Minimizing losses at red meat supply chain with circular and central slaughterhouse model

Purpose: The purpose of this paper is to find solutions to improve the red meat sector in an emerging economy, Turkey, from the circular economy point of view, and taking sustainability approach. The need for circular management within the red meat sector in Turkey is emphasized by using Grey method. As theoretical contribution of this study, the investigation of the causes of losses at the slaughter stages of the red meat supply chain leads to proposals for sustainable and circular solutions. Design/methodology/approach: Grey method is used to predict the number of slaughtered cattle and the amount of bone and blood waste in the slaughtering process between 2018 and 2020. Findings: It is revealed that according to Grey prediction calculations, although the amount of slaughtered cattle, bone and blood waste seem have decreased between 2018 and 2020, there are still significant losses in Turkish red meat sector. For bone waste, this is expected to be 56,581,200 kg in 2018, 48,235,840 kg in 2019 and 41,121,380 kg in 2020. For blood waste, it is expected to be 24,754,275 kg in 2018, 21,103,180 kg in 2019 and 17,990,604 kg in 2020. Social implications: The proposed model in the study will contribute on sector revitalization, increase in product safety, quality and hygiene, development in the management of training and education centers for farmers/labors and increase in employment. Originality/value: This paper represents policymakers with a proposal for triple bottom line (TBL) based circular and central slaughterhouse model, based on TBL, which brings social, economic and environmental benefits for the red meat sector in Turkey

Food supply chain in the era of Industry 4.0: Blockchain technology implementation opportunities and impediments from the perspective of people, process, performance and technology

Royal Academy of Engineering for supporting the authors to visit Turkey through DVFM project [DVFM 1718_1_54] titled ‘Perishable food cold chain logistics in Turkey’

HIF-driven SF3B1 induces KHK-C to enforce fructolysis and heart disease.

Fructose is a major component of dietary sugar and its overconsumption exacerbates key pathological features of metabolic syndrome. The central fructose-metabolising enzyme is ketohexokinase (KHK), which exists in two isoforms: KHK-A and KHK-C, generated through mutually exclusive alternative splicing of KHK pre-mRNAs. KHK-C displays superior affinity for fructose compared with KHK-A and is produced primarily in the liver, thus restricting fructose metabolism almost exclusively to this organ. Here we show that myocardial hypoxia actuates fructose metabolism in human and mouse models of pathological cardiac hypertrophy through hypoxia-inducible factor 1α (HIF1α) activation of SF3B1 and SF3B1-mediated splice switching of KHK-A to KHK-C. Heart-specific depletion of SF3B1 or genetic ablation of Khk, but not Khk-A alone, in mice, suppresses pathological stress-induced fructose metabolism, growth and contractile dysfunction, thus defining signalling components and molecular underpinnings of a fructose metabolism regulatory system crucial for pathological growth

iCLIP Predicts the Dual Splicing Effects of TIA-RNA Interactions

Transcriptome-wide analysis of protein-RNA interactions predicts the dual splicing effects of TIA proteins, showing that their local enhancing function is associated with diverse distal splicing silencing effects

Human and mouse essentiality screens as a resource for disease gene discovery.

The identification of causal variants in sequencing studies remains a considerable challenge that can be partially addressed by new gene-specific knowledge. Here, we integrate measures of how essential a gene is to supporting life, as inferred from viability and phenotyping screens performed on knockout mice by the International Mouse Phenotyping Consortium and essentiality screens carried out on human cell lines. We propose a cross-species gene classification across the Full Spectrum of Intolerance to Loss-of-function (FUSIL) and demonstrate that genes in five mutually exclusive FUSIL categories have differing biological properties. Most notably, Mendelian disease genes, particularly those associated with developmental disorders, are highly overrepresented among genes non-essential for cell survival but required for organism development. After screening developmental disorder cases from three independent disease sequencing consortia, we identify potentially pathogenic variants in genes not previously associated with rare diseases. We therefore propose FUSIL as an efficient approach for disease gene discovery

Pathogenic Huntingtin Repeat Expansions in Patients with Frontotemporal Dementia and Amyotrophic Lateral Sclerosis.

We examined the role of repeat expansions in the pathogenesis of frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) by analyzing whole-genome sequence data from 2,442 FTD/ALS patients, 2,599 Lewy body dementia (LBD) patients, and 3,158 neurologically healthy subjects. Pathogenic expansions (range, 40-64 CAG repeats) in the huntingtin (HTT) gene were found in three (0.12%) patients diagnosed with pure FTD/ALS syndromes but were not present in the LBD or healthy cohorts. We replicated our findings in an independent collection of 3,674 FTD/ALS patients. Postmortem evaluations of two patients revealed the classical TDP-43 pathology of FTD/ALS, as well as huntingtin-positive, ubiquitin-positive aggregates in the frontal cortex. The neostriatal atrophy that pathologically defines Huntington's disease was absent in both cases. Our findings reveal an etiological relationship between HTT repeat expansions and FTD/ALS syndromes and indicate that genetic screening of FTD/ALS patients for HTT repeat expansions should be considered

Wounding induces dedifferentiation of epidermal Gata6+ cells and acquisition of stem cell properties

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An ancestral 10-bp repeat expansion in VWA1 causes recessive hereditary motor neuropathy.

