Library

Notes: The formation of bubbles and holes in hydrogenated amorphous silicon (a-Si:H) films after isochronal annealing has been investigated. The internal stress of the bubble in an a-Si:H film has been determined by the relationship between the diameter and height of a bubble. In addition, the internal stress of the bubble has also been investigated based on the difference in hydrogen concentration between the flat and bubble areas determined by Fourier-transform infrared microspectroscopy. Consistent results are obtained from both methods regarding the magnitude of the internal stress. These results indicate that the bubble is formed by molecular hydrogen evolving from the a-Si:H film.

Notes: The threshold voltage (VT) shift of hydrogenated amorphous silicon thin-film transistors (a-Si:H TFTs) by boron doping has been investigated. In TFTs with a uniformly doped structure (SiN/B-doped a-Si:H), VT shifts to a positive voltage by boron doping, while the field-effect mobility decreases markedly. By using a step-doped structure (SiN/undoped a-Si:H/B-doped a-Si:H), the degradation of the field-effect mobility by boron doping becomes less than that of a uniformly doped TFT with the same VT shift, and a VT shift of 3.5 V was obtained without degradation of the field-effect mobility.

Notes: Using an ultrahigh-vacuum (UHV) sputtering system, we could grow two new methods of polycrystalline silicon films. The one is as-deposited polycrystalline silicon on glass at substrate temperatures under 500 °C. The other is solid-phase-crystallization by thermal annealing of as-deposited amorphous silicon films in a UHV. As-deposited polycrystalline silicon films were oriented to (220) and grain sizes were determined from half-width of x-ray diffraction to be about 40 nm. From the deposition temperature dependence of the x-ray diffraction peak intensity, the activation energy of the crystalline growth was calculated to be about 0.6 eV. Hydrogen atoms in the sputtering gas lower the reproducibility of as-deposited poly-Si. Polycrystalline silicon films produced by thermal annealing of as-deposited amorphous silicon films at 550 °C in UHV have a (111) orientation. Field-effect mobilities of the as-deposited polycrystalline silicon film and the polycrystalline silicon film by UHV thermal annealing were 5 and 18 cm2/V s, respectively. © 1995 American Institute of Physics.

Notes: We present a new doping technique using an ion shower doping system with a bucket ion source. Phosphorus atoms were implanted in polycrystalline silicon from room temperature to 300 °C. Sheet resistances were significantly reduced by raising the implantation temperature. With a crystal fraction of 85%, sheet resistance was 5×102 S−1/(D'Alembertian) as implanted. These effects were not due to pure thermal annealing by ion beam heating. A significant improvement was found in sheet resistance as a result of averaging the impurity profile by radiation enhanced diffusion and low temperature recrystallization of the implanted region by collision of atoms.

Notes: The inhibition of angiotensin II (AngII) by use of angiotensin converting enzyme (ACE) inhibitor or AngII receptor blocker is effective for prevention of the progression of renal diseases including IgA nephropathy (IgAN). AngII plays a variety of biological roles via AngII receptors. Through AngII type 1 receptor (AT1R), AngII induces vasoconstriction, cellular proliferation, extracellular matrix production and fibrosis, while it leads vasodilatation, apoptosis and inhibition of cell proliferation through AngII type 2 receptor (AT2R). Recent studies showed the local production of AngII in many tissues including the heart, vessel and kidney, suggesting that local AngII may be more important than circulating AngII in tissue injury. AngII is generated from angiotensin I by ACE or ACE independent pathway, such as chymase which is a serine protease. Since chymase was shown to be synthesized 80% of AngII in human heart, chymase also may play an important role in converting to AngII in the kidney. Although it was reported that ACE was produced in renal tissue, the localization of chymase and AngII receptors is unclear in the human kidney. To research the local renin-angiotensin system in renal tissue of patients with IgAN, we localized chymase mRNA, ACE mRNA, AT1R mRNA and AT2R mRNA by in situ hybridization and investigated the relationship between the expression of these mRNAs and tissue injury. Fresh frozen sections of renal tissue from 21 patients with IgAN were examined. The sections were fixed with 4% paraformaldehyde and hybridized with the digoxigenin (DIG)-labelled oligonucleotide probes for chymase mRNA, ACE mRNA, AT1R mRNA and AT2R mRNA. Using anti-DIG antibody, immunohistochemistry was performed to visualize the DIG-labelled probe. Colour was developed by reaction with H2O2 and 3,3′diaminobenzidine/=tetrahydrochloride. As identifying the exact locations of the cells positive for chymase mRNA, ACE mRNA and AngII receptor mRNA, we stained using periodic acid-Schiff after in situ hybridization. We classified the histological grading of the glomerular and tubulointerstitial injury. Two to five glomeruli were analysed in each biopsy tissue and the degree of injury in each glomerulus was graded from 1 to 3 based on the proportion of the lesion in the sectioned areas of each glomerulus. In the tubulointerstitium, three to five fields of cortical interstitium in each section were examined under low magnification (×200). In each designated field, we determined the degree of tubular atrophy and interstitial fibrosis from grade 1 to 3. In situ hybridization showed that the signals of chymase mRNA, ACE mRNA, AT1R mRNA and AT2R mRNA were observed in mesangial cells, glomerular epithelial cells, cells of the Bowman’s capsule, cells of crescent, tubular epithelial cells and some infiltrating mononuclear cells. In the glomeruli, the percentage of cells positive for chymase mRNA, ACE mRNA, AT1R mRNA and AT2R mRNA per glomerulus decreased as the glomerular injury progressed. Chymase mRNA and ACE mRNA were diffusely expressed in the glomeruli with mild injury. The expression significantly increased in the area of mesangial cells proliferation without mesangial matrix expansion, however, it decreased as the glomerular lesion progressed. In the tubulointerstitium, the expression of chymase mRNA, ACE mRNA and AT1R mRNA positively correlated with the degree of tubulointerstitial injury. The expression of AT2R became significantly strongest in moderate injury lesions and diminished in severe lesion. All mRNAs were highly expressed in atrophic tubuli. We also examined the relation of the cells positive for chymase mRNA and ACE mRNA on serial sections. Most cells positive for chymase mRNA also stained for ACE mRNA in the glomeruli and the tubulointerstitium. In situ hybridization for AT1R mRNA and AT2R mRNA in serial sections showed that some cells produced the both mRNAs, while other cells expressed only AT1R mRNA or AT2R mRNA. In the present study, we identified that chymase, ACE and AngII receptor were synthesized in renal tissue with IgAN. Our results suggest that AngII was generated by local ACE and ACE independent pathway (chymase) and that the regulation of local renin angiotensin system in renal tissue was different between glomerulus and tubulointerstitium. Local renin angiotensin system may contribute the progression of tissue injury in IgAN.

