Magnetic Resonance Imaging of Central Nervous System Vasculitis A Case Report of Henoch-Schönlein Purpura

ABSTRACT. A case of Henoch-Schlönlein purpura (HSP) with central nervous system vasculitis diagnosed by MRI is discussed.     

RUPTURED BRONCHUS FOLLOWING ENDOBRONCHIAL INTUBATION

A case of a ruptured bronchus, following endobronchial intubationwith a double-lumen tube, is reported. Possible contributingfactors and causes of this bronchial rupture are discussed andcareful monitoring of cuff pressures is advocated.     

Spurious Discharges Due to Late Insulation Break in Endocardial Sensing Leads for Cardioverter Defibrillators

Despite their similarity to permanent pacemaker leads, endocardial sensing leads for Cardioverter defibrillators have a relatively high failure rate. We describe four patients with endocardial rate sensing leads who developed inappropriate discharges 10–30 months after implantation due to small breaks in the lead insulation. This problem may become increasingly common as the number of Cardioverter defibrillator implants with transvenous leads continues to grow and should be considered in the differential diagnosis of late sensing failure or inappropriate device discharges.     

CHANGES IN THE DISTRIBUTION OF HISTOCHEMICALLY LOCALIZED MERCURY IN THE CNS AND IN TISSUE LEVELS OF ORGANIC AND INORGANIC MERCURY DURING THE DEVELOPMENT OF INTOXICATION IN METHYLMERCURY TREATED RATS

The development of neurotoxicity in rats after exposure to methylmercuric chloride was monitored using behavioural indices. At selected time points the cellular localization of mercury and the relative amounts of organic and inorganic mercury were determined in several regions of the CNS, and in some non-neural tissues. The CNS showed an affinity for organic mercury, the levels of inorganic mercury remaining low throughout symptomatic intoxication. Histopathological changes were not closely related to the regional tissue content of the organic or inorganic forms, nor to mercury localized histochemically at the cellular level. The stained deposits, which had focal cytoplasmic distribution, appeared in glial cells initially then in larger neurones as the intoxication progressed. These observations may represent changes in the mercury content of different cell types or reflect differences in the way that they handle a similar burden of mercury. A transitory accumulation of mercury in glial cells may be a factor contributing to the occurrence of a latent period and sequestration of mercury in cytoplasmic organelles may serve to protect some cell types from injury.     

THE CORRELATION OF ELECTRORETINOGRAPHIC AND HISTOPATHOLOGICAL FINDINGS IN THE EYES OF MICE INFECTED WITH THE 79A STRAIN OF SCRAPIE

Retinal degeneration was produced using the 79A strain of scrapie injected intracerebrally into mice of the MM inbred strain, and studied by electroretinography and light and electron microscopy during the preclinical and clinical phases of the disease. The changes in the electroretinogram (ERG), detectable in some mice at 118 days postinjection (d.p.i.), appeared to coincide with the earliest morphological evidence of photoreceptor damage. In the early stages there was a progressive reduction of b-wave amplitude without marked loss of retinal sensitivity or significant change in a- and b-wave peak implicit times. Extinction of the ERG, observed in half the mice examined at 144 d.p.i., approximated to a stage of the retinopathy in which the outer nuclear layer was reduced to about four rows of nuclei. Early morphological changes suggested that the primary lesion involved the integrity of the photoreceptor as a whole, the electrophysiological findings reflecting a primary loss of light sensitive tissue rather than impairment of the transduction mechanism or neurotransmission.     

Description of a dinucleotide repeat polymorphism in the human elastin gene and its use to confirm assignment of the gene to chromosome 7

Informative polymorphisms have been very difficult to detect in the elastin gene, and this has hampered the analysis of heritable connective tissue disorders, notably the Marfan syndrome. We have recently detected a dinucleotide repeat polymorphism in intron 17 of the human elastin gene consisting of 8 alleles with sizes between 161 and 175 bp. Analysis of 540 chromosomes from unrelated Caucasian individuals revealed a bimodal frequency distribution typical of (dC-dA)_n (dG-dT)_n repeat polymorphisms, with allele frequencies ranging from 0.004 (161 bp) to 0.574 (163 bp). As the elastin gene was originally assigned to chromosome 2q31-ter and because more recent data have suggested an assignment to 7q11.1–21.1, we have genotyped a sub-set of the CEPH pedigrees and carried out pairwise linkage analysis with markers on chromosomes 7 and 2. Lod-scores of between +3.70 and +13.69 were obtained with markers spanning 7p13-q22.1, whilst negative lod-scores were observed with the chromosome 2 markers. Analysis of type II human ovarian teratomas placed the elastin gene within 11 cM of the centromere on chromosome 7. Additionally, we detected the dinucleotide repeat in human-rodent cell hybrids containing chromosome 7, but not those containing chromosome 2. These data confirm the assignment of elastin to chromosome 7 and provide a new, highly informative marker for the analysis of heritable disorders of connective tissue for which elastin is a candidate gene.