| 1. |
- Johannsson, Gudmundur, 1960, et al.
(författare)
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Growth hormone and the metabolic syndrome.
- 1999
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Ingår i: Journal of endocrinological investigation. - 0391-4097. ; 22:5 Suppl, s. 41-6
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Forskningsöversikt (refereegranskat)abstract
- The association of several risk factors, obesity, dyslipoproteinemia, hepatic steatosis, insulin resistance and hypertension with Type 2 (non-insulin-dependent) diabetes mellitus and myocardial infarction has long been known and has been termed the "metabolic syndrome". In 1988 Reaven introduced syndrome X as the link between insulin resistance and hypertension. It has been suggested that a critical factor in the association between obesity, Type 2 diabetes and cardiovascular morbidity is the mass of intraabdominal fat. Striking similarities exist between the metabolic syndrome and untreated growth hormone (GH) deficiency in adults. The central findings in both these syndromes are abdominal/visceral obesity and insulin resistance. Other features common to both conditions are premature atherosclerosis and increased mortality from cardiovascular diseases. These similarities indicate that undetectable and low levels of GH may be of importance in the metabolic aberrations observed in both these conditions. Recent investigations have found that abdominal/visceral distribution of adipose tissue is associated with endocrine disturbances including increased activity of the hypothalamic-pituitary-adrenal axis and a blunted secretion of GH and sex steroids. Theoretically, these endocrine perturbations can be a consequence of obesity, but the endocrine aberrations may have causal effects. We studied moderately obese, middle-aged men with a preponderance of abdominal body fat. As a group, they had slight to moderate metabolic changes known to be associated with abdominal/visceral obesity. Nine months of GH treatment reduced their total body fat and resulted in a specific and a marked decrease in both abdominal subcutaneous and visceral adipose tissue. Moreover, insulin sensitivity improved and serum concentrations of total cholesterol and triglyceride decreased. Diastolic blood pressure also decreased. The finding that GH replacement in men with abdominal obesity can diminish the negative metabolic consequences of visceral obesity suggests that low levels of this hormone are of importance for the metabolic aberrations associated with visceral/abdominal obesity.
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| 2. |
- Frisén, Lars, 1939
(författare)
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High-pass resolution perimetry. A clinical review.
- 1993
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Ingår i: Documenta ophthalmologica. Advances in ophthalmology. - 0012-4486. ; 83:1, s. 1-25
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Forskningsöversikt (refereegranskat)abstract
- Review of all available reports comparing high-pass resolution perimetry (HRP) and conventional perimetry in normals and in subjects with different visual disorders reveals closely comparable aspects of sensitivity, specificity, and reliability. HRP shows important advantages concerning variability, test duration, and subject preferences. Drawbacks seem largely limited to somewhat loose renditions of visual field defects of small area and large depth. Otherwise HRP's novel format of graphic result presentation may be better suited to visual evaluation than conventional gray-scale maps with their lumping of thresholds and extensive interpolations. Several examples are provided of visual field defects due to various lesions throughout the visual system.
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| 3. |
- Ljung, R.C.R.
(författare)
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Prenatal diagnosis of haemophilia
- 1999
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Ingår i: Haemophilia. - : Wiley. - 1351-8216 .- 1365-2516. ; 5:2, s. 84-87
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Forskningsöversikt (refereegranskat)abstract
- Genotype assessment based on direct identification of the pathogenic mutation in a chorionic villi sample obtained in the 11-12th gestational week is the most reliable method for prenatal diagnosis and should be used if available. Genetic linkage studies of polymorphisms should be the second choice in the assessment of carriers and in prenatal diagnosis. Carriers of haemophilia should be offered adequate psychosocial support before, during and after the prenatal diagnostic procedures.
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| 4. |
- Basson, M D, et al.
(författare)
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Biology and management of the midgut carcinoid.
- 1993
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Ingår i: American journal of surgery. - 0002-9610. ; 165:2, s. 288-97
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Forskningsöversikt (refereegranskat)abstract
- Midgut carcinoid tumors derive from gut entoderm. These tumors may cause a complex of symptoms comprising the carcinoid syndrome by secreting a wide variety of bioactive agents in addition to serotonin. Such symptoms generally follow metastases to the liver but may also occur in primary ovarian or retroperitoneal tumors. After localization and biochemical characterization, the bioactivity of these tumors should be blocked by octreotide, sometimes in combination with other pharmacologic antagonists, so that primary resection may be performed safely. If curative resection is impossible, then a cytoreductive management scheme should be employed that includes surgical debulking and hepatic arterial embolization, followed by palliation with octreotide.
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| 5. |
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| 6. |
- Johannsson, Gudmundur, 1960, et al.
