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Purpose Against the background of increasing infrastructure loss in many rural areas, this study aims to contribute conceptually and empirically towards better understanding of rural innovation processes related to provision of public goods. Design/methodology/approach The nationally focused understanding of innovation processes leads the debate on rural development into a dilemma that this study seeks to sidestep via the concept of social innovation. Community cooperatives – a type of social enterprise that has increasingly emerged in rural areas of Germany in the past decade – offer the opportunity to examine social innovation processes. This cross-case study reveals the broad range of activities in which such cooperatives are active and analyses their social innovation processes. Findings The study shows that the social innovation governance framework enables examination of social innovation processes. Although macro-level policy has appeared to be an important instrument for financing social innovation, public actors at the micro-level seem barely able to initiate social innovation processes unless they are also private actors and, therefore, can pursue additional incentives. The social innovations studied here seem to differ in terms of their actor constellations and resource-allocation patterns, depending on whether they are concerned with the establishment or maintenance of local infrastructure. What they have in common, however, is the initiation of formalised collective-action processes that serve to legitimise social innovation. Originality/value By applying an analytical framework that is new to the literature on social innovation, the study provides insight into the activities and decision-making processes of actors involved in social innovation in rural areas. In this context, community cooperatives have rarely been studied as an interface between public, private and civil society actors or as a platform for mobilising human, social and financial capital.

The extent to which the digitalisation of agriculture will make a significant contribution to solving urgent sustainability challenges will depend on the design of political, legal and economic frameworks. In this context, social discourses play a central role as they not only reflect collective interpretations and systems of meaning but also reproduce power relations in “truth regimes” and prepare policy actions. While a critical scientific debate on unintended side effects of the digital transformation on agriculture has recently emerged, there is little knowledge about the discourse relations beyond academia. This article presents the results of a discourse analysis during a two-day online conference on the digital transformation of the agricultural value chain. We systematically visited and analysed sessions and presentations. The aim was to identify the main themes, concepts and ideas and different perspectives among actors from science and practice. The results show a wide range of perceived opportunities and challenges but also controversies, especially regarding governance issues such as regulation versus nonregulation, centralised versus decentralised data sharing, the appropriate design of data sovereignty models and trust and evolving inequalities. In addition, it became apparent that discourses on digitalisation are largely expert affairs. We discuss and conclude that a sustainability-oriented digital transformation requires a critical perspective, reflexivity and an adaptive governance approach where science–society collaborations play a central role.

Current debates on climate change have led to an increased demand for sustainable commodities. Serving this demand, sustainability certification schemes and eco-friendly labels have become prominent mechanisms of climate governance. Smallholder farmers in Jambi province, Indonesia, producing palm oil and rubber as the two dominant smallholder crops, are impacted by this distal demand. Zimmerer et al. (2018) suggest analyzing the potential sustainability in such a context with the multilevel smallholder telecoupling framework. Applying this framework to case studies from Jambi province, our first case reveals that smallholder certification for so-called sustainable palm oil does not necessarily influence smallholder towards more sustainable management practices. One explanation might be a discrepancy in sustainability perception between sender and receiver systems. The second case is the setup of an allegedly eco-friendly rubber plantation. The establishment of this model plantation is implemented by a transnational corporation in collaboration with a nature conservation organization, impacting the access to land for adjacent smallholders. The struggle over access to land is not only negotiated between smallholders and the corporation producing &ldquo, eco-friendly&rdquo, rubber but also between smallholders and big land mammals lacking access to land since the rubber plantation began to be established. We argue that the concept of sustainability as demanded by the receiving system does not mirror management practices in the sending system, even though the products reach the Global North as supposedly socially and climate-friendly. The smallholder telecoupling framework is helpful for assessing potential sustainability but can be expanded towards conflictive spillovers, second order effects, and a mismatch in sustainability perceptions in order to draw a more comprehensive picture.

Peroxisomes are essential for intermediary lipid metabolism, but the role of these organelles has been primarily studied in the liver. We recently generated aP2 – Pex5 conditional knockout mice that due to the nonselectivity of the aP2 promoter, not only had dysfunctional peroxisomes in the adipose tissue but also in the central and peripheral nervous system, besides some other tissues. Peroxisomes were however intact in the liver, heart, pancreas and muscle. Surprisingly, these mice not only showed dysfunctional white adipose tissue with increased fat mass and reduced lipolysis but also the skeletal muscle was affected including impaired shivering thermogenesis, reduced motor performance and increased insulin resistance. Non-shivering thermogenesis by brown adipose tissue was not altered. Strongly reduced levels of plasma adrenaline and to a lesser extent noradrenaline, impaired expression of catecholamine synthesizing enzymes in the adrenal medulla and reversal of all pathologies after administration of the β-agonist isoproterenol indicated that β-adrenergic signaling was reduced. Based on normal white adipose and muscle function in Nestin – Pex5 and Wnt – Pex5 knockout mice respectively, it is unlikely that peroxisome absence from the central and peripheral nervous system caused the phenotype. We conclude that peroxisomal metabolism is necessary to maintain the adrenergic tone in mice, which in turn determines metabolic homeostasis.

aP2-Cre mice have amply been used to generate conditional adipose selective inactivation of important signaling molecules. We show that the efficiency of Cre mediated recombination in adipocytes and adipose selectivity is not always guaranteed. In particular, Cre activity was found in ganglia of the peripheral nervous system (PNS), in adrenal medulla and in neurons throughout the central nervous system (CNS). Because these tissues have an important impact on adipose tissue, care should be taken when using aP2-Cre mice to define the role of the targeted genes in adipose tissue function.

