Non-Newtonian blood flow in human right coronary arteries: transient simulations

This study looks at pulsatile blood flow through four different right coronary arteries, which have been reconstructed from biplane angiograms. A non-Newtonian blood model (the Generalised Power Law), as well as the usual Newtonian model of blood viscosity, is used to study the wall shear stress in each of these arteries over the entire cardiac cycle. The difference between Newtonian and non-Newtonian blood models is also studied over the whole cardiac cycle using the recently generalised global non-Newtonian importance factor. In addition, the flow is studied by considering paths of massless particles introduced into the flow field. The study shows that, when studying the wall shear stress distribution for transient blood flow in arteries, the use of a Newtonian blood model is a reasonably good approximation. However, to study the flow within the artery in greater detail, a non-Newtonian model is more appropriate.     

Do extrafloral nectar resources, species abundances, and body sizes contribute to the structure of ant–plant mutualistic networks?

Recent research has shown that many mutualistic communities display non-random structures. While our understanding of the structural properties of mutualistic communities continues to improve, we know little of the biological variables resulting in them. Mutualistic communities include those formed between ants and extrafloral (EF) nectar-bearing plants. In this study, we examined the contributions of plant and ant abundance, plant and ant size, and plant EF nectar resources to the network structures of nestedness and interaction frequency of ant–plant networks across five sites within one geographic locality in the Sonoran Desert. Interactions between ant and plant species were largely symmetric. That is, ant and plant species exerted nearly equivalent quantitative interaction effects on one another, as measured by their frequency of interaction. The mutualistic ant–plant networks also showed nested patterns of structure, in which there was a central core of generalist ant and plant species interacting with one another and few specialist–specialist interactions. Abundance and plant size and ant body size were the best predictors of symmetric interactions between plants and ants, as well as nestedness. Despite interactions in these communities being ultimately mediated by EF nectar resources, the number of EF nectaries had a relatively weak ability to explain variation in symmetric interactions and nestedness. These results suggest that different mechanisms may contribute to structure of bipartite networks. Moreover, our results for ant–plant mutualistic networks support the general importance of species abundances for the structure of species interactions within biological communities.     

Linkage at 12q24 with systemic lupus erythematosus (SLE) is established and confirmed in Hispanic and European American families

Systemic lupus erythematosus (SLE) is a chronic, complex, and systemic human autoimmune disease, with both an environmental component and a heritable predisposition. Clinical studies, reinforced by epidemiology and genetics, show impressive variation in disease severity, expression, prevalence, and incidence by ethnicity and sex. To identify the novel SLE susceptibility loci, we performed a genomewide scan with 318 markers on 37 multiplex Hispanic families, using a nonparametric penetrance-independent affected-only allele-sharing method. Three chromosomal regions (12q24, 16p13, and 16q12-21) exceeded our predetermined threshold (Zlr>2.32; nominal P<.01) for further evaluation. Suspected linkages at 12q24, 16p13, and 16q12-21 were tested in an independent data set consisting of 92 European American (EA-1) and 55 African American (AA) families. The linkage at 12q24 was replicated in EA-1 (Zlr=3.06; P=.001) but not in AA (Zlr=0.37; P=.35). Although neither the 16p13 nor the 16q12-21 was confirmed in EA-1 or AA, the suggestive linkage (Zlr=3.06; P=.001) at 16q12-21 is sufficient to confirm the significant linkage, reported elsewhere, at this location. The evidence for linkage at 12q24 in the 129 combined (Hispanic and EA-1) families exceeded the threshold for genomewide significance (Zlr=4.39; P=5.7x10-6; nonparametric LOD=4.19). Parametric linkage analyses suggested a low-penetrance, dominant model (LOD=3.72). To confirm the linkage effect at 12q24, we performed linkage analysis in another set of 82 independent European American families (EA-2). The evidence for linkage was confirmed (Zlr=2.11; P=.017). Therefore, our results have detected, established, and confirmed the existence of a novel SLE susceptibility locus at 12q24 (designated "SLEB4") that may cause lupus, especially in Hispanic and European American families.     

云南切梢小蠹对初侵害云南松挥发物的电生理和行为反应

云南切梢小蠹Tomicus yunnanensis(Kirkendall and Faccoli)是一种蛀害云南松Pinus yunnanensis的本土害虫.为深入了解其寄主选择机制,用顶空动态法和浸提法分别提取了初侵染云南松针叶和松脂的挥发性化合物,并用气相色谱-质谱联用技术(GC-MS)、气相色谱-昆虫触角电位测量系统(GC-EAD)、生测法鉴定和筛选了对云南切梢小蠹具有活性功能的成分.结果表明:云南松针叶和松脂中共有18种化合物,均为萜烯类物质,但两者化学成分的构成有显著差异.针叶中单萜类占99.98％,主要是 α-蒎烯(80.82％)、β-蒎烯(8.78％)、D-柠檬烯(4.77％)、莰烯(2.86％)和β-月桂烯(1.42％),而松脂以单萜类和双萜类为主,前者以α-蒎烯(21.38％)、3-蒈烯(21.42％)和异松油烯(2.78％)为主要成分,后者仅有长叶松酸(51.13％)一种.云南切梢小蠹对α-蒎烯、β-蒎烯、3-蒈烯、γ-萜品烯和4-烯丙基苯甲醚有触角电位反应,其中α-蒎烯、3-蒈烯和γ-萜品烯具引诱作用,4-烯丙基苯甲醚和β-蒎烯则为驱避功能.研究可为开发植物源引诱剂或与性信息素结合进行种群监测和诱杀提供科学依据.     

