Biomechanics

Therapeutic agents used to treat osteoporosis reduce the incidence of vertebral and nonvertebral fractures in osteoporotic women. The antiremodeling agents, such as the bisphosphonates, prevent bone loss by suppressing the remodeling rate, perhaps increasing bone volume slightly, and increasing mineralization of the tissue. The anabolic agents, of which rhPTH(1–34) is the only one approved, accomplish this in a manner that is almost completely the opposite in terms of biological process. rhPTH(1–34) causes net bone gain by stimulating both modeling and remodeling, by increasing bone volume significantly through direct bone apposition to trabecular and endocortical surfaces, and by reducing the mean degree of tissue mineralization (a natural consequence of enhanced remodeling). Each of these treatments maintains or increases bone strength and is similarly effective at preventing fractures. However, because of their different mode of action, each has different consequences for bone matrix quality (defined here by microdamage accumulation and by the properties of mineral and collagen) and the mechanical properties of the tissue. Although bone's composite nature makes it a relatively tough material—more like fiberglass than glass—the accumulation of damage will nevertheless reduce its residual mechanical properties until the damage is repaired through remodeling. Agents that suppress remodeling are associated with both microdamage accumulation and increased mineralization. The biological importance of damage and mineralization to bone's mechanical properties is still a source of debate.     

A novel mutation in the last exon of ATRX in a patient with α-thalassemia myelodysplastic syndrome

Abstract:  We describe a patient with acquired alpha-thalassemia myelodysplastic syndrome (ATMDS). A previously healthy 66-year-old man presented with hemoglobin of 9.3 g/dL, mean corpuscular volume 59 fL, and a bone marrow aspirate with increased erythroid precursors and hypolobulated megakaryocytes. Hemoglobin H inclusions were seen in most red cells after 1% brilliant cresyl blue supravital stain of the peripheral blood. At the molecular level, we identified of a novel mutation in the most 3' exon of the ATRX gene ( C GA→ T GA substitution in codon 2407) resulting in a premature termination codon (p.R2407X). This case provides further evidence for a link between ATRX mutations and ATMDS, and suggests a possible role for the conserved Q-box element in ATRX function.     

Coronary artery and saphenous vein graft remodeling: A review of histologic findings after various interventional procedures—part V

Catheter balloon angioplasty is a well accepted form of nonsurgical treatment of acutely and chronically obstructed coronary artery vessels. It is also the centerpiece for various new intervention techniques. Their morphologic effect on the site of obstruction has been termed “remodeling.” Part V of this six-part series focuses on remodeling effects of balloon angioplasty on obstructed young (≤ 1 year) and old (> 1 year) saphenous vein bypass grafts.     

Aza-peptides. III. Experimental structural analysis of aza-alanme and aza-asparagine-containing peptides

To determine the structural perturbations induced by the CαH→Nα exchange in aza-peptides, we have examined by H NMR and IR spectroscopy various derivatives of the aza-analogues of alanine, aspartic acid and asparagine in different organic solvents with increasing polarity. Their general formulas are: R'-AzXaa-NR²R³, R'-Pro-AzXaa-NR²R³ and R-AzXaa-Pro-NR²R³ (where AzXaa denotes the aza-analogue of the amino acid residue Xaa = Ala, Asp, Asn; R = Boc, Z; R², R³= H, Me, iPr). The aza-analogue of an amino acid residue appears to be a strong p-turn-inducing motif, and the AzAsn carboxamide side-chain is capable of interacting, as a proton donor, with the preceding peptide carbonyl group.     

The mechanical and morphological properties of bone beneath internal fixation plates of differing rigidity

The internal fixation of diaphyseal fractures by bone plates is a well recognized treatment. The normal physiological stress of bone is reduced by plates that cause a negative balance of bone-remodeling processes. Many investigators have shown that the degree of stress protection is dependent on the rigidity of the plates. It was the aim of this study to quantify mechanical and morphological changes at different locations in a plated diaphyseal bone as a function of differing plate rigidity. Two types of plates with the same size but different materials were used. The stainless steel plates had a modulus of elasticity and bending stiffness 3.2 times higher than the carbon fiber reinforced carbon plates. Both types of plates were applied to the intact right and left femora of six foxhounds for 6 months. The stiffer stainless steel plates led to a significantly higher bone loss and correspondingly greater loss of mechanical properties. These effects were greatest directly beneath the plate and less with increasing distance from the plate.     

