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The Massachusetts page of the American Trails Website has the most comprehensive list of the state's trails and greenways with links to available web sites. If you know of a trail that should be listed, or have updates, please send them to American Trails.
Massachusetts' Long-Distance Trails:
The Massachusetts section is described as a 'primitive footpath' and runs for 90 miles through the Berkshires.
Envisioned as a 200-mile trail and greenway that circles the greater Boston area, from Kingston Bay to Plum Island. This recreation trail links parks and open spaces in the metro area. Currently, 150 miles are open and designated.
This trail will span 3,000 miles, both on and off roads, to connect Maine and Florida. The Massachusetts section runs from Salisbury to Boston, then Worcester, and through the Blackstone River corridor on to Providence.
This trail, envisioned as a 100-mile long-distance trail from the Connecticut to the Hudson that follows the corridor of the historic Native American path, is a significant link for Massachusetts. It preserves an important historic trail even traversing the original trail in one location, connects scenic landscapes, and provides users the opportunity to travel from river's edge to mountain ridge to river's edge again. Today, approximately 34 miles of the trail are open and designated in Massachusetts as woodland trail, on-road segments, and water trail on the Deerfield River. Although primarily envisioned as a hiking trail, different segments are also appropriate for cycling, snowmobiling, horseback riding, and paddling.
This multi-use trail is a work in progress, but will eventually extend 104 miles from Boston to Northampton. Just over 20 miles are already open, including the section known as the Norwottuck Trail, from Amherst to Northampton and the Wachusett Greenways sections in central Massachusetts.
The New England National Scenic Trail is a 220-mile trail route that has been in existence for over half a century. It travels through 39 communities in Connecticut and Massachusetts. Comprised of the Metacomet, Monadnock and Mattabesett Trails, the route features classic New England landscape features: long distance vistas with rural towns as a backdrop, agrarian lands, unfragmented forests, and large river valleys. The trail also travels through important Native American and colonial historical landmarks and highlights a range of diverse ecosystems and natural resources–traprock ridges, mountain summits, forested glades, vernal pools, lakes, streams and waterfalls.
This footpath extends 92 miles through Worcester County, from the Rhode Island border at Douglas to the Wapack Trail in New Hampshire.
Warner Trail
The Warner stretches 30 miles from Canton to Diamond State Park in Rhode Island. Envisioned as a woodland trail, it "offers delightful and varied outdoor experiences."
The Taconic Crest Trail winds 35 miles across the Massachusetts and New York Borders into Vermont along the Taconic Ridge.


