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Small molecules with antioxidative properties have been implicated in amyloid disorders. Curcumin is the active ingredient present in turmeric and known for several biological and medicinal effects. Adequate evidence substantiates the importance of curcumin in Alzheimer's disease and recent evidence suggests its role in Prion and Parkinson's disease. However, contradictory effects have been suggested for Huntington's disease. This difference provided a compelling reason to investigate the effect of curcumin on glutamine-rich (Q-rich) and non-glutamine-rich (non Q-rich) amyloid aggregates in the well established yeast model system. Curcumin significantly inhibited the formation of htt72Q-GFP (a Q-rich) and Het-s-GFP (a non Q-rich) aggregates in yeast. We show that curcumin prevents htt72Q-GFP aggregation by down regulating Vps36, a component of the ESCRT-II (Endosomal sorting complex required for transport). Moreover, curcumin disrupted the htt72Q-GFP aggregates that were pre-formed in yeast and cured the yeast prion, [PSI+].
Citation: Verma M, Sharma A, Naidu S, Bhadra AK, Kukreti R, Taneja V (2012) Curcumin Prevents Formation of Polyglutamine Aggregates by Inhibiting Vps36, a Component of the ESCRT-II Complex. PLoS ONE 7(8): e42923. https://doi.org/10.1371/journal.pone.0042923
Editor: Niyaz Ahmed, University of Hyderabad, India
Received: May 23, 2012; Accepted: July 13, 2012; Published: August 7, 2012
Copyright: © Verma et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Funding: Innovative Young Biotechnology Award, Department of Biotechnology, Government of India, India. VT acknowledges fellowship from Innovative Young Biotechnologist Award, Department of Biotechnology, India. MV acknowledges senior research fellowship from Indian Council of Medical Research. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Competing interests: The authors have declared that no competing interests exist.
Amyloidosis is a group of protein misfolding disorders, characterized by abnormal accumulation of insoluble fibrous protein aggregates [1]. Broadly, these amyloid proteins can be categorized as glutamine-rich (Q-rich) and non glutamine-rich (non Q-rich). Huntington's disease (HD) and Spinocerebellar ataxia [2] have been associated with expansion of Q-rich repeats. Other amyloid proteins including human prion protein (PrP), Aβ (Alzheimer disease), α-synuclein (Parkinson's disease) and Transthyretin (Transthyretin amyloidosis) lack these Q-rich regions. These amyloid proteins exhibit little or no sequence homology and are associated with a distinct clinical picture, but they share a common cross-β structure [3] suggesting a common cellular mechanism underlying the pathology of amyloid disorders.
Yeast has been well established as a successful model to decipher the molecular basis of amyloid disorders including Parkinson's disease, Alzheimer's disease, and Huntington's disease [4]–[8]. Interestingly, yeast has glutamine/asparagine (Q/N)-rich endogenous prion proteins [9] and was also shown to propagate Het-s, a non Q-rich fungal prion protein from Podospora anserina [10]. While a surfeit of research is focusing on uncovering the molecular mechanism of pathogenesis related to amyloidosis, several studies are now concentrating on therapeutic developments. Recently, both research and pharmaceutical industries are putting forth a huge effort to evaluate small molecules from natural products for their medicinal properties. Yeast is being exploited to screen for small molecule inhibitors with therapeutic potential for amyloid disorders [11], [12]. Furthermore, the ease of genetic manipulation and available tools in yeast allows dissection of the molecular pathways targeted by small molecules.
