Degradation mechanism in carbon-doped GaAs minority-carrier injection devices [HBTs]
Degradation behavior and mechanism of GaAs-based devices under minority-carrier injection has been studied by measuring the increase in the leakage current and the luminescence lifetime of minority carriers. It is found that hydrogen unintentionally incorporated in GaAs-based devices induces degrada...
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Published in | IEEE transactions on electron devices Vol. 44; no. 11; pp. 1996 - 2001 |
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Main Authors | , |
Format | Journal Article |
Language | English |
Published |
IEEE
01.11.1997
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Subjects | |
Online Access | Get full text |
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Summary: | Degradation behavior and mechanism of GaAs-based devices under minority-carrier injection has been studied by measuring the increase in the leakage current and the luminescence lifetime of minority carriers. It is found that hydrogen unintentionally incorporated in GaAs-based devices induces degradation under minority-carrier injection, i.e., increase in injection leakage current at low bias voltage. "Isolated" hydrogen donors (H/sup +/) induce rapid degradation, and even carbon-hydrogen (C-H) complexes which are believed to be electrically neutral induce slow degradation. Degradation is induced by the decomposition of the C-H complexes, enhanced by minority-carrier injection producing electrically active isolated hydrogen donors (H/sup +/). The kinetics of the leakage current increase are well explained by the decomposition kinetics of the C-H complexes. Under minority-carrier injection, H/sup +/ changes to hydrogen acceptors (H/sup - /) by capturing two electrons. Hydrogen donors (H/sup +/) and hydrogen acceptors (H/sup -/) combine and become a molecular hydrogen which Is thought to form {111} platelets. This decomposition mechanism are not due to recombination-enhanced defect reaction (REDR) but is related to charge state effects by two-electron capturing. We infer that the degradation mechanism is closely related to the leakage through the {111} platelets. |
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ISSN: | 0018-9383 1557-9646 |
DOI: | 10.1109/16.641371 |