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spinal cord injury reprograms muscle fibroadipogenic progenitors to form heterotopic bones within muscles

Bone Research 2022年第2期10卷 310-325页

作者： Hsu-Wen Tseng Dorothée Girard Kylie A.Alexander susan M.Millard Frédéric Torossian Adrienne Anginot Whitney Fleming Jules Gueguen Marie-Emmanuelle Goriot Denis Clay Beulah Jose Bianca Nowlan Allison R.Pettit Marjorie salga François Genêt Marie-Caroline Le Bousse-Kerdilès sébastien banzet Jean-Pierre Lévesque Mater Research Institute-The University of Queensland WoolloongabbaQLDAustralia Institut de Recherche Biomédicale des Armées(IRBA) INSERM UMRS-MD1197 ClamartFrance INsERM UMRs-MD 1197 Universitéde Paris-SaclayHôpital Paul BrousseVillejuifFrance INsERM UMs-44 Universitéde Paris-SaclayHôpital Paul BrousseVillejuifFrance UPOH(UnitéPéri Opératoire du Handicap Perioperative Disability Unit)Physical and Rehabilitation Medicine departmentRaymond-PoincaréHospitalAssistance Publique-Hôpitaux de Paris(AP-HP)GarchesFrance Universitéde Versailles saint Quentin en Yvelines UFR Simone Veil-SantéEND:ICAP INSERM U1179Montigny le BretonneuxFrance

The cells of origin of neurogenic heterotopic ossifications(NHOs), which develop frequently in the periarticular muscles following spinal cord injuries(sCIs) and traumatic brain injuries, remain unclear because skeletal muscle harbors two progenitor cell populations: satellite cells(sCs), which are myogenic, and fibroadipogenic progenitors(FAPs), which are mesenchymal. Lineage-tracing experiments using the Cre recombinase/Lox P system were performed in two mouse strains with the fluorescent protein Zs Green specifically expressed in either sCs or FAPs in skeletal muscles under the control of the Pax7 or Prrx1 gene promoter, respectively. These experiments demonstrate that following muscle injury, sCI causes the upregulation of PDGFRα expression on FAPs but not sCs and the failure of sCs to regenerate myofibers in the injured muscle, with reduced apoptosis and continued proliferation of muscle resident FAPs enabling their osteogenic differentiation into NHOs. No cells expressing Zs Green under the Prrx1 promoter were detected in the blood after injury, suggesting that the cells of origin of NHOs are locally derived from the injured muscle. We validated these findings using human NHO biopsies. PDGFRα+mesenchymal cells isolated from the muscle surrounding NHO biopsies could develop ectopic human bones when transplanted into immunocompromised mice, whereas CD56+myogenic cells had a much lower potential. Therefore, NHO is a pathology of the injured muscle in which sCI reprograms FAPs to undergo uncontrolled proliferation and differentiation into osteoblasts.

关键词： progenitor injuries muscles

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A PORTABLE HTs sQUID GRADIOMETER sYsTEM FOR UNsHIELDED ENVIRONMENT

A PORTABLE HTS SQUID GRADIOMETER SYSTEM FOR UNSHIELDED ENVIR...

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第8届国际材联电子材料国际研讨会

作者： Prof. Y.Zhang N.Wolters Dr. J.schubert DI. D.Lomparski M.banzet Dr. G.Panaitov Dr. H.-J. Krause Institut fuer schichten und Grenzflaechen (IsG-2) Forschungszentrum Juelich D-52425 Juelich Germany

We have developed a portable HTs rf sQUID gradiometer for different applications in unshielded environment. Applications include the recording of human magnetocardiography (MCG), detection of magnetic particles and others. In order to demonstrate the mobility of the system, the whole system including a tripod is constructed with respect to compactness and portability, and can be carried around in a travelling suitcase. The rf sQUID couples with a srTiO substrate resonator in flip-chip configuration. The resonator

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循环中内皮细胞计数是非sT段抬高急性冠脉综合征的诊断指标

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世界核心医学期刊文摘（心脏病学分册） 2005年第2期1卷 25-25页

作者： Quilici J. banzet N. Paule P. F.Dignat-George 梁磊 Lab. d’Immunologie et d’Hematologie UFR de Pharmacie 27 Bd Jean Moulin 13385 Marseille Cedex 5 France

Background shedding of endothelial cells from damaged endothelium into the bl ood occurs in a variety of vascular disorders. The purpose of this study was to evaluate the utility of circulating endothelial cell (CEC) count as a diagnostic marker of non sT elevation acute coronary syndromes(ACss). Methods and Result s CEC counts were determined immediately (H0), 4 hours (H4), and 8 hours (H8) a fter admission in 60 patients with documented non sT elevation ACs and 40 cont rol patients with no evidence of coronary artery disease. A total of 32 patients in the ACs group had elevated CEC counts (>3 cells/mL) in relation to early adm ission and single episode chest pain. Patients from the control group had norma l CEC counts. The interval between the chest pain episode and elevation was sign ificantly shorter for CEC than troponin I. No correlation was found between the 2 markers. Interestingly, a subgroup of ACs patients with initially normal tropo nin I levels had high CEC counts, thus allowing early diagnosis in 30%more case s. At H0, the mean area under the receiver operating characteristic curve was si gnificantly higher with the CEC count than with the troponin I level. At H4 and H8, the combined use of CEC and troponin was significantly better as a marker of ACs than CEC alone or troponin I alone. Conclusions This study demonstrates th at CEC count can be used as an early, specific, independent diagnostic marker fo r non sT elevation ACs. A combined strategy using CEC count and troponin I lev el could provide an effective diagnostic tool.

关键词：急性冠脉综合征内皮细胞诊断指标肌钙蛋白胸痛无冠状动脉血管内膜血管性疾病采血时间亚组

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