Optical trapping with structured light : a review

Funding: This work was supported by the National Natural Science Foundation of China (11874102 and 61975047), the Sichuan Province Science and Technology Support Program (2020JDRC0006), and the Fundamental Research Funds for the Central Universities (ZYGX2019J102). M.C. and Y.A. thank the UK Engineering and Physical Sciences Research Council for funding.Optical trapping describes the interaction between light and matter to manipulate micro-objects through momentum transfer. In the case of 3D trapping with a single beam, this is termed optical tweezers. Optical tweezers are a powerful and noninvasive tool for manipulating small objects, and have become indispensable in many fields, including physics, biology, soft condensed matter, among others. In the early days, optical trapping was typically accomplished with a single Gaussian beam. In recent years, we have witnessed rapid progress in the use of structured light beams with customized phase, amplitude, and polarization in optical trapping. Unusual beam properties, such as phase singularities on-axis and propagation invariant nature, have opened up novel capabilities to the study of micromanipulation in liquid, air, and vacuum. We summarize the recent advances in the field of optical trapping using structured light beams.Publisher PDFPeer reviewe

and susceptibility to colorectal cancer

Association between miR-27a genetic variant

Suppression of TGF-β1/Smad signaling pathway by sesamin contributes to the attenuation of myocardial fibrosis in spontaneously hypertensive rats.

This study investigated the effect of sesamin on myocardial fibrosis in spontaneously hypertensive rats (SHRs) and the possible mechanisms involved. Twenty-eight male SHRs were randomly allocated to SHR group, Ses160 group (sesamin 160 mg/kg), Ses80 group (sesamin 80 mg/kg) and Cap30 group (captopril 30 mg/kg). Seven male WKY rats were used as control. Sesamin and captopril were administered intragastrically for 12 weeks. Captopril significantly reduced systolic blood pressure and angiotensin II (Ang II) levels in SHRs, accompanied by a marked attenuation of left ventricular hypertrophy (LVH) and collagen deposition (P <0.05 or P <0.01). Though sesamin had no significant influence on Ang II levels, and the hypotensive effect was also significantly inferior to that of captopril (P <0.05 or P <0.01), however, the improvement of LVH and collagen deposition was similar to that in captopril group. Sesamin markedly reduced transforming growth factor-β1 (TGF-β1) content in cardiac tissues, with Smad3 phosphorylation decreased and Smad7 protein expression increased notably (P <0.05 or P <0.01). Protein expression of type I collagen and type III collagen, target genes of Smad3, was down-regulated markedly by sesamin (P <0.05 or P <0.01). In addition, sesamin significantly increased total antioxidant capacity and superoxide dismutase protein in cardiac tissues (P <0.05 or P <0.01), while the expression of NADPH oxidase subunit p47phox and malondialdehyde content were reduced markedly (P <0.05 or P <0.01). In vitro studies also demonstrated that sesamin was able to suppress Ang II induced phosphorylation of Smad3 and secretion of TGF-β1 and type I and type III collagen in cultured rat cardiac fibroblasts. These data suggest that sesamin is capable of attenuating hypertensive myocardial fibrosis through, at least partly, suppression of TGF-β1/Smad signaling pathway

STAMBP promotes lung adenocarcinoma metastasis by regulating the EGFR/MAPK signaling pathway

Tumor metastasis is a leading cause of death in lung adenocarcinoma (LUAD) patients, but the molecular events that regulate metastasis have not been completely elucidated. STAMBP is a deubiquitinating enzyme of the Jab1/MPN metalloenzyme family that regulates the stability of substrates in cells by specifically removing ubiquitin molecules. We found that STAMBP expression was increased in the cytoplasm of tumor cells from LUAD patients. The STAMBP level was closely associated with tumor size, lymph node invasion and neoplasm disease stage. A high STAMBP level predicted poor overall survival and disease-free survival in LUAD patients. STAMBP overexpression promoted cell migration and invasion, whereas STAMBP knockdown attenuated these processes in LUAD cells after epidermal growth factor treatment. Mechanistically, increased STAMBP expression promoted the stabilization of Epidermal growth factor receptor (EGFR), whereas STAMBP knockdown induced the degradation of EGFR. STAMBP may deubiquitinate EGFR by localizing in early endosomes and increase EGFR membrane localization in LUAD cells. The overexpression of STAMBP triggered the activation of MAPK signaling after epidermal growth factor treatment. In contrast, this activation was attenuated in STAMBP knockdown cells. Small molecule inhibitors of EGFR and MAPK signaling pathway may block STAMBP-induced cell mobility and invasion as well as ERK activation in cells. Importantly, STAMBP knockdown suppressed LUAD tumor growth and metastasis by regulating the EGFR-mediated ERK activation in a xenograft mouse model. Our findings identified STAMBP as a novel potential target for LUAD therapy

