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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: 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: 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 Altered expression of α-smooth muscle actin (α-SMA) is known to indicate the morphological, tumorigenic and immunological changes occurring in tumour and stromal cells. The purpose of this study was to analyse the dynamics of α-SMA expression in human basal cell epithelioma (BCE) cells and their surrounding stromal cells, in the process of differentiation towards cutaneous appendages such as hair, sebaceous, apocrine and eccrine glands. Using anti-α-SMA specific monoclonal antibody (MAb), 17 of 36 BCEs (47%) were shown to express α-SMA, despite the usual absence of α-SMA in all eukaryotic cells except muscle cells. Solid, adenoid and sclerosing types of BCE expressed α-SMA more frequently, and in greater amount, than cystic, keratotic and superficial types. Furthermore, the expression of α-SMA in BCE cells significantly paralleled the expression of proliferating cell nuclear antigen (PCNA) in these cells. Thus, the altered expression of α-SMA may reflect the growing properties of BCE cells under the specific cellular regulations for differentiation.In addition, we have found anti-α-SMA MAb-positive fibroblasts with smooth muscle differentiation (myofibroblasts) in desmoplastic stroma surrounding BCE nests in 13 of 36 cases (36%). Coincidental expression of α-SMA in both BCE cells and stromal cells was found in nine of the 13 cases (69%), indicating the possibility of the induction of myofibroblastic stromal changes in surrounding tissues by cytokines secreted from BCE cells [e.g. basic fibroblast growth factor (bFGF)-like factor].

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: 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.

Notes: We report the case of a 49-year-old woman suffering from a malignant neoplasm of Langerhans cells (LC), documented by immunohistochemical and ultrastructural analysis, and review the literature to examine and characterize the clinical and laboratory features, therapy, and prognosis of malignant neoplasms of LC. Langerhans cell histiocytosis is now regarded as a disorder of immune regulation or an inflammatory process, rather than as a malignant neoplasm. Although LC share certain features in common with ordinary histiocytes or interdigitating dendritic cells, they also differ significantly from these cells in other respects. Therefore, we propose designating a malignant neoplasm of LC ‘malignant Langerhans cell tumour’ and that it should be considered as a separate entity from Langerhans cell histiocytosis or other malignant histiocytoses.

Notes: Summary Based upon the detailed dissections of the lymphatic system of four adult cadavers, the lymphatic drainage of the gallbladder was divided into three pathways. 1) The cholecysto-retropancreatic pathway, which can be regarded as the main pathway, had two routes, one running spirally and posteriorly from the anterior surface of the common bile duct to the right, and the other running almost straight down from the posterior surface of the common bile duct. At the retroportal segment, these routes converged at a large lymph node, which appeared critical as the main terminal lymph node of this pathway. We designated this node the principal retroportal node. 2) The cholecysto-celiac pathway was the route by which some of the lymphatics from the gallbladder ran to the left through the hepatoduodenal ligament to reach the celiac nodes. 3) The cholecysto-mesenteric pathway was the route by which some of the lymphatics ran to the left in front of the portal vein and connected with the nodes at the superior mesenteric root. These three pathways converged with the abdomino-aortic lymph nodes near the left renal vein; in particular, the nodes in the interaortico-caval space were considered important.

Notes: Abstract Silicon carbide fibres (Nicalon) were coated with pure aluminium and aluminium alloys containing silicon. The coated fibres were annealed to produce an interfacial reaction zone between the coated layer and the fibre. The effect of this reaction zone on the tensile strength of the fibre was investigated. During the early stages of growth the reaction zone of the fibre is thin, and the strength of the fibre is controlled by inherent defects so that the fibre retains its original strength. After the early stages, notches are formed in the reaction zone of the fibre on loading at a small strain and the fibre fractures when a notch extends into the fibre. In this stage the fibre strength is dependent on the thickness of the reaction zone. An alloying addition of 1 or 5 at % Si to the aluminium matrix was found to be effective in retarding the growth rate of the reaction zone.

Notes: Abstract An investigation is carried out on the interfacial wetting behaviour and reactions between aluminium and alumina fibres (85mass% Al2O3 and 15mass% SiO2). Aluminium is coated onto alumina fibres by a vacuum evaporation technique and the surface of the fully coated fibres and the edge of the partially coated fibres are examined by scanning electron microscope after heat treatments at various temperatures. Within a temperature regime between 943 and 1273 K, occurrence of such interfacial reactions as 4Al(I) + Al2O3(s) → 3Al2O3(g) and 4Al(I) + 3SiO2(s) → 2Al2O3(s) + 3Si(s) are detected. It is found that molten aluminium can cover the alumina fibre surface but it peels off near the edge of the coating film on a partially coated fibre, showing the very weak interface cohesion. This is ascribed to the lack of a stable compound formation at the interface. Results of tensile test show that the strength of the coated fibres is degraded after heat-treating at above the melting point of aluminium. The culprits for the tensile failure of alumina fibres are evaluated by the Weibull distribution theory.