Magnetic fields at the solar wind termination shock

A transition between the supersonic solar wind and the subsonic heliosheath was observed by Voyager 1, but the expected termination shock was not seen owing to a gap in the telemetry. Here we report observations of the magnetic field structure and dynamics of the termination shock, made by Voyager 2 on 31 August-1 September 2007 at a distance of 83.7 au from the Sun (1 au is the Earth-Sun distance). A single crossing of the shock was expected, with a boundary that was stable on a timescale of several days. But the data reveal a complex, rippled, quasi-perpendicular supercritical magnetohydrodynamic shock of moderate strength undergoing reformation on a scale of a few hours. The observed structure suggests the importance of ionized interstellar atoms ('pickup protons') at the shock.     

The first hominin of Europe

The earliest hominin occupation of Europe is one of the most debated topics in palaeoanthropology. However, the purportedly oldest of the Early Pleistocene sites in Eurasia lack precise age control and contain stone tools rather than human fossil remains. Here we report the discovery of a human mandible associated with an assemblage of Mode 1 lithic tools and faunal remains bearing traces of hominin processing, in stratigraphic level TE9 at the site of the Sima del Elefante, Atapuerca, Spain. Level TE9 has been dated to the Early Pleistocene (approximately 1.2-1.1 Myr), based on a combination of palaeomagnetism, cosmogenic nuclides and biostratigraphy. The Sima del Elefante site thus emerges as the oldest, most accurately dated record of human occupation in Europe, to our knowledge. The study of the human mandible suggests that the first settlement of Western Europe could be related to an early demographic expansion out of Africa. The new evidence, with previous findings in other Atapuerca sites (level TD6 from Gran Dolina), also suggests that a speciation event occurred in this extreme area of the Eurasian continent during the Early Pleistocene, initiating the hominin lineage represented by the TE9 and TD6 hominins.     

Molecular evolution of connective tissue growth factor in Cyprinidae （Teleostei： Cypriniformes）

Connective tissue growth factor （CTGF） plays an important role in regulation of cell growth, differentiation, apoptosis and individual development in animals. The study of sequences variation and molecular evolution of CTGF gene across various species of the cyprinid could be helpful for understanding of speciation and gene divergence in this kind of fish. In this study, 19 novel sequences of CTGF gene were obtained from the representative species of the family Cyprinidae using PCR amplification, cloning and sequencing. Phylogenetic relationships of Cyprinidae were reconstructed by neighbor-joining （NJ）, maximum parsimony （MP）, maximum likelihood （ML） and Bayesian method. Oryzias latipes from the family Cyprinodontidae was assigned to be the outgroup taxon. Leuciscini and Barbini were clustered into the monophyletic lineages, respectively, with the high nodal supports. The estimation of the ratio of non-synonymous to synonymous substitution （dN/dS） for the various branches indicated that there stood the different evolution rates between the Leuciscini and the Barbini. With the ratio of dN/dS of the Leuciscini being lower than that of the Barbini, species within the Barbini were demonstrated to be subjected to the relatively less selection pressure and under the relaxable evolution background. A 6 bp indel （insertion/deletion） was found at the 5＇ end of CTGF gene of Cyprinidae, and this 6 bp deletion only appeared in the Leuciscini, which is a typical characteristic of the Leuciscini and provides evidence for the monophylogeny of the Leuciscini. For the amino acid sequences of CTGF protein, the most variations and indels were distributed in the signal region and IGFBP region of this protein, implying that these variations were correlated with the regulation of the CTGF gene expression and protein activity.     

A Cretaceous terrestrial snake with robust hindlimbs and a sacrum

It has commonly been thought that snakes underwent progressive loss of their limbs by gradual diminution of their use. However, recent developmental and palaeontological discoveries suggest a more complex scenario of limb reduction, still poorly documented in the fossil record. Here we report a fossil snake with a sacrum supporting a pelvic girdle and robust, functional legs outside the ribcage. The new fossil, from the Upper Cretaceous period of Patagonia, fills an important gap in the evolutionary progression towards limblessness because other known fossil snakes with developed hindlimbs, the marine Haasiophis, Pachyrhachis and Eupodophis, lack a sacral region. Phylogenetic analysis shows that the new fossil is the most primitive (basal) snake known and that all other limbed fossil snakes are closer to the more advanced macrostomatan snakes, a group including boas, pythons and colubroids. The new fossil retains several features associated with a subterranean or surface dwelling life that are also present in primitive extant snake lineages, supporting the hypothesis of a terrestrial rather than marine origin of snakes.     

