Junction Formation Process Research Articles

Overview of junctional complexes during mammalian early embryonic development.

Cell-cell junctions form strong intercellular connections and mediate communication between blastomeres during preimplantation embryonic development and thus are crucial for cell integrity, polarity, cell fate specification and morphogenesis. Together with cell adhesion molecules and cytoskeletal elements, intercellular junctions orchestrate mechanotransduction, morphokinetics and signaling networks during the development of early embryos. This review focuses on the structure, organization, function and expressional pattern of the cell-cell junction complexes during early embryonic development. Understanding the importance of dynamic junction formation and maturation processes will shed light on the molecular mechanism behind developmental abnormalities of early embryos during the preimplantation period.

Distinct junction transformations of pixel-arrayed long-wavelength infrared detectors by photocurrent mapping

Pixel-arrayed long-wavelength HgCdTe is of great significance in the development of infrared detection. However, the PN junction formation process for long-wavelength HgCdTe is complex. The damage induced by boron ion implantation and subsequent low-temperature annealing may results in changes in the effective doping concentration and geometry of the actual n-type implantation region. Therefore, an in-situ, non-destructive scanning-photocurrent-microscopy (SPCM) method is needed to test the performance and electroactive defects of HgCdTe devices. Here, the pixel-arrayed long-wavelength infrared detectors with n-on-p structure formed by B+ ion implantation in Hg vacancy-doped Hg0.78Cd0.22Te crystals were fabricated. The SPCM method is used to characterize the PN junction performance of long-wavelength Hg0.78Cd0.22Te array detectors. It is found that the long-wavelength device transformed from n-on-p structure to n-on-n− structure at about 175 K, and further turns into an n−-on-n-on-n− structure with the temperature increasing. In addition, when the temperature increases, the minority carrier diffusion length in the B+ ion implantation region gradually decreases with the activation of the recombination center. Our work provides an effective theoretical and experimental basis for the HgCdTe junction formation process.

In Situ Monitoring of Transmetallation in Electric Potential-Promoted Oxidative Coupling in a Single-Molecule Junction

In Situ Monitoring of Transmetallation in Electric Potential-Promoted Oxidative Coupling in a Single-Molecule Junction

Neuropathological hallmarks of fetal hydrocephalus linked to CCDC88C pathogenic variants

The prevalence of congenital hydrocephalus has been estimated at 1.1 per 1000 infants when including cases diagnosed before 1 year of age after exclusion of neural tube defects. Classification criteria are based either on CSF dynamics, pathophysiological mechanisms or associated lesions. Whereas inherited syndromic hydrocephalus has been associated with more than 100 disease-causing genes, only four genes are currently known to be linked to congenital hydrocephalus either isolated or as a major clinical feature: L1CAM, AP1S2, MPDZ and CCDC88C. In the past 10 years, pathogenic variants in CCDC88C have been documented but the neuropathology remains virtually unknown. We report the neuropathology of two foetuses from one family harbouring two novel compound heterozygous pathogenic variants in the CCDC88C gene: a maternally inherited indel in exon 22, c.3807_3809delinsACCT;p.(Gly1270Profs*53) and a paternally inherited deletion of exon 23, c.3967-?_c.4112-?;p.(Leu1323Argfs*10). Medical termination of pregnancy was performed at 18 and 23 weeks of gestation for severe bilateral ventriculomegaly. In both fetuses, brain lesions consisted of multifocal atresia-forking along the aqueduct of Sylvius and the central canal of the medulla, periventricular neuronal heterotopias and choroid plexus hydrops. The second fetus also presented lumbar myelomeningocele, left diaphragmatic hernia and bilateral renal agenesis. CCDC88C encodes the protein DAPLE which contributes to ependymal cell planar polarity by inhibiting the non-canonical Wnt signaling pathway and interacts with MPDZ and PARD3. Interestingly, heterozygous variants in PARD3 result in neural tube defects by defective tight junction formation and polarization process of the neuroepithelium. Besides, during organ formation Wnt signalling is a prerequisite for planar cell polarity pathway activation, and mutations in planar cell polarity genes lead to heart, lung and kidney malformations. Hence, candidate variants in CCDC88C should be carefully considered whether brain lesions are isolated or associated with malformations suspected to result from disorders of planar cell polarity.

