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Biomedical subjects

B Johansson

Publications and source records attributed to B Johansson.

At least 217 records · Page 12Linked to original sources
PubMed1998

Chromosomal abnormalities in secondary MDS and AML. Relationship to drugs and radiation with specific emphasis on the balanced rearrangements.

BACKGROUND AND OBJECTIVE: In therapy-related myelodysplasia (t-MDS) or acute myeloid leukemia (t-AML) balanced chromosome aberrations to bands 11q23 and 21q22 have been significantly related to previous chemotherapy with DNA topoisomerase II inhibitors. The purpose of the present study was to evaluate to what extent other balanced chromosome aberrations show the same association, and to evaluate a possible relationship to patient age and subgroups of drugs. DESIGN AND METHODS: All previously published cases of t-MDS and t-AML with any type of balanced aberration identified from Felix Mitelman's Catalog of Chromosome Aberrations in Cancer were analyzed for age and type of previous therapy, and the results were evaluated in univariate and multivariate analyses. RESULTS: A total of 422 cases were recorded, 328 had previously received well specified types of chemotherapy; 254 presented one out of five characteristic balanced aberrations, whereas 168 cases presented different uncharacteristic balanced aberrations. In univariate analysis cases with translocations to 11q23 had most often received DNA topoisomerase II inhibitors, whereas patients with the uncharacteristic balanced rearrangements most often had received alkylating agents (p < 0.00000001). Inv(16), t(15;17), and t(9;22) were likewise significantly associated with previous therapy with DNA topoisomerase II inhibitors and to almost the same extent as translocations to 21q22. Patients with translocations to 11q23 were significantly younger as compared to all other groups of patients. Translocations to 11q23 predominated following therapy with epipodophyllotoxins, whereas patients with translocations to 21q22, inv(16), t(15;17), and t(9;22) most often had received anthracyclines. In a multivariate analysis taking age into consideration, however, these drug-specific associations were no longer significant. INTERPRETATION AND CONCLUSIONS: Specific balanced chromosome aberrations in t-MDS and t-AML involving chromosome bands 11q23 and 21q22, inv(16), t(15;17), and t(9;22) are all significantly associated with previous therapy with DNA topoisomerase II inhibitors, as compared to the uncharacteristic balanced aberrations most commonly observed after therapy with alkylating agents. Younger age and not a specific type of DNA topoisomerase II inhibitor seems to predispose specifically to development of t-MDS and t-AML with translocations to chromosome band 11q23.

Acute Disease↗
PubMed1998

Fall injuries among elderly persons living at home.

Falls and their consequences are a major health problem for elderly people. The aim of this study is to describe and analyse registered fall injuries in people 65 years and older, living in their own homes, during one year. In a local health care district, injuries of such severity as to require the attention of a doctor were registered. A form designed according to the National Swedish Board of Health and Welfare classification for registration of accident injuries was used. The computer program Epiinfo was used for processing and analysis. One thousand six hundred and thirty-nine fall injuries among elderly people living at home were registered. The women accounted for 70%. The injuries occurred mostly at home or in the home area during daytime and in connection with daily routines. Fractures accounted for 46.4% of the injuries. Of the victims, 44.4% needed to make only one visit to a doctor. Additional visits and admission to hospital were more common among the women. The study reveals that most of those injured were women, and that the falls occurred during their daily routines. Registration of this kind tells nothing about the persons and the circumstances behind the accidents. In order to gain deeper knowledge, complementary investigations are necessary.

Accidental Falls↗
PubMed1997

Cytogenetic findings in metastases from colorectal cancer.

Eighteen tumor samples from 11 patients with metastatic colorectal cancer were cytogenetically analyzed after short-term culturing. Of the 13 metastases examined, 11 were from lymph nodes, 1 from the peritoneum and 1 from the lung. In 5 of the 11 patients, matched samples from the primary tumor and lymph node metastases were analyzed. Cytogenetic similarities between the primary and secondary lesions were found in all 5 cases, indicating that many of the chromosomal aberrations presumably occurred before disease spreading took place. Compared with the primaries, the metastases appeared to exhibit decreased clonal heterogeneity but, concurrently, an increase in the karyotypic complexity of individual clones. Among the aberrations recurrently found in metastatic lesions were del(1)(p34), i(17)(q10), -18, -Y, -21, +7 and +20, all of which have been seen repeatedly in previous series of primary colorectal carcinomas, and del(10)(q22) and add(16)(p13), which so far have not been associated with primary tumors and which may play a particular pathogenetic role in the metastatic process.

