Glucocorticoid-induced inhibition of osteoblastic bone formation in ewes: A biochemical and histomorphometric study

The mechanisms underlying glucocorticoid-induced osteoporosis in humans are a defect in bone formation associated with increased bone resorption. The latter may be due to elevated parathyroid hormone (PTH) levels induced by the impairment of intestinal calcium absorption caused by corticosteroids. In this study we analysed the effects of corticosteroids in old ewes, a potential model for the study of human bone turnover. Two groups of seven 9-year-old female sheep were selected. The first group was injected intramuscularly with a daily dose of 30 mg methylprednisone (MP) during the first 2 months and 15 mg during the last month. After 2 and 3 months of treatment, blood samples were taken. At the end of the experiment the animals were slaughtered and the iliac crest kept for bone histomorphometry. Serum osteocalcin (sOC) rapidly and markedly decreased in the MP-treated group compared with controls (–77%;p<0.01). In contrast, at the end of the experiment serum calcium and PTH levels were similar in both groups. Histomorphometric analysis showed a significant reduction in the wall width of trabecular packets. Dynamic parameters reflecting bone formation at the tissue and cell levels were significantly lower in the MP-treated group than in controls, with a highly significant decrease in the mineralization rate (MAR: –63%,p<0.05) and double-labeled perimeter (dLPm/B.Pm: –92%p<0.05). The bone formation rate (BFR/B.Pm) also decreased by 84% and the adjusted apposition rate (Aj.AR) by 80%. The increase in the total formation period was mainly due to an increase in the inactive period. Significant correlations were found between sOC and MAR, dLPm/B.Pm and BFR/B.Pm (withr respectively 0.67, 0.76 and 0.51). In conclusion, the effects of corticosteroid on ewe bone remodeling are essentially characterized by a major bone formation defect without evidence of secondary hyperparathyroidism, although this cannot be totally excluded by our results. Ewes treated with glucocorticoids could represent a good model for evaluating the effects of drugs candidates for all bone conditions characterized by reduced bone formation resulting from osteoblastic depression.     

竹节人参提取物抗脑缺血作用的实验研究

目的 为探讨竹节人参提取物的脑保护机制,观察竹节人参提取物对血栓形成和缺血性脑水肿的作用。方法 结扎小鼠带迷走神经的两侧颈总动脉造成急性脑缺血,结扎大鼠双侧颈总动脉造成急性不宛性脑缺血,实验性造成大鼠体内血栓形成,观察生节人参对它们的影响。结果 竹节人参提取物明显延长小鼠缺氧存活时间,明显延长小鼠因结扎带迷走神经的两侧颈总动脉造成急性脑缺血的存活时间,能减轻大鼠实验性血栓的湿重和干重,显著降低大鼠     

家兔骨生长诱导修复腭裂骨缺损的实验研究

目的　研究评价牛骨形成蛋白 (b BMP) -白蛋白 -成纤维细胞生长因子 (b FGF)复合材料修复腭裂骨缺损的可行性。方法　建立家兔腭骨缺损模型 ,将固化的 b BMP-白蛋白 - b FGF复合材料植入骨缺损区 ,通过其骨诱导作用 ,诱导新骨生成 ,修复骨缺损。经 X线、组织学观察和钙含量测定。结果　 b BMP-白蛋白 - b FGF有很强的骨诱导作用 ,可以诱导骨形成 ,实验组与对照组 X线骨修复分数评估分别为 12分 ,0分 ,组织学检查实验组骨修复完成 ,而对照组无骨修复 ,钙含量测定也有显著性差异。。结论　 b BMP-白蛋白 - b FGF复合材料可诱导修复腭骨缺损 ,有良好的临床应用前景。     

Study of platelet-rich fibrin promoting endothelial cell differentiation and angiogenesis induced by transplantation of adipose-derived stem cells

Diabetic patients are characterized by long wound healing time, and adipose stem cells (ADSCs) can secrete growth factors to promote angiogenesis and improve diabetic wound healing. In this research, we attempted to interrogate the impact of platelet-rich fibrin (PRF) on ADSCs in diabetic wound healing. ADSCs were harvested from human adipose tissues and identified through flow cytometry. After pretreatment with cultured medium supplemented with different concentrations of PRF (2.5%, 5%, and 7.5%), proliferation and differentiation capacity of ADSCs were assessed by CCK-8 assay, qRT-PCR and immunofluorescence (IF), respectively. Tube formation assay measured angiogenesis. Western blot analysis analyzed expression of endothelial markers and the extracellular signal-regulated kinase (ERK) and serine/threonine kinase (Akt) pathways in PRF-induced ADSCs. The CCK-8 experiment indicated that PRF enhanced proliferation of ADSCs in dose-dependent manner, relative to normal control group. The expression of endothelial markers and the capacity of tube formation were significantly promoted by 7.5% PRF. The release of growth factors containing vascular endothelial grow factor (VEGF) and insulin-like growth factor-1 (IGF-1) from PRF was increased with the extension of detection time. When the receptors of VEGF or/and IGF-1 were neutralized, ADSCs differentiation into endothelial cells were obviously inhibited. Additionally, PRF stimulated ERK and Akt pathways, and the inhibitors of ERK and Akt attenuated PRF-induced differentiation of ADSCs into endothelial cells. In conclusion, PRF promoted endothelial cell differentiation and angiogenesis induced by ADSCs in diabetic wound healing, which appears to give guidance for treating patients.     

