Angiography in diagnosis of subclavian vessel injury

OBJECTIVEThe far-lateral and extreme-lateral infrajugular transcondylar–transtubercular exposure (ELITE) and extreme-lateral transcondylar transodontoid (ELTO) approaches provide access to lesions of the foramen magnum, inferolateral to mid-clivus, and ventral pons and medulla. A subset of pathologies in this region require manipulation of the vertebral artery (VA)–dural interface. Although a cuff of dura is commonly left on the VA to avoid vessel injury during these approaches, there are varying descriptions of the degree of VA-dural separation that is safely achievable. In this paper the authors provide a detailed histological analysis of the VA-dural junction to guide microsurgical technique for posterolateral skull base approaches.METHODSAn ELITE approach was performed on 6 preserved adult cadaveric specimens. The VA-dural entry site was resected, processed for histological analysis, and qualitatively assessed by a neuropathologist.RESULTSHistological analysis demonstrated a clear delineation between the intima and media of the VA in all specimens. No clear plane was identified between the connective tissue of the dura and the connective tissue of the VA adventitia.CONCLUSIONSThe VA forms a contiguous plane with the connective tissue of the dura at its dural entry site. When performing posterolateral skull base approaches requiring manipulation of the VA-dural interface, maintenance of a dural cuff on the VA is critical to minimize the risk of vascular injury.

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Lymphaticovenular anastomosis for lymph vessel injury in the pelvis and groin

Microsurgery ◽

10.1002/micr.30741 ◽

2021 ◽

Author(s):

Hideki Kadota ◽

Ryo Shimamoto ◽

Seita Fukushima ◽

Yusuke Inatomi ◽

Ko Ikemura ◽

...

Keyword(s):

Lymph Vessel ◽

Vessel Injury

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Telomere damage promotes vascular smooth muscle cell senescence and immune cell recruitment after vessel injury

Communications Biology ◽

10.1038/s42003-021-02123-z ◽

2021 ◽

Vol 4 (1) ◽

Author(s):

Anna K. Uryga ◽

Mandy O. J. Grootaert ◽

Abel M. Garrido ◽

Sebnem Oc ◽

Kirsty Foote ◽

...

Keyword(s):

Dna Damage ◽

Smooth Muscle ◽

Vascular Smooth Muscle ◽

Immune Cell ◽

Cell Senescence ◽

Telomeric Dna ◽

Neointimal Formation ◽

Persistent Inflammation ◽

Vessel Injury ◽

Stress Induced Premature Senescence

AbstractAccumulation of vascular smooth muscle cells (VSMCs) is a hallmark of multiple vascular pathologies, including following neointimal formation after injury and atherosclerosis. However, human VSMCs in advanced atherosclerotic lesions show reduced cell proliferation, extensive and persistent DNA damage, and features of premature cell senescence. Here, we report that stress-induced premature senescence (SIPS) and stable expression of a telomeric repeat-binding factor 2 protein mutant (TRF2T188A) induce senescence of human VSMCs, associated with persistent telomeric DNA damage. VSMC senescence is associated with formation of micronuclei, activation of cGAS-STING cytoplasmic sensing, and induction of multiple pro-inflammatory cytokines. VSMC-specific TRF2T188A expression in a multicolor clonal VSMC-tracking mouse model shows no change in VSMC clonal patches after injury, but an increase in neointima formation, outward remodeling, senescence and immune/inflammatory cell infiltration or retention. We suggest that persistent telomere damage in VSMCs inducing cell senescence has a major role in driving persistent inflammation in vascular disease.

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