Reducing food loss and waste: Five challenges for policy and research.

Despite broad agreement in policy circles on the need to reduce food loss and waste (FLW), considerable gaps in information still exist. This paper identifies policy-relevant information gaps, summarizes recent research that tries to fill these gaps and identifies five challenges for researchers, policymakers and practitioners in reducing FLW. The five challenges identified are: (i) measuring and monitoring FLW, (ii) assessing benefits and costs of FLW reduction and the tradeoffs involved, (iii) designing FLW-related policies and interventions under limited information, (iv) understanding how interactions between stages along food value chain and across countries affect outcomes of FLW reduction efforts, (v) preparing for income transitions and the shifting relative importance of losses and waste as economies develop.

COVID-19 and impacts on global food systems and household welfare: Introduction to a special issue.

The food system, and those who depend on it, have been strongly but unevenly affected by COVID-19. Overall, the impacts on food systems, poverty, and nutrition have been caused by a combination of a generalized economic recession and disruptions in agri-food supply chains. This paper provides an overview of the contributions to this Special Issue of Agricultural Economics. The papers in this volume confirm that both income shocks and supply disruptions have affected food security and livelihoods the most where supply chains were more poorly integrated, and poverty and market informality had greater presence before COVID-19. Yet, as the pandemic still has societies worldwide in a stranglehold, outcomes remain uncertain and reliable data are still sparsely available. This Special Issue of Agricultural Economics provides new insights of the pandemics impact on food systems, household welfare, and food security, building on both model-based scenario analysis and new survey data. These methods have proven helpful in providing these insights amidst the unprecedented shock that the pandemic has caused to production systems and livelihoods worldwide. However, they also suffer from obvious limitations identified in this editorial overview paper and require substantial improvement in order to understand the changes in economic behavior and functioning of food supply chains induced by the pandemic.

Impacts of COVID-19 on global poverty, food security, and diets: Insights from global model scenario analysis.

This study assesses the impact of coronavirus disease 2019 (COVID-19) on poverty, food insecurity, and diets, accounting for the complex links between the crisis and the incomes and living costs of vulnerable households. Key elements are impacts on labor supply, effects of social distancing, shifts in demand from services involving close contact, increases in the cost of logistics in food and other supply chains, and reductions in savings and investment. These are examined using IFPRI's global general equilibrium model linked to epidemiological and household models. The simulations suggest that the global recession caused by COVID-19 will be much deeper than that of the 2008-2009 financial crisis. The increases in poverty are concentrated in South Asia and sub-Saharan Africa with impacts harder in urban areas than in rural. The COVID-19-related lockdown measures explain most of the fall in output, whereas declines in savings soften the adverse impacts on food consumption. Almost 150 million people are projected to fall into extreme poverty and food insecurity. Decomposition of the results shows that approaches assuming uniform income shocks would underestimate the impact by as much as one-third, emphasizing the need for the more refined approach of this study.

"Pivoting" by food industry firms to cope with COVID-19 in developing regions: E-commerce and "copivoting" delivery intermediaries.

Coronavirus disease 2019 and related lockdown policies in 2020 shocked food industry firms' supply chains in developing regions. Firms "pivoted" to e-commerce to reach consumers and e-procurement to reach processors and farmers. "Delivery intermediaries" copivoted with food firms to help them deliver and procure. This was crucial to the ability of the food firms to pivot. The pandemic was a "crucible" that induced this set of fast-tracking innovations, accelerating the diffusion of e-commerce and delivery intermediaries, and enabling food industry firms to redesign, at least temporarily, and perhaps for the long term, their supply chains to be more resilient, and to weather the pandemic, supply consumers, and contribute to food security. We present a theoretical model to explain these firm strategies, and then apply the framework to classify firms' practical strategies. We focus on cases in Asia and Latin America. Enabling policy and infrastructural conditions allowed firms to pivot and copivot fluidly.

Declines in moth populations stress the need for conserving dark nights.

