¿Es rentable «pensar por pensar»? Evidencia sobre innovación en España

ResumenLa evolución significativamente creciente de la investigación básica privada en EE. UU., Europa y Japón sugiere una fuerte asociación entre la capacidad de innovación y las actividades de investigación de las empresas destinadas estrictamente a trabajar en la vanguardia del conocimiento científico. Este trabajo indaga en las posibles razones de esta asociación utilizando una muestra de 8.416 empresas incluidas en el Panel de Innovación Tecnológica. Nuestros resultados ponen de manifiesto que la investigación básica mejora la habilidad de las empresas para asimilar, integrar y valorizar el conocimiento ajeno, y que de esta forma muestran sistemáticamente mayores niveles de innovación. Además, el artículo sugiere que esta capacidad para explotar el conocimiento externo puede llegar a condicionar la estrategia de la empresa a la hora de decidir operar en ciertos entornos con sistemas de propiedad intelectual más o menos desarrollados. Desde el punto de vista de la política pública, los resultados cuestionan el apoyo a las actividades de innovación más cercanas al mercado en detrimento de otras políticas con mayor capacidad para abordar externalidades relacionadas con el desarrollo del capital humano, la reducción de la incertidumbre de las inversiones, las asimetrías de información entre agentes o los problemas derivados de spillovers tecnológicos no deseados.AbstractThe significantly increasing evolution of private basic research in the U.S.A., Europe and Japan suggests a strong association between the capacity for innovation and research activities aimed strictly to work at the forefront of scientific knowledge. This paper explores the possible reasons for this association using a sample of 8,416 companies in the Spanish Technology Innovation Panel. Our results show that basic research enhances the ability of firms to assimilate, integrate and enhance other businesses’ knowledge, thus leading consistently to higher levels of innovation. In addition, the article suggests that the ability to exploit external knowledge can condition the business strategy when deciding to operate in certain environments with more or less developed intellectual property systems. From the standpoint of public policy, results question the support for innovation activities closer to the market to the detriment of other policies with greater capacity to address externalities related to the development of human capital, reducing the uncertainty of investments, addressing information asymmetries between agents or solving the problems inherent in accidental technology spillovers

La investigación básica en las empresas innovadoras españolas: un análisis exploratorio

El objetivo de este trabajo es analizar desde un punto de vista descriptivo las empresasque realizan investigación básica frente a las que no la realizan y determinar aquellas característicasque mejor las identifican. Para ello, utilizaremos los datos del Panel de Innovación TecnológicaPITEC (2003-2007). Los resultados obtenidos pueden parecer paradójicos, ya que aunque se observaque el número de empresas que realizan investigación básica es cada vez menor, estas empresasobtienen mejores resultados que aquellas que no realizan este tipo de investigación

La investigación básica en las empresas innovadoras españolas: un análisis exploratorio

El objetivo de este trabajo es analizar desde un punto de vista descriptivo las empresas que realizan investigación básica frente a las que no la realizan y determinar aquellas características que mejor las identifican. Para ello, utilizaremos los datos del Panel de Innovación Tecnológica PITEC (2003-2007). Los resultados obtenidos pueden parecer paradójicos, ya que aunque se observa que el número de empresas que realizan investigación básica es cada vez menor, estas empresas obtienen mejores resultados que aquellas que no realizan este tipo de investigación

The Role of SMEs’ Green Business Models in the Transition to a Low-Carbon Economy: Differences in Their Design and Degree of Adoption Stemming from Business Size

