Biomedical subjects

Douglas Adams

Publications and source records attributed to Douglas Adams.

3 recordsLinked to original sources

PubMed2005

Effect of platelet-rich plasma with autogenous bone graft for maxillary sinus augmentation in a rabbit model.

PURPOSE: To evaluate the effect of platelet-rich plasma (PRP) on autogenous bone graft remodeling during sinus augmentation in a rabbit model. MATERIALS: Twelve New Zealand White rabbits were divided randomly into 3 groups based on their time of sacrifice (2, 4, and 8 weeks). All animals underwent a general anesthetic and harvesting of an autogenous bone graft from the right iliac crest with subsequent bilateral maxillary sinus augmentation. PRP was prepared via standard approved technique by acquiring 21 cc of autogenous blood and performing differential centrifugation to obtain PRP. One cc of PRP was produced that was mixed with bovine topical thrombin and calcium chloride. The left maxillary sinus received only autogenous bone, while the right maxillary sinus received a mixture of PRP mixed with autogenous bone, thus each animal acted as its own control. Equal volumes of bone were inserted in each maxillary sinus. Animals were sacrificed at 2, 4, and 8 weeks and all specimens were harvested for peripheral quantitative computed tomography (pQ-CT), static, and dynamic and histomorphometric analysis. RESULTS: Student t tests were performed comparing bone density via pQ-CT analysis, histomorphometric parameters of total bone area, and bone apposition rate. PRP had no statistically significant effect on bone graft healing in maxillary sinus augmentation when compared using standard pQ-CT, static, and dynamic histologic criteria. CONCLUSION: This study fails to find a direct stimulatory effect of PRP on healing of autogenous bone grafts using pQ-CT, static, and dynamic histomorphometric analyses.

Alveolar Ridge Augmentation↗

PubMed2004

Do cyclooxygenase-2 knockout mice have primary hyperparathyroidism?

The absence of cyclooxygenase-2 (COX-2) activity in vitro reduces differentiation of both bone-forming and bone-resorbing cells. To examine the balance of COX-2 effects on bone in vivo, we studied COX-2 knockout (KO) and wild-type (WT) mice. After weaning, KO mice died 4 times faster than WT mice, consistent with reports of progressive renal failure in KO mice. Among KO mice killed at 4 months of age, some had renal failure with marked secondary hyperparathyroidism, but others appeared healthy. On the assumption that renal failure was not inevitable in COX-2 KO mice and that phenotypic differences might increase with age, we studied KO mice surviving to 10 months of age with serum creatinine levels similar to those of WT mice. In 10-month-old male KO mice, serum calcium and PTH, but not phosphorus, levels were increased compared with those in WT mice. 1,25-Dihydroxyvitamin D(3) levels were markedly elevated in KO mice. Skeletal analysis showed small nonsignificant decreases in cortical bone density by BMD and either an increase (distal femur, by microcomputed tomography) or no difference (distal femur, by static histomorphometry) in trabecular bone density in KO mice. There was a trend toward increased percent osteoblastic and osteoclastic surfaces, and on dynamic histomorphometry, the rates of trabecular bone formation and mineral apposition were increased in KO mice relative to WT mice. Similar trends were observed for most parameters in 10-month-old female COX-2 KO mice. However, rates of trabecular bone formation and mineral apposition were increased in 10-month-old WT females compared with males and did not increase further in female KO mice. These data suggest that COX-2 KO mice with intact renal function have primary hyperparathyroidism, and that effects of increased PTH and 1,25-dihydroxyvitamin D(3) to increase bone turnover may compensate for the absence of COX-2.

Animals↗

PubMedDate not supplied

Research misconduct and crime lessons from criminal science on preventing misconduct and promoting integrity.

For 200 years, criminologists theorized that delinquent and criminal acts arise from deviant psychological states (such as irrationality or immorality) and/or social conditions that produce these psychological states. This theoretical perspective, which is being duplicated in most efforts to understand and control research misconduct, has not been productive. More recently, criminological perspectives have emerged, emphasizing situational factors that enhance or restrict the opportunity for illegal or imprudent behavior. These so-called "opportunity" theories have been shown to have practical value in reducing crime rates. We explore the promise of these newer theories for the responsible conduct of research (RCR).

Crime↗