scholarly journals A Review of Thoracic Outlet Syndrome and the Possible Role of Botulinum Toxin in the Treatment of This Syndrome

Toxins ◽  
2012 ◽  
Vol 4 (11) ◽  
pp. 1223-1235 ◽  
Author(s):  
Jacqueline Foley ◽  
Heather Finlayson ◽  
Andrew Travlos
Author(s):  
Muhammad Ubaid Hafeez ◽  
Michael Moore ◽  
Komal Hafeez ◽  
Joseph Jankovic

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Renato Farina ◽  
Pietro Valerio Foti ◽  
Andrea Conti ◽  
Francesco Aldo Iannace ◽  
Isabella Pennisi ◽  
...  

AbstractVascular compression syndromes are rare alterations that have in common the compression of an arterial and/or venous vessel by contiguous structures and can be congenital or acquired. The best known are the Thoracic Outlet Syndrome, Nutcracker Syndrome, May–Thurner Syndrome, and Dunbar Syndrome. The incidence of these pathologies is certainly underestimated due to the non-specific clinical signs and their frequent asymptomaticity. Being a first-level method, Ultrasound plays a very important role in identifying these alterations, almost always allowing a complete diagnostic classification. If in expert hands, this method can significantly contribute to the reduction of false negatives, especially in the asymptomatic population, where the finding of the aforementioned pathologies often happens randomly following routine checks. In this review, we briefly discuss the best known vascular changes, the corresponding ultrasound anatomy, and typical ultrasound patterns.


2007 ◽  
Vol 49 (3) ◽  
pp. 346-352 ◽  
Author(s):  
Koichi Niwa ◽  
Kumiko Koyama ◽  
Shin-ichi Inoue ◽  
Tomonori Suzuki ◽  
Kimiko Hasegawa ◽  
...  

2014 ◽  
Vol 63 (2) ◽  
pp. 155-161 ◽  
Author(s):  
Junxia Zhang ◽  
Haiwei Wang ◽  
Lijun Zhang ◽  
Tengteng Zhang ◽  
Beibei Wang ◽  
...  

Chlamydia pneumoniae infection has been shown to be associated with the development of atherosclerosis by promoting the migration of vascular smooth muscle cells (VSMCs). However, how C. pneumoniae infection induces VSMC migration is not fully understood. A primary role of Ras-related C3 botulinum toxin substrate 1 (Rac1) is to generate a protrusive force at the leading edge that contributes to cell migration. Whether Rac1 activation plays a role in C. pneumoniae infection-induced VSMC migration is not well defined. In the present study, we therefore examined Rac1 activation in C. pneumoniae-infected rat primary VSMCs and the role of Rac1 activation in C. pneumoniae infection-induced VSMC migration. Glutathione S-transferase pull-down assay results showed that Rac1 was activated in C. pneumoniae-infected rat primary VSMCs. A Rac1 inhibitor, NSC23766 (50 µM,) suppressed Rac1 activation stimulated by C. pneumoniae infection, and thereby inhibited C. pneumoniae infection-induced VSMC migration. In addition, C. pneumoniae infection-induced Rac1 activation in the VSMCs was blocked by LY294002 (25 µM), an inhibitor of phosphatidylinositol 3-kinase (PI3K). Taken together, these data suggest that C. pneumoniae infection promotes VSMC migration, possibly through activating Rac1 via PI3K.


Eye ◽  
1991 ◽  
Vol 5 (4) ◽  
pp. 447-450 ◽  
Author(s):  
K N Hakin ◽  
J P Lee

2006 ◽  
Vol 22 (1) ◽  
pp. 87-87
Author(s):  
E Krishnan ◽  
PR Murugesan ◽  
P Ram Sankar ◽  
KS Ganesan ◽  
C Ganesan ◽  
...  

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