LONDON (AFP) — Victims of deep vein thrombosis (DVT), or “economy class syndrome,” suffered a legal setback when Britain’s de facto supreme court turned down their case for compensation.
Upholding earlier court judgements, the Law Lords on Thursday rejected claims by passengers or their families seeking to sue British Airways and other carriers for death or injury which, they say, was the result of DVT.
In the most recent ruling, the Court of Appeal said that incidents of DVT were a “non-event” and therefore could not be classed as an “accident” under the 1929 Warsaw Convention governing air travel.
Had the appeal been allowed by the Law Lords, airlines throughout the world would have faced huge damages claims.
Lord Scott, one of five peers who heard the case, said Thursday that under the Warsaw Treaty accident compensation was not recoverable “where no more can be said than that …
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Scientists from King’s College, London say they have identified a molecule that could be targeted to treat mental impairment in patients with Down syndrome. Researchers said the increased levels of the molecule myo-inositol in people with Down could be due to the presence of an extra copy of chromosome 21, which causes the syndrome.
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Since the late 1970s inflation has been on a downward trend, driven first by specific anti-inflationary monetary policies, then by the freeing up of labour markets and reduction in trade union collective bargaining power, and most recently by globalisation and the IT-enabled productivity revolution.
The world has moved from double-digit price increases in the 1970s, to a brush with deflation in 2003. Economic policymaking has evolved as the background has changed: from controlling money supply to inflation targeting, to a more pragmatic approach which recently took US rates to 1 …
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SAN DIEGO — When it comes to helping adolescents with Down syndrome and other cognitive disabilities transition to adult services, the earlier the better, William I. Cohen, M.D., advised at the annual meeting of the Society for Developmental and Behavioral Pediatrics.
Such an approach "makes perfect sense at one level, and at another level it’s very hard to do, because some families don’t start looking ahead early enough," said Dr. Cohen, director of the Down Syndrome Center of Western Pennsylvania, Pittsburgh.
"When you receive a diagnosis of a disorder that …
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Klinefelter syndrome is caused by an additional X chromosome in males (47,XXY). Clinical findings are nonspecific during childhood; thus, the diagnosis commonly is made during adolescence or adulthood in males who have small testes with hyper gonadotropic hypogonadism and gynecomastia. Virtually all men with Klinefelter syndrome are infertile.
Epidemiology
Approximately one in 1,000 boys is born with an additional X chromosome–47,XXY, the karyotype that causes Klinefelter syndrome. (1) This karyotype is detected at or before birth in 10 percent of affected boys, and it is found during adulthood in 25 percent of affected men. (2) Mmost all men with a 47,XXY karyotype will be infertile; Klinefelter syndrome accounts for 3 percent of male infertility. (30 Klinefelter syndrome is common in infertile men with oligospermia or azoospermia (5 to 10 percent). (2)
Clinical Presentation
The most overt phenotypic features of Klinefelter syndrome are caused by testosterone deficiency and, directly or indirectly, by unsuppressed follicle-stimulating and luteinizing hormones. Affected men typically have (in decreasing order of frequency): infertility, small testes, decreased facial hair, gynecomastia, decreased pubic hair, and a small penis (Table 1). (2) Because of their long legs, men with Klinefelter syndrome often are taller than predicted based on parental height. Body habitus may be feminized (Figure 1). In childhood, when there is a relative quiescence in the hormonal milieu, ascertainment of the syndrome may be difficult because the effects of hypogonadism (i.e., small external genitalia and firm testes) may be subtle or not present at all.
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Persistent androgen deficiency in adulthood may result in loss of libido, decreased muscle bulk and tone, decreased bone mineral density, a propensity for thromboembolism, and an increased risk of mortality from diabetic and cardiovascular complications. (4)
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Specific cognitive deficits in language comprehension and executive functioning are part of the Klinefelter syndrome phenotype. (5) Although most studies describe only mild cognitive impairment (e.g., mild global delay in gross and fine motor development, speech, and language), Klinefelter syndrome has been identified in 0.4 percent of boys with special education needs and no known diagnosis, and in 1.2 percent of boys with mental retardation of unknown etiology. In these cases, the boys initially were referred for consideration of fragile X syndrome. (6,7) Of note, the 0.4 percent of boys with Klinefelter syndrome in the special-education cohort is likely to represent less than half the actual prevalence, because only paternally acquired disease was identified.
Magnetic resonance imaging has identified a specific brain morphology associated with Klinefelter syndrome. (8) An increased risk of psychiatric disorders also has been reported in affected men. (9)
Diagnosis
Because most boys with Klinefelter syndrome appear similar to boys with normal karyotypes, the disorder typically is identified in adulthood, when infertility or gynecomastia are common presentations. However, by this time, a therapeutic window during adolescence for treatment of hypogonadism, cognitive impairments, and psychosocial factors has been missed. Late or incomplete puberty should prompt further examination. Testicular size can be measured with a Prader orchidometer or ultrasonography. Middle school-age boys with Klinefelter syndrome often will have elevated follicle-stimulating and luteinizing hormone levels and low plasma testosterone levels. Subclinical values on laboratory indices may be found in these patients; therefore, a karyotype with instructions to count sex chromosomes in 50 cells is useful for diagnosis, especially in patients with mosaicism.
Causes of Klinefelter Syndrome
The additional sex chromosomes in men with Klinefelter syndrome results from nondisjunction during meiosis and may have a paternal (50 to 60 percent) or maternal (40 to 50 percent) origin. This contrasts with Down syndrome, which is caused predominantly by maternal nondisjunction and inheritance of the extra chromosome 21 from the mother.
Although Klinefelter syndrome encompasses the specific clinical consequences observed in men with an XXY karyotype, there are variant karyotypes that can include additional X chromosomes (e.g., XXXY, XXXXY) or additional X and Y chromosomes (e.g., XXYY). Men with these karyotypes have similar but often more severe phenotypes compared with those with the XXY karyotype.
Physical manifestations of Klinefelter syndrome are relatively moderate compared with autosomal trisomies (e.g., Down syndrome) because when additional X chromosomes are present, one is predominantly inactivated. However, the entire X chromosome is not inactivated. As the number of X chromosomes increases, the phenotypic severity increases as well. As a result, cognitive and gonadal development is impaired, and cardiovascular and skeletal manifestations often are present.
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