医学模式的转变促进健康观念的更新

健康是人类追求的永恒目标。随着社会的发展,生物医学模式向生物心理社会医学模式转变,“没有疾病就是健康”的观念已过于陈腐,人们对健康的理解已从“没有疾病”发展到包括生理、心理、社会的完满状态,健康的涵义更为深化,健康观念得到更新。     

Cationic-amphiphilic arpromidine-derived guanidines and a histamine trifluoromethyl-toluidide derivative may activate pertussis toxin-sensitive G-proteins by a receptor-independent mechanism

Formyl peptides activate superoxide anion (O₂ ^–) formation in human neutrophils and in HL-60 cells via pertussis toxin (PTX)-sensitive guanine nucleotide-binding proteins (G-proteins), and histamine (HA) mediates inhibition of O₂ ^– formation via H₂-receptors. We have studied the effects of lipophilic arpromidine-derived guanidines, which are potent, full H₂-receptor agonists in the guinea pig atrium, on O₂ ^– formation and on activation of G-proteins in HL-60 membranes and on purified G-proteins. We have also studied the effects of a HA trifluoromethyl-toluidide derivative (HTMT), a cationic-amphiphilic HA derivative which activates O₂ ^– formation in HL-60 cells through a mechanism which is independent of known HA receptor subtypes, on G-protein activation. Guanidines, at concentrations, up to 30 mol/l inhibited and, at concentrations above 30 mol/l, enhanced formyl peptide-induce O₂ ^– formation in neutrophils. In HL-60 cells, guanidines per se activated O₂ ^– formation. The stimulatory effects of guanidines on O₂ ^– formation were not inhibited by H₁- or H₂-receptor antagonists. In HL-60 membranes, guanidines and HTMT, activated high-affinity GTPase in a PTX-sensitive manner. These substances also increased GTP hydrolysis effected by transducin and G_i/G_o-proteins. Our data suggest that lipophilic guanidines and HTMT may act as receptor-independent activators of PTX-sensitive G-proteins, resulting in stimulation of O ₂ ^– formation.     

Five- to six-year results of a prospective clinical trial using the ENDOPORE dental implant and a mandibular overdenture

This report is an update on a group of 46 clinical trial patients who each received 3 free‐standing Endopore® dental implants placed using a 2‐stage surgical approach in the anterior mandible. After an initial healing interval of 10 weeks, the implants were used in each case to retain an overdenture, and at the time of the report. all patients had passed 5 years of continuous function. The 5‐year cumulative "survival" rate based on a life table analysis was 93.4% and this remained unchanged after 6 years. The 5‐year "success rate" was 83.3% when assessed qualitatively with the published criteria of others using a four‐field table analysis categorizing every implant in the study as one of "Grade 1 Success", "survival", "unaccounted for" or "failure". Modified periodontal parameters verified continued peri‐implant soft tissue health. No implant still in function had more than 1.8 mm cumulative bone loss during the first 5 years of function. These results provide clear evidence that Endopore® implants despite their short lengths function at least as well as other dental implant 1 designs used in much longer lengths.     

Osteochondroma and secondary synovial osteochondromatosis

Secondary synovial osteochondromatosis (SOC) is a rare disorder caused by a variety of joint disorders. Two unusual cases of secondary SOC are presented. The first patient is a 43-year-old man with extensive SOC developing within a bursa surrounding an osteochondroma of the pubic bone. The second patient is a 23-year-old man who developed florid and progressive SOC of his hip joint following excision of a femoral neck osteochondroma. SOC recurred despite three excisions over a 15-month period. Imaging was useful in pre-operative diagnosis of bursal SOC in the first patient and in detecting multiple recurrences in the second patient. Both cases illustrate prominent SOC developing secondary to osteochondroma. The different hypotheses regarding bursal and secondary SOC are reviewed. Received: 8 October 1998 Revision requested: 28 October 1998 Revision received: 13 November 1998 Accepted: 16 November 1998