| 1. |
- Zeisler, H., et al.
(författare)
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Soluble fms-like tyrosine kinase-1 to placental growth factor ratio : ruling out pre-eclampsia for up to 4weeks and value of retesting
- 2019
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Ingår i: Ultrasound in Obstetrics and Gynecology. - : Wiley. - 0960-7692 .- 1469-0705. ; 53:3, s. 367-375
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Tidskriftsartikel (refereegranskat)abstract
- Objectives The soluble fms-like tyrosine kinase-1 ( sFlt-1) to placental growth factor ( PlGF) ratio is generally elevated some time before and at the clinical onset of pre-eclampsia. The PROGNOSIS study validated a sFlt-1/PlGF ratio cut-off of = 38 to rule out the onset of pre-eclampsia within 1week of testing in women with suspected disease. The aim of this study was to assess the predictive value of the sFlt-1/PlGF ratio to rule out the onset of pre-eclampsia for up to 4 weeks, and to assess the value of repeat measurements.MethodsThis was an exploratory post-hoc analysis of data from the PROGNOSIS study performed in pregnant women aged = 18 years with suspected pre-eclampsia, who were at 24+ 0 to 36+ 6weeks' gestation at their first clinic visit. Serum samples were collected at the first visit and weekly thereafter. sFlt-1 and PlGF levels were measured using Elecsys (R) sFlt-1 and PlGF immunoassays. Whether the sFlt-1/PlGF ratio cut-off of = 38 used to rule out the onset of pre-eclampsia within 1week could predict the absence of pre-eclampsia 2, 3, and 4 weeks post-baseline was assessed. The value of repeat sFlt-1/PlGF testing was assessed by examining the difference in sFlt-1/PlGF ratio 2 and 3 weeks after the first measurement in women with, and those without, pre-eclampsia or adverse fetal outcome.ResultsOn analysis of 550 women, sFlt-1/PlGF ratio = 38 ruled out the onset of pre-eclampsia 2 and 3weeks post-baseline with high negative predictive values (NPV) of 97.9% and 95.7%, respectively. The onset of pre-eclampsia within 4weeks was ruled out with a high NPV (94.3%) and high sensitivity and specificity (66.2% and 83.1%, respectively). Compared with women who did not develop pre-eclampsia, those who developed pre-eclampsia had significantly larger median increases in sFlt-1/PlGF ratio at 2 weeks (., 31.22 vs 1.45; P< 0.001) and at 3 weeks (., 48.97 vs 2.39; P< 0.001) after their initial visit. Women who developed pre-eclampsia and/or adverse fetal outcome compared with those who did not had a significantly greater median increase in sFlt-1/PlGF ratio over the same period (., 21.22 vs 1.40; P< 0.001 at 2weeks;., 34.95 vs 2.30; P< 0.001 at 3weeks).ConclusionThe Elecsys (R) immunoassay sFlt-1/PlGF ratio can help to rule out the onset of pre-eclampsia for 4 weeks in women with suspected pre-eclampsia.
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| 4. |
- Waldenstrom, U, et al.
(författare)
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Team midwife care: maternal and infant outcomes
- 2001
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Ingår i: The Australian & New Zealand journal of obstetrics & gynaecology. - : Wiley. - 0004-8666 .- 1479-828X. ; 41:3, s. 257-264
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Tidskriftsartikel (refereegranskat)
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| 7. |
- Kircher, Max, et al.
(författare)
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Kinematically complete experimental study of Compton scattering at helium atoms near the threshold
- 2020
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Ingår i: Nature Physics. - : Springer Nature. - 1745-2473 .- 1745-2481. ; 16:7, s. 756-760
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Tidskriftsartikel (refereegranskat)abstract
- Compton scattering is one of the fundamental interaction processes of light with matter. When discovered(1), it was described as a billiard-type collision of a photon 'kicking' a quasi-free electron. With decreasing photon energy, the maximum possible momentum transfer becomes so small that the corresponding energy falls below the binding energy of the electron. In this regime, ionization by Compton scattering becomes an intriguing quantum phenomenon. Here, we report on a kinematically complete experiment studying Compton scattering off helium atoms in that regime. We determine the momentum correlations of the electron, the recoiling ion and the scattered photon in a coincidence experiment based on cold target recoil ion momentum spectroscopy, finding that electrons are not only emitted in the direction of the momentum transfer, but that there is a second peak of ejection to the backward direction. This finding links Compton scattering to processes such as ionization by ultrashort optical pulses(2), electron impact ionization(3,4), ion impact ionization(5,6) and neutron scattering(7), where similar momentum patterns occur. Compton scattering experiments off helium atoms for photon energies close to the ionization threshold reveal that electrons are not only emitted in the direction of the momentum transfer but also backwards.
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| 8. |
- Mall, Moritz, et al.
(författare)
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Myt1l safeguards neuronal identity by actively repressing many non-neuronal fates
- 2017
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Ingår i: Nature. - : Springer Science and Business Media LLC. - 0028-0836 .- 1476-4687. ; 544:7649, s. 245-249
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Tidskriftsartikel (refereegranskat)abstract
- Normal differentiation and induced reprogramming require the activation of target cell programs and silencing of donor cell programs. In reprogramming, the same factors are often used to reprogram many different donor cell types. As most developmental repressors, such as RE1-silencing transcription factor (REST) and Groucho (also known as TLE), are considered lineage-specific repressors, it remains unclear how identical combinations of transcription factors can silence so many different donor programs. Distinct lineage repressors would have to be induced in different donor cell types. Here, by studying the reprogramming of mouse fibroblasts to neurons, we found that the pan neuron-specific transcription factor Myt1-like (Myt1l) exerts its pro-neuronal function by direct repression of many different somatic lineage programs except the neuronal program. The repressive function of Myt1l is mediated via recruitment of a complex containing Sin3b by binding to a previously uncharacterized N-terminal domain. In agreement with its repressive function, the genomic binding sites of Myt1l are similar in neurons and fibroblasts and are preferentially in an open chromatin configuration. The Notch signalling pathway is repressed by Myt1l through silencing of several members, including Hes1. Acute knockdown of Myt1l in the developing mouse brain mimicked a Notch gain-of-function phenotype, suggesting that Myt1l allows newborn neurons to escape Notch activation during normal development. Depletion of Myt1l in primary postmitotic neurons de-repressed non-neuronal programs and impaired neuronal gene expression and function, indicating that many somatic lineage programs are actively and persistently repressed by Myt1l to maintain neuronal identity. It is now tempting to speculate that similar 'many-but-one' lineage repressors exist for other cell fates; such repressors, in combination with lineage-specific activators, would be prime candidates for use in reprogramming additional cell types.
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