We evaluated 50 consecutive patients with acute ischemic stroke to assess the prevalence of systemic infection preceding the neurological event We analyzed the immunohematologic characteristics of patients with and without signs and/or symptoms of a preceding infectious process. Patients were examined <,7 days after cerebral infarction and evaluated for fibrinogen, anticardiolipin antibodies, fibrin D-dimer (a fragment of cross-linked fibrin), plasminogen activator inhibitor-1, and protein S. Of the 50 patients, 17 had symptoms of infection beginning <,l month before the stroke (11 had upper respiratory tract infections, three urinary tract infections, two subacute bacterial endocarditis, and one pneumonia). Compared with patients without infection, patients with infection had significant increases in fibrin D-dimer concentration (53±1.1 versus 4.7±0.9 log-transformed ng/ml,/?<0.05) and cardiolipin immunoreactivity, IgG isotype (1.8±1J versus l.l ±0.9 log-transformed phospholipid units,p<0.04), and, when studied r s 2 days after the stroke, increased fibrinogen levels (459±126 versus 360±94 mg/dl, p<0.Q5). In conclusion, infection-associated cerebral infarction is common and is associated with substantial immunohematologic abnormalities. (Stroke 1991^22:1004-1009)
These findings indicate astrocyte regulation of thrombomodulin mRNA expression in vitro and suggest an important role for the blood-brain barrier in the regulation of thrombomodulin.
Recombinant human interferon beta (rIFN-beta) inhibited in a time- and dose-dependent manner the proliferation of 18/18 human colon carcinoma cell lines in monolayer culture and 8/9 lines in a soft agar assay but had no effect on 4 human fibroblast cell lines. Maximal inhibition of cell proliferation by rIFN-beta required repetitive treatment (every 2 days) with lymphokine (50 units/ml). Furthermore, the inhibitory activity of rIFN-beta was neutralized by polyclonal antibodies against natural IFN-beta. In contrast to rIFN-beta, rIFN-alpha was inactive against all colon cell lines tested, and rIFN-gamma, with the exception of HT-29 cells, was similarly ineffective. These data demonstrate that rIFN-beta is a potent growth inhibitor of colon carcinoma cells in vitro, and suggest that studies on its mechanism of action may lead to a better understanding of the regulation of colon tumor cell proliferation.
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