Alas for Volapük

نویسنده

  • Walter Gratzer
چکیده

that his/­her monozygotic twin and a 39% chance that a dizygotic twin will also be dyscalculic. The link also exists between dyscalculics' parents and siblings: around half of the all first-degree family members of a dyscalculic also have dyscalculia (mothers, 67%; fathers, 41%; brothers, 53%; sisters, 52%), and 43% of the second-degree relatives. This prevalence is around tenfold higher than expected for the general population. However, there are no gender differences. Is there any comorbidity with other developmental problems? People that have developmental problems, such as dyslexia, attention deficit hyperactivity disorder (ADHD), neurological problems, such as epilepsy, or genetic disorders of the X chromosome, are at greater risk than the normal population of being dyscalculic. In these cases, however, the dyscalculia might be a secondary problem, and might not stem from a core deficit for numerical processing per se. For example, a child with ADHD might not be able to solve arithmetic problems successfully due to failures in planning and organisation. Aside from comorbidity with other developmental problems, it has also been suggested recently that people suffering from dyscalculia might have impaired abilities in processing other non-numerical magnitudes such as physical size. What is the consequence of dyscalculia for one's life? The consequences of poor numeracy in today's world are significant and long-lasting: initial problems in school subjects that require maths later translate into reduced employment opportunities. Not surprisingly then, poor numerical abilities correlate with an adult's economic and social status and psychological well-being (it is no coincidence that all the happy, wealthy readers of Current Biology are above normal in their numerical abilities). Surprisingly, for women, deficiencies in numerical abilities can count even more than other disorders, such as poor literacy. Can it be alleviated? In contrast to dyslexia, where the neurobiological basis has been convincingly demonstrated and some effective treatment possibilities have been introduced, remediation for dyscalculia is in its infancy. There are some current attempts to design training programs, including adaptive computer games for children, which will hopefully enable us in the long run to remediate dyscalculic behaviour. However, remediation programs still need to be validated in large group trials including a control group in order to examine placebo-like effects. The future success of remediation programs rests on accurate and early diagnosis of subtypes of dyscalculia, and referring the person to the appropriate intervention program. Hopefully, better knowledge of both normal and abnormal numerical processing at the …

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Effects of D-Doping on Characteristics of AlAs/GaAs Barriers Grown by Mba at 400 ??C

Effects of d-doping on barriers effective heights and series resistance of highly doped n-type GaAs/AIAs/GaAs/AlAs/GaAs heterostructures, grown by molecular beam epitaxy (MBE) at 400?°C, have been studied. As it was expected, inclusion of an n+ d-doped layer at each hetero-interface has reduced the barriers heights and series resistance of the structure significantly, while p+ d-doped layers ha...

متن کامل

Interaction between succinyl CoA synthetase and the heme-biosynthetic enzyme ALAS-E is disrupted in sideroblastic anemia.

The first and the rate-limiting enzyme of heme biosynthesis is delta-aminolevulinate synthase (ALAS), which is localized in mitochondria. There are 2 tissue-specific isoforms of ALAS, erythroid-specific (ALAS-E) and nonspecific ALAS (ALAS-N). To identify possible mitochondrial factors that modulate ALAS-E function, we screened a human bone marrow cDNA library, using the mitochondrial form of hu...

متن کامل

Heme deficiency in erythroid lineage causes differentiation arrest and cytoplasmic iron overload.

Erythroid 5-aminolevulinate synthase (ALAS-E) catalyzes the first step of heme biosynthesis in erythroid cells. Mutation of human ALAS-E causes the disorder X-linked sideroblastic anemia. To examine the roles of heme during hematopoiesis, we disrupted the mouse ALAS-E gene. ALAS-E-null embryos showed no hemoglobinized cells and died by embryonic day 11.5, indicating that ALAS-E is the principal...

متن کامل

Design rules for modulation-doped AlAs quantum wells

Thanks to their multi-valley, anisotropic, energy band structure, two-dimensional electron systems (2DESs) in modulation-doped AlAs quantum wells (QWs) provide a unique platform to investigate electron interaction physics and ballistic transport. Indeed, a plethora of phenomena unseen in other 2DESs have been observed over the past decade. However, a foundation for sample design is still lackin...

متن کامل

Characteristic of P-type AlAs/GaAs Bragg Mirrors Grown by MBE on (100) and (311)A Oriented Substrates

P-type GaAs/AlAs distributed Bragg mirrors have been grown using molecular beam epitaxy on (100) and (311)A GaAs substrates in a similar conditions. A comparison of I-V measurements shows that the resistance of the ungraded mirrors grown on the (311)A substrate is 35 times lower than those grown on the (100) substrate with similar structure. The effective barrier heights for both (311 )A and (1...

متن کامل

Deficient Heme and Globin Synthesis in Embryonic Stem Cells Lacking the Erythroid-Specific d-Aminolevulinate Synthase Gene

The erythroid-specific isoform of d-aminolevulinate synthase (ALAS-E) catalyzes the first step of heme biosynthesis in erythroid cells, and ALAS-E gene mutations are known to be responsible for x-linked sideroblastic anemia. To study the role of ALAS-E in erythroid development, we prepared mouse embryonic stem (ES) cells carrying a disrupted ALAS-E gene and examined the effect of the lack of AL...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • Current Biology

دوره 17  شماره 

صفحات  -

تاریخ انتشار 2007