Cryptogams in a Horticultural Setting in Scotland

The exhibiting of living cryptogams at the Royal Botanic Garden, Edinburgh and Dawyck Botanic Garden is described with the hope that from the management procedures experienced, other institutions will follow and demonstrate to the public these important components of our natural heritage

Scaling study of Si/SiGe MODFETs for RF applications

Based on the successful calibration on a 0.25 /spl mu/m strained Si/SiGe n-type MODFET, this paper presents a gate length scaling study of double-side doped Si/SiGe MODFETs. Our simulations show that gate length scaling improves device RF performance. However, the short channel effects (SCE) along with the parasitic delays limit the device performance improvements. We find that it is necessary to consider scaling (dimensions and doping) of both the lateral and vertical architecture in order to optimize the device design

Optimizations of sub-100 nm Si/SiGe MODFETs for high linearity RF applications

Based on careful calibration in respect of 70 nm n-type strained Si channel S/SiGe modulation doped FETs (MODFETs) fabricated by Daimler Chrysler, numerical simulations have been used to study the impact of the device geometry and various doping strategies on device performance and linearity. The device geometry is sensitive to both RF performance and device linearity. Doped channel devices are found to be promising for high linearity applications. Trade-off design strategies are required for reconciling the demands of high device performance and high linearity simultaneously. The simulations also suggest that gate length scaling helps to achieve higher RF performance, but decreases the linearity

Sub-100nm strained Si CMOS: device performance and circuit behavior

Using comprehensive device simulations, performance enhancement of sub-100nm strained Si MOSFETs has been investigated. Circuit behavior of conventional Si, strained Si, conventional Si SOI and strained SOI ring oscillators has been assessed

Effective mobilities in pseudomorphic Si/SiGe/Si p-channel metal-oxide-semiconductor field-effect transistors with thin silicon capping layers

The room-temperature effective mobilities of pseudomorphic Si/Si0.64Ge0.36/Si p-metal-oxidesemiconductor field effect transistors are reported. The peak mobility in the buried SiGe channel increases with silicon cap thickness. It is argued that SiO2/Si interface roughness is a major source of scattering in these devices, which is attenuated for thicker silicon caps. It is also suggested that segregated Ge in the silicon cap interferes with the oxidation process, leading to increased SiO2/Si interface roughness in the case of thin silicon caps

Restoration of IFNγR Subunit Assembly, IFNγ Signaling and Parasite Clearance in Leishmania donovani Infected Macrophages: Role of Membrane Cholesterol

Despite the presence of significant levels of systemic Interferon gamma (IFNγ), the host protective cytokine, Kala-azar patients display high parasite load with downregulated IFNγ signaling in Leishmania donovani (LD) infected macrophages (LD-MØs); the cause of such aberrant phenomenon is unknown. Here we reveal for the first time the mechanistic basis of impaired IFNγ signaling in parasitized murine macrophages. Our study clearly shows that in LD-MØs IFNγ receptor (IFNγR) expression and their ligand-affinity remained unaltered. The intracellular parasites did not pose any generalized defect in LD-MØs as IL-10 mediated signal transducer and activator of transcription 3 (STAT3) phosphorylation remained unaltered with respect to normal. Previously, we showed that LD-MØs are more fluid than normal MØs due to quenching of membrane cholesterol. The decreased rigidity in LD-MØs was not due to parasite derived lipophosphoglycan (LPG) because purified LPG failed to alter fluidity in normal MØs. IFNγR subunit 1 (IFNγR1) and subunit 2 (IFNγR2) colocalize in raft upon IFNγ stimulation of normal MØs, but this was absent in LD-MØs. Oddly enough, such association of IFNγR1 and IFNγR2 could be restored upon liposomal delivery of cholesterol as evident from the fluorescence resonance energy transfer (FRET) experiment and co-immunoprecipitation studies. Furthermore, liposomal cholesterol treatment together with IFNγ allowed reassociation of signaling assembly (phospho-JAK1, JAK2 and STAT1) in LD-MØs, appropriate signaling, and subsequent parasite killing. This effect was cholesterol specific because cholesterol analogue 4-cholestene-3-one failed to restore the response. The presence of cholesterol binding motifs [(L/V)-X1–5-Y-X1–5-(R/K)] in the transmembrane domain of IFNγR1 was also noted. The interaction of peptides representing this motif of IFNγR1 was studied with cholesterol-liposome and analogue-liposome with difference of two orders of magnitude in respective affinity (KD: 4.27×10−9 M versus 2.69×10−7 M). These observations reinforce the importance of cholesterol in the regulation of function of IFNγR1 proteins. This study clearly demonstrates that during its intracellular life-cycle LD perturbs IFNγR1 and IFNγR2 assembly and subsequent ligand driven signaling by quenching MØ membrane cholesterol

Post-intervention Status in Patients With Refractory Myasthenia Gravis Treated With Eculizumab During REGAIN and Its Open-Label Extension

OBJECTIVE: To evaluate whether eculizumab helps patients with anti-acetylcholine receptor-positive (AChR+) refractory generalized myasthenia gravis (gMG) achieve the Myasthenia Gravis Foundation of America (MGFA) post-intervention status of minimal manifestations (MM), we assessed patients' status throughout REGAIN (Safety and Efficacy of Eculizumab in AChR+ Refractory Generalized Myasthenia Gravis) and its open-label extension. METHODS: Patients who completed the REGAIN randomized controlled trial and continued into the open-label extension were included in this tertiary endpoint analysis. Patients were assessed for the MGFA post-intervention status of improved, unchanged, worse, MM, and pharmacologic remission at defined time points during REGAIN and through week 130 of the open-label study. RESULTS: A total of 117 patients completed REGAIN and continued into the open-label study (eculizumab/eculizumab: 56; placebo/eculizumab: 61). At week 26 of REGAIN, more eculizumab-treated patients than placebo-treated patients achieved a status of improved (60.7% vs 41.7%) or MM (25.0% vs 13.3%; common OR: 2.3; 95% CI: 1.1-4.5). After 130 weeks of eculizumab treatment, 88.0% of patients achieved improved status and 57.3% of patients achieved MM status. The safety profile of eculizumab was consistent with its known profile and no new safety signals were detected. CONCLUSION: Eculizumab led to rapid and sustained achievement of MM in patients with AChR+ refractory gMG. These findings support the use of eculizumab in this previously difficult-to-treat patient population. CLINICALTRIALSGOV IDENTIFIER: REGAIN, NCT01997229; REGAIN open-label extension, NCT02301624. CLASSIFICATION OF EVIDENCE: This study provides Class II evidence that, after 26 weeks of eculizumab treatment, 25.0% of adults with AChR+ refractory gMG achieved MM, compared with 13.3% who received placebo

Minimal Symptom Expression' in Patients With Acetylcholine Receptor Antibody-Positive Refractory Generalized Myasthenia Gravis Treated With Eculizumab

The efficacy and tolerability of eculizumab were assessed in REGAIN, a 26-week, phase 3, randomized, double-blind, placebo-controlled study in anti-acetylcholine receptor antibody-positive (AChR+) refractory generalized myasthenia gravis (gMG), and its open-label extension