Prenatal cocaine delays astroglial maturation: immunodensitometry shows increased markers of immaturity (vimentin and GAP-43) and decreased proliferation and production of the growth factor S-100

Exposure to cocaine during fetal development has been demonstrated to produce a variety of brain and behavioral changes. Cocaine is a potent releaser of a variety of neurotransmitters, such as serotonin, which act as developmental signals. Since serotonin plays an important role in astroglial maturation, migration, and growth factor production (e.g. S-100 beta), we proposed that these properties of astroglial cells will be altered in a brain prenatally exposed to cocaine. To observe cocaine's effects on astroglial development, we performed immunocytochemical analyses of a variety of developmental protein makers including BrdU, Gap-43, vimentin, and S100 beta. Our results demonstrate that prenatal cocaine administration produces decreased cell proliferation as measured by BrdU staining, retarded neurite outgrowth as ascertained by increased Gap-43 immunoreactivity, increased density of vimentin-positive radial glial cells, and diminished tissue S100 beta immunoreactivity. Overall, these results suggest that cocaine delays astroglial development. This delay would have profound effects on neuronal development and outgrowth and, thus, development of the entire brain.     

Transconductance and mobility of Si:B delta MOSFETs

Delta-doped MOSFETs have been fabricated in MBE-grown silicon using for the first time boron as the dopant within the delta layer. Current-voltage characteristics have been measured, and secondary ion mass spectrometry (SIMS) is used to confirm the location of the delta layer and the extent of layer broadening by diffusion during processing. Precise threshold voltages of the devices are difficult to determine since the devices (which all operate in depletion mode) take several volts to switch off. Transconductances of the devices have been measured, and it is shown how analysis of these results can yield estimates of the carrier mobility for transport along the delta layers despite the uncertainty in the threshold voltage. A clear transition is observed in the results which is attributed to the formation of a parasitic surface-channel field-effect transistor, providing conclusive evidence that the devices are conducting along a delta channel for part of the measured range of applied gate biases     

Four state binary QAM trellis code better than known codes

Presents a new one-memory quaternary four-state trellis code, and its four-state binary equivalent code based on a QAM constellation which is 0.52 dB better than the four-state Ungerboeck code.<>     

Crystal structure of tRNA-guanine transglycosylase: RNA modification by base exchange

tRNA-guanine transglycosylases (TGT) are enzymes involved in the modification of the anticodon of tRNAs specific for Asn, Asp, His and Tyr, leading to the replacement of guanine-34 at the wobble position by the hypermodified base queuine. In prokaryotes TGT catalyzes the exchange of guanine-34 with the queuine (.)precursor 7-aminomethyl-7-deazaguanine (preQ1). The crystal structure of TGT from Zymomonas mobilis was solved by multiple isomorphous replacement and refined to a crystallographic R-factor of 19% at 1.85 angstrom resolution. The structure consists of an irregular (beta/alpha)8-barrel with a tightly attached C-terminal zinc-containing subdomain. The packing of the subdomain against the barrel is mediated by an alpha-helix, located close to the C-terminus, which displaces the eighth helix of the barrel. The structure of TGT in complex with preQ1 suggests a binding mode for tRNA where the phosphate backbone interacts with the zinc subdomain and the U33G34U35 sequence is recognized by the barrel. This model for tRNA binding is consistent with a base exchange mechanism involving a covalent tRNA-enzyme intermediate. This structure is the first example of a (beta/alpha)-barrel protein interacting specifically with a nucleic acid.     

193-nm lithography

The trend in microelectronics toward printing features 0.25 μm and below has motivated the development of lithography at the 193-nm wavelength of argon fluoride excimer lasers. This technology is in its early stages, but a picture is emerging of its strengths and limitations. The change in wavelength from 248 to 193 nm will require parallel progress in projection systems, optical materials, and photo-resist chemistries and processes. This paper reviews the current status of these various topics as they have been engineered under a multiyear program at MIT Lincoln Laboratory     

Enhanced electron emission from phosphorus-doped diamond-cladsilicon field emitter arrays

Undoped and phosphorus (P)-doped diamond-clad Si field emitter arrays have been successfully fabricated using microwave plasma chemical vapor deposition (MPCVD) technology. The electron emission from the blunt diamond-clad microtips are much higher than those for the pure Si tips with sharp curvature due to a lower work function. Furthermore, the characteristics of emission current against applied voltage for the P-doped diamond-clad tips show superior emission at lower field to the undoped ones. After the examination of Auger electron spectroscopy (AES) and electrical characteristics of as-grown diamond, such a significant enhancement of the electron emission from the P-doped diamond-clad tips is attributed to a higher electron conductivity and defect densities     

The natural killer cell receptor specific for HLA-A allotypes: a novel member of the p58/p70 family of inhibitory receptors that is characterized by three immunoglobulin-like domains and is expressed as a 140-kD disulphide-linked dimer

Human natural killer (NK) cells express inhibitory receptors that are specific for different groups of HLA-C or HLA-B alleles. The majority of these receptors belong to the immunoglobulin (Ig) superfamily and are characterized by two or three extracellular Ig-like domains. Here we describe a novel inhibitory NK receptor that is specific for a group of HLA-A alleles. The HLA-A3-specific NK cell clone DP7 has been used for mice immunization. Two mAbs, termed Q66 and Q241, bound to the immunizing clone and stained only a subset of NK cell populations or clones. Among Q66 mAb-reactive clones, we further selected those that did not express any of the previously identified HLA-class I-specific NK receptors. These clones did not lyse HLA-A3+ (or -A11+) target cells, but lysis of these targets could be detected in the presence of Q66 or Q241 mAbs. On the other hand, target cells expressing other HLA-A alleles, including -A1, -A2, and -A24, were efficiently lysed. Moreover, none of the HLA-C or HLA-B alleles that were tested exerted a protective effect. Q66+, but not Q66- NK cell clones, expressed messenger RNA coding for a novel 3 Ig domain protein homologous to the HLA-C (p58) and HLA-B (p70) receptors. The corresponding cDNA (cl.1.1) was used to generate transient and stable transfectants in COS7 and NIH3T3 cell lines, respectively. Both types of transfectants were specifically stained by Q66 and Q241 mAbs. Since the cytoplasmic tail of Q66-reactive molecules was at least 11 amino acid longer than the other known p58/p70 molecules, we could generate an antiserum specific for the COOH-terminus of Q66-reactive molecules, termed PGP-3. PGP-3 immunoprecipitated, only from Q66+ NK cells, molecules displaying a molecular mass of 140 kD, under nonreducing conditions, which resolved, under reducing conditions, in a 70-kD band. Thus, differently from the other p58/p70 receptors, Q66-reactive molecules appear to be expressed as disulphide-linked dimers and were thus termed p140. The comparative analysis of the amino acid sequences of p58, p70, and p140 molecules revealed the existence of two cysteins proximal to the transmembrane region, only in the amino acid sequence of p140 molecules.