Carbon dioxide system in the Canary region during October 1995

During the cruise F/S Poseidon 212/3 (September 30-October 8, 1995) determination of carbon system variables was carried out over the section of La Palma-La Graciosa and at the ESTOC station in the Canary Island area. Total alkalinity and pH in the total scale at 25 degreesC were determined at 24 stations from surface to bottom. In this area, the presence of different water masses can be traced by the carbon system variables. NACW is defined by a strong gradient of A(T) and pH from 150 to 750 m. MW is characterised by high values of A(T) and pH between 1000 to 1200 in and AAIW signals are found at around 900 in in the strait between Gran Canaria and Fuerteventura with low A(T), low pH and a maximum of fCO(2). Assuming an atmospheric mean value of fCO(2) of 360 mu atm and an average surface value of 393 +/-7 mu atm, we can conclude that during this cruise this oceanic area tends to release CO2 into the atmosphere, acting as a weak source with a carbon flux towards the atmosphere of +8.0 +/-1.8 mmol.m(-2)d(-1). The saturation levels in the Canary Island area have been found to be higher than 3600 m for calcite and 2700 in for aragonite. The inorganic carbon/organic carbon ratio (IC/OC) varies from 0.07 at 300 m to 0.5 at 3000 m. The IC/OC ratio shows that about a 34% increase in the C-T of the deep water is contributed by the inorganic CaCO3 dissolution. The IC at 300 in is around 7 mu mol kg(-1), increasing with depth to 37.5 mu mol kg(-1) at 3700 m

Growth Rate and Associated Factors in Small Abdominal Aortic Aneurysms

AbstractObjectiveTo study the growth rate and factors influencing progression of small infrarenal abdominal aortic aneurysms (AAA).DesignObservational, longitudinal, prospective study.Patients and methodsWe followed patients with AAA <5cm in diameter in two groups. Group I (AAA 3–3.9cm, n=246) underwent annual ultrasound scans. Group II (AAA 4–4.9cm, n=106) underwent 6-monthly CT scans.ResultsWe included 352 patients (333 men and 19 women) followed for a mean of 55.2±37.4 months (6.3–199.8). The mean growth rate was significantly greater in group II (4.72±5.93 vs. 2.07±3.23mm/year; p<0.0001). Group II had a greater percentage of patients with rapid aneurysm expansion (>4mm/year) (36.8 vs. 13.8%; p<0.0001). The classical cardiovascular risk factors did not influence the AAA growth rate in group I. Chronic limb ischemia was associated with slower expansion (≤4mm/year) (OR 0.47; CI 95% 0.22–0.99; p=0.045). Diabetic patients in group II had a significantly smaller mean AAA growth rate than non-diabetics (1.69±3.51 vs. 5.22±6.11mm/year; p=0.032).ConclusionsThe expansion rate of small AAA increases with the AAA size. AAA with a diameter of 3–3.9cm expand slowly, and they are very unlikely to require surgical repair in 5 years. Many 4–4.9cm AAA can be expected to reach a surgical size in the first 2 years of follow-up. Chronic limb ischemia and diabetes are associated with reduced aneurysm growth rates

An expedient synthesis of tetrakis (cyclopropylmethyl) methane

Synthesis of tetrakis(cyclopropylmethyl)methane, a new symmetric product has been described using the radical mediated gem-diallylation of cyclopropylmethyl xanthate as a key step and its single crystal X-ray analysis established its C2-symmetry

Analysis of Kink Reduction in SOI MOSFET Using Selective Back Oxide Structure

This paper presents a complete analysis of the kink effect in SOI MOSFET and proposes a method for eliminating kink effect observed in the current-voltage output characteristics of a partially depleted SOI MOSFET device. In this method, back oxide for the device is introduced at selected regions below the source and drain and not continuously as in an SOI device giving rise to what is termed a “SELBOX” structure. Selective back oxide structure with different gap lengths and thicknesses was studied. Results obtained through numerical simulations indicate that the proposed structure can significantly reduce the kink while still preserving major advantages offered by conventional SOI structure. Although the new structure is capable of eliminating kink, for narrow gaps the device may still exhibit some kink effect. A device model that explains the kink behavior of the structure for varying gap lengths is also developed

TREM-2 plays a protective role in cholestasis by acting as a negative regulator of inflammation