Differential Impact of Acute High-Intensity Exercise on Circulating Endothelial Microparticles and Insulin Resistance between Overweight/Obese Males and Females

BackgroundAn acute bout of exercise can improve endothelial function and insulin sensitivity when measured on the day following exercise. Our aim was to compare acute high-intensity continuous exercise (HICE) to high-intensity interval exercise (HIIE) on circulating endothelial microparticles (EMPs) and insulin sensitivity in overweight/obese men and women.MethodsInactive males (BMI = 30 ± 3, 25 ± 6 yr, n = 6) and females (BMI = 28 ± 2, 21 ± 3 yr, n = 7) participated in three experimental trials in a randomized counterbalanced crossover design: 1) No exercise control (Control); 2) HICE (20 min cycling @ just above ventilatory threshold); 3) HIIE (10 X 1-min @ ∼90% peak aerobic power). Exercise conditions were matched for external work and diet was controlled post-exercise. Fasting blood samples were obtained ∼18 hr after each condition. CD62E⁺ and CD31⁺/CD42b^- EMPs were assessed by flow cytometry and insulin resistance (IR) was estimated by homeostasis model assessment (HOMA-IR).ResultsThere was a significant sex X exercise interaction for CD62E+ EMPs, CD31+/CD42b- EMPs, and HOMA-IR (all P<0.05). In males, both HICE and HIIE reduced EMPs compared to Control (P≤0.05). In females, HICE increased CD62E+ EMPs (P<0.05 vs. Control) whereas CD31+/CD42b- EMPs were unaltered by either exercise type. There was a significant increase in HOMA-IR in males but a decrease in females following HIIE compared to Control (P<0.05).ConclusionsOverweight/obese males and females appear to respond differently to acute bouts of high-intensity exercise. A single session of HICE and HIIE reduced circulating EMPs measured on the morning following exercise in males but in females CD62E+ EMPs were increased following HICE. Next day HOMA-IR paradoxically increased in males but was reduced in females following HIIE. Future research is needed to investigate mechanisms responsible for potential differential responses between males and females.     

The spleen focus-forming virus envelope glycoprotein is defective in oligomerization

The gp52 envelope glycoprotein of Friend spleen focus-forming virus (SFFV) is a recombinant molecule derived from Friend murine leukemia virus (MuLV) by various deletions, insertions, and substitutions. The SFFV gp52 glycoprotein, unlike MuLV envelope glycoproteins, is defective in transport to the cell surface. Only 3-5% of gp52 eventually reaches the cell surface as a processed form (gp65). Although gp52 lacks cytoplasmic tail residues found in MuLV glycoproteins, we have previously shown that this deletion is not responsible for its defective transport. In order to investigate the basis for the defective transport of gp52, we have examined the folding and assembly of gp52 molecules into oligomeric molecules. CV-1 cells infected with vaccinia virus recombinants expressing SFFV gp52 were pulse labeled and the cell extracts were fractionated by velocity centrifugation through sucrose gradients. Immediately after a 10-min pulse, gp52 was detected as a monomer in the upper part of the sucrose gradient (fractions 12 and 14) and it remained as such after a 2-h chase period. However, the processed form, gp65, was found in a lower part of the gradient (fraction 8) after a 2-h chase. The position of gp65 was found to correspond to the position of trimeric influenza hemagglutinin which was analyzed on a parallel sucrose gradient, suggesting that gp65 also exists as a trimer in this fraction. These results indicate that changes in the external domain of gp52 result in improper folding of the glycoprotein molecule, and suggest that this lack of oligomerization is responsible for the defective transport of the molecules. Only those molecules that do form oligomeric structures are transported to the Golgi complex and undergo further oligosaccharide processing, and transport to the cell surface.     

LIF receptor signaling limits immune-mediated demyelination by enhancing oligodendrocyte survival

Multiple sclerosis (MS) is a disabling inflammatory demyelinating disease of the central nervous system (CNS) that primarily affects young adults. Available therapies can inhibit the inflammatory component of MS but do not suppress progressive clinical disability. An alternative approach would be to inhibit mechanisms that drive the neuropathology of MS, which often includes the death of oligodendrocytes, the cells responsible for myelinating the CNS. Identification of molecular mechanisms that mediate the stress response of oligodendrocytes to optimize their survival would serve this need. This study shows that the neurotrophic cytokine leukemia inhibitory factor (LIF) directly prevents oligodendrocyte death in animal models of MS. We also demonstrate that this therapeutic effect complements endogenous LIF receptor signaling, which already serves to limit oligodendrocyte loss during immune attack. Our results provide a novel approach for the treatment of MS.