Adenocarcinoma↗
PubMed1997

A1 and A2A adenosine receptors and A1 mRNA in mouse brain: effect of long-term caffeine treatment.

The effect of oral treatment with caffeine, in doses that are known to produce marked adaptive effects, was investigated on A1 and A2A receptors in the mouse brain. Caffeine (0.1, 0.3 or 1 g/l) was added to the drinking water and the animals were sacrificed after a 14-day treatment period. Ligand binding to A1 receptors was studied, using quantitative autoradiography, with the agonist [3H]cyclohexyladenosine (CHA) and the antagonist [3H]1,3-dipropyl-8-cyclopentyl xanthine (DPCPX). Caffeine did not remain in the sections during the autoradiography experiments. Caffeine treatment (1 g/l, but not 0.1 or 0.3 g/l) tended to increase [3H]CHA binding to the CA3 subfield of the hippocampus, but in no other region studied. There was no change in the number of A1 receptors since [3H]DPCPX binding to the CA3, cerebral and cerebellar cortex was not influenced by caffeine treatment. There was similarly no change in the ability of CHA to displace [3H]DPCPX binding, suggesting that there are no major changes in the proportion of A1 receptors that are coupled to G-proteins. mRNA for the A1 receptor, measured by in situ hybridization, did not differ significantly between caffeine-treated and control mice in the structures examined. Thus, higher doses of caffeine can cause an increase in A1 agonist binding without a corresponding change in A1 mRNA or in A1 antagonist binding, suggesting that the adaptive changes seen upon prolonged caffeine treatment may be in sites different from A1 receptors. Caffeine (1 g/l) increased A2A receptors in the striatum measured as binding of the agonist [3H]CGS 21680 suggesting that up-regulation of A2A receptors may be an adaptive effect of caffeine intake.

Adenosine↗
PubMed1997

Chromosomal imbalance maps of malignant solid tumors: a cytogenetic survey of 3185 neoplasms.

To assess the distribution of gains and losses of genetic material in malignant solid neoplasms, 11 tumor types for which at least 100 short-term cultured cases with clonal chromosome aberrations had been reported in the literature were selected. The study was based on cytogenetic information from 508 breast carcinomas, 447 malignant neuroglial tumors, 435 kidney carcinomas, 333 colon carcinomas, 304 ovarian carcinomas, 303 lung carcinomas, 209 testicular germ cell tumors, 206 head and neck carcinomas, 172 malignant melanomas, 142 Wilms' tumors, and 126 neuroblastomas. In each case, the net imbalances were calculated for each chromosome band. The profiles of gains and losses revealed that all tumor types display unique combinations of imbalances. However, there is also considerable overlap among the profiles of the different diagnostic entities, indicating that similar molecular mechanisms may be operative in the development of many types of neoplasia. Deletions were more common than gains in all tumor types, with chromosomes X, Y, 4, 10, 13-15, 18, and 22 and chromosome segments 1p22-pter, 3p13-pter, 6q14-qter, 8p, 9p, and 11p being particularly often deleted in the majority of tumors. To better delineate critical lost segments, deletion profiles based only on structural rearrangements were made for chromosomes 1, 3-12, and 17, which all had on average at least four registered deletions per band. The relative distribution of losses indicated that different bands/regions are affected in different tumor types and that, often, several distinct candidate tumor suppressor gene loci can be discerned within the same chromosome arm, e.g., 1p12-13, 1p22, 1p34, and 1p36 on the short arm of chromosome 1 and 7q22, 7q32, and 7q36 on the long arm of chromosome 7. The only chromosomes or chromosome segments more often gained than deleted were chromosomes 7 and 20 and the long arms of chromosomes 1 and 12, suggesting the presence there of dominantly acting growth-regulatory genes. The data presented in this study should be valuable as a guide for molecular genetic studies on allelic imbalances and for the interpretation of results from studies using comparative genomic hybridization.

Breast Neoplasms↗
PubMed1997

Substantial genetic influence on cognitive abilities in twins 80 or more years old.

