Relationship Among MRTA, DXA, and QUS

Dual-energy X-ray absorptiometry (DXA) and quantitative ultrasound (QUS) are the accepted modalities for the evaluation of fracture risk in the clinical setting. However, neither method provides a direct measurement of bone mechanics. In this study, we investigated a prototype device, known as a mechanical response tissue analyzer (MRTA), which provides direct mechanical measurements of mechanical properties of bone. A total of 56 healthy volunteers (20 men and 36 women) between the ages of 18 and 83 were recruited. The MRTA was used to measure the cross-sectional bending stiffness (EI) of the ulna bone. Axial speed of sound (SOS) at the ulna bone was determined by QUS; bone mineral content (BMC) and bone mineral density (BMD) were determined by DXA. Correlations, regression analysis, and analyses of variance (ANOVAs) were used to compare the three modalities. These analyses revealed that although there are strong linear relationships among the data collected by the various technologies, the bone properties reflected by MRTA are not fully explained by DXA and QUS. We conclude that the total information conveyed by MRTA measurements is unique. Further research is needed to delineate the different qualities of bone strength that are captured by MRTA, but not by DXA or QUS.     

微血管密度与胃癌侵袭和转移的关系

目的 :探讨胃癌组织中微血管密度 (MVD)与胃癌生物学行为的关系。方法 :应用免疫组织化学S -P法和抗人因子Ⅷ相关抗原 (FⅧ -RAg)的抗体 ,标记 6 8例胃癌组织中的微血管 ,检测MVD。分析其与胃癌组织学类型、分化水平、浸润深度及淋巴结转移的关系。结果 :6 8例胃癌组织中FⅧ -RAg阳性表达 5 2例 ,占 76 .4 7%。FⅧ -RAg和MVD与分化水平、浸润深度 (P <0 .0 1)及淋巴结转移 (P <0 .0 0 1)密切相关。不同组织学类型中FⅧ-RAg的表达具有显著相关性 (P <0 .0 1) ,而MVD则与胃癌组织学类型无显著差异 (P >0 .0 5 )。 结论 :血管生成对胃癌的发展具有一定作用 ,FⅧ -RAg的检测和MVD可作为判断胃癌恶性程度和预后的生物学指标。     

Bone mineral density of the proximal tibia following uncemented arthroplasty

Bone mineral density (BMD, g/cm2) was measured using dual-photon absorptiometry (DPA) in selected areas of the proximal tibia following uncemented PCA knee prosthesis. In nine patients with 14 alloplastic operations, measurements were taken at 3-6-month intervals for the first 3 1/2 years after operation. There was a significant increase in BMD of about 15% during the first 6 months after operation. The following year it remained increased, although not significantly, compared with the initial values, then gradually diminished. Increased bone density after arthroplasty may be explained mainly by stimulation of bone formation from weight bearing due to improved walking ability. Stress shielding of the proximal part of the supporting tibial bone did not seem to occur.     

Treatment of osteoporosis in men

Osteoporosis in men is recognised worldwide as an important and increasing public health problem. The causes are more heterogeneous than those in women. About 50% are diagnosed as secondary cases. In some secondary forms of osteoporosis the specific diagnosis results in additional therapeutic options (e.g. androgen therapy in proven hypogonadism). The basic therapy for osteoporosis in men is no different to that in postmenopausal women, namely recommendations for counteracting modifiable risk factors, especially with regard to diet, physical exercise, and calcium and vitamin D supplementation. Concerning specific drug medications, however, even today there is still a therapeutic dilemma in male osteoporosis. While older substances (e.g. calcitonin, fluoride, alfacalcidol) are approved for both sexes, all newer medications have primarily been approved for the treatment of postmenopausal osteoporosis. Health authorities request studies in purely male populations. For new drugs, fracture data are necessary while for new substances within a class (e.g. bisphosphonates), at the very least consistent effects on bone mineral density (BMD) and bone turnover markers are requested. Due to these regulatory rules, ibandronate, teriparatide and strontium ranelate are not approved in the European Union. Some years ago, alendronate was the first bisphosphonate that was approved for the treatment of men with osteoporosis, based on consistent results from two independent male studies using a daily 10 mg dosage. Very recently risedronate was approved by the FDA and EMEA. A randomised, placebo-controlled multicentre trial of 285 male patients showed, after 2 years, a 5.8% increase in lumbar spine BMD in the risedronate 35 mg once weekly group vs 1.2% in the placebo group. In a prospective controlled study on 316 men with primary or secondary osteoporosis we found, after 12 months, a lumbar spine BMD of +4.7% vs +1.0% in controls. The number of patients with one or more new vertebral fractures was 8 in the risedronate group and 20 in the placebo group (a fracture reduction of 60%). Furthermore, we found a significantly smaller decrease in height and a steeper decrease in back pain in the risedronate group. Risedronate is the first oral bisphosphonate available for men with the more comfortable once weekly dosage.     

