Vascular Remodeling in Health and Disease

The term vascular remodeling is commonly used to define the structural changes in blood vessel geometry that occur in response to long-term physiologic alterations in blood flow or in response to vessel wall injury brought about by trauma or underlying cardiovascular diseases.1, 2, 3, 4 The process of remodeling, which begins as an adaptive response to long-term hemodynamic alterations such as elevated shear stress or increased intravascular pressure, may eventually become maladaptive, leading to impaired vascular function. The vascular endothelium, owing to its location lining the lumen of blood vessels, plays a pivotal role in regulation of all aspects of vascular function and homeostasis.5 Thus, not surprisingly, endothelial dysfunction has been recognized as the harbinger of all major cardiovascular diseases such as hypertension, atherosclerosis, and diabetes.6, 7, 8 The endothelium elaborates a variety of substances that influence vascular tone and protect the vessel wall against inflammatory cell adhesion, thrombus formation, and vascular cell proliferation.8, 9, 10 Among the primary biologic mediators emanating from the endothelium is nitric oxide (NO) and the arachidonic acid metabolite prostacyclin [prostaglandin I2 (PGI2)], which exert powerful vasodilatory, antiadhesive, and antiproliferative effects in the vessel wall

Reconstruction of the mandible with a poly(D,L-lactide) scaffold, autogenous corticocancellous bone graft, and autogenous platelet-rich plasma: an animal experiment.

Contains fulltext : 39358.pdf (publisher's version ) (Open Access)An animal study is presented, evaluating a method of mandibular reconstruction using a poly(D,Llactide) (PDLLA) scaffold. Six goats underwent a continuity resection of the mandibular angle. The defect was bridged with a preshaped PDLLA scaffold, filled with an autogenous particulate bone graft from the anterior iliac crest, and fixed with two preshaped titanium plates. To accelerate bone healing, autogenous platelet-rich plasma was mixed with the particulate bone graft. All goats had an uneventful healing. The osteosynthesis system withstood immediate loading for a period of 6 weeks until sacrifice. The particulate bone grafts within the PDLLA scaffold, which appeared to be narrowed, showed considerable resorption and replacement by fibrous tissue. In all goats, however, callus formation along the reconstructed segment was seen, providing bony continuity and maintaining the original contour of the reconstructed segment. Thus, the technique used may provide an alternative for reconstruction with revascularized composite flaps with less associated donor site morbidity

Endocrine Events Prior to Puberty in Heifers: Role of Somatotropin, Insulin-Like Growth Factor-I and Insulin-Like Growth Factor Binding Proteins

We have utilized active immunization against growth hormone releasing factor (GRF) to investigate relationships among somatotropin (ST), insulin-like growth factor-I (IGF-I), IGF binding proteins (IGFBP) and ovarian function in heifers. Active immunization against GRF (GRFi) has been demonstrated to abolish episodic release of ST and decrease serum concentrations of IGF-I. In initial experiments investigating onset of puberty, breeds of heifers differing in growth rate and reproductive traits (Angus, Charolais and Simmental) were immunized against GRF or served as controls (immunized against carrier protein, human serum albumin, HSAi). GRFi decreased rate of muscle and skeletal growth, but increased deposition of adipose tissue. In Angus and Charolais, but not Simmental heifers, GRFi at 6 mo of age significantly delayed onset of puberty beyond 18 mo of age. Retrospective analyses of serum IGF-I revealed that GRFi heifers reaching puberty at a normal age had greater pre-treatment (6 mo of age) IGF-I than GRFi heifers in which puberty was delayed. Collectively, these results strongly indicate that the bovine hypothalamic-hypophyseal-ovarian axis is particularly sensitive to changes in metabolism at or near 6 mo of age. Another series of experiments tested the hypothesis that lowering serum IGF-I via GRFi initially at 3 mo of age would increase the percentage of Angus and Simmental heifers not reaching puberty. Three mo old Angus and Simmental heifers were assigned to GRFi (n = 18), HSAi (n = 14) or received no treatment (controls, n = 16). HSAi and GRFi heifers were unilaterally ovariectomized (ULO) at 6 mo of age. As anticipated, GRFi at a younger age increased percentage of heifers not reaching puberty; over 75% of control and HSAi heifers reached puberty by 14 mo.of age compared to 22% of GRFi heifers. Serum and follicular fluid (FFL; follicles ≤ 4 mm) concentrations of IGF-I were suppressed by GRFi. Serum, but not FFL concentrations of IGF binding protein-2 (IGFBP-2) were greater in GRFi than in HSAi heifers. GRFi delayed puberty apparently by suppressing follicular growth because number of follicles ≤7 mm was significantly lower in GRFi than in HSAi heifers. In conclusion, active immunization against GRF at 3 or 6 months of age delays puberty in beef heifers. Delayed puberty was preceded by suppression of follicular growth, and decreased concentrations of IGF-I in serum and follicular fluid. Collectively, these studies demonstrate that ovarian function between 3 and 8 mo of age and subsequent onset of puberty are particularly sensitive to changes in the ST-IGF-I axis

Serum α-tocopherol concentrations in German shepherd dogs with chronic degenerative radiculomyelopathy

The concentration of serum α-tocopherol was measured in German shepherd dogs with chronic degenerative radiculomyopathy, and in German shepherd dogs and dogs of other breeds unaffected by the condition. The mean concentration was significantly higher in German shepherd dogs with the condition than in other breeds of dog unaffected by it, but it was not significantly higher than in unaffected German shepherd dogs. Estimates of components of variance indicated that the concentration varied more widely in individual affected dogs than in unaffected dogs, irrespective of breed. These results suggest that chronic degenerative radiculomyopathy in German shepherd dogs is unlikely to be due to uncomplicated vitamin E deficiency