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| 2. |
- Löfberg, H, et al.
(författare)
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gamma-trace in human pituitary adenomas
- 1984
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Ingår i: The Journal of clinical endocrinology and metabolism. - : The Endocrine Society. - 0021-972X .- 1945-7197. ; 59:1, s. 8-113
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Tidskriftsartikel (refereegranskat)abstract
- gamma-Trace, a small protein occurring in body fluids and in secretory and neuroendocrine cells, was demonstrated by immunohistochemical techniques in the cytoplasm of the tumor cells of 13 pituitary adenomas obtained at surgery and autopsy. Seven of the adenomas also contained LH immunoreactivity. FSH, TSH, and ACTH were each found in one gamma-trace-containing adenoma. gamma-Trace was also demonstrated in extracts of 1 pituitary adenoma and of 5 nontumorous adenohypophyses. The immunoreactive protein found in the extracts had a molecular weight and electrophoretic mobility characteristic of gamma-trace. Computerized amino acid sequence comparisons between the primary structure of gamma-trace and those of known hormonal peptides showed no significant similarities.
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| 3. |
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| 4. |
- Olsson, H., et al.
(författare)
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Relation between tumour size and plasma prolactin levels in premenopausal patients with breast carcinoma : A preliminary report
- 1985
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Ingår i: Acta Radiologica: Oncology. - : Informa UK Limited. - 0349-652X. ; 24:1, s. 57-59
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Tidskriftsartikel (refereegranskat)abstract
- In thirty-one premenopausal patients with carcinoma of the breast the plasma prolactin was measured after mastectomy. A highly significant correlation between tumour size and plasma prolactin levels (p<0.002) was observed after adjustment for age at diagnosis and parity. At the time of the prolactin determination no clinical signs of metastatic disease were evident, suggesting that the prolactinc levels were unrelated to the tumour burden.
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| 5. |
- Olsson, H., et al.
(författare)
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Retrospective assessment of menstrual cycle length in patients with breast cancer, in patients with benign breast disease, and in women without breast disease
- 1983
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Ingår i: Journal of the National Cancer Institute. - : Oxford University Press (OUP). - 0027-8874 .- 1460-2105. ; 70:1, s. 17-20
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Tidskriftsartikel (refereegranskat)abstract
- The length of the menstrual cycle was compared in women with breast cancer, women with benign breast disease, and controls. Older women in general tended to report shorter menstrual cycles (P < 0.05). After correction for the age difference, breast cancer patients still reported a shorter average menstrual cycle length than benign breast disease patients and controls (P < 0.006). Very short cycles (≤21 days) were present in 20% of the breast cancer patients compared to 8% of the patients with benign breast disease and 4% of the controls (P < 0.0001). Long cycles (≥30 days) were not a feature of breast cancer patients (2%), whereas 20% of the patients with benign breast disease and 28% of the controls reported such long cycles (P < 0.0001). Irregular menstrual cycles were more common in benign breast disease patients (20%) than in cancer patients (10%) and controls (8%) (P < 0.001).
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| 7. |
- Agardh, Carl-David, et al.
(författare)
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Hypoglycemic brain injury. I. Metabolic and light microscopic findings in rat cerebral cortex during profound insulin-induced hypoglycemia and in the recovery period following glucose administration
- 1980
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Ingår i: Acta Neuropathologica. - 1432-0533. ; 50:1, s. 31-41
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Tidskriftsartikel (refereegranskat)abstract
- Profound hypoglycemia causing the disappearance of spontaneous EEG activity was induced by insulin in rats. For analysis of cerebral cortical concentrations of labile phosphates, glycolytic metabolites and amino acids, the brain was frozen in situ. For microscopic analysis of the corresponding cerebral cortical areas the brain was fixed by perfusion. Hypoglycemia with an isoelectric EEG for 30 and 60 min caused severe perturbation of the cerebral energy metabolites. After both 30 and 60 min of isoelectric EEG, two microscopically different types of nerve cell injury were seen. Type I injury was characterized by angulated, darkly stained neurons with perineuronal vacuolation, mainly affecting small neurons in cortical layer 3. Type II injured neurons, mainly larger ones in layers 5–6, were slightly swollen with vacuolation or clearing (depending on the histotechnique used) of the peripheral cytoplasm, but had no nuclear changes. Recovery was induced by glucose injection. Improvement in the cerebral energy state occurred during the 30 min recovery period even after 60 min of hypoglycemia. However, the persisting reduction in the size of adenine nucleotide and amino acid pools after 30 or 180 min recovery suggested that some cells remained damaged. In confirmation many type I injured neurons persisted during the recovery suggesting an irreversible injury. The disappearance of virtually all type II injuries indicated reversibility of these histopathological changes. The microscopic changes in hypoglycemia were different from those in anoxia-ischemia suggesting a dissimilar pathogenesis in these states despite the common final pathway of energy failure.
