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Biomedical subjects

B Johansson

Publications and source records attributed to B Johansson.

At least 307 records · Page 17Linked to original sources
PubMed1996

Database and knowledge base integration--a data mapping method for Arden Syntax knowledge modules.

One of the most important categories of decision-support systems in medicine are data driven systems where the inference engine is linked to a database. It is, therefore, important to find methods that facilitate the implementation of database queries referred to in the knowledge modules. A method is described for linking clinical databases to a knowledge base with Arden Syntax modules. The method is based on a query meta-database including templates for SQL queries which is maintained by a database administrator. During knowledge module authoring the medical expert refers only to a code in the query meta-database; no knowledge is needed about the database model or the naming of attributes and relations. The method uses standard tools, such as C+2 and ODBC, which makes it possible to implement the method at many platforms and to link to different clinical databases in a standardized way.

Databases, Factual↗
PubMed1995

Cytogenetic evolution patterns in non-Hodgkin's lymphoma.

Secondary chromosomal aberrations were surveyed in non-Hodgkin's lymphomas (NHL) reported in the literature with one of the following, presently recognized, primary abnormalities: t(2;5), +3, t(3;14), del(6q), +X, and -Y. Of 2,175 NHLs with clonal karyotypic changes, 908 (42%) had one of the 13 selected primary chromosome rearrangements, and 670 (74%) of these lymphomas displayed additional abnormalities. The type and frequency of the secondary aberrations were ascertained and then correlated with both the type of primary abnormality and morphologic subtype; low-, intermediate, and high-grade according to the Working Formulation. The incidence of secondary aberrations differed not only among the primary abnormality subgroups, from 0% in del(11q) NHLs to 93% in t(3;14) lymphomas (P < .001) but also between B- and T-cell NHLs (78% versus 55%, P< .001) and among the different histologic subgroups: 66% in low-, 85% in intermediate-, and 71% in high-grade lymphomas (P < .001). The mean number of secondary changes per case also varied among the primary abnormalities, from none in del(11q) NHLs to 12.0 in inv(14) lymphomas (P < .001), and among the morphologic subtypes: 4.6 in low-, 6.7 in intermediate-, and 3.6 in high-grade NHL (P < .001). Recurrent secondary aberrations were found in 6 of the 13 primary abnormality subgroups: t(2;5), t(3;14), t(8;14), t(11;14), inv(14), and t(14;18). The most frequent secondary aberrations were +X, -Y, dup(1q), del(6q) varied both within and among the primary abnormalities; the most frequent imbalances were a gain of 1q23-31 and losses of 6q21, 6q23, and 6q25. Other common imbalances were deletions of 1p31-36, 1q31-44, 2q34-37, 7q35-36, 9p22-24, 11q23-25, 13q13-21, and duplication of 12q13-22. The distribution of the secondary changes was clearly nonrandom with the most common anomalies being -Y and +7 in t(2;5); +X, del(6q), and +7 in t(3;14); dup(1q) and +7 in t(8;14); -Y, del(6q), and -13 in t(11;14); del(6q), -17, and -18 in inv(14); and del(6q), +7, and +12 in t(14;18) NHLs. In general, the secondary aberrations were similar in lymphomas of different histologic subtypes but with the same primary abnormality, although some significant differences were discerned: +3, del(6q), +7, and +18 wee more common (P < .01) in intermediate-grade than in high-grade t(8;14) NHLs; monosomy 13 occurred only in intermediate-grade t(11;14) NHLs (P < .05); and +7 and t(8;14)/t(8;22) were more frequent (P < .01 and P< .001, respectively) in high-grade than in low- and intermediate-grade t(14;18) NHLs.(ABSTRACT TRUNCATED AT 400 WORDS)

Chromosome Aberrations↗
PubMed1995

Adenosine A2A receptors stimulate acetylcholine release from nerve terminals of the rat hippocampus.

The nature of the adenosine receptors involved in the enhancement of acetylcholine release in the hippocampus was studied. The A2A agonist, CGS 21680, increased the veratridine-evoked release of [3H]acetylcholine from hippocampal synaptosomes. This presynaptic effect of CGS 21680 was greater at 3-30 nM than at 100 nM. The excitatory effect of CGS 21680 was antagonised by the A2 antagonist, DMPX (10 microM), and by the A2A antagonist, CSC (200 nM), but not by the A1 antagonist, DPCPX (20 nM). We also found co-expression of A2A and choline acetyltransferase mRNAs in the nucleus of the diagonal band and the medial septum, where the cholinergic cell bodies that project into the hippocampus are located. These results indicate that A2A adenosine receptors are present in cholinergic nerve terminals in the hippocampus and that activation of these receptors enhances acetylcholine release.

Acetylcholine↗
PubMed1995

Cytogenetically detected clonal heterogeneity in a duodenal adenocarcinoma.

A primary duodenal adenocarcinoma, a tumor type for which no previous chromosome data existed, was cytogenetically analyzed after short-term culture. The main tumor mass was localized in the pancreatic head, but the histopathologic examination revealed its duodenal origin. A total of six abnormal, karyotypically unrelated, clones were identified. The largest exhibited clonal evolution and consisted of two subclones with massively rearranged karyotypes in the hypodiploid and hypotetraploid range. Chromosome imbalances brought about by these complex changes were gain of 1q, losses of chromosomes 6 and 9, and total or partial losses of 1p, 3p, 3q, 9p, 10p, 17p, 17q, 18q, 20p, and 20q. The remaining five smaller clones had 1-2 numerical or balanced structural chromosome aberrations. The present study thus revealed yet another epithelial tumor type characterized by karyotypically unrelated clones. For this as for other tumors, the pathogenetic significance of such cytogenetic polyclonality remains uncertain.

Adenocarcinoma↗