PubMed · 5791571
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
R Royer, G Debry, M André. [Hyperpulsatile diabetic arteriopathy].. https://pubmed.ncbi.nlm.nih.gov/5791571/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Oxidized low density lipoprotein (LDL) may be of central importance in triggering atherosclerosis. One potential pathway involves the production of nitric oxide (NO) by vascular wall endothelial cells and macrophages. NO reacts with superoxide to form peroxynitrite (ONOO-), a potent agent of LDL oxidation in vitro. ONOO- nitrates the aromatic ring of free tyrosine to produce 3-nitrotyrosine, a stable product. To explore the role of reactive nitrogen species such as ONOO- in the pathogenesis of vascular disease, we developed a highly sensitive and specific method involving gas chromatography and mass spectrometry to quantify 3-nitrotyrosine levels in proteins. In vitro studies demonstrated that 3-nitrotyrosine was a highly specific marker for LDL oxidized by ONOO-. LDL isolated from the plasma of healthy subjects had very low levels of 3-nitrotyrosine (9 +/- 7 micromol/mol of tyrosine). In striking contrast, LDL isolated from aortic atherosclerotic intima had 90-fold higher levels (840 +/- 140 micromol/mol of tyrosine). These observations strongly support the hypothesis that reactive nitrogen species such as ONOO- form in the human artery wall and provide direct evidence for a specific reaction pathway that promotes LDL oxidation in vivo. The detection of 3-nitrotyrosine in LDL isolated from vascular lesions raises the possibility that NO, by virtue of its ability to form reactive nitrogen intermediates, may promote atherogenesis, counteracting the well-established anti-atherogenic effects of NO.
Explore the source record for details and available documents.
To determine the indications for limited colon cancer surgery in each location, we reviewed the arterial branching patterns and lymph node metastases along the course of specific vascular trunks in 344 colon cancer patients who had undergone preoperative angiography and colectomy with lymph node dissection. Our conclusions are follows: Because the ileocecal artery always arises from the superior mesenteric artery and lymph node metastases of cecum cancer were limited to nodes along the ileocolic artery, cecum cancer can be cured by ileocecal resection. The right colic artery has various origins, and ascending colon cancer shows various patterns of lymph node metastases. Therefore a right hemicolectomy should be performed for ascending colon cancer. The middle colic artery forks into right and left branches, and each branch has different branching variations. If the right colic and middle colic arteries have a common trunk, a right hemicolectomy should be performed for transverse colon cancer on the right side. If the left branch of the middle colic artery has an independent replaced origin, lymph node dissection should be modified according to the variant origin. If the left colic artery and the first sigmoidal artery have a common trunk, the lymph nodes along the common trunk should be removed for sigmoid colon cancer and for descending colon cancer. Of the patients with sigmoid colon cancer, 6.3% also had lymph node metastases along the superior rectal artery. Given that the lymph nodes along the superior rectal artery are skeletonized, sigmoid colon cancer can be also cured by partial sigmoidectomy.