8 August 2015 in European Journal of Trauma and Emergency Surgery
27 January 2006 in Developmental Dynamics
We examined the role of hypoxia and HIF factors in embryonic angiogenesis and correlated the degree of hypoxia with the level of HIF and VEGF expression and blood vessel formation. Quail eggs were incubated in normoxic and hypoxic (16% O2) conditions. Tissue hypoxia marker, pimonidazol hydrochloride, was applied in vivo for 1 hr and detected in sections with Hypoxyprobe‐1 Ab. VEGF and HIF expression was detected by in situ hybridization. HIF‐1α protein was detected in sections and by Western blot. Endothelial cells were visualized with QH‐1 antibody. Hypoxic regions were detected even in normoxic control embryos, mainly in brain, neural tube, branchial arches, limb primordia, and mesonephros. The expression patterns of HIF‐1α and HIF‐1β factors followed, in general, the Hypoxyprobe‐1 marked regions. HIF‐2α was predominantly expressed in endothelial cells. Diffuse VEGF expression was detected in hypoxic areas of neural tube, myocardium, digestive tube, and most prominently in mesonephros. Growing capillaries were directed to areas of VEGF positivity. Hypoxic regions in hypoxic embryos were larger and stained more intensely. VEGF and HIF‐1 factors were proportionately elevated in Hypoxyprobe‐1 marked regions without being expressed at new sites and were followed by increased angiogenesis. Our results demonstrate that normal embryonic vascular development involves the HIF‐VEGF regulatory cascade. Experimentally increasing the level of hypoxia to a moderate level resulted in over‐expression of HIF‐1 factors and VEGF followed by an increase in the density of developing vessels. These data indicate that embryonic angiogenesis is responsive to environmental oxygen tension and, therefore, is not entirely genetically controlled. Developmental Dynamics 235:723–733, 2006.
1 October 2018 in Journal of Pain Research
Shoulder pain is a common musculoskeletal disorder of variable etiology, ranging from rotator cuff pathology to peripheral nerve entrapment. Advances in ultrasound (US) technology have allowed static and dynamic evaluation of shoulder problems and most importantly, offer real-time, radiation-free guidance for interventions. The present review aims to describe shoulder anatomy in detail using information from cadaveric models and to illustrate US-guided techniques using clearly labeled figures and videos. The review will also present evidence of specific US-guided therapies for shoulder pain by summarizing landmark studies, systematic reviews, and meta-analyses. The following shoulder structures will be covered: 1) the biceps long head tendon, 2) the acromioclavicular joint, 3) the subacromial–subdeltoid bursa, 4) the glenohumeral joint, 5) the suprascapular nerve, and 6) the axillary nerve.
25 August 2008 in The Anatomical Record
Oxygen availability is one of the necessary prerequisites for normal embryonic development. In our previous study we found that quail embryos incubated under hypoxic conditions (16% O2) die at embryonic day (ED) 9 with signs of heart failure. By ED4 and ED6 we found thinner ventricular wall and increased capillary density. We thus hypothesized that the cause of death would lie in severe myocardial and coronary maldevelopment. ED6 and 7 hypoxic hearts had thinner ventricular wall, especially left. There was a simultaneous increase in capillary density, most pronounced in the interventricular septum. This site corresponds to an area of tissue hypoxia and ensuing increased angiogenesis, and also formation of ventricular conduction system. Hypoxia had a positive effect on normal sequence of maturation of the conduction system evaluated by optical mapping at ED7. In sections from ED9 hypoxic hearts we found, in addition to thinner ventricular walls, irregularities in development of coronary tree (missing coronary ostia, absence of one coronary artery, and irregular arterial wall). This deficiency was due to decreased myocyte proliferation rather than to increased apoptosis. By Indian ink injection through the left ventricle we found in normoxic hearts regular coronary branching pattern, while in the hypoxic ones there was often only an irregular plexus. Embryonic hypoxia thus leads to increased capillarity and trabeculation to minimize diffusion distance. In the subsequent period there is a failure in organization of vascular plexus into normal vasculature, resulting in thin compact myocardium that likely leads to heart failure and embryonic death. Anat Rec, 2008.