The purpose of this paper is to analyze how SMEs define the components of their business models (value proposition, creation and capture) from the point of view of decarbonization. We analyze SMEs as a group, and study whether their size affects this process and, in both cases, we examine evolution over time. We use a database comprising 1161 observations of SMEs, 466 in 2014, and 695 in 2016. The results show that SMEs’ value propositions give an intermediate valuation to both legally required and voluntary reduction of environmental impact, irrespective of SME size and the year analyzed. Regarding value creation, SMEs adopt practically no environmental practices, and there are significant differences according to size, with more difficulties than advantages stemming from small size. The study also shows that such environmental practices are not effective in reducing carbon. This diagnosis indicates that SMEs need help from the administration if they are to play a key role in the process of transformation toward a low-carbon economy. Legislative actions involving harsher environmental protection measures might help shape value propositions that place greater importance on reducing environmental impact, whereas training actions on available environmental techniques, promotion of research on how to adapt such techniques to SMEs and the development of specific practices for SMEs might enhance environmental value creation and capture in their BMs

Overcoming the dark side of subnational start-up support policies: a pilot project for facilitating cross-border cooperation in Europe

Business start-up support policies have gained significant attention from policymakers, largely due to their immediate impacts and the positive media coverage they receive. However, the widespread adoption of these policies has often led to a fragmented landscape characterised by limited coordination, especially in countries with multi-tiered governmental structures. As a result, the full potential of public investments is hindered. This study aims to identify and address the key challenges associated with these policies, offering valuable insights drawn from a collaborative initiative within the Galicia–Northern Portugal Euroregion. The findings provide practical and scalable guidance for research institutions, businesses, and policymakers seeking to establish effective partnerships, prioritise objectives and achieve substantial impact in cross-border regions.</p

Central nicotine induces browning through hypothalamic κ opioid receptor

[ENG]Increased body weight is a major factor that interferes with smoking cessation. Nicotine, the main bioactive compound in tobacco, has been demonstrated to have an impact on energy balance, since it affects both feeding and energy expenditure at the central level. Among the central actions of nicotine on body weight, much attention has been focused on its effect on brown adipose tissue (BAT) thermogenesis, though its effect on browning of white adipose tissue (WAT) is unclear. Here, we show that nicotine induces the browning of WAT through a central mechanism and that this effect is dependent on the κ opioid receptor (KOR), specifically in the lateral hypothalamic area (LHA). Consistent with these findings, smokers show higher levels of uncoupling protein 1 (UCP1) expression in WAT, which correlates with smoking status. These data demonstrate that central nicotine-induced modulation of WAT browning may be a target against human obesityThe research leading to these results has received funding from the Xunta de Galicia (J.L.L.-G.: ED431C 2018/10; R.N.: 2015-CP080 and 2016-PG057; M.L.: 2015-CP079 and 2016-PG068); Ministerio de Economía y Competitividad (MINECO) co-funded by the FEDER Program of EU (J.L.L.-G.: BFU2015–70523; R.N.: BFU2015–70664R; C.D.: BFU2017–87721-P; M.L.: RTI2018-101840-B100; BFU2015–70454-REDT/Adipoplast and RTI2018–101840-B-I00); Instituto de Salud Carlos III (J.L.L.-G.: RD16/0011/0016; J.M.F.-R.: PI15–01934); European Molecular Biology Organization (A.D.: EMBO-Installation Grant 3037); Human Frontier Science Program (A.D.: HFSP-RGY0070/2016); Howard Hughes Medical Institute (A.D.: HHMI-208576/Z/17/Z); US National Institutes of Health (K.R.: HL084207); American Heart Association (K.R.: EIA#14EIA18860041); the University of Iowa Fraternal Order of Eagles Diabetes Research Center (K.R.); Atresmedia Corporación (R.N. and M.L.: 2017-PO004); Fundación BBVA (R.N.), European Foundation for the Study of Diabetes (R.N.); and ERC Synergy Grant-2019-WATCH-810331 (R.N.). P.S.-C. is recipient of a fellowship from Xunta de Galicia (ED481B 2018/050). L.L.-P. is recipient of a fellowship from Xunta de Galicia (ED481A-2016/094); E.R.-P. is recipient of a fellowship from MINECO (BES-2015–072743). N.M.-S. is recipient of a fellowship from Xunta de Galicia (ED481B 2016/168–0) and from the European Union’s Horizon 2020 research and innovation programme under the Marie Sklodowska-Curie actions. The CiMUS is supported by the Xunta de Galicia (2016–2019, ED431G/05). CIBER de Fisiopatología de la Obesidad y Nutrición is an initiative of ISCIIIS

