Effects of different UV radiation on photoprotective pigments and antioxidant activity of the hot‐spring cyanobacterium Leptolyngbya cf. fragilis

UV‐induced synthesis/accumulation of photoprotective pigments and antioxidant activity were investigated in the hot‐spring cyanobacterium Leptolyngbya cf. fragilis. The results indicated that UV radiation may induce biosynthesis of carotenoids, allophycocyanin, phycoerythrin, and scytonemin while phycocyanin degrades in response to longtime UV radiation. Moreover, pigment composition of L. cf. fragilis was significantly altered with increasing UV radiation times, probably due to destruction and resynthesis of accessory pigments as an adaptation strategy to UV stress. The in vitro antioxidant analysis of different extracts of UV treated cyanobacteria exhibited concentration‐dependent antioxidant activity. Ethyl acetate extract of 72 h UV treatment showed maximum total antioxidant activity (IC50 = 71.73 ± 5.3 μg mL^?1) followed by ethyl acetate control (non‐UV irradiated) extract (IC50 = 109.43 ± 2.76 μg mL^?1). This is the first report for the UV‐induced synthesis of photoprotective pigments and their antioxidant activity in L. cf. fragilis.     

Naringin prevents ultraviolet‐B radiation‐induced oxidative damage and inflammation through activation of peroxisome proliferator‐activated receptor γ in mouse embryonic fibroblast (NIH‐3T3) cells

The present study, we investigate the preventive role of naringin, a dietary flavonoid, against ultraviolet‐B (UVB) radiation (280‐320 nm) induced oxidative damage and inflammatory responses in mouse embryonic fibroblast cell lines (NIH‐3T3). In this study, 20 mJ/cm ² of UVB radiation induces cell cytotoxicity, reactive oxygen species (ROS) generation, DNA damage, and antioxidants depletion in NIH‐3T3 cells. Treatment with naringin (60 µM) prior UVB exposure prevented the cell cytotoxicity, ROS generation, DNA damage, and antioxidants depletion in NIH‐3T3 cells. Furthermore, naringin prevents UVB‐induced mitogen‐activated protein kinase families and nuclear factor‐κB (NF‐κB)‐mediated activation of inflammatory factors, that is TNF‐α, IL‐6, IL‐10, and COX‐2 in NIH‐3T3 cells. Peroxisome proliferator‐activated receptor γ (PPARγ) is an anti‐inflammatory agent and it suppressed the UVB‐mediated oxidative and inflammatory responses. In this study, naringin activates PPARγ and prevents inflammatory biomarkers in NIH‐3T3 cells. Thus, naringin prevents UVB‐mediated inflammation and oxidative damage in NIH‐3T3 cells probably over controlling NF‐κB expression and activation of PPARγ.     

Data partitioning and correction for ascertainment bias reduce the uncertainty of placental mammal divergence times inferred from the morphological clock

Bayesian estimates of divergence times based on the molecular clock yield uncertainty of parameter estimates measured by the width of posterior distributions of node ages. For the relaxed molecular clock, previous works have reported that some of the uncertainty inherent to the variation of rates among lineages may be reduced by partitioning data. Here we test this effect for the purely morphological clock, using placental mammals as a case study. We applied the uncorrelated lognormal relaxed clock to morphological data of 40 extant mammalian taxa and 4,533 characters, taken from the largest published matrix of discrete phenotypic characters. The morphologically derived timescale was compared to divergence times inferred from molecular and combined data. We show that partitioning data into anatomical units significantly reduced the uncertainty of divergence time estimates for morphological data. For the first time, we demonstrate that ascertainment bias has an impact on the precision of morphological clock estimates. While analyses including molecular data suggested most divergences between placental orders occurred near the K‐Pg boundary, the partitioned morphological clock recovered older interordinal splits and some younger intraordinal ones, including significantly later dates for the radiation of bats and rodents, which accord to the short‐fuse hypothesis.     

一氧化氮对UV-B辐射增强条件下燕麦幼苗氧化损伤的缓解作用

以燕麦品种“定燕2号”和“晋燕14号”为研究材料,研究紫外线B（ultraviolet rays-B, UV-B）辐射增强条件下,一氧化氮（nitric oxide, NO）供体硝普钠（sodium nitroprusside, SNP）对燕麦幼苗活性氧含量、膜脂过氧化和抗氧化物质含量的影响。结果表明：NO能够降低UV-B辐射增强条件下“定燕2号”和“晋燕14号”的超氧阴离子（superoxide radical, O₂^·-）产生速率、羟自由基（hydroxyl free radical, OH^·）、过氧化氢（hydrogen peroxide, H₂O₂）和丙二醛（malondialdehyde, MDA）含量。UV-B辐射时间为6 h,施加SNP时,“定燕2号”的超氧化物歧化酶（superoxide dismutase, SOD）活性和过氧化物酶（peroxidase, POD）活性、“晋燕14号”的SOD活性高于其他处理组;UV-B辐射时间为3 h,施加SNP时,“定燕2号”、“晋燕14号”的抗坏血酸过氧化物酶（ascorbate peroxidase, APX）活性显著高于0 h、12 h处理组。UV-B辐射时间为6 h,“定燕2号”的脱氢抗坏血酸（dehydroascorbic acid, DHA）含量显著高于其他处理组;而UV-B辐射时间为0 h,“晋燕14号”的DHA 含量显著高于其他处理组。NO对UV-B辐射增强下“定燕2号”和“晋燕14号”抗氧化性影响的综合测评均为：3 h>6 h>12 h>0 h。本研究结果为NO在燕麦育种、抗氧化机制等提供理论依据。     

