PubMed Health⌕ Search

Biomedical subjects

B J Bryant

Publications and source records attributed to B J Bryant.

At least 19 recordsLinked to original sources
PubMed2001

Effects of short-term use of ibuprofen or acetaminophen on bone resorption in healthy men: a double-blind, placebo-controlled pilot study.

Prostaglandins are known to be involved in the metabolism of bone, having a significant influence on bone resorption in cases of bone pathology. We therefore investigated the short-term effects of two commonly used nonsteroidal anti-inflammatory drugs (NSAIDs), ibuprofen and acetaminophen (paracetamol), on bone resorption in healthy men. In a randomized, double-blind pilot study, 28 healthy, age- and weight-matched male volunteers were treated with ibuprofen (n = 10), acetaminophen (n = 9), or a placebo (n = 9) for 3 days. As an indication of bone resorption rate, levels of the biochemical bone markers N-telopeptide (NTx) and free deoxypyridinoline (D-Pyr) were measured in urine. Differences in resorption marker levels pre- and post-NSAID use were then compared between groups. We found that NTx concentrations in the acetaminophen group were lower than placebo (p = 0.048), whereas NTx levels in the ibuprofen group were higher than in the acetaminophen group (p = 0.016). By contrast, D-Pyr concentrations in the ibuprofen group were significantly lower than in the placebo group (p = 0.009). A comparison of the percentage changes of D-Pyr:NTx ratios found that the ratio in the ibuprofen group was significantly lower than that of both the control (p = 0.0065) and acetaminophen (p = 0.01) groups. These results show the differential effects of ibuprofen and acetaminophen on urinary excretion of peptide-bound and free deoxypyridinoline cross-links of type I collagen. Short-term ibuprofen use may alter the renal handling of collagen cross-links and increase bone resorption to a greater extent than acetaminophen in normal men.

Acetaminophen↗
PubMed1992

Toxicity of monochloroacetic acid administered by gavage to F344 rats and B6C3F1 mice for up to 13 weeks.

Groups of 20 rats and 20 mice of each sex were administered monochloroacetic acid (MCAA) once daily, 5 days per week, in water by gavage for up to 13 weeks. Doses used were 0, 30, 60, 90, 120, or 150 mg/kg for rats and 0, 25, 50, 100, 150, or 200 mg/kg for mice. Compound-related deaths occurred at the four highest dose levels in rats and at the highest dose level in mice. Mean body weights of treated groups of rats and mice surviving until the end of the study were similar to those of the controls. A dose-related increase in blood urea nitrogen, alanine aminotransferase, aspartate aminotransferase, as well as a dose-related increase in the relative liver and kidney weights was observed in rats but not in mice. A dose-related increase in the incidence and severity of cardiomyopathy occurred in rats. This lesion may be related to the inhibition of heart mitochondrial aconitase activity. No compound-related lesions were observed in mice. The results of this study indicate that F344 rats are more sensitive than B6C3F1 mice; sexes within the species were equally sensitive. The no-observable-effect level was estimated as 30 mg MCAA/kg body weight for rats and 100 mg MCAA/kg body weight for mice.

Acetates↗
PubMed1990

An experience with upper-extremity vascular trauma.

In this 6-year study of 101 limbs requiring surgical intervention for upper-extremity vascular trauma, most patients were male, young, and injured by penetrating objects. Injured vessels included 13 axillary/subclavian, 23 brachial, 40 radial, and 25 ulnar arteries. Concomitant injuries included nerve injury in 50 cases, tendon laceration in 29, and bony fracture in 11. Arterial repair was accomplished by primary repair in 54 limbs, vein graft in 26 limbs, and vein patch in 3 limbs. Seventeen arterial injuries were ligated. Ancillary procedures included 30 nerve or 27 tendon repairs. The limb salvage rate was 99%. No functional deficits were noted in those cases with only a vascular injury. In 64% and 25% of patients with nerve or musculoskeletal injury, respectively, the arm was functionally impaired. Prompt diagnosis and surgical intervention eliminate vascular injury as a factor in upper-extremity limb loss or disability. Functional deficits are the result of nerve or orthopedic injuries.

Adolescent↗
PubMed1989

The CO2 laser as an intraluminal repair tool.

The CO2 laser can weld vessels together and vaporize plaque. This study evaluates its use as an intraluminal reparative tool. In 17 dogs, a 1-cm circumferential intimectomy with a 1-mm distal intimal flap was performed in both carotids. In each dog, one carotid (CON, control) underwent suture flap repair. On the contralateral side (LR, laser repair), the flap was tacked with 20 250-mW 1-sec pulses and the denuded medium was g-lased for 90 sec (250 mW continuous). Animals were randomized into five groups and sacrificed on the day of surgery (Group I, n = 3), at 3 days (Group II, n = 3), at 1 week (Group III, n = 4), at 2 weeks (Group IV, n = 4), or at 4 weeks (Group V, n = 3). Vessel patencies were 88.2 and 82.4% for CON and LR, respectively. Flap repair appeared similar. No aneurysms were noted. Histology revealed a relative absence of platelet adherence to the g-lased surfaces in Groups I and II when compared to that of mechanical methods (CON). The ratio of the thickness of the regenerated surface to the total wall thickness demonstrated hyperplasia in LR vessels (0.54 +/- 0.12) when compared to that in CON (0.30 +/- 0.15) at 2 and 4 weeks (ANOVA, P less than 0.001). Coverage with endothelial-like cells appeared complete at 4 weeks in both methods. The CO2 laser can effectively repair intimal flaps. However, our results demonstrate a significant increase in medial hyperplasia following g-lasing even in the face of minimal early platelet adherence. This may prove detrimental to the long-term patency of intraluminal CO2 laser-treated vessels.

