リュツォ・ホルム湾，プリンスオラフ海岸，及び，エンダビーランド地質調査隊報告2016-2017（JARE-58）

第58次日本南極地域観測隊（JARE-58）では，2016−2017の夏期期間にリュツォ・ホルム湾，プリンスオラフ海岸，及び，エンダビーランドにおいて地質調査をおこなった．調査隊のメンバーは，日本人地質研究者4名とアジア地域（タイ，インドネシア，モンゴル）の交換科学者3名で構成され，本吉隊長が一部期間の調査に加わった．第58次夏期観測では，「しらせ」搭載の2機の大型ヘリコプター（CH101）とともに観測隊チャーターの小型ヘリコプター（AS350）1機による野外調査の支援がなされた．本稿では，観測計画を実施するための，主に設営面での計画，準備，そして行動経過について報告する．The 58th Japanese Antarctic Research Expedition (JARE-58) conducted geological field surveys in the regions of Lützow-Holm Bay, Prince Olav Coast, and Enderby Land during the 2016−2017 austral summer season. The field party consisted of four Japanese geologists and three Asian geologists (Thai, Indonesian, Mongolian), and was joined periodically by JARE-58 expedition leader, Prof. Motoyoshi. Field parties were supported throughout the summer season by a smaller secondary helicopter (AS350) in addition to two main helicopters (CH101) stationed on the icebreaker Shirase. This report summarizes field preparations and the geological work undertaken, and highlights several key points for future planning and research

DataSheet1_Effects of litter chemical traits and species richness on soil carbon cycling changed over time.docx

Litter decomposition is the main driver of nutrient cycling process in terrestrial ecosystems. Afforestation completely altered vegetation composition and litter species, disrupting the long-term carbon balance in grassland ecosystem. However, there is a lack of understanding of how litter mixing effect (LME) affects soil carbon cycling in afforested ecosystem. Here, we investigated the effects of litter richness and quality of tree, shrub, and grass species and their litter mixture on soil CO2 fluxes. The results showed that cumulative soil CO2 flux in the early stage (1–28 days) was 1.75 times higher than that in the late stage (29–113 days), indicating litter decomposition was intensive at first and then decreased with time. Soil carbon flux changed with decomposition stages. In the early-stage of decomposition, soil CO2 flux increased with the concentrations of litter carbon, nitrogen and condense tannin. In the late phase of decomposition, all litter chemical traits were negatively related to the soil carbon flux. Additionally, plant litter richness was negatively correlated to early-stage soil CO2 flux, whereas it was positively related to late-stage soil carbon flux. Our results provide evidence that long-term carbon balance in grassland ecosystems was interrupted by afforestation, and the dominant litter chemical traits that controlling soil carbon cycling changed over time.</p

<i>In vivo</i> Cre-ER^T2 activation with tamoxifen results in apoptosis in primary <i>p53−/−</i> lymphoma.

<p>Mice with thymic lymphomas were treated with tamoxifen. Tumor sections were stained with a cleaved-Caspase 3 antibody. Apoptotic cells were stained brown color. The numbers in the top right corners represent the percentage of apoptotic cells. Data are presented as mean + standard deviation. Paired t test p<0.01, for Cre-ER^T2 post-treatment versus pre-treatment.</p

Changes in tumor volume upon tamoxifen treatment in control <i>p53−/−</i> and <i>UBC-Cre-ER^T2; p53−/−</i> mice as shown by MRI imaging.

<p>The coronal sections of the thymic lymphoma were shown with tumors labeled with white asterisks. The letter H denotes the location of heart. Post-treatment scans were performed 14 days after starting tamoxifen treatment.</p

Summary of tumor volume changes upon tamoxifen treatment.

<p>Relative tumor volume was calculated by dividing post-treatment tumor volume by pre-treatment tumor volume. Unpaired t test, p<0.001. The code number of each mouse is labeled on the x-axis.</p

PERK eIF2 alpha kinase is required to regulate the viability of the exocrine pancreas in mice-0

