Crystallization of intrinsic membrane proteins

After many years of discouraging failures, it is now possible to crystallize the intrinsic membrane proteins and to obtain structural information from diffraction studies on the crystals. The strategy for the crystallization consists of depletion of boundary phospholipids from the protein and complex formation with specific ligands.     

微创后入路治疗肩胛骨骨折的临床研究

目的:探讨微创后入路手术治疗肩胛骨骨折的临床疗效。方法:选取2009年6月~2014年1月在我院接受后路内固定手术治疗的40例肩胛骨骨折,治疗组20例,行微创后入路内固定术,对照组20例,行Judet入路内固定术。比较两组间手术时间、术中出血量、切口总长度及术后肩关节功能Constant评分。结果:40例患者均获随访,随访时间12~36个月,平均16.5个月。治疗组手术时间、术中出血量、切口总长度均优于对照组(均P0.05),术后6个月肩关节功能:治疗组优15例,良3例,可1例,差1例,优良率90%,对照组优14例,良2例,可3例,差1例,优良率80%。两组优良率比较,差异有统计学意义(P0.05)。两组均无感染、骨折延迟愈合或不愈合。对照组1例发生肩胛上神经卡压。结论:微创后入路手术操作简单,创伤小,恢复快,是一种安全有效的肩胛骨骨折手术入路。     

Assessment of cortical bone fracture resistance curves by fusing artificial neural networks and linear regression

Bone injures (BI) represents one of the major health problems, together with cancer and cardiovascular diseases. Assessment of the risks associated with BI is nontrivial since fragility of human cortical bone is varying with age. Due to restrictions for performing experiments on humans, only a limited number of fracture resistance curves (R-curves) for particular ages have been reported in the literature. This study proposes a novel decision support system for the assessment of bone fracture resistance by fusing various artificial intelligence algorithms. The aim was to estimate the R-curve slope, toughness threshold and stress intensity factor using the two input parameters commonly available during a routine clinical examination: patients age and crack length. Using the data from the literature, the evolutionary assembled Artificial Neural Network was developed and used for the derivation of Linear regression (LR) models of R-curves for arbitrary age. Finally, by using the patient (age)-specific LR models and diagnosed crack size one could estimate the risk of bone fracture under given physiological conditions. Compared to the literature, we demonstrated improved performances for estimating nonlinear changes of R-curve slope (R² = 0.82 vs. R² = 0.76) and Toughness threshold with ageing (R² = 0.73 vs. R² = 0.66).     

Browridge development in cercopithecidae: A test of two models

Theoretical discussions of primate browridge formation have resulted in several interpretations of its form and function. Lateral radiographs of adult Old World monkeys, representing most cercopithecine and colobine genera, were examined to address whether both biomechanical and spatial factors influence the development of a supraorbital torus. A linear measurement of browridge size was compared with a series of measures related to each model. Partial correlations were used to ascertain the relative independence of biomechanical (model I or II) and spatial effects upon torus formation. Allometric (size-related) shape changes were evaluated with log-linear bivariate regression analysis; subfamily differences in scaling patterns, with an analysis of covariance. When spatial and biomechanical (I or II) factors were both significantly related to brow size, additive and interactive multiple regression models were used to further assess the manner by which each set mutually affects variation in browridge dimensions. Correlation analyses were repeated with size-corrected antilogged residuals to eliminate a potentially spurious effect of skull size. Old World monkeys provide support of the spatial model. Also of interest is that skull size emerges as a primary influence on torus formation. Several alternative explanations are also put forward to account for browridge development in each subfamily.     

Functional morphology and biomechanics of cuticular fracture at the elytrophoral autotomy plane of the scaleworm Alentia gelatinosa (Annelida: Polynoidae)

Abstract. Autotomy of the elytra (scales) in the annelid Alentia gelatinosa occurs at a breakage plane near the junction between the elytron and its elytrophore (stalk), and requires fracture of the external epidermal cuticle. The mechanism of cuticular fracture was investigated by light and electron microscopy, glycoconjugate histochemistry, direct observation of autotomy in isolated preparations, and mechanical tests. The breakage plane crosses the elytrophoral wall at a cuticular thickening and passes through the subelytral cavity between the elytron and the terminal septum of the elytrophore. At the cuticular breakage zone (CBZ), the collagenous framework of the normal cuticle is replaced with non‐collagenous microfibrils. The CBZ has a complex glycoconjugate composition and includes a strongly sulfated, uronic acid‐containing glycosaminoglycan and a high proportion of disulfide or sulfydryl linkages. Tonofilament‐rich epidermal cells (tendon cells) are attached to the thick cuticle on the dorsal and ventral sides of the CBZ. Dorsal tendon cells have long processes that extend into the elytron near the roof of the subelytral cavity. Ventral tendon cells are linked by connective tissue to the longitudinal and terminal sphincter muscles of the elytrophore. Mechanical tests showed that the elytrophoral wall is not inherently weaker at the autotomy plane than elsewhere. It is hypothesized that at autotomy (i) contractile force generated by the sphincter muscle is transmitted through elytrophoral tendon cells to the ventral side of the CBZ and (ii) contraction of the longitudinal and main circular muscles of the elytrophore increases hydrostatic pressure in its lumen, everts the terminal septum, and generates tension that is transmitted through elytral tendon cells to the dorsal side of the CBZ. This results in stress concentration at the basal edge of the CBZ and initiates fracture. The distinctive microstructure and macromolecular composition of the CBZ may reduce its fracture toughness and make it more susceptible to brittle failure.     

Emerging evidence that adaptive bone formation inhibition by non-steroidal anti-inflammatory drugs increases stress fracture risk

There is mounting evidence suggesting that the commonly used analgesics, non-steroidal anti-inflammatory drugs (NSAIDs), may inhibit new bone formation with physical training and increase risk of stress fractures in physically active populations. Stress fractures are thought to occur when bones are subjected to repetitive mechanical loading, which can lead to a cycle of tissue microdamage, repair, and continued mechanical loading until fracture. Adaptive bone formation, particularly on the periosteal surface of long bones, is a concurrent adaptive response of bone to heightened mechanical loading that can improve the fatigue resistance of the skeletal structure, and therefore may play a critical role in offsetting the risk of stress fracture. Reports from animal studies suggest that NSAID administration may suppress this important adaptive response to mechanical loading. These observations have implications for populations such as endurance athletes and military recruits who are at risk of stress fracture and whose use of NSAIDs is widespread. However, results from human trials evaluating exercise and bone adaptation with NSAID consumption have been less conclusive. In this review, we identify knowledge gaps that must be addressed to further support NSAID-related guidelines intended for at-risk populations and individuals.