Picometer-differential twice-exposed element for three-dimensional measurement with extremely long depth of field.

The accuracy of optical three-dimensional (3D) shape measurement is always influenced by the defocusing of a projection or imaging system. In this paper, a novel optical element made by picometer-differential twice-exposed holography, called a picometer comb, is proposed to generate the projection pattern for 3D shape measurement. Two interference fields with picometer-scale period difference are recorded on a substrate to fabricate the picometer comb by twice-exposed laser holography; this element reconstructs the diffraction field, which is essentially the interference between the holograms of two object waves with a slight angle. This picometer comb has the advantage of the generation of a stable light field distribution with extremely long depth of field and small divergence angle. We demonstrate that this diffraction field provides a solution for non-defocusing 3D shape measurement.

Binocular vision profilometry for large-sized rough optical elements using binarized band-limited pseudo-random patterns.

In this paper, a non-contact binocular vision profilometry method is proposed to measure a rough lens with aperture of around 300mm. A series of binarized band-limited pseudo-random patterns (BBPPs) are projected onto the rough lens, we utilize the temporal encoding method so that each pixel in the captured images has its specific code word. Homologous points could be matched via stereo matching procedure, then the surface of the rough lens will be reconstructed based on triangulation method according to the previous calibration data. Compared with the three coordinate measuring machine (CMM), this method achieves a fast and cheap measurement of the large-sized rough lens, which might be highly interesting for fast and overall measurement of metre-sized rough elements in the future.

LncRNA DIGIT Accelerates Tube Formation of Vascular Endothelial Cells by Sponging miR-134.

Atherosclerosis is one of the most prevalent and important cardiac diseases, involving the heart and brain. This study aimed to explore the impacts of lncRNA Divergent to GSC induced by TGF-b family signaling (DIGIT) on vascular endothelial cells tube-formation capacity so as to reveal the potentials of DIGIT in atherosclerosis therapy. DIGIT expression in human microvascular endothelial HMEC-1 cells was silenced by transfection with shRNAs-targeted DIGIT. The effects of DIGIT silence on cell viability, migration, apoptosis, and tube formation were then assessed. Additionally, the cross-regulation between DIGIT and miR-134, and between miR-134 and Bmi-1 was detected to further reveal through which mechanism (s) DIGIT mediated HMEC-1 cells. The results showed that DIGIT silence significantly reduced cell viability, migration, tube-like structures formation, and induced apoptosis in HMEC-1 cells. DIGIT worked as a sponge for miR-134, and the anti-growth, anti-migratory, and anti-tube-formation functions of DIGIT silence on HMEC-1 cells were abolished by miR-134 suppression. Bmi-1 was a target of miR-134, and Bmi-1 upregulation abolished miR-134 overexpression-diminished cell growth, migration, and tube formation of HMEC-1 cells. Furthermore, Bmi-1 upregulation activated PI3K/AKT and Notch signaling pathways. In conclusion, our study demonstrated that lncRNA DIGIT accelerated tube formation of vascular endothelial cells through sponging miR-134. Our findings suggest that DIGIT and miR-134 may be promising molecular targets for atherosclerosis therapy.

Polymorphisms at microRNA binding sites of Ara-C and anthracyclines-metabolic pathway genes are associated with outcome of acute myeloid leukemia patients.

BACKGROUND: Gene polymorphisms at microRNA-binding sites (poly-miRTS) may affect gene transcription and expression through miRNA regulation, which is associated with cancer susceptibility, sensitivity to chemotherapy and prognosis. This study investigated the association between poly-miRTS of Ara-C/anthracycline metabolic pathways genes and the outcome of acute myeloid leukemia (AML) in Chinese patients after Ara-C-based chemotherapy. METHODS: A total of 17 poly-miRTS were selected from the SNPinfo Web Server and genotyped in 206 Chinese Han non-FAB-M3 AML patients using the SEQUENOM Mass-ARRAY system. RESULTS: Among these 17 poly-miRTS, five Ara-C metabolic gene single nucleotide polymorphisms (SNPs, NT5C2 rs10786736 and rs8139, SLC29A1 rs3734703, DCTD rs7278, and RRM1 rs1042919) were identified to significantly associate with complete AML remission and/or overall and relapse-free survival (OS and RFS, respectively), and four anthracycline-metabolic gene SNPs (ABCC1 rs3743527, rs212091, and rs212090 and CBR1 rs9024) were significantly associated with chemotherapy-related toxicities. Moreover, SLC29A1 rs3734703 was shown to associate with both chemotherapy response and survival (adjusted OR 2.561 in the overdominant model; adjusted HR 2.876 for OS and 2.357 for RFS in the dominant model). CONCLUSIONS: The data from the current study demonstrated that the poly-miRTS of Ara-C/anthracyclines metabolic genes predicted the sensitivity and side effects of AML to Ara-C-based chemotherapy and patient survival. Further study will confirm them as biomarkers for AML patients after Ara-C-based chemotherapy.

