预蠕变损伤对高温疲劳宏观裂纹扩展的影响

针对ＳＵＳ３０４不锈钢光滑试棒预先导入１０７３ Ｋ·ｃｐ－ｔｙｐｅ条件下的预蠕变疲劳损伤，然后开小切口进行时间依存性 ９２３ Ｋ·ｃｐ－ｔｙｐｅ，１０７３ Ｋ·ｃｐ－ｔｙｐｅ及循环数依存性９２３ Ｋ·ｐｐ－ｔｙｐｅ的宏观裂纹扩展试验，考察了试棒内部因预蠕变疲劳而产生的大量的粒界微小裂纹对高温疲劳宏观裂纹扩展的影响．结果如下： １．预损伤加速了９２３ Ｋ·ｃｐ－ｔｙｐｅ下的蠕变裂纹扩展，对于同一蠕变Ｊ积分范围△Ｊｃ，损伤值越大，裂纹扩展速度ｄｌ／ｄＮ也越大．这种加速起因于主裂纹与微小裂纹的合体． ２．１０７３ Ｋ·ｃｐ－ｔｙｐｅ下的预损伤材料和处女材料的ｄｌ／ｄＮ在同一△Ｊｃ。下相等．即，损伤材料的裂纹扩展速度的上限值由１０７３ Ｋ·ｃｐ－ｔｙｐｅ下的处女材料的ｄｌ／ｄＮ－△Ｊｃ关系给出． ３．在９２３ Ｋ·ｐｐ－ｔｙｐｅ条件下，对于同一疲劳Ｊ积分范围△Ｊｆ，预损伤材料的ｄｌ／ｄＮ要比处女材料快１０倍左右．一般ｐｐ－ｔｙｐｅ的破坏形式为粒内破坏．预损伤材料的场合，因为试棒内部分布有大量的微小粒界裂纹，主裂纹便沿这些破坏阻抗最小的微小裂纹边合体边扩展，主要在粒界上扩展．即微小粒界裂纹是裂纹扩展阻抗减小的主因．     

Selective coupling with K+ currents of muscarinic acetylcholine receptor subtypes in NG108-15 cells

The primary structures of two muscarinic acetylcholine receptor (mAChR) species, designated as mAChR I and mAChR II, have been elucidated by cloning and sequence analysis of DNAs complementary to the porcine cerebral and cardiac messenger RNAs, respectively. mAChR I and mAChR II expressed in Xenopus oocytes differ from each other both in acetylcholine-induced response and in antagonist binding properties. These results, together with the differential tissue location of the two mAChR mRNAs, have indicated that pharmacologically distinguishable subtypes of the mAChR represent distinct gene products. The primary structures of two additional mammalian mAChR species, designated as mAChR III and mAChR IV, have subsequently been deduced from the nucleotide sequences of the cloned cDNAs or genomic DNAs. We report here that mAChR I and mAChR III expressed in NG108-15 neuroblastoma-glioma hybrid cells, but not mAChR II and mAChR IV, efficiently mediate phosphoinositide hydrolysis, activation of a Ca2+-dependent K+ current and inhibition of the M-current, a voltage-dependent K+ current sensitive to muscarinic agonists.     

Forecasting real‐time data allowing for data revisions

A modeling approach to real‐time forecasting that allows for data revisions is shown. In this approach, an observed time series is decomposed into stochastic trend, data revision, and observation noise in real time. It is assumed that the stochastic trend is defined such that its first difference is specified as an AR model, and that the data revision, obtained only for the latest part of the time series, is also specified as an AR model. The proposed method is applicable to the data set with one vintage. Empirical applications to real‐time forecasting of quarterly time series of US real GDP and its eight components are shown to illustrate the usefulness of the proposed approach. Copyright © 2007 John Wiley & Sons, Ltd.     