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Vascular endothelial growth factor receptor-2 (VEGFR2) is a receptor tyrosine kinase that is expressed in endothelial cells and regulates angiogenic signal transduction under both physiological and pathological conditions. VEGFR2 turnover at the plasma membrane (PM) is regulated by its transport through endocytic and secretory transport pathways. Short-range cargo trafficking along actin filaments is commonly regulated by motor proteins of myosin superfamily. In the current study, performed in primary human endothelial cells, we demonstrate that unconventional myosin 1c (Myo1c; class I family member) regulates the localization of VEGFR2 at the PM. We further demonstrate that the recruitment of VEGFR2 to the PM and its colocalization with Myo1c and caveolin-1 occur in response to VEGF-A (VEGF) stimulation. In addition, VEGF-induced delivery of VEGFR2 to the cell surface requires Myo1c; surface VEGFR2 levels are reduced in the absence of Myo1c and, more importantly, are restored by the overexpression of wild-type but not mutant Myo1c. Subcellular density gradient fractionation revealed that partitioning of VEGFR2 into caveolin-1- and Myo1c-enriched membrane fractions is dependent on VEGF stimulation. Myo1c depletion resulted in increased VEGF-induced VEGFR2 transport to the lysosomes for degradation and was rescued by applying either brefeldin A, which blocks trafficking between the endoplasmic reticulum and the Golgi complex, or dynasore, an inhibitor of dynamin-mediated endocytosis. Myo1c depletion also reduced VEGF-induced VEGFR2 phosphorylation at Y1175 and phosphorylation-dependent activation of ERK1/2 and c-Src kinase, leading to reduced cell proliferation and cell migration. This is the first report demonstrating that Myo1c is an important mediator of VEGF-induced VEGFR2 delivery to the cell surface and plays a role in angiogenic signaling.
- endothelial cells
- signaling
- vascular endothelial growth factor receptor
- Myo1c
- caveolin-1
vascular endothelial growth factor receptor family members 2 (VEGFR2) and 1 (VEGFR1) are expressed primarily in the vascular endothelium. Binding of VEGF to VEGFR2 initiates signaling events that regulate diverse cellular processes such as proliferation, migration, survival, chemotaxis, and vascular permeability, which are the hallmarks of angiogenesis (44). Molecules that regulate the trafficking of intracellular vesicles and the availability of VEGFR2 at the plasma membrane (PM) may, therefore, directly regulate angiogenic events (3, 9, 16, 19, 24, 27, 42).
When bound to the ligand VEGF, VEGFR2 internalizes, traffics to endosome, and transports either to lysosome for degradation or is recycled back to the PM (3, 9, 16). Recycling has been reported to occur via both Rab4, Rab11-independent and Rab4, Rab11-dependent mechanisms (3, 16). In addition, Arf6 has been implicated in recycling VEGFR2 to the PM (19). VEGFR2 turnover at the PM is also dependent on the delivery of the newly synthesized pool of receptor via the Golgi complex (27). Caveolae, which are highly abundant in smooth muscle cells, fibroblasts, adipocytes, and endothelial cells, are heterogeneous 10–200 nm sterol- and sphingolipid-enriched domains localized in membrane rafts and play an important role in cardiovascular signaling (15, 20, 36). Ultrastructural and biochemical studies have shown that VEGFR2 localizes to caveolae, and density gradient-based fractionation studies suggest that VEGFR2 is present in caveolin-1 (Cav1)-rich membrane rafts (11, 14, 23).
Myosins are actin-based motor proteins that are involved in actin-based motility and organelle trafficking. In eukaryotes, they are required for a number of diverse functions ranging from cytokinesis to muscle contraction (41). The primary structure of an unconventional myosin (class I) consists of head (motor) domain that binds ATP, neck (regulatory) domain, followed by class-specific tail domain. (35). The neck domain contains various IQ (isoleucine-glutamine) motifs that bind calmodulin (2) and regulate the motor activity. Unlike the conventional class II myosins, class I myosins are associated with cell membranes and leading edge of migrating cells, including filopodia, lamellipodia, and membrane ruffles (5). Members of the myosin I family have also been implicated in the regulation of dynamic cellular processes such as endosomal recycling, vesicle and organelle trafficking, and calcium channel activity (18, 30, 32, 34, 43).
Myosin 1c (Myo1c) is one of nine isoforms of the human myosin I gene (17). In motile cells, Myo1c is predominantly present at the leading edge, localizing to both the cell periphery and cell surface (6). Like other unconventional myosins, Myo1c interacts with actin (7). Myo1c is involved in the transport of vesicular cargo, including the trafficking of Glut-4 glucose transporter, epithelial Na+ channel, podocyte protein Neph1, and NF-κB essential modulator (1, 7, 10, 40).
Both Myo1c and syntaxin-6 [a Golgi- and endosome-localized N-ethylmaleimide-sensitive factor-attachment protein (SNAP) receptor protein (SNARE)] are involved in the delivery of membrane raft components to the PM in fibroblasts and epithelial cells (8, 12). Although studies of endothelial cells have shown that syntaxin-6 regulates post-Golgi trafficking and delivery of VEGFR2 to the PM, thereby regulating angiogenesis (27), the role of Myo1c in VEGFR2 trafficking has not yet been investigated. The objective of this study was to determine whether Myo1c is involved in the delivery of VEGFR2 to PM and, therefore, VEGF-mediated angiogenic signaling. Our results demonstrate that Myo1c plays a role in maintaining VEGFR2 localization at the PM in response to VEGF stimulation. We further demonstrate that Myo1c and VEGFR2 colocalize in Cav1-rich membrane rafts in a VEGF-dependent manner and in Myo1c-depleted cells, VEGFR2 is degraded and the VEGF-induced angiogenic signaling associated with endothelial cell proliferation and migration is disrupted.
The rabbit monoclonal antibodies (mAbs) against human VEGFR2 (55B11) and phospho-VEGFR2 (Y1175) were purchased from Cell Signaling Technology (Danvers, MA). The rabbit polyclonal Ab against Myo1c (HPA001768), as well as cycloheximide (CHX), brefeldin A (BFA), and dynasore, were purchased from Sigma (St. Louis, MO). VEGF-A165 (VEGF) was purchased from R&D Systems (Minneapolis, MN). FuGENE 6 transfection reagent, protease inhibitor, and phosphatase inhibitor cocktail tablets were obtained from Roche Diagnostics (Indianapolis, IN). The mouse mAb against Cav1, collagen type I, and endothelial cell growth supplement were obtained from BD Biosciences (San Jose, CA). The horseradish peroxidase-labeled secondary Ab used for immunoblotting was obtained from Amersham Biosciences (Piscataway, NJ). Alexa Fluor-conjugated secondary Abs were procured from Invitrogen, Molecular Probes (Eugene, OR). Vectashield mounting medium was obtained from Vector Laboratories (Burlingame, CA). SuperSignal West Femto ECL reagent was obtained from Thermo Scientific (Rockford, IL). The mouse mAb against Myo1c (used in immunofluorescence assays), green fluorescent protein (GFP)-Myo1c, and mutant GFP-Myo1c plasmid constructs were kindly provided by Dr. Deepak Nihalani and has been previously described (1, 4, 39). All other reagents were purchased from Sigma unless stated otherwise.
Cell culture.
Primary human umbilical vein endothelial cells (HUVECs) were obtained from Lonza (Walkersville, MD) and cultured on collagen-coated plates in MCDB 131 containing 7.5% fetal bovine serum, 25 ng/ml endothelial cell growth supplement, 10 ng/ml epidermal growth factor, 2 mM l-glutamine, 1 μg/ml hydrocortisone, 50 μg/ml gentamicin, and 250 ng/ml fungizone. The cells were maintained at 37°C in a humid 95% air-5% CO2 atmosphere, split at a ratio of 1:3, and used only between passages 3 and 7. Human embryonic kidney cells expressing simian virus 40 large T antigen (293T cells) (ATCC) were maintained in Dulbecco's modified minimum essential medium containing 10% fetal bovine serum. Treatment of HUVECs with VEGF was carried out at a concentration of 50 ng/ml unless otherwise indicated. For treatment with BFA, cells stably expressing the Myo1c-targeted or control small hairpin RNA (shRNA) were treated with 1 μg/ml of BFA.
Generation of stable Myo1c knockdown HUVECs.
A plasmid containing shRNA against Myo1c was purchased from Sigma (Catalog number TRCN0000122927 NM_033375.3). Lentiviral particles were generated by cotransfecting the Myo1c shRNA-expressing plasmid, envelope plasmid (pMD2.G), and packaging plasmid (pCMV-dR8.74) into HEK-293T cells using Fugene HP transfection reagent (Roche). At 48 h posttransfection, lentivirus-containing supernatant was collected and filtered through a 0.45-μM syringe filter. Early passage HUVECs were transduced with lentiviral supernatant in the presence of 8 μg/ml polybrene (Sigma). Later (24 h), the medium was replaced, and the cell population stably expressing the shRNA was enriched via puromycin (1 μg/ml) selection for 3 days. Knockdown of the Myo1c protein was confirmed by immunoblotting.
Membrane raft preparation.
Raft-enriched membrane fractions were prepared by OptiPrep density gradient centrifugation as described in the study of Katoh et al. (22). Briefly, confluent HUVECs (grown in 10-cm dishes) were scraped and pelleted after washing with phosphate-buffered saline (PBS). The pellet was lysed for 30 min on ice in lysis buffer containing 25 mM Tris·HCl (pH 7.4), 125 mM NaCl, 12.5 mM EDTA, 1% Triton X-100, and inhibitor of protease and phosphatases, and all steps were performed at 4°C on ice. The lysate was adjusted to contain 40% OptiPrep by adding four volumes of 50% OptiPrep in the same lysis buffer and placed at the bottom of an ultracentrifuge tube. Optiprep (40%)-containing lysate (0.525 ml) was overlaid with 0.75 ml of 30% Optiprep in lysis buffer and 0.225 ml lysis buffer without OptiPrep, respectively, forming a 0–40% discontinuous OptiPrep gradient when centrifuged at 55,000 rpm for 2 h in a swinging bucket, S55S rotor (Beckman Instruments, Fullerton, CA). For analysis of the resulting gradient, 13 equal volume fractions of 100 μl each were carefully collected from the top of the gradient, and proteins were resolved by SDS-PAGE and analyzed by immunoblotting.
Cell-surface biotinylation.
To measure the pool of VEGFR2 at the PM, we covalently labeled cell-surface proteins with a membrane-impermeant biotinylation reagent (NHS-SS-biotin; Pierce, Rockford, IL) using methods previously described (27). All steps were performed at 4°C. Cells were washed three times in PBS and then incubated with 0.15 mg/ml sulfo-NHS-SS-biotin in PBS for 10 min. The unreacted biotinylation reagent was quenched by washing once with a buffer containing (in mM) 25 Tris (pH 8), 137 NaCl, 5 KCl, 2.3 CaCl2, 0.5 mM MgCl2, and 1 mM Na2 HPO4. The cells were then again washed three times with PBS and resuspended in radioimmunoprecipitation assay buffer containing a protease inhibitor cocktail. The resulting lysates were centrifuged at 14,000 g for 10 min at 4°C. A sample taken from the supernatant at this point represented total cellular VEGFR2. Streptavidin-sepharose high-performance beads (GE Healthcare) were added to the remaining supernatant (100 μl packed beads per 500 μl lysate) and left on a rotator at 4°C for 2 h. The beads were collected by centrifugation at 14,000 g for 10 s at 4°C, and the supernatant was removed. The beads were then washed three times in lysis buffer at 4°C, and protein was extracted from the beads by heating at 95°C in SDS-PAGE sample buffer.
Cultured cells were washed twice with ice-cold PBS and lysed in radioimmunoprecipitation assay buffer supplemented with inhibitors of proteases and phosphatases for 30 min on ice and centrifuged at 13,000 g for 20 min before supernatants were collected. The protein concentration was estimated using the Bio-Rad DC Protein Assay kit (Bio-Rad). Proteins (10–25 μg) per lane were resolved by SDS-PAGE and transferred to a polyvinylidene difluoride membrane. After blocking with 5% (wt/vol) nonfat dried skimmed milk powder in TBS plus Tween-20 buffer, the membrane was incubated with the appropriate primary Abs at 4°C overnight and then with secondary Ab for 1 h at room temperature (RT). Ab binding was visualized by developing the blot with enhanced chemiluminescence reagent. The bands were visualized using ChemiDocIt (UVP) and then analyzed using ImageJ 1.42q software (http://rsbweb.nih.gov/ij/).
Immunofluorescence assay and image analysis.