General and specific cognitive abilities were studied in intact Swedish same-sex twin pairs 80 or more years old for whom neither twin had major cognitive, sensory, or motor impairment. Resemblance for 110 identical twin pairs significantly exceeded resemblance for 130 fraternal same-sex twin pairs for all abilities. Maximum-likelihood model-fitting estimates of heritability were 62 percent for general cognitive ability, 55 percent for verbal ability, 32 percent for spatial ability, 62 percent for speed of processing, and 52 percent for memory. There was also evidence for the significant influence of idiosyncratic experience as the environmental component that most determines individual differences in cognitive abilities late in life.

Aged↗
PubMed1997

Impact of autonomic neuropathy on circulatory instability during liver transplantation for familial amyloidotic polyneuropathy.

BACKGROUND: Circulatory instability with severe hypotension frequently complicates liver transplantation in patients with familial amyloidotic polyneuropathy. Autonomic dysfunction is found early in the course of the disease by analysis of beat-to-beat heart rate variability (HRV). The aim of the present study was to investigate the impact of autonomic neuropathy on intraoperative circulatory instability during liver transplantation for familial amyloidotic polyneuropathy. METHODS: Twenty-two patients were evaluated at the Department of Medicine, Umea University Hospital, by spectral analysis of HRV and later received liver transplants at Huddinge University Hospital. The low-and high-frequency bands obtained by spectral analysis of HRV in the supine and upright positions, respectively, were used as representative of sympathetic and parasympathetic activity. Circulatory instability during transplantation was defined as a fall in systolic arterial blood pressure below 70 mmHg for more than 5 min during the preanhepatic phase. RESULTS: Both arrhythmia preventing spectral analysis of HRV and a sympathetic variability peak below 2.5 mHz2 were significantly more common among patients with intraoperative circulatory instability (P=0.03 and 0. 004, respectively). A diminished increase in pulse rate when tilting the patients from the supine to the upright position was also more pronounced among patients with circulatory instability (P<0.05). CONCLUSIONS: The majority of patients who will develop circulatory instability with a pronounced fall in arterial blood pressure can be identified by Poincare plots of R-R intervals and spectral analysis of HRV. A low sympathetic peak or arrhythmia precluding spectral analysis of HRV is significantly related to operative circulatory instability.

Amyloid Neuropathies↗
PubMed1997

Intermediate filament proteins in adult human arteries.

BACKGROUND: The cytoskeleton of cells in blood vessel walls contains desmin, vimentin, and cytokeratins. The distribution of these proteins in human vessels is not fully known. We have mapped the distribution of intermediate filament proteins in human arterial walls. METHODS: Monoclonal antibodies targeted at the intermediate filament proteins desmin, vimentin, and cytokeratins were used, and the distribution of these proteins was studied by immunohistochemistry. RESULTS: In the muscular arteries, most smooth muscle cells in the media expressed both desmin and vimentin; in the elastic arteries, the proportion of desmin-labelled cells was lower and preferentially located to the periphery of the media. In general, the desmin immunoreactivity within the intima was weak, but some smooth muscle cells and smooth muscle cells in the musculoelastic layer showed strong immunoreactivity. The vasa vasorum exhibited a heterogeneous desmin-labelling pattern. The vimentin antibodies labelled the endothelium and showed a heterogeneous staining pattern in the other layers of the arterial wall. Cytokeratin was detected in occasional cells in the media of muscular arteries, in many adluminal cells and cell clusters in the coronary intima, and in smooth muscle cells in the media of the elastic arteries. CONCLUSIONS: Vimentin is widely distributed in vascular smooth muscle cells, whereas the distribution of desmin and cytokeratin varies. Each artery studied had an intermediate filament pattern typical for the anatomical location. There were no interindividual variations in the distribution of intermediate filament proteins.

Adult↗
PubMed1997

Deletions of CDKN1B and ETV6 in acute myeloid leukemia and myelodysplastic syndromes without cytogenetic evidence of 12p abnormalities.

Seventy-nine acute myeloid leukemias (AML) and myelodysplastic syndromes without cytogenetic evidence of 12p aberrations were investigated by fluorescence in situ hybridization with probes for ETV6 and CDKN1B (previously called TEL and KIP1, respectively) to ascertain whether abnormalities of these genes are frequently undetected by standard chromosome banding analyses and, if so, whether they are associated with specific karyotypic patterns and morphologic features. One of sixty cytogenetically aberrant myeloid malignancies, an AML with a complex karyotype including del(5q) and del(20q), showed a hemizygous interstitial deletion of the ETV6 and CDKN1B loci. No concomitant rearrangement of the other ETV6 allele was detected. Two of nineteen cytogenetically normal AML displayed a hemizygous interstitial deletion involving CDKN1B, but not ETV6. Thus, cryptic deletions of these genes seem to be rare in cytogenetically abnormal myeloid malignancies without 12p aberrations (2%), whereas they may be more frequent in karyotypically normal AML (10%). Furthermore, the present findings show that the deletions may be narrow, not including the ETV6 gene, and indirectly suggest that CDKN1B, or a closely located genomic segment, is the target of 12p deletions.