Curcumin, a polyphenol present in the spice turmeric, is known to have broad biological and medicinal effects including efficient anti-oxidant, anti-inflammatory and anti-proliferative activities. Overwhelming evidence now suggest that curcumin can be exploited for potential drug development for prevention and treatment of several disorders including cancer, obesity, aging, and neurodegenerative diseases. The neuroprotective effect of curcumin has been extensively studied in Aβ amyloid pathology. It binds and inhibits formation of Aβ fibrils in vitro [13] and reverses amyloid pathology in transgenic Alzheimer's disease (AD) animal models [14], [15]. In addition, curcumin has an inhibitory effect on the aggregation of α-synuclein [16], [17] and in vitro conversion of prion protein (PrP) together with the inhibition of protease-resistant PrP formation in cell culture [18]. Hence, it appeared very likely that curcumin could inhibit aggregation of expanded polyglutamine repeats in the huntingtin protein. Instead, it has previously been shown to promote aggregation of expanded polyglutamine in exon 1 of the huntingtin protein [19]. Thus, the therapeutic effect of curcumin in Huntington's disease is still questionable. In the present study, we sought to evaluate the anti-aggregation potential of curcumin for both Q-rich and non Q-rich amyloid proteins using established yeast models. Here, we find that curcumin acts through VPS36, which is a component of the ESCRT-II complex and prevents aggregation of exon 1 of the huntingtin protein with expanded glutamine repeats.
Materials and Methods
Yeast strains, Plasmids and Chemical compounds
VL2, a [psi−][pin−] and a weak [PSI+] [pin−] strain in 74-D694 background (ade1-14, ura3-52, leu2-3, 112 trp1-289, his3-200) was a gift from Susan Liebman. Yeast deletion strains and BY4741 were purchased from Invitrogen. The TAP (Tandem Affinity Purification)-tagged strains for VPS36 (Cat# YSC1178-7501934) and VPS4 (Cat# YSC1178-7503327). were procured from Open Biosystems. Deletion of VPS36 was created in the VL2 strain by short flanking homology primers [20]. The sequences of primers used for deletion are:
- Forward:ATGGAGTACTGGCATTATGTGGAAACTACGTCATCGGGCCCGAGGAGAACTTCTAGTATATC
- Reverse:TCCCACTCAGTTGCTTGTCTATCAGTAAATCGCCTTCATCGTGCGTATATAGTTTCGTCTACCC
The exon 1 of human HTT gene cloned in the p426-GAL1 vector with expanded polyglutamine (htt72Q-GFP) was a gift from Susan Lindquist. The C-terminal prion domain of the Het-s gene fused with GFP is cloned under a galactose promoter in a 2 micron vector [10]. The plasmids were transformed into yeast by standard Lithium Acetate protocol [21].
Curcumin (Cat# C1386) , morin hydrate (Cat# M4008) and ascorbic acid (Cat# A4403) were all procured from Sigma. α-Tocopherol was procured from INTAS Pharmaceuticals. Curcumin and α-tocopherol were dissolved in Dimethyl sulfoxide (DMSO), morin was dissolved in methanol and ascorbic acid in sterile water.
IC50 of compounds
The 50% inhibitory concentration (IC50) of the chemical compounds was calculated by adding different concentrations of molecules to yeast culture in early log phase (0.2 OD). The treatment was done for 14 hours at 30°C and OD600 was taken. The IC50 (curcuminIC50 = 62.5 µM, morinIC50 = 475 µM, α-tocopherolIC50 = 650 µM, ascorbic acidIC50 = 5 mM) was determined by plotting percentage survival versus concentration. The concentrations below IC50 for each compound were used in all the experiments.
Quantification of amyloid aggregates in yeast by fluorescent microscopy
A [psi−][pin−] strain transformed with htt72Q-GFP or Het-s-GFP was grown in Synthetic media lacking uracil and tryptophan, respectively. Cells were then re-inoculated in Synthetic Raffinose +2% Galactose (SRaf+Gal) and grown till early log phase. Cells were transiently treated (8 hours) with different concentrations of compounds. Cell growth becomes slow during this period but the cells are then replenished with fresh inducing media and incubated for 16 hours at 30°C. After replenishment, there was no difference in growth in the treated and untreated cultures. Cells with aggregates were analyzed using a Nikon Ti-E inverted fluorescent microscope and manually counted. The percentage of cells with aggregates was calculated by counting more than 300 cells for each treatment per transformant.
To calculate the percentage of cells with htt72Q-GFP aggregates in deletion strains and BY4741 (wild type, WT), cells were grown for 48 hours in inducing media (SRaf+Gal) at 30°C and analyzed under the fluorescent microscope.