Animals↗
PubMed1988

A CASE-SAR study of mammalian hepatic azoreduction.

A group of 36 aryl azo dyes were examined for their ability to be reduced by rat liver microsomal azoreductase. This group of azo dyes featured a variety of substituents, including sulfonic acid, phenol, nitro, amide, and methyl functionalities on phenyl, alpha-naphthyl, and beta-naphthyl rings. Reduction rates for each dye were obtained using a spectrophotometric method and anaerobic incubation conditions. These rates ranged from 0 to 7.35 nmol dye reduced/min.mg protein. The reduction rates and dye structures provided the data for a CASE-SAR (computer automated structure evaluation-structure-activity relationship) fragment analysis, and three major structure fragments associated with the ability of this group of azo dyes to be reduced were identified. The three CASE fragments correctly label 92% of the azo dye structures as active or inactive and may be useful in future predictions of the ability of azo dyes to undergo reduction by rat liver azoreductase.

Animals↗
PubMed1987

Morphological transforming activity and metabolism of cyclopenta-fused isomers of benz[a]anthracene in mammalian cells.

4 isomeric cyclopenta-derivatives of benz[e]anthracene (benz[a]aceanthrylene, benz[j]aceanthrylene, benz[l]aceanthrylene, and benz[k]acephenanthrylene) were examined for their ability to morphologically transform C3H10T1/2CL8 mouse-embryo fibroblasts. All of these polycyclic aromatic hydrocarbons studied except benz[k]acephenanthrylene transformed C3H10T1/2CL8 cells to both type II and type III foci in a concentration-dependent fashion. Benz[j]aceanthrylene was the most active, equivalent in activity to benzo[a]pyrene on a molar basis, in producing dishes of cells with transformed foci (94% at 1.0 microgram/ml). Benz[e]aceanthrylene, and benz[l]aceanthrylene produced 58% and 85% of the dishes with foci respectively at 10 micrograms/ml. Metabolism studies with [3H]benz[j]aceanthrylene in C3H10T1/2CL8 cells in which unconjugated, glucuronic acid conjugated, and sulfate conjugated metabolites were measured indicated that the dihydrodiol precursor to the bay-region diol-epoxide, 9,10-dihydroxy-9,10-dihydrobenz[j]aceanthrylene, was the major dihydrodiol formed (55%). Smaller quantities of the cyclopenta-ring dihydrodiol, 1,2-dihydroxy-1,2-dihydrobenz[j]aceanthrylene (14%), and the k-region dihydrodiol, 11,12-dihydroxy-11,12-dihydrobenz[j]aceanthrylene (5%) were also formed. Similar studies with [14C]benz[l]aceanthrylene indicated that the k-region dihydrodiol, 7,8-dihydroxy-7,8-dihydrobenz[l]aceanthrylene was the major metabolite formed (45%). The cyclopenta-ring dihydrodiol, 1,2-dihydroxy-1,2-dihydrobenz[l]aceanthrylene and 4,5-dihydroxy-4,5-dihydrobenz[l]aceanthrylene were formed in minor amounts (less than 6%). Therefore, metabolism at the cyclopenta-ring of B(j)A and B(l)A is a minor pathway in C3H10T1/2CL8 cells in contrast to previously reported studies with cyclopenta[cd]pyrene in which the cyclopenta-ring dihydrodiol was the major metabolite. These results suggest that routes of metabolic activation other than oxidation at the cyclopenta-ring such as bay region or k-region activation may play an important role with these unique polycyclic aromatic hydrocarbons in C3H10T1/2CL8 cells.

Animals↗
PubMed1986

Quantitative analysis of the metabolism of benzo(a)pyrene by transformable C3H10T1/2CL8 mouse embryo fibroblasts.

