Ab initio surface core-level shifts and surface segregation energies.
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Journal Article↗
Biomedical subjects
B Johansson
Publications and source records attributed to B Johansson.
Deep layer-resolved core-level shifts in the beryllium surface.
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Journal Article↗
Age- and gender-related heterogeneity of cancer chromosome aberrations.
The karyotype of a neoplasm is known to be associated not only with the histopathologic subtype of the tumor but also with previous cytotoxic exposure and with the geographic place of origin of the patient. Some data also indicate that cytogenetic patterns vary with age and gender. To further investigate whether the frequencies of cancer chromosome aberrations differ between children and adults or between men and women, clinical and karyologic data on 14,141 neoplasms with clonal chromosome changes reported in the literature were assessed. In cytogenetically well-characterized neoplasias, recognized primary and secondary chromosome aberrations were selected, and their frequencies were calculated in men, women, children (< or = 15 years), and adults (> 15 years). In general, the frequencies of the various aberrations did not differ between men and women or between children and adults, but a few exceptions were found. In refractory anemia (RA) and RA with excess of blasts or in transformation, del(5q) was more common among women. In acute lymphoblastic leukemia (ALL-L1 + L2), t(1;19) was more frequently detected in women and del(6q) more common among men. In Philadelphia chromosome positive chronic myeloid leukemia, gain of an extra der(22)t(9;22) occurred more frequently among men. Four primary aberrations were more common in children than in adults: t(8;21) in acute myeloid leukemia (AML-M2), -7 in AML-M4, der(11q) in AML-M5, and t(8;14) in ALL-L3. On the other hand, der(16q) in AML-M4 and t(9;22) in ALL-L1 + L2 were more common in adults. The only secondary cancer chromosome aberration showing a variation with age was loss of the Y chromosome in AML-M2 with t(8;21), being more common in children than in adults. These variations might be spurious and level out when more data are collected, but more probably they reflect, for reasons presently unknown, that different genetic mechanisms may be operative in children and adults--and even in men and women--in the development of some tumors.
Adult↗
Local-moment collapse in compressed samarium metal.
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Journal Article↗
Cytogenetic analysis of 52 colorectal carcinomas--non-random aberration pattern and correlation with pathologic parameters.
Cytogenetic analysis of short-term cultures from 52 colorectal carcinomas revealed a normal karyotype in 13 and clonal chromosome aberrations in 39 tumors. In the abnormal group, 13 tumors had simple numerical changes only, whereas 26 had at least one structural rearrangement with or without concomitant numerical changes. The most common numerical abnormalities were, in order of decreasing frequency, +7, -18, -Y, +8, +13 and -14. The most common structural rearrangements affected, again in order of decreasing frequency, chromosomes 8, 1, 6, 7, 17, 3, 11, 13, 14, 16, 2 and 10. The chromosome bands most frequently involved in the structural changes were 8q10, 17p11, 11q13, 8p11, 6q21, 7p15, 7q36, 12q13, 13q10, and 16q13. The most frequent genomic imbalances brought about by the structural rearrangements were losses from chromosome arms 8p, 1p, 6q, 17p, 7p, and 16q, as well as gains of 7q, 8q, 13q, and 11q. A statistically significant (p < 0.05) correlation between the karyotypic pattern and tumor grade was found, with the poorly differentiated carcinomas generally having more massive chromosomal abnormalities.
Adult↗
Striatal D2/acetylcholine interactions: PET studies of the vesamicol receptor.
The regional cerebral distribution of [18F]NEFA, an aminobenzovesamicol (ABV), was studied in primates with PET. The binding was stereoselective and could be blocked but not displaced with vesamicol. The regional distribution pattern at late times, striatum > cortex > cerebellum, was corroborated by in vitro autoradiography using [3H]ABV and is consistent with known patterns of cholinergic innervation. Pretreatment with sigma 1 or D1 antagonists did not affect the striatal uptake, whereas D2 antagonists markedly augmented the uptake. This is consistent with the known induction of acetylcholine turnover in the striatum in response to D2-receptor blockade and demonstrates that the amount of [18F]-(-)-NEFA incorporated was influenced by the cholinergic activity in the target neurones.
