Betel Nut Chewing Is Strongly Associated With General and Central Obesity in Chinese Male Middle‐aged Adults

Betel nut chewing has been reported to increase the risk of cardiovascular disease and all‐cause mortality. The reason is unclear. In this study, we investigated the association between betel nut chewing and general obesity (BMI ≥25 kg/m²) and central obesity (waist circumference (WC) ≥90 cm). A total of 1,049 male subjects, aged ≥40 years, were recruited from Taichung city in Taiwan in 2004. The relationships between betel nut chewing and general and central obesity were studied by multiple linear and logistic regression analyses. The prevalence of current and former betel nut chewing was 7.0 and 10.5% in our male Taiwanese cohort. Current/former betel nut chewers had a higher prevalence of general and central obesity when compared with individuals who had never chewed betel nut. Adjusted for age, diabetes, hypertension, lipids, smoking, alcohol drinking, physical activity, income, and education level, the odds ratios (ORs; 95% confidence intervals) of general and central obesity among the lower consumption of betel nut chewers were 1.78 (1.07, 2.96) and 1.19 (0.70, 2.02), respectively, compared to 2.01 (1.18, 3.41) and 1.89 (1.10, 3.23), respectively, among higher consumption chewers compared to individuals who had never chewed betel nut. The increasing ORs of general and central obesity with higher betel nut consumption revealed dose–response effects. Using multiple linear regression analyses, after adjusting for potential confounders, betel nut consumption was statistically significantly associated with BMI and WC. In conclusion, betel nut chewing was independently associated with general and central obesity in Taiwanese men. Dose–response effects of the association between betel nut consumption and general obesity as well as central obesity were found.     

Effects of brain‐derived neurotrophic factor on dopaminergic function and motor behavior during aging

Brain‐derived neurotrophic factor (BDNF) is critical in synaptic plasticity and in the survival and function of midbrain dopamine neurons. In this study, we assessed the effects of a partial genetic deletion of BDNF on motor function and dopamine (DA) neurotransmitter measures by comparing Bdnf^+/? with wildtype mice (WT) at different ages. Bdnf^+/? and WT mice had similar body weights until 12 months of age; however, at 21 months, Bdnf^+/? mice were significantly heavier than WT mice. Horizontal and vertical motor activity was reduced for Bdnf^+/? compared to WT mice, but was not influenced by age. Performance on an accelerating rotarod declined with age for both genotypes and was exacerbated for Bdnf^+/? mice. Body weight did not correlate with any of the three behavioral measures studied. Dopamine neurotransmitter markers indicated no genotypic difference in striatal tyrosine hydroxylase, DA transporter (DAT) or vesicular monoamine transporter 2 (VMAT2) immunoreactivity at any age. However, DA transport via DAT (starting at 12 months) and VMAT2 (starting at 3 months) as well as KCl‐stimulated DA release were reduced in Bdnf^+/? mice and declined with age suggesting an increasingly important role for BDNF in the release and uptake of DA with the aging process. These findings suggest that a BDNF expression deficit becomes more critical to dopaminergic dynamics and related behavioral activities with increasing age.     

Incidence of Fungal Necrotrophic and Biotrophic Pathogens in Pioneer and Shade‐tolerant Tropical Rain Forest Trees

This study assessed the hypothesis that plant life history traits determine the incidence of fungal biotrophic and necrotrophic pathogens in pioneer vs. shade‐tolerant tropical plant species. Considering that pioneer species mainly invest in induced defenses, we expected a negative relationship between the incidence of biotrophic and necrotrophic pathogens; in contrast, as shade‐tolerant species invest heavily in constitutive defenses, we expected to find no correlation between the incidence of biotrophic and necrotrophic pathogens. These ideas were evaluated by assessing standing levels of fungal damage in a set of pioneer and shade‐tolerant species from the Lacandona tropical rain forest (Mexico). The results showed that among pioneer plant species, leaves with biotrophic lesions were between 34 and 44 percent more abundant than those with necrotic lesions. In contrast, among shade‐tolerant species, the proportions of leaves with necrotic lesions were 17–23 percent higher than those of leaves with injuries caused by biotrophic pathogens. Our study suggests that tropical tree species might present different defense strategies depending on the life‐style of the pathogens that attack them, and the life history strategy of the attacked host plant species. Thus, the host constitutive and induced defenses, as well as the mechanisms used by different types of pathogens to circumvent those defenses maybe responsible for the patterns of attack observed in perennial tropical plants. Abstract in Spanish is available at http://www.blackwell‐synergy.com/loi/btp .     

