Performance of Small-Fruited Pumpkin Cultivars in Maine

A small-fruited (2-4 lb) or “pie” type pumpkin variety trial was established in the spring of 2009 at Highmoor Farm in Monmouth, ME. Three replications of seven varieties were direct-seeded on 18 June through black plastic mulch. Plots were 18 feet long with three feet between plants and six feet between rows. All fertilizer was applied according to soil test recommendations and incorporated prior to mulch application and seeding. Fruit were harvested on 18 September. Top performing varieties in terms of yield per plot included ‘Chucky’, ‘Small Sugar’, and ‘Field Trip’. ‘Fall Splendor’ produced the largest fruit in the trial, followed by ‘Winter Luxury’ and ‘Mystic Plus’. ‘Field Trip’ and ‘Fall Splendor’ had the highest stem quality in the trial and ‘Field Trip’, ‘Mystic Plus’ and ‘Fall Splendor’ were rated highest for exterior color and ribbing. The results of this trial suggest that ‘Field Trip’, ‘Mystic Plus’ and ‘Fall Splendor’ offer very high quality fruit with acceptable yields for pie-type pumpkins, while ‘Chucky’ offers acceptable fruit quality and very high yields.https://digitalcommons.library.umaine.edu/extension_ag/1000/thumbnail.jp

Warburg Micro syndrome is caused by RAB18 deficiency or dysregulation

RAB18, RAB3GAP1, RAB3GAP2 and TBC1D20 are each mutated in Warburg Micro syndrome, a rare autosomal recessive multisystem disorder. RAB3GAP1 and RAB3GAP2 form a binary ‘RAB3GAP’ complex that functions as a guanine-nucleotide exchange factor (GEF) for RAB18, whereas TBC1D20 shows modest RAB18 GTPase-activating (GAP) activity in vitro. Here, we show that in the absence of functional RAB3GAP or TBC1D20, the level, localization and dynamics of cellular RAB18 is altered. In cell lines where TBC1D20 is absent from the endoplasmic reticulum (ER), RAB18 becomes more stably ER-associated and less cytosolic than in control cells. These data suggest that RAB18 is a physiological substrate of TBC1D20 and contribute to a model in which a Rab-GAP can be essential for the activity of a target Rab. Together with previous reports, this indicates that Warburg Micro syndrome can be caused directly by loss of RAB18, or indirectly through loss of RAB18 regulators RAB3GAP or TBC1D20

Loss of ALDH18A1 function is associated with a cellular lipid droplet phenotype suggesting a link between autosomal recessive cutis laxa type 3A and Warburg Micro syndrome

Autosomal recessive cutis laxa type 3A is caused by mutations in ALDH18A1, a gene encoding the mitochondrial enzyme Δ(1)-pyrroline-5-carboxylate synthase (P5CS). It is a rare disorder with only six pathogenic mutations and 10 affected individuals from five families previously described in the literature. Here we report the identification of novel compound heterozygous missense mutations in two affected siblings from a Lebanese family by whole-exome sequencing. The mutations alter a conserved C-terminal domain of the encoded protein and reduce protein stability as determined through Western blot analysis of patient fibroblasts. Patient fibroblasts exhibit a lipid droplet phenotype similar to that recently reported in Warburg Micro syndrome, a disorder with similar features but hitherto unrelated cellular etiology

Structural and Functional Deficits in a Neuronal Calcium Sensor-1 Mutant Identified in a Case of Autistic Spectrum Disorder

Neuronal calcium sensor-1 (NCS-1) is a Ca2+ sensor protein that has been implicated in the regulation of various aspects of neuronal development and neurotransmission. It exerts its effects through interactions with a range of target proteins one of which is interleukin receptor accessory protein like-1 (IL1RAPL1) protein. Mutations in IL1RAPL1 have recently been associated with autism spectrum disorders and a missense mutation (R102Q) on NCS-1 has been found in one individual with autism. We have examined the effect of this mutation on the structure and function of NCS-1. From use of NMR spectroscopy, it appeared that the R102Q affected the structure of the protein particularly with an increase in the extent of conformational exchange in the C-terminus of the protein. Despite this change NCS-1(R102Q) did not show changes in its affinity for Ca2+ or binding to IL1RAPL1 and its intracellular localisation was unaffected. Assessment of NCS-1 dynamics indicated that it could rapidly cycle between cytosolic and membrane pools and that the cycling onto the plasma membrane was specifically changed in NCS-1(R102Q) with the loss of a Ca2+ -dependent component. From these data we speculate that impairment of the normal cycling of NCS-1 by the R102Q mutation could have subtle effects on neuronal signalling and physiology in the developing and adult brain

Evaluation of saliency tracking as an alternative for health monitoring in PMSM-drives under nonstationary conditions