Guide Cells Support Muscle Regeneration and Affect Neuro-Muscular Junction Organization.

Muscular regeneration is a complex biological process that occurs during acute injury and chronic degeneration, implicating several cell types. One of the earliest events of muscle regeneration is the inflammatory response, followed by the activation and differentiation of muscle progenitor cells. However, the process of novel neuromuscular junction formation during muscle regeneration is still largely unexplored. Here, we identify by single-cell RNA sequencing and isolate a subset of vessel-associated cells able to improve myogenic differentiation. We termed them ‘guide’ cells because of their remarkable ability to improve myogenesis without fusing with the newly formed fibers. In vitro, these cells showed a marked mobility and ability to contact the forming myotubes. We found that these cells are characterized by CD44 and CD34 surface markers and the expression of Ng2 and Ncam2. In addition, in a murine model of acute muscle injury and regeneration, injection of guide cells correlated with increased numbers of newly formed neuromuscular junctions. Thus, we propose that guide cells modulate de novo generation of neuromuscular junctions in regenerating myofibers. Further studies are necessary to investigate the origin of those cells and the extent to which they are required for terminal specification of regenerating myofibers.

Laminin-driven Epac/Rap1 regulation of epithelial barriers on decellularized matrix

Decellularized tissues offer a unique tool for developing regenerative biomaterials or in vitro platforms for the study of cell-extracellular matrix (ECM) interactions. One main challenge associated with decellularized lung tissue is that ECM components can be stripped away or altered by the detergents used to remove cellular debris. Without characterizing the composition of lung decellularized ECM (dECM) and the cellular response caused by the altered composition, it is difficult to utilize dECM for regeneration and specifically, engineering the complexities of the alveolar-capillary barrier. This study takes steps towards uncovering if dECM must be enhanced with lost ECM proteins to achieve proper epithelial barrier formation. To achieve this, the epithelial barrier function was assessed on dECM coatings with and without the systematic addition of several key basement membrane proteins. After comparing barrier function on collagen I, fibronectin, laminin, and dECM in varying combinations as an in vitro coating, the alveolar epithelium exhibited superior barrier function when dECM was supplemented with laminin as evidenced by trans-epithelial electrical resistance (TEER) and permeability assays. Increased barrier resistance with laminin addition was associated with upregulation of Claudin-18, E-cadherin, and junction adhesion molecule (JAM)-A, and stabilization of zonula occludens (ZO)-1 at junction complexes. The Epac/Rap1 pathway was observed to play a role in the ECM-mediated barrier function determined by protein expression and Epac inhibition. These findings revealed potential ECM coatings and molecular therapeutic targets for improved regeneration with decellularized scaffolds. Statement of significanceEfforts to produce a transplantable organ-scale biomaterial for lung regeneration has not been entirely successful to date, due to incomplete cell-cell junction formation, ultimately leading to severe edema in vivo. To fully understand the process of alveolar junction formation on ECM-derived biomaterials, this research has characterized and tailored decellularized ECM (dECM) to mitigate reductions in barrier strength or cell attachment caused by abnormal ECM compositions or detergent damage to dECM.These results indicate that laminin-driven Epac signaling plays a vital role in the stabilization of the alveolar barrier. Addition of laminin or Epac agonists during alveolar regeneration can reduce epithelial permeability within bioengineered lungs.

