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Dardanus brachyopsForest 1962, is redescribed in detail on the basis of specimens recently collected from Japan and a paratype specimen from Madagascar, with a color photograph of a living individual. Supplemental information on female morphology is provided. Fleshy membranous protuberances on the abdomens of DardanusPaul'son 1875 species are discussed. Zoogeographical aspects of Japanese species of Dardanusare also considered.

Background: The clinicopathologic features of colorectal liver metastases that invade the bile duct were evaluated. Methods: From 1992 to 1996, 149 patients who underwent a first hepatic resection were studied for a total of 377 colorectal liver metastases. Twenty-one second hepatic resections in these patients were also analyzed. Results: Bile duct invasion was histologically observed in 62 (42%) of 149 patients with first colorectal liver metastasis. Eighteen patients (12%) had gross extension of the tumor in the bile duct ranging from 4 mm to 42 mm (median 17.0 mm). Histologically, two thirds (12 of 18) of the tumors with macroscopic bile duct invasion were well-differentiated adenocarcinomas with a tendency for less vascular involvement. The actuarial 3- and 5-year survivals were 62% and 57% for patients with no bile duct invasion, 56% and 48% for patients with microscopic bile duct invasion, and 94% and 80% for patients with macroscopic bile duct invasion. The 5-year survival rate was better for patients with macroscopic bile duct invasion than for those with only microscopic (P = .02) or no bile duct invasion (P = .03). In a multivariate analysis, macroscopic bile duct invasion was an independent prognostic variable for favorable outcome after hepatic resection. Conclusions: Macroscopic bile duct invasion of colorectal liver metastases may reflect an indolent biologic behavior, warrants an aggressive surgical approach, and confers a better prognosis. (Surgery 1999;126:829-34.)

In previous studies we determined the nucleotide sequence of the gene cluster containing lys20, hacA (lys4A), hacB (lys4B), orfE, orfF, rimK, argC, and argB of Thermus thermophilus, an extremely thermophilic bacterium. In this study, we characterized the role of each gene in the cluster by gene disruption and examined auxotrophy in the disruptants. All disruptants except for the orfE disruption showed a lysine auxotrophic phenotype. This was surprising because this cluster consists of genes coding for unrelated proteins based on their names, which had been tentatively designated by homology analysis. Although the newly found pathway contains alpha-aminoadipic acid as a lysine biosynthetic intermediate, this pathway is not the same as the eukaryotic one. When each of the gene products was phylogenetically analyzed, we found that genes evolutionarily-related to the lysine biosynthetic genes in T. thermophilus were all present in a hyperthermophilic and anaerobic archaeon, Pyrococcus horikoshii, and formed a gene cluster in a manner similar to that in T. thermophilus. Furthermore, this gene cluster was analogous in part to the present leucine and arginine biosyntheses pathways. This lysine biosynthesis cluster is assumed to be one of the origins of lysine biosynthesis and could therefore become a key to the evolution of amino acid biosynthesis.

Neosurugatoxin (NSTX) which contains two sugars (myoinositol and xylopyranose) and bromine in the chemical structure, has been shown previously to be a selective antagonist of nicotinic receptors in guinea pig ileum and in murine brain. To study the role of sugar moiety and bromine in the antinicotinic activity by NSTX, we have examined the action of NSTX (compound I) and the structurally related compounds (compound II, III and IV) on the nicotine-induced contraction of guinea pig isolated ileum and on specific [3H]nicotine binding in rat forebrain membranes. Among four compounds examined, compound I was the most potent in inhibiting the nicotine-induced contraction of guinea pig isolated ileum (pA2 = 9.1 +/- 0.1, pD2' = 8.0 +/- 0.1) and also in inhibiting specific [3H]nicotine binding in rat forebrain (IC50 = 83 +/- 9 9 nM). Compared to compound I, compound II and III which are devoid of one and two sugars, respectively, in the chemical structure of compound I were 2 or 3 times less potent in the antinicotinic activity in both tissues, and compound IV which lacks bromine in addition to two sugars was two orders of magnitude less potent. Thus, the present study demonstrates that bromine rather than sugar moiety in the chemical structure of compound I (NSTX) is an important determinate of its high affinity for nicotinic receptors.

Genes for indoleacetic acid production (iaaM and iaaH) are necessary for gall induction by the olive pathogen Pseudomonas savastanoi. In strain 2009 these determinants are borne on plasmid pIAA1. To map and characterize the genes, fragments of pIAA1 generated by EcoRI endonuclease treatment were cloned in Escherichia coli by using plasmid RSF1010 as vector. We isolated a recombinant plasmid encoding iaaM, the locus for tryptophan 2-monooxygenase. This plasmid, called pLUC1, was characterized by restriction endonuclease hydrolysis. It contained a 2.75-kilobase-pair segment of pIAA1. By cloning this segment in the EcoRI site of pBR328 and pBRH3B we showed that efficient expression of iaaM was dependent on the orientation with respect to the vector promoters, and thus determined the direction of transcription. To more finely map iaaM and confirm the orientation of transcription, plasmid pLUC1 was subjected to transposon Tn/mutagenesis. The promoter-distal end of iaaM was mapped between coordinates at 1.7 and 2.15 kilobase pairs of the cloned segment.

