CVD金刚石薄膜的界面能量分析

分析了CVD金刚石薄膜的界面能量情况,并由此研究了金刚石成核几率、晶核取向、附着强度与基底材料结构和性能的关系     

PdCu／ZSM－5催化剂上乙醇一步合成乙酸乙酯反应机理的研究

本文采用程序升温脱附（ＴＰＤ）法、程序升温表面反应（ＴＰＳＲ）法和微反－色谱技术。综合考察了在ＰｄＣｕ／ＺＳＭ－５催化剂上，乙醇、乙醛、乙酸、氧等的吸附、脱附性能，以及不同条件下反应产物的分布规律，推测出乙醇在该催化剂上气相催化一步合成乙酸乙酯过程中的复杂网络图及反应机理，为改善此催化剂性能和进行动力学研究提供了重要信息和依据．     

Clarke导数与Dinin导数

本文讨论了Ｃｌａｒｋｅ导数与Ｄｉｎｉ导数的关系，这一结果为利用Ｃｌａｒｋｅ导数研究函数性质提供了新方法．     

Immunoactive TSH in the amniotic fluid of the rat

Summary Amniotic fluid was obtained from 19-day-old rat fetuses by aspiration. Pooled samples measured at 4 different dilutions demonstrated parallelism with standard rat TSH. It is concluded that rat amniotic fluid has TSH immunoactivity.This work was supported by Hong Kong University Research Grant No. 335/034/5727.The authors wish to acknowledge with thanks the gift of rat TSH RIA kit from Dr A. F. Parlow and the Rat Pituitary Programme of NIAMDD.     

羰基簇合物途径制备的碳载Pt-Co催化剂阴极抗甲醇性能

通过Pt和Co羰基簇合物途径制备了碳载Pt—Co(Pt-Co／C)复合催化剂．其金属粒子的平均粒径小．相对结晶度很低．与商业化的E-TEK Pt／C催化剂相比,该催化剂具有较好的抗甲醇性能和电催化氧还原活性．     

Paxillin binds schwannomin and regulates its density-dependent localization and effect on cell morphology

Neurofibromatosis type 2 is an autosomal dominant disorder characterized by tumors, predominantly schwannomas, in the nervous system. It is caused by mutations in the gene NF2, encoding the growth regulator schwannomin (also known as merlin). Mutations occur throughout the 17-exon gene, with most resulting in protein truncation and undetectable amounts of schwannomin protein. Pathogenic mutations that result in production of defective schwannomin include in-frame deletions of exon 2 and three independent missense mutations within this same exon. Mice with conditional deletion of exon 2 in Schwann cells develop schwannomas, which confirms the crucial nature of exon 2 for growth control. Here we report that the molecular adaptor paxillin binds directly to schwannomin at residues 50-70, which are encoded by exon 2. This interaction mediates the membrane localization of schwannomin to the plasma membrane, where it associates with beta 1 integrin and erbB2. It defines a pathogenic mechanism for the development of NF2 in humans with mutations in exon 2 of NF2.     

Axisymmetric fundamental solutions for a finite layer with impeded boundaries

Axisymmetrie fundamental solutions that are applied in the consolidation calculations of a finite clay layer with impeded boundaries were derived. Laplace and Hankel integral transforms were utilized with respect to time and radial coordinates, respectively in the analysis. The derivation of fundamental solutions considers two boundary-value problems involving unit point loading and ring loading in the vertical. The solut-ions are extended to circular distributed and strip distributed normal load. The computation and analysis of set-tlements, vertical total stress and excess pore pressure in the consolidation layer subject to circular loading are presented.     

Msx2 deficiency in mice causes pleiotropic defects in bone growth and ectodermal organ formation

The composite structure of the mammalian skull, which forms predominantly via intramembranous ossification, requires precise pre- and post-natal growth regulation of individual calvarial elements. Disturbances of this process frequently cause severe clinical manifestations in humans. Enhanced DNA binding by a mutant MSX2 homeodomain results in a gain of function and produces craniosynostosis in humans. Here we show that Msx2-deficient mice have defects of skull ossification and persistent calvarial foramen. This phenotype results from defective proliferation of osteoprogenitors at the osteogenic front during calvarial morphogenesis, and closely resembles that associated with human MSX2 haploinsufficiency in parietal foramina (PFM). Msx2-/- mice also have defects in endochondral bone formation. In the axial and appendicular skeleton, post-natal deficits in Pth/Pthrp receptor (Pthr) signalling and in expression of marker genes for bone differentiation indicate that Msx2 is required for both chondrogenesis and osteogenesis. Consistent with phenotypes associated with PFM, Msx2-mutant mice also display defective tooth, hair follicle and mammary gland development, and seizures, the latter accompanied by abnormal development of the cerebellum. Most Msx2-mutant phenotypes, including calvarial defects, are enhanced by genetic combination with Msx1 loss of function, indicating that Msx gene dosage can modify expression of the PFM phenotype. Our results provide a developmental basis for PFM and demonstrate that Msx2 is essential at multiple sites during organogenesis.     

Functional haploinsufficiency of the human homeobox gene MSX2 causes defects in skull ossification

The genetic analysis of congenital skull malformations provides insight into normal mechanisms of calvarial osteogenesis. Enlarged parietal foramina (PFM) are oval defects of the parietal bones caused by deficient ossification around the parietal notch, which is normally obliterated during the fifth fetal month. PFM are usually asymptomatic, but may be associated with headache, scalp defects and structural or vascular malformations of the brain. Inheritance is frequently autosomal dominant, but no causative mutations have been identified in non-syndromic cases. We describe here heterozygous mutations of the homeobox gene MSX2 (located on 5q34-q35) in three unrelated families with PFM. One is a deletion of approximately 206 kb including the entire gene and the others are intragenic mutations of the DNA-binding homeodomain (RK159-160del and R172H) that predict disruption of critical intramolecular and DNA contacts. Mouse Msx2 protein with either of the homeodomain mutations exhibited more than 85% reduction in binding to an optimal Msx2 DNA-binding site. Our findings contrast with the only described MSX2 homeodomain mutation (P148H), associated with craniosynostosis, that binds with enhanced affinity to the same target. This demonstrates that MSX2 dosage is critical for human skull development and suggests that PFM and craniosynostosis result, respectively, from loss and gain of activity in an MSX2-mediated pathway of calvarial osteogenic differentiation.     

西藏芒康县盐井化探异常分布规律及找矿标志

盐井属于藏东昌都地区芒康县,地处于著名的三江成矿区;藏东地质构造复杂,成矿条件优越,具备形成铜、金、铅、锌、银矿的地质背景,是中国重要的多金属成矿带。根据1∶20万区域化探异常特征优选了芒康县盐井开展1∶5万地球化学测量,Au、Cu、Ag、Pb元素套叠好,异常强度大,属于典型的矿致异常,找矿前景十分广阔,是该区重要找矿靶区。