Influence of hydrogen on the structural stability of annealed ultrathin Si/Ge amorphous layers

Semiconductor structures based on Si and Ge are generally submitted to hydrogenation because H passivates the dangling bonds of Si and Ge. By this way the devices prepared from those semiconductors, e.g., solar cells, have much better electrical properties. However, H stability is still a critical issue. In fact, there is wide evidence that H is very unstable against illumination as well as heat treatment. It has been seen that H out effuses from the samples under such treatments. As this causes unsaturation of the dangling bonds the electrical properties worsen significantly. In this work we will show that in the case of ultrathin Si/Ge amorphous layers the H thermal instability also affects the structural stability even up to the micrometric scale depending on the H content. Such type of structure can also be used to prepare SiGe alloys by mixing the layers with heat treatments. The samples were amorphous multilayers (MLs) of alternating ultrathin (3 nm) layers of Si and Ge deposited by sputtering on (100) oriented Si substrate. The total thickness of the MLs was 300 nm. The samples were hydrogenated by introducing H in the sputter chamber with flow rates varying from 0.8 to 6 ml/min. The MLs underwent different heat treatments, from the one at 350 ?C for 1 h up to the one at 250 ?C for 0.5 h + 450 ?C for 5 h. The samples were analysed by AFM, TEM, energy filtering TEM and Small-Angle X-Ray Diffraction (SAXRD). AFM showed that upon annealing the structure of the samples degrades with formation of surface bumps whose size increases by increasing the annealing temperature and/or time, for the same H content, or by increasing the H content for the same annealing conditions. For high H content and/or annealing conditions AFM showed that the bumps have blown up giving rise to craters. This suggests that H was released from its dangling bonds to Si and Ge and formed H bubbles in the MLs because of the energy supplied by the annealing. Additional energy for the break of the Si-H and Ge-H bonds could be the one supplied by the recombination of thermally generated carriers associated with the band gap fluctuations caused by the not uniform distribution of H in the MLs. The first sites of H accumulation are very likely nanocavities certainly present in the amorphous MLs. By TEM it has been seen that layer intermixing occurred which could be the first step of H bubbles formation. SAXRD measurements as well as TEM energy filtering maps for Si and Ge showed that Si and Ge interdiffusion took place in an asymmetric way as Si was seen to diffuse to the Ge layers whereas Ge did not diffuse to the Si layers. This might be due to the higher density of free dangling bonds in the Ge layers created by annealing because the binding energy of the Ge-H bond is smaller than the one of the Si-H bond

The Gasotransmitter Hydrogen Sulfide (H₂S) Prevents Pathologic Calcification (PC) in Cartilage.

Pathologic calcification (PC) is a painful and disabling condition whereby calcium-containing crystals deposit in tissues that do not physiologically calcify: cartilage, tendons, muscle, vessels and skin. In cartilage, compression and inflammation triggered by PC leads to cartilage degradation typical of osteoarthritis (OA). The PC process is poorly understood and treatments able to target the underlying mechanisms of the disease are lacking. Here we show a crucial role of the gasotransmitter hydrogen sulfide (H <sub>2</sub> S) and, in particular, of the H <sub>2</sub> S-producing enzyme cystathionine γ-lyase (CSE), in regulating PC in cartilage. Cse deficiency (Cse KO mice) exacerbated calcification in both surgically-induced (menisectomy) and spontaneous (aging) murine models of cartilage PC, and augmented PC was closely associated with cartilage degradation (OA). On the contrary, Cse overexpression (Cse tg mice) protected from these features. In vitro, Cse KO chondrocytes showed increased calcification, potentially via enhanced alkaline phosphatase (Alpl) expression and activity and increased IL-6 production. The opposite results were obtained in Cse tg chondrocytes. In cartilage samples from patients with OA, CSE expression inversely correlated with the degree of tissue calcification and disease severity. Increased cartilage degradation in murine and human tissues lacking or expressing low CSE levels may be accounted for by dysregulated catabolism. We found higher levels of matrix-degrading metalloproteases Mmp-3 and -13 in Cse KO chondrocytes, whereas the opposite results were obtained in Cse tg cells. Finally, by high-throughput screening, we identified a novel small molecule CSE positive allosteric modulator (PAM), and demonstrated that it was able to increase cellular H <sub>2</sub> S production, and decrease murine and human chondrocyte calcification and IL-6 secretion. Together, these data implicate impaired CSE-dependent H <sub>2</sub> S production by chondrocytes in the etiology of cartilage PC and worsening of secondary outcomes (OA). In this context, enhancing CSE expression and/or activity in chondrocytes could represent a potential strategy to inhibit PC

Critical Strain Region Evaluation of Self-Assembled Semiconductor Quantum Dots

A novel peak finding method to map the strain from high resolution transmission electron micrographs, known as the Peak Pairs method, has been applied to In(Ga) As/AlGaAs quantum dot (QD) samples, which present stacking faults emerging from the QD edges. Moreover, strain distribution has been simulated by the finite element method applying the elastic theory on a 3D QD model. The agreement existing between determined and simulated strain values reveals that these techniques are consistent enough to qualitatively characterize the strain distribution of nanostructured materials. The correct application of both methods allows the localization of critical strain zones in semiconductor QDs, predicting the nucleation of defects, and being a very useful tool for the design of semiconductor device

InAs/InP/InSb Nanowires as Low Capacitance n-n Heterojunction Diodes

Nanowire diodes have been realized by employing an axial heterojunction between InAs and InSb semiconductor materials. The broken-gap band alignment (type III) leads to a strong rectification effect when the current-voltage (I-V) characteristic is inspected at room temperature. The additional insertion of a narrow InP barrier reduces the thermionic contribution, which results in a net decrease of leakage current in the reverse bias with a corresponding enhanced rectification in terms of asymmetry in the I-V characteristics. The investigated diodes compare favorably with the ones realized with p-n heterostructured nanowires, making InAs/InP/InSb devices appealing candidates to be used as building blocks for nanowire-based ultrafast electronics and for the realization of photodetectors in the THz spectral range

CD11b Signaling Prevents Chondrocyte Mineralization and Attenuates the Severity of Osteoarthritis.