Acetylcholine↗
Break-down of Hund's third rule for induced magnetism in U metal.
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Journal Article↗
[Acupuncture therapy in stroke. Patients experience significant improvement].
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Activities of Daily Living↗
Long-term caffeine treatment leads to a decreased susceptibility to NMDA-induced clonic seizures in mice without changes in adenosine A1 receptor number.
The effects of long-term caffeine treatment on N-methyl-D-aspartate (NMDA)-induced seizures in mice were studied. Caffeine was added (0.3 g/l) to drinking water for 14 days and the mice ingested 60-70 mg/kg/day. During the treatment, the plasma concentrations of methylxanthines (caffeine, theophylline and/or paraxanthine, theobromine) were measured. NMDA (150 mg/kg i.p.) was administered to control mice and to mice during and after the caffeine administration. A1 adenosine receptor density in the gyrus dentatus of hippocampus, measured by quantitative receptor autoradiography with [3H]cyclohexyl adenosine as the ligand, was not significantly altered after long-term caffeine treatment. NMDA-induced clonic seizures, wet dog shakes and mortality were significantly reduced at the end of long-term caffeine treatment but returned towards control at 1 and 2 days after withdrawal. At the end of caffeine treatment, tonic seizures were also absent. These results show that long-term treatment with caffeine in a dose that gives plasma levels of 6-10 microM decreases the effects of NMDA on e.g. seizure susceptibility, and that this effect cannot be ascribed to changes of A1 adenosine receptor density.
Animals↗
Cytogenetic aberrations in colorectal adenocarcinomas and their correlation with clinicopathologic features.
BACKGROUND: Little is known about the karyotypes of colorectal carcinomas and, in particular, about how the cytogenetic findings correlate with clinicopathologic features. METHODS: Short-term cultures from 49 colorectal adenocarcinomas were analyzed cytogenetically. The karyotypes were correlated with grade, stage, lymphocytic infiltration, and site (using the chi-square test), with patient age and tumor size (using the Student t test), and with survival (using the log-rank or Mantel-Haenszel test). RESULTS: Normal karyotypes were detected in 17, simple numeric changes in 22, and multiple structural and numeric abnormalities in 10. The most common numeric aberrations were +7, -Y, -18, and -22. The most common structural rearrangements were, in decreasing order of frequency, of chromosomes 1 (eight samples, leading to loss of 1p material in five), 3, 11, 17, 6, 8, 13, and 20. Marked or moderate lymphocytic infiltration was seen significantly less often (P < 0.05) in tumors with complex chromosomal abnormalities than in those with simple anomalies or normal karyotypes. The subset of patients who had tumors with multiple chromosomal abnormalities had a significantly shorter survival time (P < 0.025) than those who had lesions with simple changes or normal karyotypes. CONCLUSIONS: Loss of 1p material is the most consistent chromosomal change in colorectal carcinomas but probably represents a progressional rather than a primary event. Structural changes of chromosomes 3 and 11 seem to be more common in tumors located in the distal part of the large intestine. The significantly shorter survival time of patients with complex aberrations indicates that the karyotype could be used as a prognostic parameter in patients with colorectal cancer.
Adenocarcinoma↗
Trisomy 7 in nonneoplastic cells.