Microscopy studies were performed as previously described (27). Briefly, cells grown on acid-washed glass coverslips were fixed with 4% paraformaldehyde in Dulbecco's modified PBS for 25 min at RT, after which the reaction was quenched by adding 100 mM glycine in PBS and incubating for a further 15 min at RT. The cells were then permeabilized with 0.1% Triton X-100 in PBS for 2 min at RT, blocked with PBS containing 5% glycine and 5% normal goat or donkey serum for 60 min, and incubated with primary Abs overnight at 4°C. Coverslips were incubated for 1 h in a 1:200 dilution of either Alexa Fluor 488- or Alexa Fluor 594-conjugated secondary A and mounted using Vectashield mounting medium containing 4,6-diamidino-2-phenylindole. Fluorescence images were acquired using Zeiss LSM 700-inverted confocal microscope (Carl Zeiss) with a Plan-Apochromat 63×/1.40 oil objective or Plan-Apochromat 40×/1.3 oil objective (Zeiss) in x, y-, and z-planes. Epifluorescence images were acquired using a Leica spinning disk confocal microscope equipped with a Hamamatsu EM-CCD digital camera (Hamamatsu Photonics). The acquired images were processed using Metamorph image processing software (Molecular Device, Downingtown, PA). For a given experiment, all photomicrographs were exposed and processed identically for each fluorophore. Background fluorescence correction was done using unlabeled specimens. For double and triple Ab labeling experiments, control samples were labeled identically with the individual fluorophores and exposed identically to the dual/triple-labeled samples at each wavelength to verify that there was no crossover between emission signals for different channels at the exposure settings used.
For quantitative colocalization studies, individual cells (overlaid image of 2 or 3 wavelengths) were mapped and pasted into a new image file. The individual images recorded following excitation at two to three different wavelengths were then separated, and a lower threshold was set individually for each image to ensure that background fluorescence was reduced to zero. The thresholded (background subtracted) images were then analyzed using the quantitative colocalization function of the Metamorph software. The total pixel intensity of the thresholded protein 1 that colocalized with protein 2 or protein 3 was quantified and displayed as either a percentage of the total pixel intensity of protein 1 staining over the entire cell or that of a selected region of interest (e.g., PM or perinuclear Golgi) within a cell. This method was used for 10 cells per condition from three separate experiments.
Real-time quantitative RT-PCR analysis for VEGFR2 mRNA expression.
Endothelial cells stably expressing either scrambled shRNA (scr-shRNA) or shMyo1c were used to isolated total RNA using a Qiagen RNeasy kit (Qiagen) and quantified. cDNA was synthesized from total RNA using the iScript cDNA synthesis kit (Bio-Rad). Thermocycler conditions included a 5-min incubation at 25°C, a 30-min incubation at 42°C, and a 5-min incubation at 85°C. The cDNAs were subjected to quantitative PCR analysis with the following 5′→3′ primers (sense and antisense, respectively): VEGFR2, 5′-CACCACTCAAACGCTGACTA-3′ and 5′-CACCACTCAAACGCTGACAT-3′ (amplicon length, 74 bp); and human 18S rRNA (housekeeping gene) CCTTGGATGTGGTAGCCGTTT and AACTTTCGATGGTAGTCGCCG (amplicon length, 105 bp). Primers were designed using Primer Express software (Applied Biosystems). The assay was performed in a 96-well optical plate with a final reaction volume of 20 μl, including synthesized cDNA (20 ng), oligonucleotide primers (100 μM each), and 2× SYBR Green/ROX PCR master mix (Bio-Rad). Samples were run on an ABI PRISM Sequence Detection System (model 7000, Applied Biosystems). PCR conditions were one cycle for 10 min at 95°C, followed by 30–45 cycles (15–25 cycles for 18S rRNA) of 30 s denaturation at 95°C, 1 min annealing at 55–60°C, and 1 min extension at 72°C. Samples were checked for nonspecific products or primer/dimer amplification by melting curve analysis. The threshold cycle (Ct) values for VEGFR2 and 18S in all of the samples (analyzed in triplicate) were normalized on the basis of the abundance of the 18S transcript. Relative expression is expressed as 2−dCt, where dCt = (cycle threshold for the soluble fms-like tyrosine kinase 1) − (cycle threshold for the 18S rRNA transcript).
Cell proliferation assay.
HUVECs (2 × 104) were seeded in 96-well plates. After 24 h, they were either left untreated or were infected with syntaxin 6-cyto or syntaxin 16-cyto. After infection for 6 h, the cells were serum (0.1%) starved for 6 h and then treated with VEGF at 50 ng/ml for 24 h. Proliferation was measured using 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) colorimetric assay according to the manufacturer's recommendations (Promega). The absorbance at 490 nm was determined using a Spectra Fluor PLUS (Molecular Devices, Sunnyvale, CA). For each group, samples were prepared in triplicate. The data are presented as the fold increase over control levels.
Cell migration assay.
Harvested endothelial cells (2 × 104) were replated in triplicate onto the 0.1% collagen-coated upper chamber of a Transwell filter with 8-μm pores (6.5 mm, polycarbonate, Costar), and the chamber was placed in serum-free medium for 6 h. Serum-free medium containing VEGF (100 ng/ml) was added to the lower chamber to stimulate chemotaxis. After 4–6 h, the cells were fixed with 4% paraformaldehyde in PBS. Cells on the upper side of the filter (those that had not migrated) were removed with a cotton swab, and cells on the underside of the filter were stained with 2% crystal violet in 10% ethanol. After the cells were extensively washed in water to remove excess crystal violet, the filters were dried overnight. The number of cells that had migrated was determined by eluting the crystal violet dye from the stained cells on the underside of the filter in 250 μl of 10% acetic acid (for 15 min), followed by optical density measurement 562 nm. In parallel, cells were separately plated to transwell filters without any serum in the lower chamber (in triplicate) to control for the total number of cells that were simply attached. Relative cell migration was determined by normalizing the number of cells that had migrated to the total number of the cells adhering to transwell filters.
Statistical analysis.
All values are expressed as means ± SD. Statistical significance was determined using a two-sided Student's t-test and GraphPad Prism software (GraphPad Software, version 4.0; San Diego, CA). Unless stated otherwise, a value of P < 0.05 was considered significant.
VEGFR2 colocalizes with Myo1c and Cav1 at the PM and cofractionates with Cav1-enriched membrane rafts.
To establish what role, if any, Myo1c plays in VEGFR2 trafficking, we first assessed the localization of these two proteins in primary endothelial cells. Immunolocalization of the endogenous proteins revealed that VEGFR2 colocalizes with Myo1c and Cav1 at the PM (Fig. 1A). Quantitative analysis revealed ≥75% colocalization with Myo1c and ≥35% colocalization with Cav1 of VEGFR2 at the cell periphery (Fig. 1B). These results indicate that under normal conditions, VEGFR2 associates with Myo1c and Cav1 at the PM, consistent with observations made by other investigators that VEGFR2 and Myo1c are both present in membrane rafts (8, 23). We further investigated whether VEGFR2, Myo1c, and Cav1 colocalize in membrane rafts. OptiPrep gradient fractionation was performed to identify membranes enriched for the raft-associated protein Cav1. Our results show that among 13 fractions collected from the top of the gradient, fractions 3 and 4 were enriched in Cav1. Approximately 30 to 40% of total VEGFR2 cofractionated with Myo1c in Cav1-positive membrane-raft fractions (Fig. 1, C and D). These finding are consistent with VEGFR2 and Myo1c colocalization and VEGFR2 and Cav1 colocalization at the PM (Fig. 1, A and B). These results strengthen the possibility that PM pool of VEGFR2 associates with Myo1c- and Cav1-rich domains.
VEGF stimulation induces the recruitment of VEGFR2 to Myo1c and Cav1-containing membrane rafts.
VEGF-A is a ligand for VEGFR2 and is known to initiate internalization and transport of the latter to the late endosomes and lysosomes for degradation (9). In addition, VEGF stimulation mobilizes VEGFR2 from internal organelles such as the Golgi complex for subsequent delivery to the PM (27). We wanted to determine whether localization of VEGFR2 along with Myo1c and Cav1 to the PM from Golgi could be modulated by stimulating cells with VEGF. Therefore, serum-starved HUVECs were pretreated with CHX (to prevent new VEGFR2 synthesis and transport to the Golgi) and then with VEGF (30 min in the presence of CHX), and the localization of VEGFR2 at Golgi and PM was monitored. Immunofluorescence analysis showed that in serum-starved endothelial cells, the majority of VEGFR2 colocalized (≥80%) with Golgi marker trans-Golgi network 46 (TGN46) (Fig. 2, A and B); however, upon VEGF stimulation, the amount of VEGFR2 at the PM was even greater (Fig. 2, A and C), and its colocalization with Myo1c and Cav1 increased (to ≥75 and ≥35%, respectively, Fig. 2C). Localization of Myo1c to the PM and the extent of its colocalization with Cav1 did not alter in response to VEGF stimulation (Fig. 2, A and C). These results suggest that VEGF alters the subcellular localization of VEGFR2 and may recruit the receptor to Cav1-enriched regions at the PM.
To confirm and complement these findings, we used a density gradient fractionation approach analyzing the redistribution of VEGFR2 to Myo1c- and Cav1-containing membrane rafts upon VEGF stimulation. Cells were either serum starved or stimulated with VEGF and then processed for fractionation using OptiPrep density gradient centrifugation. The analysis of collected fractions suggests that in the absence of VEGF, ∼80 to 90% of cell-associated VEGFR2 partitioned in endosome (EEA1 enriched) and Golgi fractions (TGN46 enriched), which lack Cav1 and Myo1c (Fig. 3, A and B). However, upon stimulation with VEGF-A (30 min), ≥50% of total VEGFR2 redistributed to Myo1c- and Cav1-containing PM (syntaxin 4 enriched) fractions (Fig. 3, C and D). These results indicate that VEGFR2 is enriched in Myo1c-containing PM raft fractions in response to VEGF stimulation.
Myo1c depletion results in decreased cell-surface and total cellular VEGFR2 levels.
Since VEGF stimulation enhances partitioning of VEGFR2 into Myo1c-containing fractions, we investigated the possibility that Myo1c regulates the subcellular localization of VEGFR2. For this experiment, we transduced primary endothelial cells with lentivirus encoding a shRNA (shMyo1c) specific for human Myo1c. Cells stably expressing shMyo1c were selected using puromycin. In a similar fashion, we also generated cells stably expressing a scr-shRNA as a control. The shMyo1c stable cells showed 75–85% knockdown of Myo1c protein relative to controls (Fig. 4, A and B).
We used these Myo1c knockdown and control cell lines to examine the role of Myo1c in localizing VEGFR2 at the cell surface and its effect on total cellular level of VEGFR2. Cell-surface biotinylation revealed a ≥70% reduction at the cell surface and a ≥75% reduction in the total pool of VEGFR2 in Myo1c-depleted cells relative to controls following stimulation with VEGF (Fig. 4, C and D). The intracellular localization of VEGFR2 was significantly altered in the shMyo1c-expressing stable line compared with control, as the VEGFR2 levels at PM and its perinuclear accumulation were reduced (Fig. 4F). To understand the mechanism by which intracellular VEGFR2 levels are reduced in Myo1c-depleted cells, we first analyzed the expression of VEGFR2 mRNA in scr-shRNA and shMyo1c-expressing stable lines by quantitative real-time RT-PCR. Expression levels were similar in shMyo1c and scr-shRNA stable lines (Fig. 4E), suggesting that the decrease in the levels of VEGFR2 in the shMyo1c stable line relative to controls was not due to reduced mRNA expression.
To distinguish between the possibilities that Myo1c is required for VEGF-induced delivery or maintenance of VEGFR2 at the cell surface, we overexpressed GFP-tagged wild-type murine Myo1c (GFP-Myo1c) and mutant GFP-Myo1c (dominant negative form that lacks ATP and actin-binding domains) in shMyo1c stable cells. GFP-Myo1c overexpression in these cells rescued cell-surface VEGFR2, resulting in a fivefold increase relative to that in Myo1c-depleted cells in response to VEGF stimulation (Fig. 4, F and G). However, overexpression of mutant GFP-Myo1c failed to rescue VEGFR2 at the cell surface in Myo1c-depleted cells. Our data also show that overexpression of mutant GFP-Myo1c reduces PM and total VEGFR2 levels in control (scr-shRNA), an effect similar to that observed upon Myo1c depletion (Fig. 4, F and G). These results suggest that functional Myo1c is essential for maintaining normal cellular levels of VEGFR2.
