Theoretical predictions of structural phase transitions in Cr, Mo, and W.
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Journal Article↗
Biomedical subjects
B Johansson
Publications and source records attributed to B Johansson.
Photoelectron spectra and magnetic moments in UPdSn: Theory.
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Journal Article↗
Localisation of the breast-ovarian cancer susceptibility gene (BRCA1) on 17q12-21 to an interval of < or = 1 cM.
A breast-ovarian cancer susceptibility gene, BRCA1, which is responsible for disease in approximately 45% of breast cancer families and most families that contain breast and ovarian cancer, has been assigned by genetic linkage to 17q12-21. Here, we report the analysis of three marker-disease recombinants in families that contain breast and ovarian cancer, two of which strongly suggest a location for BRCA1 telomeric to D17S702, a microsatellite polymorphism, and a third which suggests a location centromeric to EDH17B, the gene encoding estradiol-17B dehydrogenase. If the interpretation of these recombinants is correct, the results localise BRCA1 to an interval of < or = 1 cM.
Adult↗
Isochromosomes in neoplasia.
In order to ascertain the frequency and distribution of isochromosomes in neoplasia, we surveyed the cytogenetic data from 20,007 tumors with clonal chromosome aberrations reported in the literature. Tumor types for which at least 50 cases with acquired aberrations and 10 cases with isochromosomes had been reported were selected, yielding a total of 18,160 neoplasms. Of these, 1,792 cases (9.9%) displayed a total of 2,014 isochromosomes. The 9 most common isochromosomes (detected in at least 50 cases) were, in decreasing order of frequency, i(17q), i(8q), i(1q), i(12p), i(6p), i(7q), i(9q), i(5p), and i(21q). The frequency of isochromosomes varied among the different tumor types, with the highest incidence in germ cell neoplasms (60%) and the lowest in chronic myeloproliferative disorders (2.3%). Also, the spectrum of isochromosomes differed among the neoplasms. The most common isochromosomes in the different tumor types were i(11q), i(17q), and i(21q) in acute myeloid leukemia; i(9q), i(17q), and i(22q) in chronic myeloid leukemia; i(17q) in chronic myeloproliferative disorders; i(X)(q13), i(17q), and i(21q) in myelodysplastic syndromes; i(7q), i(9q), and i(17q) in acute lymphoblastic leukemia; i(1q), i(7q), i(8q), and i(17q) in chronic lymphoproliferative disorders; i(1q), i(6p), i(9p), i(17q), and i(21q) in Hodgkin's disease; i(1q), i(6p), and i(17q) in non-Hodgkin's lymphoma; i(1q), i(8q), and i(17q) in adenocarcinoma; i(1q), i(3q), i(5p), and i(8q) in squamous cell carcinoma; i(5p), i(8q), and i(11q) in transitional cell carcinoma; i(1q), i(7q), and i(17q) in Wilms' tumor; i(1q), i(12p), and i(17q) in germ cell neoplasms; i(1p), i(1q), i(6p), and i(17q) in sarcoma; i(5p), i(6p), i(7p), and i(21q) in mesothelioma; i(1q), i(6p), and i(17q) in malignant neurogenic neoplasms; i(1q), i(6p), and i(17q) in retinoblastoma; and i(1q), i(6p), and i(8q) in malignant melanoma.
Chromosome Aberrations↗
Fusion of the FUS gene with ERG in acute myeloid leukemia with t(16;21)(p11;q22).
