Poleward migration of tropical corals inhibited by future trends of seawater temperature and calcium carbonate (CaCO3) saturation.

Poleward range expansion of marine organisms is commonly attributed to anthropogenic ocean warming. However, the extent to which a single species can migrate poleward remains unclear. In this study, we used molecular data to examine the current distribution of the Pocillopora damicornis species complex in Taiwan waters and applied niche modeling to predict its potential range through the end of the 21st Century. The P. damicornis species complex is widespread across shallow, tropical and subtropical waters of the Indo-Pacific regions. Our results revealed that populations from subtropical nonreefal coral communities are P. damicornis, whose native geographical ranges are approximately between 23°N and 35°N. In contrast, those from tropical reefs are P. acuta. Our analysis of 50 environmental data layers demonstrated that the concentrations of CaCO3 polymorphs had the greatest contributions to the distributions of the two species. Future projections under intermediate shared socioeconomic pathways (SSP) 2-4.5 and very high (SSP5-8.5) scenarios of greenhouse gas emissions showed that while sea surface temperature (SST) isotherms would shift northwards, saturation isolines of two CaCO3 polymorphs, calcite (Ωcal) and aragonite (Ωarag), would shift southwards by 2100. Subsequent predictions of future suitable habitats under those conditions indicated that distinct delimitation of geographical ranges for the two species would persist, and neither would extend beyond its native geographical zones, indicating that tropical Taiwan waters are the northern limit for P. acuta. In contrast, subtropical waters are the southern limit for P. damicornis. We concluded that the decline in CaCO3 saturation would make high latitudes less inhabitable, which could be one of the boundary elements that limit poleward range expansion driven by rising SSTs and preserve the latitudinal diversity gradient (LDG) on Earth. Consequently, poleward migration of tropical reef corals to cope with warming oceans should be reevaluated.

Dexmedetomidine infusion for emergence coughing prevention in patients undergoing an endovascular interventional procedure: A randomized dose-finding trial.

OBJECTIVE: Dexmedetomidine has been introduced in emergence coughing, agitation, and shivering prevention. This study aimed to investigate the optimal dose of dexmedetomidine for emergence cough prophylaxis. METHODS: In this randomized, double-blinded, and prospective trial, 356 patients scheduled for an endovascular interventional procedure were randomly assigned to 0.3 (D 0.3), 0.4 (D 0.4), 0.5 (D 0.5), and 0.6 (D 0.6) µg·kg-1·h-1 dexmedetomidine rate, or saline control (C), from anesthesia induction until the end of surgery. The primary outcomes measured were cough grade and frequency. Additionally, groups were compared according to mean arterial pressure (MAP), heart rate, agitation, shivering, postoperative nausea and vomiting (PONV), extubation time, sedation scores, and postoperative first night sleep quality (secondary outcomes). RESULTS: A total of 351 patients were included in the analysis. The respective incidences of D 0.3, D 0.4, and D 0.5 versus C group were: 78.6%, 68.6%, 53.4% and 42.9% vs 89.7% for cough (p = 0.002, p < 0.001, and p < 0.001 between group D 0.4, D 0.5 and D 0.6 vs C, respectively); 30%, 27.1%, 20.5%, 15.7% vs 44.1% for agitation (p = 0.04, p = 0.003, and p < 0.001 between group D 0.4, D 0.5 and D 0.6 vs C, respectively); 8.6%, 7.1%, 6.8%, 5.7% vs 22.1% for shivering (p = 0.027, p = 0.013, p = 0.01, and p = 0.01 between D 0.3, D 0.4, D 0.5 and D 0.6 vs C, respectively); and 52.9%, 57.1%, 42.5%, 44.3% vs 61.8% for poor sleep quality (p = 0.02 and p = 0.04 between group D 0.5 and D 0.6 vs C, respectively). D 0.4, D 0.5 and D 0.6 showed lower MAP during extubation, compared with the C group. Also, D 0.5 and D 0.6 presented a slight delay in extubation (3.1 and 3.3 min longer than C; p = 0.002 and p < 0.001, respectively). Meanwhile, the frequency of atropine, vasopressor administration, PONV and dizziness were similar to the control. CONCLUSIONS: Both 0.5 and 0.6 µg·kg-1·h-1 dexmedetomidine infusion rates effectively mitigated emergence coughing with prolonged extubation time, besides sleep disturbance. D 0.4, D 0.5, and D 0.6 reduced agitation and sustained hemodynamic stability. Finally, the four doses applied were effective in shivering attenuation.

