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| 2. |
- Wennergren, Göran, 1947, et al.
(författare)
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The decline in the incidence of SIDS in Scandinavia and its relation to risk-intervention campaigns. Nordic Epidemiological SIDS Study.
- 1997
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Ingår i: Acta paediatrica (Oslo, Norway : 1992). - : Wiley. - 0803-5253 .- 1651-2227. ; 86:9, s. 963-8
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Tidskriftsartikel (refereegranskat)abstract
- A prospective case-control study of sudden infant death syndrome (SIDS) in Norway, Denmark and Sweden between September 1, 1992 and August 31, 1995 comprised 244 cases and 869 matched controls. After the introduction of risk-intervention campaigns, the SIDS incidence decreased from 2.3/1000 live births in Norway, 1.6 in Denmark and 1.0 in Sweden to 0.6/1000 or fewer in all the Scandinavian countries in 1995. The decrease paralleled a decline in the prone sleeping position and there was an accompanying parallel fall in total postneonatal mortality in all three countries. Thus, the risk-reducing campaigns for SIDS have been successful not only in Norway and Denmark, starting from relatively high incidences, but also in Sweden, starting from a low incidence. During the study period, a gradual increase was observed for the effects of prone sleeping, smoking and bottle-feeding as risk factors for SIDS.
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| 6. |
- Alm, Bernt, 1951, et al.
(författare)
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A case-control study of smoking and sudden infant death syndrome in the Scandinavian countries, 1992 to 1995. The Nordic Epidemiological SIDS Study.
- 1998
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Ingår i: Archives of disease in childhood. - 1468-2044. ; 78:4, s. 329-34
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Tidskriftsartikel (refereegranskat)abstract
- To establish whether smoking is an independent risk factor for sudden infant death syndrome (SIDS), if the effect is mainly due to prenatal or postnatal smoking, and the effect of smoking cessation.The analyses were based on data from the Nordic epidemiological SIDS study, a case-control study with 244 cases and 869 controls. Odds ratios were computed by conditional logistic regression analysis.Smoking emerged as an independent risk factor for SIDS, and the effect was mainly mediated through maternal smoking in pregnancy (crude odds ratio 4.0 (95% confidence interval 2.9 to 5.6)). Maternal smoking showed a marked dose-response relation. There was no effect of paternal smoking if the mother did not smoke. Stopping or even reducing smoking was beneficial. SIDS cases exposed to tobacco smoke were breast fed for a shorter time than non-exposed cases, and feeding difficulties were also more common.Smoking is an independent risk factor for SIDS and is mainly mediated through maternal smoking during pregnancy. Stopping smoking or smoking less may be beneficial in reducing the risk of SIDS.
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| 7. |
- Alm, Bernt, 1951, et al.
(författare)
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Caffeine and alcohol as risk factors for sudden infant death syndrome. Nordic Epidemiological SIDS Study.
- 1999
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Ingår i: Archives of disease in childhood. - : BMJ. - 1468-2044 .- 0003-9888. ; 81:2, s. 107-11
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Tidskriftsartikel (refereegranskat)abstract
- To assess whether alcohol and caffeine are independent risk factors for sudden infant death syndrome (SIDS).Analyses based on data from the Nordic epidemiological SIDS study, a case control study in which all parents of SIDS victims in the Nordic countries from 1 September 1992 to 31 August 1995 were invited to participate with parents of four controls, matched for sex and age at death. Odds ratios (ORs) were calculated by conditional logistic regression analysis.The crude ORs for caffeine consumption > 800 mg/24 hours both during and after pregnancy were significantly raised: 3.9 (95% confidence interval (CI), 1.9 to 8.1) and 3.1 (95% CI, 1.5 to 6.3), respectively. However, after adjustment for maternal smoking in 1st trimester, maternal age, education and parity, no significant effect of caffeine during or after pregnancy remained. For maternal or paternal alcohol use, no significant risk increase was found after adjusting for social variables, except for heavy postnatal intake of alcohol by the mother, where the risk was significantly increased.Caffeine during or after pregnancy was not found to be an independent risk factor for SIDS after adjustment for maternal age, education, parity, and smoking during pregnancy. Heavy postnatal but not prenatal intake of alcohol by the mother increased the risk.
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| 10. |
- Daltveit, A K, et al.
(författare)
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Sociodemographic risk factors for sudden infant death syndrome: associations with other risk factors. The Nordic Epidemiological SIDS Study.
