Evidence map›Paper›PMID 27478409›Full record

ArticleBMC clinical pathology2016

The study of calcified atherosclerotic arteries: an alternative to evaluate the composition of a problematic tissue reveals new insight including metakaryotic cells.

Silvia Fittipaldi, Francesco Vasuri, Alessio Degiovanni, Rodolfo Pini, Mauro Gargiulo, Andrea Stella, Gianandrea Pasquinelli, William G Thilly, Elena V Gostjeva

Open access · hybridAbstract read
In one paragraph

Article in BMC clinical pathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.5field-weighted citation impact, top 32% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 2 countries.

Silvia FittipaldiDepartment of Experimental, Diagnostic and Specialty Medicine (DIMES); S. Orsola-Malpighi Hospital, Bologna University, Via Massarenti 9, I 40139 Bologna, Italy ; Laboratory in Metakaryotic Biology (LIMB), Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA USA.
Francesco VasuriDepartment of Experimental, Diagnostic and Specialty Medicine (DIMES); S. Orsola-Malpighi Hospital, Bologna University, Via Massarenti 9, I 40139 Bologna, Italy.
Alessio DegiovanniDepartment of Experimental, Diagnostic and Specialty Medicine (DIMES); S. Orsola-Malpighi Hospital, Bologna University, Via Massarenti 9, I 40139 Bologna, Italy.
Rodolfo PiniDepartment of Experimental, Diagnostic and Specialty Medicine (DIMES); S. Orsola-Malpighi Hospital, Bologna University, Via Massarenti 9, I 40139 Bologna, Italy.
Mauro GargiuloDepartment of Experimental, Diagnostic and Specialty Medicine (DIMES); S. Orsola-Malpighi Hospital, Bologna University, Via Massarenti 9, I 40139 Bologna, Italy.
Andrea StellaDepartment of Experimental, Diagnostic and Specialty Medicine (DIMES); S. Orsola-Malpighi Hospital, Bologna University, Via Massarenti 9, I 40139 Bologna, Italy.
Gianandrea PasquinelliDepartment of Experimental, Diagnostic and Specialty Medicine (DIMES); S. Orsola-Malpighi Hospital, Bologna University, Via Massarenti 9, I 40139 Bologna, Italy.
William G ThillyLaboratory in Metakaryotic Biology (LIMB), Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA USA.
Elena V GostjevaLaboratory in Metakaryotic Biology (LIMB), Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA USA.
Policlinico S.Orsola-Malpighi · ITMarch of Dimes · USMassachusetts Institute of Technology · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCalcifications of atherosclerotic plaques represent a controversial issue as they either lead to the stabilization or rupture of the lesion. However, the cellular key players involved in the progression of the calcified plaques have not yet been described. The primary reason for this lacuna is that decalcification procedures impair protein and nucleic acids contained in the calcified tissue. The aim of our study was to preserve the cellular content of heavily calcified plaques with a new rapid fixation in order to simplify the study of calcifications.

methodsHere we applied a fixation method for fresh calcified tissue using the Carnoy's solution followed by an enzymatic tissue digestion with type II collagenase. Immunohistochemistry was performed to verify the preservation of nuclear and cytoplasmic antigens. DNA content and RNA preservation was evaluated respectively with Feulgen staining and RT-PCR. A checklist of steps for successful image analysis was provided. To present the basic features of the F-DNA analysis we used descriptive statistics, skewness and kurtosis. Differences in DNA content were analysed with Kruskal-Wallis and Dunn's post tests. The value of P < 0.05 was considered significant.

resultsTwenty-four vascular adult tissues, sorted as calcified (14) or uncalcified (10), were processed and 17 fetal tissues were used as controls (9 soft and 8 hard). Cells composing the calcified carotid plaques were positive to Desmin, Vimentin, Osteocalcin or Ki-67; the cellular population included smooth muscle cells, osteoblasts and osteoclasts-like cells and metakaryotic cells. The DNA content of each cell type found in the calcified carotid artery was successfully quantified in 7 selected samples. Notably the protocol revealed that DNA content in osteoblasts in fetal control tissues exhibits about half (3.0 ng) of the normal nuclear DNA content (6.0 ng).

conclusionTogether with standard histology, this technique could give additional information on the cellular content of calcified plaques and help clarify the calcification process during atherosclerosis.

Indexed as

AtherosclerosisCalcificationDNA quantificationImmunohistochemistryMetakaryotic cellsOsteogenesis

Identifiers

PMID27478409
PMCPMC4966787
OpenAlexW2478188254

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.