Energy efficiency, productivity and exporting: firm-level evidence in Latin America

This work explores the relationship between energy efficiency, productivity and exporting for a sample of firms located in thirty Latin American and Caribbean (LAC) countries. This relationship has not been studied in depth although it is important and relevant to policymaking. We apply a standard constant returns to scale Cobb-Douglas production function with labor, capital, and knowledge expanded to exports and energy efficiency. We also investigate the relationship between energy efficiency and exporting and take heterogeneity by firms and industries into account. Firm-level data come from the national representative World Bank Enterprise Survey (WBES). Our empirical analysis finds heterogeneous results by firm size and industrial sector both in the relationship between energy efficiency and productivity and between energy efficiency and exporting. These outcomes are robust to different measures of energy efficiency and controlling for heterogeneity among countries and provinces. By providing for the first time an extensive investigation of energy intensity and firm performance for such a large sample of LAC countries, this work contributes to the lively debate on LAC energy efficiency and weak productivity. By adopting a broader productivity and international trade perspective, it opens the ground to a rethinking of the priorities of energy saving policies and their environmental impacts

Network Analysis of World Trade using the BACI-CEPII dataset

In this paper we explore the BACI-CEPII database using Network Analysis. Starting from the visualization of the World Trade Network, we then define and describe the topology of the network, both in its binary version and in its weighted version, calculating and discussing some of the commonly used network's statistics. We finally discuss some specic topics that can be studied using Network Analysis and International Trade data, both at the aggregated and sectoral level. The analysis is done using multiple software (Stata, R, and Pajek). The scripts to replicate part of the analysis are included in the appendix, and can be used as an handson tutorial. Moreover,the World Trade Network local and global centrality measures, for the unweighted and the weighted version of the Network, calculated using the bilateral aggregate trade data for each country (178 in total) and each year (from 1995 to 2010,) can be downloaded from the CEPII webpage

An immunohistochemically positive E-cadherin status is not always predictive for a good prognosis in human breast cancer

BACKGROUND: in primary breast cancers dichotomic classification of E-cadherin expression, according to an arbitrary cutoff, may be inadequate and lead to loss of prognostic significance or contrasting prognostic indications. We aimed to assess the prognostic value of high and low E-cadherin levels in a consecutive case series (204 cases) of unilateral node-negative non-lobular breast cancer patients with a 8-year median follow-up and that did not receive any adjuvant therapy after surgery. METHODS: expression of E-cadherin was investigated by immunohistochemistry and assessed according to conventional score (0, 1+, 2+, 3+). Multiple correspondence analysis was used to visualise associations of both categorical and continuous variables. The impact of E-cadherin expression on patients outcome was evaluated in terms of event-free survival curves by the Kaplan-Meier method and proportional hazard Cox model. RESULTS: respect to intermediate E-cadherin expression values (2+), high (3+) or low (0 to 1+) E-cadherin expression levels had a negative prognostic impact. In fact, both patients with a low-to-nil (score 0 to 1+) expression level of E-cadherin and patients with a high E-cadherin expression level (score 3+) demonstrated an increased risk of failure (respectively, hazard ratio (HR)=1.71, confidence interval (CI)=0.72-4.06 and HR=4.22, CI=1.406-12.66) and an interesting association with young age. CONCLUSIONS: the findings support the evidence that high expression values of E-cadherin are not predictive for a good prognosis and may help to explain conflicting evidence on the prognostic impact of E-cadherin in breast cancer when assessed on dichotomic basis