- 1998
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Ingår i: Acta paediatrica (Oslo, Norway : 1992). - 0803-5253. ; 87:3, s. 284-90
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Tidskriftsartikel (refereegranskat)abstract
- The aim of this study was to investigate associations between sudden infant death syndrome (SIDS) and social factors in the Nordic countries. A case-control study was conducted in Denmark, Norway and Sweden: The Nordic Epidemiological SIDS Study. Parents of 244 SIDS infants and 869 control infants matched on gender, age at death and place of birth filled in questionnaires. The dataset was analysed by conditional logistic regression. In univariate analysis, the following sociodemographic factors were associated with an increased risk of SIDS: low maternal age [odds ratio (OR) 7.8; 2.8-21.5], high birth order (OR 4.4; 2.5-7.5), single motherhood (OR 2.9; 1.7-5.0), low maternal education (OR 4.5; 2.8-7.1), low paternal education (OR 3.0; 1.9-4.7), maternal unemployment (OR 2.4; 1.8-3.4) and paternal unemployment (OR 4.0; 2.7-5.9). In a multivariate analysis where maternal smoking was also included, only paternal unemployment, young maternal age and high birth order remained significantly associated with SIDS. Housing conditions were not associated with SIDS. However, the risk of SIDS was high if the family had lived in their present home for only a few years (OR 2.3; 1.3-4.1). Sociodemographic differences remain a major concern in SIDS in a low-incidence situation and even in an affluent population with adequate health services.
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| 11. |
- de Zegher, F, et al.
(författare)
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Androgens and fetal growth
- 1998
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Ingår i: Hormone research. - : S. Karger AG. - 0301-0163. ; 50:4, s. 243-244
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Tidskriftsartikel (refereegranskat)abstract
- Boys are heavier than girls at term birth. Children with a 46,XY karyotype and androgen insensitivity syndrome (clinically complete form and/or proven mutations in the androgen receptor gene) were found to have a birth weight comparable to that of girls. These findings support the hypothesis that the difference in birth weight between boys and girls is generated by androgen action.
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| 13. |
- Helweg-Larsen, K, et al.
(författare)
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Interactions of infectious symptoms and modifiable risk factors in sudden infant death syndrome. The Nordic Epidemiological SIDS study.
- 1999
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Ingår i: Acta paediatrica (Oslo, Norway : 1992). - 0803-5253. ; 88:5, s. 521-7
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Tidskriftsartikel (refereegranskat)abstract
- The aim of the study was to investigate the effect of infection on sudden infant death syndrome (SIDS) and to analyse whether modifiable risk factors of SIDS, prone sleeping, covered head and smoking act as effect modifiers. In a consecutive multicentre case-control study of SIDS in Denmark, Norway and Sweden, questionnaires on potential risk factors for SIDS were completed by parents of SIDS victims, and for at least two controls matched for gender, age and place of birth. All SIDS cases were verified by an autopsy. The study comprised 244 SIDS cases and 869 controls, analysed by conditional logistic regression. Significantly more cases than controls presenting symptoms of infectious diseases during the last week and/or last day were treated with antibiotics and had been seen by a physician. The finding is consistent with the hypothesis of an infectious mechanism in SIDS induced by local microorganism growth and toxin or cytokine production, and also adds further support to a possible association between infection and SIDS by loss of protective mechanisms, such as arousal. The risk of SIDS among infants with the combined presence of infectious symptoms and either of the other modifiable risk factors, prone sleeping, head covered or parental smoking, was far greater than the sum of each individual factor. These risk factors thus modify the dangerousness of infection in infancy.
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| 17. |
- Nilsson, K O, et al.
(författare)
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Improved final height in girls with Turner's syndrome treated with growth hormone and oxandrolone.
- 1996
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Ingår i: Journal of Clinical Endocrinology and Metabolism. - : The Endocrine Society. - 0021-972X .- 1945-7197. ; 81, s. 635-
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Tidskriftsartikel (refereegranskat)abstract
- The spontaneous growth process in Turner's syndrome is characterized by a progressive decline in height velocity during childhood and no pubertal growth spurt. Therefore, therapy aimed at improving height during childhood as well as increasing final height is desirable for most girls with Turner's syndrome. Forty-five girls with Turner's syndrome, 9-16 yr of age (mean age, 12.2 yr), were allocated to three study groups. Group 1 (n = 13) was initially treated with oxandrolone alone; after 1 yr of treatment, GH without (group 1a; n = 6) or with (group 1b; n = 7) ethinyl estradiol was added. Group 2 (n = 17) was treated with GH plus oxandrolone. Group 3 (n = 15) was treated with GH, oxandrolone, and ethinyl estradiol. The dosage were: GH, 0.1 IU/kg.day; oxandrolone, 0.05 mg/kg.day; and ethinyl estradiol, 100 ng/kg.day. A height of 150 cm or more was achieved in 61%, 75%, and 60% of the girls in groups 1, 2, and 3, respectively. The most impressive increase in height was seen in group 2. In this group the mean final height was 154.2 cm (SD = 6.6), which is equivalent to a mean net gain of 8.5 cm (SD = 4.6) over the projected final height. In group 3, in which ethinyl estradiol was included from the start of therapy, the initially good height velocity decelerated after 1-2 yr of treatment. Their mean final height was 151.1 (SD = 4.6) cm, equivalent to a mean net gain of 3.0 cm (SD = 3.8). A similar growth-decelerating effect of ethinyl estradiol was seen in group 1b. We conclude that in girls with Turner's syndrome who are older than 9 yr of age, treatment with GH in combination with oxandrolone results in significant growth acceleration, imitating that in normal puberty, leading to a more favorable height during childhood. This mode of treatment also results in a significantly increased final height, permitting a great number of the girls to attain a final height of more than 150 cm. However, early addition of estrogen decelerates the height velocity and reduces the gain in height.