Statistics and Mechanisms of Intermittent Plasticity in FCC and BCC Microcrystals

Plastic deformation in crystalline materials consists of an ensemble of collective dislocation glide processes, which lead to strain burst emissions in micro-scale samples. To unravel the combined role of crystalline structure, sample size and temperature on these processes, we performed a comprehensive set of strict displacement-controlled micropillar compression experiments in conjunction with large-scale molecular dynamics and physics-based discrete dislocation dynamics simulations. The results indicate that plastic strain bursts consist of numerous individual dislocation glide events, which span over minuscule time intervals. The size distributions of these events follow a power-law function which bifurcates from an incipient slip regime of uncorrelated glide (spanning ≈ 2.5 decades of slip sizes) to a large avalanche domain of collective glide (spanning ≈ 4 decades of emission probability) at a critical slip magnitude sc. This critical slip size characterizes the transition between bulk-like and localized plasticity. In face-centered cubic (FCC) metals, sc is essentially governed by the interplay between dislocation annihilation, cross-slip and junction formation processes developing as a function of microcrystal size and stacking fault width in Al, Ni and Cu. Dislocation starvation then rules the avalanche statistics in smaller microcrystals. In body-centered cubic (BCC) metals, sc evaluates the combined role of temperature and the applied stress level upon the glide of the sluggish screw dislocations via cross-kinking mechanisms. Different sc values result in BCC Ta and W due to the distinctive thermal and stress-dependent activation of cross-kinking. These FCC and BCC dislocation glide mechanisms determine the evolution from self-organized to stress-tuned avalanching processes.

From PERC to Tandem: POLO- and p+/n+ Poly-Si Tunneling Junction as Interface Between Bottom and Top Cell

We present a novel cell concept that combines the tandem cell approach with the passivated emitter and rear cells (PERC) mainstream technology. As an interface between Si bottom and top cell, we utilize passivating n <sup xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">+</sup> -type polysilicon on oxide (POLO) contacts and a p <sup xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">+</sup> poly-Si/n <sup xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">+</sup> poly-Si tunneling junction. Our full area PERC+ Si bottom cells are fabricated within a typical industrial process sequence where the POCl3 diffusion and SiNx deposition are replaced by the POLO junction formation processes. The implied open-circuit voltage iVoc that is measured on these devices reaches up to 708 mV (684 mV) under 1 sun (under filtered spectrum to simulated top cell absorption). On sister cells with planar front side, the respective iVoc values are 718 mV (696 mV). In order to understand the device physics of our ultra-abrupt p <sup xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">+</sup> poly-Si/n <sup xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">+</sup> poly-Si tunneling junction, we determined the carrier lifetime in the poly-Si by time-resolved photoluminescence. The extracted lifetimes of 42-54 ps enter as input parameter for numerical Sentaurus Device simulations. These simulations reveal the importance of band-to-band and trap-assisted tunneling for a low tunneling junction resistivity of 2.95 mΩ·cm <sup xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">2</sup> . Experimentally, an upper limit for the combined junction resistance of the p <sup xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">+</sup> poly-Si/n <sup xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">+</sup> poly-Si/SiOx stack of 100 mΩ·cm <sup xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">2</sup> is determined.

Dislocation Networks and the Microstructural Origin of Strain Hardening

When metals plastically deform, the density of line defects called dislocations increases and the microstructure is continuously refined, leading to the strain hardening behavior. Using discrete dislocation dynamics simulations, we demonstrate the fundamental role of junction formation in connecting dislocation microstructure evolution and strain hardening in face-centered cubic (fcc) Cu. The dislocation network formed consists of line segments whose lengths closely follow an exponential distribution. This exponential distribution is a consequence of junction formation, which can be modeled as a one-dimensional Poisson process. According to the exponential distribution, two non-dimensional parameters control microstructure evolution, with the hardening rate dictated by the rate of stable junction formation. Among the types of junctions in fcc crystals, we find that glissile junctions make the dominant contribution to strain hardening.