Regulation of myelopoiesis by proinflammatory cytokines in infectious diseases

Hematopoiesis is hierarchically orchestrated by a very small population of hematopoietic stem cells (HSCs) that reside in the bone-marrow niche and are tightly regulated to maintain homeostatic blood production. HSCs are predominantly quiescent, but they enter the cell cycle in response to inflammatory signals evoked by severe systemic infection or injury. Thus, hematopoietic stem and progenitor cells (HSPCs) can be activated by pathogen recognition receptors and proinflammatory cytokines to induce emergency myelopoiesis during infection. This emergency myelopoiesis counterbalances the loss of cells and generates lineage-restricted hematopoietic progenitors, eventually replenishing mature myeloid cells to control the infection. Controlled generation of such signals effectively augments host defense, but dysregulated stimulation by these signals is harmful to HSPCs. Such hematopoietic failure often results in blood disorders including chronic inflammatory diseases and hematological malignancies. Recently, we found that interleukin (IL)-27, one of the IL-6/IL-12 family cytokines, has a unique ability to directly act on HSCs and promote their expansion and differentiation into myeloid progenitors. This process resulted in enhanced production of neutrophils by emergency myelopoiesis during the blood-stage mouse malaria infection. In this review, we summarize recent advances in the regulation of myelopoiesis by proinflammatory cytokines including type I and II interferons, IL-6, IL-27, granulocyte colony-stimulating factor, macrophage colony-stimulating factor, and IL-1 in infectious diseases.     

Heterogeneous responses of canine basilar and middle cerebral arteries to serotonin at normal and high CO2 tension.

The responses of basilar arteries (BAs) to serotonin were attenuated by high PCO2 (86 +/- 1 mm Hg) and the pH matched acidotic solution (PCO2 37 +/- 1 mm Hg), whereas the responses of middle cerebral arteries (MCAs) were not. High PCO2 decreased the basal tone of both arteries, and the changes in basal tone due to high PCO2 were not influenced by 3 x 10(-7) M imipramine, 10(-5) M pargyline or 10(-4) M aspirin. The responses of BAs to serotonin were attenuated by high PCO2 in the presence of imipramine, pargyline and aspirin. The responses of MCAs to serotonin were not influenced by high PCO2 in the presence of pargyline and aspirin, but attenuated by high PCO2 in the presence of imipramine.     

Seasonality in human sleep

The timing of sleep and sleep EEG parameters in 10 healthy male subjects were investigated in four seasons under controlled conditions. The phase of nocturnal sleep was delayed about one and a half hours in winter as compared to that in summer. The duration of stage 4 sleep decreased and REM sleep increased significantly in winter compared with summer. The seasonality in the timing of sleep can be explained by photoperiodic time cues, but the changes in sleep EEG parameters are diffucult to explain in terms of photoperiod.     

Cloning, sequencing and expression of complementary DNA encoding the muscarinic acetylcholine receptor

Cloning and sequence analysis of DNA complementary to porcine cerebral messenger RNA encoding the muscarinic acetylcholine receptor predict the complete amino-acid sequence of this protein. Expression of the complementary DNA produced functional muscarinic receptor in Xenopus oocytes. The muscarinic receptor is homologous with the beta-adrenergic receptor and rhodopsin in both amino-acid sequence and suggested transmembrane topography.     

Structure of the inositol 1,4,5-trisphosphate receptor binding core in complex with its ligand

In a variety of cells, the Ca2+ signalling process is mediated by the endoplasmic-reticulum-membrane-associated Ca2+ release channel, inositol 1,4,5-trisphosphate (InsP3) receptor (InsP3R). Being ubiquitous and present in organisms ranging from humans to Caenorhabditis elegans, InsP3R has a vital role in the control of cellular and physiological processes as diverse as cell division, cell proliferation, apoptosis, fertilization, development, behaviour, memory and learning. Mouse type I InsP3R (InsP3R1), found in high abundance in cerebellar Purkinje cells, is a polypeptide with three major functionally distinct regions: the amino-terminal InsP3-binding region, the central modulatory region and the carboxy-terminal channel region. Here we present a 2.2-A crystal structure of the InsP3-binding core of mouse InsP3R1 in complex with InsP3. The asymmetric, boomerang-like structure consists of an N-terminal beta-trefoil domain and a C-terminal alpha-helical domain containing an 'armadillo repeat'-like fold. The cleft formed by the two domains exposes a cluster of arginine and lysine residues that coordinate the three phosphoryl groups of InsP3. Putative Ca2+-binding sites are identified in two separate locations within the InsP3-binding core.