Bone remodeling during the development of osteoporosis in paraplegia

Summary Osteoporosis developing during the first weeks after the onset of traumatic paraplegia was studied with cortical and cancellous samples of iliac crest and tibia of 14 patients, and compared to normals. We used a procedure of bone particle fractionation (according to degree of mineralization) that allowed us to establish a profile reflecting the metabolic remodeling of bone and to analyze the organic matrix of the newly synthesized tissue. In paraplegics, we observed a large increase in the proportion of little calcified bone in the cortical as well as in the cancellous bone. Based on amino acid analyses, we found a decreased number of hydroxyproline residues in the newly synthesized organic matrix from paraplegia bone resulting either from an alteration of the prolyl hydroxylation or from the presence of an excess of noncollagen polypeptides. These results, together with previously published data reporting increased urinary hydroxylproline and calcium kinetic parameters, suggest an enhanced rate of skeletal remodeling in acute paraplegia. When investigated 2 years after injury, the patterns of distribution approach that of normal subjects.     

Biochemical Markers of Bone Turnover in Camurati–Engelmann Disease: A Report on Four Cases in One Family

Moderate increases in ``classical' biochemical markers of bone turnover have been described only in some patients with Camurati–Engelmann disease. However, the determination of the following ``new' markers has not been previously performed: serum osteocalcin (BGP), bone alkaline phosphatase (BAP), carboxyterminal propeptide of type I procollagen (PICP), aminoterminal propeptide of type I procollagen (PINP), tartrate-resistant acid phosphatase (TRAP), telopeptide carboxyterminal of type I collagen (ICTP), urinary pyridinoline (PYR), crosslinked N-telopeptides of type I collagen (NTX), and Crosslaps (CL). Such a determination may improve the evaluation of the disease activity. To evaluate the usefulness of biochemical markers of bone turnover reflecting Camurati–Engelmann disease activity we measured the levels of all these markers in four affected patients. The results were compared with bone scintigraphic indices of disease activity. Except for PICP and TRAP, bone formation and resorption markers were abnormal in all patients and were related to bone scan indices of disease activity. Among the markers of bone formation PINP, BAP, and BGP showed the highest values, whereas NTX and CL were the most sensitive markers of bone resorption. These results suggest that the determination of NTX or CL, and PINP or either BAP and BGP, associated with bone scan evaluation, provides the best assessment of Camurati–Engelmann disease activity. Received: 14 June 1996 / Accepted: 31 December 1996     

重油和沥青中饱和碳的定量估计

建立了较完整的估计重油和沥青中饱和碳浓度数方法，其中包括环烷桥头碳、环烷甲基取代碳、环烷烷基（≥Ｃ２）取代碳等。基于理论分析，建立了估计环间的桥链和各种平均结构参数的方法，包括平均芳环环核数和环烷环环核数、芳环和环烷环烷工取代度、单元片上芳环和环烷环数。从实验数据出发，提出了烷基链长分布的公式。     

转化生长因子-β在哮喘气道炎症与重塑中的作用

Transforming growth factor-β(TGF-β) was reported to be increased in asthma in some studies. Accumulation of TGF-β in airway promotes smooth muscle cell mitogenesis and hyperplasia, and in-duces fibroblast and myofibroblast and smooth muscle proliferation as well as increase in protein synthesis in connective tissue(such as collagen deposition on the reticular basement membrane). The autocrine induction of collagen expression by smooth muscle may contribute to the thickening of the reticular basement membrane, irre-versible f‘throsis and remodeling seen in the airways in some asthmatics. TGF-β is considered to be a major fi-brogenic cytokine. It can increase smooth muscle mass and lead to severe bronchial obstruction in an asthma at-tack.     

STUDY OF MORPHOLOGICAL CHANGES OF HEART IN VIRAL MYOCARDITIS CAUSED BY REPETITIVE INFECTION OF CVB3m

Objective To investigate the morphological changes of heart in viral myocarditis caused by repetitive infection of CVB3m. Methods 4-week-old mice were infected four times intraperitoneally with a timedependent dose and killed at the 10th, 30th and 60th day after the final infection respectively, then we examined the heart changes and collagen hyperplasia by HE, VG stain and 1HC. Results Heart damage appeared very serious at the tenth day, even there were small necrotic foci at the day of 30th, but we could not see any injury of heart 2 months later after final infection. Collagen turned up at the tenth day and there was much more collagen in heart and increased PCVA, CVF index at the sixtieth day. The 1HC of collagen demonstrated the collagen I hyperplasia was much obvious compared to collagen Ⅲ. Conclusion It strongly indicated that repetitive infection of CVB3m could lead to heart fibrosis and ventricular remodeling, which resulted in decreased systolic and diastolic function of heart.