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| 18. |
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| 19. |
- Oyen, N, et al.
(författare)
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Combined effects of sleeping position and prenatal risk factors in sudden infant death syndrome: the Nordic Epidemiological SIDS Study.
- 1997
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Ingår i: Pediatrics. - 1098-4275. ; 100:4, s. 613-21
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Tidskriftsartikel (refereegranskat)abstract
- Prone sleeping is a strong risk factor for sudden infant death syndrome (SIDS). We investigated whether the combined effect of prone sleeping position and prenatal risk factors further increased the SIDS risk.In the Nordic Epidemiological SIDS Study, parents of SIDS victims in Denmark, Norway, and Sweden completed a questionnaire on potential risk factors for SIDS. Forensic pathologists verified the SIDS diagnosis. Four controls of the same gender, age, and place of birth were selected. This matched case-control study, which included 244 SIDS cases and 869 controls from 1992 to 1995, was analyzed by conditional logistic regression.Odds ratios (ORs) for prone and side sleeping compared with supine sleeping for the last sleep were 13.9 (95% confidence interval 8.2-24) and 3.5 (2.1-5.7). Infants 13 to 24 weeks old had particularly high risk in prone and side sleeping, at 28.5 (7.9-107) and 5.9 (1.6-22). OR for prone sleeping was higher in girls, at 30.4 (11-88), than in boys, 10.3 (5.5-19). We found strong combined effects of sleeping position and prenatal risk factors (more than multiplicative). The OR for prone and side sleeping was increased for infants with birth weight <2500 g, at 83 (25-276) and 36.6 (13-107); for preterm infants, at 48.8 (19-128) and 40.5 (14-115); and for intrauterine growth retarded, at 38.8 (14-108) and 9.6 (4.3-22), compared with supine position in infants without these prenatal factors. The combined effect of nonsupine positions and intrauterine growth retarded was highest among 13- to 24-week-old infants. Effects of combined presence of nonsupine sleeping positions and each of the factors of smoking in pregnancy, young maternal age, higher parity, low level of maternal education, and single motherhood were more than additive. Attributable fractions in the population for prone and side sleeping were 18.5% and 26.0%.Both prone and side sleeping increased the risk of SIDS. The risk was increased further in low birth weight infants, preterm infants, and infants at the age of 13 to 24 weeks, suggesting that SIDS may be triggered by nonsupine sleeping in infants with prenatal risk factors during a vulnerable period of postnatal development.
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| 20. |
- Perez, M T, et al.
(författare)
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Localisation of neuronal nitric oxide synthase-immunoreactivity in rat and rabbit retinas
- 1995
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Ingår i: Experimental Brain Research. - 0014-4819. ; 104:2, s. 17-207
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Tidskriftsartikel (refereegranskat)abstract
- The distribution of neuronal nitric oxide synthase (NOS) immunoreactivity was examined in rat and rabbit retinas and was compared with the distribution of nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase reactivity and vasoactive intestinal peptide (VIP) immunoreactivity. An antibody raised against a C-terminal fragment of a cloned rat cerebellar NOS was used to localise NOS immunoreactivity. NOS immunoreactive cells were not detected in rat retinas at postnatal day 1 or 4, but were seen from postnatal day 7 onwards. NOS immunolabelling was seen in a small population of cells in the proximal inner nuclear layer. Most of the labelled cells had the position of amacrine cells and were seen to send processes into the inner plexiform layer. A few labelled cells were at times also seen in the ganglion cell layer, which are likely to correspond to displaced amacrine cells. The same NOS-labelling pattern was seen in rat and rabbit retinas. NADPH-diaphorase staining was observed in both species, in photoreceptor inner segments, in cells with the position of horizontal cells, in a subset of amacrine and displaced amacrine cells, in large cell bodies in the ganglion cell layer, in both plexiform layers, and in endothelium. Colocalisation of NOS immunoreactivity and NADPH-diaphorase staining was only observed among amacrine cells. However, not all NADPH-diaphorase-reactive amacrine cells were found to be NOS immunoreactive. VIP immunoreactivity was also localised in rat retinas in a subpopulation of amacrine cells, but no colocalisation of NOS and VIP immunoreactivity was observed. Our observations indicate that only amacrine cells contain the NOS form recognisable by the antibody used, and suggest that different isoforms of neuronal NOS may be present in retinal cells. Further, the onset of NOS expression in rat amacrine cells appears to occur independently of neuronal activity.