Preparation of High Thermo-Stability and Compactness Microencapsulated Phase Change Materials with Polyurea/Polyurethane/Polyamine Three-Composition Shells through Interfacial Polymerization.

In the preparation of microencapsulated phase change materials (MicroPCMs) with a three-composition shell through interfacial polymerization, the particle size, phase change behaviors, core contents, encapsulation efficiency morphology, thermal stability and chemical structure were investigated. The compactness of the MicroPCMs was analyzed through high-temperature drying and weighing. The effect of the core/shell ratio and stirring rate of the system was studied. The results indicated that the microcapsules thus-obtained possessed a spherical shape and high thermal stability and the surfaces were intact and compact. Furthermore, in the emulsification stage, the stirring speed had a significant influence on the microcapsules' particle size, and smaller particles could be obtained under the higher stirring speed, and the distributions were more uniform in these cases. When the core/shell ratio was lower than 4, both the core content and the encapsulation efficiency was high. Additionally, when the core/shell ratio was higher than 4, the encapsulation efficiency was decreased significantly. The three-composition shell greatly increased the compactness of microcapsules, and when the core/shell ratio was adjusted to 3, the mass loss of the MicroPCMs was lower than 6% after drying at 120 °C for 1 h. After the microencapsulation, double exothermic peaks appeared on the crystallization curve of the MicroPCMs, the crystallization mechanism was changed from the heterogeneous nucleation to the homogeneous nucleation and the super cooling degree was enhanced.

Tuberculosis Diagnosis by Metagenomic Next-generation Sequencing on Bronchoalveolar Lavage Fluid: a cross-sectional analysis.

BACKGROUND: Metagenomic next-generation sequencing (mNGS) is an effective diagnostic method for infectious diseases, however, its clinical utility for tuberculosis (TB) diagnosis remains to be demonstrated. METHODS: A total of 322 bronchoalveolar lavage fluid (BALF) samples were collected from 311 suspected and confirmed pulmonary TB patients and tested by mNGS, acid-fast bacillus (AFB) smear by microscopy, Xpert® MTB/RIF (Xpert), mycobacterium culture and bacterial/fungal culture. Diagnostic performance of mNGS was compared with conventional methods for detection of Mycobacterium tuberculosis complex (MTBC) and other pathogens in BALF. Underlying factors associated with positive detection in pulmonary TB patients were investigated. RESULTS: mNGS, Xpert and culture presented a high proportion of complete matching for MTBC detection (244/322, 75.8%). In pulmonary TB patients pre-treatment the sensitivity of MTBC detection by mNGS, Xpert, culture and smear was 59.9% (85/142), 69.0% (98/142), 59.9% (85/142) and 24.6% (35/142), respectively, and 79.6% overall; MTBC was detected by mNGS in 33.2% (5/34) Xpert and culture negative samples. Positive MTBC detection by mNGS was affected by Vitamin D, erythrocyte sedimentation rate, TB initial treatment/retreatment, and cavity in chest imaging (χ2 = 37.42, P < 0.001), but not by prior anti-TB therapy within 3 months. mNGS was able to detect new potential pathogens in 8.7% (28/322) of samples. CONCLUSIONS: Combining mNGS with conventional detection methods could increase the detection rate for MTBC. Additionally, mNGS could identify pathogens in a non-targeted approach for better diagnosis of coinfection.

Corrigendum to "Loss of SNHG4 Attenuated Spinal Nerve Ligation-Triggered Neuropathic Pain through Sponging miR-423-5p".

[This corrects the article DOI: 10.1155/2020/2094948.].

Astaxanthin promotes M2 macrophages and attenuates cardiac remodeling after myocardial infarction by suppression inflammation in rats.