Osteoarthritis (OA) is a progressive joint disease that is strongly associated with calcium-containing crystal formation (mineralization) by chondrocytes leading ultimately to cartilage calcification. However, this calcification process is poorly understood and treatments targeting the underlying disease mechanisms are lacking. The CD11b/CD18 integrin (Mac-1 or αMβ2), a member of the beta 2 integrin family of adhesion receptors, is critically involved in the development of several inflammatory diseases, including rheumatoid arthritis and systemic lupus erythematosus. We found that in a collagen-induced arthritis, CD11b-deficient mice exhibited increased cartilage degradation compared to WT control animals. However, the functional significance of CD11b integrin signaling in the pathophysiology of chondrocytes remains unknown. CD11b expression was found in the extracellular matrix and in chondrocytes in both healthy and damaged human and murine articular cartilage. Primary murine CD11b KO chondrocytes showed increased mineralization when induced in vitro by secondary calciprotein particles (CPP) and quantified by Alizarin Red staining. This increased propensity to mineralize was associated with an increased alkaline phosphatase (Alp) expression (measured by qRT-PCR and activity assay) and an enhanced secretion of the pro-mineralizing IL-6 cytokine compared to control wild-type cells (measured by ELISA). Accordingly, addition of an anti-IL-6 receptor antibody to CD11b KO chondrocytes reduced significantly the calcification and identified IL-6 as a pro-mineralizing factor in these cells. In the same conditions, the ratio of qRT-PCR expression of collagen X over collagen II, and that of Runx2 over Sox9 (both ratio being indexes of chondrocyte hypertrophy) were increased in CD11b-deficient cells. Conversely, the CD11b activator LA1 reduced chondrocyte mineralization, Alp expression, IL-6 production and collagen X expression. In the meniscectomy (MNX) model of murine knee osteoarthritis, deficiency of CD11b led to more severe OA (OARSI scoring of medial cartilage damage in CD11b: 5.6 ± 1.8, in WT: 1.2 ± 0.5, p < 0.05, inflammation in CD11b: 2.8 ± 0.2, in WT: 1.4 ± 0.5). In conclusion, these data demonstrate that CD11b signaling prevents chondrocyte hypertrophy and chondrocyte mineralization in vitro and has a protective role in models of OA in vivo

Tuning morphology and magnetism in epitaxial L10-FePt films

In this work, well-ordered epitaxial FePt thin ¿lms have been grown by RF sputtering on two different substrates (MgO (100) and SrTiO3 (100)) and the effect of different lattice parameters between the substrate and FePt ¿lm on morphology and magnetic behavior has been considered. Growth conditions have been optimized to obtain different morphologies and magnetic behaviors

The protective role of the 3-mercaptopyruvate sulfurtransferase (3-MST)-hydrogen sulfide (H₂S) pathway against experimental osteoarthritis.

Osteoarthritis (OA) is characterized by the formation and deposition of calcium-containing crystals in joint tissues, but the underlying mechanisms are poorly understood. The gasotransmitter hydrogen sulfide (H <sub>2</sub> S) has been implicated in mineralization but has never been studied in OA. Here, we investigated the role of the H <sub>2</sub> S-producing enzyme 3-mercaptopyruvate sulfurtransferase (3-MST) in cartilage calcification and OA development. 3-MST expression was analyzed in cartilage from patients with different OA degrees, and in cartilage stimulated with hydroxyapatite (HA) crystals. The modulation of 3-MST expression in vivo was studied in the meniscectomy (MNX) model of murine OA, by comparing sham-operated to MNX knee cartilage. The role of 3-MST was investigated by quantifying joint calcification and cartilage degradation in WT and 3-MST <sup>-/-</sup> meniscectomized knees. Chondrocyte mineralization in vitro was measured in WT and 3-MST <sup>-/-</sup> cells. Finally, the effect of oxidative stress on 3-MST expression and chondrocyte mineralization was investigated. 3-MST expression in human cartilage negatively correlated with calcification and OA severity, and diminished upon HA stimulation. In accordance, cartilage from menisectomized OA knees revealed decreased 3-MST if compared to sham-operated healthy knees. Moreover, 3-MST <sup>-/-</sup> mice showed exacerbated joint calcification and OA severity if compared to WT mice. In vitro, genetic or pharmacologic inhibition of 3-MST in chondrocytes resulted in enhanced mineralization and IL-6 secretion. Finally, oxidative stress decreased 3-MST expression and increased chondrocyte mineralization, maybe via induction of pro-mineralizing genes. 3-MST-generated H <sub>2</sub> S protects against joint calcification and experimental OA. Enhancing H <sub>2</sub> S production in chondrocytes may represent a potential disease modifier to treat OA

Correction to: New eco-friendly low-cost binders for Li-ion anodes

The article New eco-friendly low-cost binders for Li-ion anodes, written by D. Versaci, R. Nasi, U. Zubair, J. Amici, M. Sgroi, M. A. Dumitrescu, C. Francia, S. Bodoardo and N. Penazzi, was originally published electronically on the publisher's internet portal (currently SpringerLink)