Background: Hypotonia-Cystinuria syndrome (HCS) and 2p21 deletion syndrome are 2 recessive contiguous gene deletion syndromes associated with cystinuria type I. The deletions differ in size and the number of genes involved. In HCS patients, only SLC3A1 and PREPL are disrupted. In the 2p21 deletion syndrome 2 additional genes (C2orf34 and PPM1B) are lost. Objective: Clinical and molecular analysis of 2 siblings who presented with an atypical HCS phenotype. Methods: Molecular analysis of the SLC3A1/PREPL locus was performed in the patients using qPCR methods. Results: HCS in both siblings was confirmed with the deletion screen of the SLC3A1/PREPL locus. Fine mapping of the breakpoint revealed a deletion of 77.4 kb, including 3 genes: SLC3A1, PREPL and C2orf34. Features not present in classical HCS were a mild/moderate mental retardation and a respiratory chain complex IV deficiency documented in patient 2. Conclusions: We report the first patients with a deletion of SLC3A1, PREPL and C2orf34. They present with a phenotype intermediate between HCS and 2p21 deletion syndrome. These patients facilitate the elucidation of the contribution of each gene to the phenotype in the different 2p21 deletion syndromes.

Peroxisome deficiency in men causes severe pathology in several organs, particularly in the brain and liver, but it is still unknown how metabolic abnormalities trigger these defects. In the present study, a mouse model with hepatocyte-selective elimination of peroxisomes was generated by inbreeding Pex5-loxP and albumin-Cre mice to investigate the consequences of peroxisome deletion on the functioning of hepatocytes. Besides the absence of catalase-positive peroxisomes, multiple ultrastructural alterations were noticed, including hepatocyte hypertrophy and hyperplasia, smooth endoplasmic reticulum proliferation, and accumulation of lipid droplets and lysosomes. Most prominent was the abnormal structure of the inner mitochondrial membrane, which bore some similarities with changes observed in Zellweger patients. This was accompanied by severely reduced activities of complex I, III, and V and a collapse of the mitochondrial inner membrane potential. Surprisingly, these abnormalities provoked no significant disturbances of adenosine triphosphate (ATP) levels and redox state of the liver. However, a compensatory increase of glycolysis as an alternative source of ATP and mitochondrial proliferation were observed. No evidence of oxidative damage to proteins or lipids nor elevation of oxidative stress defence mechanisms were found. Altered expression of peroxisome proliferator-activated receptor alpha (PPAR-α) regulated genes indicated that PPAR-α is activated in the peroxisome-deficient cells. In conclusion, the absence of peroxisomes from mouse hepatocytes has an impact on several other subcellular compartments and metabolic pathways but is not detrimental to the function of the liver parenchyma. Supplementary material for this article can be found on the HEPATOLOGYwebsite (http://interscience.wiley.com/jpages/0270-9139/suppmat/index.html). (HEPATOLOGY 2005.)

Mice with inactivation of the D-specific multifunctional protein 2 (MFP2), a crucial enzyme of peroxisomal beta-oxidation, develop multiple pathologies in diverse tissues already starting in the postnatal period. Gene expression profiling performed on liver of 2-day-old pups revealed up-regulation of PPAR alpha responsive genes in knockout mice. Surprisingly, also genes involved in cholesterol biosynthesis were markedly induced. Real-time PCR confirmed the induction of PPAR alpha target genes and of HMGCR and SREBP2, both involved in cholesterol synthesis, in lactating and in adult MFP2 knockout mice. In accordance, the rate of cholesterol biosynthesis was significantly increased in liver of knockout mice but the hepatic cholesterol concentration was unaltered. In MFP2/PPAR alpha double knockout mice, up-regulations of SREBP2 and HMGCR were markedly attenuated. These data demonstrate a tight interrelationship between induction of PPAR alpha by endogenous ligands and up-regulation of genes of cholesterol biosynthesis through increased expression of SREBP2.

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In coronary artery disease (CAD) the individual variation in aerobic power and the response to physical training are largely unexplained.1 The gene coding for the angiotensin converting enzyme (ACE) is expressed in several types of somatic cells, including vascular cells, heart, lung, and muscles.2 Intron 16 contains a polymorphism characterised by the presence (insertion (I)) or absence (deletion (D)) of a 287 bp Alu repeat sequence,3 which has been associated with endurance related phenotypes and the response to training.4 The objective of the present study was to investigate the role of ACE I/D polymorphism on aerobic power and its response to physical training in patients with CAD enrolled in the CAREGENE (cardiac rehabilitation and genetics of exercise performance) study. Biologically unrelated white patients with CAD (mean (SE) age 56 (0.3) years) who had achieved evident exhaustion during graded cycle ergometer testing before and after three months of physical training (three sessions weekly) from 1990 through 2001 (n = 1095) were eligible for inclusion. The methods for graded exercise testing and training have been …