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Biomedical subjects

G Wallin

Publications and source records attributed to G Wallin.

At least 55 records · Page 3Linked to original sources
PubMed1997

[Rehabilitation of discharged patients is beneficial. Medical and economical analysis].

Even after the Swedish "Adel"-reform in 1992, large Swedish emergency hospitals still have many "bed-blockers" waiting to be discharged for further care by the social services. In Malmö a special ward, run by the social services, was created in 1994 for the purpose of treating, rehabilitating and planning the discharge of "bed-blockers" from the university hospital. The "bed-blockers" treated at this ward during an 18 month period (patient group, n = 223) were compared with a control group of "bed-blockers" (n = 285) who were not admitted to this ward. Although the patients in the patient group seemed to be more sick and handicapped than those in the control group, emergency in-hospital care during a follow-up period of one year was four times greater in the control group than in the patient group. Economic analysis showed that rehabilitation of the patient group was cheap and effective. The study has shown that municipal care of "bed-blockers" needs to be improved and better organised.

Activities of Daily Living↗
PubMed1996

Deletions of the long arm of chromosome 10 in progression of follicular thyroid tumors.

Previous studies of follicular thyroid tumors have shown loss of heterozygosity (LOH) on the short arm of chromosome 3 in carcinomas, and on chromosome 10 in atypical adenomas and carcinomas, but not in common adenomas. We studied LOH on these chromosomal arms in 15 follicular thyroid carcinomas, 19 atypical follicular adenomas and 6 anaplastic (undifferentiated) carcinomas. Deletion mapping of chromosome 10 using 15 polymorphic markers showed that 15 (37.5%) of the tumors displayed LOH somewhere along the long arm. Thirteen of these tumors showed deletions involving the telomeric part of chromosome 10q, distal to D10S187. LOH on chromosome 3p was found in 8 (20%) cases. Seven of these also showed LOH on chromosome 10q. In eight cases LOH was seen on chromosome 10q but not 3p. In comparison, the retinoblastoma gene locus at chromosome 13q showed LOH in 22% of the tumors. Most of these also had deletions on chromosome 10q. The results indicate that a region at the telomeric part of 1Oq may be involved in progression of follicular thyroid tumors.

Adenocarcinoma, Follicular↗
PubMed1996

Stromal fibroblasts adjacent to invasive thyroid tumors: expression of gelatinase A but not stromelysin 3 mRNA.

Thyroid tumors vary widely in biologic behavior, they range from benign adenomas to rapidly growing anaplastic carcinomas. Among thyroid neoplasms, the follicular tumor is especially suited as a model for studies of tumor cell invasion; the distinction between adenomas and carcinomas relies mainly on the presence of capsular and vascular invasion. Matrix metalloproteinases play an important role in tumor cell invasion, as they are able to degrade basement membrane and extracellular matrix components. Twenty-nine thyroid tumors of varying type and aggressiveness were selected for analysis of relative molecular weight 72,000-dalton type IV collagenase (gelatinase A) expression by mRNA in situ hybridization. Strong gelatinase A mRNA expression was seen in 10 of 14 follicular carcinomas, in none of six follicular adenomas, in all four anaplastic carcinomas, and in four of five papillary carcinomas. The expression was restricted to fibroblasts in the stroma adjacent or close to invading tumor cells. Twelve of the tumors were also investigated for expression of stromelysin 3 mRNA, no expression of which was detected in any tumor. The findings suggest that gelatinase A contributes to the invasive process and spread of aggressive thyroid tumors.

Adenocarcinoma↗
PubMed1996

EGF-receptors in human normal and pathological thyroid tissue.

Expression of the epidermal growth factor receptor (EGFR) was studied in cryosections from human thyroid tissues. Normal tissue (4 cases), nodular goitre (12), toxic goitre (9), adenoma (9), follicular carcinoma (1), papillary carcinoma (7) and poorly differentiated carcinoma (1) were used for immunohistochemistry. Northern blot analysis was performed in two nodular goitres, three adenomas, two papillary carcinomas, one follicular carcinoma and the adjacent normal tissue in five cases as well as in two cell lines from anaplastic carcinomas. Epidermal growth factor receptor immunoreactivity was detected in all tissues examined. The amount of EGFR mRNA did not differ between normal and abnormal tissues. However, the EGFR staining was weaker in normal thyroid tissue compared to the adjacent neoplastic areas suggesting an upregulation at the posttranslational level in the latter. A strong staining was also seen in hyperfunctioning thyroid glands. The EGFR location was mainly basal or basolateral in all thyroid tissues with normal histology and in toxic diffuse goitre. Pericellular and sometimes cytoplasmatic staining was seen in neoplastic tissues. In nodular goitre the staining was both basal, lateral and apical and varied in intensity. Our data suggest that a non-polarized location of EGFR probably indicates a loss of the normal epithelial cell polarity and could be interpreted as an early sign of dedifferentiation. Furthermore, a role for the EGFR is proposed, not only in the development of thyroid neoplasias but also in goitre formation.