Background & Aims: Inflammation, particularly that mediated by bacterial components translocating from the gut to the liver and binding to toll-like receptors (TLRs), is central to cholestatic liver injury. The triggering receptor expressed on myeloid cells-2 (TREM-2) inhibits TLR-mediated signaling and exerts a protective role in hepatocellular injury and carcinogenesis. This study aims to evaluate the role of TREM-2 in cholestasis.Methods: TREM-2 expression was analyzed in the livers of pa-tients with primary biliary cholangitis (PBC) or primary scle-rosing cholangitis (PSC), and in mouse models of cholestasis. Wild-type (WT) and Trem-2 deficient (Trem-2-/-) mice were subjected to experimental cholestasis and gut sterilization. Pri-mary cultured Kupffer cells were incubated with lipopolysac-charide and/or ursodeoxycholic acid (UDCA) and inflammatory responses were analyzed.Results: TREM-2 expression was upregulated in the livers of patients with PBC or PSC, and in murine models of cholestasis. Compared to WT, the response to bile duct ligation (BDL)-induced obstructive cholestasis or alpha-naphtylisothiocyanate (ANIT)-induced cholestasis was exacerbated in Trem-2-/-mice. This was characterized by enhanced necroptotic cell death, in-flammatory responses and biliary expansion. Antibiotic treat-ment partially abrogated the effects observed in Trem-2-/-mice after BDL. Experimental overexpression of TREM-2 in the liver of WT mice downregulated ANIT-induced IL-33 expression and neutrophil recruitment. UDCA regulated Trem-1 and Trem-2 expression in primary cultured mouse Kupffer cells and damp-ened inflammatory gene transcription via a TREM-2-dependent mechanism.Conclusions: TREM-2 acts as a negative regulator of inflamma-tion during cholestasis, representing a novel potential thera-peutic target.Lay summary: Cholestasis (the reduction or cessation of bile flow) causes liver injury. This injury is exacerbated when gut-derived bacterial components interact with receptors (spe-cifically Toll-like receptors or TLRs) on liver-resident immune cells, promoting inflammation. Herein, we show that the anti-inflammatory receptor TREM-2 dampens TLR-mediated signaling and hence protects against cholestasis-induced liver injury. Thus, TREM-2 could be a potential therapeutic target in cholestasis.Spanish Carlos III Health Institute (ISCIII) [J.M. Banales (FIS PI18/01075, PI21/00922 and Miguel Servet Program CPII19/00008); M.J. Perugorria (FIS PI14/00399, PI17/00022 and PI20/00186); J.J.G. Marin (FIS PI16/00598 and PI19/00819); P.M. Rodrigues (Sara Borrell CD19/00254)] cofinanced by “Fondo Europeo de Desarrollo Regional” (FEDER); “Instituto de Salud Carlos III” [CIBERehd: M.J. Monte, J.J.G. Marin, J.M. Banales, M.J. Perugorria, P. Aspichueta, P.M. Rodrigues and L. Bujanda], Spain; “Diputación Foral de Gipuzkoa” (M.J. Perugorria: DFG18/114), Department of Health of the Basque Country (M.J. Perugorria: 2019111024, 2015111100 and J.M. Banales: 2021111021), “Euskadi RIS3” (J.M. Banales: 2019222054, 2020333010, 2021333003), and Department of Industry of the Basque Country (J.M. Banales: Elkartek: KK-2020/00008); “Junta de Castilla y Leon” (J.J.G. Marin: SA063P17). La Caixa Scientific Foundation (J.M. Banales: HR17-00601). “Fundación Científica de la Asociación Española Contra el Cáncer” (AECC Scientific Foundation, to J.M. Banales and J.J.G. Marin); “Centro Internacional sobre el Envejecimiento” (J.J.G. Marin: OLD-HEPAMARKER, 0348_CIE_6_E); Fundació Marato TV3 (J.J.G. Marin: Ref. 201916-31). O Sharif was funded by the Austrian Science Fund (FWF-P35168). Work in the lab of T. Luedde was funded by the European Research Council (ERC) (Grant Agreement 771083), the German Research Foundation (DFG – LU 1360/3-2 (279874820), LU 1360/4-(1461704932) and SFB-CRC 1382-Project A01) and the German Ministry of Health (BMG – DEEP LIVER 2520DAT111). Contributions of M. Marzioni were funded by the Università Politecnica delle Marche PSA2017_UNIVPM grant. Contributions of DAM were supported by programme grants from CRUK (C18342/A23390) and MRC (MR/K0019494/1 and MR/R023026/1). MJ Perugorria was funded by the Spanish Ministry of Economy and Competitiveness (MINECO: “Ramón y Cajal” Programme RYC-2015-17755), I. Labiano, A. Agirre-Lizaso, P. Olaizola, A. Echebarria and F. González-Romero by the Basque Government (PRE_2016_1_0152, PRE_2018_1_0184, PRE_2016_1_0269 PRE_2020_1_0080, PRE_2018_1_0120, respectively), I. Olaizola by the Ministry of Universities (FPU 19/03327) and A. Esparza-Baquer by the University of the Basque Country (PIF2014/11). The funding sources had no involvement in study design, data collection and analysis, decision to publish, or preparation of the article

TREM-2 defends the liver against hepatocellular carcinoma through multifactorial protective mechanisms

