The cross section of the process e+ e−→ KS KL π0 has been studied with the CMD-3 detector at the VEPP-2000 electron-positron collider in the center-of-mass energy range from 1.1 to 2 GeV. Preliminary ...results on the total cross section of the process are presented.
The barrel electromagnetic calorimeter of the CMD-3 detector consists of two subsystems: the Liquid Xenon calorimeter and the calorimeter based on CsI scintillation crystals. Its structure and main ...characteristics are presented. The energy calibration procedures of the combined calorimeter are described.
Calorimetry of the CMD-3 detector Shebalin, V.E.; Akhmetshin, R.R.; Anisenkov, A.V. ...
Nuclear instruments & methods in physics research. Section A, Accelerators, spectrometers, detectors and associated equipment,
07/2016, Letnik:
824
Journal Article
Recenzirano
CMD-3 is a general purpose detector designed to study e+e− annihilation into hadrons. It is mounted at VEPP-2000 collider which operates in the wide energy range, Ec.m.s=0.32−2GeV. The calorimetry at ...the detector is based on three subsystems: closest to the beam pipe barrel Liquid Xenon calorimeter, outer barrel calorimeter based on CsI scintillation crystals and the endcap calorimeter made of BGO scintillation crystals. We describe the structure of the calorimeters, their electronics and the energy calibration procedures.
OBJECTIVE—Carotid plaque instability is a major cause of ischemic stroke, but detailed knowledge about underlying molecular pathways is still lacking. Here, we evaluated large-scale transcriptomic ...and protein expression profiling in a biobank of carotid endarterectomies followed by characterization of identified candidates, as a platform for discovery of novel proteins differentially regulated in unstable carotid lesions.
APPROACH AND RESULTS—Genes highly upregulated in symptomatic versus asymptomatic plaques were selected from Affymetrix microarray analyses (n=127 plaques), and tissue microarrays constructed from 34 lesions were assayed for 21 corresponding proteins by immunohistochemistry. Quantification of stainings demonstrated differential expression of CD36, CD137, and DOCK7 (P<0.05) in unstable versus stable lesions and the most significant upregulation of a proprotein convertase, PCSK6 (P<0.0001). Increased expression of PCSK6 in symptomatic lesions was verified by quantitative real-time polymerase chain reaction (n=233), and the protein was localized to smooth muscle α-actin positive cells and extracellular matrix of the fibrous cap by immunohistochemistry. PCSK6 expression positively correlated to genes associated with inflammation, matrix degradation, and mitogens in microarrays. Stimulation of human carotid smooth muscle cells in vitro with cytokines caused rapid induction of PCSK6 mRNA.
CONCLUSIONS—Using a combination of transcriptomic and tissue microarray profiling, we demonstrate a novel approach to identify proteins differentially expressed in unstable carotid atherosclerosis. The proprotein convertase PCSK6 was detected at increased levels in the fibrous cap of symptomatic carotid plaques, possibly associated with key processes in plaque rupture such as inflammation and extracellular matrix remodeling. Further studies are needed to clarify the role of PCSK6 in atherosclerosis.
RATIONALE:In the search for markers and modulators of vascular disease, microRNAs (miRNAs) have emerged as potent therapeutic targets.
OBJECTIVE:To investigate miRNAs of clinical interest in patients ...with unstable carotid stenosis at risk of stroke.
METHODS AND RESULTS:Using patient material from the BiKE (Biobank of Karolinska Endarterectomies), we profiled miRNA expression in patients with stable versus unstable carotid plaque. A polymerase chain reaction–based miRNA array of plasma, sampled at the carotid lesion site, identified 8 deregulated miRNAs (miR-15b, miR-29c, miR-30c/d, miR-150, miR-191, miR-210, and miR-500). miR-210 was the most significantly downregulated miRNA in local plasma material. Laser capture microdissection and in situ hybridization revealed a distinct localization of miR-210 in fibrous caps. We confirmed that miR-210 directly targets the tumor suppressor gene APC (adenomatous polyposis coli), thereby affecting Wnt (Wingless-related integration site) signaling and regulating smooth muscle cell survival, as well as differentiation in advanced atherosclerotic lesions. Substantial changes in arterial miR-210 were detectable in 2 rodent models of vascular remodeling and plaque rupture. Modulating miR-210 in vitro and in vivo improved fibrous cap stability with implications for vascular disease.