(Invited) Ultrathin-Body Ge-on-Insulator Mosfet and TFET Technologies

CMOS and tunneling FETs (TFETs) utilizing Ge-On-Insulator (GOI) channels on Si substrates are expected as one of the promising device options for low-power integrated systems. In this paper, we present viable device and process technologies of GOI MOSFETs and TFETs on the Si CMOS platform. High compressive strain, favorable in p-MOSFET applications, is introduced in GOI films by optimizing the Ge condensation process, which is one of the most promising technologies to form ultrathin-body GOI devices. Also, source engineering in GOI layers to realize superior tunnel junctions with steep impurity profiles is developed for TFET applications. The electrical characteristics of GOI MOSFETs and TFETs are presented and analyzed from the viewpoints of applied strain and source junction properties, respectively. One strategy to reduce Vdd is to increase Ion of MOSFETs by employing low effective mass (high velocity) channels. From this viewpoint, Ge/III-V materials are promising. The critical issues for Ge MOSFETs on Si platform are high quality Ge channel formation and application of strain, which are mandatory for overcoming the performance of strained Si/SiGe CMOS. As a technology of the Ge channel formation, we are focusing on the Ge condensation [1]. We previously reported that GOI crystallinity can be enhanced by combining high temperature condensation with intermixing annealing processes [2]. However, no strain was left in the GOI structures because of severe strain relaxation during Ge condensation [1-3], which not only causes defects in the GOI layers but also prevents from enhancing hole mobility in pMOSFETs. Thus, we have proposed and demonstrated a new condensation method with minimized temperature cycles and slow temperature cooling rate [4]. We found that the amount of compressive strain in GOI significantly increases with reducing the cooling rate of GOI after condensation. It was also found that higher compressive strain is obtained by thinning SiGe layers included in starting substrates before condensation [5]. We fabricated 10 nm-thick UTB GOI structure with strain of ~1.7% by using Si/40-nm-thick Si0.75Ge0.25/ SOI starting substrates under the improved condensation recipe. GOI pMOSFETs fabricated on the GOI substrates exhibited the peak hole mobility of as high as 342 cm2/Vs, thanks to high compressive strain. Furthermore, 4.5-nm-thick ETB GOI pMOSFETs with hole mobility enhancement of 3.1 against fully-relaxed GOI ones were achieved without strain relaxation by employing digital thinning with ECR plasma oxidation. Ge is also promising for TFET applications, because of the smaller bandgap and effective mass. Another advantage of Ge is a possibility to realize both n- and p-channel FETs simultaneously, allowing to provide the complementary TFETs in one single material, as similar to Si. However, Ge TFETs previously reported exhibited insufficient characteristics with high Ioff [6, 7]. We recently demonstrated the operation of Ge n- and p-TFETs with the source junctions formed by BF2 implantation and P solid phase diffusion from SOG, respectively [8-10]. It was found that steep source impurity profiles can increase Ion of TFETs [9, 10]. A snowplow effect of NiGe combined with low-energy BF2 + implantation realized an abrupt junction with B profile abruptness less than 5nm/dec and a high doping concentration of around 1021 cm3 by optimizing the Ni thickness. GOI n-TFETs with these source junctions exhibited the Ion/Ioff ratio of 743 and the subthreshold slope of 239 mV/dec at room temperature. It was also found that P diffusion can realize both the high impurity concentration (> 7x1019 cm3) and the steep impurity profile (> 10nm/dec) because of the dopant-concentration-dependent diffusion coefficient. This result indicates that P is a suitable dopant for the source formation of Ge p-TFETs. Using this P diffusion process, Ge p-TFETs with Ion higher than 1.7 μA/μm was obtained at room temperature. However, still high Ioff and S.S. must be much improved by optimizing the source junction formation process and reducing the defect density included in the junctions and the MOS interfaces. This work was supported by JST-CREST Grant Number JPMJCR1332, Japan, and a Grant-in-Aid for Scientific Research (17H06148) from MEXT.

Adsorption of Expanded Pyridinium Molecules at the Electrified Interface and Its Effect on the Electron-Transfer Process.