The somatic mutation theory of tumorigenesis states that mutations are necessary for tumor development. On the other hand, acquired, clonal chromosomal alterations are occasionally detected in otherwise normal, nonneoplastic cells--for example, loss of sex chromosomes occurs in bone marrow cells and lymphocytes in elderly individuals--and it is therefore evident that not all mutations are by themselves sufficient for neoplasia to occur. Thus, the finding of an acquired, clonal chromosomal abnormality does not constitute proof that a lesion is neoplastic. Trisomy 7 has, as the sole clonal chromosomal aberrations, been reported in a wide variety of epithelial tumor types but also in some mesenchymal and neurogenic neoplasms. It has been suggested to be a primary, i.e., tumor-initiating, abnormality in tumors of the bladder, brain, colon, kidney, lung, ovary, prostate, and thyroid. But data from cytogenetic studies of solid tumors, macroscopically normal tissue in the proximity of solid tumors, and nonneoplastic lesions now question the importance of a solitary +7 as a neoplasia-associated change. Most solid tumors in which trisomy 7 has been found as the sole change in one clone have also displayed other, cytogenetically unrelated, clones with complex karyotypic abnormalities. Such karyotypic differences among coexisting clones could indicate that the neoplasm is polyclonal, that the cytogenetically disparate clones have emerged during tumor progression from one original clone carrying submicroscopic genomic changes only, or that the clone with +7 does not represent the tumor parenchyma. The latter interpretation is supported by the finding of cells with trisomy 7 in macroscopically normal tissue outside tumors of the brain, kidney, and lung.(ABSTRACT TRUNCATED AT 250 WORDS)
Cell Transformation, Neoplastic↗
Cytogenetic deletion maps of hematologic neoplasms: circumstantial evidence for tumor suppressor loci.
Research in oncogenetics has led to the identification of two major classes of tumor-associated genes, oncogenes and tumor suppressor genes. In a wide variety of solid tumor types, mutations of both groups of genes have been implicated in the tumorigenic process. In hematologic neoplasms, on the other hand, most attention has focused on illegitimate activation of oncogenes, e.g., deregulation leading to disturbed transcriptional activity and structural rearrangements resulting in hybrid genes. Whether loss or mutational inactivation of tumor suppressor genes also plays an essential role in the genesis of tumors of the hematopoietic system has received less attention. Because such inactivation can be the result of karyotypically detectable loss of chromosomal material, cytogenetic studies may prove helpful in pinpointing genomic sites that harbor tumor suppressor genes. The present study is based on a total of 12,473 cytogenetically abnormal hematologic neoplasms reported in the literature to date. Among these, we selected the 6,422 cases with sole clonal chromosomal abnormalities in order to include only aberrations of importance in the genesis, rather than in the progression, of these neoplasms. All tumors with monosomies or structural abnormalities resulting in loss of chromosomal material were compiled, and for every such structural aberration, i.e., deletion, unbalanced translocation, isochromosome, and ring chromosome, the chromosome bands lost were ascertained. This cytogenetic deletion mapping revealed that the most commonly lost chromosomes were Y and 7 in acute myeloid leukemia (AML), myelodysplastic syndromes (MDS), and chronic myeloproliferative disorders (MPD); X, Y, 7, 20, and 21 in acute lymphocytic leukemia (ALL); X, Y, and 17 in chronic lymphoproliferative disorders (LPD); and X and Y in non-Hodgkin's lymphoma (NHL). Chromosome segments/bands lost due to unbalanced structural abnormalities in at least 5% of the cases were 5q13-33, 7q22-36, 9q13-31, 11q23-25, 12p12-13, 17p11-13, and 20q11-13 in AML; 5q13-35 and 20q11-13 in MDS; 5q22-23, 7q22, 13q12-22, 17p11-13, and 20q11-13 in MPD; 6q15-27, 9p11-24, 12p12-13, and 19p13 in ALL; 6q16-27, 11q21-25, 13q13-14, and 14q32 in LPD; and 6q21-27, 11q13-25, and 14q24-32 in NHL. Based on these findings, three conclusions can be drawn. First, there is no good correspondence between total and partial monosomies, the only exception being -7 and 7q-, both of which are common in myeloid neoplasms. This indicates different pathogenetic effects of total and partial losses.(ABSTRACT TRUNCATED AT 400 WORDS)
Chromosome Aberrations↗
Detection of hepatitis C virus (HCV) RNA by PCR related to HCV antibodies in serum and liver histology in Swedish blood donors.