VEGFR2 level in Myo1c-depleted cells is restored by treatment with either BFA, dynasore, or chloroquine.
To determine the mechanism by which loss of Myo1c alters cellular distribution of VEGFR2 in response to VEGF, we inhibited endoplasmic reticulum (ER) -to-Golgi transport by subjecting cells to treatment with BFA for 2 h (that results in resorption of the Golgi complex into ER, Fig. 5A) (21, 27). We then assessed the intracellular distribution of VEGFR2 in the presence or absence of VEGF in cell lines stably expressing either scr-shRNA or shMyo1c by immunofluorescence imaging. Myo1c-depleted cells showed a decrease in intracellular VEGFR2 levels only in response to VEGF stimulation (Fig. 5, B and C). In response to VEGF, BFA-treated shMyo1c-expressing cells showed increased intracellular accumulation of VEGFR2 (relative to that in mock-treated cells) within punctate vesicular structures (Fig. 5, B and C). As expected, in the control group, BFA treatment resulted in the accumulation of VEGFR2 in perinuclear area and corresponding loss of prominent Golgi-like perinuclear staining (Fig. 5B). Quantitation revealed 75% increase in intracellular accumulation of VEGFR2 in BFA-treated, VEGF-exposed shMyo1c stable cells (Fig. 5C). The PM level of VEGFR2 was reduced in control and Myo1c-depleted cells after BFA treatment most likely because of a block in membrane trafficking between ER and Golgi complex (Fig. 5, A, B, and D).
We next investigated whether Myo1c depletion affects the targeting of endocytic VEGFR2 pool (PM-localized) for degradation. We used dynasore, a small-molecule reversible inhibitor of dynamin 1 and 2 to inhibit clathrin-dependent and -independent endocytic pathways (Fig. 5A) (26, 29). We expected that if Myo1c has a role in regulating VEGF-induced trafficking of endocytic VEGFR2, then dynasore treatment should trap VEGFR2 at the PM and prevent its degradation in Myo1c-depleted cells. Indeed, dynasore treatment increased the PM expression of VEGFR2 by ≥200% in controls and Myo1c-depleted cells in response to VEGF (Fig. 5, B and D). In addition, dynasore treatment also rescued intracellular upregulation of VEGFR2 levels in Myo1c-depleted cells exposed to VEGF; these receptors were trapped in the Golgi complex and at the PM (Fig. 5B). Quantitation of the images revealed a ≥75% VEGF-mediated increase in intracellular accumulation of VEGFR2 in dynasore-treated shMyo1c stable cells (Fig. 5C). Golgi accumulation of VEGFR2 upon dynasore treatment suggests that dynamin GTPase is required for VEGFR2 to exit the Golgi complex. These results indicate that blocking membrane transport from ER to Golgi complex or anterograde transport from Golgi prevents Myo1c depletion-induced VEGFR2 reduction following stimulation with VEGF. We previously showed that blocking syntaxin 6-regulated post-Golgi trafficking of VEGFR2 targets this receptor to the lysosomes for degradation (27). We next investigated whether the decreased VEGFR2 level in Myo1c-depleted cells is due to a block in VEGF-induced VEGFR2 delivery to the PM. We found that treatment with chloroquine [an inhibitor of lysosomal hydrolases that effectively blocks VEGFR2 degradation in lysosomes (27, 38)] rescued intracellular levels of VEGFR2 in Myo1c-depleted cells treated with VEGF (Fig. 5, E and F). Thus VEGF appears to stimulate delivery of the post-Golgi and endocytic pools of VEGFR2 to the PM via a Myo1c-dependent mechanism, and in the absence of Myo1c, VEGFR2 appears to move from PM to lysosomes where it is processed for degradation.
Myo1c is required for VEGF-induced endothelial cell proliferation and migration.
The functional significance of Myo1c depletion was first assessed in response to VEGF-induced endothelial cell proliferation. Endothelial cells stably expressing shMyo1c showed a ≥3-fold reduction in VEGF-induced cell proliferation relative to wild-type HUVECs and scr-shRNA-expressing cells (Fig. 6A). The effect of Myo1c depletion on endothelial cell migration was also determined. Specifically, directed cell migration in the presence or absence of VEGF was analyzed using the Boyden chamber assay. The stable endothelial line expressing shMyo1c showed a ≥2-fold reduction in migration to the lower chamber in response to VEGF relative to HUVECs and scr-shRNA-expressing cells (Fig. 6B). These results suggest that Myo1c is required for maintaining VEGFR2 at the cell surface where it can associate with VEGF and transmit cell proliferation and migration signals. VEGF-induced phosphorylation of VEGFR2 has been shown to regulate endothelial cell migration via Src activation and cell proliferation via mitogen-activated protein kinase/extracellular signal-regulated kinase-1/2 (ERK1/2) activation (28, 37). We found that in Myo1c knockdown cells, levels of phosphorylated VEGFR2 (pY1175), c-Src (pY419, active), and Erk1/2 (active) kinases were reduced (Fig. 6, C and D). These experiments indicate that Myo1c participates in the regulation of dynamic endothelial cell processes such as proliferation and migration by regulating the signaling events downstream of VEGFR2.
VEGFR2 is expressed at the endothelial cell surface and regulates angiogenesis in response to VEGF. Binding of VEGF to VEGFR2 at the cell surface initiates signal transduction and alters receptor localization and its distribution in distinct domains within the PM. Membrane rafts located at the cell surface (caveolae) are enriched for Cav1. Previous biochemical and ultrastructural studies have demonstrated that VEGFR2 is present in both raft and nonraft regions of cell membranes. The motor protein Myo1c is a member of unconventional myosin family and has been shown to localize at the leading edge of motile cells (13, 33). Our analysis reveals that a significant fraction of total Myo1c colocalizes with Cav1 at the cell surface in primary human endothelial cells. We show that exposure of cells to VEGF-A increases the recruitment of VEGFR2 to Myo1c- and Cav1-rich cell-surface membrane rafts. Importantly, Myo1c depletion drastically reduces total cellular VEGFR2 concentration in response to VEGF treatment, but does not alter VEGFR2 mRNA levels. Given the importance of VEGFR2 in angiogenesis our study represents a key advancement in the study of angiogenic receptors regulation.
Cell-surface VEGFR2 exists in a dynamic state, and its levels are maintained by internalization, recycling, secretory transport, and delivery of receptor to the PM (3, 9, 16, 19, 24, 27, 42). In response to VEGF stimulation, endothelial cells mobilize VEGFR2 from the Golgi complex for subsequent transport to the PM (27), which most likely involves intermediate vesicular compartments. In both adipocytes and epithelial cells, Myo1c is involved in PM delivery of transmembrane cargo proteins such as NF-κB essential modulator, Glut-4, and Neph1 (1, 7, 33). We observed that in human endothelial cells, Myo1c and VEGFR2 colocalize at the PM and cofractionate with PM-rich domains by density gradient analysis. We further demonstrate that VEGFR2 colocalizes with Myo1c at PM in a VEGF-dependent fashion. In epithelial cells, Myo1c localizes to membrane rafts (8), which is in agreement with our data showing colocalization of Myo1c with Cav1 at the PM of endothelial cells. Previous subcellular fractionation of aortic endothelial cells had shown that VEGFR2 is partitioned into Cav1-enriched membrane raft fractions but that VEGFR2 is mobilized out of raft membranes following activation by VEGF (23). In contrast, our data suggest that VEGFR2 is redistributed from the nonraft to raft fractions in response to VEGF. Our results are supported by immunolocalization studies demonstrating that VEGFR2 is recruited to PM and colocalizes with Myo1c and Cav1 in response to VEGF. We also observed that a fraction of VEGFR2 in the perinuclear region colocalizes with TGN46 (indicating that it is present in the Golgi) and that VEGF-stimulation leads to reduced colocalization at these locations and increased colocalization with Myo1c and Cav1 at PM. Our results and previous studies by other investigators have prompted us to hypothesize that VEGF mobilizes inactive intracellular VEGFR2 from Golgi for delivery to the PM that is mediated through a Myo1c-dependent mechanism for subsequent receptor activation and signaling (11, 23).
Previous studies indicating the involvement of Myo1c in translocation of Glut-4 and Neph1 to the PM (1, 7) and ours demonstrating restoration of cell-surface VEGFR2 levels in Myo1c-depleted cells in which Myo1c is overexpressed support our hypothesize that Myo1c is required for the delivery of VEGFR2 to PM in endothelial cells. When cells are depleted of Myo1c, the PM pool of VEGFR2 is reduced in a VEGF-dependent manner as is the total intracellular pool of VEGFR2. Since our data indicate that Myo1c depletion altered neither expression of the VEGFR2 mRNA nor trafficking of the protein between the ER and Golgi but it did affect the delivery of receptor to the PM, we postulate that loss of Myo1c may lead to a transient accumulation of VEGFR2 destined for PM delivery in vesicles at the interface between actin cytoskeleton and PM [site at which Myo1c is thought to contribute to exocytic delivery of cargo to the PM (30)] and that it may eventually be rerouted for subsequent degradation in lysosomes. Notably, in a previous study we observed that blocking post-Golgi VEGFR2 trafficking by inhibiting syntaxin 6 function reroutes receptor from PM to lysosomes. Since Myo1c is known to regulate short-range transport events, it is likely that VEGF stimulation causes a pool of VEGFR2 to be recycled back to the PM shortly after endocytosis in a Myo1c-dependent manner. This is supported by the finding that blocking endocytosis prevented Myo1c depletion-induced VEGFR2 degradation. We previously showed that syntaxin 6 plays a role in the post-Golgi trafficking of VEGFR2 for subsequent transport via intermediate vesicular compartments along the secretory pathway before being delivered to the PM (27). Alternatively, Myo1c may play a role in the delivery of VEGF-responsive secretory post-Golgi pool of VEGFR2 to the PM. Therefore, our study indicates that Myo1c plays a critical role in rapid VEGF-induced VEGFR2 recruitment to the PM from endocytic and secretory pools and thus participates in the regulation of endothelial cell dynamics.
VEGF binding to VEGFR2 leads to phosphorylation of VEGFR2 and activation of MAPKs including ERK1/ERK2 to promote endothelial cell proliferation. VEGF-induced activation of VEGFR2 also stimulates Src phosphorylation in endothelial cells (31). Here we report for the first time that loss of Myo1c can antagonize both VEGF-induced endothelial cell proliferation and migration. Reduced proliferation in Myo1c-depleted cells is most likely due to decreased total and phosphorylated (Y1175) VEGFR2, which accounts for the reduced ERK1/ERK2 phosphorylation (activation). VEGF also induces the formation of a complex by VEGFR2, VEGFR-associated protein (also known as TSAD), and c-Src; this interaction has been suggested to regulate Src activation and endothelial cell migration (28). Reduced Src activation in Myo1c-depleted cells may be due to the absence of active VEGFR2. Myo1c has been shown to regulate the delivery of membrane-raft contents at the PM (8) and c-Src activation has been shown to require membrane rafts (25). Hence, Myo1c may regulate not only VEGFR2 trafficking but also c-Src activation. Given the limited information available on the role of unconventional myosins in VEGFR2 trafficking and angiogenesis, our study provides significant advancement in this field. This is the first study that demonstrates the role of Myo1c in regulating VEGF-induced angiogenic signal transduction by regulating VEGFR2 localization at the endothelial cell surface.
This work was supported in part by National Institutes of Health Grants R01-HL-089599 (to A. Choudhury) and R01-DK-087956 (to D. Nihalani).
No conflicts of interest, financial or otherwise, are declared by the author(s).
A.T., J.-J.J., and S.M.I. performed experiments; A.T., J.-J.J., S.M.I., and A.C. analyzed data; A.T., J.-J.J., S.M.I., and A.C. interpreted results of experiments; A.T., J.-J.J., and S.M.I. prepared figures; A.T., J.-J.J., S.M.I., and A.C. drafted manuscript; A.T., J.-J.J., S.M.I., D.N., and A.C. edited and revised manuscript; A.T., J.-J.J., S.M.I., D.N., and A.C. approved final version of manuscript; A.C. conception and design of research.
We thank Dr. Christine Blaumueller for editorial contributions.
- Copyright © 2013 the American Physiological Society