Inhibition of carnitine palmitoyl-transferase 1A in hepatic stellate cells protects against fibrosis

Background & Aims The pathogenesis of liver fibrosis requires activation of hepatic stellate cells (HSCs); once activated, HSCs lose intracellular fatty acids but the role of fatty acid oxidation and carnitine palmitoyltransferase 1A (CPT1A) in this process remains largely unexplored. Methods CPT1A was found in HSCs of patients with fibrosis. Pharmacological and genetic manipulation of CPT1A were done in HSCs human cell lines and primary HCSs. Finally, we induced fibrosis in mice lacking CPT1A specifically in HSCs. Results Here we show that CPT1A expression is elevated in HSCs of patients with NASH, showing a positive correlation with the fibrosis score. This was corroborated in rodents with fibrosis, as well as in primary human HSCs and LX-2 cells activated by transforming growth factor β1 (TGFβ1) and fetal bovine serum (FBS). Furthermore, both pharmacological and genetic silencing of CPT1A prevent TGFβ1- and FBS-induced HSC activation by reducing mitochondrial activity. The overexpression of CPT1A, induced by saturated fatty acids and reactive oxygen species, triggers mitochondrial function and the expression of fibrogenic markers. Finally, mice lacking CPT1A specifically in HSCs are protected against fibrosis, induced by a choline-deficient high fat diet, a methionine- and choline-deficient diet, or treatment with carbon tetrachloride. Conclusions These results indicate that CPT1A plays a critical role in activation of HSCs and is implicated in the development of liver fibrosis, making it a potentially actionable target for fibrosis treatment. Lay summary We show that CPT1A located in HSCs is elevated in patients and mice models with fibrosis, and that CPT1A induces the activation of these cells. Inhibition of CPT1A ameliorates fibrosis by preventing the activation of HSCs

Inhibition of ATG3 ameliorates liver steatosis by increasing mitochondrial function

Background & aims: Autophagy-related gene 3 (ATG3) is an enzyme mainly known for its actions in the LC3 lipidation process, which is essential for autophagy. Whether ATG3 plays a role in lipid metabolism or contributes to non-alcoholic fatty liver disease (NAFLD) remains unknown. Methods: By performing proteomic analysis on livers from mice with genetic manipulation of hepatic p63, a regulator of fatty acid metabolism, we identified ATG3 as a new target downstream of p63. ATG3 was evaluated in liver samples from patients with NAFLD. Further, genetic manipulation of ATG3 was performed in human hepatocyte cell lines, primary hepatocytes and in the livers of mice. Results: ATG3 expression is induced in the liver of animal models and patients with NAFLD (both steatosis and non-alcoholic steatohepatitis) compared with those without liver disease. Moreover, genetic knockdown of ATG3 in mice and human hepatocytes ameliorates p63- and diet-induced steatosis, while its overexpression increases the lipid load in hepatocytes. The inhibition of hepatic ATG3 improves fatty acid metabolism by reducing c-Jun N-terminal protein kinase 1 (JNK1), which increases sirtuin 1 (SIRT1), carnitine palmitoyltransferase 1a (CPT1a), and mitochondrial function. Hepatic knockdown of SIRT1 and CPT1a blunts the effects of ATG3 on mitochondrial activity. Unexpectedly, these effects are independent of an autophagic action. Conclusions: Collectively, these findings indicate that ATG3 is a novel protein implicated in the development of steatosis. Lay summary: We show that autophagy-related gene 3 (ATG3) contributes to the progression of non-alcoholic fatty liver disease in humans and mice. Hepatic knockdown of ATG3 ameliorates the development of NAFLD by stimulating mitochondrial function. Thus, ATG3 is an important factor implicated in steatosis. Keywords: ATG3; NAFLD; NASH; lipid metabolism; mitochondria; sirtuin 1