过氧化物酶体增殖物激活受体γC161T基因多态性与糖皮质激素性骨质疏松症的关系

目的 探讨中国人过氧化物酶体增殖物激活受体γ(PPARγ)基因外显子6 C161T多态性与糖皮质激素性骨质疏松症(GIO)的相关关系。方法 应用聚合酶链反应-限制性片段长度多态性(PCR-RELP)方法测定208例正常健康人（Ⅰ组）、168例非GIO患者（Ⅱ组）和104例GIO患者（Ⅲ组）PPARγ基因外显子6 C161T的基因型。应用双能X线骨密度仪(DEXA)测定股骨、腰椎等部位的骨密度。 结果 外显子6 C161T有CC、CT、TT 3种基因型。GIO组CC基因型频率显著低于正常对照组；CT和TT基因型频率显著高于正常对照组。非GIO组、应用激素组（GIO组＋非GIO组）与正常对照组比较，各基因型频率差异均无统计学意义。正常对照组C161T的CC基因型组各部位的骨密度有高于CT和TT基因型组的趋势，但差异无统计学意义。非GIO组和GIO组C161T的CC基因型组腰椎的骨密度明显高于CT和TT基因型组 (P ＜ 0.05)，分别为非GIO组CC型（1.04±0.17） g/cm2，CT+TT型（1.02±0.07） g/cm2；GIO组CC型（0.94±0.12） g/cm2，CT+TT型（0.83±0.08） g/cm2。经年龄、体重指数等因素校正后，差异仍有统计学意义(P ＜ 0.05）。 结论 PPARγ基因C161T基因型在正常人和应用激素患者之间无明显差异，它可能与肾小球肾炎的发病无关。C161T基因型在GIO组和正常对照组之间差异有统计学意义，它可能与糖皮质激素性骨质疏松症的发病有关。PPARγ基因C161T多态性与应用糖皮质激素患者腰椎的骨密度有关。等位基因C可能是骨量的保护因子，它可能与应用糖皮质激素后骨量的丢失有关。     

体表面积、体质量指数对老年骨质疏松的影响

目的探讨体表面积（BS）、体质量、体质量指数（BMI）对老年人骨密度（BMD）的影响。方法用双能X线骨密度仪测定1794例老年人腰椎、髋关节的BMD值，并对其与BS等指标进行相关回归分析。结果BS大的老年人其BMD大于BS小者，有显著性差异。在各种指标与BMD的相关性比较中，BS与BMD的相关性最好，其后依次为：体质量、身高、OSTA得分（亚洲人自我骨质疏松筛查工具）、BMI。结论BS比BMI等指标更能反映出人体体型对老年人BMD的影响。     

Homocysteinylation of low-density lipoproteins (LDL) from subjects with Type 1 diabetes: effect on oxidative damage of human endothelial cells.

