1 - 2 February 2014 has grown to become the world's largest biomedical optics and biophotonics exhibition. The exhibition sold out in 2013 with more than 220 companies.
Photonics West exhibition, 4 - 6 February, 2014 is the flagship event for companies in the photonics industry. The exhibition sold out in 2013 with more than 1230 companies.
SPIE Photonics West—find the latest research and products in photonics, biomedical optics, MEMs, optoelectronics, industrial lasers, and more. We look forward to seeing you in February 2014.
Important Dates
Abstracts Due:22 July 2013Late abstracts may be accepted; subject to chair approval. Contact: Program Coordinator
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Yesterday Sony published figures for the last three months of 2008. They revealed sales of all three consoles were down year-on-year, with only PS3 software showing an increase. Bad news for Sony, you might think - but David Reeves would disagree.
We sat down with the Sony Computer Entertainment Europe boss to ask why he's happy with the figures, and who he believes is winning the console battle. Plus, when we can expect a price cut, what's next for PSP and whether Sony has started work on PlayStation 4.
Eurogamer: What's your reaction to the Q3 financial figures?
David Reeves: On PS3, the target is still 10 million sell-in. PS3 was the number one priority, and the Corporation is going to meet that target. We're very happy about it overall.
PSP was not hit so much by demand, but by economic factors. I can only talk specifically about Europe, but we've lost volume in Russia. A lot of retailers there have been sucked up by oligarchs, and they didn't have the financial support. They were not able to buy in the product, even though the demand was there.
Also unemployment has rocketed in Spain, and to some extent in Italy. The demand was not there. Not just for us - for Nintendo or Microsoft, it's exactly the same.
Eurogamer: Why do you think sales of PS3 have fallen year-on-year?
David Reeves: We've said it would be 10 million, and it is 10 million. We had a price decrease in the previous year, and we didn't have a price decrease this year. Xbox 360 did, and Nintendo was already quite low.
The plan wasn't necessarily to hit sales, it was to hit a profit target - to do better than break even in Q3. The financial results show a break even in Q3 for Sony Computer Entertainment worldwide. So rather than then going for market share and sales, we went for profit, at least to break even.
Eurogamer: But the fact is PS3 sales fell year-on-year. Do you think the console might have peaked?
David Reeves: Absolutely not. We're two-and-a-half years into a ten-year cycle. For October, November and December we were in a holding pattern, especially with the pricing. We had to demonstrate we could make a profit with the business model, and that's what we've done.
Eurogamer: In an interview with us in July 2007, you predicted that PS3 would be "far and away the winner" by March 2008...
David Reeves: In March 2008, we were a long way ahead of Microsoft. We launched PS3 six months later [in Europe] than the US, we launched 18 months later than Xbox 360 and we were beating Microsoft in terms of installed base - so that came true.
Eurogamer: How about now? According to NPD, Xbox 360 outsold PS3 2-to-1 in the US last month. Microsoft is claiming to be ahead by 1 million units in Europe. Can you really say Sony is the winner?
David Reeves: I don't want to talk about the competition too much, but Xbox 360 is not ahead by a million units. We sold through 500,000 PS3s in November. We sold through 1.1 million units in December. Our installed base now is very close to 8.5 million units in PAL territories. Our numbers show we are absolutely neck-and-neck.
What happened was, we overtook them, and they dropped the price. It's almost as if we've gone ten rounds as Mohammed Ali and we're still standing, because we didn't drop the price. We held firm.
Now, going into the remaining rounds and the next seven years, we are going to be very strong. The last few weeks have shown we are clearly number two in the market. I'm as confident as I was before.
Eurogamer: Sony Computer Entertainment boss Kaz Hirai was recently quoted as saying the Xbox 360 "lacks longevity". Do you agree?
David Reeves: I'm not going to comment on that. I simply don't know what their plans are. I'm not going to be as arrogant as to comment on either Nintendo or Xbox 360.
Eurogamer: Do you think what Kaz Hirai said was arrogant?
David Reeves: I don't think so. He was probably misquoted, because I don't think Kaz would say that.