Adenocarcinoma, Follicular↗
PubMed1996

Alterations of p53 and expression of WAF1/p21 in human thyroid tumors.

We have investigated p53 expression in 178 thyroid tumors from 162 patients by immunohistochemistry using two antibodies, DO1 and CM1. In addition, 35 tumors were analyzed for expression of WAF1/p21, one of the downstream mediators of p53. Only 15 tumors (8.4%) had greater than 10% of tumor cell nuclei positively stained for p53. Six of 14 Hürthle tumors and three of 34 papillary thyroid carcinomas showed staining of p53 in the cytoplasm. A total of 40 tumors, including all p53 positive tumors, and all anaplastic and poorly differentiated tumors were screened for mutations in exons 5-8 of the TP53 gene by constant denaturing gel electrophoresis and subsequent sequence analysis. A mutation was detected in five tumors only: one anaplastic carcinoma, one poorly differentiated follicular carcinoma (negative by p53 immunohistochemistry), one atypical follicular adenoma, and two papillary thyroid carcinoma metastases, of which the primary tumors had no detectable mutation. We conclude that p53 immunohistochemistry cannot be used for diagnostic and prognostic purposes in thyroid tumors. The tumors with TP53 mutation showed a markedly reduced WAF1/p21 expression. Three anaplastic carcinomas with highly expressed p53, but with no detectable mutation, also showed high expression of WAF1/p21. This may be explained by overexpression of wild-type p53, possibly due to the patients' preoperative treatment, including external radiation of the neck region. The results indicate that WAF1/p21 immunohistochemistry contributes to the information of the functional status of p53, and may facilitate the interpretation of results from p53 immunohistochemistry in these tumors.

Base Sequence↗
PubMed1996

Graves' hyperthyroidism: treatment with antithyroid drugs, surgery, or radioiodine--a prospective, randomized study. Thyroid Study Group.

To analyze the benefits and risks of three common treatments, we randomly assigned 179 patients with Graves' hyperthyroidism as follows: 60 patients, 20-34 yr of age (young adults), received antithyroid drugs for 18 months (medical) or subtotal thyroidectomy (surgical), and 119 patients, 35-55 yr of age (old adults), received medical, surgical, or radioiodine (iodine-131) treatment. The follow-up time was at least 48 months. Antithyroid drugs, surgery, or iodine-131 treatment normalized the mean serum hormone levels within 6 weeks. The risk of relapse was highest in the medically treated young and old adults (42% vs. 34%), followed by that in those treated with iodine-131 (21%) and that in the surgically treated young and old adults (3% vs 8%), respectively. Elevated TSH receptor antibodies at the end of medical therapy or increasing TSH receptor antibodies values after medical or surgical treatment increased the probability of relapse. Development or worsening of ophthalmopathy was not associated with relapse per se. Ninety percent of the subjects in all groups were satisfied with the treatment they received. No significant difference in sick-leave due to Graves' or other diseases was seen during the first 2 yr after initiation of therapy. The increased risk of ophthalmopathy in patients with high serum T3 levels, especially when treated with iodine-131, and the relatively high frequency of relapse after treatment with antithyroid drugs are important factors to consider when selecting therapy for Graves' disease.

Absenteeism↗
PubMed1995

Loss of neurofibromatosis type I (NF1) gene expression in pheochromocytomas from patients without NF1.

The neurofibromatosis type 1 (NF1) gene encodes a tumor-suppressor protein termed neurofibromin, which, in adults, is expressed predominantly in neurons, Schwann cells, and the adrenal medulla. Loss of NF1 gene expression has been reported in Schwann cell tumors (neurofibrosarcomas) from patients with NF1 as well as in malignant melanomas and neuroblastomas from patients without NF1. Previously, we demonstrated the lack of neurofibromin expression in six pheochromocytomas from patients with NF1, supporting the idea that neurofibromin might be an essential regulator of cell growth in these cells. To determine whether NF1 gene expression is similarly altered in pheochromocytomas from patients without NF1, we examined 20 pheochromocytomas for the presence of NF1 RNA and neurofibromin by reverse-transcribed polymerase chain reaction (RT-PCR) and immunohistochemistry, respectively. Reduced or absent NF1 gene expression was documented in 7 of these 20 tumors (35%) including 1 of 4 sporadic tumors, 3 of 10 tumors from patients with multiple endocrine neoplasia (MEN) 2A, 2 of 4 tumors from patients with MEN2B, and 1 of 2 tumors from patients with von Hippel-Lindau syndrome. In addition, most of these tumors expressed predominantly the type 1 NF1 isoform (75% type 1 NF1 isoform expression) as opposed to other neural crest-derived tissues such as adrenal gland and Schwann cells, which express predominantly type 2 NF1. This type 1 isoform predominance was also observed in the rat pheochromocytoma PC12 cell line, suggesting that this change in isoform expression may be associated with the genesis of these tumors.(ABSTRACT TRUNCATED AT 250 WORDS)

Base Sequence↗
PubMed1995

Allelotyping of follicular thyroid tumors.

