Geometric error modeling and compensation for high precision composite optical measurement systems.

Composite optical measurement systems are widely used in the field of precision measurement due to their combination of inspection with high accuracy, speed, wide range, real-time, and other advantages. Whereas errors are prevalent in measurements, in order to improve detection accuracy, the systems must be compensated for geometric errors in three-dimensional space. Aiming at the complex situation of multi-probes and multi-zooms in the composite optical measurement system, the current error modelling methods are difficult to be directly applied, so this paper establishes a unified three-dimensional volumetric error model based on the theory of multi-body system and combined with the principle of geometric optics, performs the error verification through the direct measurement method, and finally realises the compensation of geometric error in the continuous space of the whole measurement range. Eventually, the accuracy of the proposed error model and the effectiveness of the error compensation method were verified by a laser interferometer and standard objects to be measured, and the integrated geometric error of the system was decreased by 76.55%, which effectively improved the accuracy of the system. The error modelling and compensation method proposed in this paper provides a new idea for the error compensation of the zoom measurement system, and at the same time, it is universal for the measurement systems of different structures and motion forms, which can be widely used in the field of precision measurement.

Brick tea consumption and its relationship with fluorosis in Tibetan areas.

Brick tea-type fluorosis (BTF) due to a high intake of brick tea is possible in Tibetan populations, and dental fluorosis (DF) and skeletal fluorosis (SF) are its primary manifestations. To determine the prevalence of DF and SF and their relationships with brick tea intake in Tibetan populations, a literature review was conducted for studies published between 1994 and 2021. The available evidence revealed that brick tea may be produced from older stems and leaves of the tea plant and that the fluoride content of brick tea exceeds the national standard. The harsh environment of the plateau has led to limited food sources for the local Tibetan people who form the habit of drinking tea leaves as a satiation solution to digest greasy food and replenish vitamins, and regular consumption of brick tea leads to excessive exposure of Tibetan residents to fluoride. Studies in Tibet showed that the prevalence of DF in children was 14.06-75.93% in different districts, and the overall pooled prevalence of DF was 26.08%. The prevalence of SF in adults was 19.90-74.77% in different Tibetan districts, and the overall pooled prevalence of SF was 33.84%. The analysis of risk factors showed that the prevalence of BTF may be related to high-altitude and different working and living conditions, and BTF in children may be associated with fluoride intake during mothers' pregnancy and lactation. With the development of bioinformatics research, gene polymorphisms were suspected to be related to susceptibility to fluorosis in Tibetan populations. The study of BTF in Tibetan people needs to be further investigated and standardized, and additional studies evaluating the pathogenesis and preventive measures of BTF are warranted.

CircRNA protein tyrosine phosphatase receptor type a suppresses proliferation and induces apoptosis of lung adenocarcinoma cells via regulation of microRNA-582-3p.

Circular RNAs (circRNAs) are associated with cancer progression. The present study aimed to examine the function of circRNA protein tyrosine phosphatase receptor type A (circRNA_PTPRA) in lung cancer cells and elucidate the underlying molecular mechanisms. The levels of circRNA_PTPRA and microRNA (miRNA/miR)-582-3p were measured in lung cancer tissue and cells using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Cell proliferation and apoptosis were evaluated using an 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry, respectively. The expression of cyclin D1, caspase-3, and cleaved caspase-3 was assessed via western blotting. The sites of circRNA_PTPRA/miR-582-3p interaction were identified using StarBase, and validated using a dual-luciferase reporter assay. We observed that circRNA_PTPRA levels were remarkably decreased, and miR-582-3p expression was up-regulated in lung cancer tissues and cells. circRNA_PTPRA directly interacts with miR-582-3p and downregulates miR-582-3p expression in lung cancer cells. Moreover, an miR-582-3p inhibitor decreased lung cancer cell proliferation and promoted apoptosis. The overexpression of circRNA_PTPRA decreased cell proliferation and increased apoptotic cell numbers, whereas miR-582-3p overexpression reversed these effects. These findings demonstrate that the up-regulation of circRNA_PTPRA significantly reduces lung cancer cell proliferation and induces apoptosis by regulating miR-582-3p expression.

The recombination zone adjusted by the gradient doping of TPA-DCPP for efficient and stable deep red organic light emitting diodes.