This paper evaluates the capability of saliency tracking to assess the health condition of permanent magnet synchronous motor (PMSM) drives operating under nonstationary conditions. The evaluated scheme is based on saliency tracking methods, which are associated to the accurate sensorless control of AC drives without zero speed limitations. In this work two representative saliency tracking architectures are evaluated: High Frequency (HF) injection, and PWM transient excitation. Although a monitoring approach based on HF injection was previously reported, a comparative study to evaluate the most representative saliency tracking schemes to assess health condition in drives was still missing. The aim of this work is to fill out this gap by evaluating and comparing two saliency-based monitoring schemes (one based on HF-injection and the other based on PWM transient excitation) to evaluate their performance in the presence of inter-turn winding faults. Simulation and experimental results are presented which confirm that both schemes offer excellent detection capabilities and that are suitable for drives operating under nonstationary conditions including standstill operation. Significant differences are also found for instance, PWM transient excitation offers improved accuracy since the approach is not affected by the inverter nonlinearities and is suitable for full-speed range applications. The main drawback here is complexity and the hardware requirements. Schemes based on HF-injection proved to be very simple and provide comparable results; however a good performance is only guaranteed for the zero-to-medium speed range applications which limit their applicability

Condition monitoring approach for permanent magnet synchronous motor drives based on the INFORM method

This paper proposes a monitoring scheme based on saliency tracking to assess the health condition of PMSM drives operating under non stationary conditions. The evaluated scheme is based on the INFORM methodology, which is associated to the accurate sensorless control of PM drives without zero speed limitation. The result is a monitoring scheme that is able to detect faults that would be very difficult to evaluate under nonstationary conditions. A relevant aspect of the proposed scheme is that it remains valid for full speed range, and can be used for standstill operation. Additionally, the approach is insensitive to the inverter nonlinearities which enhance the detection capabilities further respect to similar topologies. In this work the proposed approach is evaluated numerically and experimentally in the presence of incipient winding faults and inter-turn short circuits in a PM conventional drive. The obtained results show quick response and excellent detection capabilities not only in the detection of faults, but to determine their magnitude which is vital to avoid further degradation

Comparative proximity biotinylation implicates the small GTPase RAB18 in sterol mobilization and biosynthesis

Loss of functional RAB18 causes the autosomal recessive condition Warburg Micro syndrome. To better understand this disease, we used proximity biotinylation to generate an inventory of potential RAB18 effectors. A restricted set of 28 RAB18-interactions were dependent on the binary RAB3GAP1-RAB3GAP2 RAB18-guanine nucleotide exchange factor (GEF) complex. 12 of these 28 interactions are supported by prior reports and we have directly validated novel interactions with SEC22A, TMCO4 and INPP5B. Consistent with a role for RAB18 in regulating membrane contact sites (MCSs), interactors included groups of microtubule/membrane-remodelling proteins, membrane-tethering and docking proteins, and lipid-modifying/transporting proteins. Two of the putative interactors, EBP and OSBPL2/ORP2, have sterol substrates. EBP is a Δ8-Δ7 sterol isomerase and ORP2 is a lipid transport protein. This prompted us to investigate a role for RAB18 in cholesterol biosynthesis. We find that the cholesterol precursor and EBP-product lathosterol accumulates in both RAB18-null HeLa cells and RAB3GAP1-null fibroblasts derived from an affected individual. Further, de novo cholesterol biosynthesis is impaired in cells in which RAB18 is absent or dysregulated, or in which ORP2 expression is disrupted. Our data demonstrate that GEF-dependent Rab-interactions are highly amenable to interrogation by proximity biotinylation and may suggest that Micro syndrome is a cholesterol biosynthesis disorder

Rab18 and a Rab18 GEF complex are required for normal ER structure

The ancestral Rab GTPase Rab18 and both subunits of the Rab3GAP complex are mutated in the human neurological and developmental disorder Warburg Micro syndrome. Here, we demonstrate that the Rab3GAP complex is a specific Rab18 guanine nucleotide exchange factor (GEF). The Rab3GAP complex localizes to the endoplasmic reticulum (ER) and is necessary for ER targeting of Rab18. It is also sufficient to promote membrane recruitment of Rab18. Disease-associated point mutations of conserved residues in either the Rab3GAP1 (T18P and E24V) or Rab3GAP2 (R426C) subunits result in loss of the Rab18 GEF and membrane-targeting activities. Supporting the view that Rab18 activity is important for ER structure, in the absence of either Rab3GAP subunit or Rab18 function, ER tubular networks marked by reticulon 4 were disrupted, and ER sheets defined by CLIMP-63 spread out into the cell periphery. Micro syndrome is therefore a disease characterized by direct loss of Rab18 function or loss of Rab18 activation at the ER by its GEF Rab3GAP

THISTLE:trial of hands-on Interprofessional simulation training for local emergencies: a research protocol for a stepped-wedge clustered randomised controlled trial

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