Eurogamer: He also said Sony still has "official leadership" of the industry. Isn't it really about who's shifting the most boxes? Doesn't that sound a bit arrogant?
David Reeves: I look at it differently. In the videogames industry, we've all been winners for the last two years. We've had more people coming in who have never played games before. The industry is not recession-proof, but it has done extremely well.
Eurogamer: But there are more and more stories about people being made redundant and studios being shut down. Just today, for example, Kuju has announced impending redundancies. Is the industry really doing well when people are losing their jobs and studios are shutting down?
David Reeves: It's a function of the economic situation that you are going to find people who are resilient, who do not play with their pricing, who are very efficient. Those people in that particular studio, they don't have a job, but I think in a few weeks you'll find them housed in other studios.
Of course there are going to be some people who fold. But the videogames industry is inherently very healthy. It's not a question of survival of the fittest, it's the survival of people who are professional, and don't just go around cutting their prices and destroying the market.
Eurogamer: Is the PS3 going to remain the most expensive console on the market?
David Reeves: I think it will, yes. I'm not saying there are going to be any price cuts at all in the short term or the medium term. I'm not saying we don't need to do it - we are expensive. It is possible that as the cost [of manufacturing] comes down, we will be able to do it.
But we're protecting ourselves with a very hard shell to get through the next one or two years of an economic situation. If you're experienced, you know you have to go into that mode - it's like being an armadillo. You have to be hard, and then you will come out when the sun comes out.
If, as an industry, we can get through the next six to seven months, we're going to find a massive uplift in September and October. I'm very optimistic about it.
Eurogamer: Let's imagine an average consumer, someone who's not an early adopter, not a hardcore gamer, who doesn't care about Blu-ray. They walk into a shop and see three games machines on the shelf, and yours is the most expensive. At times like these, aren't you concerned the price will affect their decision?
David Reeves: The price will affect their decision. Yes, if I haven't got that much money to spend, I will go for, let's say, the green machine. Because the salesman will say, "Well, it's got all the games," and he wants to sell that machine.
But there are people who come in having done their research, thinking, 'PS3 has got all the games, it's free to go online, it's got a Blu-ray player. I know I'm not going to have to ring up the customer careline saying I've got three red lights.'
We recognised that those numbers would go down because we did not drop the price. But we reached the targets we expected to reach under those assumptions.
Eurogamer: Will you cut the price of PS3 this year?
David Reeves: As the cost of manufacturing comes down, we will look at it, as we've looked at it in the past. I'm not going to say we're going to do anything short term or anything long term on the price. At the moment, we have a value-added strategy.
Eurogamer: So can we expect to see more SKUs, perhaps with different hard drive specs, sold at different prices?
David Reeves: I'm not going to comment on that, simply because I don't have that detailed knowledge.
Eurogamer: Would Sony ever consider licensing out the PS3 technology? Could we see a Sony laptop or Blu-ray player, or even a machine manufactured by another company, which plays PS3 games?
David Reeves: I wouldn't rule it out, but I haven't thought of it myself. We don't have any plans to do that.
Eurogamer: Let's talk about software, specifically with regard to exclusivity. In the US, GTAIV sold 3.3 million on Xbox 360 and 1.9 million on PS3. When you look at those figures, do you regret giving up that exclusivity?
David Reeves: Those are US figures, right? Well, it wasn't the same in Europe.
I don't think we were in a position not to give up exclusivity. You can't live on exclusivity forever; in the end, you've got to be master of your own destiny. We've invested in studios like Media Molecule and gained exclusivity that way. We've made studios like Evolution and Guerrilla wholly-owned.
At the beginning, we had very few IPs and relied on other people for exclusivity. Now, our strategy is to have 15 to 20 IPs by the time we get to 2009, 2010. We don't have to go to Capcom or Take-Two and ask for an exclusive. And I don't think we could afford it anyway. In the cold light of day, I would do exactly as those publishers have done and go multi-platform.
Eurogamer: So what if, say, Konami came to you and said, 'We want to take Metal Gear Solid multi-platform'?