Report: Analysis on pathogen distribution and drug-resistance of incision infection caused by vascular operation.

To investigate pathogen distribution and drug resistance of incision infection caused by vascular operation to reduce postoperative incision infection, this paper retrospectively reviewed and analyzed 635 in-hospital patients taking vascular operation during Jan. 2008 and Dec. 2012. Analyzed data were statistically processed by SPSS 13.0 software, which resulted in 16 infected cases with 2.52% infection rate. A total of 27 pathogens wasisolated from specimens submitted for inspection, including 17 strains of Gram positive bacteria (62.96%) and 10 Gram negative bacteria (37.04%). Besides high sensitivity to imipenem, all bacteria were able to resist antibacterial drugs. Incision infection is proved in this research to be reduced effectively by some means, like complication correction before operation and reasonable application of antibacterial drugs after operation. While during an operation, it is necessary to operate strictly in a bacterium-free environment and wash incisions thoroughly.

Circ_0009910 promotes imatinib resistance through ULK1-induced autophagy by sponging miR-34a-5p in chronic myeloid leukemia.

BACKGROUND: The occurrence in drug resistance of chronic myeloid leukemia (CML) was accompanied by autophagy activation. Abnormal circular RNAs (circRNAs) participated in this progression. This study attempted to investigate the potential role of circ_0009910 in imatinib resistance of CML cells. METHODS: The expression of circ_0009910 and miR-34a-5p was measured by quantitative real-time polymerase chain reaction (qRT-PCR). The characterization of circ_0009910 was investigated using oligo (dT)18 primers, Actinomycin D and RNase R. Cell viability (IC50 value) and apoptosis were assessed by Cell Counting Kit-8 (CCK8) assay and flow cytometry assay, respectively. The relative protein expression was quantified by western blot. The relationship among miR-34a-5p, circ_0009910 and ULK1 was predicted by online bioinformatics tool, and verified by dual-luciferase reporter assay and RNA immunoprecipitation (RIP). RESULTS: The expression of circ_0009910 was up-regulated in the serum of imatinib-resistance CML patients and K562/R cells, and associated with unfavorable clinicopathologic features. Circ_0009910 in K562 and K562/R cells was mainly localized in the cytoplasm. Circ_0009910 knockdown inhibited cell proliferation and autophagy, but induced apoptosis in K562/R cells. Circ_0009910 targeted miR-34a-5p to regulate ULK1. MiR-34a-5p depression rescued the effects of circ_0009910 knockdown on apoptosis and autophagy in K562/R cells. CONCLUSION: Circ_0009910 accelerated imatinib-resistance in CML cells by modulating ULK1-induced autophagy via targeting miR-34a-5p, providing a potential target in imatinib resistance of CML.

Exosomes derived from oxLDL-stimulated macrophages induce neutrophil extracellular traps to drive atherosclerosis.

This study aimed to investigate the role and underlying mechanism of exosomes secreted by oxidized low-density lipoprotein (oxLDL)-stimulated macrophages in the progression of atherosclerosis (AS). Exosomes from peripheral blood of AS patients or oxLDL-treated macrophages were co-cultured with human neutrophils. Neutrophil extracellular traps (NETs) were detected by immunofluorescence staining. The levels of inflammatory cytokines were quantified by enzyme-linked immunosorbent assay (ELISA). The expression levels of miR-146a and superoxide dismutase 2 (SOD2) were determined by quantitative real-time PCR (qRT-PCR) and western blot. The generation of intracellular reactive oxygen species (ROS) was observed by using dichlorofluorescin diacetate (DCFH-DA). ApoE-deficient mice were fed with high-fat diet (HFD) to induce AS. Atherosclerotic plaques were evaluated by Oil red O (ORO) and hematoxylin-eosin (HE) staining. Our results showed that miRNA-146a was enriched in serum-derived exosomes of AS patients and oxLDL-treated macrophage THP-1-derived exosomes. Importantly, exosomal miR-146a secreted by oxLDL-treated macrophages promoted ROS and NETs release via targeting SOD2. In addition, intravenous administration of oxLDL-treated THP-1 cells-derived exosomes into AS mice significantly deteriorated AS in vivo. Our findings indicate that exosomal miR-146a derived from oxLDL-treated macrophages promotes NETs formation via inducing oxidative stress, which might provide a novel scientific basis for the understanding of AS progression.

