PubMed Health⌕ Search

Biomedical subjects

S B Combs

Publications and source records attributed to S B Combs.

6 recordsLinked to original sources
PubMed1997

Symptoms of neck artery compromise: case presentations of risk estimate for treatment.

OBJECTIVE: To discuss the use of magnetic resonance angiography (MRA) imaging as a definitive means to assess vascular patency and the relative value of various vertebral artery screening maneuvers. CLINICAL FEATURES: Two female patients suffered head and neck trauma with possible vertebral artery insufficiency. Positive vertebral artery screening tests with consistent symptoms were present in both cases. One patient had a congenitally narrowed vertebral artery, whereas the second had no evidence of vascular anomaly. INTERVENTION AND OUTCOME: Conservative chiropractic management using manipulation and rehabilitation led to favorable outcome in both cases. The patient with vascular compromise received a treatment plan avoiding neck manipulation. The second case received manipulation per clinical indications from neck findings. CONCLUSION: MRA imaging may be more important to critical decision making than are the various vertebral artery screening tests in patients with positional vertigo on combined neck extension and rotation.

Adult↗
PubMed1994

Effects of ascorbic acid on proliferation and collagen synthesis in relation to the donor age of human dermal fibroblasts.

Several events are associated with cellular aging: alterations in the extracellular matrix, loss of the cell's proliferative capacity, and decreased responsiveness to growth factors. In skin, a major component of the extracellular matrix is collagen; an important regulator of collagen synthesis is ascorbic acid, which may also have growth factor-like properties. To investigate the relationship of the extracellular matrix and proliferative capacity to aging, we examined the effects of ascorbic acid on cell proliferation and collagen expression in dermal fibroblasts from donors of two age classes, newborn (3-8 d old) and elderly (78-93 years old). In the absence of ascorbic acid (control) proliferative capacities were inversely related to age; newborn cell lines proliferated faster and reached greater densities than elderly cell lines. However, in the presence of ascorbic acid both newborn and elderly cells proliferated at a faster rate and reached higher densities than controls. To determine whether there are age-related differences in extracellular matrix production and ascorbic acid responsiveness we examined and found that collagen biosynthesis (collagenase-digestible protein) was inversely related to age, but the stimulation by ascorbic acid appeared age independent. The increase in collagen synthesis was reflected by coordinate increases in steady-state pro alpha 1(I) and pro alpha 1(III) collagen mRNAs, suggesting a pretranslational mechanism. Ascorbic acid appears capable of overcoming the reduced proliferative capacity of elderly dermal fibroblasts, as well as increasing collagen synthesis in elderly cells by similar degrees as in newborn cells even though basal levels of collagen synthesis are age dependent.

Aged↗
PubMed1987

Influence of dietary vitamin E on nutritional pancreatic atrophy in selenium-deficient chicks.

Studies were conducted to determine the relationship between dietary vitamin E (VE) and the development of nutritional pancreatic atrophy (NPA) in selenium (Se)-deficient chicks. Selenium- and VE-depleted chicks reared on a low Se, amino acid-based diet containing 100 IU VE (as all-rac-alpha-tocopheryl acetate) per kilogram were found to have exceedingly low pancreatic activities of Se-dependent glutathione peroxidase (SeGSHpx) at 8 d of age. Supplementation of the purified diet with 500 or 1,000 IU VE/kg prevented both NPA and the associated growth depression. Use of graded dietary VE levels showed that addition of at least 300 IU/kg was required to overcome the growth depression associated with severe Se deficiency. Although tissue alpha-tocopherol concentrations increased linearly with increasing dietary levels of VE, the response in pancreas was less than (about one-half of) those in liver and heart and, unlike the response in heart, was not affected by dietary Se level. That protection against NPA involved the antioxidant action of VE was suggested by results showing that NPA is promoted by high dietary levels of linoleic acid, that high VE levels correct membrane unsaturated fatty acid losses due to Se deficiency and that NPA is prevented by high levels of other antioxidants. It is suggested that the normally low activities of SeGSHpx and concentrations of alpha-tocopherol in the pancreas may predispose that organ to lesions due to oxidative stress under conditions of severe nutritional Se deficiency that results in further depletion of SeGSHpx. This situation may be overcome by feeding VE at 15-20-fold excesses over the levels normally regarded as nutritionally required.

Animals↗