David Reeves: That's totally their decision. We're not going to fall over ourselves just to try and keep that exclusive. We have to stand on our own two feet.
Eurogamer: So you wouldn't spend a lot of time and money trying to keep MGS exclusive to PS3?
David Reeves: I don't think we would. I'm not ruling it out, but we would sooner invest that money in two years' time, in having another major IP like Resistance or LittleBigPlanet.
Heavy Rain is a good example. That will be, de facto, an exclusive; we haven't just given them a paper bag full of cash, we've built up a solid, long-term relationship.
Eurogamer: Speaking of LittleBigPlanet - did it sell as well as you expected?
David Reeves: It exceeded in the post orders and online. Selling it in, during peak, was quite difficult, but we sold in exactly what we thought we would. Subsequent orders have been very high; LittleBigPlanet has a very long tail.
Eurogamer: What did you think of the reaction to PlayStation Home? Do you think the release came at the right time?
David Reeves: I would have liked to introduce the open beta at the beginning of September. We wanted to make some modifications so gamers could take more advantage of things like Trophies that were in place, but weren't tested.
Now we're trying to sprinkle the dust over. We've got avatars, pavilions and spaces, and now you're going to see the content. It's still only open beta, it's not a full launch. I don't know how long it will remain in open beta, but we're now starting to get the rich content.
You talked about people going into stores - I've heard people in GAME say, "But this one's got Home. I've heard of that, I'll buy that." I don't know how many people buy PS3 because of Home, but I'd like to think it's a lot.
PR Executive: We've got 1.5 million unique registrants in the SCEE areas for Home, and more than 3.4 million worldwide.
David Reeves: Between 13th December and 13th January, there were over one million dollars' worth of micro-transactions in Home. So don't forget, it's a commercial venture as well.
Eurogamer: How's the software line-up looking for Christmas 2009? Have you got many big titles still to be announced?
David Reeves: There are a couple. You can probably guess, but we have not formally announced them. They will most likely be announced in the next four to six weeks. They may even keep some for E3 or Cologne.
Eurogamer: Moving on to the PSP - also back in July 2007, you said it needed "better and more original games". Do you think that need has been met?
David Reeves: No, I don't.
Eurogamer: Why do you think that is? What could Sony be doing to solve that problem?
David Reeves: The competition has been such that publishers have had four consoles, plus PC, to publish for. They did not put their chips on PSP, certainly in the US and Europe.
In Japan, a lot of publishers put their chips on PSP. So games like Monster Hunter, Phantasy Star Portable and Dissidia have caused enormous spikes for PSP in Japan. But there haven't been big platform drivers in Europe.
Now I can look you in the face and say, the line-up for PSP in 2009 is two or three times stronger than it was last year. We ran out of steam on games around August, September last year. We didn't have a Monster Hunter or a Dissidia. But probably from March to July, you're going to see that type of thing starting to kick in.
Eurogamer: I did a quick search of all the announced games on Games Press the other day. There are 44 listed for PSP, and 185 for DS. That's a worrying margin of difference, isn't it?
David Reeves: I don't know. It depends on the quality of the games, doesn't it? People come out on DS and want to compete against Nintendo first-party, and that's a tough thing.
It's like when you watch six year-old boys play football, and they all follow the ball right the way across the field. Sometimes developers and publishers do that, and that's what they've done with DS.
Eurogamer: Publishers have even stopped doing PSP versions of their biggest titles. The most recent Tomb Raider, Call of Duty and James Bond games didn't come out on your handheld - but they all came out on DS. How concerned are you about that?
David Reeves: I worry about it, but it comes back to how thin they have to spread the butter. It would have been nice if some of those had come out, and I think they will eventually, but they can only place their chips on so many slots.
Eurogamer: The iPhone and the App Store are doing very well at the moment. How do you plan to compete?
David Reeves: If you look at the statistics, more than 80 per cent of those games come in through telecommunications, as opposed to being downloaded. We are not planning to have any SIM card in any of our devices, so we have to think whether it would be as successful if we did something similar.
