Low-loss singlemode PECVD silicon nitride photonic wire waveguides for 532-900 nm wavelength window fabricated within a CMOS pilot line

PECVD silicon nitride photonic wire waveguides have been fabricated in a CMOS pilot line. Both clad and unclad single mode wire waveguides were measured at lambda = 532, 780, and 900 nm, respectively. The dependence of loss on wire width, wavelength, and cladding is discussed in detail. Cladded multimode and singlemode waveguides show a loss well below 1 dB/cm in the 532-900 nm wavelength range. For singlemode unclad waveguides, losses < 1 dB/cm were achieved at lambda = 900 nm, whereas losses were measured in the range of 1-3 dB/cm for lambda = 780 and 532 nm, respectively

Characterization of PECVD Silicon Nitride Photonic Components at 532 and 900 nm Wavelength

Low temperature PECVD silicon nitride photonic waveguides have been fabricated by both electron beam lithography and 200 mm DUV lithography. Propagation losses and bend losses were both measured at 532 and 900 nm wavelength, revealing sub 1dB/cm propagation losses for cladded waveguides at both wavelengths for single mode operation. Without cladding, propagation losses were measured to be in the 1-3 dB range for 532 nm and remain below 1 dB/cm for 900 nm for single mode waveguides. Bend losses were measured for 532 nm and were well below 0.1 dB per 90 degree bend for radii larger than 10 mu m

Hydrophilic Monomethyl Auristatin E Derivatives as Novel Candidates for the Design of Antibody-Drug Conjugates

Peer reviewe

Direct Imaging of Graphene Edges: Atomic Structure and Electronic Scattering

We report an atomically-resolved scanning tunneling microscopy (STM) investigation of the edges of graphene grains synthesized on Cu foils by chemical vapor deposition (CVD). Most of the edges are macroscopically parallel to the zigzag directions of graphene lattice. These edges have microscopic roughness that is found to also follow zigzag directions at atomic scale, displaying many ~120 degree turns. A prominent standing wave pattern with periodicity ~3a/4 (a being the graphene lattice constant) is observed near a rare-occurring armchair-oriented edge. Observed features of this wave pattern are consistent with the electronic intervalley backscattering predicted to occur at armchair edges but not at zigzag edges

A modelling framework for the assessment of the impacts of alternative policy and management options on the sustainability of Finnish agrifood systems

Recently, a new project focussing on integrated assessment modelling of agrifood systems (IAM-Tools) has been launched at MTT Agrifood Research Finland to gather, evaluate, refine and develop these component models and to link tem in an IAM framework for Finnish conditions

Regulation of stem cell differentiation by histone methyltransferases and demethylases

The generation of different cell types from stem cells containing identical genetic information and their organization into tissues and organs during development is a highly complex process that requires defined transcriptional programs. Maintenance of such programs is epigenetically regulated and the factors involved in these processes are often essential for development. The activities required for cell-fate decisions are frequently deregulated in human tumors, and the elucidation of the molecular mechanisms that regulate these processes is therefore important for understanding both developmental processes and tumorigenesis

Mitochondrial degeneration and not apoptosis is the primary cause of embryonic lethality in ceramide transfer protein mutant mice

Ceramide transfer protein (CERT) functions in the transfer of ceramide from the endoplasmic reticulum (ER) to the Golgi. In this study, we show that CERT is an essential gene for mouse development and embryonic survival and, quite strikingly, is critical for mitochondrial integrity. CERT mutant embryos accumulate ceramide in the ER but also mislocalize ceramide to the mitochondria, compromising their function. Cells in mutant embryos show abnormal dilation of the ER and degenerating mitochondria. These subcellular changes manifest as heart defects and cause severely compromised cardiac function and embryonic death around embryonic day 11.5. In spite of ceramide accumulation, CERT mutant mice do not die as a result of enhanced apoptosis. Instead, cell proliferation is impaired, and expression levels of cell cycle–associated proteins are altered. Individual cells survive, perhaps because cell survival mechanisms are activated. Thus, global compromise of ER and mitochondrial integrity caused by ceramide accumulation in CERT mutant mice primarily affects organogenesis rather than causing cell death via apoptotic pathways

Association of Early Beta-amyloid Accumulation and Neuroinflammation Measured with [11C]PBR28 in Elderly Individuals Without Dementia

OBJECTIVE: To examine whether early β-amyloid (Aβ) accumulation and metabolic risk factors are associated with neuroinflammation in elderly individuals without dementia. METHODS: We examined 54 volunteers (mean age 70.0, 56% women, 51% APOE ε4 carriers) with a TSPO-tracer [11C]PBR28 to assess neuroinflammation and with [11C]Pittsburgh compound B (PiB) to assess cerebral Aβ accumulation. [11C]PBR28 and [11C]PiB standardized uptake value ratios (SUVRs) were quantified in six regions of interests by using the cerebellar cortex as a pseudo-reference/reference region, respectively. Fasting venous glucose, insulin, and high sensitivity C-reactive protein (hs-CRP) values were determined. Homeostatic model assessment of insulin resistance (HOMA-IR) was calculated. A subset of individuals (n=11) underwent CSF sampling, and Aβ40, Aβ42, total-tau, phospho-tau, soluble TREM2 and YKL-40 levels were measured. RESULTS: Among the whole study group, no significant association was found between [11C]PiB and [11C]PBR28 SUVR composite scores (slope 0.02, p=0.30). However, higher [11C]PiB binding was associated with higher [11C]PBR28 binding among amyloid negative ([11C]PiB composite score ≤1.5) (TSPO-genotype, age and sex adjusted slope 0.26, p=0.008) but not among amyloid positive participants (slope: -0.004, p=0.88). Higher CSF sTREM2 (rs 0.72, p=0.01) and YKL-40 (rs=0.63, p=0.04) concentrations were associated with a higher [11C]PBR28 composite score. Higher body mass index, HOMA-IR, and hs-CRP were associated with higher [11C]PBR28 binding in brain regions where Aβ accumulation is first detected in Alzheimer's disease (AD). CONCLUSIONS: While there was no association between amyloid and neuroinflammation in the overall study group, neuroinflammation was associated with amyloid among the subgroup at early stages of amyloid pathology