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| 22. |
- Rudolph, P, et al.
(författare)
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Correlation between p53, c-erbB-2, and topoisomerase II alpha expression, DNA ploidy, hormonal receptor status and proliferation in 356 node-negative breast carcinomas : prognostic implications
- 1999
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Ingår i: Journal of Pathology. - 0022-3417. ; 187:2, s. 16-207
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Tidskriftsartikel (refereegranskat)abstract
- Various new prognostic indicators have been identified for mammary carcinomas, but the issue of their significance remains unsettled. The prognostic impact of p53, c-erbB-2, and topoisomerase II alpha expression was investigated in relation to standard prognostic factors for carcinomas of the breast and to the tumour cell growth fraction. Paraffin-embedded specimens of 356 node-negative infiltrating ductal carcinomas were stained immunohistochemically using a polyclonal antiserum to c-erbB-2, and the monoclonal antibodies DO-1 (p53), Ki-S4 (topoisomerase II alpha), and Ki-S5 (Ki-67). The patients were followed for a median duration of 99 months. Both p53 and c-erbB-2 were significantly associated with high tumour grade, large tumour size, DNA aneuploidy, lack of steroid hormone receptors, young age, and increased topoisomerase II alpha and Ki-67 expression levels. The correlation of p53 and c-erbB-2 was not significant. Topoisomerase II alpha and Ki-67 scores closely paralleled each other, indicating that both reflect the proliferative activity of tumour cells. A univariate analysis of overall (OS), specific (SS), and disease-free survival (DFS) revealed all the above-mentioned parameters to be statistically significant except patient age, which was relevant only to overall survival. Multivariate analysis with inclusion of all covariates selected tumour size and proliferation (topoisomerase II alpha and Ki-67) indices as independent predictors of survival in all three models. No additional information was gained by p53 or c-erbB-2. It is concluded that the proliferative activity, as assessed by topoisomerase II alpha or Ki-67 immunostaining, is the most useful indicator of breast cancer prognosis, except for tumour size.
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| 23. |
- Rudolph, P, et al.
(författare)
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Immunologic proliferation marker Ki-S2 as prognostic indicator for lymph node-negative breast cancer
- 1999
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Ingår i: Journal of the National Cancer Institute. - : Oxford University Press (OUP). - 1460-2105 .- 0027-8874. ; 91:3, s. 8-271
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Proper treatment of lymph node-negative breast cancer depends on an accurate prognosis. To improve prognostic models for this disease, we evaluated whether an immunohistochemical marker for proliferating cells, Ki-S2 (a monoclonal antibody that binds to a 100-kd nuclear protein expressed in S, G2, and M phases of the cell cycle), is an accurate indicator of prognosis.METHODS: We studied 371 Swedish women with lymph node-negative breast cancer; the median follow-up time was 95 months. The fraction of tumor cells in S phase was assessed by flow cytometry, and tumor cell proliferation was measured immunohistochemically with the monoclonal antibodies Ki-S2 and Ki-S5 (directed against the nuclear antigen Ki-67). A combined prognostic index was calculated on the basis of the S-phase fraction, progesterone receptor content, and tumor size.RESULTS: In multivariate analyses that did or did not (263 and 332 observations, respectively) include the S-phase fraction and the combined prognostic index, the Ki-S2 labeling index (percentage of antibody-stained tumor cell nuclei) emerged as the most statistically significant predictor of overall survival, disease-specific survival, and disease-free survival (all two-sided P<.0001). In the risk group defined by a Ki-S2 labeling index of 10% or less, life expectancy was not statistically significantly different from that of age-matched women without breast cancer, whereas the group with a high Ki-S2 labeling index had an increased risk of mortality of up to 20-fold.CONCLUSIONS: Cellular proliferation is a major determinant of the biologic behavior of breast cancer. Prognosis is apparently best indicated by the percentage of cells in S through M phases of the cell cycle. Measurement of the Ki-S2 labeling index of a tumor sample may improve a clinician's ability to make an accurate prognosis and to identify patients with a low risk of recurrence who may not need adjuvant therapy.
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