To elucidate further the genetic mechanisms for follicular thyroid tumor development and progression, we allelotyped follicular thyroid tumors and other thyroid lesions from 92 patients. In general, a low frequency of loss of heterozygosity (LOH) was found, the highest being for chromosomes 3q, 10q, 11p, 11q, 13q, and 22q (10%-15%). However, detailed study of LOH of these chromosome arms with regard to the different histopathological diagnoses indicates that a locus on chromosome 10q may be involved in follicular thyroid tumor progression. In addition, the majority of Hürthle cell adenomas showed LOH on either chromosome 3q or 18q, in contrast to the other tumor types. This discrepancy in genetic alterations may contribute to the divergent clinical features occurring in these tumors.

Adenocarcinoma, Follicular↗
PubMed1995

Autonomic and thermal sensory symptoms and dysfunction after stroke.

BACKGROUND AND PURPOSE: Symptoms interpreted as unilateral disturbances of autonomic function, such as coldness, dryness, sweating, and trophic changes, are well known but incompletely understood clinical problems after stroke. The present study provides data related to the incidence and mechanisms behind such symptoms. METHODS: Temperature perception thresholds, skin temperatures, evaporation rates, and skin blood flow responses were measured bilaterally in 37 stroke patients aged 58 +/- 13 years (mean +/- SD) and in a control group of 15 patients aged 64 +/- 15 years with a single transient ischemic attack. RESULTS: Of the 37 stroke patients, 43% reported a sensation of coldness in the contralesional side of the body. Basal skin blood flow and temperature were relatively lower in the contralesional side. There was an excess of evaporation in the contralesional side after brain stem lesions and in the ipsilesional side after hemispheric lesions. Vasomotor reflex asymmetries occurred in 34% of the patients and were due to weak vasodilator or vasoconstrictor reflexes in the ipsilesional side. These abnormalities correlated significantly to sensations of unilateral coldness, hypalgesia, and thermohypesthesia in the contralesional side and anatomically to lesions in spinothalamo-cortical pathways. CONCLUSIONS: Focal central nervous system lesions due to stroke may result in symptoms and measurable evidence of unilateral disturbance of skin sympathetic function. Vasomotor asymmetries are probably due to lesions of vasomotor pathways descending uncrossed. Subjective coldness may be due to disturbed central processing.

Aged↗
PubMed1995

Mutations of codon 918 in the RET proto-oncogene correlate to poor prognosis in sporadic medullary thyroid carcinomas.

The hereditary multiple endocrine neoplasia syndromes types 2A and B (MEN 2A and B) were recently linked to germline mutations in the RET proto-oncogene, altering one of five cysteine residues in exon 10 or 11 (MEN 2A), or substituting a methionine for a threonine at codon 918 in exon 16 (MEN 2B). The latter mutation also occurs somatically in some sporadic medullary thyroid carcinomas (MTC), and has in a previous study been correlated with a less favorable clinical outcome. In the present study, 46 MTCs were selected for investigation of the codon 918 mutation. The mutation was found in 29 tumors (63%), and was significantly correlated with a poor outcome, with regard to distant metastasis or tumor recurrence (p < 10(-4)). Two tumors showed multifocal growth and C-cell hyperplasia, and these patients were therefore also investigated for germline mutations in exons 10, 11 and 16. The codon 918 mutation was found only in the tumors, thus of somatic origin. The RET codon 918 mutation may have prognostic impact, and therefore preoperative assessment may influence decision-making in the treatment of patients suffering from MTC.

Base Sequence↗
PubMed1994

Combined doxorubicin, hyperfractionated radiotherapy, and surgery in anaplastic thyroid carcinoma. Report on two protocols. The Swedish Anaplastic Thyroid Cancer Group.