[EN] Objective Hepatocellular carcinoma (HCC) is a prevalent and aggressive cancer usually arising on a background of chronic liver injury involving inflammatory and hepatic regenerative processes. The triggering receptor expressed on myeloid cells 2 (TREM-2) is predominantly expressed in hepatic non-parenchymal cells and inhibits Toll-like receptor signalling, protecting the liver from various hepatotoxic injuries, yet its role in liver cancer is poorly defined. Here, we investigated the impact of TREM-2 on liver regeneration and hepatocarcinogenesis. Design TREM-2 expression was analysed in liver tissues of two independent cohorts of patients with HCC and compared with control liver samples. Experimental HCC and liver regeneration models in wild type and Trem-2-/- mice, and in vitro studies with hepatic stellate cells (HSCs) and HCC spheroids were conducted. Results TREM-2 expression was upregulated in human HCC tissue, in mouse models of liver regeneration and HCC. Trem-2-/- mice developed more liver tumours irrespective of size after diethylnitrosamine (DEN) administration, displayed exacerbated liver damage, inflammation, oxidative stress and hepatocyte proliferation. Administering an antioxidant diet blocked DEN-induced hepatocarcinogenesis in both genotypes. Similarly, Trem-2-/- animals developed more and larger tumours in fibrosis-associated HCC models. Trem-2-/- livers showed increased hepatocyte proliferation and inflammation after partial hepatectomy. Conditioned media from human HSCs overexpressing TREM-2 inhibited human HCC spheroid growth in vitro through attenuated Wnt ligand secretion. Conclusion TREM-2 plays a protective role in hepatocarcinogenesis via different pleiotropic effects, suggesting that TREM-2 agonism should be investigated as it might beneficially impact HCC pathogenesis in a multifactorial manner.Spanish Ministry of Economy and Competitiveness and ’Instituto de Salud Carlos III’ grants (MJP (PI14/00399, PI17/00022 and Ramon y Cajal Programme RYC-2015–17755); JMB (PI12/00380, PI15/01132, PI18/01075, Miguel Servet Programme CON14/00129 and CPII19/00008) cofinanced by ’Fondo Europeo de Desarrollo Regional’ (FEDER); CIBERehd: MJP, JMB and LB), Spain; IKERBASQUE, Basque foundation for Science (MJP and JMB), Spain; ’Diputación Foral de Gipuzkoa’ (MJP: DFG18/114, DFG19/081; JMB: DFG15/010, DFG16/004); BIOEF (Basque Foundation for Innovation and Health Research: EiTB Maratoia BIO15/CA/016/ BD to JMB); Department of Health of the Basque Country (MJP: 2015111100 and 2019111024; JMB: 2017111010), Euskadi RIS3 (JMB: 2016222001, 2017222014, 2018222029, 2019222054, 2020333010) Department of Industry of the Basque Country (JMB: Elkartek: KK-2020/00008) and AECC Scientific Foundation (JMB). AE-B was funded by the University of the Basque Country (UPV/EHU) (PIF2014/11) and by the short-term training fellowship Andrew K Burroughs (European Association for the Study of the Liver, EASL). IL and AA-L were funded by the Department of Education, Language Policy and Culture of the Basque Government (PRE_2016_1_0152 and PRE_2018_1_0184). OS and SK were funded by the Austrian Science Fund (FWF25801-B22, FWF-P35168 to OS and L-Mac: F 6104-B21 to SK). FO and DAM were funded by a UK Medical Research Council programme Grant MR/R023026/1. DAM was also funded by the CRUK programme grant C18342/A23390, CRUK/AECC/AIRC Accelerator Award A26813 and the MRC MICA programme grant MR/R023026/1. JBA is supported by the Danish Medical Research Council, Danish Cancer Society, Nordisk Foundation, and APM Foundation. CJO’R and PM-G are supported by Marie Sklodowska-Curie Programme and EASL Sheila Sherlock postdoctoral fellowships

Ultrasensitive and fast voltammetric determination of iron in seawater by atmospheric oxygen catalysis in 500 l samples

[eng] A new method based on adsorptive cathodic stripping voltammetry with catalytic enhancement for the determination of total dissolved iron in seawater is reported. It was demonstrated that iron detection at the ultratrace level (0.1 nM) may be achieved in small samples (500 μL) with high sensitivity, no need for purging, no added oxidant, and a limit of detection of 5 pM. The proposed method is based on the adsorption of the complex Fe/2,3-dihydroxynaphthalene (DHN) exploiting the catalytic effect of atmospheric oxygen. As opposite to the original method (Obata, H.; van den Berg, C. M. Anal. Chem. 2001, 73, 2522−2528), atmospheric oxygen dissolved in solution replaced bromate ions in the oxidation of the iron complex: removing bromate reduces the blank level and avoids the use of a carcinogenic species. Moreover, the new method is based on a recently introduced hardware that enables the determinations to be performed in 500 μL samples. The analyses were carried out on buffered samples (pH 8.15, HEPPS 0.01 M), 10 μM DHN and iron quantified by the standard addition method. The sensitivity is 49 nA nM−1 min−1 with 30 s deposition time and the LOD is equal to 5 pM. As a result, the whole procedure for the quantification of iron in one sample requires around 7.5 min. The new method was validated via analysis on two reference samples (SAFe S and SAFe D2) with low iron content collected in the North Pacific Ocea