BACKGROUND: Cardiac remodeling after acute myocardial infarction (AMI) is an important process. The present study aimed to assess the protective effects of astaxanthin (ASX) on cardiac remodeling after AMI. METHODS: The study was conducted between April and September 2018. To create a rat AMI model, rats were anesthetized, and the left anterior descending coronary artery was ligated. The rats in the ASX group received 10 mg·kg·day ASX by gavage for 28 days. On the 1st day after AMI, but before ASX administration, six rats from each group were sacrificed to evaluate changes in the heart function and peripheral blood (PB) levels of inflammatory factors. On the 7th day after AMI, eight rats from each group were sacrificed to evaluate the PB levels of inflammatory factors and the M2 macrophage count using both immunofluorescence (IF) and flow cytometry (FC). The remaining rats were observed for 28 days. Cardiac function was examined using echocardiography. The inflammatory factors, namely, tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), and IL-10, were assessed using enzyme-linked immunosorbent assay. The heart weight/body weight (BW), and lung weight (LW)/BW ratios were calculated, and myocardial fibrosis in the form of collagen volume fraction was measured using Masson trichrome staining. Hematoxylin and eosin (H&E) staining was used to determine the myocardial infarct size (MIS), and TdT-mediated dUTP nick-end labeling staining was used to analyze the myocardial apoptosis index. The levels of apoptosis-related protein, type I/III collagen, transforming growth factor ß1 (TGF-ß1), metalloproteinase 9 (MMP9), and caspase 3 were assessed by Western blotting. Unpaired t-test, one-way analysis of variance, and non-parametric Mann-Whitney test were used to analyze the data. RESULTS: On day 1, cardiac function was worse in the ASX group than in the sham group (left ventricular end-systolic diameter [LVIDs]: 0.72 ±â€Š0.08 vs. 0.22 ±â€Š0.06 cm, t = -11.38; left ventricular end-diastolic diameter [LVIDd]: 0.89 ±â€Š0.09 vs. 0.48 ±â€Š0.05 cm, t = -9.42; end-systolic volume [ESV]: 0.80 [0.62, 0.94] vs. 0.04 [0.03, 0.05] mL, Z = -2.89; end-diastolic volume [EDV]: 1.39 [1.03, 1.49] vs. 0.28 [0.22, 0.32] mL, Z = -2.88; ejection fraction [EF]: 0.40 ±â€Š0.04 vs. 0.86 ±â€Š0.05, t = 10.00; left ventricular fractional shortening [FS] rate: 0.19 [0.18, 0.20] %FS vs. 0.51 [0.44, 0.58] %FS, Z = -2.88, all P < 0.01; n = 6). The levels of inflammatory factors significantly increased (TNF-α: 197.60 [133.89, 237.94] vs. 50.48 [47.21 57.10] pg/mL, Z = -2.88; IL-1ß: 175.23 [160.74, 215.09] vs. 17.78 [16.83, 19.56] pg/mL, Z = -2.88; IL-10: 67.64 [58.90, 71.46] vs. 12.33 [11.64, 13.98] pg/mL, Z = -2.88, all P < 0.01; n = 6). On day 7, the levels of TNF-α and IL-1ß were markedly lower in the ASX group than in the AMI group (TNF-α: 71.70 [68.60, 76.00] vs. 118.07 [106.92, 169.08] pg/mL, F = 42.64; IL-1ß: 59.90 [50.83, 73.78] vs. 151.60 [108.4, 198.36] pg/mL, F = 44.35, all P < 0.01, n = 8). Conversely, IL-10 levels significantly increased (141.84 [118.98, 158.36] vs. 52.96 [42.68, 74.52] pg/mL, F = 126.67, P < 0.01, n = 8). The M2 macrophage count significantly increased (2891.42 ±â€Š211.29 vs. 1583.38 ±â€Š162.22, F = 274.35, P < 0.01 by immunofluorescence test; 0.96 ±â€Š0.18 vs. 0.36 ±â€Š0.05, F = 46.24, P < 0.05 by flowcytometry test). On day 28, cardiac function was better in the ASX group than in the AMI group (LVIDs: 0.50 [0.41, 0.56] vs. 0.64 [0.56, 0.74] cm, Z = -3.60; LVIDd: 0.70 [0.60, 0.76] vs. 0.80 [0.74 0.88] cm, Z = -2.96; ESV: 0.24 [0.18, 0.45] vs. 0.58 [0.44, 0.89] mL, Z = -3.62; EDV: 0.76 [0.44, 1.04] vs. 1.25 [0.82, 1.46] mL, Z = -2.54; EF: 0.60 ±â€Š0.08 vs. 0.50 ±â€Š0.12, F = 160.48; %FS: 0.29 [0.24, 0.31] vs. 0.20 [0.17, 0.21], Z = -4.43, all P < 0.01; n = 16). The MIS and LW/BW ratio were markedly lower in the ASX group than in the AMI group (myocardial infarct size: 32.50 ±â€Š1.37 vs. 50.90 ±â€Š1.73, t = 23.63, P < 0.01, n = 8; LW/BW: 1.81 ±â€Š0.15 vs. 2.17 ±â€Š0.37, t = 3.66, P = 0.01, n = 16). The CVF was significantly lower in the ASX group than in the AMI group: 12.88 ±â€Š2.53 vs. 28.92 ±â€Š3.31, t = 10.89, P < 0.01, n = 8. The expression of caspase 3, TGF-ß1, MMP9, and type I/III collagen was lower in the ASX group than in the AMI group (caspase 3: 0.38 ±â€Š0.06 vs. 0.66 ±â€Š0.04, t = 8.28; TGF-ß1: 0.37 ±â€Š0.04 vs. 0.62 ±â€Š0.07, t = 6.39; MMP9: 0.20 ±â€Š0.06 vs. 0.40 ±â€Š0.06, t = 4.62; type I collagen: 0.42 ±â€Š0.09 vs. 0.74 ±â€Š0.07, t = 5.73; type III collagen: 0.13 ±â€Š0.02 vs. 0.74 ±â€Š0.07, t = 4.32, all P < 0.01; n = 4). CONCLUSIONS: ASX treatment after AMI may promote M2 macrophages and effectively attenuate cardiac remodeling by inhibiting inflammation and reducing myocardial fibrosis.

