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We have used photoexcitation-dependent radiative efficiency measurements to investigate the rates of defect-related, radiative, and Auger recombination in lattice-matched In[sub x]Ga[sub 1-x]As/InAs[sub y]P[sub 1-y] double heterostructures on InP substrates. Temperature dependence is used to discern the underlying mechanisms responsible for the nonradiative recombination processes. We find that defect-related recombination decreases with an increase in the temperature when the epistructure is lattice matched to the substrate (x = 0.53). In contrast, when the epistructure is lattice mismatched to the substrate, defect-related recombination increases slowly with the temperature. The difference between the lattice-matched and mismatched cases is related to fundamental changes in the defect-related density of states function. The temperature dependence in the lattice-mismatched structures is attributed to two competing effects: wider carrier diffusion, which augments the capture rate, and thermally activated escape, which reduces the occupation of shallow traps. The band gap and temperature dependence of the Auger rate demonstrate that the conduction to heavy hole band/ splitoff to heavy hole band mechanism generally dominates Auger recombination in undoped low-band gap In[sub x]Ga[sub 1-x]As. With this interpretation, our results give a spin-orbit valence split-off band effective mass of m[sub so] = (0.12 ± 0.02)m[sub 0]. [ABSTRACT FROM AUTHOR]

Study design:Prospective repeated-measures longitudinal study.Objectives:To determine if an 8-week course of an oral anabolic steroid can positively effect body composition or pulmonary function in healthy individuals with chronic tetraplegia.Setting:United States.Methods:Oxandrolone (20 mg per day) was administered for 8 weeks to 10 men with motor complete tetraplegia. Dual X-ray absorptiometry scans, pulmonary function tests (PFTs), serum lipids and liver function tests (LFTs) were obtained at baseline, 4, 8, 12 and 20 weeks. To analyze change over time, a repeated measures General Linear Model and nonparametric tests were utilized.Results:Following treatment, total lean body mass (LBM) increased 1.9% and LBM of the arms increased 5.4%. Total body fat decreased 1.5%, and increased 3.9% in the arms and, on average, combined measures of PFTs improved 2.2%. High-density lipoprotein cholesterol decreased 31.8%, low density lipoprotein cholesterol increased 41.2%, and LFTs increased 9.7–65.6% while on therapy but all trended to baseline at 20 weeks.Conclusion:Baseline body composition was characterized by a high proportion of fat and a body mass index that underestimated chronic disease risk. Treatment with oxandrolone was associated with modest improvements in PFTs and in arm and total body LBM. Unfavorable changes in serum lipids and LFTs indicate that reported benefits of using oxandrolone in this population must be carefully weighed against potential adverse effects. [ABSTRACT FROM AUTHOR]

Seventy-seven persons with a variety of heritable chondrodysplasias were screened for gross rearrangements of the structural gene encoding the major cartilage collagen, collagen II. None was found. Segregation of the locus (COL2A1) was studied in 19 pedigrees using three restriction site dimorphisms (shown by PvuII, HindIII, and BamHI) and a length polymorphism as linkage markers. Discordant segregation between COL2A1 and the mutant locus was seen in pedigrees with multiple epiphyseal dysplasia, autosomal recessive spondyloepiphyseal dysplasia tarda, hypochondroplasia, pseudoachondroplasia, diaphyseal aclasis, and trichorhinophalangeal syndrome. One pedigree with diastrophic dysplasia was weakly concordant. Autosomal dominant spondyloepiphyseal dysplasia tarda and metaphyseal chondrodysplasia (type Schmid) were not informative. We conclude that mutations of the collagen II gene are not a common feature of the heritable chondrodysplasias. Since the chondrocyte binding protein, chondrocalcin, is also encoded at COL2A1 our conclusions apply equally to this gene. [ABSTRACT FROM PUBLISHER]

We have measured the excitation-dependent radiative efficiency in a set of lattice-matched In[sub x]Ga[sub 1-x]As/InAs[sub y]P[sub 1-y] double heterostructures incrementally lattice mismatched to InP substrates. We find that the overall rate of defect-related recombination shows little change from the lattice-matched case. However, the excitation-dependent transition between defect-related and radiative recombination changes dramatically with mismatch. While a simple defect recombination model assuming defect levels concentrated near the middle of the band gap fits well for the lattice-matched material, the model does not fit the shape of the efficiency curve for the mismatched structures. We show that the addition of band edge exponential tails to the defect-related density of states gives a much better theoretical fit. [ABSTRACT FROM AUTHOR]