On the origin of rhythmic contractile activity of the esophagus in early achalasia, a clinical case study

A patient with early achalasia presented spontaneous strong rhythmic non-propulsive contractions at ~ 7/min, independent of swallows. Our aim was to evaluate characteristics of the rhythmic contractions, provide data on the structure of pacemaker cells in the esophagus and discuss a potential role for interstitial cells of Cajal (ICC) in the origin of rhythmicity. We hypothesize that intramuscular ICC (ICC-IM) are the primary pacemaker cells. The frequency but not the amplitude of the rhythmic contractions was inhibited by the phosphodiesterase inhibitor drotaverine consistent with cAMP inhibiting pacemaker currents in ICC-IM. The frequency increased by wet swallows but not dry swallows, consistent with stretch causing increase in slow wave frequency in ICC-IM. New studies on archival material showed that ICC-IM were present throughout the human esophageal musculature and were not diminished in early achalasia. Although ICC-IM exhibited a low density, they were connected to PDGFRα-positive fibroblast-like cells with whom they formed a dense gap junction coupled network. Nitrergic innervation of ICC was strongly diminished in early achalasia because of the loss of nitrergic nerves. It therefore appears possibly that ICC-IM function as pacemaker cells in the esophagus and that the network of ICC and PDGFRα-positive cells allows for coupling and propagation of the pacemaker activity. Loss of nitrergic innervation to ICC in achalasia may render them more excitable such that its pacemaker activity is more easily expressed. Loss of propagation in achalasia may be due to loss of contraction-induced aboral nitrergic inhibition

Effect of sesamin on Ang II induced Smad3 phosphorylation.

<p>Rat cardiac fibroblasts were isolated from 0 to 3-day-old neonatal rats. Following incubation with sesamin (1.0, 10.0 and 100.0 μmol/L) for 12 h, cells were exposed to Ang II (0.1μmol/L) for 24 h. Cell lysates were subjected to western blot analysis for Smad3 phosphorylation as detailed in the Methods section. Levels of p-Smad3 protein were normalized to that of total Smad3 protein. Data were presented as percentage of that in control group (mean ± SD, n = 3). a <i>P</i> <0.05, b <i>P</i> <0.01 vs. control group; c <i>P</i> <0.05, d <i>P</i> <0.01 vs. Ang II group.</p

Effect of sesamin on left ventricular mass index (LVMI) in rats.

<p>After 12 weeks of supplementation with sesamin or captopril, rats were anaesthetized with pentobarbital sodium and sacrificed, followed by dissection of left ventricles. LVMI is calculated as the ratio of left ventricular weight to body weight (mg/g). Data were presented as mean±SD (n = 7). b <i>P</i> <0.01 vs. WKY group; c <i>P</i> <0.05, d <i>P</i> <0.01 vs. SHR group.</p

Effect of sesamin on Ang II induced secretion of TGF-β₁ and type I and type III collagen in cardiac fibroblasts (mean±SD, n = 6).

<p>a <i>P</i> <0.05</p><p>b <i>P</i> <0.01 vs. Control group</p><p>c <i>P</i> <0.05</p><p>d <i>P</i> <0.01 vs. Ang II group</p><p>Effect of sesamin on Ang II induced secretion of TGF-β₁ and type I and type III collagen in cardiac fibroblasts (mean±SD, n = 6).</p