subset: commoncrawl


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August 26, 2014
Student Outreach Children's Clinic
Aug. 26 Clinic Geared to Children's Back-To-School Needs
6–9 p.m.
Please Note: This event has already occurred.
Those without medical insurance are encouraged to attend our Student Outreach Children's Clinic Tuesday, Aug. 26 from 6 p.m. to 9 p.m.
The clinic will be held at the School of Medicine's Family Medicine Center, located on the University of Nevada, Reno campus on the corner of 17th street and East Stadium Way (just north of Mackay Stadium). You can take RTC bus route 7 to North Virginia Street or the free Sierra Spirit bus.
Student Outreach Clinics are a free service providing much needed care for Washoe County's medically uninsured population. The August 26th clinic is specially geared towards the needs of children. No appointment is necessary. Patients will be seen on a first-come, first-served basis. Early arrival is recommended. Spanish translators are available as needed.
Under the direct supervision of licensed faculty and community physicians, medical students from the University of Nevada School of Medicine offer monthly Student Outreach Clinics providing free care to the medically uninsured.
Visit the Student Outreach Clinic website for more information.
- Category
- Clinic
- Audience
- General Public
- Student
- Region
- North (Reno Area)


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i want to try some roms on this scl, but not sure if they are the same thing, couldnt find a specific page regarding scl so my wild guess is that is the same as this, am i right?
As falex said, the "two" phones are the same.The important thing here is the Number. Think of it as a kind of series number. I9000 = SGS, I9003 = SGSL, I9100 = SGS II, and so on.
Sent from my GT-I9003 using XDA App
Well The Sig generally needs a little correction. Haven't done it yet.
Sent from my GT-I9003 using XDA App
XDA Developers was founded by developers, for developers. It is now a valuable resource for people who want to make the most of their mobile devices, from customizing the look and feel to adding new functionality.
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Ever wanted to meet the cStreet Campaigns team IRL? Now's your chance! Below are a few upcoming events we're organizing or will be at.
Torontonians with Vision Party
(Toronto, Nov 15): Come watch the returns with us on Vancouver election night. Watch the world's most handsome mayor get re-elected with his troupe of amazing progressives.
Enter your email below to subscribe to our digital magazine, Tactics
CanRoots East
(Toronto, Nov 28-20): Bringing together activists and organizers from a wide variety of incredible organizations, join us to share stories, gain new skills, and trade ideas for building a more progressive, engaged Canada. cStreet's own CEO Amy Leaman will be leading a workshop.
Learn more about CanRoots & register >
Let us know you'll be there >
(Washington, DC, Dec 13-15): cStreet will be at RootsCamp on December 13 and 14 in Washington, DC, alongside a bunch of progressive organizers, data geeks, and activists of all levels to meet and share knowledge, build skills, and grow networks.
Learn more about RootsCamp & register >
Let us know you'll be there >


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After nearly two decades of having only bats, rats and the occasional tramp as inhabitants, the former Midland Grand Hotel beside London's St Pancras station is at last about to open its doors to paying guests in May, re-christened the St Pancras Renaissance Hotel London . The restoration of the grand Victorian-Gothic structure cost more than £150 million, but a recent visit showed it was money well spent.
There are a few casualties, including some original romantic murals that have been papered over. But most of the detailing has been painstakingly preserved. Sir George Gilbert Scott's wide stone cantilevered staircase – down which Sarah Miles and Dirk Bogarde swept when filming The Servant – has been sandblasted, so it looks like the inside of a snail's shell, and its intricate balustrade polished. The arched forecourt on which taxis parked has been artfully covered to create the reception area, and the adjoining old ticket hall, with its dark- panelled walls and soaring church-like windows, is now a bar.
On every floor, rooms open up to reveal elaborate and unique detailing. In the Ladies Smoking Room – the first public room in London set aside for women to enjoy tobacco in public – ceilings have been painted with fine patterns in a faded palette; in the dining room, the iron cornicing has been so thoroughly cleaned it resembles fine white lace; and on stairwells, the Brinton carpets have been rewoven in antique-looking colours. Best of all, the room just inside the building's triple-arched side entrance now has jewel-coloured Gothic ceilings and 22-carat gilded cornices beneath which diners will imbibe cocktails before adjourning to the 120-seat fine-dining restaurant.
The only new rooms are the 189 bedrooms in the extension to the rear, and bathrooms for the 38 Victorian suites in the original building. "When the hotel opened in 1871," says Royden Stock , the building's caretaker for more than 13 years, "there were only eight baths, in four rooms. Most people, if they wanted a wash, would ring for water to be brought to their rooms."
Thankfully the bathrooms aren't the only things to have been modernised. The hotel's plumbing and electrics have been entirely replaced, too. "In its day, there would have been only gas lamps in here," Stock says. "And the lifts quite often wouldn't get all the way to their destinations. I'm not sure guests would put up with that now..."
- More information at www.stpancrasrenaissance.com


text:
Engineering jobs remain strong, financially lucrative
While unemployment remains high, the demand and pay for engineers--especially electrical engineers--remain high.
Engineering jobs are a hot commodity, even in the wake of the Great Recession. Demand for people who can build, engineer, and design infrastructure in major projects all over the country remains very strong.
According to the Bureau of Labor Statistics there are more than 2.3 million jobs in the architecture and engineering fields, which often work close together on numerous projects. Electrical engineers, in particular, have 148,770 jobs as of May 2010, making it one of the largest in the field. Only civil and mechanical engineers totaled more in terms of personnel (margin of error 0.4%).
The pay isn't too bad, either. According to PayScale, the median starting pay for an entry-level worker in electrical engineering field is $60,800. Median overall pay is tied for fourth amongst all listed positions at $104,000 per year. Only aerospace, chemical, and petroleum (tops at $157,000) average more than electrical engineers.
Blue bars represent 'Starting Median Pay' - Silver bars represent 'Mid-Career Median Pay'
Annual pay for Bachelors graduates without higher degrees. Typical starting graduates have 2 years of experience; mid-career have 15 years. See full methodology for more.
The chart from PayScale also shows that of the top 10 college majors in terms of pay, seven of them are in the engineering field. All of the top 10 are either in math or science. With an added emphasis in recent years on math and science, especially with the U.S. test scores at an all-time low compared to the rest of the industrialized world, the people who excel in both and have a desire to join the engineering field will likely be rewarded with their hard work.
- Edited by Chris Vavra, Consulting-Specifying Engineer, www.csemag.com
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Before the calendar turned, 2016 already had the makings of a pivotal year for manufacturing, and for the world.
There were the big events for the year, including the United States as Partner Country at Hannover Messe in April and the 2016 International Manufacturing Technology Show in Chicago in September. There's also the matter of the U.S. presidential elections in November, which promise to shape policy in manufacturing for years to come.
But the year started with global economic turmoil, as a slowdown in Chinese manufacturing triggered a worldwide stock hiccup that sent values plummeting. The continued plunge in world oil prices has resulted in a slowdown in exploration and, by extension, the manufacture of exploration equipment.
Read more: 2015 Salary Survey


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text:
After 57-years the blonde bombshell has been transformed to reflect her diverse customer base.
The iconic toy is now available in three new body-types including petite, curvy and tall. The changes to Barbie's image also include 7 new skin tones, 22 eye colours and 24 new hairstyles including a curls and a half-shaved gender-neutral hair cut.
Source | Twitter @Barbie
The changes to Barbie's body type come after decades of criticism that her proportions are unobtainable and promote unhealthy body-image for young girls. While studies have shown Barbie only has a small impact on body-image it has been proven that given her proportions Barbie would not be able to stand-up if scaled up to life-size.
Source: BBC.co.uk
Over the last few years Mattel has faced a decline in sales as parents seek out toys that are more in line with their values. In a TIME cover story on Barbie's transformation Senior Vice President of Mattel, Evelyn Mazzocco says that many millennial parents consider Barbie "out of touch", "materialistic" and "not diverse"
Mattel believes the new dolls begin to address the criticism Barbie has faced for promoting unrealistic body standards, while also promoting a more inclusive images that girls can relate to.
In a statement about the new collection, Mazzocco said;
"We are excited to literally be changing the face of the brand - these new dolls represent a line that is more reflective of the world girls see around them - the variety in body type, skin tones and style allows girls to find a doll that speaks to them,"
The transformation was a huge undertaking for Mattel, who named the operation "Project Dawn" in order to keep it top secret. The in-depth report from TIME details the stages of the project including some troubling market research sessions involving young girls. In one session, the girls as young as 6 would undress the 'curvy' and laugh at it mercilessly.
Now released, the collection is being applauded for its progress. However, Mattel also expects to have some backlash and have set up a specified helpline to deal with complaints related to the new collection of dolls.
The new collection is available online HERE and will be in stores later this year.


text:
North-South Trade: Is Africa Unusual?
We estimate a gravity model to address the question of whether Africa's bilateral trade with industrial countries is 'unusual' compared with other developing country regions. Our main finding is that the unusually low level of African trade is explained by economic size, geographical distance and population. This result holds after controlling for a country's access to the sea, composition of exports, linguistic ties with industrial countries and trade policies. If anything, the average African country tends to 'overtrade' compared with developing countries in other regions, although the degree to which Africa overtrades had steadily declined over the past two-and-one-half decades. Copyright 1999 by Oxford University Press.
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Volume (Year): 8 (1999)
Issue (Month): 2 (July)
Pages: 228-256
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Outdoor Photographer – December 2016Nov 20
Outdoor Photographer is the premier magazine about outdoor photography. Our photography technique articles are geared to helping you capture the best wildlife, travel and outdoor sports photography. Review photography tips and keep up with digital photography as applied to nature photography; stay current with the latest in photography equipment. You can also explore our readers' favorite places that offer the best in photography locations.
Outdoor Photographer – December 2016
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text: I'll be in the parks for about a day and a half this coming weekend, and am trying to figure out what to prioritize and what to skip. It looks like the Captain America meet and greet is up and running, and I'm wondering if that's all it is, or if there are props from the new film to see as well. I don't like meeting characters, but I want to stop by if they have things from the movie to check out.