Demographic census confirms a stable population of the critically-endangered caryophyllid coral Polycyathus chaishanensis (Scleractinia; Caryophyllidae) in the Datan Algal Reef, Taiwan.

Polycyathus chaishanensis is a symbiotic caryophyllid coral described from a single population in a tidal pool off Chaishan, Kaohsiung, Taiwan. Due to its rarity, P. chaishanensis was declared a critically-endangered species under the Taiwan Wildlife Protection Act. In May 2017, a P. chaishanensis colony was discovered in the intertidal area of the Datan Algal Reef, Taoyuan, Taiwan. To determine whether this is a stable population in the algal reef, a demographic census-including data on occurrence, distribution, and colony size-was carried out in the algal reef in southern Taoyuan. Intertidal censuses and sediment collections were conducted at five different sections-Baiyu, Datan G1, Datan G2, Yongxing, and Yongan algal reefs-during the monthly spring low tide from July 2018 to January 2019. In total, 84 colonies-23 in Datan G1 and 61 in Datan G2-were recorded from a tidal range of - 160 to - 250 cm, according to the Taiwan Vertical Datum 2001 compiled by the Central Weather Bureau. No P. chaishanensis was found in Baiyu, Yongxing, or Yongan. The P. chaishanensis colony sizes ranged from 2.55 to 81.5 cm in diameter, with the larger P. chaishanensis present in the lower intertidal zone. Sediment was extremely high, with monthly site averages ranging from 3,818.26 to 29,166.88 mg cm-2 day-1, and there was a significant difference between sites and months, both of which affected the distribution of P. chaishanensis in the algal reef. Our study confirms the existence of a second population of P. chaishanensis in Taiwan, highlighting the importance of the Datan Algal Reef for the survival and protection of this critically-endangered caryophyllid coral and why it is so urgent that the reef should be conserved.

Loss of SNHG4 Attenuated Spinal Nerve Ligation-Triggered Neuropathic Pain through Sponging miR-423-5p.

Neuropathic pain is an intractable comorbidity of spinal cord injury. Increasing noncoding RNAs have been implicated in neuropathic pain development. lncRNAs have been recognized as significant regulators of neuropathic pain. lncRNA Small Nucleolar RNA Host Gene 4 (SNHG4) is associated with several tumors. However, the molecular mechanisms of SNHG4 in neuropathic pain remain barely documented. Here, we evaluated the function of SNHG4 in spinal nerve ligation (SNL) rat models. We observed that SNHG4 was significantly upregulated in SNL rat. Knockdown of SNHG4 was able to attenuate neuropathic pain progression via regulating behaviors of neuropathic pain including mechanical and thermal hyperalgesia. Moreover, knockdown of SNHG4 could repress the neuroinflammation via inhibiting IL-6, IL-12, and TNF-α while inducing IL-10 levels. Additionally, miR-423-5p was predicted as the target of SNHG4 by employing bioinformatics analysis. miR-423-5p has been reported to exert significantly poorer in several diseases. However, the role of miR-423-5p in the development of neuropathic pain is needed to be clarified. Here, in our investigation, RIP assay confirmed the correlation between miR-423-5p and SNHG4. Meanwhile, we found that miR-423-5p was significantly decreased in SNL rat models. SNHG4 regulated miR-423-5p expression negatively. As exhibited, the loss of miR-423-5p contributed to neuropathic pain progression, which was rescued by the silence of SNHG4. Therefore, our study indicated SNHG4 as a novel therapeutic target for neuropathic pain via sponging miR-423-5p.

Leptoria phrygia in Southern Taiwan shuffles and switches symbionts to resist thermal-induced bleaching.

