Flow-induced release of adenosine 5′-triphosphate from endothelial cells of the rat mesenteric arterial bed

Adenosine 5q75u9/xxlarge8242.gif" alt="prime" align="BASELINE" BORDER="0">-triphosphate (ATP) was released into the perfusate of rat isolated mesenteric arterial beds during each of two consecutive increases in flow. There was no significant difference between the amounts of ATP released on each occasion. Substance P was also released into the perfusate by increased flow, although its release was more variable. Removal of the endothelium of the mesenteric vessels with sodium deoxycholate led to a significant reduction (74%) in the amount of ATP released compared with the release before the endothelium had been removed. This suggests that the ATP released into the mesenteric arterial perfusate during increased flow arises from endothelial cells.     

Bromocriptine-induced removal of endoplasmic membranes from prolactinoma cells

Summary Adenomatous prolactin cells lose 39% of their cytoplasm volume within 7 days after the beginning of bromocriptine treatment. A simultaneous reduction of the rough-surfaced endoplasmic reticulum and the Golgi apparatus occurs. Their membranes are removed by rapid transport along the secretory pathway to the cell surface and to lysosomal destruction.We thank Prof. E. del Pozo, Sandoz Ltd, Basle, for the generous gift of injectable bromocriptine, Prof. E.R. Weibel, Dept. of Anatomy, University of Bern, for his technical advice, Dr U. Helfenstein, Institute of Biostatistics, University of Zürich, for his help in the statistical evaluation of the results and the EMDO-Foundation, Zürich, for financial support.     

The susceptibility to exercise-induced muscle damage increases as rats grow larger

Summary Glucose-6-phosphate dehydrogenase and N-acetyl-q314647668080567/xxlarge946.gif" alt="beta" align="MIDDLE" BORDER="0">-glucosaminidase activities were both elevated after eccentric exercise indicating that this type of exercise causes muscle damage. Muscle damage as measured by glucose-6-phosphate dehydrogenase activity in the vastus intermedius was greater and occurred later in larger rats indicating that the susceptibility to muscle damage is increased and the repair process delayed in older and larger animals.     

CVD 矩阵与 n-宽度的(p,q)问题

证明了ｄ２ｋ＝δ２ｋ＝ｄ２ｋ≥ｂ２ｋ，其中ｄ２ｋ、δ２ｋ、ｂ２ｋ分别表示Ａ（ＢＭｐ）在ｌＮｇ中的ｋｏｌｍｏｇｒｏｖ、线性、Ｂｅｒｎｓｔｅｉｎ型２ｋ－宽度，ｄ２ｋ表示ＡＴ（ＢｌＮｑ′）在ｌＭｐ′中Ｇｅｌ′ｆａｎｄ型２ｋ－宽度，这里Ａ（ＢＭｐ）＝｛Ａｘ：ｘ∈ＡｌＭｐ，‖ｘ‖ｐ≤１｝，其中Ａ是一个Ｎ×Ｍ的ＣＶＤ矩陈（Ｎ＞Ｍ＝ｒａｎｋＡ，Ｍ是奇数），１ｐ＋１ｐ′＝１，１ｑ＋１ｑ′＝１（１≤ｑ≤ｐ＜＋∞，ｐ≠１）．     

连续鞅极大算子加Ap,q权特征性刻划

本文对连续鞅的极大算子的加双权Ａｐ，ｑ权有界性进行了估计，从而把调和分析极大算子加Ａｐ，ｑ权特征刻划引入到连续鞅里。     

The genomic basis of the Williams – Beuren syndrome

The Williams-Beuren syndrome is a genomic disorder (prevalence: 1/7,500 to 1/20,000), caused by a hemizygous contiguous gene deletion on chromosome 7q11.23. Typical symptoms comprise supravalvular aortic stenosis, mental retardation, overfriendliness and visuospatial impairment. The common deletion sizes range of 1.5–1.8 mega base pairs (Mb), encompassing app. 28 genes. For a few genes, a genotype-phenotype correlation has been established. The best-explored gene within this region is the elastin gene; its haploinsufficiency causes arterial stenosis. The region of the Williams-Beuren syndrome consists of a single copy gene region (~1.2 Mb) flanked by repetitive sequences – Low Copy Repeats (LCR). The deletions arise as a consequence of misalignment of these repetitive sequences during meiosis and a following unequal crossing over due to high similarity of LCRs. This review presents an overview of the Williams-Beuren syndrome region considering the genomic assembly, chromosomal rearrangements and their mechanisms (i.e. deletions, duplications, inversions) and evolutionary and historical aspects. Received 11 July 2008; received after revision 15 October 2008; accepted 16 October 2008     

Bose—Einstein关联的方向性

本文研究了Ｂｏｓｅ—Ｅｉｎｓｔｅｉｎ关联的方向性。运用一种简捷的方法，从一般的源分布讨论ｑ的角分布，得到一个确定发射源形状的公式。运用参数η＝（Ｎ＿１＋Ｎ＿２）／（Ｎ＿１＋Ｎ＿２）和ａ＝ｒ＿（ｘｙ）／ｒ＿ｚ，很容易确定源的形状。由此对Ａｋｅｓｓｏｎ数据进行处理，得到一个纵向扩展源。进一步对此结果进行了讨论和处理。     

关于整函数增长性的一些注记

我们推广C.T.Rajagopal关于整函数实部最大模的一个定理,并对金忆丹一文中的一个主要结果予以简明的重证。     

单支方法的收敛性与稳定性

本文针对Ｂａｎａｃｈ空间中一类非刚性问题，构造了一类单支方法，证明了该方法是稳定的，且当其ｑ阶相容时是ｑ阶收敛的，此外，还给出了该方法的一个整体截断误差的先验界。     

高度平面图的L(p,q)—标号

研究高度平面图G的L(p,q)-标号问题，证明了高度平面图h1-图的L(p,q)-标号数满足:λ(G;p,q)(2q-1)Δ+6(p-q)；h2-图的L(p,q)-标号数满足:λ(G;p,q)(2q-1)Δ+8p-6q-1. 对于L(2,1)标号问题Griggs和Yeh有一著名猜想：对最大度为Δ的任意图有λ(G)Δ2. 此猜想对高度平面图是正确的.