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Structural defects and microstrain in GaN induced by Mg ion implantation (1998)

Pong, B. J. ; Pan, C. J. ; Teng, Y. C. ; [et al.]

[S.l.] : American Institute of Physics (AIP)

Journal of Applied Physics 83 (1998), S. 5992-5996

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ISSN: 1089-7550

Source: AIP Digital Archive

Topics: Physics

Notes: The optical and structural characteristics of GaN films implanted with Mg and Be ions, grown by low-pressure metalorganic chemical vapor deposition were studied. The low temperature (20 K) photoluminescence (PL) spectra of annealed Mg implanted GaN show a 356 nm near band edge emission, a 378 nm donor-acceptor (D-A) transition with phonon replicas, and a 528 nm green band deep level emission. The origin of the 528 nm green band emission and the 378 nm D-A emission might be attributed, respectively, to the Mg implantation induced clustering defect and the vacancy defect in GaN film. Observations of in-plane and out-of-plane x-ray diffraction spectra for as-grown undoped, Mg implanted and rapid thermal annealed GaN suggest that ion implantation induced anisotropic strain may be responsible for the observed PL emission characteristics. © 1998 American Institute of Physics.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1063/1.367465

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Type-1c glycogen storage disease is not caused by mutations in the glucose-6-phosphate transporter gene (1999)

Lin, B. ; Hiraiwa, H. ; Pan, C.-J. ; [et al.]

Springer

Human genetics 〈Berlin〉 105 (1999), S. 515-517

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ISSN: 1432-1203

Source: Springer Online Journal Archives 1860-2000

Topics: Biology , Medicine

Notes: Abstract. Glycogen storage disease type 1 (GSD-1) is a group of autosomal recessive disorders caused by deficiencies in glucose-6-phosphatase (G6Pase) and the associated substrate/product transporters. Molecular genetic studies have demonstrated that GSD-1a and GSD-1b are caused by mutations in the G6Pase enzyme and a glucose-6-phosphate transporter (G6PT), respectively. While kinetic studies of G6Pase catalysis predict that the index GSD-1c patient is deficient in a pyrophosphate/phosphate transporter, the existence of a separate locus for GSD-1c remains unclear. We have previously shown that the G6Pase gene of the index GSD-1c patient is intact; we now show that the G6PT gene of this patient is normal, strongly suggesting the existence of a distinct GSD-1c locus.