Symbiodiniaceae communities in some corals often shuffle or switch after severe bleaching events, one of the major threats to coral survival in a world with climate change. In this study we reciprocally transplanted five Leptoria phrygia colonies between two sites with significantly different temperature regimes and monitored them for 12 months. Our ITS2 amplicon deep sequencing demonstrated that L. phrygia acclimatized to maintain a strong and stable association with Durusdinium D17, D. trenchii, and D. glynnii, but also remained flexible and formed a short-term association with different Cladocopium. Most interestingly, two colonies shuffled between Durusdinium and Cladocopium without the occurrence of bleaching; one colony even switched its dominant Cladocopium after generic shuffling. Both dominant Cladocopium were originally rare with relative abundances as low as 0.024%. This is the first record of adult corals switching dominant symbiont without bleaching.

Propofol Attenuates Hypoxia/Reoxygenation-Induced Apoptosis and Autophagy in HK-2 Cells by Inhibiting JNK Activation.

PURPOSE: The aim of this study was to investigate whether propofol could attenuate hypoxia/reoxygenation-induced apoptosis and autophagy in human renal proximal tubular cells (HK-2) by inhibiting JNK activation. MATERIALS AND METHODS: HK-2 cells were treated with or without propofol or JNK inhibitor SP600125 for 1 hour and then subjected to 15 hours of hypoxia and 2 hours of reoxygenation (H/R). Cell viability and LDH release were measured with commercial kits. Cell apoptosis was evaluated by flow cytometry. The expressions of p-JNK, cleaved-caspase-3, Bcl-2, and autophagy markers LC3 and p62 were measured by Western blot or immunofluorescence. RESULTS: HK-2 cells exposed to H/R insult showed higher cell injury (detected by increased LDH release and decreased cell viability), increased cell apoptosis index and expression of cleaved-caspase-3, a decrease in the expression of Bcl-2 accompanied by increased expression of p-JNK and LC3II, and a decrease in expression of p62. All of these alterations were attenuated by propofol treatment. Similar effects were provoked upon treatment with the JNK inhibitor SP600125. Moreover, the protective effects were more obvious with the combination of propofol and SP600125. CONCLUSION: These results suggest that propofol could attenuate hypoxia/reoxygenation induced apoptosis and autophagy in HK-2 cells, probably through inhibiting JNK activation.

TLR7 mediates increased vulnerability to ischemic acute kidney injury in diabetes.

OBJECTIVE: Diabetes is a risk factor for acute kidney injury (AKI). However, its mechanism of pathogenesis has not been elucidated. The aim of the study was to investigate the role of inflammation and the toll-like receptor 7 (TLR7) in ischemic AKI for diabetes. METHODS: A high glucose hypoxia-reoxygenation model of human renal tubular epithelial (HK-2) cells was used to generate AKI induced by ischemia-reperfusion in diabetes. The activity of cells was measured by CCK-8 assay and LDH activity. Inflammatory cytokines were assessed by ELISA. TLR7, MyD88, and NF-κB expressions were examined by western blotting. Apoptosis was evaluated by flow cytometry. RESULTS: The high glucose group and low glucose group were subjected to hypoxia-reoxygenation. The low glucose group developed only mild cell damage, apoptosis, and inflammatory response. In contrast, an equivalent hypoxia-reoxygenation injury provoked severe cell damage, apoptosis, and inflammatory response in the high glucose group. Expression of TLR7 and its related proteins were measured in the high glucose group before and after hypoxia-reoxygenation. The high glucose group exhibited more significant increases in TLR7 expression following hypoxia-reoxygenation than the low glucose group. In addition, the expression of TLR7 and its related proteins after hypoxia-reoxygenation were higher in the high glucose group than in the low glucose group. Inhibition of TLR7 provides significant protection against ischemic injury in diabetes. CONCLUSION: Our results suggest that diabetes increases the vulnerability to ischemia-induced renal injury. This increased vulnerability originates from a heightened inflammatory response involving the TLR7 signal transduction pathway.