Adsorption properties of a series of redox-active expanded pyridinium molecules were studied at an electrified interface by cyclic and alternating current voltammetry methods. It was shown that the adsorbed state can sufficiently block N-pyramidalization of the pyridinium redox center of 2',6'-diphenyl-[4,1':4',4''-terpyridin]-1'-ium tetrafluoroborate (2), leading to a change of the mechanism from a single two-electron-transfer process to stepwise transfer of two electrons. Chemically locked molecules 1, 9-(pyridin-4-yl)benzo[ c]benzo[1,2]quinolizino[3,4,5,6- ija][1,6]naphthyridin-15-ium tetrafluoroborate (ring fusion), and 3, 3,5-dimethyl-2',6'-diphenyl-[4,1':4',4''-terpyridin]-1'-ium tetrafluoroborate (steric hindrance) do not enable N-pyramidalization of the redox center upon electron transfer (ET) and serve as references. It was shown that 1 follows Langmuir-type adsorption around a potential of zero charge and that 1-3 form a close-packed film with some repulsive interactions between individual molecules at potentials where ET takes place. It has been suggested that all three molecules lie flat on the electrode surface, with the lowest free energy of adsorption found for 2. Maximum surface concentration Γ* equal to (1.4 ± 0.1) × 10-10 mol·cm-2 was found for 1, (1.5 ± 0.1) × 10-10 mol·cm-2 for 2, and (1.6 ± 0.1) × 10-10 mol·cm-2 for 3. These findings will help to clarify the role of molecular contacts with conducting substrate in the single-molecule electron-transport measurements of 1-3 during the metal-molecule-metal junction formation process.

Impact of junction formation processes on single molecular conductance.

We have investigated the electric conductance and atomic structure of single molecular junctions of pyrazine (Py), 4,4'-bipyridine (BiPy), fullerene (C60), and 1,4-diaminobutane (DAB). The single molecular junctions were fabricated by breaking Au contacts between an Au tip and the Au electrode surface in the presence of the target molecules (breaking process) or approaching the Au tip to the Au electrode surface covered by the molecules (making process). In the making process, no major conductance state was observed in the conductance histogram for DAB, while single conductance states were observed for the π-conjugated molecules of Py (10 mG0, G0∼ 77.45 μΩ-1), BiPy (3 mG0), and C60 (5 mG0). In contrast to the making process, two major conductance states were observed for Py (1 mG0 and 0.3 mG0), BiPy (0.6 mG0 and 0.2 mG0), and C60 (30 mG0 and 3 mG0) in the breaking process. The observed conductance behavior could be explained by the characters of the anchoring unit of molecules. In the making process, anchoring of molecules cannot be established by the point contact between the Au electrode and the localized lone pair of the N atom of DAB, Py, and BiPY, while molecules anchor on the Au electrode by using the plane-like contact between the Au electrode and the delocalized π electrons in the aromatic ring of Py, BiPY, and C60, which explains the difference in the observed conductance behavior between DAB and the π conjugated molecules of Py, BiPY, and C60 in the making process. In the breaking process, the delocalized π-electrons of Py, BiPY, and C60 can make a contact with the Au electrode surface and the lone pair on the N atom of DAB as well as Py and BiPY can bind to Au atoms, and therefore, single molecular junctions were formed for all systems. The present results indicate that the π-plane is important for making metal-molecule contacts and for the formation of the single molecular junction in the making process.

