Characterization of Malignant Portal Vein Thrombosis with Contrast-Enhanced Ultrasonography

We prospectively evaluated the effectiveness of contrast-enhanced ultrasonography (CEUS) for differentiation of benign versus malignant portal vein thrombosis (PVT). We studied a total of 43 patients with chronic liver disease, hepatocellular carcinoma-suggestive nodules and confirmed PVT, in whom the nature of the PVT was confirmed by follow-up imaging (US, computed tomography and/or magnetic resonance imaging) performed up to 6 mo after CEUS. PVT was assessed by US, Doppler US and CEUS with respect to vessel wall disruption and/or invasion, color Doppler vascularization, pulsed Doppler vascularization pattern and CEUS enhancement and vascularization pattern, and thrombi were classified as benign or malignant based on these findings. Follow-up studies revealed malignant PVT in 22 of the 43 patients (51%) and benign PVT in 21 patients (49%). CEUS findings were consistent with follow-up studies in 41 of the 43 patients (95%), with κ?=?0.903 (p < 0.0001), sensitivity?=?91% and specificity?=?100%, indicating that CEUS can be confidently used to differentiate benign from malignant portal vein thrombosis in the setting of chronic liver disease.     

Mitochondrial encephalomyopathies: biochemical approach.

Thanks to recent advances in the molecular genetics of mitochondrial encephalomyopathies, we can now begin to correlate genetic lesions with biochemical defects. In the fatal infantile myopathy due to cytochrome c oxidase (COX) deficiency, an autosomal recessive condition, immunocytochemical studies have shown an isolated defect of subunit VIIa, which is 1 of the only 2 tissue-specific subunits of human COX. In muscle biopsies from patients with Kearns-Sayre syndrome, a multisystem disorder characterized by deletions of the mitochondrial DNA (mtDNA), the activities of all mitochondrial enzymes containing mtDNA-encoded subunits are decreased. The results of Northern analysis, in situ hybridization, and immunocytochemistry in muscle, and of mitochondrial protein synthesis in cultured fibroblasts suggest that partially deleted mtDNAs are transcribed but not translated, probably due to lack of indispensable tRNAs.     

Manifestations of insulin-dependent diabetes mellitus in the periodontium of young Brazilian patients

The periodontal condition of patients with insulin-dependent diabetes mellitus was evaluated in terms of plaque, gingival indices, pocket depth, and alveolar bone loss. Thirty male and female diabetic patients aged 5 to 18 years were compared with 30 non-diabetic subjects and correlated with sex and age. Statistical analyses of the data showed that the mean plaque index was significantly higher (P less than 0.01) among the diabetic patients (1.23) than among the control subjects (0.81). The plaque index was significantly higher (P less than 0.01) among diabetic females (1.34) than among diabetic males (1.10), whereas no sex differences were observed in the control group. The arithmetic means obtained for gingival index were statistically higher (P less than 0.01) for the diabetics (0.58) when compared with the controls (0.15), but no significant differences were obtained when the values were correlated with sex and age. Pocket depth did not differ statistically between groups. When pocket depth was correlated with sex, a statistically significant difference (P less than 0.05) was observed only for the palatal region, with a depth of 2.1 mm in female patients and 1.92 mm in male patients. When pocket depth was correlated with age, a positive correlation (P less than 0.01) was detected in the diabetic group for all regions investigated, whereas the correlation was not significant in the control group. Mean alveolar bone loss was higher in the anterior upper (1.94 mm) and anterior lower (1.87 mm) regions of the diabetic group when compared to the controls (1.52 and 1.37 mm respectively), the difference being significant at the 5% level of probability.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of unilateral cortex lesions on gene expression of rat cortical cholecystokinin neurons.

In rat neocortex, the gene encoding preprocholecystokinin is expressed in interneurons which also synthetize gamma-aminobutyric acid. An injury to the meninges and the underlying cortex increased the concentration of mRNA coding for preprocholecystokinin in all ipsilateral cortical areas. Simultaneous treatment of the rats with the anti-inflammatory agent diclofenac did not affect the injury-induced change in gene expression indicating that inflammatory processes were not involved. The injury also enhanced the expression of the immediate early gene c-fos in the ipsilateral cortex in a time-dependent manner. There was an increase in c-fos mRNA 1 h after the operation, which was no longer observed 3 h later. Twenty-four hours after the operation, cells containing c-fos mRNA were found in cortical layers II, III, V and VI. The neurons which showed an increased expression of preprocholecystokinin were also in these layers. The N-methyl-D-aspartate (NMDA) receptor antagonist MK-801 prevented the injury-induced increases in both preprocholecystokinin and c-fos gene expression, indicating that stimulation of this glutamate receptor subtype may initiate the changes in expression of both genes. It is hypothetized that the immediate early gene c-fos is activated first and this then leads to the increase in preprocholecystokinin mRNA.     

Mitochondrial myopathy of childhood associated with depletion of mitochondrial DNA.

We have studied five children with mitochondrial myopathy manifesting within or soon after the first year of life. Muscle biopsies showed ragged-red fibers and decreased respiratory chain activity. All five patients had a severe decrease (2 to 34% of normal) in the amount of muscle mitochondrial DNA (mtDNA). The depletion of mtDNA correlated with absence of mtDNA-encoded translation products and with loss of cytochrome c oxidase enzyme activity in individual muscle fibers. This mitochondrial myopathy of childhood illustrates one phenotypic expression of a novel pathogenetic mechanism in mitochondrial diseases, the specific depletion of mtDNA in affected tissues.     

Volar plate osteosynthesis in typical and atypical distal radius fractures]

28 patients with a fracture of the distal end of the radius were treated by a T-plate osteosynthesis through the volar approach. There were 7 unstable distal metaphyseal fractures and 21 dislocated intra-articular fractures. 21 patients were investigated 6 months to 8 years after operation according to the scheme of Sarmiento. 17 patients had a good or excellent result, 4 patients a fair or poor result. 2 patients developed a Sudeck's dystrophy (Algodystrophy), one of them with a radial-ulnar bone bridge. The volar application of the plate is indicated for flexion and extension fractures. In cases with compression of the dorsal cortex a bone graft is indicated to improve a stable osteosynthesis. A conventional tomography on two views helps to diagnose exactly an intra-articular fracture and to decide whether to use a plate or pins and external fixation after open reduction. Remanipulation or an operation 2 weeks after trauma increases the risk of a Sudeck's dystrophy and leads to a poor result.     

Arthrogryposis as a possible mechanism of scrotoschisis acquired in utero

A congenital defect of the scrotal wall with consequent testicular exstrophy is an exceptional finding. The etiopathogenesis of this defect is debated. We report a newborn male with arthrogryposis who presented with an exstrophied testicle. The association of these two conditions seems to establish a cause-effect relationship mediated by mechanical factors, i.e., in utero compression of the scrotum by the feet. It is likely that a similar mechanism could also be advocated to explain the previous cases reported in the literature.