2-D dopant profiling in VLSI devices using dopant-selectiveetching: an atomic force microscopy study

We report a detailed mapping of a 2-D dopant profile on a fully processed industrial sample with large dynamic range and high spatial resolution by utilizing a dopant-selective etching process and Atomic Force Microscopy. The experimental results show excellent agreement with those obtained from SRP and SIMS as corroborative methods. We also discuss the most critical factors which influence the applicability, reproducibility, and reliability of this method     

Nonlinear dynamics of femtosecond optical solitary wave propagationat the zero dispersion point

A perturbed nonlinear Schrodinger equation, describing nonlinear pulse propagation of femtosecond duration in optical fibers at the zero dispersion point, is considered. This equation is reduced to an ordinary differential equation, which is treated by means of Hamiltonian dynamics techniques. Conditions for solitary wave formation, as well as the solutions themselves, namely, a bright soliton, a rarefaction soliton, and a pair of dark solitons, are derived analytically. The shifts of the solitary wave velocity, the angular frequency, and the wavenumber, as well as the peak power required to launch a bright soliton are also obtained. The connection among the point initial conditions of the pulse and the type of solitary wave that can be excited is finally presented     

Full-wave computation of constitutive parameters for losslesscomposite chiral materials

Composite chiral materials are realized by embedding large numbers of handed inclusions within a host material. A computational methodology is presented whereby the effective constitutive parameters of artificial chiral materials are computed while accounting for all self and mutual interactions among the inclusions. This technique combines a full-wave, Monte-Carlo scattering solution for randomly oriented inclusions together with an analytical solution for the scattering by a canonically-shaped body having a properly chosen constitutive model. It is believed that the effective constitutive parameters shown in this paper are the first full-wave computation of these quantities to appear in the literature     

Immunological properties of Weil-Felix test negative sera from patients with Japanese spotted fever

Sera from 4 out of 19 patients with the Japanese spotted fever were negative to OX2 antigen of Weil-Felix (WF) test. These WF test negative sera were analyzed by ELISA and immunoblot used whole cells and lipopolysaccharides (LPS) of rickettsiae and Proteus strains as antigens. These acute-phase sera have already possessed the IgG antibodies against LPS of Proteus OX2 strain, whereas IgM antibodies in these acute- and convalescent-phase sera did not react with this LPS. On the other hand, the reactivity of IgM antibodies of the convalescent-phase sera in the 2 patients with LPS of Proteus OX19 strain increased as compared with that of the acute-phase sera by ELISA, and these IgM antibodies also showed the reactivity with bands of OX19-LPS in the immunoblot. On the basis of these results, it is interpreted that the WF test negative sera from patients with Japanese spotted fever are due to the presence of IgG antibodies against OX2-LPS in the sera.     

Angiotensin II regulates the expression of plasminogen activator inhibitor-1 in cultured endothelial cells. A potential link between the renin-angiotensin system and thrombosis

Plasminogen activator-inhibitor C-1 (PAI-1) plays a critical role in the regulation of fibrinolysis, serving as the primary inhibitor of tissue-type plasminogen activator. Elevated levels of PAI-1 are a risk factor for recurrent myocardial infarction, and locally increased PAI-1 expression has been described in atherosclerotic human arteries. Recent studies have shown that the administration of angiotensin converting enzyme inhibitors reduces the risk of recurrent myocardial infarction in selected patients. Since angiotensin II (Ang II) has been reported to induce PAI-1 production in cultured astrocytes, we have hypothesized that one mechanism that may contribute to the beneficial effect of angiotensin converting enzyme inhibitors is an effect on fibrinolytic balance. In the present study, we examined the interaction of Ang II with cultured bovine aortic endothelial cells (BAECs) and the effects of this peptide on the production of PAI-1. 125I-Ang II was found to bind to BAECs in a saturable and specific manner, with an apparent Kd of 1.4 nM and Bmax of 74 fmol per mg of protein. Exposure of BAECs to Ang II induced dose-dependent increases in PAI-1 antigen in the media and in PAI-1 mRNA levels. Induction of PAI-1 mRNA expression by Ang II was not inhibited by pretreating BAECs with either Dup 753 or [Sar1, Ile8]-Ang II, agents that are known to compete effectively for binding to the two major angiotensin receptor subtypes. These data indicate that Ang II regulates the expression of PAI-1 in cultured endothelial cells and that this response is mediated via a pharmacologically distinct form of the angiotensin receptor.     

Subarachnoid haemorrhage induced proliferation of leptomeningeal cells and deposition of extracellular matrices in the arachnoid granulations and subarachnoid space. Immunhistochemical study

Subarachnoid haemorrhage (SAH) often leads to subarachnoid fibrosis and resultant normal pressure hydrocephalus; however, how subarachnoid fibrosis occurs is unknown. We examined the changes within arachnoid granulations (AGs) and the subarachnoid space (SAS) chronologically at the parasagittal region obtained from patients with SAH at autopsy and made comparison with controls by immunostaining for cytokeratin, specific marker for leptomeningeal cells and by the elastica Masson-Goldner methods. Within a week some AGs were torn, and many inflammatory cells filled the AGs and SAS. Cytokeratin positive cells were scarce. During the next two weeks cytokeratin positive cells increased. After three weeks, AGs and SAS were filled by dense deposits of extracellular matrices surrounded by multiple layers of leptomeningeal cells.