ASOSIASI LAMUN DAN ECHINODERMATA PADA EKOSISTEM PADANG LAMUN CAGAR ALAM LEUWEUNG SANCANG, JAWA BARAT

ABSTRACTThe Leuweung Sancang Nature Reserve has ecosystem diversity, including seagrass beds, with a variaety of natural resources that are important to be preserved. Apart from being a food source for herbivorous organisms, seagrass beds also function as shelter and breed for many marine invertebrates, including Echinoderms. Association between Echinoderms and seagrass was observed in this study to investigate the interaction. Sampling was carried out in 1x1 m2 plots which were placed in 3  transect  lines  of 250 m long, with a plot intervals of 25 m on each transect line.  The transect line extended from the beach heading to the shore, and was carried out in 4 different stations, namely Ciporeang, Cipunaga, Cikolomberan, and Cipangikisan. Observation had been done to determine diversity, density, coverage, and evenness of both seagrass and Echinoderms, thus to study the correlation between them. The results showed that there were 2 seagrass species, Thalassia hempricii and Cymodocea rotundata, and there were 2 families of Echinoderms: Ophiocomidae and Holothuridae. Result of Rank–Spearman correlation coefficient showed possitive association between seagrass and echinoderms in all stations being observed, but only in Cikolomberan that showed significantly high association.Keywords:  association, Echinoderms, Leuweung Sancang, seagrass.ABSTRAKCagar alam Leuweung Sancang memiliki keanekaragaman ekosistem, termasuk padang lamun, dengan berbagai sumber daya alam di dalamnya yang penting untuk dijaga kelestariannya. Selain sebagai sumber makanan bagi organisme herbivor, padang lamun juga berfungsi sebagai tempat berlindung dan berkembang biak bagi banyak invertebrata laut, termasuk Echinodermata. Keterkaitan antara Echinodermata dan lamun diobservasi pada studi ini untuk dipelajari untuk melihat interaksinya. Pengambilan sampel dilakukan dalam plot 1 x 1 m2 yang ditempatkan pada 3 garis transek masing-masing sepanjang 250 m dengan interval plot sejauh 25 m pada setiap garis transek. Garis transek terbentang dari pantai menuju laut, dan dilakukan pada 4 stasiun yang berbeda, yaitu Ciporeang, Cipunaga, Cikolomberan, Cipangikisan. Pengamatan dilakukan untuk menentukan keragaman, kepadatan, frekuensi, tutupan dan kemerataan lamun dan Echinodermata, untuk kemudian dilihat asosiasinya. Hasil menunjukkan bahwa di keempat stasiun pengamatan ditemukan 2 spesies lamun yaitu Thalassia hempricii dan Cymodocea rotundata dan 2 famili Echinodermata: Ophiocomidae dan Holothuridae. Hasil koefisien korelasi Rank-Spearman pada keempat stasiun pengamatan menunjukan adanya asosiasi positif antara lamun dan Echinodermata, namun hanya di Cikolomberan yang memiliki asosiasi tinggi dan signifikan.Kata kunci: asosiasi, Echinodermata, Leuweung Sancang, lamun

Both base excision repair and O-6-methylguanine-DNA methyltransferase protect against methylation-induced colon carcinogenesis

Methylating agents are widely distributed environmental carcinogens. Moreover, they are being used in cancer chemotherapy. The primary target of methylating agents is DNA, and therefore, DNA repair is the first-line barrier in defense against their toxic and carcinogenic effects. Methylating agents induce in the DNA O[superscript 6]-methylguanine (O[superscript 6]MeG) and methylations of the ring nitrogens of purines. The lesions are repaired by O[superscript 6]-methylguanine-DNA methyltransferase (Mgmt) and by enzymes of the base excision repair (BER) pathway, respectively. Whereas O[superscript 6]MeG is well established as a pre-carcinogenic lesion, little is known about the carcinogenic potency of base N-alkylation products such as N3-methyladenine and N3-methylguanine. To determine their role in cancer formation and the role of BER in cancer protection, we checked the response of mice with a targeted gene disruption of Mgmt or N-alkylpurine-DNA glycosylase (Aag) or both Mgmt and Aag, to azoxymethane (AOM)-induced colon carcinogenesis, using non-invasive mini-colonoscopy. We demonstrate that both Mgmt- and Aag-null mice show a higher colon cancer frequency than the wild-type. With a single low dose of AOM (3 mg/kg) Aag-null mice showed an even stronger tumor response than Mgmt-null mice. The data provide evidence that both BER initiated by Aag and O[superscript 6]MeG reversal by Mgmt are required for protection against alkylation-induced colon carcinogenesis. Further, the data indicate that non-repaired N-methylpurines are not only pre-toxic but also pre-carcinogenic DNA lesions.Deutsche Forschungsgemeinschaft (DFG) (FOR 527)Deutsche Forschungsgemeinschaft (DFG) (DFG KA 724/13-3)Deutsche Forschungsgemeinschaft (DFG) (WI 3304/1-1

Epithelial p38α Controls Immune Cell Recruitment in the Colonic Mucosa

Intestinal epithelial cells (IECs) compose the first barrier against microorganisms in the gastrointestinal tract. Although the NF-κB pathway in IECs was recently shown to be essential for epithelial integrity and intestinal immune homeostasis, the roles of other inflammatory signaling pathways in immune responses in IECs are still largely unknown. Here we show that p38α in IECs is critical for chemokine expression, subsequent immune cell recruitment into the intestinal mucosa, and clearance of the infected pathogen. Mice with p38α deletion in IECs suffer from a sustained bacterial burden after inoculation with Citrobacter rodentium. These animals are normal in epithelial integrity and immune cell function, but fail to recruit CD4+ T cells into colonic mucosal lesions. The expression of chemokines in IECs is impaired, which appears to be responsible for the impaired T cell recruitment. Thus, p38α in IECs contributes to the host immune responses against enteric bacteria by the recruitment of immune cells