WAVE regulates Cadherin junction assembly and turnover during epithelial polarization

Actin is an integral component of epithelial apical junctions, yet the interactions of branched actin regulators with apical junction components are still not clear. Biochemical data have shown that α−catenin inhibits Arp2/3-dependent branched actin. These results suggested that branched actin is only needed at earliest stages of apical junction development. We use live imaging in developing C. elegans embryos to test models for how WAVE-induced branched actin collaborates with other apical junction proteins during the essential process of junction formation and maturation. We uncover both early and late essential roles for WAVE in apical junction formation. Early, as the C. elegans intestinal epithelium becomes polarized, we find that WAVE components become enriched concurrently with the Cadherin components and before the DLG-1 apical accumulation. Live imaging of F-actin accumulation in polarizing intestine supports that the Cadherin complex components and branched actin regulators work together for apical actin enrichment. Later in junction development, the apical accumulation of WAVE and Cadherin components is shown to be interdependent: Cadherin complex loss alters WAVE accumulation, and WAVE complex loss increases Cadherin accumulation. To determine why Cadherin levels rise when WVE-1 is depleted, we use FRAP to analyze Cadherin dynamics and find that loss of WAVE as well as of the trafficking protein EHD-1/RME-1 increases Cadherin dynamics. EM studies in adults depleted of branched actin regulators support that WVE-1 maintains established junctions, presumably through its trafficking effect on Cadherin. Thus we propose a developmental model for junction formation where branched actin regulators are tightly interconnected with Cadherin junctions through their previously unappreciated role in Cadherin transport.

Rare Deleterious PARD3 Variants in the aPKC-Binding Region are Implicated in the Pathogenesis of Human Cranial Neural Tube Defects Via Disrupting Apical Tight Junction Formation.

Increasing evidence that mutation of planar cell polarity (PCP) genes contributes to human cranial neural tube defect (NTD) susceptibility prompted us to hypothesize that rare variants of genes in the core apical-basal polarity (ABP) pathway are risk factors for cranial NTDs. In this study, we screened for rare genomic variation of PARD3 in 138 cranial NTD cases and 274 controls. Overall, the rare deleterious variants of PARD3 were significantly associated with increased risk for cranial NTDs (11/138 vs.7/274, P<0.05, OR=3.3). These NTD-specific variants were significantly enriched in the aPKC-binding region (6/138 vs. 0/274, P<0.01). The East Asian cohort in the ExAC database and another Chinese normal cohort further supported this association. Over-expression analysis in HEK293T and MDCK cells confirmed abnormal aPKC binding or interaction for two PARD3 variants (p.P913Q and p.D783G), resulting in defective tight junction formation via disrupted aPKC binding. Functional analysis in human neural progenitor cells and chick embryos revealed that PARD3 knockdown gave rise to abnormal cell polarity and compromised the polarization process of neuroepithelial tissue. Our studies suggest that rare deleterious variants of PARD3 in the aPKC-binding region contribute to human cranial NTDs, possibly by disrupting apical tight junction formation and subsequent polarization process of the neuroepithelium.