Serum samples from 103 blood donors or patients with slightly increased serum levels of liver enzymes were tested for antibodies to hepatitis C virus (anti-HCV) using second generation tests and for HCV RNA by the polymerase chain reaction (PCR). PCR was in a nested configuration, using primer pairs from the 5'-nontranslated region. The anti-HCV antibody was found by enzyme linked immunosorbent assay (ELISA) in 93 patients. The anti-HCV confirmatory second generation recombinant immunoblot assay (RIBA) was positive in 44, indeterminate in 34 and negative in 25 subjects. Histopathological examination of the liver was carried out in 51 subjects. HCV RNA was detected in serum of 39/41 (95%) RIBA positive patients, and in 7/34 (21%) RIBA indeterminate subjects, but in none of the RIBA negative subjects. All but one of the PCR positive patients with a RIBA indeterminate pattern exhibited the C22 band. HCV RNA was found in the serum of all but one patients with chronic active or persistent hepatitis, but also in one RIBA positive subject with normal liver tissue. These results imply that most patients with antibodies to two or more HCV antigens by RIBA will have a chronic replicative HCV infection associated with viraemia. HCV viraemia can also be present in some patients, who have antibodies to only one HCV antigen particularly the C22 epitope.
Adult↗
Encephalitis in immunocompetent patients due to herpes simplex virus type 1 or 2 as determined by type-specific polymerase chain reaction and antibody assays of cerebrospinal fluid.
A herpes simplex virus type 2 (HSV 2) etiology was sought in 93 consecutive cases of herpes simplex encephalitis (HSE) in immunocompetent post neonate patients. Antibodies to HSV 2 glycoprotein G antigen were determined by an enzyme-linked immunosorbent assay (ELISA) and HSV 2 DNA in cerebrospinal fluid (CSF) by a nested polymerase chain reaction (PCR) assay with primer pairs in the glycoprotein G gene. Evidence of HSV 2 infection was found in 6 patients; HSV 2 DNA was demonstrated in CSF and the intrathecal HSV 2 antibody response confirmed the findings. Five of the 6 patients with HSV 2 encephalitis presented a clinical picture, CSF, EEG, and CT findings characteristic of severe HSE. An atypically mild clinical course was seen in one patient. HSV 2 should be considered as an etiological agent in the viral diagnosis of HSE. With a combination of nested PCR assays for HSV 1 (primer pairs in the glycoprotein D gene) and HSV 2 in 10 microliters of CSF with no other preparation than freeze-thawing, HSV 1 or HSV 2 DNA was detected in 88 out of 93 (95%) of the first CSF specimens collected after the onset of neurological HSV disease. These findings extend and confirm previous results with PCR as a rapid and sensitive tool for early diagnosis of HSE.
Adolescent↗
Effect of long term caffeine treatment on A1 and A2 adenosine receptor binding and on mRNA levels in rat brain.
The effect of long-term oral treatment with caffeine on A1 and A2 receptors in the rat brain was studied. Caffeine was added to the drinking water and the animals were sacrificed after a 12 day treatment period. The plasma caffeine concentration was close to 100 microM. A1 receptors were studied using quantitative autoradiography with [3H]cyclohexyladenosine (CHA). Caffeine treatment increased the number of A1 receptors in the CA3 subfield of the hippocampus from 337 to 393 fmol/mg with no change in KD (0.692 vs. 0.675 nM). A1 mRNA was measured using Northern blots and quantitative in situ hybridization. There was no increase in A1 mRNA. A2a receptors, located in dopamine rich regions of the rat brain, were studied with quantitative autoradiography using [3H]CGS 21680 as the ligand, and the A2a mRNA was determined using quantitative in situ hybridization. Caffeine treatment produced no significant change in either receptor number or mRNA, even though the apparent Bmax tended to increase from 322 +/- 8 to 352 +/- 8 fmol/mg. The results show that treatment with caffeine in a dose that causes tolerance to several effects of caffeine and increases some effects of adenosine analogues increases the number of A1 receptors without any change in A1 mRNA, suggesting that the adaptive changes are at a post-translational level. There were no significant changes in A2 receptors indicating that the two types are regulated differently and/or that the amount of endogenous agonist is sufficient to regulate A1, but not A2 receptors.