TLR7 mediates increased vulnerability to ischemic acute kidney injury in diabetes

SUMMARY OBJECTIVE Diabetes is a risk factor for acute kidney injury (AKI). However, its mechanism of pathogenesis has not been elucidated. The aim of the study was to investigate the role of inflammation and the toll-like receptor 7 (TLR7) in ischemic AKI for diabetes. METHODS A high glucose hypoxia-reoxygenation model of human renal tubular epithelial (HK-2) cells was used to generate AKI induced by ischemia-reperfusion in diabetes. The activity of cells was measured by CCK-8 assay and LDH activity. Inflammatory cytokines were assessed by ELISA. TLR7, MyD88, and NF-κB expressions were examined by western blotting. Apoptosis was evaluated by flow cytometry. RESULTS The high glucose group and low glucose group were subjected to hypoxia-reoxygenation. The low glucose group developed only mild cell damage, apoptosis, and inflammatory response. In contrast, an equivalent hypoxia-reoxygenation injury provoked severe cell damage, apoptosis, and inflammatory response in the high glucose group. Expression of TLR7 and its related proteins were measured in the high glucose group before and after hypoxia-reoxygenation. The high glucose group exhibited more significant increases in TLR7 expression following hypoxia-reoxygenation than the low glucose group. In addition, the expression of TLR7 and its related proteins after hypoxia-reoxygenation were higher in the high glucose group than in the low glucose group. Inhibition of TLR7 provides significant protection against ischemic injury in diabetes. CONCLUSION Our results suggest that diabetes increases the vulnerability to ischemia-induced renal injury. This increased vulnerability originates from a heightened inflammatory response involving the TLR7 signal transduction pathway.

RESUMO OBJETIVO O diabetes é um fator de risco para a lesão renal aguda (LRA). No entanto, seu mecanismo de patogênese não foi elucidado. O objetivo do estudo foi investigar o papel da inflamação e do receptor Toll-like 7 (TLR7) na LRA isquêmica no diabetes. MÉTODOS Um modelo de hipóxia-reoxigenação de células epiteliais tubulares renais humanas (HK-2) na presença de concentrações altas de glicose foi utilizado para gerar LRA induzida por isquemia-reperfusão em diabetes. A atividade das células foi medida pelo ensaio Cell Counting Kit-8 (CCK-8) e pela atividade da lactato desidrogenase (LDH). As citocinas inflamatórias foram avaliadas por ensaio imunoenzimático (Elisa). A expressão de TLR7, do fator de diferenciação mieloide 88 (MyD88) e do fator de transcrição nuclear-κB (NF-κB) foi examinada por Western blotting. A apoptose foi avaliada por citometria de fluxo. RESULTADOS Os grupos glicose alta e glicose baixa foram submetidos à hipóxia-reoxigenação. O grupo de baixa glicose desenvolveu apenas danos celulares ligeiros, apoptose e uma resposta inflamatória. Em contraste, no grupo de alta glicose, uma lesão equivalente de hipóxia-reoxigenação provocou danos celulares graves, apoptose e uma resposta inflamatória. A expressão de TLR7 e suas proteínas relacionadas foi medida no grupo de alta glicose antes e após a hipóxia-reoxigenação. O grupo de alta glicose exibiu maiores aumentos na expressão de TLR7 após hipóxia-reoxigenação do que o grupo de baixa glicose. Além disso, a expressão de TLR7 e suas proteínas relacionadas após a hipóxia-reoxigenação foi maior no grupo com alto nível de glicose do que no grupo com baixo nível de glicose. A inibição do TLR7 fornece proteção significativa contra a lesão isquêmica no diabetes. CONCLUSÃO Nossos resultados sugerem que o diabetes aumenta a vulnerabilidade à lesão renal induzida por isquemia. Essa vulnerabilidade acrescida tem por origem uma resposta inflamatória aumentada envolvendo a via de transdução de sinal do TLR7.

Temporal variation and photochemical efficiency of species in Symbiodinaceae associated with coral Leptoria phrygia (Scleractinia; Merulinidae) exposed to contrasting temperature regimes.

The Symbiodinaceae are paradoxical in that they play a fundamental role in the success of scleractinian corals, but also in their dismissal when under stress. In the past decades, the discovery of the endosymbiont's genetic and functional diversity has led people to hope that some coral species can survive bleaching events by associating with a stress-resistant symbiont that can become dominant when seawater temperatures increase. The variety of individual responses encouraged us to scrutinize each species individually to gauge its resilience to future changes. Here, we analyse the temporal variation in the Symbiodinaceae community associated with Leptoria phrygia, a common scleractinian coral from the Indo-Pacific. Coral colonies were sampled from two distant reef sites located in southern Taiwan that differ in temperature regimes, exemplifying a 'variable site' (VS) and a 'steady site' (SS). We investigated changes in the relative abundance of the dominant symbiont and its physiology every 3-4 months from 2016-2017. At VS, 11 of the 12 colonies were dominated by the stress-resistant Durusdinium spp. (>90% dominance) and only one colony exhibited co-dominance between Durusdinium spp. and Cladocopium spp. Every colony displayed high photochemical efficiency across all sampling periods, while showing temporal differences in symbiont density and chlorophyll a concentration. At SS, seven colonies out of 13 were dominated by Cladocopium spp., five presented co-dominance between Durusdinium spp./Cladocopium spp. and only one was dominated by Durusdinium spp. Colonies showed temporal differences in photochemical efficiency and chlorophyll a concentration during the study period. Our results suggest that VS colonies responded physiologically better to high temperature variability by associating with Durusdinium spp., while in SS there is still inter-colonial variability, a feature that might be advantageous for coping with different environmental changes.