(Keynote) FDSOI Past, Present and Future

FDSOI is quickly becoming a technology offering that can deliver next generation performance with superior low power operation at a significant cost advantage. Researchers have actively pursued alternatives to conventional bulk and PDSOI transistors for well over 10 years. However, there was not enough compelling need to change until conventional CMOS scaling dramatically slowed. Beyond the 28nm node new device architectures were needed to continue the scaling trend. FDSOI was always thought to be an attractive option since of all the alternative approaches it is the most similar to conventional bulk or PDSOI. This is mainly due to the fact that it is planar and thus much of the process and design methodology can be re used from previous nodes. On the other hand several key issues for FDSOI were known and thought to be fundamental challenges. Specifically silicon consumption, high external resistance and parasitic capacitance were identified as major hurdles. FDSOI relies upon the thin channel to control short channel effects. For example a channel thickness of approximately 6nm is required to maintain good electrostatics for a transistor with Lg=20nm. Maintaining thin silicon in the channel while still preserving silicon in the source-drain regions is a big process challenge. We have carefully optimized several key process steps including the spacer etch process to eliminate excessive silicon consumption. As shown in Fig. 1 the zero loss spacer process features a partial etch using reactive ion etching. In order to minimize silicon consumption, the spacer etch is terminated before the spacer material is completely removed from the horizontal surfaces and the dry etch cannot consume silicon. The residual spacer material is removed as part of the pre epi clean for raised source-drain. Since the wet etch for the pre-clean is highly selective to the silicon, there is no silicon consumption. High external resistance was thought to be a significant challenge for FDSOI mainly in part due to the silicon consumption from the spacer process but also from the junction formation process. Ion implantation is well known to cause damage in thin silicon even with high temperature activation anneal. The silicon damage caused by the ion implantation can also cause defective epitaxial growth during the raised source drain process. We have solved the challenge of junction formation for FDSOI by developing an implant last scheme. After the spacer module is completed the raised-source and drain is formed. Since the ion implant is done into the thick raised-source drain, the damage created is healed during the activation anneal. Parasitic capacitance is another known issue for devices with raised-source drain. We have developed a facetted epi process which eliminates a significant component of the additional parasitic capacitance caused by the raised-source drain (Fig. 2). 1 We have also developed several key elements that enable high performance FDSOI circuits. In-situ doped SiGeB for raised source-drain has been developed to reduce contact resistance and form abrupt junctions for pFETs. SiGe channel is another innovation we have developed to enable high performance by increasing hole mobility. Fig. 3 shows the benefit of the strained SiGe raised source-drain and the SiGe channel.2 FDSOI is scalable and can be used for several technology nodes. Gate length scaling for FDSOI can be accomplished by thinning the silicon. Reverse back bias can also be used to improve short channel effects and enable scaling. Figure 4 shows the improvement in short channel control as the silicon is thinned down to 3.5nm Remarkably the external resistance of the devices is not compromised as evidenced by the Ion vs Ioff comparison to devices with 6nm channel thickness. The same figure also shows the improvement in electrostatic behavior with reverse back bias.3 Additional improvements in FDSOI performance can be achieved by strained silicon on insulator technology. Figure 5 shows the benefit of the strained silicon channel for nFETs.4 Table 1 shows a comparison of state of the art FDSOI research transistors to FinFETs.5It is interesting to note that the FDSOI devices can achieve competitive drive currents at dramatically shorter gate-lengths thereby improving circuit performance. It is also interesting to note the FinFETs are normalized to the footprint which is 30% greater than the effective channel width. References K. Cheng et. al. IEDM 2010.K. Cheng et. al. IEDM 2013.A. Khakifirooz et. al. EDL 2012.A. Khakifirooz et. al. VLSI 2012.Q. Liu et. al. IEDM 2014. Figure 1

A comparative study of the effects of sputtering deposition conditions for ZnO surface electrode layers on Cu(In,Ga)Se2 and CuGaSe2 solar cells

The effects of post p-n junction formation processes, namely transparent conducting oxide (TCO) layer deposition conditions on Cu(In,Ga)Se2 (CIGS) and CuGaSe2 (CGS) solar cell device properties were comparatively studied. It was found that CIGS devices were relatively insensitive to the presence of oxygen and heat during TCO layer deposition, whereas CGS devices were extremely sensitive to oxygen and heat, resulting in a degradation of device performance in the presence of them. The use of the relatively low TCO deposition temperature (Ts) of 80°C led to significant improvements in the fill factor values of CGS devices compared to the case for Ts ~180°C, though the open circuit voltage was reduced. These results suggest that TCO deposition conditions can be an important parameter which critically affects ternary CGS solar cell device properties. It is, therefore, suggested that TCO layer deposition conditions for CGS devices should be optimized independently of that for conventional narrow-gap CIGS devices.