Given the global continuous rise, artificial light at night is often considered a driving force behind moth population declines. Although negative effects on individuals have been shown, there is no evidence for effects on population sizes to date. Therefore, we compared population trends of Dutch macromoth fauna over the period 1985-2015 between moth species that differ in phototaxis and adult circadian rhythm. We found that moth species that show positive phototaxis or are nocturnally active have stronger negative population trends than species that are not attracted to light or are diurnal species. Our results indicate that artificial light at night is an important factor in explaining declines in moth populations in regions with high artificial night sky brightness. Our study supports efforts to reduce the impacts of artificial light at night by promoting lamps that do not attract insects and reduce overall levels of illumination in rural areas to reverse declines of moth populations.

A new species in the genus Notata Hampson, 1891 (Lepidoptera: Erebidae, Arctiinae, Lithosiini).

A new species in the genus Notata Hampson, 1891, N. kokoda spec. nov., is discovered from Papua New Guinea. An overview of the genus is given and the new species is described. Of all species pictures of the adults and genitalia are displayed.

The genus Orieosia Bucsek, 2012 also found in New Guinea, with description of two new species (Lepidoptera: Erebidae, Arctiinae, Lithosiini).

The genus Orieosia Bucsek, 2012 appears to be present in New Guinea too. Four species have been discovered in New Guinea to belong to this formerly believed to be Oriental genus. Two already known species, Lambula hypopolius Rothschild, 1916 and Utriculofera tetrastigmata Rothschild, 1916, are transferred to the genus Orieosia Bucsek, 2012. Orieosia stenoptera spec. nov. and O. albigrisea spec. nov. are described as new to science. Nomenclatorial confusion with Holocraspedon hypopolius (Rothschild, 1916) is discussed.

Two new species of the subgenus Cryptanaema de Vos of the genus Cyana Walker from eastern Indonesia (Lepidoptera: Erebidae: Arctiinae: Lithosiini: Nudariina).

Two new species of the subgenus Cryptanaema de Vos, 2017 of the genus Cyana Walker, 1854 are described from eastern Indonesia: Cyana (Cryptanaema) ngata sp. n. (Western New Guinea) and Cyana (Cryptanaema) sibela sp. n. (Maluku Islands). Adults, male and female genitalia of the new and similar species are illustrated.

Agricultural subsidies and global greenhouse gas emissions.

Agricultural production is strongly affected by and a major contributor to climate change. Agriculture and land-use change account for a quarter of total global emissions of greenhouse gases (GHG). Agriculture receives around US$600 billion per year worldwide in government support. No rigorous quantification of the impact of this support on GHG emissions has been available. This article helps fill the void. Here, we find that, while over the years the government support has incentivized the development of high-emission farming systems, at present, the support only has a small impact in terms of inducing additional global GHG emissions from agricultural production; partly because support is not systematically biased towards high-emission products, and partly because support generated by trade protection reduces demand for some high-emission products by raising their consumer prices. Substantially reducing GHG emissions from agriculture while safeguarding food security requires a more comprehensive revamping of existing support to agriculture and food consumption.

The Processed food revolution in African food systems and the Double Burden of Malnutrition.