Adenosine↗
Pharmacokinetics of peptichemio in myeloma patients: release of m-L-sarcolysin in vivo and in vitro.
Peptichemio (PTC) is a mixture of six synthetic oligopeptides, each of which contains the alkylating residue m-[di(2-chloroethyl)amino]-L-phenylalanine (L-mSL). The fate of PTC was investigated in eight patients with multiple myeloma after intravenous infusion of the drug. The quantitative analysis of the plasma samples was performed by liquid chromatography with fluorometric detection. L-mSL was rapidly released from the peptides and reached its maximal plasma concentration at the end of the infusion. Its median elimination half-life was 1.73 (range, 0.72-2.41) h. It was possible to follow the concentration of only one of the peptides, L-mSL-L-Arg(NO2)-L-Nval.OEt, during and shortly after the infusion of PTC. The stability of L-mSL and the peptides was studied in buffer solution (pH 7.3), plasma, and blood. The stability of some of the peptides was drastically decreased in blood, the degradation half-lives being only about 1 min. We conclude that L-mSL plays an important role in the mechanism of action of PTC.
Aged↗
Sequence analysis of selected regions of the env (V3 loop and gp41) and gag (p7) reading frames of Ethiopian human immunodeficiency virus type 1 strains.
Amplified polymerase chain reaction (PCR) products, corresponding to the V3 loop and gp41 of the env, and p7 of the gag region, from proviral DNA of several Ethiopian and Swedish HIV-1 strains were sequenced. Of the six amino acids (GPGRAF) that constitute the principal neutralizing determinant (PND) within the V3 loop, the Ethiopian isolates all showed two amino acid changes (GPGQTF). Four to five other substitutions were found in the amino acids flanking the PND. Substitution of alanine (A) for threonine (T) should result in a change in the predicted secondary structure, i.e., disappearance of a coil structure. Percentage similarity data on a stretch of 22 amino acids within the V3 loop showed a concordance of the Ethiopian HIV-1 isolates with the sequences of published macrophage-T-cell tropic HIV isolates. Additionally derived protein sequences in two other regions showed two common substitutions in p7 and one to two substitutions in gp41 compared to a recent consensus sequence. These changes are hitherto unique for the Ethiopian strains, and suggest the presence of a clustering of a divergent HIV-1 strain in Addis Ababa, Ethiopia.
Amino Acid Sequence↗
The neurotoxin-like sequence of human immunodeficiency virus gp120: a comparison of sequence data from patients with and without neurological symptoms.
A region of the human immunodeficiency virus type 1 (HIV-1) envelope glycoprotein gp 120 has been claimed previously to be homologous to parts of snake venom neurotoxins and rabies virus glycoprotein ("the neurotoxic loop"). We have determined DNA sequences directly from a polymerase chain reaction amplified fragment corresponding to this region of HIV-1 gp 120 and have translated these to protein sequences. This was performed with the prototype HIVSF2 isolate and several Swedish HIV-1 strains, which were precultivated from blood cells or cerebrospinal fluid (CSF) or were directly obtained from CSF cells of patients with and without neurological symptoms. The results show that there are sequence similarities between a short segment of gp120 of clinical HIV-1 strains and the neurotoxic loop. The strains of patients with neurological symptoms did not, however, show a genetic shift of their sequences towards a greater similarity to the sequences of snake venom neurotoxins and rabies virus glycoprotein as compared to the strains of asymptomatic individuals.
AIDS Dementia Complex↗