Porous silicon formation by hole injection from a back side p+/n junction for electrical insulation applications

In this paper, we propose to study the formation of porous silicon (PS) in low doped (1 × 1014 cm−3) n-type silicon through hole injection from a back side p+/n junction in the dark. This technique is investigated within the framework of electrical insulation. Three different types of junctions are investigated. The first one is an epitaxial n-type layer grown on p+ doped silicon wafer. The two other junctions are carried out by boron diffusion leading to p+ regions with junction depths of 20 and 115 μm. The resulting PS morphology is a double layer with a nucleation layer (NL) and macropores fully filled with mesoporous material. This result is unusual for low doped n-type silicon. Morphology variations are described depending on the junction formation process, the electrolyte composition, the anodization current density and duration. In order to validate the more interesting industrial potentialities of the p+/n injection technique, a comparison is achieved with back side illumination in terms of resulting morphology and experiments confirm comparable results. Electrical characterizations of the double layer, including NL and fully filled macropores, are then performed. To our knowledge, this is the first electrical investigation in low doped n type silicon with this morphology. Compared to the bulk silicon, the measured electrical resistivities are 6–7 orders of magnitude higher at 373 K.

Manufacturing 100-µm-thick silicon solar cells with efficiencies greater than 20% in a pilot production line

Reducing wafer thickness while increasing power conversion efficiency is the most effective way to reduce cost per Watt of a silicon photovoltaic module. Within the European project 20 percent efficiency on less than 100-µm-thick, industrially feasible crystalline silicon solar cells (“20plµs”), we study the whole process chain for thin wafers, from wafering to module integration and life-cycle analysis. We investigate three different solar cell fabrication routes, categorized according to the temperature of the junction formation process and the wafer doping type: p-type silicon high temperature, n-type silicon high temperature and n-type silicon low temperature. For each route, an efficiency of 19.5% or greater is achieved on wafers less than 100 µm thick, with a maximum efficiency of 21.1% on an 80-µm-thick wafer. The n-type high temperature route is then transferred to a pilot production line, and a median solar cell efficiency of 20.0% is demonstrated on 100-µm-thick wafers.

Modeling of junction formation in scaled Si devices

In this article, modeling of junction formation in scaled Si device is shown. An atomistic kinetic Monte Carlo (KMC) diffusion modeling is used for the analysis of dopant diffusion and defects during shallow junction formation processes. Dopant diffusion and defect evolution during sub-millisecond non-melt laser annealing (NLA) are studied in both experiments and an atomistic kMC diffusion modeling. Pre-amorphization implant is often used for ultra shallow junction formation. It is shown that Solid Phase Epitaxial Regrowth (SPER) annealing stage plays an important role for dopant diffusion in junction formation process. As Ge implant energy is increased, damage structure and IV composition of Amorphous Pockets are changed and this affects the dopant diffusion and activation behavior. KMC simulations show that B, As deactivation is induced by the formation of dopant-defect complexes, such as B n I m , As n V m , As n I m , As n , during millisecond annealing time range. Both experiments and KMC show that defect evolution during millisecond annealing time range. Fluorine, Carbon co-implant effects are also modeled using KMC.

Cadherin controls nectin recruitment into adherens junctions by remodeling the actin cytoskeleton.

The mechanism that coordinates activities of different adhesion receptors is poorly understood. We investigated this mechanism by focusing on the nectin-2 and E-cadherin adherens junction receptors. We found that, cadherin was not required for the basic process of nectin junction formation because nectin-2 formed junctions in cadherin-deficient A431D cells. Formation of nectin-2 junctions in these cells, however, became regulated by cadherin as soon as E-cadherin was re-expressed. E-cadherin recruited nectin-2 into adherens junctions, where both proteins formed distinct but tightly associated clusters. Live-cell imaging showed that the appearance of E-cadherin clusters often preceded that of nectin-2 clusters at sites of junction assembly. Inactivation of E-cadherin clustering by different strategies concomitantly suppressed the formation of nectin clusters. Furthermore, cadherin significantly increased the stability of nectin clusters, thereby making them resistant to the BC-12 antibody, which targets the nectin-2 adhesion interface. By testing different E-cadherin-α-catenin chimeras, we showed that the recruitment of nectin into chimera junctions is mediated by the actin-binding domain of α-catenin. Our data suggests that E-cadherin regulates assembly of nectin junctions through α-catenin-induced remodeling of the actin cytoskeleton around the cadherin clusters.