scholarly journals Splanchnic Aneurysms & Possible Etiology

2019 ◽  
Vol 2 (1) ◽  
pp. 1-7
Author(s):  
Nicholas J. Demos ◽  
Patrick McGovern ◽  
Peter Smith ◽  
Victoria Demos

Four cases are reported with splanchnic aneurysms of the branches of the main arteries. Three of the cases presented as emergencies. Possible rupture was present in Case 2 and true rupture in Case 4. The etiology of Cases 1 and 2 may have been a floxacin antibiotics, Table 1. This report is the first clinical chronological association of the antibiotics and arterial and aortic pathology. This association was supported by nationwide research by Pasternak, 11. Detailed experimental work done on mice showed connective tissue fragmentation and arterial cell injury. Apparently, the above antibiotic induced mitochondrial DNA damage and dysfunction, 9.

2003 ◽  
Vol 285 (5) ◽  
pp. L1018-L1025 ◽  
Author(s):  
Arti Shukla ◽  
Michael Jung ◽  
Maria Stern ◽  
Naomi K. Fukagawa ◽  
Douglas J. Taatjes ◽  
...  

To test the hypothesis that asbestos-mediated cell injury is mediated through an oxidant-dependent mitochondrial pathway, isolated mesothelial cells were examined for mitochondrial DNA damage as determined by quantitative PCR. Mitochondrial DNA damage occurred at fourfold lower concentrations of crocidolite asbestos compared with concentrations required for nuclear DNA damage. DNA damage by asbestos was preceded by oxidant stress as shown by confocal scanning laser microscopy using MitoTracker Green FM and the oxidant probe Redox Sensor Red CC-1. These events were associated with dose-related decreases in steady-state mRNA levels of cytochrome c oxidase, subunit 3 (COIII), and NADH dehydrogenase 5. Subsequently, dose-dependent decreases in formazan production, an indication of mitochondrial dysfunction, increased mRNA expression of pro- and antiapoptotic genes, and increased numbers of apoptotic cells were observed in asbestos-exposed mesothelial cells. The possible contribution of mitochondrial-derived pathways to asbestos-induced apoptosis was confirmed by its significant reduction after pretreatment of cells with a caspase-9 inhibitor. Apoptosis was decreased in the presence of catalase. Last, use of HeLa cells transfected with a mitochondrial transport sequence targeting the human DNA repair enzyme 8-oxoguanine DNA glycosylase to mitochondria demonstrated that asbestos-induced apoptosis was ameliorated with increased cell survival. Studies collectively indicate that mitochondria are initial targets of asbestos-induced DNA damage and apoptosis via an oxidant-related mechanism.


Epidemiology ◽  
2009 ◽  
Vol 20 ◽  
pp. S99
Author(s):  
Ruey-Hong Wong ◽  
Pei-Lin Huang ◽  
Yu-Hsuan Yeh ◽  
Yu-Ching Chen ◽  
Yi-Jie Liu ◽  
...  

Lupus ◽  
2014 ◽  
Vol 23 (11) ◽  
pp. 1133-1141 ◽  
Author(s):  
L López-López ◽  
M Nieves-Plaza ◽  
M del R Castro ◽  
YM Font ◽  
CA Torres-Ramos ◽  
...  

2001 ◽  
Vol 38 (2-3) ◽  
pp. 153-158 ◽  
Author(s):  
Barry J. Barclay ◽  
Carrie L. DeHaan ◽  
Ursula G.G. Hennig ◽  
Oksana Iavorovska ◽  
Reid W. von Borstel ◽  
...  

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