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The influences of biaxial and uniaxial strain on the ultraviolet emission efficiencies of both c- and m-plane AlxGa1-xN films with different Al concentrations are investigated under the framework of k·p perturbation theory. The optimal high efficiency windows, for ultraviolet light emissions are quantitatively estimated. c-plane AlxGa1-xN modified by uniaxial strain, shows more advantages over biaxial-strained AlxGa1-xN. This is due to the relatively more flexible tuning range and the advantage of obtaining pure linear polarization, which can be utilized to design polarized emission devices. For m-plane AlxGa1-xN, there are always in-plane polarized emissions under both biaxial and uniaxial strain conditions, thus, it is more likely to obtain high surface emission efficiency. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To study elderly hypertensive patients with trace albuminuria (urine albumin to creatinine ratio (UACR)) and the relationship between the occurrence of new cardiovascular events, to provide a basis for early prevention in elderly patients with high blood pressure. PATIENTS AND METHODS: A total of 3564 elderly patients with high blood pressure were enrolled in the study. Based on UACR, patients were divided into four groups (group A: 0.05-3.20 mg/g; group B:3.21-10.04 mg/g; group C: 10.05-19.33 and group D: 19.34-30.00 mg/g). All patients underwent follow-up for an average period of 3.8 years. Four groups were compared for new cardiovascular events and they were correlated with UACR. RESULTS: Through multivariate Cox proportional hazards regression analysis, the relative risk of cardiocerebrovascular events, cerebral infarction and acute myocardial infarction (mi), in group D was 1.74 times (p < 0.05), 1.66 times (p < 0.05) and 2.48 times (p < 0.05), respectively. UACR level in females and those with higher age, body mass index, systolic blood pressure, fasting blood glucose, TG, TC, LDL-C levels and lower HDL-C were higher. During follow-up, patients from group D with sudden cardiac death, acute myocardial infarction, cerebral hemorrhage, cerebral infarction occurrence was significantly higher than group A (x2 = 79.3, p = 79.3) CONCLUSIONS: According to UACR level, we can perform early prevention for elderly patients with high blood pressure, thus reducing the occurrence of cerebral infarction and myocardial infarction. [ABSTRACT FROM AUTHOR]

We investigated the polarization and temperature dependence of photoluminescence (PL) of m-plane GaN grown on γ-LiAlO2 (100) substrate. The calculated electronic band structure with k•p Hamiltonian points out the energy splitting as well as polarization selection originate from the m-plane GaN epilayer under anisotropic strain. The polarization-angle dependence PL spectra are found to be selected from in-plane x- and z-polarized emission, corresponding to T1 and T2 transition. And the intensity distribution of the fitting peaks satisfies the Malus’ law. An S-shape energy evolution of near band edge peak on temperatures is observed, which originates from the transition between the localized holes and electrons in triangular potentials induced by basal stacking faults. [ABSTRACT FROM AUTHOR]

The m-plane GaN films grown on LiAlO2(100) by metal-organic chemical vapor deposition exhibit anisotropic crystallographic properties. The Williamson–Hall plots point out they are due to the different tilts and lateral correlation lengths of mosaic blocks parallel and perpendicular to GaN[0001] in the growth plane. The symmetric and asymmetric reciprocal space maps reveal the strain of m-plane GaN to be biaxial in-plane compress [variant_greek_epsilon]xx=-0.79% and [variant_greek_epsilon]zz=-0.14% with an out-of-plane dilatation [variant_greek_epsilon]yy=0.38%. This anisotropic strain further separates the energy levels of top valence band at Γ point. The energy splitting as 37 meV as well as in-plane polarization anisotropy for transitions are found by the polarized photoluminescence spectra at room temperature. [ABSTRACT FROM AUTHOR]

The nonpolar m-plane (1100) thin film GaN and InGaN/GaN light-emitting diodes (LEDs) grown by metal-organic chemical vapor deposition on LiAlO2 (100) substrates are reported. The LEDs emit green light with output power of 80 μW under a direct current of 20 mA for a 400×400 μm2 device. The current versus voltage (I-V) characteristic of the diode shows soft rectifying properties caused by defects and impurities in the p-n junction. The electroluminescence peak wavelength dependence on injection current, for currents in excess of 20 mA, saturates at 515–516 nm. This proves the absence of polarization fields in the active region present in c-plane structures. The light output intensity versus current (L-I) characteristic of the diode exhibits a superlinear relation at low injection current caused by nonradiative centers providing a shunt path and a linear light emission zone at high current level when these centers are saturated. [ABSTRACT FROM AUTHOR]

Objective: The phenotype and genotype of a pedigree with Glanzmann thrombasthenia caused by compound heterozygous mutation in the ITGA2B gene and its molecular pathogenesis were explored. Methods: The platelet aggregation rate of the proband and his family was detected by using a platelet aggregation test with adenosine diphosphate, collagen, epinephrine, arachidonic acid, and ristocetin. The expression levels of CD41 (αⅡb), CD61 (β3), and CD42b (GPⅠb) on the platelet surface was detected by flow cytometry. Gene sequencing technology was used for the genetic identification of the family. RT-PCR was used in the detection of mRNA splicing, and qRT-PCR was used in detecting the relative mRNA level of the ITGA2B gene. Bioinformatics analysis was used to evaluate the pathogenicity of mutation sites and their effects on protein structure and function. The expressions of total αⅡb and β3 in platelets were analyzed by Western blot. Results: Except ristocetin, the other four inducers could not induce platelet aggregation in the proband. Flow cytometry showed that the expression levels of αⅡb and β3 were only 0.25% and 9.76%, respectively, on the platelet surface of the proband, whereas GPⅠb expression was relatively normal. The expression levels of glycoproteins in the other family members were almost normal. c.480C>G and c.2929C>T mutations were detected in the proband through gene sequencing. The c.480C>G mutation was inherited from his mother, and the c.2929C>T mutation was inherited from his father. The RT-PCR and sequencing results showed that the c.480C>G mutation caused mRNA splicing in the proband and his mother, resulting in the deletion of 99 bases in c.476G-574A (p.S160-S192). qRT-PCR showed that the c.2929C>T variant reduced the mRNA level of the ITGA2B gene in the proband and his father. Bioinformatics analysis suggested that the c.480C>G mutation might form a binding sequence with hnRNP A1 protein and generate the 5'SS splice site. The three-dimensional structural model of the αⅡb subunit showed that the β-propeller domain of the p.S160-S192 deletion lost two β-strands and one α-helix in blade 2. The c.2929C>T nonsense mutation caused premature translation termination and produced a truncated protein with the deletion of p.R977-E1039, including the cytoplasmic domain, transmembrane domain, and a β chain of the extracellular Calf-2 domain. The total αⅡb expression of the proband was absent, and the relative expression of β3 was 11.36% of the normal level. Conclusion: The compound heterozygous mutation c.480C>G in exon 4 and c.2929C>T in exon 28 of the ITGA2B gene probably underlies Glanzmann thrombasthenia in this pedigree.