It has been shown that the gene ERG in 21q22 is rearranged in the t(16;21)(p11;q22) associated with acute myeloid leukemia (AML). ERG is a member of the ETS gene family and is fused with EWS in a subset of Ewing's sarcomas. EWS in 22q12 has a very high homology with FUS (also called TLS) in 16p11; the latter gene is rearranged in the t(12;16)(q13;p11) that characterizes myxoid liposarcoma. To investigate whether FUS is involved in the t(16;21) of AML, we used the Southern blot technique and polymerase chain reaction (PCR) to examine the bone marrow of a 3-year-old boy with a t(16;21)(p11;q22)-positive AML. Hybridization of Southern blot filters containing digested DNA with probes for FUS and ERG showed both germline and aberrant fragments. Using specific primers for the 5' part of FUS and the 3' part of ERG, we amplified a 4.4 kb genomic FUS/ERG DNA fragment from the leukemic sample. In a second PCR experiment, in which we used primers upstream of the 5' part of ERG and downstream of the 3' part of FUS, a 5.6 kb fragment was amplified. Blotting and hybridization with specific probes for FUS and ERG revealed that the amplified fragments consisted of FUS/ERG and ERG/FUS hybrid DNA. Both PCR fragments, when used as probes, detected germline ERG and FUS as well as aberrant fragments on Southern blot filters. The results suggest that the t(16;21) in AML leads to rearrangement and fusion of the FUS and ERG genes.(ABSTRACT TRUNCATED AT 250 WORDS)
Base Sequence↗
Tirilazad reduces brain edema after middle cerebral artery ligation in hypertensive rats.
Tirilazad (3 mg/kg i.v.) or vehicle was given 10 min, 3 and 12 hours after ligation of the right middle cerebral artery in male spontaneously hypertensive rats (n = 12 in each group). Brain specific gravity was determined in 23 predetermined cortical regions covering the core and penumbra areas 24 hours after the occlusion. The specific gravity was significantly higher in tirilazad-treated rats than in controls (p < 0.0001). When individual regions of the two groups were compared, the difference was significant in 9 of the 23 samples predominantly, but not exclusively, in the penumbra zone.
Animals↗
Laparoscopic Rosetti fundoplication.
Early experiences with laparoscopic fundoplication using the Rosetti technique are presented and compared with retrospective results from conventional fundoplication procedures. A 360 degrees floppy fundoplication was laparoscopically constructed without division of short gastric vessels. We have performed 60 consecutive procedures. Conversion to open surgery was done in seven cases due to anatomical reasons and in two due to progressive subcutaneous emphysema and CO2-retention. The complication rate was low. The range of postoperative hospital stay is 1-4 days for non-converted patients. Symptomatic follow up has hitherto been performed in 41 patients with a follow-up time of 3-9 months. Regurgitation and heartburn had disappeared in all but one patient. The follow-up results do not differ from those achieved in patients operated upon with the conventional open Nissen (N = 41), Toupét (N = 9) or Rosetti (N = 36) technique. Pre and postoperative control of 24h pH and lower esophageal sphincter pressure (LESP) in 19 laparoscopically treated patients showed normalisation of LESP in all cases and postoperative 24h pH < 4 ranging between 0 and 3%. Assessment of quality of life showed postoperative results in accordance with normal population for all treated groups.
Esophagogastric Junction↗
Experiences from the use of data-driven decision support in different environments.
The paper reports experiences from the implementation and use of data-driven decision support based on the Arden Syntax in three different environments: in a health-care centre, in a clinical laboratory, and in a research department. Methods and tools used for realization of decision support systems (DSSs) are shortly presented, and integration aspects of the DSS with running clinical applications and existing patient databases are discussed. The application areas are also described, together with validation procedures for the developed knowledge modules.
Artificial Intelligence↗
The dynamics of local tissue damage induced by Bothrops asper snake venom and myotoxin II on the mouse cremaster muscle: an intravital and electron microscopic study.