The extracellular matrix comprises a network of macromolecules such as collagens, proteoglycans and glycoproteins. VWA1 (von Willebrand factor A domain containing 1) encodes a component of the extracellular matrix that interacts with perlecan/collagen VI, appears to be involved in stabilizing extracellular matrix structures, and demonstrates high expression levels in tibial nerve. Vwa1-deficient mice manifest with abnormal peripheral nerve structure/function; however, VWA1 variants have not previously been associated with human disease. By interrogating the genome sequences of 74 180 individuals from the 100K Genomes Project in combination with international gene-matching efforts and targeted sequencing, we identified 17 individuals from 15 families with an autosomal-recessive, non-length dependent, hereditary motor neuropathy and rare biallelic variants in VWA1. A single disease-associated allele p.(G25Rfs*74), a 10-bp repeat expansion, was observed in 14/15 families and was homozygous in 10/15. Given an allele frequency in European populations approaching 1/1000, the seven unrelated homozygote individuals ascertained from the 100K Genomes Project represents a substantial enrichment above expected. Haplotype analysis identified a shared 220 kb region suggesting that this founder mutation arose >7000 years ago. A wide age-range of patients (6-83 years) helped delineate the clinical phenotype over time. The commonest disease presentation in the cohort was an early-onset (mean 2.0 ± 1.4 years) non-length-dependent axonal hereditary motor neuropathy, confirmed on electrophysiology, which will have to be differentiated from other predominantly or pure motor neuropathies and neuronopathies. Because of slow disease progression, ambulation was largely preserved. Neurophysiology, muscle histopathology, and muscle MRI findings typically revealed clear neurogenic changes with single isolated cases displaying additional myopathic process. We speculate that a few findings of myopathic changes might be secondary to chronic denervation rather than indicating an additional myopathic disease process. Duplex reverse transcription polymerase chain reaction and immunoblotting using patient fibroblasts revealed that the founder allele results in partial nonsense mediated decay and an absence of detectable protein. CRISPR and morpholino vwa1 modelling in zebrafish demonstrated reductions in motor neuron axonal growth, synaptic formation in the skeletal muscles and locomotive behaviour. In summary, we estimate that biallelic variants in VWA1 may be responsible for up to 1% of unexplained hereditary motor neuropathy cases in Europeans. The detailed clinical characterization provided here will facilitate targeted testing on suitable patient cohorts. This novel disease gene may have previously evaded detection because of high GC content, consequential low coverage and computational difficulties associated with robustly detecting repeat-expansions. Reviewing previously unsolved exomes using lower QC filters may generate further diagnoses

GWAS meta-analysis of intrahepatic cholestasis of pregnancy implicates multiple hepatic genes and regulatory elements

Intrahepatic cholestasis of pregnancy (ICP) is a pregnancy-specific liver disorder affecting 0.5–2% of pregnancies. The majority of cases present in the third trimester with pruritus, elevated serum bile acids and abnormal serum liver tests. ICP is associated with an increased risk of adverse outcomes, including spontaneous preterm birth and stillbirth. Whilst rare mutations affecting hepatobiliary transporters contribute to the aetiology of ICP, the role of common genetic variation in ICP has not been systematically characterised to date. Here, we perform genome-wide association studies (GWAS) and meta-analyses for ICP across three studies including 1138 cases and 153,642 controls. Eleven loci achieve genome-wide significance and have been further investigated and fine-mapped using functional genomics approaches. Our results pinpoint common sequence variation in liver-enriched genes and liver-specific cis-regulatory elements as contributing mechanisms to ICP susceptibility

Exploring barriers to smart and sustainable circular economy: The case of an automotive eco-cluster

The transition process from linear economy to circular economy (CE) has brought many challenges and barriers. The three core concepts, which are smartness, sustainability, and circularity, need to be intertwined and adapted by companies to overcome these barriers. Based on this intertwined structure, this paper presents the concept of Smart and Sustainable Circular Economy (SSCE) at the macro-level and addresses the barriers of SSCE under four main aspects: technology, producers, consumers, and policy. Moreover, these four aspects are investigated for small and medium-sized enterprises of an Eco-Cluster in the automotive industry. The fuzzy DEMATEL method is used to uncover, analyse, and discuss the influencing and affected SSCE barriers critically. Finding these SSCE barriers gives an insight into the underlying problems of CE practices, as the only way to ensure an opportunity to achieve SSCE goals is to overcome them. The principal results show that problems of ownership issues in an Eco-Cluster, lack of governmental support and administrative burden, and lack of effective execution of environmental regulations are found as causal barriers that are difficult to change. Furthermore, lack of integration and collaboration among supply chain partners, ineffective CE framework adoption, and product complexity for CE principles are classified as effect barriers that are easily affected by the other factors and the implications can be shown in the short-term. Besides, the cooperation between supply chain partners can be encouraged to provide a solution to the lack of integration and collaboration between supply chain partners and the adoption of an ineffective CE framework