Eurogamer: There do seem to be some issues with your download service. For example, when LocoRoco 2 came out, it was cheaper to buy the boxed version from Play.com than to buy it as a download from the PlayStation Store.
David Reeves: I was not aware of that... How do we anticipate how much the retail trade is going to discount? That's an art, not a science. It may be that we have to have differential pricing.
Eurogamer: Shouldn't the prices be different anyway? If you buy the download version of a game, you're not paying for the production of a disc, box or manual, nor are there any retailer overheads. Shouldn't you be getting it cheaper?
David Reeves: You could argue the same with iTunes. You don't have to get in your car and go out, queue up at the store, buy it and come back. You can just download it, and there it is. That's what children do all the time. If we have to think boxed products, I think we're dinosaurs.
Eurogamer: Back in 2007, you said it was "definitely possible later" that we could see a PSP with a built-in hard drive. Now it's 2009, are we talking sooner rather than later?
David Reeves: It's still possible, but it's going to be later rather than sooner.
Eurogamer: Not this year, then?
David Reeves: No, I'm not saying that. You didn't give me your timeline - whether it's minutes, weeks, months or years...
Eurogamer: Is it minutes, weeks, months or years?
David Reeves: There is no timeframe. I stand by what I said. It is possible, yes, to have a fixed hard drive or flash memory. But what's happened is, the rate at which memory stick prices have come down have surprised everyone.
Eurogamer: You were recently quoted as saying Sony's priority for 2009 is to "start making money". How do you plan to do that?
David Reeves: Europe certainly will make money this fiscal year, from Sony Computer Entertainment's point of view. We are already on track to do that. Even with the recession we've got to ramp it up, to keep that install base and that momentum going. The priority now is still to make money, or at least to get to break even.
Eurogamer: Have you had your first meeting about PlayStation 4 yet?
David Reeves: I have never even heard it mentioned. I think people are concentrating so much on what's happening now that they're not even thinking about it.
David Reeves is president of Sony Computer Entertainment Europe.


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The Pkmn Masters
Welcome to The Pokemon Masters
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A world filled with only immortals. The rich live freely, yet not every one has the same luck. . . being pets to their masters and fulfilling their every desire!
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The Dark Masters Guild is a chill guild of the digimon masters online game.
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An English Forum Dedicated to Show Lo / Lo Chih Hsiang / Show Luo / Luo Zhi Xiang / Xiao Zhu
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The Swift Masters - Wom Realms Clan Website
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This is the forum for TMA or The Masters Academy for The Wrestling Game.
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Free forum : Forum for Uchiha Masters Clan members
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A portal for all Mike and Rainie fans to gather =)
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Free forum : Gamers unite around this Round Table of discussion for the creation of a new Role-play video game.
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Free forum : Stay up to dates on the latest Yu Gi Oh news & touraments or just discuss Yu Gi Oh strategies with your fellow duelist.
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Guild of Digimon Masters Online
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Online community for people who are interested in trucks or simulator games, such as Euro Truck Simulator 2, Scania Truck Driving Simulator, German Truck Simulator, 18 wos Extreme trucker and others.
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a place for people who love to roleplay and feel like they need a challenge as well as some fun.
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Forum gratis : Free forum : The time has come for the mandolorians to rise again as the true masters of the galaxie. Join or vanish!
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Forum gratis : YOU KNOW THAT DRAGONS ARE MYTHICAL POKÉMON! THEY'RE HARD TO MASTER, BUT THEIR POWERS ARE SUPERIOR! THEY'RE VIRTUALLY INDESTRUCTIBLE!
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Mornings start simply over northern Minnesota's Lake Vermilion. Motorboats putter across 40,000 acres of open water as deer graze at the edge of thick pine forests. The blue water ripples ever so slightly. Somewhere in the distance, a loon calls. And just down the road from Pehrson Lodge, the town of Cook (population: 500) is waking up. Valerie Ohotto pours coffee at the Montana Cafe as men in baseball caps and blue jeans tuck into sausage patties as big as their hands.
Pictured: Walleye, northern and smallmouth bass draw anglers to Lake Vermilion.
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