Silicon nitride metalenses for unpolarized high-NA visible imaging

As one of nanoscale planar structures, metasurface has shown excellent superiorities on manipulating light intensity, phase and/or polarization with specially designed nanoposts pattern. It allows to miniature a bulky optical lens into the chip-size metalens with wavelength-order thickness, playing an unprecedented role in visible imaging systems (e.g. ultrawide-angle lens and telephoto). However, a CMOS-compatible metalens has yet to be achieved in the visible region due to the limitation on material properties such as transmission and compatibility. Here, we experimentally demonstrate a divergent metalens based on silicon nitride platform with large numerical aperture (NA~0.98) and high transmission (~0.8) for unpolarized visible light, fabricated by a 695-nm-thick hexagonal silicon nitride array with a minimum space of 42 nm between adjacent nanoposts. Nearly diffraction-limit virtual focus spots are achieved within the visible region. Such metalens enables to shrink objects into a micro-scale size field of view as small as a single-mode fiber core. Furthermore, a macroscopic metalens with 1-cm-diameter is also realized including over half billion nanoposts, showing a potential application of wide viewing-angle functionality. Thanks to the high-transmission and CMOS-compatibility of silicon nitride, our findings may open a new door for the miniaturization of optical lenses in the fields of optical fibers, microendoscopes, smart phones, aerial cameras, beam shaping, and other integrated on-chip devices.Comment: 16 pages, 7 figure

LATS kinase-mediated CTCF phosphorylation and selective loss of genomic binding.

Chromatin topological organization is instrumental in gene transcription. Gene-enhancer interactions are accommodated in the same CTCF-mediated insulated neighborhoods. However, it remains poorly understood whether and how the 3D genome architecture is dynamically restructured by external signals. Here, we report that LATS kinases phosphorylated CTCF in the zinc finger (ZF) linkers and disabled its DNA-binding activity. Cellular stress induced LATS nuclear translocation and CTCF ZF linker phosphorylation, and altered the landscape of CTCF genomic binding partly by dissociating it selectively from a small subset of its genomic binding sites. These sites were highly enriched for the boundaries of chromatin domains containing LATS signaling target genes. The stress-induced CTCF phosphorylation and locus-specific dissociation from DNA were LATS-dependent. Loss of CTCF binding disrupted local chromatin domains and down-regulated genes located within them. The study suggests that external signals may rapidly modulate the 3D genome by affecting CTCF genomic binding through ZF linker phosphorylation

Characterization of dendritic morphology and neurotransmitter phenotype of thoracic descending propriospinal neurons after complete spinal cord transection and GDNF treatment

After spinal cord injury (SCI), poor regeneration of damaged axons of the central nervous system (CNS) causes limited functional recovery. This limited spontaneous functional recovery has been attributed, to a large extent, to the plasticity of propriospinal neurons, especially the descending propriospinal neurons (dPSNs). Compared with the supraspinal counterparts, dPSNs have displayed significantly greater regenerative capacity, which can be further enhanced by glial cell line-derived neurotrophic factor (GDNF). In the present study, we applied a G-mutated rabies virus (G-Rabies) co-expressing green fluorescence protein (GFP) to reveal Golgi-like dendritic morphology of dPSNs. We also investigated the neurotransmitters expressed by dPSNs after labeling with a retrograde tracer Fluoro-Gold (FG). dPSNs were examined in animals with sham injuries or complete spinal transections with or without GDNF treatment. Bilateral injections of G-Rabies and FG were made into the 2nd lumbar (L2) spinal cord at 3 days prior to a spinal cord transection performed at the 11th thoracic level (T11). The lesion gap was filled with Gelfoam containing either saline or GDNF in the injury groups. Four days post-injury, the rats were sacrificed for analysis. For those animals receiving G-rabies injection, the GFP signal in the T7-9 spinal cord was visualized via 2-photon microscopy. Dendritic morphology from stack images was traced and analyzed using a Neurolucida software. We found that dPSNs in sham injured animals had a predominantly dorsal-ventral distribution of dendrites. Transection injury resulted in alterations in the dendritic distribution with dorsal-ventral retraction and lateral-medial extension. Treatment with GDNF significantly increased the terminal dendritic length of dPSNs. The density of spine-like structures was increased after injury, and treatment with GDNF enhanced this effect. For the group receiving FG injections, immunohistochemistry for glutamate, choline acetyltransferase (ChAT), glycine, and GABA was performed in the T7-9 spinal cord. We show that the majority of FG retrogradely-labeled dPSNs were located in the Rexed Lamina VII. Over 90% of FG-labeled neurons were glutamatergic, with the other three neurotransmitters contributing less than 10% of the total. To our knowledge this is the first report describing the morphologic characteristics of dPSNs and their neurotransmitter expressions, as well as the dendritic response of dPSNs after transection injury and GDNF treatment

Analysis of safety and effect of reconstructing anterior and middle columns by single posterior approach in treating lumbar burst fractures