Olive (or oleander) knot is a plant disease incited by Pseudomonas savastanoi. Disease symptoms consist of tumorous outgrowths induced in the plant by bacterial production of indole-3-acetic acid (IAA). Synthesis of IAA occurs by the following reactions: L-tryptophan leads to indoleacetamide leads to indoleacetic acid, catalyzed by tryptophan 2-monooxygenase and indoleacetamide hydrolase, respectively. Whereas the enzymology of IAA synthesis is well characterized, nothing is known about the genetics of the system. We devised a positive selection for the presence of tryptophan 2-monooxygenase based on its capacity to use as a substrate the toxic tryptophan analogue 5-methyltryptophan. Efficient curing of the bacterium of tryptophan 2-monoxygenase, indoleacetamide hydrolase, and IAA production was obtained by acridine orange treatment. Further, loss of capacity to produce IAA by curing was correlated with loss of a plasmid of 34 X 10(6) molecular weight. This plasmid, here called pIAA1, when reintroduced into Iaa- mutants by transformation, restored tryptophan 2-monooxygenase and indoleacetamide hydrolase activities and production of IAA.

Specific [3H]nicotine binding to rat forebrain membranes was saturable and of high affinity, and it exhibited pharmacological specificity as well as stereoselectivity for nicotinic agents. There was a regional variation of specific [3H]nicotine binding in rat brain. Low concentrations of neosurugatoxin markedly inhibited specific [3H]nicotine binding in rat forebrain (IC50 = 78 nM) and the competition curve by the toxin was biphasic (pseudo-Hill slope, 0.44). Approximately 50% of [3H]nicotine binding in rat forebrain was inhibited by low concentrations (0.3-100 nM) of neosurugatoxin and the residual binding was inhibited by higher concentrations (0.3-10 microM). In the presence of 3 nM, 100 nM, and 1 microM neosurugatoxin, there was a concentration-dependent (28, 54, and 71%, respectively) loss of [3H]nicotine-binding sites (Bmax) in rat forebrain with little change in the dissociation constant (Kd). The blockade of brain [3H]nicotine-binding sites induced by neosurugatoxin was not reversed by washing. Further, the toxin (10 microM) considerably accelerated the dissociation of [3H]nicotine from its receptor sites initiated by nonlabeled (-)nicotine. These observations suggest that neosurugatoxin may allosterically regulate [3H]nicotine binding rather than competing directly. In contrast to a marked inhibition of [3H]nicotine binding, neosurugatoxin (100 nM-10 microM) had no effect on brain [3H]quinuclidinyl benzilate binding. In conclusion, the present study has shown that [3H]nicotine selectively labels nicotinic cholinergic receptors in rat brain and that neosurugatoxin is a potent noncompetitive antagonist of these receptors.

Objective: We evaluated a bovine jugular vein graft with a natural trileaflet valve for right ventricular outflow tract reconstruction in a canine study for an entire year. Methods: Heparinized bovine jugular vein grafts with a natural valve cross-linked with a hydrophilic polyepoxy compound of 18 to 20 mm in internal diameter were implanted in the right ventricular-pulmonary arterial position in eight dogs, and the main natural pulmonary artery was ligated. Anticoagulants were not used after implantation. Five grafts were retrieved on day 182 after implantation and the other three grafts on days 196, 375, and 385, respectively, and were inspected by macroscopic and microscopic observation. Cardiac catheterization, followed by angiography and echocardiography, was done just before graft retrieval. Results: No graft kinking or regurgitation of the valve was observed. Echocardiography showed natural valve motion without thickening of the leaflets. Blood pressure in the conduits ranged from 18/9 to 31/4 mm Hg, in the right ventricle from 18/4 to 40/0 mm Hg, and the gradient varied from 0 to 14 mm Hg. The explanted conduits maintained their original shape, softness, and pliability with good coaptation of valves, without calcification or degenerative changes, except for one leaflet with slight deformation. In microscopic observation, endothelial cells lined the luminal surface of the conduit except for the areas adjacent to the valve. Conclusion: The graft worked perfectly as a right ventricular-pulmonary arterial valved conduit without anticoagulant therapy for a long time. J Thorac Cardiovasc Surg 1997;114:224-33

A 1.3-kilobase-pair DNA element, IS51, causes a loss of virulence in the plant pathogen Pseudomonas syringae pv. savastanoi. This sequence, IS51, was first discovered in a plasmid-borne iaaM locus, which together with iaaH directs the synthesis of a virulence factor, indoleacetic acid. The spontaneous insertion of IS51 in iaaM resulted in the loss of indoleacetic acid production, attenuation of virulence, and the loss of both enzyme activities coded by iaaM and iaaH. Using a cloned IS51 element as a probe, we found that numerous homologous sequences are present in different strains of this bacterium, on both chromosomal and plasmid DNAs. By artificially positioning IS51 between a tetracycline resistance gene and a promoter region, we showed that IS51 terminated transcription in Escherichia coli.