Deep-red organic light-emitting diodes (DR-OLEDs) or near-infrared organic light-emitting diodes (NIR-OLEDs) have a wide range of applications in real life, such as special light sources for plant growth in agriculture, optical communications, infrared imaging, infrared medical imaging and other fields. However, the device performance of DR-OLEDs is still far behind that of red, green and blue OLEDs. In addition to the well-known energy gap law, the location of the recombination region also has a significant impact on the device performance. If the recombination area is too close to the cathode, the electrons in the electron transport layer will easily cause exciton quenching. In this study, for the first time, we adopted a quantum well-like structure by changing the host (CBP) and guest (TPA-DCPP) thicknesses as the light-emitting layer to manage the position of the recombination zone, and then improved the carrier injection and transportation as well as increased the exciton recombination rate. Furthermore, we introduced a hole trap layer to reduce the current density and suppress the recombination zone movement; finally, we prepared high-brightness and high-efficiency DR-OLEDs based on the TADF material with a wavelength of 674 nm, a maximum brightness of 1151 cd m-2 and a maximum EQE of 4.4%.

Color-Tunable Organic Light Emitting Diodes for Deep Blue Emission by Regulating the Optical Micro-Cavity.

Nowadays, most blue organic light emitting diodes (OLEDs) are fabricated by using sky-blue emitters which are more easily synthesized when compared with other deep blue emitters. Herein, we put forward a new idea of using an optical micro-cavity based on metal electrodes to regulate electroluminance (EL) spectra of sky-blue organic light emitting diodes to obtain a saturated deep blue emission with a narrowed full-width at half-maximum (FWHM). First, we simulate micro-cavity OLEDs and find that the transmission of the anode plays an important role in the forward emission. Meanwhile, the optical path of micro-cavity OLEDs as well as the phase shifting from electrodes influence the EL spectra and induce the extra intensity enhancement. The results show that when the resonant cavity optical path is regulated by changing the thickness of emitting layer (EML) from 25 nm to 75 nm in the micro-cavity, the EL peak of blue OLEDs has a redshift from 479 nm to 493 nm with FWHM shifting from 69.8 nm to 83.2 nm, when compared to the device without the micro-cavity, whose approximate EL peak and FWHM are 487 nm and 87 nm, respectively. However, the efficiency of electroluminescence decreases in micro-cavity OLEDs. We speculate that this is on account of the ohmic contact between ITO and Ag, the surface plasma effect and the rough morphology induced by Ag electrodes.

Decreased expression of SOX17 is associated with tumor progression and poor prognosis in breast cancer.

The SOX17 (SRY-related HMG-box) transcription factor is involved in a variety of biological processes and is related to the tumorigenesis and progression of multiple tumors. However, the clinical application of SOX17 for breast cancer prognosis is currently limited. The aim of this study was to investigate the clinicopathologic and prognostic significance of SOX17 expression in human breast cancer. qPCR and western blot assays were performed to measure the expression of SOX17 in breast cancer cell lines and 30 matched pairs of breast cancer and corresponding noncancerous tissues. A SOX17 overexpression cell model was used to examine changes in cell growth in vitro. Immunohistochemical analyses were performed to retrospectively examine the prognostic impact of SOX17 expression in 187 additional breast cancer patients. Our results showed that SOX17 expression was decreased at both the messenger RNA (mRNA) and protein levels in the breast cancer cell lines and tissues, and that SOX17 overexpression could strongly suppress cell growth in vitro. Furthermore, the lack of SOX17 protein expression was strongly correlated with higher tumor grade (P = 0.002), lymph node metastasis (P < 0.001), and tumor node metastasis (TNM) stage (P = 0.001) and had poorer disease-free survival (DFS) and overall survival (OS) compared to normal SOX17 expression (P = 0.002 and 0.001, respectively). Univariate and multivariate analyses indicated that lower SOX17 expression was an independent prognostic factor for DFS (P = 0.007; HR = 2.854; 95 % CI 1.326-6.147) and OS (P = 0.005; HR = 5.035; 95 % CI 1.648-15.385) for breast cancer. Our findings indicate that SOX17 expression is a useful prognostic biomarker for breast cancer.

miR-451 regulates FoxO3 nuclear accumulation through Ywhaz in human colorectal cancer.

BACKGROUND AND OBJECTIVE: Our previous studies reported that miR-451 could protect against erythroid oxidant stress target gene-Ywhaz (14-3-3zeta) via inhibiting FoxO3 in the erythropoiesis. This study aimed to investigate the potential mechanism underlying the regulatory effect of miR-451 on human colorectal cancer (CRC) cells. METHODS: In this study, expressions of miR-451 and Ywhaz in CRC tissues and adjacent normal tissues were detected by quantitative real-time PCR (qRT-PCR) and immunohistochemistry respectively. Human colon cancer cell lines were transfected with miR-451-MSCV-PIG retroviral vector to restore miR-451 expression. Ywhaz-3'UTR luciferase reporter assay confirmed Ywhaz as a direct target gene of miR-451. HCT116 cells and H29 cells were transfected with -shRNA-Ywhaz (pSGU6-Ywahz-shRNA-GFP) and the protein level of FoxO3 in the nucleus and cytoplasm was detected via Western blot assay. The anti-tumor effects of miR-451 were further verified in nude mice. RESULTS: miR-451 was significantly down-regulated in human colon cancer tissues and cell lines (HCT116 and HT29), and inversely correlated with Dukes stage of colon cancer. Ywhaz was a candidate target gene of miR-451 and able to stimulate tumor growth via binding to FoxO3, inhibiting the FoxO3 nuclear accumulation. CONCLUSION: miR-451 may inhibit the colon cancer growth in vitro and in vivo, likely through directly targeting Ywhaz and indirectly regulating the nuclear accumulation of FoxO3.