ObjectiveTo explore the safety and effect of the technique of reconstructing anterior and middle columns by posterior approach in treating lumbar burst fractures.MethodsFrom July 2005 to January 2007, 22 cases (18 males and 4 females, aged 28-57 years, 42.7 years on average) of lumbar burst fractures were treated with surgical procedures in our hospital. Based on the routine posterior approach, one of the transverse processes of the injured vertebra was incised to get access to the lateral side of the injured vetebral body. After all the displaced fracture fragments were cleared away and the spinal canal was decompressed, the titanium mesh packed with autografts was implanted from the lateral side to reconstruct the anterior and middle columns. The adjacent above and below segments of the vetebral body were fixed with transpedicular screws. The operation time, intraoperative blood loss, vertebral height, degree of kyphotic deformity and comprised spinal canal were documented.ResultsThe average operation time was 3.5 hours (ranging 2.8-5.8 hours) and the average blood loss was 820 ml (ranging 650-2 100 ml). All the cases were followed up for 17.2 months on average (ranging 12-28 months). The height of the injured vetebral body was restored from 24 % (12%45%) preoperatively to 96% (95%-99%) postoperatively (P<0.05). The natural spinal curvatures and spinal canal were restored. Three cases were involved in transient iatrogenic nerve root injury and 1 case was involved in the loosening of the connected rod of the pedicle screw system 3 months postoperatively.ConclusionsThe technique of implanting the titanium mesh by posterior approach is effective and safe enough to reconstruct the anterior and middle columns in treating lumbar burst fractures

Unilateral Microinjection of Acrolein into Thoracic Spinal Cord Produces Acute and Chronic Injury and Functional Deficits

Although lipid peroxidation has long been associated with spinal cord injury (SCI), the specific role of lipid peroxidation-derived byproducts such as acrolein in mediating damage remains to be fully understood. Acrolein, an α-β unsaturated aldehyde, is highly reactive with proteins, DNA, and phospholipids and is considered as a second toxic messenger that disseminates and augments initial free radical events. Previously, we showed that acrolein increased following traumatic SCI and injection of acrolein induced tissue damage. Here, we demonstrate that microinjection of acrolein into the thoracic spinal cord of adult rats resulted in dose-dependent tissue damage and functional deficits. At 24 h (acute) after the microinjection, tissue damage, motoneuron loss, and spinal cord swelling were observed on sections stained with Cresyl Violet. Luxol fast blue staining further showed that acrolein injection resulted in dose-dependent demyelination. At 8 weeks (chronic) after the microinjection, cord shrinkage, astrocyte activation, and macrophage infiltration were observed along with tissue damage, neuron loss, and demyelination. These pathological changes resulted in behavioral impairments as measured by both the Basso, Beattie, and Bresnahan (BBB) locomotor rating scale and grid walking analysis. Electron microscopy further demonstrated that acrolein induced axonal degeneration, demyelination, and macrophage infiltration. These results, combined with our previous reports, strongly suggest that acrolein may play a critical causal role in the pathogenesis of SCI and that targeting acrolein could be an attractive strategy for repair after SCI

CSRP2 transcript levels after consolidation therapy increase prognostic prediction ability in B-cell acute lymphoblastic leukaemia

Quantification of measurable residual disease (MRD) correlates with the risk of leukemia recurrence in adults with B-cell acute lymphoblastic leukemia (ALL). However, it remains unknown whether collecting data on cysteine and glycine-rich protein 2 (CSRP2) transcript levels, after completing the second course of consolidation, improves prognosis prediction accuracy. A total of 204 subjects with B-cell ALL were tested for CSPR2 transcripts after completing the second course of consolidation using quantitative real-time polymerase chain reaction (qRT-PCR) and divided into high (N = 32) and low (N = 172) CSRP2 expression cohorts. In multivariable analyses, subjects with high expression of CSRP2 had a higher 5-year cumulative incidence of relapse (CIR) (hazard ratio [HR] = 2.57, 95% confidence interval [CI] 1.38-4.76; P = 0.003), lower 5-year relapse-free survival (RFS) (HR = 3.22, 95% CI 1.75-5.93; P < 0.001), and overall survival (OS) (HR = 4.59, 95% CI 2.64-7.99; P < 0.001) in the whole cohort, as well as in the multi-parameter flow cytometry (MPFC) MRD-negative cohort (for CIR, HR = 2.70, 95% CI 1.19-6.12; for RFS, HR = 4.37, 95% CI 1.94-9.85; for OS, HR = 4.90, 95% CI 2.43-9.90; all P < 0.05). Prognostic analysis showed that allogeneic hematopoietic stem cell transplantation (allo-HSCT) could significantly improve the prognosis of patients with high CSRP2 expression (allo-HSCT vs chemotherapy: 5-year CIR, 52% vs 91%; RFS, 41% vs 9%; OS, 38% vs 20%; all P < 0.05). Our data indicate that incorporating data from CSPR2 transcript levels to the MRD-testing at the end of the second course of consolidation therapy enhances prognosis prediction accuracy in adults with B-cell ALL