Fluid shear stress‐induced JNK activity leads to actin remodeling for cell alignment

Fluid shear stress (FSS) exerted on endothelial cell (EC) surfaces induces actin cytoskeleton remodeling through mechanotransduction. This study was designed to determine whether FSS activates Jun N‐terminal kinase (JNK), to examine the spatial and temporal distribution of active JNK relative to the actin cytoskeleton in ECs exposed to different FSS conditions, and to evaluate the effects of active JNK on actin realignment. Exposure to 15 and 20 dyn/cm² FSS induced higher activity levels of JNK than the lower 2 and 4 dyn/cm² flow conditions. At the higher FSS treatments, JNK activity increased with increasing exposure time, peaking 30 min after flow onset with an eightfold activity increase compared to cells in static culture. FSS‐induced phospho‐JNK co‐localized with actin filaments at cell peripheries, as well as with stress fibers. Pharmacologically blocking JNK activity altered FSS‐induced actin structure and distribution as a response to FSS. Our results indicate that FSS‐induced actin remodeling occurs in three phases, and that JNK plays a role in at least one, suggesting that this kinase activity is involved in mechanotransduction from the apical surface to the actin cytoskeleton in ECs. J. Cell. Physiol. 226: 110–121, 2010. © 2010 Wiley‐Liss, Inc.     

Effect of ice melting on bacterial carbon fluxes channelled by viruses and protists in the Arctic Ocean

During the last few years, extensive sea ice melting in the Arctic due to climate change has been detected, which could potentially modify the organic carbon fluxes in these waters. In this study, the effect of sea ice melting on bacterial carbon channelling by phages and protists has been evaluated in the northern Greenland Sea and Arctic Ocean. Grazing on bacteria by protists was evaluated using the FLB disappearance method. Lysis of bacteria due to viral infections was measured using the virus reduction approach. Losses of bacterial production caused by protists (PMM_BP) dominated losses caused by viruses (VMM_BP) throughout the study. Lysogenic viral production was detected in 7 out of 21 measurements and constituted from 33.9 to 100.0% of the total viral production. Significantly higher PMM_BP and lower VMM_BP were detected in waters affected by ice melting compared with unaffected waters. Consequently, significantly more bacterial carbon was channelled to the higher trophic levels in affected waters (13.05 ± 5.98 μgC l⁻¹ day⁻¹) than in unaffected waters (8.91 ± 8.33 μgC l⁻¹ day⁻¹). Viruses channelled 2.63 ± 2.45 μgC l⁻¹ day⁻¹ in affected waters and 4.27 ± 5.54 μgC l⁻¹ day⁻¹ in unaffected waters. We conclude that sea ice melting in the Arctic could modify the carbon flow through the microbial food web. This process may be especially important in the case of massive sea ice melting due to climate change.     

Identification of toxicological biomarkers of di(2‐ethylhexyl) phthalate in proteins secreted by HepG2 cells using proteomic analysis