Notes: The antigenicity of premelanosomes, which are specific organelles for melanin biosynthesis in the cytoplasm of malignant melanoma cells, has been revealed by the blastogenic responses of lymphocytes from melanoma-bearing Syrian (golden) hamsters, using the lymphocyte stimula tion assay. The lymphocytes from these hamsters have also been found to exhibit cytotoxic effects on cultured melanoma cells as shown by the microcytotoxic assay technique.

Notes: This paper describes two types of photodiode arrays using indium-tin-oxide/amorphous silicon (ITO/a-Si:H) junctions for a contact-type linear image sensor. One type is a photodiode array of separated ITO electrodes, an a-Si:H stripe layer, and a common metal (Cr) electrode. The other consists of a common ITO electrode, an a-Si:H stripe layer, and separated Cr electrodes. We investigated the bias dependence of the photocurrent and its spatial distribution for the two types of diode array. Our results indicate that the photocarriers generated around the element for a common ITO electrode type deteriorate the resolving power of the diode array, which can be improved by using separated ITO electrodes. A separated ITO electrode increases the modulation transfer function and the fineness of linear image sensors.

Notes: We investigated the effect of hydrogen ion shower doping on polycrystalline silicon thin-film transistors (p-Si TFTs). Hydrogen atoms were introduced to the channel region of p-Si TFTs by PH3/H2 ion shower doping of the source/drain contact. Hydrogen concentration in the channel region can be controlled by altering the gate metal thickness. Hydrogen atoms affect the TFT's threshold voltage shifts until it becomes negative, in n-type TFTs. The threshold voltage shift depends on the hydrogen content of the channel region in p-Si TFTs. This is explained by the existence of Si−3 trap states in the grain boundaries. © 1995 American Institute of Physics.

Notes: The effect of silicon nitride (SiN) deposition on hydrogenated amorphous silicon (a-Si:H) has been investigated to find the origin of the difference of a-Si:H/SiN interface properties caused by the order of deposition. Sheet conductance of the on-state in inverted staggered (a-Si:H on SiN) thin-film transistors (TFTs) increases gradually with the substrate temperature (Tsub) of SiN, but decreases rapidly with the Tsub of SiN in staggered TFTs (SiN on a-Si:H). Photoluminescence experiments indicated that the degradation in staggered TFTs was due to the creation of defects in a-Si:H by the deposition of the SiN overlayer. It was shown by Fourier transform infrared attenuated total reflection that the origin of the defects was hydrogen effusion from a-Si:H.

Notes: Summary It has been proposed that basic fibroblast growth factor (bFGF) is an autocrine growth factor of melanoma cells, in contrast with normal melanocytes where bFGF acts as a paracrine growth factor. As this notion is mostly based on the different requirements for bFGF in cultures of benign and malignant pigment cells in vitro, we performed an immunohistochemical study to examine bFGF expression in vivo using paraffin sections from naevus cell naevi (NCN) and malignant melanoma (MM). All the NCN (n=7) showed strong and homogeneous expression of bFGF protein, whereas the primary MMs (n=5) showed heterogeneous expression, with a population of negative cells. Metastatic MMs (n=5) also showed heterogeneous expression, and had a greater population of negative cells. These results suggest that bFGF has some, as yet unidentitied, role in the growth of benign NCN, and that overexpression of bFGF is neither a prerequisite for melanoma genesis nor for progression to metastatic MM.