Compilation of Selected Vegetable Crop Reports Dealing with Research and Demonstration Plots Located at the Muck Crops Branch, 1983

Spinach cultivar trials, 1982 ; Celery cultivar trials, 1982 / James M. Pisarczyk and Richard L. Hassell -- Potato cultivar trials, 1982 / James M. Pisarczyk -- Celery transplant study, 1982 / Richard L. Hassell -- Parsley 1982 variety trials ; Onion 1982 variety trials ; Broccoli variety trials, 1982 / Richard L. Hassell -- Carrot variety trials, 1982 / R. Mack Riedel and Richard C. Henne -- Control of early blight of celery with fungicides, 1982 ; Control of crucifer downy mildew with fungicide sprays, 1982 / Randall C. Rowe and Richard L. Hassell -- Synergistic interaction between species of lesion nematodes and Verticillium dahliae, 1982 / R. M. Riedel and R. C. Rowe -- Transplants vs. bare-root in controlling root-knot nematode / R. M. Riedel -- Rotations for control of root-knot nematode / R. M. Riedel and J. A. Chatfield -- Fertilizer guidelines for vegetable crops grown on muck soils in Ohio / William M. Brooks, E. C. Wittmeyer and Richard Hassel

Abrupt reversal in emissions and atmospheric abundance of HCFC-133a (CF3CH2Cl)

Hydrochlorofluorocarbon HCFC-133a (CF3CH2Cl) is an anthropogenic compound whose consumption for emissive use is restricted under the Montreal Protocol. A recent study showed rapidly increasing atmospheric abundances and emissions. We report that, following this rise, the at- mospheric abundance and emissions have declined sharply in the past three years. We find a Northern Hemisphere HCFC-133a increase from 0.13 ppt (dry air mole fraction in parts-per-trillion) in 2000 to 0.50 ppt in 2012–mid-2013 followed by an abrupt reversal to 0.44 ppt by early 2015. Global emissions derived from these observations peaked at 3.1 kt in 2011, followed by a rapid decline of 0.5 kt yr−2 to 1.5 kt yr−1 in 2014. Sporadic HCFC-133a pollution events are detected in Europe from our high-resolution HCFC-133a records at three European stations, and in Asia from sam- ples collected in Taiwan. European emissions are estimated to be <0.1 kt yr−1 although emission hotspots were identi- fied in France

Intracellular curvature-generating proteins in cell-to-cell fusion

Cell-to-cell fusion plays an important role in normal physiology and in different pathological conditions. Early fusion stages mediated by specialized proteins and yielding fusion pores are followed by a pore expansion stage that is dependent on cell metabolism and yet unidentified machinery. Because of a similarity of membrane bending in the fusion pore rim and in highly curved intracellular membrane compartments, in the present study we explored whether changes in the activity of the proteins that generate these compartments affect cell fusion initiated by protein fusogens of influenza virus and baculovirus. We raised the intracellular concentration of curvature-generating proteins in cells by either expressing or microinjecting the ENTH (epsin N-terminal homology) domain of epsin or by expressing the GRAF1 (GTPase regulator associated with focal adhesion kinase 1) BAR (Bin/amphiphysin/Rvs) domain or the FCHo2 (FCH domain-only protein 2) F-BAR domain. Each of these treatments promoted syncytium formation. Cell fusion extents were also influenced by treatments targeting the function of another curvature-generating protein, dynamin. Cell-membrane-permeant inhibitors of dynamin GTPase blocked expansion of fusion pores and dominant-negative mutants of dynamin influenced the syncytium formation extents. We also report that syncytium formation is inhibited by reagents lowering the content and accessibility of PtdIns(4,5)P2, an important regulator of intracellular membrane remodelling. Our findings indicate that fusion pore expansion at late stages of cell-to-cell fusion is mediated, directly or indirectly, by intracellular membrane-shaping proteins

The Coarse-Grained Plaque: A Divergent Aβ Plaque-Type in Early-Onset Alzheimer’s Disease

