We examined mechanisms of recovery from aphasia in seven nonfluent aphasic patients, who were successfully treated with melodic intonation therapy (MIT) after a lengthy absence of spontaneous recovery. We measured changes in relative cerebral blood flow (CBF) with positron emission tomography (PET) during hearing and repetition of simple words, and during repetition of MIT-loaded words. Without MIT, language tasks abnormally activated right hemisphere regions, homotopic to those activated in the normal subject, and deactivated left hemisphere language zones. In contrast, repeating words with MIT reactivated Broca's area and the left prefrontal cortex, while deactivating the counterpart of Wernicke's area in the right hemisphere. The recovery process induced by MIT in these patients probably coincides with this reactivation of left prefrontal structures. In contrast, the right hemisphere regions abnormally activated during simple language tasks seem to be associated with the initial persistence of the aphasia. This study supports the idea that abnormal activation patterns in the lesioned brain are not necessarily related to the recovery process.

No abstract

No abstract

Aorto-bifemoral bypass using a total laparoscopic approach can be performed safely. As all new techniques, a learning curve is observed. This new technique should be evaluated in a larger randomised trial to assess its clinical value in comparison to conventional surgery.

Since CBF patterns in children are related to maturational changes in brain function, these results indicate a delayed frontal maturation in childhood autism. Such a delayed brain maturational process is consistent with the clinical data and cognitive performance of autistic children.

Gammopathies were found to be present in 25 0.3%) of 192 HIV-negative renal transplant recipients ~Ith more than 30 months follow-up prospectively inves-?gated for monoclonal or oligoclonal immunoglobulins Emlg) by agarose gel electrophoresis and immunofixation. 1 leven patients had only one monoclonal band, whereas 4 had two or more bands. Of these bands, 60% were IgG kappa, 29% IgG lambda and 11 % IgM lambda or kappa, and 90% did not exceed 2 g/1. Most gammopathies occurred early post-transplant (median 5 months) and they Were always transient. Some predisposing factors for mig ~mergence could be identified: 1. age, but only in women, :duration of dialysis, 3. occurrence of prior cytomegalo-Vtru~ infection, and 4. immunosuppressive regimen in-l~dmg cyclosporine. Serological evidence for active EBV } 0 e~tion was obtained in ten patients, but in six cases in-ec~ton occurred subsequent to the finding of mig. In eight

SummaryIn 10 patients with nephrotic syndrome (NS), the coagulation inhibitors, the fibrinolytic system and several functions of the fibrinogen-fibrin molecule were studied.Among the coagulation inhibitors, only antithrombin III (AT III) was found decreased and correlated with serum-albumin levels. Venous occlusion test provoked a normal tissue plasminogen activator (tPA) release in all patients. The plasminogen activator inhibitor (PAI) had an increased activity in 5 out of the 10 patients.Thrombin and reptilase times were found abnormal in most patients. The thrombin time (TT) prolongation correlated with serum albumin levels and was corrected by adding purified albumin.The fibrinogen was purified from each of the 10 patients’ plasma. Only 2 of them showed abnormal polymerization in purified system, suggesting dysfibrinogenaemia. Other functions (thrombin binding, tPA stimulating activity, lysis by purified plasmin) were found normal except in one of the 2 patients with dysfibrinogenaemia whose fibrinogen lysis by plasmin was delayed.It is concluded that an abnormal fibrinogen molecule is not the most frequent explanation for thrombin time prolongation in NS.

SUMMARYThe aim of the present study was to investigate the prevalence of C4 and C2 deficiencies and to characterize genomic alterations in C4 genes in a large cohort of 125 unselected patients with SLE. We determined the protein concentration and functional activity of C2 and C4, as well as the C4 phenotype. C4 genotyping included Taq 1 restricted fragment lengh polymorphism (RFLP) analysis and polymerase chain reaction using sequence-specific primers (SSP-PCR). Type I C2 deficiency was diagnosed by PCR. Overall, 79´2% of the patients exhibited abnormalities of the C4 genes including deletion, nonexpression, gene conversion and duplication. Among C4-deficient patients (n 66, 52´8% prevalence), 41´0% of the patients exhibited a C4A deficiency and 59´0% a C4B deficiency. Half of the C4 deficiencies were due to a gene deletion. There was a strong association between C4A and C4B gene deletion and the presence of the DRB1*03 allele. Among the silent C4A genes, only two cases were related to a 2-bp insertion in exon 29 of the C4A gene. A gene conversion was demonstrated in eight patients (6´4%). One patient had a homozygous C4A deficiency. Three (2´4%) patients presented with a heterozygous type I C2 deficiency and none with homozygous deficiency. Our results argue against a specific role for C4A gene deficiency in determining disease susceptibility among patients with SLE that are C4-deficient.