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Notes: Low-temperature processing for high-performance solar cells based on hydrogenated microcrystalline silicon (μc-Si:H) has been developed using a conventional rf plasma-enhanced chemical vapor deposition (PECVD) technique at an excitation frequency of 13.56 MHz under a high deposition pressure condition. Among pin type solar cells, it is found that deposition temperature of i-layer at 140 °C is effective particularly for improving open circuit voltage (Voc), surprisingly without deteriorating short circuit current or fill factor. Carrier density of undoped μc-Si abruptly decreases for deposition temperatures lower than 180 °C, and the improvement of Voc is ascribed to a decrease of shunt leakage current arising from the oxygen-related donors. This implies that oxygen-related donors can be passivated at low deposition temperatures and that hydrogen plays an important role for the passivation. We propose a simple model for the hydrogen passivation of oxygen related donors. We apply this passivation technique to solar cells, and consequently a conversion efficiency of 8.9% (Voc=0.51 V, Jsc=25 mA/cm−1, FF=0.70) has been obtained in spite of an oxygen concentration of 2×1019 cm−3 in combination with device optimization such as a p-layer. Effect of deposition temperature of i-layer upon other solar cell parameter, short circuit current, and fill factor is also discussed. © 2001 American Institute of Physics.

Notes: We have developed hydrogenated microcrystalline silicon germanium, which exhibits a red-shifted absorption spectrum relative to hydrogenated microcrystalline silicon, as a candidate material for the bottom cell of amorphous silicon-based tandem solar cells. Optical absorption, x-ray diffraction, and Raman scattering spectra are presented in addition to optoelectronic properties and light-induced changes. © 1996 American Institute of Physics.

Notes: We have investigated the role of hydrogen in hydrogenated microcrystalline silicon (μc-Si:H) formation using hydrogen plasma treatments, in particular examining the possibility of subsurface reaction due to permeating hydrogen atoms, which leads to the crystallization of hydrogenated amorphous silicon (a-Si:H). It is demonstrated that the hydrogen plasma treatment of a-Si:H film on the anode using a cathode covered by a-Si:H film, which is inevitably coated during the deposition period, gives rise to the deposition of μc-Si:H over the a-Si:H layer, i.e., chemical transport takes place. It is also found that the pure hydrogen plasma treatment using a clean cathode induces only etching of the a-Si:H layer. These results imply that the present hydrogen plasma condition does not cause crystallization of a-Si:H but only etching, and that careful experimentation is required to determine the real subsurface reaction due to atomic hydrogen. © 1997 American Institute of Physics.

Notes: The optical gains in AlGaInP/GaInP strained quantum wells using valence band structures by the second-order k⋅p method, with and without spin-orbit split-off (SO) band effect have been calculated. It was easy to overestimate the optical gain without considering the SO-band effect, because a small spin-orbit splitting energy for GaInP makes higher nonparabolicity of the valence bands. The SO-band effect is particularly significant under tensile strain, since the SO band makes the effective mass very large due to the large interaction between the SO and light hole bands. © 1995 American Institute of Physics.

Notes: Background: Nitric oxide synthase activity is increased in the stomach in association with Helicobacter pylori infection and portal hypertension, but the mechanism by which nitric oxide contributes to mucosal damage remains unclear. Aim: To examine whether nitric oxide injures gastric mucosal cells and whether cellular glutathione affects nitric oxide-induced cytotoxicity. Methods: A confluent monolayer of RGM-1 gastric mucosal cells was exposed to nitric oxide donors (NOC5 or NOC12). Cell viability was determined by trypan blue dye exclusion, lactate dehydrogenase release and supravital staining with Hoechst 33342 and propidium iodide. The kinetics of the reduced/oxidized forms of glutathione were also measured, as well as the effect of glutathione-depletion or glutathione-precursor treatment on nitric oxide-induced cytotoxicity. Results: Excess exogenous nitric oxide produced by NOC5 or NOC12 induced necrosis in RGM-1 cells in a time- and concentration-dependent manner. The level of reduced glutathione drastically decreased prior to the loss of cell viability and remained low, but oxidized glutathione was not affected. Glutathione depletion increased necrosis of both NOCs in an NOC-concentration-related fashion, while pre-treatment with γ-glutamylcysteine ethyl ester reduced their necrotic susceptibility. Conclusion: Exogenous nitric oxide induced necrosis in gastric mucosal cells, and intracellular reduced glutathione protects gastric mucosal cells from damage by nitric oxide.