LBP reduces theinflammatory injuryof kidney in septic rat and regulates the Keap1-Nrf2∕ARE signaling pathway1.

PURPOSE: To investigate the influence of lycium barbarum polysaccharides (LBP), a functional derivative from lycium barbarum, on septic kidney injury. METHODS: The SD male rats were randomly divided into 8 groups. The concentration of IL-1ß, IL-6, IL-8, TNF-α, NF-κB and ROS, in kidney cortex homogenates after 12 h treatments were determined by enzyme-linked immunosorbent assay and ROS test kit, respectively. Morphology observation of kidney tissue was conducted with HE staining. The mRNA and protein expression levels of Nrf2, HO-1, NQO1, NF-κB, and Keap1 in kidney tissues were determined by qRT-PCR and Western blot, respectively. RESULTS: LPS treatment significantly increased the oxidative stress. After LBP treatment, the ROS content reduced significantly in a dose-depend manner. However, the levels of HO-1, NQO1 and Nrf2 as molecular elements that respond to oxidative stress were further increased. Also, administration of LBP increased the levels of NF-κB and Keap1, and decreased the levels of Nrf2 in the Keap 1-Nrf2∕ARE signaling pathway. By administrating the brusatol, the inhibition of Nrf2 enhanced the expression of NF-κB, inhibits the antioxidant responses, and further reverse the protective effect of LBP on the LPS induced septic kidney injury. CONCLUSION: Lycium barbarum polysaccharides can reduce inflammation and activate the antioxidant responses via regulating the level of pro-inflammatory cytokines and the Keap1-Nrf2/ARE signaling pathway.

LBP reduces theinflammatory injuryof kidney in septic rat and regulates the Keap1-Nrf2∕ARE signaling pathway

Abstract Purpose: To investigate the influence of lycium barbarum polysaccharides (LBP), a functional derivative from lycium barbarum, on septic kidney injury. Methods: The SD male rats were randomly divided into 8 groups. The concentration of IL-1β, IL-6, IL-8, TNF-α, NF-κB and ROS, in kidney cortex homogenates after 12 h treatments were determined by enzyme-linked immunosorbent assay and ROS test kit, respectively. Morphology observation of kidney tissue was conducted with HE staining. The mRNA and protein expression levels of Nrf2, HO-1, NQO1, NF-κB, and Keap1 in kidney tissues were determined by qRT-PCR and Western blot, respectively. Results: LPS treatment significantly increased the oxidative stress. After LBP treatment, the ROS content reduced significantly in a dose-depend manner. However, the levels of HO-1, NQO1 and Nrf2 as molecular elements that respond to oxidative stress were further increased. Also, administration of LBP increased the levels of NF-κB and Keap1, and decreased the levels of Nrf2 in the Keap 1-Nrf2∕ARE signaling pathway. By administrating the brusatol, the inhibition of Nrf2 enhanced the expression of NF-κB, inhibits the antioxidant responses, and further reverse the protective effect of LBP on the LPS induced septic kidney injury. Conclusion: Lycium barbarum polysaccharides can reduce inflammation and activate the antioxidant responses via regulating the level of pro-inflammatory cytokines and the Keap1-Nrf2/ARE signaling pathway.

Correction: Complete chloroplast genome sequence of common bermudagrass (Cynodon dactylon (L.) Pers.) and comparative analysis within the family Poaceae.

[This corrects the article DOI: 10.1371/journal.pone.0179055.].

Complete chloroplast genome sequence of common bermudagrass (Cynodon dactylon (L.) Pers.) and comparative analysis within the family Poaceae.

