Decreased corpus callosum size in sickle cell disease: relationship with cerebral infarcts and cognitive functioning.

We assessed midsagittal corpus callosum size in sickle cell disease (SCD) and its relationship to lesion volume, lesion location, and cognitive functioning. Twenty-eight children with SCD and 16 demographic controls completed magnetic resonance imaging (MRI) and neuropsychological testing. Corpus callosum (CC) size was smaller for children with silent infarcts (n = 8) or overt stroke (n = 8) than for those without visible infarcts (n = 12) or control participants. Lesion volume was a robust predictor of IQ and other cognitive scores; total CC size did not typically add explanatory power for these measures. The size of the rostral body of the CC, however, independently predicted measures of distractibility, speeded production, and working memory. Posterior CC size was also decreased among many of the children with SCD, even in the absence of visible infarcts in this region. Brain morphology appears to provide additional information about SCD-related effects on the brain above and beyond visible infarcts.     

Increased corneal temperature caused by MR imaging of the eye with a dedicated local coil.

To determine the existence of tissue heating-associated risks to the eye with magnetic resonance (MR) imaging performed at high specific absorption rates (SARs), corneal temperature was measured in 14 patients immediately before and after MR imaging performed with a 1.5-T, 64-MHz unit and a quadrature-driven body coil for radio-frequency transmission and a receive-only local coil designed for eye imaging. Fast spin-echo pulse sequences were used predominantly. Estimated peak SARs ranged from 3.3 to 8.4 W/kg. A statistically significant (P < .001) increase in average corneal temperature (32.2 degrees C +/- 0.7 before imaging, 33.1 degrees C +/- 0.6 after) was associated with MR imaging of the eye. The changes in corneal temperature ranged from 0.2 degrees to 1.8 degrees C (average, 0.9 degrees C). The highest corneal temperature measured after MR imaging was 35.1 degrees C. MR imaging performed with a dedicated local coil at the SARs studied produced elevations in corneal temperature that were physiologically inconsequential and below the temperature threshold (41 degrees to 55 degrees C) for radio-frequency radiation-induced cataractogenesis.     

A clinical and radiologic study of autotransplanted impacted canines

The aim of the present study was to evaluate the clinical and radiologic results of 20 autotransplantations of impacted canines performed in the Orthodontic and Pedodontic Department of the University of Geneva between 1979 and 1988. The sample, divided into two different age groups (group A: 13–20 years; group B: 20–48 years), demonstrated persistence of pulp vitality in 80% of the cases in group A, whereas routine endodontic treatment was instituted in all cases of group B. Periodontal healing was noted in 90% of the cases in group A, and in 70% of the cases in group B. The present clinical and radiologic data indicate that impacted canines can be transplanted at any age with good prognosis and are an alternative to orthodontic repositioning in selected cases of canine impaction.     

Non-redundancy of cytidine deaminases in class switch recombination

Class switch recombination (CSR), somatic hypermutation, and gene conversion are immunoglobulin diversification mechanisms that are strictly dependent on the activity of the activation-induced cytidine deaminase (AID). The precise role and substrate(s) of AID in these processes remain to be well defined. The closest homologue of AID is APOBEC-1, a bona fide mRNA-editing enzyme, which shares with AID the ability to deaminate cytidines within single-stranded DNA in vitro and in prokaryotic cells. To determine whether APOBEC-1 can therefore substitute for AID in activated B cells, we expressed human AID, a catalytic mutant thereof, and rat APOBEC-1 in AID-deficient murine B cells. Whereas AID rescued CSR, neither the inactive mutant nor APOBEC-1 could complement AID deficiency. This indicates that cytidine deaminase activity is necessary but not sufficient to initiate CSR, and suggests that AID is specifically targeted to its cognate substrate, the immunoglobulin genes or a distinct mRNA, by an as-yet-unknown mechanism.