The acute tissue damaging effects of Bothrops asper snake venom and a myotoxic Lys-49 phospholipase A2 (myotoxin II) on the mouse cremaster muscle were studied by intravital and electron microscopy. Both venom and myotoxin induced local contractions of the muscle fibres within 10-60 sec after exposure, which disappeared after 1-2 min. This observation is consistent with the hypothesis that Bothrops myotoxins act initially at the sarcolemma by affecting its permeability and allowing an influx of calcium. The venom also induced an early but transient vasoconstriction of arterioles. The development of edema was monitored using i.v. FITC-dextran as a marker. Plasma leakage started after about 2 min of exposure to venom or myotoxin, was extensive by 4-5 min, and originated from small venules and their adjoining capillary segments. The venom induced formation of thrombi and emboli in venules, but not in arterioles. Haemorrhage appeared after 4-6 min of exposure, the bleedings always originating from capillaries and small venules. The microbleedings were explosive, appearing as rapid bursts of erythrocytes into the extravascular space, and suggesting a per rhexis type of haemorrhage. This was confirmed by electron microscopy evaluation of the same microvessels observed intravitally, which showed erythrocyte extravasation through gaps in damaged endothelial cells. Other phenomena in the microcirculation included blood-flow disturbances, crenation and sphering of erythrocytes, and stasis with dense packing of cells in capillary networks. Muscle necrosis, caused by either venom or myotoxin, started 3-4 min after application. The first sign of damage in the fibres was the development of a narrow, transverse band with local loss of striation. This was followed by slow retraction of myofibrils until there was a complete transverse rupture of the fibre. This process was often repeated along the same fibre, leaving a row of fragments separated by spaces apparently devoid of myofibrillar material. The results confirm the rapid tissue damaging effects of B. asper venom, implying that potentially useful blocking agents must be administered early and have the ability to diffuse rapidly into the tissues.
Animals↗
Trisomy 19 as the sole chromosomal anomaly in hematologic neoplasms.
Trisomy 19 was found as the sole chromosomal aberration in three hematologic malignancies: one chronic myelomonocytic leukemia and two cases of of immunophenotypically immature acute myeloid leukemia (AML). A compilation of previously published hematologic neoplasms with +19 as the only change reveals that this anomaly is strongly associated with myeloid malignancies; 25 of 31 cases have been myelodysplastic syndromes (MDS) or AML. Eight of the 11 MDS cases have been either refractory anemia (RA) or RA with excess of blasts, and four of the 14 AML cases have had preleukemic myelodysplastic cases phase, with the +19 accruing during the time of leukemic transformation. The AML cases have, in general, been either or early maturation arrest, i.e. undifferentiated or AML-M1/M2, or of myelomonocytic-monoblastic origin, i.e., AML-M4/M5. None of the MDS or AML cases with +19 had had a previous history of radio- or chemotherapy. We conclude that trisomy 19, as the sole anomaly, is a characteristic abnormality in de novo myeloid malignancies. No clinical features seem to characterize patients with +19 AML and MDS and the prognostic impact of the aberration remains to be elucidated.
Acute Disease↗
Abnormal karyotypes in three carcinomas of the gallbladder.
Short-term cultures from three carcinomas of the gallbladder were cytogenetically analyzed. All three had an abnormal karyotype. The modal chromosome number was near- or hypertriploid in two tumors and near diploid in the third. Structural rearrangements of chromosomes 1 and 3, loss of material from the long arm of chromosome 18, and loss of chromosome 21 material were common to all three tumors and would seem to be the best candidates for nonrandom karyotypic changes in carcinomas of the gallbladder.
Aged↗
Cytogenetic characterization of a periampullary adenocarcinoma of the pancreas, its liver metastasis, and a cell line established from the metastasis and a cell line established from the metastasis in a patient with Gardner's syndrome.
A cell line was established from a liver metastasis of a periampullary pancreatic carcinoma in a patient with Gardner's syndrome. The primary tumor, the liver metastasis, and passages 6 and 15 of the cell line were characterized cytogenetically. The only aberration common to all samples was a der(15)t(8;15); this was probably the primary chromosomal abnormality. Loss of the short arm of chromosome 19 was also found in all samples but was brought about by different aberrations in the primary tumor and the metastasis. The secondary aberrations characteristic of clonal evolution often included further gain of 8q material but losses from 1p, 6q, and chromosomes 17 and 18, all of which have been seen before in sporadic pancreatic and colorectal carcinomas. This is the first cell line established from a tumor in a Gardner's syndrome patient and also the first characterization of an abnormal tumor karyotype associated with this autosomal dominant cancer syndrome.
