Cognitive processing in migraine: a failure to find facilitation in patients with aura

Recent interest in cognitive processing in migraine has been based on the assumption that cortical hyperexcitability in migraine with aura may manifest itself in the form of response time advantages in migraine as compared to controls. The study reported here attempted to replicate and extend the findings of Wray and colleagues (Brain 1995;118:25–35). Using identical cognitive tasks, three experiments failed to find differences between migraine with aura patients and controls: furthermore, an additional group of patients without aura were also statistically indistinguishable from controls with respect to response times. Error rates were consistently high across experiments, indicating that subjects were responding at or near chance levels. These findings cast doubt on the utility of straightforward cognitive psychological methods for the study of cortical hyperexcitability in migraine. Some theoretical difficulties concerning the interpretation of response times in the context of migraine pathophysiology are discussed.     

雌激素治疗与冠状动脉钙化

背景：冠状动脉中的钙化斑块是动脉粥样硬化程度的一个标记物，并能预测未来发生心血管疾病的风险。在一项随机临床试验中，我们研究了雌激素治疗与冠状动脉钙化的关系。     

Progressive hearing loss and vestibular dysfunction caused by a homozygous nonsense mutation in CLIC5

In a consanguineous Turkish family diagnosed with autosomal recessive nonsyndromic hearing impairment (arNSHI), a homozygous region of 47.4 Mb was shared by the two affected siblings on chromosome 6p21.1-q15. This region contains 247 genes including the known deafness gene MYO6. No pathogenic variants were found in MYO6, neither with sequence analysis of the coding region and splice sites nor with mRNA analysis. Subsequent candidate gene evaluation revealed CLIC5 as an excellent candidate gene. The orthologous mouse gene is mutated in the jitterbug mutant that exhibits progressive hearing impairment and vestibular dysfunction. Mutation analysis of CLIC5 revealed a homozygous nonsense mutation c.96T>A (p.(Cys32Ter)) that segregated with the hearing loss. Further analysis of CLIC5 in 213 arNSHI patients from mostly Dutch and Spanish origin did not reveal any additional pathogenic variants. CLIC5 mutations are thus not a common cause of arNSHI in these populations. The hearing loss in the present family had an onset in early childhood and progressed from mild to severe or even profound before the second decade. Impaired hearing is accompanied by vestibular areflexia and in one of the patients with mild renal dysfunction. Although we demonstrate that CLIC5 is expressed in many other human tissues, no additional symptoms were observed in these patients. In conclusion, our results show that CLIC5 is a novel arNSHI gene involved in progressive hearing impairment, vestibular and possibly mild renal dysfunction in a family of Turkish origin.     

Patterns of substance use on a college campus: a 14-year comparison study

In 1972, a drug incidence survey was conducted at a private southern university. Pooled results of this random survey of 1,032 students revealed that on at least one occasion, 90% of the students had tried alcohol, 70% had used tobacco, and 61% had experimented with marijuana. Use of amphetamines (38%), hallucinogens (28%), barbiturates (19%), and cocaine (10%) was much lower. To evaluate the apparent change in trends of drug usage, a follow-up study was undertaken in 1986 at the same school. The results showed a decline in amphetamine and barbiturate use. The greatest differences were seen in the nearly fourfold increase in one-time use of cocaine between 1972 and 1986 and the sixteenfold increase in students who used cocaine more than 10 times. It was noteworthy that one-third of the students who used marijuana had done so by the 9th grade. Similar early experimentation was noted with a majority of the other drugs.     

Transferrin saturation and recovery from coma in cerebral malaria

To determine if the elevated transferrin saturations found in some patients with severe malaria are associated with an adverse outcome in cerebral malaria, we retrospectively measured baseline saturations in stored serum samples from 81 Zambian children with strictly defined cerebral malaria. The children had been treated with quinine, sulfadox- ine-pyrimethamine, and intravenous infusions of either placebo (n = 39) or the iron chelator, desferrioxamine B (n = 42), in a previously reported trial (Gordeuk et al, N Engl J Med 327:1473, 1992). More than one-third of children in both the placebo- and iron chelator-treated groups had transferrin saturations exceeding 43%, which is 3 standard deviations above the expected mean for age. Among children receiving quinine and placebo, those with elevated transferrin saturations had a delayed estimated median time to recover full consciousness (68.2 hours) compared with those with saturations < or = 43% (25.4 hours; P = .006). The addition of iron chelation to quinine therapy in children with high saturations appeared to hasten recovery (P = .046). We conclude that increased transferrin saturations may be associated with delayed recovery from coma during standard therapy for cerebral malaria and that serum iron and total iron binding capacity should be measured in future studies.