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| 8. |
- Agardh, Carl-David, et al.
(författare)
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Hypoglycemic brain injury: metabolic and structural findings in rat cerebellar cortex during profound insulin-induced hypoglycemia and in the recovery period following glucose administration
- 1981
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Ingår i: Journal of Cerebral Blood Flow and Metabolism. - 1559-7016. ; 1:1, s. 71-84
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Tidskriftsartikel (refereegranskat)abstract
- Previous results have shown that severe, prolonged hypoglycemia leads to neuronal cell damage in, among other structures, the cerebral cortex and the hippocampus but not the cerebellum. In order to study whether or not this sparing of cerebellar cells is due to preservation of cerebellar energy stores, hypoglycemia of sufficient severity to abolish spontaneous EEG activity was induced for 30 and 60 min. At the end of these periods of hypoglycemia, as well as after a 30 min recovery period, cerebellar tissue was sampled for biochemical analyses or for histopathological analyses or for histopathological analyses by means of light and electron microscopy. After 30 min of hypoglycemia. the cerebellar energy state, defined in terms of the phosphocreatine, ATP, ADP, and AMP concentrations, was better preserved than in the cerebral cortex. After 60 min, gross deterioration of cerebellar energy state was observed in the majority of animals, and analyses of carbohydrate metabolites and amino acids demonstrated extensive consumption of endogenous substrates. In spite of this metabolic disturbance, histopathologic alterations were surprisingly discrete. After 30 min, no clear structural changes were observed. After 60 min, only small neurons in the molecular layer (basket cells) were affected, while Purkinje cells and granule cells showed few signs of damage. The results support our previous conclusion that the pathogenesis of cell damage in hypoglycemia is different from that in hypoxia-ischemia and indicate that other mechanisms than energy failure must contribute to neuronal cell damage in the brain.
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| 10. |
- Auer, R., et al.
(författare)
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The dentate gyrus in hypoglycemia : Pathology implicating excititoxin-mediated neuronal necrosis
- 1985
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Ingår i: Acta Neuropathologica. - 0001-6322. ; 67:3-4, s. 279-288
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Tidskriftsartikel (refereegranskat)abstract
- A detailed light- and electron-microscopic study of the damage to the rat dentate gyrus in hypoglycemia was undertaken, in view of the previously advanced hypothesis that hypoglycemic nerve cell injury is mediated by a released neurotoxin. The distribution of neuronal necrosis showed a relationship to the subarachnoid cisterns. Electron microscopy of the dentate granule cells and their apical dendrites revealed dendrosomal, axon-sparing neuronal pathology. Dentate granule cells were affected first in the dendrites in the outer layer of the stratum moleculare, sparing axons of passage and terminal boutons. Subsequently, the neuronal perikarya were affected, and Wallerian degeneration of axons followed. Cell membrane abnormalities preceded the appearance of mitochondrial flocculent densities and degradation of the cytoskeleton, and are suggested to be early lethal changes. The observed early dendrotoxic changes, and the dendrosomal, axon-sparing nature of the lesion implicate an excitotoxin-mediated neuronal necrosis in hypoglycemia.
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