Background and Purpose-The purpose of the present study was to assess the incidence and clinical significance of the intraparenchymal hyperdense areas on the posttherapeutic CT scan just after intra-arterial reperfusion therapy. Methods-Seventy-seven patients with acute middle cerebral artery occlusion were studied prospectively with posttherapeutic CT. Hyperdense areas were classified into three groups: those in the lentiform nucleus, insular cortex and cerebral cortex. We investigated the incidence of hyperdense areas and hemorrhagic transformations and assessed whether location of hyperdense areas may play a role in the incidence of hemorrhagic transformations. We also evaluated correlation between early CT signs and hyperdense areas. Results-Forty-five hyperdense areas were seen in 37 of the 77 patients (48.1%): 19 of the 45 (42.2%) were confirmed to be hematomas themselves, 6 (13.4%) showed later conversion to petechial hemorrhages, and 20 (44.4%) showed rapid disappearance without hemorrhagic transformations. Eleven of the 37 patients (29.7%) had neurological worsening due to massive hematoma (symptomatic hemorrhage), whereas none of the 40 patients without hyperdense areas had symptomatic hemorrhage. The incidence of hemorrhage among hyperdense areas was significantly lower in the insular cortex than in the other 2 regions (PϽ0.01). On the other hand, hyperdense areas in the lentiform nucleus had a significantly higher incidence of neurological worsening (PϽ0.05). There was a significant correlation between early CT signs and hyperdense areas (PϽ0.0001). Conclusions-The presence of hyperdense areas was a significant risk factor for severe hemorrhagic transformations, although only 29.7% of patients with hyperdense areas had symptomatic hemorrhage. On the contrary, the absence of hyperdense areas was a reliable negative predictor for symptomatic hemorrhage.

Background and aims: Imbalance between pro-and anti-inflammatory cytokines produced by intestinal T cells induces inflammatory bowel diseases (IBD). However, the importance of regulation of cytokine signalling in IBD has not been fully clarified. We have demonstrated that suppressor of cytokine signalling 1 (SOCS1) is expressed in inflamed tissues in an experimental colitis model. In the present study, we investigated the role of SOCS1 in colitis models to clarify the mechanism of IBD development. Methods: Intestinal T cells in transgenic mice expressing high levels of SOCS1 in lymphocytes (SOCS1Tg mice) were characterised by flow cytometric analysis and cytokine production from intestinal T cells was determined by ELISA. 2,4,6-Trinitrobenzene sulphonic acid (TNBS) induced colitis was induced in SOCS1Tg mice and severity was compared with control littermates by measurement of survival rates. Intracellular signalling was assessed by western blotting analysis. Results: SOCS1Tg mice developed colitis spontaneously with age. Young SOCS1Tg mice less than 15 weeks of age, before the onset of colitis, were susceptible to TNBS induced colitis. Intestinal T cells of SOCS1Tg mice showed increased interferon c and tumour necrosis factor a production and decreased transforming growth factor b production. Expression of cytotoxic T lymphocyte associated antigen 4 (CTLA-4), a negative regulator of T cell activation, in SOCS1Tg mice was severely impaired at the protein level although mRNA levels of CTLA-4 in SOCS1Tg mice were comparable with those in control mice. Conclusions: Our data suggest that SOCS1 plays an important role in the regulation of colitis by controlling intestinal T cell activation mediated through CTLA-4 expression.

Using a microdialysis technique, the rat striatum was perfused with NSD-1015, an inhibitor of aromatic L-amino acid decarboxylase, and the amount of L-3,4-dihydroxyphenylalanine (L-DOPA) and 5-hydroxytryptophan (5-HTP) accumulating in dialysate was measured as an index of in vivo activities of tyrosine hydroxylase and tryptophan hydroxylase. NSD-1015 increased the concentration of L-DOPA much higher than that of 5-HTP in a dose-related manner (1-100 mumol/L). In order to examine the relationship between dopaminergic and serotonergic neurons in the striatum, either 5-HTP or L-DOPA was injected intraperitoneally to rats pretreated with benserazide, an inhibitor of peripheral decarboxylase. 5-HTP administration increased 5-HTP, but decreased L-DOPA in a dose-dependent manner. Conversely, 5-HTP concentration decreased in an association with the increased content of L-DOPA following L-DOPA administration. The decrease of 5-HTP caused by L-DOPA administration was not as remarkable as that of L-DOPA by 5-HTP injection. These results suggest that L-DOPA and 5-HTP, the precursor amino acids for catecholamines and indoleamines, could affect mutually each other neuronal activity through the inhibition of their rate-limiting enzymes.

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Surgery with curative intent should be considered for patients with Stage IV CRC defined by the P1 factor or H factor.