Aberrant protamine 1/protamine 2 ratios in sperm of infertile human males

Summary Protamines were extracted from the sperm of fertile and infertile human males and the relative proportion of protamines 1, 2, and 3 were determined by scanning microdensitometry following electrophoresis of total protamine in polyacrylamide gels. The proportion of the three protamines was found to be similar in sperm obtained from different normal males. The distribution of protamines in sperm obtained from a select group of infertile males producing an elevated level of large sperm heads, in contrast, was different from that of the fertile males.     

A relationship between the yeast cell cycle genes CDC4 and CDC36 and the ets sequence of oncogenic virus E26

We report here significant primary sequence homology among the predicted translational products of three genes: CDC4 , CDC36 and ets. CDC4 and CDC36 are Saccharomyces cerevisiae cell division cycle genes, while ets is a transformation-specific sequence of avian erythroblastosis virus E26. The deduced primary structures of the three gene products were compared by computer to a large data base of known and predicted protein sequences. The search revealed 22.0-25.5% identity over regions of 140-206 codons, respectively between the different pairwise combinations. For these particular sequences, these identity scores fall 3.4-4.0 standard deviations above the empirically-determined mean values of fortuitous similarity. S. cerevisiae calls require CDC36 and CDC4 in order to complete two early events in the cell cycle: execution of start ( CDC36 ) and spindle pole body separation ( CDC4 ). In virus E26, the ets sequence is linked in frame with delta gag and mybE in the tripartite structure 5'-delta gag- mybE -ets-3', comprising the E26 transforming oncogene. The homologies described here suggest that the biochemical functions or regulation of the CDC4 , CDC36 and ets products may be related.     

Maternal imprinting of the mouse Snrpn gene and conserved linkage homology with the human Prader-Willi syndrome region.

Prader-Willi syndrome (PWS) is associated with paternal gene deficiencies in human chromosome 15q11-13, suggesting that PWS is caused by a deficiency in one or more maternally imprinted genes. We have now mapped a gene, Snrpn, encoding a brain-enriched small nuclear ribonucleoprotein (snRNP)-associated polypeptide SmN, to mouse chromosome 7 in a region of homology with human chromosome 15q11-13 and demonstrated that Snrpn is a maternally imprinted gene in mouse. These studies, in combination with the accompanying human mapping studies showing that SNRPN maps in the Prader-Willi critical region, identify SNRPN as a candidate gene involved in PWS and suggest that PWS may be caused, in part, by defects in mRNA processing.     

局部遮挡目标的识别

提出一种局部遮挡目标的识别方法。该方法利用多边形近似方法将目标轮廓分段，抽取目标轮廓每一小段的不变矩作特征，利用动态规划技术在段间距离表中寻找最佳路径，确定所有的匹配对，这些匹配对序列构成了目标与模型的局部匹配，可从局部匹配中计算匹配可信度。该方法简单、有效、抗噪声能力较强，是一种较好的局部目标识别方法。     

A giant planet orbiting the 'extreme horizontal branch' star V 391 Pegasi

After the initial discoveries fifteen years ago, over 200 extrasolar planets have now been detected. Most of them orbit main-sequence stars similar to our Sun, although a few planets orbiting red giant stars have been recently found. When the hydrogen in their cores runs out, main-sequence stars undergo an expansion into red-giant stars. This expansion can modify the orbits of planets and can easily reach and engulf the inner planets. The same will happen to the planets of our Solar System in about five billion years and the fate of the Earth is matter of debate. Here we report the discovery of a planetary-mass body (Msini = 3.2M(Jupiter)) orbiting the star V 391 Pegasi at a distance of about 1.7 astronomical units (au), with a period of 3.2 years. This star is on the extreme horizontal branch of the Hertzsprung-Russell diagram, burning helium in its core and pulsating. The maximum radius of the red-giant precursor of V 391 Pegasi may have reached 0.7 au, while the orbital distance of the planet during the stellar main-sequence phase is estimated to be about 1 au. This detection of a planet orbiting a post-red-giant star demonstrates that planets with orbital distances of less than 2 au can survive the red-giant expansion of their parent stars.     

Label-free immunodetection with CMOS-compatible semiconducting nanowires

Semiconducting nanowires have the potential to function as highly sensitive and selective sensors for the label-free detection of low concentrations of pathogenic microorganisms. Successful solution-phase nanowire sensing has been demonstrated for ions, small molecules, proteins, DNA and viruses; however, 'bottom-up' nanowires (or similarly configured carbon nanotubes) used for these demonstrations require hybrid fabrication schemes, which result in severe integration issues that have hindered widespread application. Alternative 'top-down' fabrication methods of nanowire-like devices produce disappointing performance because of process-induced material and device degradation. Here we report an approach that uses complementary metal oxide semiconductor (CMOS) field effect transistor compatible technology and hence demonstrate the specific label-free detection of below 100 femtomolar concentrations of antibodies as well as real-time monitoring of the cellular immune response. This approach eliminates the need for hybrid methods and enables system-scale integration of these sensors with signal processing and information systems. Additionally, the ability to monitor antibody binding and sense the cellular immune response in real time with readily available technology should facilitate widespread diagnostic applications.     