Trends in brain cancers (glioma) in New Zealand from 1995 to 2020, with reference to mobile phone use

BackgroundSome case-control studies have suggested substantial increased risks of glioma in association with mobile phone use; these risks would lead to an increase in incidence over time.MethodsIncidence rates of glioma from 1995 to 2020 by age, sex, and site in New Zealand (NZ) recorded by the national cancer registry were assessed and trends analysed. Phone use was based on surveys.ResultsIn these 25 years there were 6677 incident gliomas, giving age-standardised rates (WHO world standard) of 6.04 in males, and 3.95 in females per 100,000. The use of mobile phones increased rapidly from 1990 to more than 50% of the population from about 2000, and almost all the population from 2006. The incidence of glioma from ages 10–69 has shown a small decrease over the last 25 years, during which time the use of mobile phones has become almost universal. Rates in the brain locations receiving most radiofrequency energy have also shown a small decrease. Rates at ages of 80 and over have increased.ConclusionThere is no indication of any increase related to the use of mobile phones. These results are similar to results in Australia and in many other countries. The increase in recorded incidence at ages over 80 is similar to that seen in other countries and consistent with improved diagnostic methods.     

Possible adaptive and non-adaptive radiation in three plant genera in the Japanese archipelago

The adaptive radiation of flowering plants as manifested by the floral diversity has long been considered associated with the diversity of plant–pollinator interactions, because changes in plant–pollinator interactions are hypothesized as one of the major mechanisms driving plant ecological speciation. To understand the relative contributions of various mechanisms for plant radiation, including pollinator changes, it is useful to study a plant group for which comparative study of the species life history across the whole lineage is feasible. To this end, we will focus on the plant lineages that have presumably radiated in the Japanese archipelago, namely, the genera Asimitellaria, Asarum, and Arisaema. By comparing these three genera, we will comment on the possible modes of adaptive radiation and diversification among the endemic flora of Japan.     

The speciation view: Disentangling multiple causes of adaptive and non-adaptive radiation in terms of speciation

Biological diversification often includes burst of lineage splitting. Such “radiation” has been known to act as evolutionary arenas with the potential to generate unique phylogenetic clusters and further novel groups. Although these radiations when accompanied by ecological diversification, so-called “adaptive radiation” have persisted as a central premise in evolutionary biology, the ecological and genetic mechanism of such rapid diversification has remained unclear. There are several critical definitions for the pattern of adaptive radiation, and those provide delimitation of adaptive and non-adaptive radiation. That being said, only a few studies have provided any clear demarcations in our understanding of the adaptive and non-adaptive causes of radiation from the mechanism of speciation. Here, we review the current consensus for the causes of adaptive radiation, especially along with the recent theoretical synthesis of “ecological speciation.” Further, we suggest the signature of adaptive and non-adaptive radiation in the earliest stages of diversification from the viewpoint of speciation. These criteria from the speciation view are useful to find the cases with the signatures of adaptive/non-adaptive radiation.     

Enhanced UV‐B radiation during pupal stage reduce body mass and fat content,while increasing deformities,mortality and cell death in female adults of solitary bee Osmia bicornis

The effects of enhanced UV‐B radiation on the oogenesis and morpho‐anatomical characteristics of the European solitary red mason bee Osmia bicornis L. (Hymenoptera: Megachilidae) were tested under laboratory conditions. Cocooned females in the pupal stage were exposed directly to different doses (0, 9.24, 12.32, and 24.64 kJ/m²/d) of artificial UV‐B. Our experiments revealed that enhanced UV‐B radiation can reduce body mass and fat body content, cause deformities and increase mortality. Following UV exposure at all 3 different doses, the body mass of bees was all significantly reduced compared to the control, with the highest UV dose causing the largest reduction. Similarly, following UV‐B radiation, in treated groups the fat body index decreased and the fat body index was the lowest in the group receiving the highest dose of UV radiation. Mortality and morphological deformities, between untreated and exposed females varied considerably and increased with the dose of UV‐B radiation. Morphological deformities were mainly manifested in the wings and mouthparts, and occurred more frequently with an increased dose of UV. Cell death was quantified by the Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay (DNA fragmentation) during early stages of oogenesis of O. bicornis females. The bees, after UV‐B exposure exhibited more germarium cells with fragmented DNA. The TUNEL test indicated that in germarium, low doses of UV‐B poorly induced the cell death during early development. However, exposure to moderate UV‐B dose increased programmed cell death. In females treated with the highest dose of UV‐B the vast majority of germarium cells were TUNEL‐positive.