废弃玻璃骨料混凝土梁抗剪性能研究

运用简支梁的抗剪试验分别研究了用玻璃粗集料和玻璃细集料取代混凝土中粗骨料和细骨料对混凝土梁斜截面的破坏形态和抗剪承载力的影响。试验结果表明:玻璃集料混凝土梁的剪切破坏形态与普通混凝土梁基本相同;玻璃细集料混凝土梁与普通混凝土梁初始抗弯刚度基本相同,粗集料混凝土梁相对较小;玻璃集料混凝土梁的开裂荷载与普通集料混凝土梁接近;废弃玻璃细集料混凝土梁的抗剪承载力比普通混凝土梁高5%左右,废弃玻璃粗集料混凝土梁抗剪承载力比普通混凝土梁低13%左右。     

Action mechanisms of a new erythrocyte-derived depressing factor

To investigate the action mechanisms of a new erythrocyte-derived depressing factor (EDDF), the focus is placed on the effect of EDDF on both cytosolic and nuclear free calcium (Ca²⁺) transportation in vascular smooth muscle cell (VSMC), as well as the apoptosis and cell cycle of VSMC of rats. EDDF has been extracted from human erythrocytes. The changes of Ca²⁺ levels in cytoplasm ([Ca²⁺]_i) and nucleus ([Ca²⁺]_n) have been observed using a laser scanning confocal microscope together with fluo-3/AM as a calcium indicator. Flow cytometric technique was used to study the effect of EDDF on cell cycle and apoptosis of VSMC. [Ca²⁺], and [Ca²⁺]_n were significantly decreased through several different pathways: ( i ) it reduced the Ca²⁺ influx by blocking L-type voltage-dependent calcium channel (L-VDC) and R-type voltage-dependent calcium channel (R-VDC); (ii) it inhibited the Ca²⁺ release from inositol 1, 4, 5-trisphosphate (IP₃) sensitive calcium store; and (iii) activated Ca²⁺-ATPase of sarcoplasmic reticulum (SR) and promoted the transportation of Ca²⁺ from cytoplasm to SR. However, EDDF seemed to have little inhibitory effect on the Ca²⁺ release from ryonodine sensitive calcium pool. It was also found that EDDF (10⁻⁴ g/mL) significantly decreased the proportion of S phase of human umbilical vein (HUV) and inhibited the proliferation of VSMC induced by angiotensin II (Angll, 10⁻⁵ mol/L). The apopotosis did not occur when VSMC was cultured under normal condition. While VSMC apoptosis was induced by Angll (10⁻⁵ mol/L) and EDDF (10⁻⁴ g/mL) seemed to have little effect on it. The inhibitory effect of EDDF on the elevation of [Ca²⁺]_i and [Ca²⁺]_n of VSMC might play an essential role in its action mechanisms and the ways it affects the Ca²⁺ handling of VSMC demonstrate that EDDF was different from other endogenous blood pressure regulators and some known antihypertensive drugs. EDDF could inhibit the proliferation of VSMC, which indicated that it might be beneficial to the prevention and treatment of hypertension and arteriosclerosis.     

Interaction between integrin αIIbβ3 and synthesized cyclic hexapeptide containing RGD

The RGD sequence generally exists in the extracellular matrix proteins and can be recognized by many integrin proteins. The binding ability of immobilized biotinylated cyclic hexapeptide [cyclo(-Arg-Gly-Asp-D-Phe-Lys-Gly-)] containing RGD to integrin α_αbβ₃ was tested by the methods of ELISA and SPR. Results showed that a spacer of 1.48–2.2 nm between the peptide and the biotin residue was long enough to send the RGD sequence into the binding center embccedded within α_IIbβ₃, and the equilibrium dissociation constant was 1.1 μm. The work provides an ideal model system for the research of cell adhesion on solid surfaces.     

Emerging topics and new perspectives on HLA-G

Following the Fifth International Conference on non-classical HLA-G antigens (HLA-G), held in Paris in July 2009, we selected some topics which focus on emerging aspects in the setting of HLA-G functions. In particular, HLA-G molecules could play a role in: (1) various inflammatory disorders, such as multiple sclerosis, intracerebral hemorrhage, gastrointestinal, skin and rheumatic diseases, and asthma, where they may act as immunoregulatory factors; (2) the mechanisms to escape immune surveillance utilized by several viruses, such as human cytomegalovirus, herpes simplex virus type 1, rabies virus, hepatitis C virus, influenza virus type A and human immunodeficiency virus 1 (HIV-1); and (3) cytokine/chemokine network and stem cell transplantation, since they seem to modulate cell migration by the downregulation of chemokine receptor expression and mesenchymal stem cell activity blocking of effector cell functions and the generation of regulatory T cells. However, the immunomodulatory circuits mediated by HLA-G proteins still remain to be clarified.     

Exome sequencing identifies MAX mutations as a cause of hereditary pheochromocytoma

Hereditary pheochromocytoma (PCC) is often caused by germline mutations in one of nine susceptibility genes described to date, but there are familial cases without mutations in these known genes. We sequenced the exomes of three unrelated individuals with hereditary PCC (cases) and identified mutations in MAX, the MYC associated factor X gene. Absence of MAX protein in the tumors and loss of heterozygosity caused by uniparental disomy supported the involvement of MAX alterations in the disease. A follow-up study of a selected series of 59 cases with PCC identified five additional MAX mutations and suggested an association with malignant outcome and preferential paternal transmission of MAX mutations. The involvement of the MYC-MAX-MXD1 network in the development and progression of neural crest cell tumors is further supported by the lack of functional MAX in rat PCC (PC12) cells and by the amplification of MYCN in neuroblastoma and suggests that loss of MAX function is correlated with metastatic potential.