Hsa-microRNA-101 suppresses migration and invasion by targeting Rac1 in thyroid cancer cells.

MicroRNAs (miRNAs) are 22- to 25-nucleotide non-coding RNA molecules that function as negative regulators of gene expression. In previous years, increasing evidence has arisen implicating the involvement of miRNAs in carcinogenesis. In previous studies, the role of miRNA-101 (miR-101) in tumors has been identified as a tumor suppressor and, until now, the role of miR-101 and Rac1 in thyroid cancer has remained undefined. This study revealed that miR-101 is significantly downregulated in papillary thyroid carcinoma (PTC) tissue and thyroid cancer cell lines, and that the downregulated miR-101 is associated with lymph node metastasis. Infection with the miR-101 murine stem cell virus may markedly inhibit cell migration and invasion in TPC-1 and HTH83 thyroid cancer cell lines. Rac1 was demonstrated to be negatively regulated by miR-101 at the post-transcriptional level, via a specific target site within the 3' untranslated region by dual-luciferase reporter assay. The expression of Rac1 was also observed to inversely correlate with miR-101 expression in PTC tissues; knockdown of Rac1 by shRNA inhibited thyroid cancer cell migration and invasion, resembling that of miR-101 overexpression. Thus, these findings suggested that miR-101 acts as a novel suppressor by targeting the Rac1 gene and inhibiting thyroid cancer cell migration and invasion.

Atorvastatin inhibits myocardin expression in vascular smooth muscle cells.

Atorvastatin (ATV), an inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A reductase, is widely prescribed as a lipid-lowering drug. It also inhibits the RhoA-Rho-associated kinase pathway in vascular smooth muscle (SM) cells and critically inhibits SM function. Myocardin is a coactivator of serum response factor, which upregulates SM contractile proteins. The RhoA-Rho-associated kinase pathway, which directly triggers SM contraction, also increases myocardin gene expression. Therefore, we investigated whether ATV inhibits myocardin gene expression in SM cells. In mice injected with ATV (IP 20 µg/g per day) for 5 days, myocardin gene expression was significantly downregulated in aortic and carotid arterial tissues with decreased expression of myocardin target genes SM α-actin and SM22. Correspondingly, the contractility of aortic rings in mice treated with ATV or the Rho-associated kinase inhibitor Y-27632 was reduced in response to treatment with either KCl or phenylephrine. In cultured mouse and human aortic SM cells, KCl treatment stimulated the expression of myocardin, SM α-actin, and SM22. These stimulatory effects were prevented by ATV treatment. ATV-induced inhibition of myocardin expression was prevented by pretreatment with either mevalonate or geranylgeranylpyrophosphate but not farnesylpyrophosphate. Treatment with Y-27632 mimicked ATV effects on the gene expression of myocardin, SM α-actin, and SM22, further suggesting a role for the RhoA-Rho-associated kinase pathway in ATV effects. Furthermore, ATV treatment inhibited RhoA membrane translocation and activation; these effects were prevented by pretreatment with mevalonate. We conclude that ATV inhibits myocardin gene expression in vivo and in vitro, suggesting a novel mechanism for ATV inhibition of vascular contraction.

[Expressions of FHIT and PTEN and their significance in prostate cancer].

OBJECTIVE: To investigate the expressions of the FHIT and PTEN genes and their significance in prostate cancer. METHODS: The expressions of FHIT and PTEN were detected in 85 cases of prostate cancer and 30 cases of benign prostatic nodular hyperplasia by immunohistochemistry of PV-6000. RESULTS: The positive expression rates of FHIT and PTEN were 34.1% and 42.4% in prostate cancer, significantly lower than 96.7% and 90.0% in benign prostatic nodular hyperplasia (P <0.01). Statistically significant differences were found in the positive expression rates of FHIT and PTEN among different Gleason grades, 44.4% and 55.6% in well differentiated, 38.9% and 44.4% in moderately differentiated, and 25.0% and 37.5% in lowly differentiated prostate cancer (P <0.05). But the expression of FHIT. CONCLUSION: FHIT and PTEN may play a certain role in the was not correlated with that of PTEN in the prostate cancer tissue (P >0.05). development, progression and infiltration of prostate cancer.