Notes: Background: Neutrophil–endothelial cell interactions mediated by adhesion molecules may be involved in gastric mucosal inflammation associated with Helicobacter pylori or nonsteroidal anti-inflammatory drugs. Aim: To investigate the effects of proton pump inhibitors and histamine-2 receptor antagonists (HRA) on neutrophil-endothelial cell adhesive interactions induced by H. pylori water extract (HPE) or interleukin-1β (IL-1β). Methods: Human peripheral neutrophils and umbilical vein endothelial cells were incubated with either proton pump inhibitors (lansoprazole and omeprazole) or HRA (famotidine and ranitidine). Neutrophil surface expression of CD11b and CD18 and endothelial cell intercellular adhesion molecule-1 (ICAM-1) and vascular adhesion molecule-1 (VCAM-1) were assessed by flow cytometry and an enzyme immunoassay, respectively. Neutrophil adherence was defined as the ratio of exogenous neutrophils that adhered to the endothelial monolayers. Results: The expression of CD11b and CD18 on neutrophils and neutrophil-dependent adhesion to endothelial cells elicited by HPE were inhibited by lansoprazole and omeprazole at clinical relevant doses, and the expression of ICAM-1 and VCAM-1 on endothelial cells and endothelial-dependent neutrophil adherence induced by IL-1β were also inhibited by lansoprazole and omeprazole at similar doses. Famotidine and ranitidine had no effect on neutrophil–endothelial cell interactions. Conclusions: These results indicate that proton pump inhibitors can attenuate neutrophil adherence to endothelial cells via inhibiting the expression of adhesion molecules, suggesting that proton pump inhibitors may have anti-inflammatory activity.

Notes: Background Transforming growth factor-β1 (TGF-β1) is generally considered to play an important role in the pathogenesis of chronic inflammation and fibrosis.Objective and methods This study was designed to determine mechanisms of reduced responsiveness of guinea-pig tracheal smooth muscle to β-adrenoceptor agonists by TGF-β1, using isometric tension records and tissue cAMP measurement. Moreover, we examined the involvement of the signal transduction processes of TGF-β superfamily in the desensitization of β-adrenoceptors.Results After exposure to 0.2–2000 pm TGF-β1 for 4–8 h, the inhibitory effects of 1 µm isoprenaline (ISO) and 10 µm forskolin on 1 µm MCh-induced contraction were markedly reduced in a concentration-dependent fashion. The desensitization by TGF-β1 was greater against ISO than for forskolin. The values of EC75 for the curves for ISO after exposure to the normal bathing solution and TGF-β1 were 0.039 ± 0.02 and 0.38 ± 0.28 µm, respectively. The values of EC50 for the curves for forskolin under these conditions were 0.50 ± 0.12 and 0.89 ± 0.21 µm, respectively. On the other hand, the inhibitory effects of phosphodiesterase inhibitors such as theophylline and rolipram were not attenuated after exposure to TGF-β1. Concentration–inhibition curve for ISO was shifted to the right after exposure to 2000 pm TGF-β1 for 8 h more than that curve for forskolin. In contrast, the curve for theophylline was not shifted to the right by TGF-β1. When the tissues were incubated with TGF-β1 in the presence of IFN-γ, an intracellular antagonist of TGF-β signalling, IFN-γ inhibited the reduced response to ISO and forskolin after exposure to TGF-β1 in a concentration-dependent fashion. After exposure to TGF-β1, the effects of cAMP accumulation of ISO was significantly reduced, however, neither forskolin-nor theophylline-induced cAMP accumulation was affected. IFN-γ had no significant effect on cAMP accumulation either to ISO or forskolin.Conclusions Impairment of the β-adrenoceptors/adenylyl cyclase pathway are involved in heterologous desensitization of β-adrenoceptors induced by TGF-β1 in airway smooth muscle. IFN-γ functionally suppresses this phenomenon via cAMP-independent processes. Phosphodiesterase is still intact under this condition.

Notes: A 58-year-old woman gave a 6-month history of porphyria-like photosensitivity. Fractioned porphyrin analysis by high performance liquid chromatography revealed elevated concentrations of all urinary porphyrins and faecal protoporphyrin. Hepatocellular carcinoma had developed in an otherwise normal liver. Tumour tissue fluoresced strongly under fluorescence microscopy, exhibiting elevated activity of three haem-biosynthetic enzymes, δ-aminolevulinic acid (ALA) synthase, ALA dehydratase and porphobilinogen deaminase. This patient did not satisfy any of the criteria for inherited porphyria. The patient's symptoms were relieved after excision of the liver tumour. This strongly suggests that excessive porphyrin synthesis originated from the tumour tissue. Primary porphyria-like photosensitivity occurs as a paraneoplastic phenomenon, secondary to hepatocellular carcinoma.