Optical tweezing of microparticles and cells using silicon-photonics-based optical phased arrays.

Integrated optical tweezers have the potential to enable highly-compact, low-cost, mass-manufactured, and broadly-accessible optical manipulation when compared to standard bulk-optical tweezers. However, integrated demonstrations to date have been fundamentally limited to micron-scale standoff distances and, often, passive trapping functionality, making them incompatible with many existing applications and significantly limiting their utility, especially for biological studies. In this work, we demonstrate optical trapping and tweezing using an integrated OPA for the first time, increasing the standoff distance of integrated optical tweezers by over two orders of magnitude compared to prior demonstrations.

Silicon-photonics-enabled chip-based 3D printer.

Imagine if it were possible to create 3D objects in the palm of your hand within seconds using only a single photonic chip. Although 3D printing has revolutionized the way we create in nearly every aspect of modern society, current 3D printers rely on large and complex mechanical systems to enable layer-by-layer addition of material. This limits print speed, resolution, portability, form factor, and material complexity.

Integrated visible-light polarization rotators and splitters for atomic quantum systems.

In this work, we design and experimentally demonstrate the first, to the best of our knowledge, integrated polarization splitters and rotators at blue wavelengths. We develop compact and efficient designs for both a polarization splitter and rotator at a 422-nm wavelength, an important laser-cooling transition for Sr ions. These devices are fabricated in a 200-mm wafer-scale process and experimentally demonstrated, resulting in a measured polarization-splitter transverse-electric thru-port coupling of 98.

FAK family proteins regulate breast cancer metastasis distinct mechanisms.

Breast cancer is the most commonly diagnosed malignancy and the major leading cause of tumor-related deaths in women. It is estimated that the majority of breast tumor-related deaths are a consequence of metastasis, to which no cure exists at present. The FAK family proteins Proline-rich tyrosine kinase (PYK2) and focal adhesion kinase (FAK) are highly expressed in breast cancer, but the exact cellular and signaling mechanisms by which they regulate tumor cell invasiveness and consequent metastatic dissemination are mostly unknown.

Circulating succinate-modifying metabolites accurately classify and reflect the status of fumarate hydratase-deficient renal cell carcinoma.

Germline or somatic loss-of-function mutations of fumarate hydratase (FH) predispose patients to an aggressive form of renal cell carcinoma (RCC). Since other than tumor resection there is no effective therapy for metastatic FH-deficient RCC, an accurate method for early diagnosis is needed. Although MRI or CT scans are offered, they cannot differentiate FH-deficient tumors from other RCCs.

Feedback between mechanosensitive signaling and active forces governs endothelial junction integrity.

The formation and recovery of gaps in the vascular endothelium governs a wide range of physiological and pathological phenomena, from angiogenesis to tumor cell extravasation. However, the interplay between the mechanical and signaling processes that drive dynamic behavior in vascular endothelial cells is not well understood. In this study, we propose a chemo-mechanical model to investigate the regulation of endothelial junctions as dependent on the feedback between actomyosin contractility, VE-cadherin bond turnover, and actin polymerization, which mediate the forces exerted on the cell-cell interface.

A novel Pyk2-derived peptide inhibits invadopodia-mediated breast cancer metastasis.

Dissemination of cancer cells from the primary tumor into distant body tissues and organs is the leading cause of death in cancer patients. While most clinical strategies aim to reduce or impede the growth of the primary tumor, no treatment to eradicate metastatic cancer exists at present. Metastasis is mediated by feet-like cytoskeletal structures called invadopodia which allow cells to penetrate through the basement membrane and intravasate into blood vessels during their spread to distant tissues and organs.

FAK-Mediated Signaling Controls Amyloid Beta Overload, Learning and Memory Deficits in a Mouse Model of Alzheimer's Disease.

The non-receptor focal adhesion kinase (FAK) is highly expressed in the central nervous system during development, where it regulates neurite outgrowth and axon guidance, but its role in the adult healthy and diseased brain, specifically in Alzheimer's disease (AD), is largely unknown. Using the 3xTg-AD mouse model, which carries three mutations associated with familial Alzheimer's disease (APP KM670/671NL Swedish, PSEN1 M146V, MAPT P301L) and develops age-related progressive neuropathology including amyloid plaques and Tau tangles, we describe here, for the first time, the in vivo role of FAK in AD pathology. Our data demonstrate that while site-specific knockdown in the hippocampi of 3xTg-AD mice has no effect on learning and memory, hippocampal overexpression of the protein leads to a significant decrease in learning and memory capabilities, which is accompanied by a significant increase in amyloid β (Aβ) load.

Pyk2 regulates cell-edge protrusion dynamics by interacting with Crk.

Focal adhesion kinase (FAK) is well established as a regulator of cell migration, but whether and how the closely related proline-rich tyrosine kinase 2 (Pyk2) regulates fibroblast motility is still under debate. Using mouse embryonic fibroblasts (MEFs) from Pyk2 mice, we show here, for the first time, that lack of Pyk2 significantly impairs both random and directed fibroblast motility. Pyk2 MEFs show reduced cell-edge protrusion dynamics, which is dependent on both the kinase and protein-protein binding activities of Pyk2.

NBPF1 independently determine the risk stratification and prognosis of patients with neuroblastoma.

Neuroblastoma is the most frequent extracranial malignant solid tumor in children, and the 5 year OS of high risk neuroblastoma patients was less than 15%. This study aimed to identify biomarkers for risk stratification and prognosis prediction in neuroblastoma.149 low risk samples, 108 intermediate risk samples and 619 high risk samples were included in our study, and NBPF1 gene was found to be significantly correlated with risk levels and OS.

Complement and coagulation cascades pathway correlates with chemosensitivity and overall survival in patients with soft tissue sarcoma.

Chemotherapy is an indispensable method in treatment of Soft tissue sarcomas (STS), but variability in sensitivity as a result of tumor heterogeneity is a key factor in determining patient outcome. Several studies have investigated the phenomenon of chemotherapy resistance in STS, while its precise complex mechanism is still unknown. This study aims to identify potential biomarkers for predicting the STS chemosensitivity, with the goal of both aiding patient treatment determination in the clinic and providing insight into key parts of the underlying mechanism.

Expression of CXCR4 and MMP-2 is associated with poor prognosis in patients with osteosarcoma.

Background: Osteosarcoma is a primary malignant tumor with a high tendency to form metastasis and poor prognosis. Consequently, finding effective early indicators of metastases is crucial for identifying and treating high-risk patients. CXCR4 and MMP-2 have been found to strongly correlate with invasion and metastasis of malignant tumors, including osteosarcoma.