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Find It: Papaya Seed Dressing Mix
Today my dear friend FabSugar brought over a sad empty packet of Papaya Seed Dressing Mix. Apparently both she and her mom picked up a few packets when they were in Hawaii this Thanksgiving and have just run out. She wanted to know if I could help her track it down and lucky for her (and the rest of you), I have!
The Papaya Seed Dressing Mix is available in a 2 oz. bag. To prepare, you just add the mix to white wine vinegar (Fab used champagne vinegar for a better kick!) and then dilute with water. According to FabSugar, this dressing is similar to a light vinaigrette, only with a subtle papaya flavor that is not too sweet - like many other fruit flavored dressings.
There was a tiny bit of mix left in the packet that FabSugar gave me, however it wasn't enough to make any dressing. The mix is white with black flecks and is a granular blend of salt, sugar, onion powder, garlic powder, dehydrated papaya seeds, spices and a gum stabilizer. Out of curiosity I decided to taste it. It was salty, with a kick of sweet and you could definitely taste the garlic and onion powders. I think I may try to make my own flavoring mix someday, but until then we can always order Papaya Seed Dressing Mix for $2.50 a bag. It's also available in a low-calorie version: six 1.2 oz bags for $14.50.
Update: The link for the regular version of the Papaya Seed Dressing now says "Under Construction." Seems a bit weird... you can also buy it at the 2nd link, but you have to buy several bags.
How about you, do you have any weird food items that you need help finding? Drop me a line and I'll see what I can do!


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How do I eat this? A guide to difficult foodsAugust 8, 2014 Updated: August 10, 2014 5:19pm
Photo: Photos By William Luther / San Antonio Express-News
SAN ANTONIO — There are so many ways to commit a food faux pas.
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text:
- Do you need to share your ArcGIS project or parts of this project with colleagues or customers that don't have ArcGIS software?
- Do you need to share your geodata securely - so that no one could modify or extract it from the file that you provide?
CarryMap is a unique solution for reproducing your ArcGIS maps as self sufficient distributable electronic map applications for desktop computers, Apple iOS, and Android devices (CarryMap application for iOS and Android devices is available at App Store and Google Play Market, respectively).
How to use CarryMap mobile maps on iOS devices (pdf, 2 MB)
How to use CarryMap mobile maps on Android devices (pdf, 2 MB)
How to use CarryMap mobile maps on iOS devices - Chinese (pdf, 1 MB)
With CarryMap you get the professional production tool for making spatially enabled guides, exploration plans, field work maps, recreation and attraction plans for navigation and information support purposes. All that you can easily supply to any non GIS user having neither specific GIS software nor professional GIS skills and experience.
- Reproduce your ArcGIS map document or part of it as a searchable exe-file for unlimited distribution available for wide range of users. You can send it, burn to a CD or put up to your web site for download. The output maps data can be imported back to ArcGIS.
- Output map applications can be run on any Windows computer, Windows Mobile, iOS or Android.
- Compressed and protected spatial data, friendly user interface, advanced search capabilities accompanied with GPS navigation - you can have it all in just one executable file.
- Managing the access to the electronic map with passwords and time limits you have capabilities to safely distribute your spatial data.
Make your mobile maps more usable and interactive with the possibility of adding hyperlinks in the Identify dialog. Create your maps using different skin colors or add your own company logo to the map. This way the maps you create can be designed in a unified corporate style.
Based on the CarryMap technology Data East developed Zoo Nsk – a free application for the Novosibirsk zoo, one of the three biggest zoos in Russia. The application is available for Android and Apple iOS smart phones and tablets. With Zoo Nsk you can track your current location, find your favorite animals, see their description with photo, plan your own zoo visit route, as well as get detailed information about all attractions, cafes, and other services provided on site.
Learn more


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DeGeneres Loses Talk-Show Crown at Daytime Emmys
Ellen DeGeneres has lost her crown as the Queen of daytime TV — the hosts of The View ended her four-year run as Best Talk-Show Host at the Daytime Emmy Awards.
The beloved funnywoman had held on to the prize since 2005, but faltered at the ceremony on Sunday when she came up against The View's feisty foursome Whoopi Goldberg, Joy Behar, Elisabeth Hasselbeck and Barbara Walters.
But it wasn't all bad for DeGeneres — her daily talk show pulled back by picking up four awards during the night.
Fellow talk-show hosts Rachael Ray and Tyra Banks also walked away with prizes, winning Best Entertainment and Best Informative program for their respective TV shows.
Soap opera The Bold and the Beautiful took Best Drama, while Best Actor went to The Young and the Restless' Christian LeBlanc and Susan Haskell, from One Life to Live, was named Best Actress.
Haskell was also celebrating after her show scooped the most awards of the night, tied with All My Children — winning five Emmys in total.
PBS' Sesame Street received the lifetime achievement award in recognition of its 40-year run.
The ceremony was hosted by Ugly Betty star Vanessa Williams at the Orpheum Theater in Los Angeles.
(c) 2009 WORLD ENTERTAINMENT NEWS NETWORK LTD. All global rights reserved. No unauthorized copying or re-distributing permitted.


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Dunn not keen on trade talk
By Bill Ladson / MLB.com
Nationals first baseman Adam Dunn admitted that he doesn't like it when asked if he will be dealt before the Trade Deadline. Dunn is in the last year of a two-year $20 million deal.
Dunn said nothing has been done in terms of getting a contract extension.
"I hear this every single year. This is part of baseball and signing two-year deals that I hate," Dunn said. "There is always a possibility of getting traded, but that is out of my control. I think we have a very good nucleus of guys here. I don't think we need to break up that corps."
General manager Mike Rizzo said the Nationals continue to have interest in signing Dunn to an extension. He said the team is pleased with his offense and defense, which has improved dramatically this season.
"We're looking into it," Rizzo said about Dunn's contract status. "We've been talking about him since Spring Training.
"Like I said, we are looking at every way to improve the club.
"We like where Adam's at offensively and defensively. He's a big part of the clubhouse and a big part of the middle of the lineup."
Nats ponder Trade Deadline options
WASHINGTON -- General manager Mike Rizzo said the Nationals could be buyers or sellers before the July 31st Trade Deadline. He wouldn't get into specifics, but said they are looking to make deals that would help the Nationals in the long term. A year ago, for example, the Nationals traded for center fielder Nyjer Morgan and reliever Sean Burnett and the club was already out of the race.
"If that means buying, we would buy. If that means selling, we will sell. That hasn't changed since Opening Day," Rizzo said.
Rizzo acknowledged that the team's biggest need is starting pitching.
"That's everyone's biggest need and we are included in that," Rizzo said. "We need more starting pitching. Premier, front-line starting pitching is what everybody needs to get to the next level of championship-caliber clubs. We are no different."
Zimmermann has simulated game
WASHINGTON -- Nationals right-hander Jordan Zimmermann, on the disabled list because of elbow reconstruction, had his second simulated game and pitched two innings without any problems.
General manager Mike Rizzo said Zimmermann is expected to start his rehab assignment in a couple of weeks.
"Zimmermann is, according to his rehab calendar, probably a couple weeks away from going on a rehab start," Rizzo said. "We haven't thought about where he is going to go."
Tuesday could be bullpen game
WASHINGTON -- With left-hander John Lannan in the Minor Leagues, the Nationals need a pitcher for next Tuesday against the Braves in Atlanta. Washington is thinking about using a bullpen-by-committee using right-handers Miguel Batista, Joel Peralta and left-hander Sean Burnett. The club also hasn't ruled out calling up right-hander Craig Stammen or left-hander Matt Chico for the start.
Bill Ladson is a reporter for MLB.com and writes an MLBlog, All Nats All the time. This story was not subject to the approval of Major League Baseball or its clubs.


text:
For the terms and conditions of Breeze Mastercard introductory balance transfer and purchase rate offer refer to the "Things you should know" section at the bottom of this page.
Bankwest Breeze Mastercard
Low rate
- After any intro period, an ongoing balance transfer and purchase rate of 12.99% p.a. applies
- Add up to 3 additional card holders for no extra cost
- Free worldwide emergency card replacement
Intro purchase and balance transfer rate for 13 months (2% balance transfer fee applies).
Limited time only for new Breeze Mastercard customers


text:
12 stories on funding, e-commerce, supercomputing, SA trends, new reports
Is the volume and selling price of domain names containing African terms is a harbinger of what's to come in terms of Africa's e-commerce industry?
Can a uniquely African social network instigate revolution with the zeal of a Facebook or Twitter? The challenges facing African social networks stem more a lack of planning and focus than from a lack of technology.
The cost of an Internet shutdown in Kenya, African online marketing spreads, cloud computing in SA
Africa's IPv4, Zimbabwean Internet banking
Sudanese protest scheduled on Facebook, YouTube video already posted of Sudanese protests
oAfrica is a showcase of the dynamic African digital landscape. We addresse a variety of aspects of African Internet connectivity with an understanding that every nation has different tools and ideologies to utilize. Although every African citizen may not have the chance to access the Internet for years to come, African digital opportunities are rapidly expanding. We do our best to objectively share those stories.


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It's a Saturday afternoon. I'm going to my favorite clothing retailer. As soon as I walk inside, I hear a beep. It's a "Welcome Back, Kate!" in-app message. Curiously, I click the in-app message. Afterward, I'm redirected to the retailer's mobile hybrid app. I see my loyalty points listed. In fact, I've already accumulated 250 points. Therefore, I've also leveled up a "Fashionista" status because I visited the store more than 3 times in November. Additionally, I opened the app more than 5 times and explored the new Fall arrivals both in their store and app.
How did the retailer know that I entered their shop? And how did they know I'm inside their store without opening their app initially?
The retailer set up proximity marketing in order to engage me. So then, what is proximity marketing? It's a type of marketing that leverages technologies like beacons, geo-fencing, geo-targeting, NFC, BlueTooth and more in order to identify different mobile-powered or IoT-powered devices nearby or a certain geographic range. Therefore, if the proximity marketing technology pairs well with the right mobile solution, marketers can unlock revenue-driven, engagement opportunities. Depending on the marketer's mobile strategy, such engagement opportunities can potentially influence shoppers to buy more in-store, accumulate more points, participate in gamification and so forth.
There are countless creative ways retailers can do in a proximity marketing strategy. The bottom line is that as long as I'm engaged, rewarded, or enticed, I'll keep coming back for more.
To find out more, download the FREE "Proximity Brief" below.DOWNLOAD MY BRIEF