African consumers have purchased increasing amounts of processed food over the past 50 years. The opportunity cost of time of women and men has increased as more of them work outside the home, driving them to buy processed food and food prepared away from home to save arduous home-processing and preparation labor. In the past several decades, this trend has accelerated with a surge on the supply side of the processing sector and small and medium enterprises (SMEs) and large private companies making massive aggregate investments. Packaged, industrialized, ultra-processed foods and sugar-sweetened beverages (SSBs) are a growing proportion of the processed food consumed. Also, in the past several decades, overweight and obesity have joined the long-standing high levels of stunting and wasting among children and extreme thinness among women of childbearing age. Together these phenomena have formed a double burden of malnutrition (DBM). The DBM has emerged as an important health problem in sub-Saharan Africa. The rise of the DBM and the increase in ultra-processed food consumption are linked. Policy makers face a dilemma. On the one hand, purchases of processed food are driven by long-term factors, such as urbanization, increased income, and employment changes, and thus policy cannot change the pursuit of convenience and labor-saving food. Moreover, much processed food, like packaged milk, is a boon to nutrition, and the processed food system is a major source of jobs for women. On the other hand, the portion (some 10-30%) of processed food that is ultra-processed is a public health challenge, and policy must address its detrimental effects on disease burden. The global experience suggests that double duty actions are most important as are selected policies focused on healthy weaning foods for addressing stunting and taxes on SSBs, nutrition labeling, and other measures can steer consumers away from unhealthy ultra-processed foods to addressing obesity and possibly child nutrition and stunting. We recommend that African governments consider these policy options, but note that the current extreme fragmentation of the processing sector, consisting of vast numbers of informal SMEs in sub-Saharan Africa, and the limited administrative/implementation capacity of many African governments require pursuing this path only gradually.

Axonal inclusions in spinocerebellar ataxia type 3.

Protein aggregation is a major pathological hallmark of many neurodegenerative disorders including polyglutamine diseases. Aggregation of the mutated form of the disease protein ataxin-3 into neuronal nuclear inclusions is well described in the polyglutamine disorder spinocerebellar ataxia type 3 (SCA3 or Machado-Joseph disease), although these inclusions are not thought to be directly pathogenic. Neuropil aggregates have not yet been described in SCA3. We performed a systematic immunohistochemical study of serial thick sections through brains of seven clinically diagnosed and genetically confirmed SCA3 patients. Using antibodies against ataxin-3, p62, ubiquitin, the polyglutamine marker 1C2 as well as TDP-43, we analyzed neuronal localization, composition and distribution of aggregates within SCA3 brains. The analysis revealed widespread axonal aggregates in fiber tracts known to undergo neurodegeneration in SCA3. Similar to neuronal nuclear inclusions, the axonal aggregates were ubiquitinated and immunopositive for the proteasome and autophagy associated shuttle protein p62, indicating involvement of neuronal protein quality control mechanisms. Rare TDP-43 positive axonal inclusions were also observed. Based on the correlation between affected fiber tracts and degenerating neuronal nuclei, we hypothesize that these novel axonal inclusions may be detrimental to axonal transport mechanisms and thereby contribute to degeneration of nerve cells in SCA3.

CD8(+)/perforin/granzyme B(+) effector cells infiltrating cerebellum and inferior olives in gluten ataxia.

Up to 8% of patients with gluten sensitivity (GS) develop neurological symptoms such as ataxia, dementia, seizures or peripheral neuropathy. The underlying immunological mechanisms still remain to be elucidated. We here report the case of a 68-year-old male patient suffering from progressive ataxia and dementia associated with chronic diarrhea and both elevated IgG and IgA antigliadin-antibodies. At autopsy, frequent argyrophilic glial and neuronal inclusions within the basal nucleus of Meynert were considered as the structural correlative for the cognitive decline. Significant neuronal loss in the cerebellar cortex and the inferior olives was accompanied by infiltrating CD8(+)/perforin(+)/granzyme B(+) cells as well as reactive astrogliosis and microglial activation. These CD8(+) cytotoxic T and NK cells are likely to act as effector cells responsible for neuronal cell death in patients with gluten sensitivity and neurological disease and might therefore at least partly be responsible for cerebellar symptoms in gluten ataxia. In conclusion, our results, showing an absence of B- or plasma cells but multiple CD8(+) as well as granzyme B and perforin expressing cells in ataxia-associated brain areas, suggest that there are also prominent cytotoxic effects in neuropathogenesis of GS.

Polarised asymmetric inheritance of accumulated protein damage in higher eukaryotes.

