Estimation of sex from the hyoid body in skeletal individuals from archeological sites

Recent forensic studies have shown that the hyoid bone is a sexually dimorphic element of the human skeleton. Given the advanced techniques of collecting human remains in archeological and forensic contexts, the recovery of hyoid bones is now more frequent in skeletal samples. For that reason the authors propose a new method for estimating sex based on hyoid bodies from archeological sites.     

Rootstock genotype succession influences apple replant disease and root-zone microbial community composition in an orchard soil

Apple replant disease (ARD) is a soil-borne disease complex that affects young apple trees in replanted orchards, resulting in stunted growth and reduced yields. Newly developed rootstock genotypes with tolerance to ARD may help to control this disease. We determined the effects of rootstock genotype rotations during orchard renovation, by investigating root-zone soil microbial consortia and the relative severity of ARD on seven rootstock genotypes (M.9, M.26, G.30, G.41, G.65, G.935, and CG.6210) planted in soil where trees on four of those same rootstocks (M.9, M.26, G.30 and CG.6210) had grown for the previous 15 years. Rootstock genotyping indicated that genetic distances among rootstocks were loosely correlated with their differential responses to ARD. Root-zone fungal and bacterial community composition, assessed by DNA fingerprinting (T-RFLP), differed between M.26 and CG.6210. Soil bacterial communities were influenced most by which rootstock had grown in the soil previously, while fungal communities were influenced more by the current replanted rootstock. In a clone library of bacteria from M.26 and CG.6210 root-zone soil, β-Proteobacteria was the most abundant phylum (25% of sequences). Sequences representing the Burkholderia cepacia complex were obtained only from CG.6210 soil. Rootstock genotypes that were grown in the orchard soil previously affected subsequent ARD severity, but replanting with the same or closely related rootstocks did not necessarily exacerbate this disease problem. Our results suggest that genotype-specific interactions with soil microbial consortia are linked with apple rootstock tolerance or susceptibility to ARD.     

IAP antagonists target cIAP1 to induce TNFalpha-dependent apoptosis

XIAP prevents apoptosis by binding to and inhibiting caspases, and this inhibition can be relieved by IAP antagonists, such as Smac/DIABLO. IAP antagonist compounds (IACs) have therefore been designed to inhibit XIAP to kill tumor cells. Because XIAP inhibits postmitochondrial caspases, caspase 8 inhibitors should not block killing by IACs. Instead, we show that apoptosis caused by an IAC is blocked by the caspase 8 inhibitor crmA and that IAP antagonists activate NF-kappaB signaling via inhibtion of cIAP1. In sensitive tumor lines, IAP antagonist induced NF-kappaB-stimulated production of TNFalpha that killed cells in an autocrine fashion. Inhibition of NF-kappaB reduced TNFalpha production, and blocking NF-kappaB activation or TNFalpha allowed tumor cells to survive IAC-induced apoptosis. Cells treated with an IAC, or those in which cIAP1 was deleted, became sensitive to apoptosis induced by exogenous TNFalpha, suggesting novel uses of these compounds in treating cancer.     

Authors need to be prudent when assigning names to microbial isolates

Antonie van Leeuwenhoek -     

Macrophage apoAI protects against dyslipidemia-induced dermatitis and atherosclerosis without affecting HDL

Tissue cholesterol accumulation, macrophage infiltration, and inflammation are features of atherosclerosis and some forms of dermatitis. HDL and its main protein, apoAI, are acceptors of excess cholesterol from macrophages; this process inhibits tissue inflammation. Recent epidemiologic and clinical trial evidence questions the role of HDL and its manipulation in cardiovascular disease. We investigated the effect of ectopic macrophage apoAI expression on atherosclerosis and dermatitis induced by the combination of hypercholesterolemia and absence of HDL in mice. Hematopoietic progenitor cells were transduced to express human apoAI and transplanted into lethally irradiated LDL receptor^−/−/apoAI^−/− mice, which were then placed on a high-fat diet for 16 weeks. Macrophage apoAI expression reduced aortic CD4⁺ T-cell levels (−39.8%), lesion size (−25%), and necrotic core area (−31.6%), without affecting serum HDL or aortic macrophage levels. Macrophage apoAI reduced skin cholesterol by 39.8%, restored skin morphology, and reduced skin CD4⁺ T-cell levels. Macrophage apoAI also reduced CD4⁺ T-cell levels (−32.9%) in skin-draining lymph nodes but had no effect on other T cells, B cells, dendritic cells, or macrophages compared with control transplanted mice. Thus, macrophage apoAI expression protects against atherosclerosis and dermatitis by reducing cholesterol accumulation and regulating CD4⁺ T-cell levels, without affecting serum HDL or tissue macrophage levels.     

Characterization of acute phase proteins and oxidative stress response to road transportation in the dog

Haptoglobin (Hp), serum amyloid A (SAA), C-reactive protein (CRP), white blood cells (WBC), reactive oxygen metabolites (ROMs), the antioxidant barrier (Oxy-adsorbent) and thiol groups of plasma compounds (SHp) were measured in ten dogs that had been transported a distance of about 230 km within 2 h (experimental group) and in ten dogs that had not been subjected to road transportation (control group). Blood was collected via cephalic venipuncture before road transportation (T0), after road transportation (T1), and more than 6 (T6) and 24 (T24) hours after road transportation in the experimental group (Group A) and at the same time points in the control group (Group B). The GLM (general linear model) Repeated Measures procedure showed a significant difference between the two groups (P<0.0001) and a significant rise (P<0.0001) in the concentrations of Hp, SAA, CRP, WBC, ROMs, Oxy-adsorbent and SHp after road transportation in Group A, underlining that physiological and homeostatic mechanisms are modified differently at various sampling times.     

Daily hypoxia increases basal monocyte HSP72 expression in healthy human subjects

Heat shock protein 72 (HSP72) performs vital roles within the body at rest and during periods of stress. In vitro, research demonstrates HSP72 induction in response to hypoxia. Recently, in vivo, an acute hypoxic exposure (75 min at 2,980 m) was sufficient to induce significant increases in monocyte expressed HSP72 (mHSP72) and a marker of oxidative stress in healthy human subjects. The purpose of the current study was to identify the impact of 10 consecutive days of hypoxic exposures (75 min at 2,980 m) on mHSP72 and erythropoietin (EPO) expression, markers of oxidative stress, and maximal oxygen consumption in graded incremental aerobic exercise. Eight male subjects were exposed to daily normobaric hypoxic exposures for 75 min at 2,980 m for 10 consecutive days, commencing and ceasing at 0930 and 1045, respectively. This stressor was sufficient to induce significant increases in mHSP72, which was significantly elevated from day 2 of the hypoxic exposures until 48 h post-final exposure. Notably, this increase had an initial rapid (30% day on day compared to baseline) and final slow phase (16% day on day compared to baseline) of expression. The authors postulate that 7-day hypoxic exposure in this manner would be sufficient to induce near maximum hypoxia-mediated basal mHSP72 expression. Elevated levels of mHSP72 are associated with acquired thermotolerance and provide cross tolerance to non-related stressors in vivo, the protocol used here may provide a useful tool for elevating mHSP72 in vivo. Aside from these major findings, significant transient daily elevations were seen in a marker of oxidative stress, alongside sustained increases in EPO expression. However, no physiologically significant changes were seen in maximal oxygen consumption or time to exhaustion.