BACKGROUND: Anaplastic carcinoma of the thyroid (ACT) rarely can be cured, but every effort should be made to improve prognosis and, above all, prevent death due to suffocation or large local tumor ulceration. METHODS: From 1984 to 1992, 33 consecutive patients with ACT were treated prospectively according to a combined treatment program consisting of hyperfractionated radiotherapy, doxorubicin, and debulking surgery. Preoperative radiotherapy was administered to a target dose of 30 Gy and postoperatively to a total dose of 46 Gy. Radiotherapy was performed 5 days a week. The daily fraction was 1.0 Gy x 2 until 1988, after which it was 1.3 Gy x 2. Otherwise, the therapy remained unchanged. Twenty milligrams of doxorubicin were administered intravenously per week. Debulking surgery was possible in 23 patients (70%). RESULTS: No patient failed to complete the protocol because of toxicity. There were no signs of local recurrence in 16 patients (48%). In only eight patients (24%) was death attributed to local failure. In four patients, survival with no evidence of disease exceeded 2 years. Improvement in local tumor control was marginally significant (P = 0.08) in the 17 patients treated in the latter part of the study, with no sign of local disease in 11 patients and deaths due to local failure in only 2 patients. The improved local control could not be attributed to any differences between the two series. CONCLUSION: Combination modality treatment of ACT is feasible and effective despite the patients' advanced age and locally advanced disease. There was a tendency for local control to be improved after accelerated radiotherapy.

Aged↗
PubMed1994

Technetium-99m methoxyisobutylisonitrile localizes an ectopic ACTH-producing tumour: case report and review of the literature.

Extensive investigation including whole-body examinations with computed tomography and magnetic resonance imaging did not detect the suspected ectopic ACTH-producing tumour in a patient with advanced Cushing's syndrome and hypokalemic alkalosis. Gamma camera examination with technetium-99m methoxyisobutylisonitrile (MIBI) depicted the tumour, which was localized in the anterior neck and mediastinum. This was later verified by surgery. 99mTc-MIBI is normally used for myocardial scintigraphy. Its accumulation is unspecific and merely reflects metabolic activity. Despite this, the present case shows that examination with this agent can provide important information with regard to tumour localization in a given situation, thereby serving as a complement to other imaging modalities. The current literature on 99mTc-MIBI for tumour diagnosis is reviewed.

ACTH Syndrome, Ectopic↗
PubMed1994

Somatic and MEN 2A de novo mutations identified in the RET proto-oncogene by screening of sporadic MTC:s.

Since germline mutations in the RET proto-oncogene (RET) predisposing to tumor development in Familial Medullary Thyroid Carcinoma (FMTC), Multiple endocrine neoplasia type 2A (MEN 2A), and Multiple endocrine neoplasia type 2B (MEN 2B) were reported, it has become possible to identify gene carriers with a very high degree of accuracy. Mutations in FMTC and MEN 2A exclusively affect cysteine residues in exon 10 and 11 of RET, whereas in MEN 2B codon 918 in exon 16 is involved. This latter mutation has also been described in a subset of apparently sporadic medullary thyroid carcinomas (MTC). Mutations in MEN 2B often occur as de novo germline mutations, whereas de novo mutations have not yet been described in FMTC or MEN 2A. We analyzed ten MTC:s and ten pheochromocytomas, all clinically judged to be sporadically occurring, by direct DNA sequencing of exons 10, 11, and 16 of RET. This analysis revealed a de novo germline mutation of codon 634 in exon 11 in a patient with MTC. In addition, somatic mutations of codon 918 in exon 16 in six of the remaining MTC:s were found. Interestingly, the presence of this somatic mutation was associated with a significantly less favorable clinical outcome.

Adult↗
PubMed1994

Expression of thyrotropin receptor and thyroid hormone receptor messenger ribonucleic acid in normal, hyperplastic, and neoplastic human thyroid tissue.

In the first part of this study, we examined TSH receptor (TSHR) and thyroid hormone receptor (T3R beta) messenger ribonucleic acid (mRNA) levels in normal, hyperplastic, and neoplastic human thyroid tissue. Tumor specimens from patients with different thyroid carcinomas and thyroid adenomas, and tissues from patients with Graves' disease and from normal thyroid glands were analyzed by solution hybridization and Northern blot using complementary RNA probes. In the second part of the study, mRNA analysis of T3R was extended to include the expression levels of each of the four T3R isoforms alpha 1, alpha 2, beta 1, and beta 2. In neoplastic thyroid tissue such as papillary and follicular carcinomas, the expression of both TSHR and T3R beta mRNA per microgram total RNA was significantly lower than that in normal thyroid tissue. The decrease in T3R beta mRNA was shown to represent a specific and significant decrease in T3R beta 2 mRNA levels in particular, but also in the expression levels of T3R beta 1 mRNA. No differences were found in the expression levels of T3R alpha 1 or -alpha 2 mRNA. Furthermore, no differences in TSHR or T3R mRNA levels were found in thyroid tissue from patients with Graves' disease compared to normal thyroid tissue. It is concluded that the reduction of TSHR and T3R mRNA in specific neoplastic thyroid tissues might be associated with the differentiation state of these tumors and that the decrease in T3R mRNA levels is due to a specific decrease in the expression levels of the T3R beta gene.

Adenocarcinoma, Follicular↗