Common bermudagrass (Cynodon dactylon (L.) Pers.) belongs to the subfamily Chloridoideae of the Poaceae family, one of the most important plant families ecologically and economically. This grass has a long connection with human culture but its systematics is relatively understudied. In this study, we sequenced and investigated the chloroplast genome of common bermudagrass, which is 134,297 bp in length with two single copy regions (LSC: 79,732 bp; SSC: 12,521 bp) and a pair of inverted repeat (IR) regions (21,022 bp). The annotation contains a total of 128 predicted genes, including 82 protein-coding, 38 tRNA, and 8 rRNA genes. Additionally, our in silico analyses identified 10 sets of repeats longer than 20 bp and predicted the presence of 36 RNA editing sites. Overall, the chloroplast genome of common bermudagrass resembles those from other Poaceae lineages. Compared to most angiosperms, the accD gene and the introns of both clpP and rpoC1 genes are missing. Additionally, the ycf1, ycf2, ycf15, and ycf68 genes are pseudogenized and two genome rearrangements exist. Our phylogenetic analysis based on 47 chloroplast protein-coding genes supported the placement of common bermudagrass within Chloridoideae. Our phylogenetic character mapping based on the parsimony principle further indicated that the loss of the accD gene and clpP introns, the pseudogenization of four ycf genes, and the two rearrangements occurred only once after the most recent common ancestor of the Poaceae diverged from other monocots, which could explain the unusual long branch leading to the Poaceae when phylogeny is inferred based on chloroplast sequences.

Winding paths to simplicity: genome evolution in facultative insect symbionts.

Symbiosis between organisms is an important driving force in evolution. Among the diverse relationships described, extensive progress has been made in insect­bacteria symbiosis, which improved our understanding of the genome evolution in host-associated bacteria. Particularly, investigations on several obligate mutualists have pushed the limits of what we know about the minimal genomes for sustaining cellular life. To bridge the gap between those obligate symbionts with extremely reduced genomes and their non-host-restricted ancestors, this review focuses on the recent progress in genome characterization of facultative insect symbionts. Notable cases representing various types and stages of host associations, including those from multiple genera in the family Enterobacteriaceae (class Gammaproteobacteria), Wolbachia (Alphaproteobacteria) and Spiroplasma (Mollicutes), are discussed. Although several general patterns of genome reduction associated with the adoption of symbiotic relationships could be identified, extensive variation was found among these facultative symbionts. These findings are incorporated into the established conceptual frameworks to develop a more detailed evolutionary model for the discussion of possible trajectories. In summary, transitions from facultative to obligate symbiosis do not appear to be a universal one-way street; switches between hosts and lifestyles (e.g. commensalism, parasitism or mutualism) occur frequently and could be facilitated by horizontal gene transfer.

Early-Onset Convulsive Seizures Induced by Brain Hypoxia-Ischemia in Aging Mice: Effects of Anticonvulsive Treatments.

Aging is associated with an increased risk of seizures/epilepsy. Stroke (ischemic or hemorrhagic) and cardiac arrest related brain injury are two major causative factors for seizure development in this patient population. With either etiology, seizures are a poor prognostic factor. In spite of this, the underlying pathophysiology of seizure development is not well understood. In addition, a standardized treatment regimen with anticonvulsants and outcome assessments following treatment has yet to be established for these post-ischemic seizures. Previous studies have modeled post-ischemic seizures in adult rodents, but similar studies in aging/aged animals, a group that mirrors a higher risk elderly population, remain sparse. Our study therefore aimed to investigate early-onset seizures in aging animals using a hypoxia-ischemia (HI) model. Male C57 black mice 18-20-month-old underwent a unilateral occlusion of the common carotid artery followed by a systemic hypoxic episode (8% O2 for 30 min). Early-onset seizures were detected using combined behavioral and electroencephalographic (EEG) monitoring. Brain injury was assessed histologically at different times post HI. Convulsive seizures were observed in 65% of aging mice post-HI but not in control aging mice following either sham surgery or hypoxia alone. These seizures typically occurred within hours of HI and behaviorally consisted of jumping, fast running, barrel-rolling, and/or falling (loss of the righting reflex) with limb spasms. No evident discharges during any convulsive seizures were seen on cortical-hippocampal EEG recordings. Seizure development was closely associated with acute mortality and severe brain injury on brain histological analysis. Intra-peritoneal injections of lorazepam and fosphenytoin suppressed seizures and improved survival but only when applied prior to seizure onset and not after. These findings together suggest that seizures are a major contributing factor to acute mortality in aging mice following severe brain ischemia and that early anticonvulsive treatment may prevent seizure genesis and improve overall outcomes.

Complete Genome Sequence of Agrobacterium tumefaciens Ach5.

Agrobacterium tumefaciens is a phytopathogenic bacterium that causes crown gall disease. The strain Ach5 was isolated from yarrow (Achillea ptarmica L.) and is the wild-type progenitor of other derived strains widely used for plant transformation. Here, we report the complete genome sequence of this bacterium.