711. |
- Wennerholm, U. B., et al.
(författare)
-
Induction of labour at 41 weeks versus expectant management and induction of labour at 42 weeks (SWEdish Post-term Induction Study, SWEPIS) : multicentre, open label, randomised, superiority trial
- 2020
-
Ingår i: Geburtshilfe und Frauenheilkunde. - : Georg Thieme Verlag KG. - 0016-5751 .- 1438-8804. ; 80:10, s. E76-E76
-
Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- Objective: To evaluate if induction of labour at 41 weeks improves perinatal and maternal outcomes in women with low risk pregnancies compared with expectant management and induction at 42 weeks.Methods: A multicenter, randomised controlled superiority trial.Women with low risk singleton pregnanies (n = 2760) were randomised to either induction or expectant management group. The primary outcome was a composite perinatal outcome including one or more of stillbirth, neonatal mortality, Apgar score < 7 at five minutes, pH < 7.00 or metabolic acidosis (pH < 7.05 and base deficit >12 mmol/L) in the umbilical artery, hypoxic ischaemic encephalopathy, intracranial haemorrhage, convulsions, meconium aspiration syndrome, mechanical ventilation within 72 hours, obstetric brachial plexus injury. Primary analysis was by intention to treat.Results: The study was stopped early owing to a significantly higher rate of perinatal mortality in the expectant management group (no deaths compared to six deaths, p = 0.03). The primary outcome did not differ: 2.4 % (33/1381) in the induction group and 2.2 % (31/1379) in the expectant management group (RR 1.06, 95 %CI 0.65 to 1.73; p = 0.90). The proportion of caesarean delivery, instrumental vaginal delivery, or any major maternal morbidity did not differ between the groups.Conclusions: There was no significant difference in the primary composite outcome when comparing induction at 41 weeks with expectant management and induction at 42. However, a reduction of the secondary outcome perinatal mortality was observed without increasing adverse maternal outcomes. To offer induction at 41 weeks could be one of few interventions that reduces the rate of stillbirths.
|
|
712. |
|
|
713. |
|
|
714. |
- Wennmalm, K, et al.
(författare)
-
A gene signature in breast cancer
- 2007
-
Ingår i: The New England journal of medicine. - 1533-4406. ; 356:18, s. 1887-1888
-
Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
|
|
715. |
|
|
716. |
- Wennmalm, K, et al.
(författare)
-
Stromal signature identifies basal breast cancers
- 2009
-
Ingår i: Nature medicine. - : Springer Science and Business Media LLC. - 1546-170X .- 1078-8956. ; 15:3, s. 237-238
-
Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
|
|
717. |
- Wikström, P, et al.
(författare)
-
Alterations of transforming growth factor beta1 (TGF-beta1) and TGFbeta receptor expressions with progression in Dunning rat prostatic adenocarcinoma sublines.
- 1999
-
Ingår i: Urological research. - 0300-5623 .- 1434-0879. ; 27:3, s. 185-93
-
Tidskriftsartikel (refereegranskat)abstract
- Transforming growth factor-beta1 (TGF-beta1) inhibits epithelial cell proliferation in the normal prostate. Prostate tumours express high levels of TGF-beta1, and seem to acquire resistance to its anti-proliferative effects with tumour progression. In this study, TGFbeta variations with tumour progression were examined in the Dunning prostatic adenocarcinoma model. Expression of TGF-beta1 and TGFbeta receptor type I and type II (TGFbeta-RI and TGFbeta-RII) in rat dorsolateral prostate (DLP) and Dunning tumour sublines (PAP, AT-1, AT-2, AT-3 and MatLyLu) was examined in vitro and in vivo, using competitive reverse transcription-polymerase chain reaction (RT-PCR), Northern and Western blot, and immunohistochemistry. All tumours expressed elevated levels of TGF-beta1 and TGFbeta-RI mRNA, when compared with the DLP (P < or = 0.05). All tumours except MatLyLu also expressed elevated levels of TGFbeta-RII mRNA (P < or = 0.05). Interestingly, TGFbeta-RII protein levels were very low in the highly metastatic AT-3 and MatLyLu tumours in vivo, when compared with levels in the PAP, AT-1, and AT-2 tumours. This difference was not detected for the AT-1, AT-2, and AT-3 cells in vitro. Immunostaining of TGF-beta1, TGFbeta-RI, and TGFbeta-RII was localised principally in normal and tumour epithelial cells, and occasionally in smooth muscle cells. In conclusion, high expression of TGF-beta1 and TGFbeta-RI and low expression of TGFbeta-RII may contribute to tumour progression and metastasis in the Dunning prostatic adenocarcinoma model.
|
|
718. |
|
|
719. |
|
|
720. |
|
|