Acute Disease↗
PubMed1997

Comparative genomic hybridization reveals frequent gains of 20q, 8q, 11q, 12p, and 17q, and losses of 18q, 9p, and 15q in pancreatic cancer.

Comparative genomic hybridization (CGH) was used to screen for genomic imbalances in 24 exocrine pancreatic carcinomas, including II low-passage cell lines (4-8 subcultures) and 13 uncultured samples. Aberrations were found in all cell lines and in seven of the 13 biopsies. The most frequent changes in the cell lines were gains of 20q (91%), 11q (64%), 17q (64%), 19q (64%), 8q, 12p, 14q, and 20p (55%), and losses of 18q (100%), 9p (91%), 15q(73%), 21q (64%), 3p (55%), and 13q (55%). High-levels gains (tumor to normal ratio over 1.5) were detected at 3q, 6p, 7q, 8q, 12p, 19q, and 20q. Among the tumor biopsies, overrepresentations of 7p and 8q were most common (31%), followed by 5p, 5q, 11p, 11q, 12p, and 18q (23%), whereas the most frequent losses involved 18p and 18q (31%) and 6q and 17p (23%). The genetic changes in nine samples obtained from metastatic lesions did not differ significantly from those in 15 primary carcinomas. Most of the gains and losses detected in this CGH study correspond well to those identified in previous cytogenetic and molecular genetic investigations of pancreatic carcinomas. However, frequent gain of 12p and loss of 15q have not been previously reported. Molecular genetic analyses of these chromosome arms are warranted, and may lead to the discovery of novel genes important in pancreatic carcinogenesis.

Aged↗
PubMed1997

Early cognitive markers of the incidence of dementia and mortality: a longitudinal population-based study of the oldest old.

This study examines whether cognitive markers at prior examinations are indicative of subsequent dementia and mortality. The sample was composed of subjects aged 84-90 at baseline who were reexamined three times over a 6-year period on a comprehensive biobehavioral battery. Dementia was evaluated at each examination using DSM-III-R criteria. Results indicated that incident cases of dementia had lower cognitive scores both 2 and 4 years prior to diagnosis, compared to non-demented survivors. Evidence for terminal decline was also found, as people who subsequently died also had lower cognitive performance at prior examinations, compared to non-demented survivors. The findings suggest that mild cognitive dysfunction is an important clinical finding among the oldest old and may herald either the onset of dementia or mortality.

Aged↗
PubMed1997

Prevalence of diabetic retinopathy in children and adolescents with IDDM. A population-based multicentre study.

Vision-threatening diabetic retinopathy can be prevented if it is diagnosed before becoming too advanced. Since diabetic retinopathy has been reported to occur only rarely before the end of pubertal development, children and adolescents are seldom included in screening programmes. We invited 780 children and adolescents with insulin-dependent diabetes mellitus diagnosed before the age of 15.0 years (disease duration of < 12 years) and who were older than 9.0 years at the time of examination from eight regions of Sweden. Retinal examination was performed with stereoscopic fundus photograph. The photograph were rated according to a modified Airlie House classification. The dropouts (223/780, 28.6%) were significantly older and with a longer duration of diabetes than the examined children (p < 0.001 and 0.001, respectively). Photographs from 557 patients aged (median [interquartile range]:14.6 [12.4-17.0]) years and with a diabetes duration of 8.0 (5.5-9.9) years were evaluated. Retinopathy was demonstrated in 81 patients (14.5%):66 with background retinopathy, 2 with microaneurysms and hard exudates, 12 with preproliferative retinopathy, 1 with proliferative retinopathy. Preproliferative retinopathy was diagnosed in a 12.8-year-old girl in pubertal stage 3 and an 11.8-year-old boy in pubertal stage 2, and proliferative retinopathy was found in a 21.5-year-old girl. Retinopathy was demonstrated in 6% and 18% of patients in pubertal stages 1 and 5, respectively. The overall prevalence of retinopathy in this population may even be higher since the dropouts were older and had a longer duration of diabetes. Since background and preproliferative retinopathy were found in children before puberty, we recommend including children and adolescents in screening programmes for diabetic retinopathy from the age of 10 years.