(författare)
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Growth hormone and the acquisition of bone mass.
- 1997
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Ingår i: Hormone research. - 0301-0163. ; 48 Suppl 5, s. 72-7
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Forskningsöversikt (refereegranskat)abstract
- Bone remodelling is a continuous, closely coupled process of bone resorption followed by bone formation. This process is regulated by factors and hormones which include GH, IGF-I and gonadal steroids. GH deficiency in childhood results in short stature and delayed bone maturation and a reduced peak bone mass might account for reduced BMC and BMD. Possible pathophysiological mechanisms for reduced bone mass in both childhood- and adult-onset GH deficiency are discussed. GH treatment effects on bone metabolism include increased remodelling, with increases in BMC, BMD and bone area. Increases in BMC and BMD are delayed while these changes are incorporated into the skeleton. BMC increases to a greater extent than BMD. At a cellular level, GH and IGF-I have direct and indirect effects on osteoblast and osteoclast precursors and fully differentiated cells. Osteoblasts possess both oestrogen and androgen receptors and bone loss accelerates with the loss of gonadal function. There are gender differences in GH effects on bone. BMD is related to fracture risk in the hip and lumbar spine in women. GH treatment might decrease fracture risk at a level comparable to oestrogen or bisphosphonate treatment. Patients with the lowest BMD prior to treatment derive the greatest benefit from GH therapy.
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| 7. |
- Kristjánsson, Sigurdur, 1955, et al.
(författare)
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Inflammatory markers in childhood asthma.
- 1996
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Ingår i: Annals of medicine. - 0785-3890. ; 28:5, s. 395-9
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Forskningsöversikt (refereegranskat)abstract
- The importance of airway inflammation in the pathogenesis of asthma is clearly established. Studies in adults as well as in children have led to the concept that asthma is a chronic inflammatory disease. Airway inflammation is found even in mild asthma. Bronchoconstriction and hyper-reactivity appear to be secondary to the release of inflammatory mediators. The changed view of the pathogenesis of asthma and current emphasis on anti-inflammatory treatment have raised a need for markers that reflect the inflammatory status in the airways. This is of special importance in paediatric practice because lung function tests are less easily performed in young children, and it is preferable to keep steroid doses as low as possible. The eosinophil granulocyte has a multitude of proinflammatory functions and plays a key role in the asthmatic inflammation. It secretes toxic proteins and produces cytokines, which have important roles in airway inflammation. Use of eosinophil granula proteins to monitor inflammation is now finding its place. Measurement of eosinophil cationic protein (ECP) seems to be a valuable complement to the recording of lung function. For paediatric use, measurement of urinary eosinophil protein X (EPX) is promising because it does not require blood sampling.
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| 8. |
- Olsson, I, et al.
(författare)
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Cell differentiation in acute myeloid leukemia
- 1996
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Ingår i: European Journal of Haematology. - : Wiley. - 0902-4441 .- 1600-0609. ; 57:1, s. 1-16
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Forskningsöversikt (refereegranskat)abstract
- Acute myeloid leukemia (AML) is characterized by a differentiation block leading to accumulation of immature cells. Chromosomal translocations in AML affect transcription factors that are involved in regulation of myeloid differentiation. Aberrant expression of these factors interferes with differentiation events and has a role in the pathogenesis of AML through superactivation or (dominant negative) repression of genes regulating proliferation and differentiation or by interference with assembly of the transcription complex for these genes. The maturation arrest can be reversed by certain agents as judged by results from investigations of myeloid leukemic cell lines and from treatment of acute promyelocytic leukemia (APL) patients with all-trans retinoic acid. Inactivation of the p53 and retinoblastoma (Rb) tumor suppressor genes is also associated with the pathogenesis of leukemia through effects on the cell cycle, and manipulation of these genes can affect differentiation of AML cells. With differentiation therapy, when successful as in APL, the leukemic cell mass is reduced to allow restoration of normal hematopoiesis and clinical remission, but the disease is not cured. However, initial reduction of the cell mass by maturation can increase the probability for cure with chemotherapy. Overexpression of suppressor genes may increase the probability for differentiation. Most probably, particular molecular defects of subgroups of AML have to be explored to find optimal strategies for treatment including both blocking the cell cycle, promoting terminal differentiation, and inducing apoptosis as well as strengthening the immune response.
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| 9. |
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| 10. |
- Wennergren, Göran, 1947
(författare)
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Impact of viral infection on bronchial hyperresponsiveness.
- 1996
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Ingår i: Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology. - 0905-6157. ; 7:9 Suppl, s. 10-3
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Forskningsöversikt (refereegranskat)
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