<p><b>Copyright information:</b></p><p>Taken from "PERK eIF2 alpha kinase is required to regulate the viability of the exocrine pancreas in mice"</p><p>http://www.biomedcentral.com/1471-2121/8/38</p><p>BMC Cell Biology 2007;8():38-38.</p><p>Published online 29 Aug 2007</p><p>PMCID:PMC2072952.</p><p></p>y packed in wild-type (A, P20). In contrast, acinar cells have become degranulated giving a light pink appearance to the cytoplasm in the pancreas (B, P20). The same phenotype is seen in acinar cell-specific PERK knockout (C, P19, ). (D) Enlarged views of dying oncotic cells seen in (B) and (C). Some cells have lost nuclear staining (upper arrow) while others retain nuclear staining (lower arrow) (E) At P19, this particular mouse has already lost most of the exocrine pancreas although typically this degree of atrophy is not seen until 3–4 months of age. Arrows indicate examples of the smaller number of acini remaining. (F) In older mice (P162), acinar cells have been replaced by other cell types including adipocytes. Only a few dark pink acini are seen. Islets (arrows) still maintain an apparent normal structure. The animal also showed a normal glucose clearance rate. Red arrow indicates a few remaining acini. (G) In some cases, mutant acinar cells dedifferentiate into duct-like structures (P31) with abnormally large centroacinar ducts (black arrows). In the beginning of this process, duct cells still contain zymogen granules (right panel, white arrow). In some of these duct-like structures the presumptive acinar cells have completely lost zymogen granules (right panel, white arrow). (H) Conditional deletion of the gene in 3-month-old mice also results in the appearance of oncotic cells. Two oncotic acinar cells are enlarged (inset) with lower left still exhibiting nuclear staining while the cell in the upper right shows a nuclear ghost. H&E staining. A-C, H, 200x; E, 100x; F, 80x; D, G, 600x

(A, B) Acinar cells in the pancreas have numerous TUNEL-positive cells (A, P31 wild-type; B, P22 )

<p><b>Copyright information:</b></p><p>Taken from "PERK eIF2 alpha kinase is required to regulate the viability of the exocrine pancreas in mice"</p><p>http://www.biomedcentral.com/1471-2121/8/38</p><p>BMC Cell Biology 2007;8():38-38.</p><p>Published online 29 Aug 2007</p><p>PMCID:PMC2072952.</p><p></p> Note that the TUNEL staining pattern strikingly differs between the two genotypes. TUNEL, green; DAPI, blue; background, red. (C, D) Adjacent serial sections (3μ) of the pancreas (P19). Pale pink (oncotic) acinar cells identified by H&E staining (C) correspond to cells positive for ApoE (D); see arrows as an examples of several cells. ApoE, red; DAPI, blue; background, green. (E, F) The KO pancreas has significant leukocyte infiltration (E, wild-type; F, , P74). Dark purple acid phosphatase staining indicates infiltrated leukocytes including macrophages (see arrows) in F but not E. The background cellular staining is methylene blue

Microclimatic conditions during the experimental period from 2010 to 2013 at the study site: natural rainfall, artificial rainfall (water addition) and mean temperature.

<p>Microclimatic conditions during the experimental period from 2010 to 2013 at the study site: natural rainfall, artificial rainfall (water addition) and mean temperature.</p

Hyperuricemia and Risk of Incident Hypertension: A Systematic Review and Meta-Analysis of Observational Studies

<div><p>Background</p><p>Observational studies of the relationship between hyperuricemia and the incidence of hypertension are controversial. We conducted a systematic review and meta-analysis to assess the association and consistency between uric acid levels and the risk of hypertension development.</p><p>Methods</p><p>We searched MEDLINE, EMBASE, CBM (Chinese Biomedicine Database) through September 2013 and reference lists of retrieved studies to identify cohort studies and nested case-control studies with uric acid levels as exposure and incident hypertension as outcome variables. Two reviewers independently extracted data and assessed study quality using Newcastle-Ottawa Scale. Extracted information included study design, population, definition of hyperuricemia and hypertension, number of incident hypertension, effect sizes, and adjusted confounders. Pooled relative risks (RRs) and corresponding 95% confidence intervals (CIs) for the association between hyperuricemia and risk of hypertension were calculated using a random-effects model.</p><p>Results</p><p>We included 25 studies with 97,824 participants assessing the association between uric acid and incident hypertension in our meta-analysis. The quality of included studies is moderate to high. Random-effects meta-analysis showed that hyperuricemia was associated with a higher risk of incident hypertension, regardless of whether the effect size was adjusted or not, whether the data were categorical or continuous as 1 SD/1 mg/dl increase in uric acid level (unadjusted: RR = 1.73, 95% CI 1.46∼2.06 for categorical data, RR = 1.22, 95% CI 1.03∼1.45 for a 1 SD increase; adjusted: RR = 1.48, 95% CI 1.33∼1.65 for categorical data, RR = 1.15, 95% CI 1.06∼1.26 for a 1 mg/dl increase), and the risk is consistent in subgroup analyses and have a dose-response relationship.</p><p>Conclusions</p><p>Hyperuricemia may modestly increase the risk of hypertension incidence, consistent with a dose-response relationship.</p></div