A non‐linear dynamic model for multiplicative seasonal‐trend decomposition

A non‐linear dynamic model is introduced for multiplicative seasonal time series that follows and extends the X‐11 paradigm where the observed time series is a product of trend, seasonal and irregular factors. A selection of standard seasonal and trend component models used in additive dynamic time series models are adapted for the multiplicative framework and a non‐linear filtering procedure is proposed. The results are illustrated and compared to X‐11 and log‐additive models using real data. In particular it is shown that the new procedures do not suffer from the trend bias present in log‐additive models. Copyright © 2002 John Wiley & Sons, Ltd.     

Decidual cell reaction in ovariectomized-adrenalectomized rats

Enhancement of decidual cell reaction (DCR) following adrenalectomy was reversed by corticosterone as well as indomethacin. The results suggest the adrenal involvement in DCR through uterine prostaglandin production.     

p53-induced inhibition of Hif-1 causes cardiac dysfunction during pressure overload

Cardiac hypertrophy occurs as an adaptive response to increased workload to maintain cardiac function. However, prolonged cardiac hypertrophy causes heart failure, and its mechanisms are largely unknown. Here we show that cardiac angiogenesis is crucially involved in the adaptive mechanism of cardiac hypertrophy and that p53 accumulation is essential for the transition from cardiac hypertrophy to heart failure. Pressure overload initially promoted vascular growth in the heart by hypoxia-inducible factor-1 (Hif-1)-dependent induction of angiogenic factors, and inhibition of angiogenesis prevented the development of cardiac hypertrophy and induced systolic dysfunction. Sustained pressure overload induced an accumulation of p53 that inhibited Hif-1 activity and thereby impaired cardiac angiogenesis and systolic function. Conversely, promoting cardiac angiogenesis by introducing angiogenic factors or by inhibiting p53 accumulation developed hypertrophy further and restored cardiac dysfunction under chronic pressure overload. These results indicate that the anti-angiogenic property of p53 may have a crucial function in the transition from cardiac hypertrophy to heart failure.     

Loss of the autophagy protein Atg16L1 enhances endotoxin-induced IL-1beta production

Systems for protein degradation are essential for tight control of the inflammatory immune response. Autophagy, a bulk degradation system that delivers cytoplasmic constituents into autolysosomes, controls degradation of long-lived proteins, insoluble protein aggregates and invading microbes, and is suggested to be involved in the regulation of inflammation. However, the mechanism underlying the regulation of inflammatory response by autophagy is poorly understood. Here we show that Atg16L1 (autophagy-related 16-like 1), which is implicated in Crohn's disease, regulates endotoxin-induced inflammasome activation in mice. Atg16L1-deficiency disrupts the recruitment of the Atg12-Atg5 conjugate to the isolation membrane, resulting in a loss of microtubule-associated protein 1 light chain 3 (LC3) conjugation to phosphatidylethanolamine. Consequently, both autophagosome formation and degradation of long-lived proteins are severely impaired in Atg16L1-deficient cells. Following stimulation with lipopolysaccharide, a ligand for Toll-like receptor 4 (refs 8, 9), Atg16L1-deficient macrophages produce high amounts of the inflammatory cytokines IL-1beta and IL-18. In lipopolysaccharide-stimulated macrophages, Atg16L1-deficiency causes Toll/IL-1 receptor domain-containing adaptor inducing IFN-beta (TRIF)-dependent activation of caspase-1, leading to increased production of IL-1beta. Mice lacking Atg16L1 in haematopoietic cells are highly susceptible to dextran sulphate sodium-induced acute colitis, which is alleviated by injection of anti-IL-1beta and IL-18 antibodies, indicating the importance of Atg16L1 in the suppression of intestinal inflammation. These results demonstrate that Atg16L1 is an essential component of the autophagic machinery responsible for control of the endotoxin-induced inflammatory immune response.     

利用近红外彩色成像技术监测松萎蔫病 Katsunori Nakamura, Mamoru Takehana, Tsuneo Itagaki, Hayato Tashiro,Kazumasa Ohta,Osamu Nakakita

有效监测患病株方法的缺失是导致对松萎蔫病难以成功控制的主要原因之一。利用航空手段调查该病导致的针叶颜色变化已被证明是一种可靠的方法。为了克服该方法固有的缺点，笔者引用了近红外彩色胶片航拍方法。该项技术在获得正摄航拍图像时，通过图像处理可以增强松针颜色变化，获得较直接拍摄图像更明显的色差。因为图像可以在室内仔细处理，因此能解决飞行时间缺乏等问题。但是，该方法也存在对被压木无法获得其影像而漏检的缺陷。笔者研发的计算机软件可以将目标树标记在计算机图像文件上，并且标记树的地理位置数据和背景航拍图像并传输到装有内置GPS接收器的掌上电脑中，借助软件产生的图像导航定位系统，有利于地面接近标记树，从而可以现场检查和校正标记树的数据，并将修正数据传回至主机。此方法利用最新航拍图像技术建立对每株树处理和管理的连续资料，大大改善了防控松萎蔫病的措施。     

Recent progress in understanding the diversity of the human ov-serpin/clade B serpin family

The inhibitory mechanism against proteases is important in the maintenance of homeostasis or health in the body. The human ovalbumin serpin (ovserpin)/ clade B serpin family is one group of the human serpins, a family of serine protease inhibitors. They have acquired diversity in the profiles of target proteases, inhibitory mechanisms, and localization patterns during their evolution. Most serpins target serine proteases, however, some ov-serpins target only cysteine proteases or both serine and cysteine proteases and furthermore, several ov-serpins do not possess inhibitory activities. Although the ov-serpins act primarily as intracellular serpins, some show extracellular and nuclear localizations. Such diversity enables the ov-serpins to play multiple physiological roles in the body. Recent analyses have revealed that the functions of human ov-serpins are more diversified than we previously knew. In this article, we describe recent progress in our understanding of how the human ov-serpin/clade B serpin family demonstrates diversity.