Adenocarcinoma, Papillary↗
Translocation (3;21)(q26;q22) in therapy-related myelodysplasia following drugs targeting DNA-topoisomerase II combined with alkylating agents, and in myeloproliferative disorders undergoing spontaneous leukemic transformation.
Translocation (3;21)(q26;q22) has been observed only rarely in de novo myelodysplasia (MDS) and de novo acute myeloid leukemia (AML), but, including the two new cases in the present study, the aberration has now been identified in at least 10 cases of t-MDS or t-AML. All these 10 patients had previously received alkylating agents, in nine patients combined with a drug targeting at DNA-topoisomerase II (doxorubicin in eight cases). Eight of the ten patients presented with t-MDS. A further 20 patients with various myeloproliferative disorders and an identical t(3;21) have been reported. In these cases, t(3;21) was not related to any specific type of previous therapy but was associated with transformation from chronic stage disease to overt AML.
Alkylating Agents↗
Acute myeloid leukemia (AML-M1) with multiple trisomies and t(8;21)(q22;q22).
Cytogenetic analysis of an acute myeloid leukemia (AML-M1) showed the karyotype 53,XY, +6, +8,t(8;21)(q22;q22), +9, +10, +13, +19, +21. Only one AML with a massively hyperdiploid karyotype (> 50 chromosomes) and t(8;21) has been published before. A comparison of the two cases reveals similarities both with regard to the morphologic subtype (M1) and to which chromosomes were trisomic (+6, +8, +13, +19, and +21 were found in both cases). We surmise that the t(8;21) was the primary chromosomal abnormality and that the set of multiple trisomies occurred secondarily; this pattern of clonal evolution may have favored a more immature leukemic phenotype in these two cases than is regularly seen in t(8;21)-associated leukemias.
Child↗
Colorimetric detection of competitive PCR products for quantification of hepatitis C viremia.
A method based on competitive polymerase chain reaction (PCR) and colorimetric detection of the amplified products was developed to quantify hepatitis C virus (HCV) genomes. Serum samples were obtained from patients who were treated with interferon alpha (IFN-alpha). After reverse transcription of the HCV RNA, the cDNA was coamplified with a serially diluted cloned HCV competitor DNA using nested PCR. The competitor DNA consisted of the amplified region of the wild type HCV cDNA with an internal region substituted with the lac operator (lacO) sequence. The PCR products were quantitated specifically by a colorimetric solid-phase assay. The results suggest that the method is well suited for analysing the kinetics of the anti-HCV effects during IFN-alpha treatment. The quantification assay is simple, reliable and suitable for quantitating HCV genomes in a large number of clinical samples.
Base Sequence↗
Enhancement of thrombolysis by ultrasound.
Drug-induced early reperfusion in acute myocardial infarction reduces myocardial damage and decreases mortality. A further beneficial effect may be achieved if the time from start of thrombolytic treatment to reperfusion, on average 45 min, can be shortened. With this purpose in mind, we have analysed the effect of ultrasound on the reperfusion time in an experimental model in vitro. A cylindrical fibrin thrombus with a 2 mm diameter and a 20 microL volume was made by thrombin activation of a pure 0.5% fibrinogen solution in a soft silicone tube. The tube was placed in a low pressure perfusion system and maintained at 37 degrees C. The thrombi were then exposed to hydrostatic loading with a streptokinase concentration of 5000 units/mL. Reperfusion times (RT) were measured from time of Streptokinase exposure to fluid passage, identified by the photoelectric technique. RT increased significantly with increasing thrombus age (r = 0.92, p < 0.05) and was 34-45 min (95% confidence limits) at a thrombus age of 1 h and 102-122 min at a thrombus age of 2 h. RT was unaffected by temperatures between 33 and 45 degrees C but increased with higher temperatures. All investigations of ultrasound effects were performed with 1 h old thrombi and at 37 degrees C. RT decreased by 49% (p < 0.01) as an effect of exposure to 1 MHz ultrasound at 1 W/cm2 SATA. Intermittent ultrasound exposure for 10 microseconds/ms with the same intensity and frequency shortened RT by 54% (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
Blood Circulation↗
Differences in the regional and cellular localization of c-fos messenger RNA induced by amphetamine, cocaine and caffeine in the rat.