CONCLUSIONS:An unstable carotid plaque at risk of stroke is characterized by low expression of miR-210. miR-210 contributes to stabilizing carotid plaques through inhibition of APC, ensuring smooth muscle cell survival. We present local delivery of miR-210 as a therapeutic approach for prevention of atherothrombotic vascular events.
Overview of the CMD-3 recent results Ryzhenenkov, A E; Akhmetshin, R R; Amirkhanov, A N ...
Journal of physics. Conference series,
04/2020, Letnik:
1526, Številka:
1
Journal Article
Recenzirano
Odprti dostop
The CMD-3 detector started data taking at the electron-positron collider VEPP-2000 in December 2010 with a goal to collect about 1 fb−1. The collected data sample corresponds to an integrated ...luminosity of 200 pb−1 in the center-of-mass energy range from 0.32 up to 2 GeV. This paper reports recent results on the hadronic cross sections measurements with the CMD-3 detector.
The Super C-
τ
(SCT) Factory at Novosibirsk is a project of new colliding beam experiment proposed in Budker Institute of Nuclear Physics. Electron-positron collider based on Crab-Waist technique for ...operation energy range 2–5 GeV in center of mass is suggested. The luminosity up to 10
35
cm
−1
s
−1
(in 100 times higher than in operated today experiments in this energy region) is expected. To perform broad experimental program of the project successfully the excellent particle identification (PID) system is needed. A number of options are under consideration. Three of them are described in the paper: Focusing Aerogel RICH (FARICH) detector, threshold Cherenkov counters based on ASHIPH (Aerogel SHifter PHotomultiplier) technique with 6000 litres of aerogel of two refractive indexes and time-of-flight counters with TOP (Time of Propagation) approach with time resolution better than 30 ps. Comparison of PID capabilities with help of parametric simulation is given.
Understanding the processes behind carotid plaque instability is necessary to develop methods for identification of patients and lesions with stroke risk. Here, we investigated molecular signatures ...in human plaques stratified by echogenicity as assessed by duplex ultrasound.
Lesion echogenicity was correlated to microarray gene expression profiles from carotid endarterectomies (n=96). The findings were extended into studies of human and mouse atherosclerotic lesions in situ, followed by functional investigations in vitro in human carotid smooth muscle cells (SMCs).
Pathway analyses highlighted muscle differentiation, iron homeostasis, calcification, matrix organization, cell survival balance, and
(BCL2 B-cell lymphoma 2-associated transcription factor 1) as the most significant signatures.
was downregulated in echolucent plaques, positively correlated to proliferation and negatively to apoptosis. By immunohistochemistry, BCLAF1 was found in normal medial SMCs. It was repressed early during atherogenesis but reappeared in CD68+ cells in advanced plaques and interacted with BCL2 by proximity ligation assay. In cultured SMCs,
was induced by differentiation factors and mitogens and suppressed by macrophage-conditioned medium.
silencing led to downregulation of BCL2 and SMC markers, reduced proliferation, and increased apoptosis. Transdifferentiation of SMCs by oxLDL (oxidized low-denisty lipoprotein) was accompanied by upregulation of BCLAF1, CD36, and CD68, while oxLDL exposure with
silencing preserved MYH (myosin heavy chain) 11 expression and prevented transdifferentiation.
was associated with expression of cell differentiation, contractility, viability, and inflammatory genes, as well as the scavenger receptors
and
. BCLAF1 expression in CD68+/BCL2+ cells of SMC origin was verified in plaques from MYH11 lineage-tracing atherosclerotic mice. Moreover,
downregulation associated with vulnerability parameters and cardiovascular risk in patients with carotid atherosclerosis.
Plaque echogenicity correlated with enrichment of distinct molecular pathways and identified
, previously not described in atherosclerosis, as the most significant gene. Functionally, BCLAF1 seems necessary for survival and transdifferentiation of SMCs into a macrophage-like phenotype. The role of BCLAF1 in plaque vulnerability should be further evaluated.
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