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POOLER, Ga. {AP} Police investigating rumors of a bomb plot at a middle school raided the homes of 11 students and arrested a 14-year-old boy who had several guns, Nazi posters, $4,900 in cash and bomb recipes in his room.
Investigators said Thursday they found no explosives at the school or in the students' homes and still were investigating whether there was a conspiracy to bomb West Chatham Middle School.
"I don't think we can say right now they had the intent. We know that they had the means," said Pooler Police Chief Butch Chan.
"If you go to a 14-year-old child's home and you find evidence on how to make a bomb and you find seven weapons and (nearly) $5,000 in his house, I think the evidence speaks for itself," he said.
The 14-year-old, whose name was not released because of his age, was charged with possession of a firearm by a minor for two handguns police found in his room.
The boy also had two shotguns and three rifles in his closet, but minors can legally possess such weapons under Georgia law.
The boy's father told The Associated Press on Thursday that the handguns belong to his son-in-law, who is visiting from Illinois. The pistols were stashed in his son's room to keep them away from younger children, he said.
"He is not a violent kid," the father said.
The boy pulled bomb-making recipes off the Internet only to demonstrate to his father how easily teens could find such instructions online, the father said.
As for the drawing of Adolf Hitler seized from the boy's room, the father said his son once wrote a school report on Adolf Hitler, and got a good grade for it. He said his son claimed the $4,900 belonged to a friend.
None of the other 10 students was arrested in Wednesday night's raids, prompted by students who warned police of rumors that their classmates planned to bomb the school Thursday.
But police say there may be more arrests and charges. They're calling the students the "Gothic Gang" and labeled the students outsiders who favor black clothing, Nazi and satanic paraphernalia.
"I think this group gets away from the wannabe stage to the fact that they may have been actually laying plans to do something here," Chan said.
Classes were held as normal Thursday at the school in Pooler, 10 miles west of Savannah. But a steady stream of scared parents pulled their children out of class on the final day before spring break.
"If your child was here and you read about this, would you leave your child here, or pick him up?" Karen Davidson said as she left with her eighth-grade son. "It's just scary."
Principal Paula Cleckler said she believes there was no immediate danger to students.
"There was some dabbling in and looking at how to do this, maybe looking at some of the chemistry," Cleckler said. "Was there an imminent threat today? From what was found, I do not think so."
The 14-year-old boy was being held at a juvenile detention center. A hearing was scheduled Monday to determine if he would be released to his parents.
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Posted 4 years ago
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Hello Friends!
Hope I don't get blown out of the house before I finish this posting, we're having a hurricane here on Cape Cod. Do you believe it, another storm, and more ferocious that any other we had in the Winter.
I found this a couple of weeks ago, and even though it's been cut at the wheels, :(, I love it.
It's a heavy little beast.
Any idea where it may have come from,....was it a hood ornament? ( it has that kind of wear ). and WHY on earth would someone have cut it's wheels? Oh well.
Thanks for taking a look,
p.s. I forgot to mention that it has a hole on the underside,....it screwed onto something.


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Would you like to save as your currency permanently or for this visit only?
Property Location With a stay at Hotel Sarangbang, you'll be centrally located in Seoul, steps from Ssamji-gil and Mokin Museum. This hotel is close to Gyeongbok Palace and Dongdaemun Market. Rooms Make yourself at home in one of the 24 individually furnished guestrooms, featuring refrigerators and LCD televisions. Computers with complimentary wired and wireless Internet keep you connected


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Earthquakes and Other Disaster Movies
For some completely unprovoked reason, Hollywood.com has decided to take a look back at the 1974 Charlton Heston film, Earthquake. Among the most iconic additions to the disaster genre, the movie strung together a handful of vignettes, pitting average everyday big-name celebrities against a ripple in the California plates.
Natural disaster movies are gripping for many reasons—the first and foremost of which: they have a slightly larger chance of occurring to you and your loved ones than do zombie outbreaks or alien attacks—and it's always fun to imagine how you'd measure up to the Charlton Hestons, Tommy Lee Joneses and, to a lesser extent, Bill Paxtons if these situations were to actually occur.
Thus, in the completely arbitrary spirit of earthquakes and other natural phenomena, we've made a list of a few more classic movies in the genre:
The thing that keeps this from being in the same spirit as most disaster movies is that Helen Hunt and Bill Paxton actually go looking for trouble. Nevertheless, Twister is incurably memorable—the Flying Cows Phenomenon is a hard thing to erase from memory.
This is a pair of movies that, in the same vein as Armageddon and Deep Impact, came out so close together and were so similar in theme and plot that I have a difficult time remembering what happened in which. So I'll just lump them together and pretend they were one movie: Tommy Lee Jones and Pierce Brosnan team up to stop a Volcano from erupting in the Pacific Northwest and Los Angeles. Collectively, they have a dead fiancée and a young daughter, as well as an antagonistic boss and a friend named Emmitt. All in all, everyone important doesn't get lava'd.
There's a storm. Boat goes flying. Captain goes down with the ship. The kids are fine.
There's a lot of snow because people don't know how to turn lights off. The disastrousness of the disaster is overshadowed by the disastrousness of humans in this movie—but the real disaster is the "I just want my son back" storyline Dennis Quaid enlists as he treks across the tundra to rescue Jake Gyllenhaal from swimming around with a pretty girl.
Bill Paxton was in this movie, too. And again, I found it kind of hard to feel bad for him. A bunch of jackasses find it necessary to run around on mountains, taking pictures of animals or yetis or Buddhists or something, and then—BAM! Avalanche. A few of them die, but none of the ones you're really supposed to be all that invested in; that's just the way it goes. If you ever find yourself in a natural disaster, don't worry about your loved ones. It's only the marginally dislikable characters who get avalanched/perfect stormed/volcanoed/twisted/earthquaked. And that's the real lesson to take away from this all.


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The Gloucester hooker, Olivier Azam, will appear before a disciplinary committee next week after being cited for allegedly kicking the England captain, Steve Borthwick, in the head during the defeat at Saracens last Sunday.
Borthwick left the field after the incident and was treated at a specialist eye hospital in London before being ruled out of action for two to four weeks because of intense swelling. Azam will appear before a three-man panel in Bristol next Tuesday.
Saracens claimed after the match that the kick had been made deliberately but Azam said he was reacting to someone who had grabbed his ankle and that, far from taking aim, he did not realise that he had made contact with Borthwick.
Gloucester, who have lost their last three Premiership matches, face another forward being unavailable after the No8, Adam Eustace, was cited for an alleged stamp on the scrum-half, Justin Marshall, during the same match. The panel is in for a busy night with the Bath wing, Joe Maddock, called to answer a charge of making a dangerous tackle on the Leicester second-row, Geoff Parling, at the Recreation Ground last Saturday.
Leicester will be without their captain, Geordan Murphy, for the rest of the year after he dislocated his left shoulder in a collision with Maddock on Saturday. The Ireland international has had surgery and will be out of action for between three and four months.
Another shoulder victim, the Wasps and England flanker Tom Rees, will know on Wednesday when he will be able to play again after having surgery in the summer. Wasps had hoped their captain would be back in action by now but his rehabilitation has not gone as planned.
Harlequins today signed the Northampton centre, Nils Mordt, to act as cover for another player who has had surgery, the England midfielder Jordan Turner-Hall, who will be out of action until the new year.
Meanwhile the England manager, Martin Johnson, will travel to France tonight watch the match between Stade Français and Brive. With James Haskell and Jamie Noon on show, Johnson believes he can no longer just rely on videotape with this autumn's internationals fast approaching and will accompany his assistant coaches John Wells and Graham Rowntree on the trip.
"It's a good idea to see the game and it's easy to get there and back again," he said. "When you are playing over there you are out of the mix compared to being in the Premiership but we do monitor their form and are trying to develop relationships with their clubs."


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Ed Gray, a prominent sportswriter for the Boston Herald, outed himself Tuesday in a column in the newspaper. "I'm out because I no longer, in good conscience, choose to ignore the unabashed homophobia that is so cavalierly tolerated within the world of sports," he said. "I'm out because the silence of a closeted gay man only serves to give his implicit approval to bigotry. I'm out because I refuse to continue hiding from the truth that an openly gay man has as much right as a straight man to play sports or report on them."
"In the cases of both a gay athlete and a gay sportswriter, homophobic athletes always come up with the same sorry excuse to justify the perpetuation of prejudice on the basis of sexual orientation--the locker room," Gray continued. "What, exactly, does a straight athlete have to fear from a gay teammate or sportswriter? Any man secure in his heterosexuality should not have a care in the world when a gay man is present in the locker room. He is there only to earn a living, not to infiltrate the locker room in a covert operation to 'convert' straight athletes. There are infinitely more friendly and healthy environments in which a self-respecting gay man would prefer to explore his sexuality than a locker room full of straight guys."


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Darkside bikie raids0:54
Victorian police have arrested Hells Angels bikie members after conducting a series of raids linked to its newest Darkside chapter on the Mornington Peninsula
SIX accused Hells Angels members arrested in a series of police raids have been remanded in custody at an out-of-sessions court hearing at the St Kilda Rd police complex.
Three — president of the Hells Angels Darkside chapter Mohammed Khodr, 26, Logo Afuie, 27, and Cuong Hoang, 28 — were automatically denied bail after being charged last night with trafficking commercial quantities of drugs of dependence.
Mr Khodr, of Balwyn North, was charged with 24 offences, including trafficking a large commercial quantity drug of dependence, trafficking a commercial quantity drug of dependence, 10 counts of trafficking drug of dependence, 10 counts of possessing drug of dependence, prohibited person possessing a firearm and ammunition and possessing a handgun.
He did not apply for bail.
Mr Afuie, of Tarneit, was charged with 13 offences — trafficking a commercial quantity drug of dependence, six counts of trafficking a drug of dependence and six counts possessing a drug of dependence.
The pair were arrested when a search warrant was executed on Mr Khodr's Balwyn North home earlier in the day.
Mr Hoang, of St Albans, faces eight charges — four counts of trafficking a commercial quantity drug of dependence and four counts possessing a drug of dependence.
Michael "Spaghetti" Barboro, 54, of Sydenham, was also charged with two counts of trafficking drug of dependence, two counts possessing drug of dependence and possessing a long-arm firearm.
James Turner, 27, of Craigieburn faces charges of trafficking and possessing a drug of dependence, possessing ammunition and possessing proceeds of crime, while Dimi Sovolos, 24, of Lower Templestowe was charged with theft of a motor vehicle, possessing proceeds of crime, trafficking drugs of dependence and handling stolen goods.
All will appear in court later today. More charges are expected to laid against the group.
It is understood six further accused Hells Angels members and associates were also bailed last night.
The charges came as a result of an investigation into Mr Khodr's drug and firearm trafficking activity launched by Echo Taskforce in June 2013, the court heard.
Echo Taskforce Sen-Det Daniel Prato said police had intercepted three of Mr Khodr's mobile phones as part of the investigation.
Sen-Det Prato said raids were carried out across the six men's Melbourne homes, uncovering drugs, drug equipment, money, unregistered firearms and ammunition.
About 140 grams of methylamphetamine and a quantity of cash were discovered in a car at Mr Khodr's Balwyn North residence, where he and Mr Afuie were arrested.
Originally published as Hells Angels in court after police raids


