Output power density of 5.1/mm at 18 GHz with an AlGaN/GaN HEMT on Si substrate

Microwave frequency capabilities of AlGaN/GaN high electron mobility transistors (HEMTs) on high resistive silicon (111) substrate for power applications are demonstrated in this letter. A maximum dc current density of 1 A/mm and an extrinsic current gain cutoff frequency (F/sub T/) of 50 GHz are achieved for a 0.25 /spl mu/m gate length device. Pulsed and large signal measurements show the good quality of the epilayer and the device processing. The trapping phenomena are minimized and consequently an output power density of 5.1 W/mm is reached at 18 GHz on a 2/spl times/50/spl times/0.25 /spl mu/m/sup 2/ HEMT with a power gain of 9.1dB.     

Chlorine gas induced acute lung injury in isolated rabbit lung

This study was designed to investigate the pathogenesis of chlorine gas (Cl2) induced acute lung injury and oedema. Isolated blood-perfused rabbit lungs were ventilated either with air (n=7) or air plus 500 parts per million (ppm) of Cl2 (n=7) for 10 min. Capillary pressure, measured by analysing the pressure/time transients of pulmonary arterial, venous and double (both arterial and venous) occlusions, was unchanged in both groups. In Cl2-exposed lungs, the fluid filtration rate increased from -0.228+/-0.25 to 1.823+/-1.23 mL min(-1) x 100 g(-1) (p<0.001) and the filtration coefficient increased from 0.091+/-0.01 to 0.259+/-0.07 mL x min(-1) x cmH2O(-1) x 100 g(-1) (p<0.001). No changes were observed in the control lungs. The extravascular lung water/blood-free dry weight ratio was 8.6+/-1.6 in the Cl2 group and 4.0+/-0.5 in the control group (p<0.001), confirming that the increase in lung weight was related to accumulation of extravascular fluid. Although the alveolar flooding by oedema is explained, in part, by the Cl2-induced epithelial injury, our results suggest that Cl2 exposure induces acute lung injury and oedema due to an increased microvascular permeability.     

Evidence of surface states for AlGaN/GaN/SiC HEMTs passivated Si<Subscript>3</Subscript>N<Subscript>4</Subscript> by CDLTS

In AlGaN/GaN heterostructure field-effect transistors (HEMTs) structures, the surface defects and dislocations may serve as trapping centers and affect the device performance via leakage current and low frequency noise. This work demonstrates the effect of surface passivation on the current-voltage characteristics and we report results of our investigation of the trapping characteristics of Si₃N₄-passivated AlGaN/GaN HEMTs on SiC substrates using the conductance deep levels transient spectroscopy (CDLTS) technique. From the measured of CDLTS we identified one electron trap had an activation energy of 0.31 eV it has been located in the AlGaN layer and two hole-likes traps H ₁, H ₂. It has been pointed out that the two hole-likes traps signals did not originate from changes in hole trap population in the channel, but reflected the changes in the electron population in the surface states of the HEMT access regions.     

Abnormalities of nasal potential difference measurement in Liddle''s syndrome

Vascular endothelial growth factor (VEGF) production was analysed in megakaryocytic cell lines and CD34+ haematopoietic progenitors following treatment with thrombopoietin (TPO). In CMK cells TPO caused a time- and dose-dependent increase in the levels of VEGF released into the medium. A similar effect was observed in UT-7/mpl cells transfected with the TPO receptor c-Mpl, but not in parental UT-7 cells. In CD34+ haematopoietic progenitor cell cultures TPO stimulated VEGF mRNA expression and VEGF protein release. Production of VEGF in CD34+ cultures increased with TPO-induced megakaryocytic differentiation, but not with erythroid or myelomonocytic differentiation induced respectively by erythropoietin and granulocyte-macrophage colony-stimulating factor. These results demonstrate that TPO stimulates VEGF release in c-Mpl-expressing cells and suggest that this process is an integral feature of the megakaryocytic differentiation programme.     

AlGaN-GaN HEMTs on Si with power density performance of 1.9 W/mm at 10 GHz

AlGaN-GaN high electron mobility transistors (HEMTs) on silicon substrate are fabricated. The device with a gate length of 0.3-/spl mu/m and a total gate periphery of 300 /spl mu/m, exhibits a maximum drain current density of 925 mA/mm at V/sub GS/=0 V and V/sub DS/=5 V with an extrinsic transconductance (g/sub m/) of about 250 mS/mm. At 10 GHz, an output power density of 1.9 W/mm associated to a power-added efficiency of 18% and a linear gain of 16 dB are achieved at a drain bias of 30 V. To our knowledge, these power results represent the highest output power density ever reported at this frequency on GaN HEMT grown on silicon substrates.     

In vivo quantitation of epithelial lining fluid in dog lung

We used an original saturation bronchoalveolar lavage (SBAL) technique (Eur. Respir. J. 1995;8[Suppl. 19]398S) to quantitate lung epithelial lining fluid volume (VELF) in dogs in two separate experiments: control and after oleic-acid-induced injury. We confirmed the hypothesis that 99mTc-DTPA, infused at constant plasma activity, reaches equilibrium with epithelial lining fluid after 90 min. We performed eight sequential lavages 215 min after beginning the infusion of 99mTc-DTPA. 99mTc-DTPA activity (Qn) in the lavage fluid increased linearly with time, suggesting transport from the plasma into the alveoli during lavage. We extrapolated Qn to time zero (Q0), when 99mTc-DTPA was not affected by lavage. VELF was calculated from: VELF = Q0/Cp, (Cp: 99mTc-DTPA mean plasma activity). 125I-albumin was used as a nondiffusible alveolar indicator to measure the fluid volume present in the lavaged segment (Vt,n). Vt,n plateaud for n >= 4. VELF/Vt,n(n = 5,8) was 1.7 +/- 0.4 and 25.0 +/- 4.4% (p < 0.05) in control and injury experiments, respectively. SBAL allowed reliable measurements of VELF and detection of alveolar edema fluid in the injured lung.     

Gallium nitride MEMS resonators: how residual stress impacts design and performances

Microsystem Technologies - Starting from Gallium Nitride epitaxially grown on silicon, pre-stressed micro-resonators with integrated piezoelectric transducers have been designed, fabricated, and...     

Genetic study of renal artery fibromuscular dysplasia

The aim of this study was to conduct a formal pedigree analysis of the involvement of the elastin gene in families. From 140 subjects with renal FMD documented on angiography, family cases with documented renal artery fibromuscular dysplasia (FMD) and to test pedigrees were constructed and familial cases defined by angiographic evidence of FMD in at least one sibling. Familial screening was made either by echodoppler for asymptomatic subjects or by digital intravenous angiography for hypertensive subjects. Linkage analysis at the elastin gene locus was performed in these families with two polymorphic markers: one diallelic RFLP located in exon 16 and one multiallelic CA repeat located in intron 17 of the elastin gene. Fourteen pedigrees (10%) were obtained including nine sibling pairs, four trios and one vertical transmission from a father to his daughter. Most affected subjects were females (84%) but familial cases were more frequently bilateral than sporadic cases (80% vs 49%, p = 0.07). Pedigrees analysis was compatible with an autosomal dominant mode of inheritance and suggested in these families an age and sex-dependent incomplete penetrance model. Linkage analysis resulted in a maximum two-point lod score of 0.06 at theta = 0.20 using the dinucleotide CA repeat. Analysis of the diallelic marker revealed similar frequencies in affected and non affected subjects. This study highlights the role of genetics factors in approximately 10% of FMD cases. The elastin gene does not seem to be involved in the pathogenesis of FMD.