De-Trending Time Series for Astronomical Variability Surveys

We present a de-trending algorithm for the removal of trends in time series. Trends in time series could be caused by various systematic and random noise sources such as cloud passages, changes of airmass, telescope vibration or CCD noise. Those trends undermine the intrinsic signals of stars and should be removed. We determine the trends from subsets of stars that are highly correlated among themselves. These subsets are selected based on a hierarchical tree clustering algorithm. A bottom-up merging algorithm based on the departure from normal distribution in the correlation is developed to identify subsets, which we call clusters. After identification of clusters, we determine a trend per cluster by weighted sum of normalized light-curves. We then use quadratic programming to de-trend all individual light-curves based on these determined trends. Experimental results with synthetic light-curves containing artificial trends and events are presented. Results from other de-trending methods are also compared. The developed algorithm can be applied to time series for trend removal in both narrow and wide field astronomy.Comment: Revised version according to the referee's second revie

An Algorithm Informed by the Parathyroid Hormone Level Reduces Hypocalcemic Complications of Thyroidectomy

Ó The Author(s) 2010. This article is published with open access at Springerlink.com Background Measurement of the parathyroid hormone (PTH) level following total thyroidectomy (TTx) may allow prediction of postoperative hypocalcemia. We present an algorithmic method of managing hypocalcemia preemptively, based on the PTH level 1 h after operation. Materials and methods We examined 423 consecutive patients undergoing TTx at a single institution. A subset of patients were managed using an algorithm involving routine postoperative oral calcium administration and the early addition of oral calcitriol in patients with a low 1-h postoperative PTH level. Algorithm patients were compared to a concurrent, conventionally managed group. Outcomes measured included serum calcium levels, symptoms of hypocalcemia, postoperative complications, and receipt of intravenous (IV) calcium. Results The algorithm was applied in 135 patients, and 288 patients were managed conventionally. Critically low calcium levels (total calcium \7.5 mg/dl [1.88 mmol/l] or ionized calcium \0.94 mmol/l) were less common in algorithm patients (10.6 % vs. 25.3%; p \ 0.005). Much of this difference was attributable to the protective impact of the algorithm on patients undergoing TTx for cancer, 30% of whom developed critically low calcium levels when managed conventionally. Among patients requiring IV calcium, algorithm patients received fewer doses (1.29 vs

Non-essential role for TLR2 and its signaling adaptor Mal/TIRAP in preserving normal lung architecture in mice

Myeloid differentiation factor 88 (MyD88) and MyD88-adaptor like (Mal)/Toll-interleukin 1 receptor domain containing adaptor protein (TIRAP) play a critical role in transducing signals downstream of the Toll-like receptor (TLR) family. While genetic ablation of the TLR4/MyD88 signaling axis in mice leads to pulmonary cell death and oxidative stress culminating in emphysema, the involvement of Mal, as well as TLR2 which like TLR4 also signals via MyD88 and Mal, in the pathogenesis of emphysema has not been studied. By employing an in vivo genetic approach, we reveal here that unlike the spontaneous pulmonary emphysema which developed in Tlr42/2 mice by 6 months of age, the lungs of Tlr22/2 mice showed no physiological or morphological signs of emphysema. A more detailed comparative analysis of the lungs from these mice confirmed that elevated oxidative protein carbonylation levels and increased numbers of alveolar cell apoptosis were only detected in Tlr42/2 mice, along with up-regulation of NADPH oxidase 3 (Nox3) mRNA expression. With respect to Mal, the architecture of the lungs of Mal2/2 mice was normal. However, despite normal oxidative protein carbonylation levels in the lungs of emphysema-free Mal2/2 mice, these mice displayed increased levels of apoptosis comparable to those observed in emphysematous Tlr42/2 mice. In conclusion, our data provide in vivo evidence for the non-essential role for TLR2, unlike the related TLR4, in maintaining the normal architecture of the lung. In addition, we reveal that Mal differentially facilitates the anti-apoptotic, but not oxidant suppressive, activities of TLR4 in the lung, both of which appear to be essential for TLR4 to prevent the onset of emphysema