Alzheimer’s disease (AD) is characterized by amyloid-beta (Aβ) deposits, which come in myriad morphologies with varying clinical relevance. Previously, we observed an atypical Aβ deposit, referred to as the coarse-grained plaque. In this study, we evaluate the plaque’s association with clinical disease and perform in-depth immunohistochemical and morphological characterization. The coarse-grained plaque, a relatively large (Ø ≈ 80 µm) deposit, characterized as having multiple cores and Aβ-devoid pores, was prominent in the neocortex. The plaque was semi-quantitatively scored in the middle frontal gyrus of Aβ-positive cases (n = 74), including non-demented cases (n = 15), early-onset (EO)AD (n = 38), and late-onset (LO)AD cases (n = 21). The coarse-grained plaque was only observed in cases with clinical dementia and more frequently present in EOAD compared to LOAD. This plaque was associated with a homozygous APOE ε4 status and cerebral amyloid angiopathy (CAA). In-depth characterization was done by studying the coarse-grained plaque’s neuritic component (pTau, APP, PrPC), Aβ isoform composition (Aβ40, Aβ42, AβN3pE, pSer8Aβ), its neuroinflammatory component (C4b, CD68, MHC-II, GFAP), and its vascular attribution (laminin, collagen IV, norrin). The plaque was compared to the classic cored plaque, cotton wool plaque, and CAA. Similar to CAA but different from classic cored plaques, the coarse-grained plaque was predominantly composed of Aβ40. Furthermore, the coarse-grained plaque was distinctly associated with both intense neuroinflammation and vascular (capillary) pathology. Confocal laser scanning microscopy (CLSM) and 3D analysis revealed for most coarse-grained plaques a particular Aβ40 shell structure and a direct relation with vessels. Based on its morphological and biochemical characteristics, we conclude that the coarse-grained plaque is a divergent Aβ plaque-type associated with EOAD. Differences in Aβ processing and aggregation, neuroinflammatory response, and vascular clearance may presumably underlie the difference between coarse-grained plaques and other Aβ deposits. Disentangling specific Aβ deposits between AD subgroups may be important in the search for disease-mechanistic-based therapies

New insights into the genetic etiology of Alzheimer's disease and related dementias

Characterization of the genetic landscape of Alzheimer's disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/'proxy' AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE ε4 allele

Multiancestry analysis of the HLA locus in Alzheimer’s and Parkinson’s diseases uncovers a shared adaptive immune response mediated by HLA-DRB1*04 subtypes

Across multiancestry groups, we analyzed Human Leukocyte Antigen (HLA) associations in over 176,000 individuals with Parkinson’s disease (PD) and Alzheimer’s disease (AD) versus controls. We demonstrate that the two diseases share the same protective association at the HLA locus. HLA-specific fine-mapping showed that hierarchical protective effects of HLA-DRB1*04 subtypes best accounted for the association, strongest with HLA-DRB1*04:04 and HLA-DRB1*04:07, and intermediary with HLA-DRB1*04:01 and HLA-DRB1*04:03. The same signal was associated with decreased neurofibrillary tangles in postmortem brains and was associated with reduced tau levels in cerebrospinal fluid and to a lower extent with increased Aβ42. Protective HLA-DRB1*04 subtypes strongly bound the aggregation-prone tau PHF6 sequence, however only when acetylated at a lysine (K311), a common posttranslational modification central to tau aggregation. An HLA-DRB1*04-mediated adaptive immune response decreases PD and AD risks, potentially by acting against tau, offering the possibility of therapeutic avenues

Synchronous Hermaphroditism and Self-Fertilization in a Captive Shortnose Sturgeon

The shortnose sturgeon Acipenser brevirostrum is a federally listed endangered fish species endemic to the East Coast of North America, where captive fish are cultured for recovery efforts. During routine evaluations of broodfish for spawning potential, a single hermaphroditic shortnose sturgeon was discovered. Motile sperm and approximately 7,600 eggs were manually stripped from the individual simultaneously. Eggs were fertilized with the fish’s own sperm (self-fertilized) and with the sperm of two unrelated males (cross-fertilized). Both self- and cross-fertilization procedures were successful. Viable fry hatched from 9% of the eggs produced by self-fertilization and from 2% of those produced by cross-fertilization. Fry survival through 180 d posthatch was 1% in the self-fertilization treatment and 11% in the cross-fertilization treatment. Endoscopic evaluation of gonads confirmed the presence of ovotestes with discrete regions of active testicular and ovarian tissues. The present account provides empirical evidence including gross anatomical and histological photodocumentation that advances knowledge of this rare condition in a fish species threatened with extinction