Male rats were treated i.p. with either 5 mg/kg amphetamine, 3 and 30 mg/kg cocaine or 100 mg/kg caffeine and killed after 30 min. Brains were sectioned and processed for radioactive in situ hybridization histochemistry for the labelling of either c-fos, enkephalin, substance P, neurokinin B, choline acetyltransferase, somatostatin or adenosine A2A receptor messenger RNA. The distribution of c-fos messenger RNA was investigated both at the regional level using film autoradiography, and at the cellular level using emulsion autoradiography. All drug treatments except 3 mg/kg cocaine induced an increased level of c-fos messenger RNA in cells that had a neuron-like morphology. The cells that contained the c-fos messenger RNA were identified by making pairs of 5-microns sections in which one section was processed for c-fos messenger RNA and the other was processed for one of the other messenger RNA species. After amphetamine treatment, only some 10% of the cells in the striatum were labelled, and to a variable extent. Instead there was prominent labelling of a band in the cortex that runs parallel to the cortical surface. There was also a moderate degree of labelling in the nucleus accumbens. c-fos-positive cells were substance P-positive and negative for enkephalin or A2A receptor messenger RNA. Cocaine (30 mg/kg) induced a modest labelling in the caudate-putamen, as well as in the accumbens. With cocaine treatment (30 mg/kg), about 30% of striatal neuron-like cells were c-fos labelled. Most c-fos-positive cells were substance P-positive, but none of the c-fos-positive cells were enkephalin-positive or A2A-receptor-positive. Cocaine (3 mg/kg) had no significant effect on c-fos. Caffeine gave rise to a strong hybridization signal in the caudate-putamen, particularly the dorsolateral part. No other region examined differed significantly from control. With caffeine treatment, about 73% of neuron-like cells were c-fos labelled in the lateral striatum, but labelling was much less pronounced in the medial part or in the accumbens. c-fos-labelled cells were found in enkephalin-positive and enkephalin-negative, substance P-positive and substance P-negative, neurokinin B-positive and neurokinin B-negative groups. No choline acetyltransferase-positive or somatostatin-positive cells were found that were also c-fos-positive with any of the treatments. We conclude that each of the different CNS stimulant drugs induces a highly specific pattern of c-fos messenger RNA.(ABSTRACT TRUNCATED AT 400 WORDS)
Amphetamine↗
On the point of action for sympatho-adrenergic inhibition of duodenal alkaline secretion in the rat.
Experiments were performed on chloralose anaesthetized rats. A duodenal segment was decentralized by means of bilateral vagotomy and splanchnicotomy. The mucosal alkaline secretion by the segment was measured using an in situ pH-stat titration. The duodenal alkaline secretion was raised by about 100% utilizing two different secretagogues; vasoactive intestinal polypeptide (VIP) and prostaglandin E2 (PGE2). Direct splanchnic nerve stimulation (10 Hz, 5 min, bilaterally), or exogenous administration of the alpha-2-adrenoceptor agonist clonidine (15 micrograms h-1 kg-1), inhibited the secretion stimulated by PGE2, but not by VIP. The results suggest that the sympathetic nerves exert their inhibitory effect mainly on enteric secretomotor neurones.
Animals↗