Preparation and measurement of three-qubit entanglement in a superconducting circuit

Traditionally, quantum entanglement has been central to foundational discussions of quantum mechanics. The measurement of correlations between entangled particles can have results at odds with classical behaviour. These discrepancies grow exponentially with the number of entangled particles. With the ample experimental confirmation of quantum mechanical predictions, entanglement has evolved from a philosophical conundrum into a key resource for technologies such as quantum communication and computation. Although entanglement in superconducting circuits has been limited so far to two qubits, the extension of entanglement to three, eight and ten qubits has been achieved among spins, ions and photons, respectively. A key question for solid-state quantum information processing is whether an engineered system could display the multi-qubit entanglement necessary for quantum error correction, which starts with tripartite entanglement. Here, using a circuit quantum electrodynamics architecture, we demonstrate deterministic production of three-qubit Greenberger-Horne-Zeilinger (GHZ) states with fidelity of 88 per cent, measured with quantum state tomography. Several entanglement witnesses detect genuine three-qubit entanglement by violating biseparable bounds by 830?±?80 per cent. We demonstrate the first step of basic quantum error correction, namely the encoding of a logical qubit into a manifold of GHZ-like states using a repetition code. The integration of this encoding with decoding and error-correcting steps in a feedback loop will be the next step for quantum computing with integrated circuits.     

Deregulated cyclin E induces chromosome instability.

Cyclin E, a regulatory subunit of cyclin-dependent kinase 2 (Cdk2), is an important regulator of entry into S phase in the mammalian cell cycle. In normal dividing cells, cyclin E accumulates at the G1/S-phase boundary and is degraded as cells progress through S phase. However, in many human tumours cyclin E is overexpressed and the levels of protein and kinase activity are often deregulated relative to the cell cycle. It is not understood how alterations in expression of cyclin E contribute to tumorigenesis. Here we show that constitutive cyclin-E overexpression in both immortalized rat embryo fibroblasts and human breast epithelial cells results in chromosome instability (CIN). In contrast, analogous expression of cyclin D1 or A does not increase the frequency of CIN. Cyclin-E-expressing cells that exhibit CIN have normal centrosome numbers. However, constitutive overexpression of cyclin E impairs S-phase progression, indicating that aberrant regulation of this process may be responsible for the CIN observed. These results indicate that downregulation of cyclin-E/Cdk2 kinase activity following the G1/S-phase transition may be necessary for the maintenance of karyotypic stability.     

急性肝功能衰竭的猪动物模型

目的：建立一个比较接近人类条件的急性肝衰竭模型。用于人工肝脏治疗的疗效和安全性的测试。方法：以右旋半乳糖来制造猪肝衰竭的大型动物模型,分组３组给药,剂量分别为０．５、１和０．７５g/kg。观察其临床表现、生理生化指标和病理改变。结果：３组实验都能引出与人的临床和生化指标变化相伫的肝功能衰竭的表现,以０．７５g/kg组最为理想。结论：以０．７５g/kg的半乳糖胺制造的急性肝功能衰竭的猪动物模型,符合人工肘脏研究对动物模型的要求。     

Birc2 (cIap1) regulates endothelial cell integrity and blood vessel homeostasis

Integrity of the blood vessel wall is essential for vascular homeostasis and organ function. A dynamic balance between endothelial cell survival and apoptosis contributes to this integrity during vascular development and pathological angiogenesis. The genetic and molecular mechanisms regulating these processes in vivo are still largely unknown. Here, we show that Birc2 (also known as cIap1) is essential for maintaining endothelial cell survival and blood vessel homeostasis during vascular development. Using a forward-genetic approach, we identified a zebrafish null mutant for birc2, which shows severe hemorrhage and vascular regression due to endothelial cell integrity defects and apoptosis. Using genetic and molecular approaches, we show that Birc2 positively regulates the formation of the TNF receptor complex I in endothelial cells, thereby promoting NF-kappaB activation and maintaining vessel integrity and stabilization. In the absence of Birc2, a caspase-8-dependent apoptotic program takes place that leads to vessel regression. Our findings identify Birc2 and TNF signaling components as critical regulators of vascular integrity and endothelial cell survival, thereby providing an additional target pathway for the control of angiogenesis and blood vessel homeostasis during embryogenesis, regeneration and tumorigenesis.