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The distribution of virus-infected cells in the organs of Rock Bream naturally infected with megalocytivirus is reported. Examination of sections of liver, spleen and kidney stained by haematoxylin and eosin (HE) and periodic acid Schiff (PAS) revealed the presence of swollen and degenerate cells having morphology consistent with leucocytes. Many of these cells were shown to contain viral DNA by in-situ hybridization (ISH). Cells containing viral DNA were also found in the connective tissue of other organs in which there was no prominent infiltrate of degenerate leucocytes. Viral DNA was also found in the cytoplasm of leucocytes in blood smears. Transmission electron microscopy (TEM) confirmed the presence of viral particles in the cells within tissue and free within blood. The tissue distribution of virus in this infection is suggested to reflect the infiltration of virus-infected leucocytes.

The magnesium isotope effects were investigated by chemical ion exchange with a hydrous manganese(IV) oxide. The capacity of manganese(IV) oxide was 0.5 meq g(-1). The distribution coefficient of magnesium ions on the MnO(2) was determined by a batch method. The heavier isotopes of magnesium were enriched in the solution phase, while the lighter isotopes were enriched in the hydrous MnO(2) phase. The separation factor was determined according to the method of Glueckauf from the elution curve and isotopic assays. The separation factors of (24)Mg(2+)-(25)Mg(2+), (24)Mg(2+)-(26)Mg(2+), and (25)Mg(2+)-(26)Mg(2+) isotope pair fractionations were 1.011, 1.021, and 1.011, respectively.

The strong transactivation activity of the C-terminal half (amino acids 76-152) of Nm23 was reported previously. Here we examined a structural domain preventing or necessary to its transactivation activity. The C-terminal 1/4 (amino acids 109-152) was sufficient for transactivation, but the C-terminal half with a longer N-terminal extension (amino acids 58-152) caused the loss of the transactivation ability. Furthermore, coexpression of the N-terminal half with the C-terminus of Nm23-H1 blocked the transactivation activity of the C-terminal half, where direct interaction of both truncated proteins was demonstrated in vitro. Transactivation activities in the C-terminal halves of the known mutants (P96S, H118F, S120G, and S120A) exhibiting differential antimetastasis effects were also tested. Significant reduction of transactivation activity was observed only in H118F, indicating that NPD kinase active-site histidine is required. This suggests that transactivation potential of Nm23 is related to NDP kinase activity but not to metastasis suppressor activity., ((c) 2001 Elsevier Science.)

The KpnAI restriction-modification (R-M) system has been identified in Klebsiella pneumoniae strain M5a1. The restriction gene of KpnAI was first cloned into pBR322 using an r-m+ M5a1 derivative and phage SBS for screening. Subsequently, an adjacent DNA fragment showing modification activity was cloned into pUC19. A total of 7.2 kb DNA sequencing data revealed three open reading frames, corresponding to hsdR, hsdM and hsdS genes of type I R-M systems. The predicted hsdR, hsdM and hsdS-coded peptides shared 95%, 98% and 44% identity, respectively, with the corresponding peptides of the recently identified StySBLI system, a prototype of the type ID family. This high homology suggests that KpnAI is also a member of the type ID family. The KpnAI system seems to be the first type I system identified in Klebsiella species.

The prevention, management, and prognosis of patients with transient ischemic attack or stroke caused by extracranial cerebrovascular disease depend on the underlying pathophysiologic mechanisms involved. Atherosclerotic vascular disease is the predominant pathophysiologic mechanism. Management of this entity remains controversial and should be individualized. Recent data have clearly confirmed that carotid endarterectomy is better than medical therapy. Patients with a critically tight carotid stenosis appropriate in location to their symptoms are considered for carotid endarterectomy. This procedure should be performed only in the setting of excellent neuroradiologic support and surgical expertise, however, with a cumulative complication risk of less than 3%. Intimal dissection appears to be associated with a good prognosis with or without treatment. However, patients with symptoms should receive short-term therapy with antiplatelet or anticoagulant agents to prevent distal embolization. Corticosteroids are the drugs of choice for treatment of patients with extracranial arteritis. The presence of fibromuscular dysplasia in the cerebrovascular system has not proved to be a definitive risk for stroke or transient ischemic attack.

It has been well established that elevated dietary tryptophan (TRP) levels can increase brain serotonin concentrations, thereby influencing serotonergic transmission. We previously examined interaction between dietary substrate (TRP: 0.15 and 0.6%) and the cofactor precursor (pyridoxine HCl: 3 and 3,000 mg/kg) on brain serotonin metabolism, observing significant increases in serotonin concentrations from such dietary interaction. The present experiments were designed to explore possible behavioral consequences of the substrate-cofactor interaction. After the IP injection of fenfluramine (FA: at 5, 10, 15, and 20 mg/kg), serotonin-mediated behavior traits and the appearance of flushing were observed in rats fed experimental diets as stated above. With a 5 mg/kg dose of FA, a differential dietary effect was most visible. However, at higher FA levels (15 and 20 mg/kg), such dietary effects were no longer discernible. The appearance of flushing was also dependent on dietary TRP intake and the dosage of FA. These results indicate a clear substrate-cofactor interaction on certain serotonin-mediated behavior traits in the rat.

We studied the metabolic effects of high dietary intakes of pyridoxine and of the substrate-cofactor interaction between dietary histidine or tryptophan and pyridoxine in rat brain. In the substrate-cofactor interaction study, histamine and serotonin levels were determined in rats fed elevated or requirement levels of substrate (histidine: 0.3% and 0.8%, tryptophan: 0.15% and 0.6%) and excess or requirement levels of pyridoxine HCl (7 mg vs. 3,000 mg/kg). Excess pyridoxine intake caused a differential effect on brain histamine concentration--inhibitory with the requirement level of histidine (-29%), and stimulatory (+21%) with the elevated level of histidine. When dietary tryptophan was fed at the requirement level, excess pyridoxine caused essentially no changes in hypothalamic serotonin and 5HIAA (-2%, -2%). With elevated tryptophan intake, excess pyridoxine significantly increased serotonin and 5HIAA (+32%, +20%) in the hypothalamus. These results indicate a clear interaction between substrate and coenzyme precursor which influences brain metabolism of histamine and serotonin.