Aims/hypothesis Obesity and insulin resistance are associated with low-grade chronic inflammation. Glucagon-like peptide-1 (GLP-1) is known to reduce insulin resistance. We investigated whether GLP-1 has anti-inflammatory effects on adipose tissue, including adipocytes and adipose tissue macrophages (ATM). Methods We administered a recombinant adenovirus (rAd) producing GLP-1 (rAd-GLP-1) to an ob/ob mouse model of diabetes. We examined insulin sensitivity, body fat mass, the infiltration of ATM and metabolic profiles. We analysed the mRNA expression of inflammatory cytokines, lipogenic genes, and M1 and M2 macrophage-specific genes in adipose tissue by real-time quantitative PCR. We also examined the activation of nuclear factor κB (NF-κB), extracellular signalregulated kinase 1/2 and Jun N-terminal kinase (JNK) in vivo and in vitro. Results Fat mass, adipocyte size and mRNA expression of lipogenic genes were significantly reduced in adipose tissue of rAd-GLP-1-treated ob/ob mice. Macrophage populations (F4/80 + and F4/80 + CD11b + CD11c + cells), as well as the expression and production of IL-6, TNF-α and monocyte chemoattractant protein-1, were significantly reduced in adipose tissue of rAd-GLP-1-treated ob/ob mice. Expression of M1-specific mRNAs was significantly reduced, but that of M2-specific mRNAs was unchanged in rAd-GLP-1-treated ob/ob mice. NF-κB and JNK activation was significantly reduced in adipose tissue of rAd-GLP-1-treated ob/ob mice. Lipopolysaccharide-induced inflammation was reduced by the GLP-1 receptor agonist, exendin-4, in 3T3-L1 adipocytes and ATM. Conclusions/interpretation We suggest that GLP-1 reduces macrophage infiltration and directly inhibits inflammatory pathways in adipocytes and ATM, possibly contributing to the improvement of insulin sensitivity.

<p><strong>Abstract.</strong> Recently, the drastic climate changes have increased the importance of wildfire monitoring and damage assessment as well as the possibility of wildfire occurrence. Estimation of wildfire damage provides the information on wildfire-induced ecological changes and supports the decision-making process for post-fire treatment activities. For accurate wildfire damage assessment, the discrimination between disaster-induced and natural changes is crucial because they usually coupled together.</p> <p>In this study, Sentinel-2 images were employed to assess the damage from a wildfire, which occurred in the coniferous forest of Gangneung, Gangwon Province, South Korea on April 2019. The images were captured from both Sentinel-2A and -2B, shortening the temporal interval of available pre- and post-fire images. Multi-temporal image analysis was performed in both object and pixel-based with two commonly used spectral indices, NDVI and NBR. Additional image pair from the same period of 2018 was used to distinguish the fire-affected regions from the naturally changed area and compared with the results from using only one pair of images from 2019. The experimental results showed that the change detection performance could be affected by the number of image pairs and spectral indices used to discriminate burned region from unburned region. Thus it verified the significance of adequately employing annual multi-pair satellite images for wildfire damage assessment.</p>

<p><strong>Abstract.</strong> Combining pre-disaster optical and post-disaster synthetic aperture radar (SAR) data is regarded as desirable for timely damage assessment, which is essential for the prompt rescue operation. Due to the extreme differences between the two data, however, this combination has not been practically used in the previous research. In this paper, a method to assess the various types of damage caused by disasters using the desirable data combination, particularly pre-disaster very high resolution optical data and post-disaster polarimetric SAR data. The proposed method is a rule-based classification, and uses diverse components derived from the two data such as normalized difference vegetation index, polarization orientation angle, SPAN, and entropy. The proposed method was applied to the case study of the 2011 tsunami in Japan. The experimental results demonstrated the potential of the proposed method to assesses the types of tsunami-induced damage in urban and vegetated areas. The achievement in this paper is expected to facilitate efficient and fast disaster-induced complex damage assessment.</p>

High mobility group box 1" (HMGB1) is a well-known nuclear protein that stabilizes DNA and facilitates gene transcription, but at outside the membrane, it functions as an alarmin, causing an inflammatory response in combination with other cytokines. Recently, we confirmed that HMGB1 shows the proinflammatory activity depending on the redox status, which is in the reduced, disulfide, or oxidized form. The reduced-HMGB1 exerts a chemoattractive effect, and the disulfide-HMGB1 has proinflammatory cytokine activity, but the oxidized form has no inflammatory activity. In our previous study, the proinflammatory effect of disulfide-HMGB1 was seen under the poly(I:C)-induced inflammation in keratinocyte, but reduced-HMGB1 showed the suppressive effect of poly(I:C)-induced inflammation. In addition, HMGB1 contains two homologous DNA-binding domains, the A and B-boxes. HMGB1 B-box induces strong proinflammatory activities, but HMGB1 A-box is a specific antagonist for HMGB1 and exerts an anti-inflammatory effect in macrophage. However, the direct effects of HMGB1 A-box and B-box for keratinocytes were not well elucidated. To investigate those effects, we established recombinant peptides for HMGB1 A-box and B-box. HMGB1 A and B-box alone did not induce inflammatory cytokines for keratinocyte on own. On the other hand, HMGB1 A-box had suppressive effect for IL-6 and IFN-beta expression on poly (I:C) induced inflammation in keratinocyte, but HMGB1 B-box had no inflammatory in keratinocytes. From these results, it is possible that HMGB1 A-box could become a new antiinflammatory material for some inflammatory skin diseases.

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The nucleotide excision repair (NER) system removes pyrimidine (6-4) pyrimidone photoproducts [(6-4)PPs] and cyclobutane pyrimidine dimers (CPDs) from DNA in the form of small (w30-nt-long), excised, damage-containing DNA oligonucleotides (sedDNAs). However, the detection of UV photoproduct-containing sedDNAs as a biochemical read-out for NER activity has thus far been limited to defined in vitro cell-free systems and to cultured cells. Using small punch biopsies of human skin, we show here that the sedDNA products of NER can be isolated, detected, and quantified in skin epidermis within minutes of UVB exposure and following low, sub-erythemal doses of UVB. Interestingly, a partially degraded form of the sedDNAs can be detected in human skin epidermis for several hours following UVB irradiation, which indicates that sedDNA degradation occurs slowly following their release from epidermal genomic DNA. Treatment of skin explants with spironolactone, which depletes the epidermis of the essential NER protein XPB (xeroderma pigmentosum group B), inhibits sedDNA generation following UVB exposure. Our results indicate that the detection of sedDNAs offers a sensitive and quantitative assay for nucleotide excision repair activity in human skin samples and may therefore be useful for determining how genetic, environmental, and pharmacological factors contribute to inter-individual differences in NER activity in human skin.

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