The effects of di(2‐ethylhexyl) phthalate (DEHP) on proteins secreted by HepG2 cells were studied using a proteomic approach. HepG2 cells were exposed to various concentrations of DEHP (0, 2.5, 5, 10, 25, 50, 100, and 250 μM) for 24 or 48 h. 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyl tetrazolium bromide (MTT) and comet assays were then conducted to determine the cytotoxicity and genotoxicity of DEHP, respectively. The MTT assay showed that 10 μM DEHP was the maximum concentration that did not cause cell death. In addition, the DNA damage in HepG2 cells exposed to DEHP was found to increase in a dose‐ and time‐dependent fashion. Proteomic analysis using two different pI ranges (4–7 and 6–9) and large size 2‐DE revealed the presence of 2776 protein spots. A total of 35 (19 up‐ and 16 down‐regulated) proteins were identified as biomarkers of DEHP by ESI‐MS/MS. Several differentiated protein groups were also found. Proteins involved in apoptosis, transportation, signaling, energy metabolism, and cell structure and motility were found to be up‐ or down‐regulated. Among these, the identities of cystatin C, Rho GDP inhibitor, retinol binding protein 4, gelsolin, DEK protein, Raf kinase inhibitory protein, triose phosphate isomerase, cofilin‐1, and haptoglobin‐related protein were confirmed by Western blot assay. Therefore, these proteins could be used as potential biomarkers of DEHP and human disease associated with DEHP.     

Proliferation of myofibroblasts in the stroma of renal oncocytoma

Objectives: Myofibroblasts are a vital component of stroma of many malignant neoplasms, but it is not yet established whether stromal myofibroblasts also exist in benign tumours such as oncocytoma of the kidney. Materials and methods: Histomorphological and immunohistochemical analysis of 16 renal oncocytomas diagnosed at Chang Gung Memorial Hospital, Taiwan, has been performed. Results: Renal oncocytomas were composed of oncocytes, large cells with granular eosinophilic cytoplasm, arranged mostly in sheets, in tubulocystic or combined pattern. Few oncocytes appeared to be undergoing proliferation or apoptosis. MIB‐1 and active caspase 3 indices were low, but higher in tumour than in surrounding non‐tumour parenchyma (MIB‐1: 0.93 ± 0.09 versus 0.46 ± 0.07, P < 0.001 and active caspase 3: 0.76 ± 0.08 versus 0.41 ± 0.09, P < 0.001). Wnt/β‐catenin signalling was not implicated in this neoplasm, as there was no loss of E‐cadherin membranous localization or expression of intranuclear β‐catenin in the cells. Clumps of oncocytes were stained with periodic acid Schiff and had collagen I‐, collagen III‐ and fibronectin‐positive, but desmin‐ and human caldesmon‐negative stromas. Importantly, α‐smooth muscle actin (SMA)‐immunostaining established the myofibroblastic nature of many of the stromal cells. Some of the myofibroblasts were also positive for MIB‐1, indicating a proliferative role for them in the stroma. Conclusions: Renal oncocytomas were composed of two independent compartments: benign oncocytes and pronounced fibrotic stroma, which consisted of proliferating myofibroblasts (SMA‐ and MIB‐1‐positive) which were associated with excessive deposition of extracellular matrix (periodic acid Schiff‐component, collagen I‐, collagen III‐ and fibronectin‐positive, and desmin‐ and human caldesmon‐negative).     

Does urbanization affect selective pressures and life‐history strategies in the common blackbird (Turdus merula L.)?

Urbanization, one of the most extreme land‐use alterations, is currently spreading, and the number of species confronting these changes is increasing. However, contradictory results of previous studies impede a clear interpretation of which selective pressure (nest predation or food limitation) is more important in urban habitats compared with natural situations, and whether birds can confront them by adjusting their life‐history strategies. We investigated life‐history syndromes of three common blackbird (Turdus merula) populations differing in their human influence (urban, rural, and woodland). We analysed daily nest predation and nestling starvation rates to assess the relative importance of these selection pressures in each habitat. Simultaneously, several life‐history traits were investigated to determine if T. merula seem adapted to their main source of selection. Food limitation was more important in the city, whereas nest predation was the most important selective force in the forest. The rural habitat was characterized by an intermediate influence of these two factors. Life‐history syndromes, as the covariation of a suite of traits, confirmed these results because T. merula seem well adapted to the main cause of selection in each habitat. Our results are consistent with urbanization imposing new challenges on birds, and that they adaptively respond to them. © 2010 The Linnean Society of London, Biological Journal of the Linnean Society, 2010, 101 , 759–766.