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Blane Klemek column: Hands off usually best policy for wildlife
It's a common occurrence. A fawn is found by a well meaning person who thinks that the animal has been abandoned by its mother. The person carries the young deer home and calls the DNR to ask what they should do.
The correct action is frequently the most difficult thing for anyone to do; that is, leave the animal alone, where it was found, and walk away. After all, what mother would leave a vulnerable baby all alone, right?
The fact is, deer routinely do this. Fawns instinctively know they must hide, and their mothers instinctively know how to communicate this message to their fawns: "Hide, hide right now, and stay hidden until I return and tell you it's safe." It's Nature's way and it works quite well.
But we human beings are compassionate creatures, and there's nothing wrong with that whatsoever. Yet, when it comes to wildlife intervention, some of our actions are unnecessary and harmful.
Take me for example. I have been monitoring this spring and summer a pair of American kestrels that accepted an artificial nest box that my son and I had built especially for their species a couple of years ago. It has been interesting and enjoyable to observe the pair throughout their courtship and nest site selection.
It was almost two months ago that the female kestrel had laid five speckled, brownish eggs in the box. Weeks later all five eggs had hatched and five white, down-covered kestrels lay quietly in the nest box. Throughout the ensuing days, I found myself spending a lot of time observing the entrance hole hoping to catch sight of the parents bringing food to the fast-growing chicks.
Then came the torturous heat wave of mid-July.
By this time the five chicks were close to fledging, but the demands that their near adult-sized bodies required - perhaps too much for the confines of the nest box and the oppressive heat - took a toll as their parents tried keeping the brood nourished and hydrated.
I could clearly see that the chicks were stressed when I climbed the ladder to peek inside the nest box on hot day, and I actually thought about intervening. I thought I should "rescue" one or more of the weakest looking chicks and "do something." But, as hard as it was, I left them alone.
What happened next was something I've known all along was possible under the circumstances: the chicks turned on each other. Because one day, in fact only a few days after I had initially contemplated an intervention, I was shocked to discover upon opening the box that only two chicks were alive.
The other three chicks were dead, their bodies almost completely gone save for a few feathers and entrails. It was a prime example of "siblicide," a behavior common in some species of birds as a means of brood reduction brought on by stressors such as shortage of food. Just two days later the surviving chicks had fledged and were gone. At this writing, I can hear the adult kestrels vocalizing near the nest site, evidently caring for their two fledged offspring.
But I'm not perfect. Sometimes, against my better judgment, I do interfere with Mother Nature once in a while - in fact, just last month. While on the job assisting a contractor on a trail mowing project, I was operating an all-terrain vehicle on a narrow, little-used and overgrown wooded trail.
A portion of the trail about 10 feet wide and 20 feet long was inundated with water from a recent rain. As I steered the vehicle alongside the water hole, I noticed a single duckling skittering across the surface of the water in an attempt to escape and hide in the vegetation. I stopped the machine, dismounted and captured the little duck - a common goldeneye. The bird wasn't much more than a day or two old.
I guessed that the duckling had lost its way after hatching from its tree cavity nest, probably unable to keep up with its mother and siblings. Or, it simply waited too long to leave the cavity in the first place. Regardless, the duckling was now inside my front shirt pocket, buttoned closed, without a clue of its fate, much less what was happening.
My plan was to release the little fellow in the nearby beaver pond, the closest body of water from the puddle where I found the stranded little duck.
"Maybe," I thought, "just maybe the duckling will vocalize loud enough to attract the attention of its mother."
It was, from my perspective anyway, worth a try.
So that's what I did. I released the duckling and watched as it paddled itself furiously with its webbed feet across the pond, peeping loudly as it swam, until the bird disappeared into the emergent vegetation. And then I left.
About an hour later I returned to the area with the four-wheeler to wait for the contractor's return to the trail. As I sat in the quiet woods, birds everywhere were singing and vocalizing. As I waited, I heard the faint call of a hen goldeneye emanating through the woods from the nearby beaver pond.
I listened.
Seconds later, lo and behold, I was astonished when I heard the call of a lone duckling answering the hen's call. And soon, both were excitedly vocalizing to one another.
When I reached the edge of the beaver pond to search for the two ducks, I witnessed the impossible reunion of the hen goldeneye and the lone duckling. (My duckling?) I was thrilled as I stood and watched the two birds disappear, together, with the hen in the lead and the little duckling following closely behind.
And so it goes. We can no sooner change human nature as we can change Mother Nature. Sometimes we help and sometimes we should - perhaps - reconsider as we get out and enjoy the great outdoors.
Blane Klemek is the Bemidji area assistant wildlife manager, DNR Division of Fish & Wildlife. He can be reached at email@example.com


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20 Games Like Tokyo Road Race()
Spintires: MudRunner
Like Spintires before it, Spintires: MudRunner puts players in the driver seat and dares them to take charge of incredible all-terrain vehicles, venturing across extreme Siberian landscapes with only a map and compass as guides! This edition comes complete with a brand new Sandbox Map joining the original game's 5 environments, a total graphical overhaul, a new Challenge mode with 9 new dedicated maps, 13 new vehicles and other comprehensive improvements.
Need For Speed: Payback
"This explosive adventure is filled with intense heist missions, high stakes car battles, epic cop pursuits and jaw dropping set pieces. It's blockbuster gameplay never before seen from the series, fueled by a gripping story of betrayal and revenge. With Need for Speed: Payback, it's no longer just about being the first to cross the finish line or racing to prove to be the best, it's about building the perfect ride, getting behind the wheel and playing out an action driving fantasy.
Set in the underworld of Fortune Valley, players will drive as three distinct characters reunited by a quest for vengeance against The House, a nefarious cartel that rules the city's casinos, criminals and cops. They will take on a variety of challenges and events as Tyler, the Racer; Mac, the Showman; and Jess, the Wheelman to earn the respect of the underground. Featuring the deepest customization from the series, players can truly craft a personalized and unique ride, or spend hours finding and tuning an abandoned derelict into a supercar. They can then push their cars to the limit and raise the stakes by betting on their own performance, where they can either multiply their winnings or risk losing it all."
Car Mechanic Simulator 2018
Build and expand your repair service empire in this incredibly detailed and highly realistic simulation game, where attention to car detail is astonishing. Find classic, unique cars in the new Barn Find module and Junkyard module. You can even add your self-made car in the Car Editor.
Micro Machines World Series
Micro Machines World Series will retain the manic social game play of the classic series, but will bring a new dimension to the experience with stunning HD visuals – taking you to the much-loved household environments as they've never been seen before.
As well as bringing to you the classic game modes like Race and Elimination, Micro Machines World Series will introduce a new style of game play to the series: Battle Mode. The all-new Battle Arenas will allow you to wreak mass destruction on a miniature scale against your friends or the AI. Meanwhile, Team Play lets you work together using your vehicles' unique skills with modes such as 'King of the Hill' or 'Capture the Flag'!
Need for Speed: The Run
Need for Speed The Run lures players into an underground world of illicit, high-stakes racing. The heat is on - and it isn't just the fuzz who are after you. Entering the race is just the beginning as you blow across borders, weave through dense urban traffic, rocket down icy mountain passes and navigate narrow canyons at breakneck speeds. Powered by DICE's state-of-the-art Frostbite 2 engine, Need for Speed The Run takes the action racing genre to new heights with stunning visuals and car physics that hug the road even at top speeds all built around a gripping storyline. The cars are hot, the racing is intense and the story will have you at the edge of your seat… all the way from the Golden Gate Bridge to the Empire State building.
71 / 100433.55
Absolute Drift: Zen Edition
A unique racing game about mastering the art of drifting.
Journey from apprentice to master drifter as you hone your skill in a gorgeous minimalist world. Travel from airports and docks to a floating metropolis in search of new cars and ever greater challenges. Chill out to over 3 hours of electronic music by C41 and NYTE. Push yourself to the limit on drifting tracks and wild mountain roads while you work to unlock the elite Midnight events. Your driving skills will be challenged at every turn until you finally become a master drifter.
The Crew 2
The newest iteration in the revolutionary franchise, The Crew 2 captures the thrill of the American motorsports spirit in one of the most exhilarating open worlds ever created. Welcome to Motornation, a huge, varied, action-packed, and beautiful playground built for motorsports throughout the entire US of A. Enjoy unrestrained exploration on ground, sea, and sky. From coast to coast, street and pro racers, off-road explorers, and freestylers gather and compete in all kinds of disciplines. Join them in high-octane contests and share every glorious moment with the world.
Speed Race GP-5
The fourth release in Taito's Speed Race series.
MaXXed Out Racing
MaXXed Out Racing was released for the PlayStation 2 in Europe. In Japan, it is known as Simple 2000 Series Ultimate Vol. 3: Saisoku! Zokusha King.
Cosmic Highway
A racing game coming to Wii U from Maestro Interactive Games
Toy Cars
Toy Cars is a top-down racing game developed for the PC and XBox Live Indie Games. It's been conceived as both a homage and an evolution of classic top-down arcade racers. In it players control pocket-sized vehicles around table-top tracks built from all manner of everyday objects.
Trigger Rally
Trigger Rally is an open source rally racing game.
Endless Racing Game
Endlessly race in a top-down perspective before the time runs out.
Double S.T.E.A.L. The Second Clash
Double S.T.E.A.L. The Second Clash is a Car Combat game.