Disease-associated misfolded proteins or proteins damaged due to cellular stress are generally disposed via the cellular protein quality-control system. However, under saturating conditions, misfolded proteins will aggregate. In higher eukaryotes, these aggregates can be transported to accumulate in aggresomes at the microtubule organizing center. The fate of cells that contain aggresomes is currently unknown. Here we report that cells that have formed aggresomes can undergo normal mitosis. As a result, the aggregated proteins are asymmetrically distributed to one of the daughter cells, leaving the other daughter free of accumulated protein damage. Using both epithelial crypts of the small intestine of patients with a protein folding disease and Drosophila melanogaster neural precursor cells as models, we found that the inheritance of protein aggregates during mitosis occurs with a fixed polarity indicative of a mechanism to preserve the long-lived progeny.

Proteasome subunit proteins and neuropathology in tauopathies and synucleinopathies: Consequences for proteomic analyses.

Accumulation of proteins in inclusions in neurological disorders is partly due to dysfunction of the ubiquitin-proteasome system. Proteasomal dysfunction may be caused by misexpression of one or more of its subunits. A large number of antibodies reactive with proteasome subunits were screened on material from patients exhibiting tau- and synucleinopathies. Many antisera against proteasomal subunits (11S activator, 19S regulator ATPase/non-ATPase, and 20S alpha and beta resulted in a distinct nuclear and/or cytoplasmic staining of the entorhinal-hippocampal area and the temporal cortex of Alzheimer's disease (AD) patients. In particular an antibody directed against 19S regulator ATPase subunit 6b (S6b) specifically stained the neurofibrillary tangles and dystrophic neurites in AD, Down syndrome and aged nondemented controls. In other tauopathies (Pick's disease, frontotemporal dementia, progressive supranuclear palsy and argyrophilic grain disease), neuronal and/or glial inclusions were also S6b immunoreactive. In contrast, in synucleinopathies (Lewy body disease (LBD) and multiple system atrophy) no S6b staining was seen. Real time quantitative PCR on the temporal cortex of AD patients revealed a significant increase in S6b subunit mRNA. This increase was not found in the gyrus cinguli anterior of patients with LBD. This differential expression of S6b most likely will result in different proteomic patterns. Here we present evidence to show that S6b coexists with a reporter for proteasomal dysfunction (ubiquitin(+1)), and we conclude that S6b transcript up-regulation and the dysfunction in tauopathies may be functionally related.

Consistent affection of the central somatosensory system in spinocerebellar ataxia type 2 and type 3 and its significance for clinical symptoms and rehabilitative therapy.

The spinocerebellar ataxias type 2 (SCA2) and type 3 (SCA3) are progressive, currently untreatable and ultimately fatal ataxic disorders, which belong to the group of neurological disorders known as CAG-repeat or polyglutamine diseases. Since knowledge regarding the involvement of the central somatosensory system in SCA2 and SCA3 currently is only fragmentary, a variety of somatosensory disease signs remained unexplained or widely misunderstood. The present review (1) draws on the current knowledge in the field of neuroanatomy, (2) describes the anatomy and functional neuroanatomy of the human central somatosensory system, (3) provides an overview of recent findings regarding the affection of the central somatosensory system in SCA2 and SCA3 patients, and (4) points out the underestimated pathogenic role of the central somatosensory system for somatosensory and somatomotor disease symptoms in SCA2 and SCA3. Finally, based on recent findings in the research fields of neuropathology and neural plasticity, this review supports currently applied and recommends further neurorehabilitative approaches aimed at maintaining, improving, and/or recovering adequate somatomotor output by enforcing and changing somatosensory input in the very early clinical stages of SCA2 and SCA3.

Ataxin-3 represses transcription via chromatin binding, interaction with histone deacetylase 3, and histone deacetylation.