Risk factors for operative morbidity and mortality in gastric cancer patients undergoing total gastrectomy.

AIM: To study the risk factors for morbidity and mortality following total gastrectomy. METHODS: We retrospectively reviewed the records of 125 consecutive patients who underwent total gastrectomy for gastric cancer at the Second Affiliated Hospital of Zhejiang University School of Medicine between January 2003 and March 2008. RESULTS: The overall morbidity rate was 20.8% (27 patients) and the mortality rate was 3.2% (4 patients). Morbidity rates were higher in patients aged over 60 [odds ratio (OR) 4.23 (95% confidence interval (CI) 1.09 to 12.05)], with preoperative comorbidity [with vs without, OR 1.25 (95% CI 1.13 to 8.12)], when the combined resection was performed [combined resection vs total gastrectomy only, OR 2.67 (95% CI 1.58 to 5.06)]. CONCLUSION: Age, preoperative comorbidity and combined resection were independently associated with the rate of morbidity after total gastrectomy for gastric cancer.

Effects of integrin α5ß1 on the proliferation and migration of human aortic vascular smooth muscle cells.

Integrin (ITG) α5ß1 is a dominant fibronectin receptor that is abundantly expressed on the surface of vascular smooth muscle cells (VSMCs). However, the association between integrin α5ß1 and the proliferation and migration of VSMCs has yet to be elucidated. The aim of the present study was to characterize the roles of ITGα5 and ITGß1 in the proliferation and migration of VSMCs, and to determine the effects of ITGα5ß1 on integrin-linked kinase (ILK) and focal adhesion kinase (FAK) mRNA expression. Lentiviral expression vectors as well as RNA interference vectors of ITGα5 and ITGß1 were successfully constructed and transfected into VSMCs to obtain ITGα5­ and ITGß1­overexpressing or -silenced cells, respectively. Cell cycle distribution, proliferation and migration were analyzed in the transfected VSMCs in order to clarify the roles of ITGß1 and ITGα5 in the proliferation and migration of VSMCs. ITGß1 was markedly associated with the proliferation and migration of VSMCs, and FAK was shown to be involved in the signaling pathways of ITGß1. ITGα5 did not exert any effects on VSMCs. The results of the present study may provide a possible therapeutic target for the prevention and treatment of early vascular disease associated with VSMCs.

Diagnosis and Treatment of Vascular Surgery Related Infection.

Surgical site infection (SSI) is an important component of infections acquired from hospital. The most significant feature of vascular surgery different from other surgeries is frequent application of artificial grafts. Once SSI occurs after vascular operations with grafts, it might results in a serious disaster. Staphylococcus aureus and coagulase-negative Staphylococcus are the most common pathogenic bacteria for SSI after vascular surgery. Although SSI in vascular surgery often lacks of typical clinical characters, some clinical symptoms, laboratory data and certain imaging procedures may help to diagnose. In most cases of SSI after vascular procedures, the artificial grafts must be removed and sensitive antibiotics should be administered. However, for different cases, personalized management plan should be made depending on the severity and location of SSI.

Meta-analysis of the association between angiotensin-converting enzyme I/D polymorphism and aortic aneurysm risk.

BACKGROUND: Angiotensin-converting enzyme (ACE) I/D polymorphism has been indicated to be correlated with aortic aneurysm (AA) susceptibility, but study results are still debatable. Thus, a meta-analysis was conducted. METHODS: Databases including PubMed, Embase, Web of Science, and Chinese National Knowledge Infrastructure (CNKI) were searched. Data were extracted and pooled odds ratios (OR) with 95% confidence intervals (CI) were calculated. RESULTS: Ten studies with 3557 cases and 5231 controls were included in this meta-analysis. The association between ACE I/D genotype and AA risk was significant (OR=1.30; 95%CI, 1.07-1.57; p<0.01; I(2)=68%). When stratified by ethnicity, a significantly elevated risk was observed in Caucasians (OR=1.31; 95%CI, 1.07-1.61; p<0.01; I(2)=71%). In the abdominal AA subgroup, a significantly increased risk was observed (OR=1.29; 95%CI, 1.03-1.62; p=0.02; I(2)=73%). However, ACE I/D polymorphism was not associated with thoracic AA risk (OR=1.33; 95%CI, 0.85-2.07; p=0.21; I(2)=52%). Subgroup analysis on blood pressure status showed that an increased risk was found in hypertensive patients (OR=1.52; 95%CI, 1.02-2.26; p=0.04; I(2)=0%) but not in normotensive subjects (OR=1.46; 95%CI, 0.72-2.96; p=0.30; I(2)=25%). CONCLUSIONS: In conclusion, this meta-analysis suggested that ACE I/D polymorphism is a risk factor for AA.