BACKGROUND: Homocysteine (Hcy) is an independent risk factor for cardiovascular disease (CVD). Individuals with Type 1 and Type 2 diabetes are more susceptible to the effects of homocysteine than non-diabetic subjects. The interaction between homocysteine-thiolactone (Hcy-thiolactone), a reactive product of Hcy, and low-density lipoproteins (LDL) induces the formation of homocystamide-LDL adducts (Hcy-LDL) and it has been suggested that homocysteinylation could increase atherogenicity of lipoproteins. AIM: The aim of the study was to compare the effect of in vitro homocysteinylation of LDL isolated from healthy control subjects (C-LDL) and from Type 1 diabetic patients (DM-LDL) and to investigate the effect of homocysteinylated LDL (Hcy-C-LDL and Hcy-DM-LDL) on peroxynitrite production of endothelial cells. METHODS: The in vitro homocysteinylation of LDL isolated from control (n = 12) and DM subjects (n = 12) was carried out by incubating lipoproteins with Hcy-thiolactone. The reaction was verified by quantifying the increase in sulphydryl groups (-SH groups) in Hcy-LDL with respect to control LDL. Control and homocysteinylated LDL were incubated with human aortic endothelial cells (HAEC) in culture. Peroxynitrite production in cells treated in different experimental conditions was assayed by a fluorimetric method. RESULTS: The increase in -SH groups after incubation with homocysteine was greater in LDL from diabetic subjects compared with LDL from control subjects (P < 0.001). In addition, peroxynitrite production from HAEC incubated with Hcy-LDL from diabetic patients was greater than after incubation with Hcy-LDL from control subjects and untreated LDL from diabetic patients (P < 0.001). CONCLUSIONS: These results show that LDL from diabetic patients is more susceptible to in vitro homocysteinylation than LDL from non-diabetic individuals and demonstrate that the compositional changes in Hcy-LDL from diabetic subjects have cytotoxic effects on human endothelial cells.     

肿瘤微血管密度与肝癌病理及预后关系

目的 探讨肿瘤微血管密度（MVD）与肝细胞性肝癌临床病理及预后的关系。方法对30例肝细胞性肝癌根治性切除病理组织切片进行苏木精伊红染色．并用CD34单克隆抗体进行免疫组化染色，计数被CD34抗体染色的肿瘤血管内皮细胞数，以测定MVD。对MVD与临床病理因素及术后生存率关系进行分析。结果 单因素分析结果表明．MVD水平与肿瘤大小、TNM分期都是影响肝细胞性肝癌预后的因素；多因素分析结果表明．肝癌大小及肿瘤分期是肝细胞性肝癌独立预后因素。结论 MVD是肝细胞性肝癌一种预后因素。     

Cyclic tensile stretch load and oxidized low density lipoprotein synergistically induce lectin-like oxidized ldl receptor-1 in cultured bovine chondrocytes, resulting in decreased cell viability and proteoglycan synthesis.

Mechanical stimulation is known to be an essential factor in the regulation of cartilage metabolism. We tested the hypothesis that expression of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) can be modulated by cyclic tensile stretch load in chondrocytes. Cyclic loading of repeated stretch stress at 10 cycles per minute with 10 kPa of stress for 6 h induced expression of LOX-1 to 2.6 times control in cultured bovine articular chondrocytes, equivalent to the addition of 10 microg/mL oxidized low density lipoprotein (ox-LDL) (2.4 times control). Application of the cyclic load to the chondrocytes along with 10 microg/mL ox-LDL resulted in synergistically increased LOX-1 expression to 6.3 times control. Individual application of cyclic loading and 10 microg/mL ox-LDL significantly suppressed chondrocytes viability (84.6% +/- 3.4% and 80.9% +/- 3.2% of control at 24 h, respectively; n = 3; p < 0.05) and proteoglycan synthesis [81.0% +/- 7.1% and 85.7% +/- 5.2% of control at 24 h, respectively; p < 0.05 when compared with 94.6% +/- 4.6% for native-LDL (n = 3)]. Cyclic loading and 10 microg/mL ox-LDL synergistically affected cell viability and proteoglycan synthesis, which were significantly suppressed to 45.6% +/- 4.9% and 48.7% +/- 6.7% of control at 24 h, respectively (n = 3; p < 0.01 when compared with individual application of cyclic loading or 10 microg/mL ox-LDL). In this study, we demonstrated synergistic effects of cyclic tensile stretch load and ox-LDL on cell viability and proteoglycan synthesis in chondrocytes, which may be mediated through enhanced expression of LOX-1 and which has important implications in the progression of cartilage degeneration in osteoarthritis.