The metabolism of benzo(a)pyrene [B(a)P] to organic soluble and water soluble metabolites by transformable C3H10T1/2CL8 mouse embryo fibroblasts was studied as a function of time, B(a)P concentration, and cell density. The total formation of organic-soluble and water-soluble metabolites increased with incubation time from 4 to 48 h and with B(a)P concentration from 4 to 40 microM. As cell density increased, the metabolic rate decreased for organic-soluble and water-soluble products between 6,300 and 54,000 cells/cm2 probably due to decreases in B(a)P concentrations to values below saturation. Specific organic-soluble metabolites identified were B(a)P-pre-9,10-diols, B(a)P-9,10-diol, B(a)P-7,8-diol, B(a)P-3,6-quinone, B(a)P-3-phenol, and B(a)P-9-phenol. Water-soluble metabolites were subjected to enzymatic hydrolysis with beta-glucuronidase and aryl sulfatase to identify specific conjugated products. The sulfate conjugated metabolites identified were B(a)P-7,8-diol, B(a)P-pre-9,10-diols, B(a)P-9,10-diol, and B(a)P-3,6-quinone. The beta-glucuronic acid metabolites identified were B(a)P-pre-9,10-diols, B(a)P-3,6-quinone, and B(a)P-3-phenol. Patterns of metabolite formation rates are discussed as to their possible effect on morphological transformation rates in C3H10T1/2 cells with respect to incubation time and cell density.

Animals↗
PubMed1986

Metabolism of benzo(a)pyrene in monolayer cultures of human bronchial epithelial cells from a series of donors.

Benzo(a)pyrene [B(a)P] metabolism was measured in monolayer cultures of human bronchial epithelial cells derived from 18 specimens of explanted tissue. Bronchial epithelial cells converted B(a)P to dihydrodiols, phenols, quinone derivatives, and polyhydroxylated forms. Sulfate and glucuronide conjugates of B(a)P metabolites were also detected. Both total metabolism and distribution of metabolites showed a 10-fold or greater variation in cultures from different specimens. When the data were divided according to smoking status, however, no differences in total metabolism, extent of conjugation, or distribution of metabolites could be demonstrated between the two groups. Wide variation (over 1000-fold) in the cytotoxicity of B(a)P towards cells derived from different specimens was demonstrated but could not be directly correlated to the extent of metabolic activation. The results suggest that human bronchial epithelial cells which are newly grown from explanted tissue of smokers in culture do not demonstrate enzymatic induction. Variation among individuals observed in these studies probably represents basal differences in metabolic capability.

Benzo(a)pyrene↗
PubMed1984

Metabolism of alpha-naphthoflavone by rat, mouse, rabbit, and hamster liver microsomes.

The metabolism of alpha-naphthoflavone (ANF) was studied in hepatic microsomes from rats, mice, rabbits, and hamsters, species in which ANF exerts its biological activities. The major metabolites produced by all species were ANF-5,6-oxide, ANF-6-phenol, and ANF-7,8-dihydrodiol. Minor metabolites produced by all species were ANF-5,6-dihydrodiol, ANF-7-phenol, and ANF-9-phenol. In general, the total rates of metabolism were similar within all species: 22-32 nmol ANF metabolized/15 min/mg protein. Mouse liver microsomes were approximately 1.7 to 2.9 times as active as the other species on a nanomole of cytochrome P-450 basis. The major sites of enzymatic oxidation were the 5,6 and 7,8 bonds of ANF where for all species, 49-71% and 15-46% of the total metabolism occurred, respectively.

Animals↗
PubMed1983

Reanalysis and clarification of the structures of alpha-naphthoflavone dihydrodiols formed by uninduced and induced rat liver microsomes from Charles River CD and Sprague-Dawley rats.

The structures of alpha-naphthoflavone (ANF) dihydrodiols formed by uninduced and induced rat liver microsomes are identified by conversion of the metabolically formed ANF-dihydrodiols to the corresponding phenols. Comparison of these phenols with synthetic standards provides an unambiguous method for structural identification. The results of these studies are that hepatic microsomes from uninduced or phenobarbital, Aroclor-1254, 3-methylcholanthrene, or 5,6-benzoflavone induced Sprague-Dawley or Charles River CD rats each produce a major and a minor ANF-dihydrodiol identified as ANF-7,8-dihydrodiol and ANF-5,6-dihydrodiol, respectively.

Animals↗
PubMed1976

Leukemia allotransplants in canine fetuses: influence of host age and immune responsiveness.

Myelomonocytic leukemia cells allografted prenatally in some developing purebred Beagle fetuses elicited tumors postnatally in some of the pups. The later in gestation that the inoculum was delivered, the less was the disposition to eventual leukemia, indicating that fetal host age at the time of grafting and tumorigenesis are correlated. The leukemogenic transplants may have grown because of fetal immunoinsufficiency or because they were tolerogenic in the developing immune system. Limited immunologic data for exclusion of the latter possibility are reported.

Animals↗
PubMed1975

Thymus lymphocytes. Efflux and restoration phases after peripheral exposure of mice to phytohaemagglutinin.

Juvenile Swiss mice experienced significant diminutions in thymic content of both small, non-proliferating and larger, proliferating lymphocytes within 12 hours after intraperitoneal injection of phytohaemagglutinin. These alterations, which may predate alterations in lymphocyte traffic and morphology elsewhere, were interpreted as being the consequence of a massive thymus lymphocyte emigration, not of in situ cytolysis, and were effaced by intrathymic lymphocyte restoration toward control numbers by 24 hours.

Animals↗