Ataxin-3 (AT3), the disease protein in spinocerebellar ataxia type 3 (SCA3), has been associated with the ubiquitin-proteasome system and transcriptional regulation. Here we report that normal AT3 binds to target DNA sequences in specific chromatin regions of the matrix metalloproteinase-2 (MMP-2) gene promoter and represses transcription by recruitment of the histone deacetylase 3 (HDAC3), the nuclear receptor corepressor (NCoR), and deacetylation of histones bound to the promoter. Both normal and expanded AT3 physiologically interacted with HDAC3 and NCoR in a SCA3 cell model and human pons tissue; however, normal AT3-containing protein complexes showed increased histone deacetylase activity, whereas expanded AT3-containing complexes had reduced deacetylase activity. Consistently, histone analyses revealed an increased acetylation of total histone H3 in expanded AT3-expressing cells and human SCA3 pons. Expanded AT3 lost the repressor function and displayed altered DNA/chromatin binding that was not associated with recruitment of HDAC3, NCoR, and deacetylation of the promoter, allowing aberrant MMP-2 transcription via the transcription factor GATA-2. For transcriptional repression normal AT3 cooperates with HDAC3 and requires its intact ubiquitin-interacting motifs (UIMs), whereas aberrant transcriptional activation by expanded AT3 is independent of the UIMs but requires the catalytic cysteine of the ubiquitin protease domain. These findings demonstrate that normal AT3 binds target promoter regions and represses transcription of a GATA-2-dependent target gene via formation of histone-deacetylating repressor complexes requiring its UIM-associated function. Expanded AT3 aberrantly activates transcription via its catalytic site and loses the ability to form deacetylating repressor complexes on target chromatin regions.

Altered Sphingolipid Balance in Capillary Cerebral Amyloid Angiopathy.

BACKGROUND: The majority of patients with Alzheimer's disease (AD) exhibit amyloid-ß (Aß) deposits at the brain vasculature, a process referred to as cerebral amyloid angiopathy (CAA). In over 51% of AD cases, Aß also accumulates in cortical capillaries, which is termed capillary CAA (capCAA). It has been postulated that the presence of capCAA in AD is a specific subtype of AD, although underlying mechanisms are not yet fully understood. Sphingolipids (SLs) are implicated in neurodegenerative disorders, including AD. However, to date it remains unknown whether alterations in the SL pathway are involved in capCAA pathogenesis and if these differ from AD. OBJECTIVE: To determine whether AD cases with capCAA have an altered SL profile compared to AD cases without capCAA. METHODS: Immunohistochemistry was performed to assess the expression and localization of ceramide, acid sphingomyelinase (ASM), and sphingosine-1-phosphate receptors (S1P1, S1P3). In addition, we determined the concentrations of S1P as well as different chain-lengths of ceramides using HPLC-MS/MS. RESULTS: Immunohistochemical analysis revealed an altered expression of ceramide, ASM, and S1P receptors by reactive astrocytes and microglial cells specifically associated with capCAA. Moreover, a shift in the balance of ceramides with different chain-lengths and S1P content is observed in capCAA. CONCLUSION: Here we provide evidence of a deregulated SL balance in capCAA. The increased levels of ASM and ceramide in activated glia cells suggest that the SL pathway is involved in the neuroinflammatory response in capCAA pathogenesis. Future research is needed to elucidate the role of S1P in capCAA.

Relationship of apolipoprotein E and age at onset to Parkinson disease neuropathology.

Previous studies investigating the association between apolipoprotein E (APOE) genotypes and Parkinson disease (PD) have yielded conflicting results, and only a few have addressed APOE as a possible determinant of PD pathology. Therefore, we aimed to evaluate the relationship between APOE and PD as well as APOE and PD pathology. We studied 108 pathologically verified patients with PD and 108 controls pair-matched for age and gender. Allele frequencies of APOE differed between patients with PD and controls (p = 0.02). The frequency of epsilon4 allele increased (p = 0.01), whereas that of epsilon3 allele decreased with advancing PD pathology (p = 0.002). Only age of PD onset was an independent predictor for the rate of progression of PD pathology in which late-onset patients appeared to reach end point PD pathology more rapidly than early-onset patients (p = 0.001). In conclusion, our findings suggest that APOE may express its effect on the risk of PD by modifying the occurrence of PD pathology, but age of PD onset seems to be the principal determinant of the progression rate of PD pathology.