Adolescent↗
PubMed1997

Clonal CD5-positive B lymphocytes in myelodysplastic syndrome with systemic vasculitis and trisomy 8.

Bone marrow and peripheral blood from a myelodysplastic syndrome (MDS) patient with trisomy 8 and associated systemic vasculitis was investigated for clonal lymphoid lineage involvement using simultaneous metaphase and interphase fluorescence in situ hybridization (FISH) and immunocytochemistry with antibodies against CD13 (granulocytic), glycophorin A (GPA, erythroid), and the lymphocytic antigens CD3. CD5, CD20, and CD22. Trisomy 8 was detected in 55% of CD13+, 40% of GPA+, 6% of CD5+, and 5% of CD20/22+, but not in CD3+ cells. In a complementary experiment using interphase FISH on bone marrow cells sorted by flow cytometry, 13% of CD5/CD19 double-positive cells (76% purity) were found to be trisomic. The results indicate the existence of a small CD5-positive B-lymphoid clone as part of the MDS process in this patient. Since CD5/19-positive cells have been proposed to be autoantibody producing, this finding might be a clue to the pathogenesis underlying the propensity for MDS patients to develop immune-mediated complications.

B-Lymphocytes↗
PubMed1997

Human papillomavirus findings in relation to cervical intraepithelial neoplasia grade: a study on 476 Stockholm women, using PCR for detection and typing of HPV.

Among human papillomavirus (HPV) types found in humans, there is a strong association between HPV 16, 18, 31, and 33, and cervical cancer. The relationship between various grades of dysplasia and HPV type is less clear. To elucidate this point, the authors tested 476 cytological and histological samples from cervix with polymerase chain reaction (PCR) for HPV using consensus primer My 09-11 and type-specific primers. All cases were divided into groups on the basis of cytology: "normal cases" (ie, women with other disease than cervical intraepithelial neoplasia [CIN]), and CIN I, II, and III. Out of the "normal cases," in which women with a previous history of condyloma and dysplasia were included, 69% had HPV with type 6 as the most common one. Of all CIN I cases, 71% were HPV positive, and HPV type 6 and 16 were equally common. In CIN II cases, HPV 16 was the most common type, whereas HPV 6 accounted for only 7.5% of cases in this group as single virus type. HPV 16 was also the most common type in the CIN III group, followed by type 33. Double and even multiple infections occurred in all groups.

Adolescent↗
PubMed1997

Clinical significance of cytogenetic findings in solid tumors.

Chromosome analysis of solid tumors is becoming an increasingly useful tool to help establish a correct diagnosis and to provide prognostically important information. Characteristic karyotypic patterns in terms of degree of cytogenetic complexity and type of nonrandom abnormalities may help to distinguish neoplasia from a nonneoplastic lesion and to differentiate between a benign and a malignant tumor. More importantly, the presence of a specific or pathognomonic change may confirm or refute a suspected diagnosis, provide an alternative, unsuspected diagnosis, and trace the origin of a metastasis. Presently, specific cytogenetic abnormalities may be of substantial, and sometimes decisive, help in four groups of differential diagnostic dilemmas: (1) Benign vs. malignant epithelial tumors of the kidney, thyroid gland, salivary glands, and ovary; (2) Benign vs. malignant mesenchymal tumors of adipose and muscle tissue; (3) Differentiation between various malignant bone and soft tissue tumors: and (4) Diagnosis of undifferentiated small-cell round-cell tumors. In addition to the diagnostic value, karyotypic findings may provide prognostic information. Thus, the presence of an abnormal clone and/or complex rearrangements is a poor prognostic sign in, e.g., carcinomas of the ovary, prostate, bladder, colon, and pancreas. Furthermore, characteristic cytogenetic aberrations are now known to be valuable prognostic parameters in malignant melanoma, malignant fibrous histiocytoma, germ cell tumors, neuroblastoma, and squamous cell carcinoma of the head and neck region. Many of the correlation analyses are preliminary, but they all point in the same direction, namely that cytogenetic studies will soon play the same essential role in the management of patients with solid tumors as they do today in hematologic oncology.

Chromosome Aberrations↗