Instrumental delivery and ultrasound: a multicentre randomised controlled trial of ultrasound assessment of the fetal head position versus standard care as an approach to prevent morbidity at instrumental delivery

Objectives: To determine whether the use of ultrasound can reduce the incidence of incorrect diagnosis of the fetal head position at instrumental delivery and subsequent morbidity. Design: Two-arm, parallel, randomised trial, conducted from June 2011 to December 2012. Setting: Two maternity hospitals in the Republic of Ireland. Sample: 514 nulliparous women at term (≥37 weeks' gestation) with singleton cephalic pregnancies, aiming to deliver vaginally were recruited prior to induction of labour or in early labour. Methods: If instrumental delivery was required, women who had provided written consent were randomised to receive clinical assessment (standard care) or ultrasound scan and ultrasound assessment (ultrasound). Main outcome: Incorrect diagnosis of the fetal head position. Results: The incidence of incorrect diagnosis was significantly lower in the ultrasound group than the standard care group (4/257, 1.6% versus 52/257, 20.2%, odds ratio 0.06, 95% confidence interval (CI) 0.02 to 0.19, p value <0.001). The decision to delivery interval was similar in both groups (ultrasound mean 13.8 minutes, SD 8.7, versus standard care mean 14.6 minutes, SD 10.1, p value 0.35). The incidence of maternal and neonatal complications,4 failed instrumental delivery and caesarean section was not significantly different between the two groups. Conclusions: An ultrasound assessment prior to instrumental delivery reduced the incidence of incorrect diagnosis of the fetal head position without delaying delivery but did not prevent morbidity. A more integrated clinical skills-based approach is likely to be required to prevent adverse outcomes at instrumental delivery

High prevalence of bronchiectasis is linked to HTLV-1-associated inflammatory disease.

BACKGROUND: Human T-lymphotropic virus type 1 (HTLV-1), a retrovirus, is the causative agent of HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) and adult T-cell leukaemia/lymphoma (ATLL). The reported association with pulmonary disease such as bronchiectasis is less certain. METHODS: A retrospective case review of a HTLV-1 seropositive cohort attending a national referral centre. The cohort was categorised into HTLV-1 symptomatic patients (SPs) (ATLL, HAM/TSP, Strongyloidiasis and HTLV associated inflammatory disease (HAID)) and HTLV-1 asymptomatic carriers (ACs). The cohort was reviewed for diagnosis of bronchiectasis. RESULT: 34/246 ACs and 30/167 SPs had been investigated for respiratory symptoms by computer tomography (CT) with productive cough +/- recurrent chest infections the predominant indications. Bronchiectasis was diagnosed in one AC (1/246) and 13 SPs (2 HAID, 1 ATLL, 10 HAM/TSP) (13/167, RR 19.2 95 % CI 2.5-14.5, p = 0.004) with high resolution CT. In the multivariate analysis ethnicity (p = 0.02) and disease state (p < 0.001) were independent predictors for bronchiectasis. The relative risk of bronchiectasis in SPs was 19.2 (95 % CI 2.5-14.5, p = 0.004) and in HAM/TSP patients compared with all other categories 8.4 (95 % CI 2.7-26.1, p = 0.0002). Subjects not of African/Afro-Caribbean ethnicity had an increased prevalence of bronchiectasis (RR 3.45 95 % 1.2-9.7, p = 0.02). CONCLUSIONS: Bronchiectasis was common in the cohort (3.4 %). Risk factors were a prior diagnosis of HAM/TSP and ethnicity but not HTLV-1 viral load, age and gender. The spectrum of HTLV-associated disease should now include bronchiectasis and HTLV serology should be considered in patients with unexplained bronchiectasis

Effect of promoter architecture on the cell-to-cell variability in gene expression

According to recent experimental evidence, the architecture of a promoter, defined as the number, strength and regulatory role of the operators that control the promoter, plays a major role in determining the level of cell-to-cell variability in gene expression. These quantitative experiments call for a corresponding modeling effort that addresses the question of how changes in promoter architecture affect noise in gene expression in a systematic rather than case-by-case fashion. In this article, we make such a systematic investigation, based on a simple microscopic model of gene regulation that incorporates stochastic effects. In particular, we show how operator strength and operator multiplicity affect this variability. We examine different modes of transcription factor binding to complex promoters (cooperative, independent, simultaneous) and how each of these affects the level of variability in transcription product from cell-to-cell. We propose that direct comparison between in vivo single-cell experiments and theoretical predictions for the moments of the probability distribution of mRNA number per cell can discriminate between different kinetic models of gene regulation.Comment: 35 pages, 6 figures, Submitte