An intestinal epithelial defect conferring ER stress results in inflammation involving both innate and adaptive immunity

We recently characterized Winnie mice carrying a missense mutation in Muc2, leading to severe endoplasmic reticulum stress in intestinal goblet cells and spontaneous colitis. In this study, we characterized the immune responses due to this intestinal epithelial dysfunction. In Winnie, there was a fourfold increase in activated dendritic cells (DCs; CD11c+ major histocompatibility complex (MHC) class IIhi) in the colonic lamina propria accompanied by decreased colonic secretion of an inhibitor of DC activation, thymic stromal lymphopoietin (TSLP). Winnie also displayed a significant increase in mRNA expression of the mucosal TH17 signature genes Il17a, IL17f, Tgfb, and Ccr6, particularly in the distal colon. Winnie mesenteric lymph node leukocytes secreted multiple TH1, TH2, and TH17 cytokines on activation, with a large increase in interleukin-17A (IL-17A) progressively with age. A major source of mucosal IL-17A in Winnie was CD4+ T lymphocytes. Loss of T and B lymphocytes in Rag1-/- × Winnie (RaW) crosses did not prevent spontaneous inflammation but did prevent progression with age in the colon but not the cecum. Adoptive transfer of naive T cells into RaW mice caused more rapid and severe colitis than in Rag1-/-, indicating that the epithelial defect results in an intestinal microenvironment conducive to T-cell activation. Thus, the Winnie primary epithelial defect results in complex multicytokine-mediated colitis involving both innate and adaptive immune components with a prominent IL-23/TH17 response, similar to that of human ulcerative colitis

Innate Immune Activation in Intestinal Homeostasis

Loss of intestinal immune regulation leading to aberrant immune responses to the commensal microbiota are believed to precipitate the chronic inflammation observed in the gastrointestinal tract of patients with inflammatory bowel diseases (IBD), Crohn's disease and ulcerative colitis. Innate immune receptors that recognize conserved components derived from the microbiota are widely expressed by both epithelial cells and leucocytes of the gastrointestinal tract and play a key role in host protection from infectious pathogens; yet precisely how pathogenic and commensal microbes are distinguished is not understood. Furthermore, aberrant innate immune activation may also drive intestinal pathology, as patients with IBD exhibit extensive infiltration of innate immune cells to the inflamed intestine, and polymorphisms in many innate immunity genes influence susceptibility to IBD. Thus, a balanced interaction between the microbiota and innate immune activation is required to maintain a healthy mutualistic relationship between the microbiota and the host, which when disturbed can result in intestinal inflammation

Intestinal Epithelial-Derived TAK1 Signaling Is Essential for Cytoprotection against Chemical-Induced Colitis

We have previously reported that intestinal epithelium-specific TAK1 deleted mice exhibit severe inflammation and mortality at postnatal day 1 due to TNF-induced epithelial cell death. Although deletion of TNF receptor 1 (TNFR1) can largely rescue those neonatal phenotypes, mice harboring double deletion of TNF receptor 1 (TNFR1) and intestinal epithelium-specific deletion of TAK1 (TNFR1KO/TAK1(IE)KO) still occasionally show increased inflammation. This indicates that TAK1 is important for TNF-independent regulation of intestinal integrity.In this study, we investigated the TNF-independent role of TAK1 in the intestinal epithelium. Because the inflammatory conditions were sporadically developed in the double mutant TNFR1KO/TAK1(IE)KO mice, we hypothesize that epithelial TAK1 signaling is important for preventing stress-induced barrier dysfunction. To test this hypothesis, the TNFR1KO/TAK1(IE)KO mice were subjected to acute colitis by administration of dextran sulfate sodium (DSS). We found that loss of TAK1 significantly augments DSS-induced experimental colitis. DSS induced weight loss, intestinal damages and inflammatory markers in TNFR1KO/TAK1(IE)KO mice at higher levels compared to the TNFR1KO control mice. Apoptosis was strongly induced and epithelial cell proliferation was decreased in the TAK1-deficient intestinal epithelium upon DSS exposure. These suggest that epithelial-derived TAK1 signaling is important for cytoprotection and repair against injury. Finally, we showed that TAK1 is essential for interleukin 1- and bacterial components-induced expression of cytoprotective factors such as interleukin 6 and cycloxygenase 2.Homeostatic cytokines and microbes-induced intestinal epithelial TAK1 signaling regulates cytoprotective factors and cell proliferation, which is pivotal for protecting the intestinal epithelium against injury