Analysis of htt72Q-GFP aggregates by sedimentation and centrifugation assays
In the sedimentation assay, yeast cells with htt72Q-GFP aggregates were harvested and lysed using 1× lysis buffer (50 mM TrisCl, 50 mM KCl, 10 mM MgCl2, 5% glycerol). 150 µl of cell lysate normalized for total protein was loaded on 20% to 70% sucrose step-gradient and centrifuged for one hour at 14000 rpm. 150 µl of different fractions were carefully taken out, boiled at 95°C and run on 12% SDS-PAGE. The blot was probed with anti-GFP antibody (Cat # G6795, Sigma).
In the centrifugation assay, cell lysate normalized for total protein was centrifuged at 17,500 rpm for 1 hour at 4°C. Supernatant fraction was aspirated and the pellet was resuspended in the same volume of 1× lysis buffer. The total, supernatant and pellet fractions were resolved on 12% SDS-PAGE and analyzed by immunoblotting using anti-GFP antibody. β-actin, a housekeeping protein was used as loading control.
Expression levels of VPS36 and VPS4 in the presence of curcumin
For protein levels, TAP tagged yeast strains for VPS36 and VPS4 were grown in rich media, re-inoculated in Synthetic complete media. Cells were treated with 20 µM and 40 µM of curcumin at 0.2 OD and incubated for 16 hours at 30°C. Protein was isolated, normalized, immunoblotted and probed with anti-TAP antibody. β-actin was used as loading control. Anti-Tap antibody was from Open Biosystems.
For mRNA levels, [psi−][pin−] cells were treated with 20 µM and 40 µM of curcumin and incubated for 16 hours at 30°C. Cells were lysed by lyticase and RNA was isolated by the Guanidinium thiocynate-phenol-chloroform extraction protocol (TRIzol method) using TRI reagent from Sigma (Cat#T9424) [22]. cDNA was prepared using High Capacity cDNA kit (Applied Biosystems) and real time PCR was carried out using SYBR Green (Fast SYBR from Applied Biosystems). ACT1 was used as an endogenous control.
Analyzing the effect of curcumin on yeast prion by antibiogram assay
Yeast cells contain an endogenous prion protein, Sup35, a translational termination factor. When Sup35 is functional (non-prion form), it terminates at the premature stop codon on the ade1-14 allele. This inhibits adenine biosynthesis and results in accumulation of red pigment in the cell which gives red color to yeast cells on rich media. When Sup35 is non-functional (prion form), it no longer terminates at the stop codon on the ade1-14 allele, adenine biosynthesis takes place and cells appear pink (weak [PSI+]) to white in color (strong [PSI+]) on rich media [23].
Log phase culture of a weak [PSI+] strain was grown in YPD broth and uniformly spread on YPD plates. Plates were allowed to air dry for 30 minutes and sterile filter paper discs soaked with different concentrations of curcumin were placed on it. A sterile filter soaked with DMSO and 10 mM guanidine hydrochloride was used as negative and positive controls, respectively. These plates were incubated for 2 days at 30°C and then kept at 4°C for 2–3 days. Curing of weak [PSI+] was monitored by change in coloration of the colonies.
Curcumin inhibits both Q-rich (htt72Q-GFP) and non Q-rich (Het-s-GFP) aggregate formation in yeast
The inhibitory effect of curcumin has been well established for non Q-rich amyloid proteins including Alzheimer's [13] but has been shown to promote aggregation of mutant huntingtin [19]. The difference in action of curcumin on two different types of amyloid proteins prompted us to re-examine the effect of curcumin on existing yeast models for both Q-rich and non Q-rich amyloid proteins. The effect of curcumin was analyzed on htt72Q-GFP and Het-s-GFP aggregation by fluorescent microscopy in a [psi−][pin−] strain (Figure S1). More than 2-fold decrease at 20 µM and >3-fold decrease at 40 µM of curcumin were consistently observed for cells with htt72Q-GFP aggregates (Figure 1A). In case of Het-s-GFP aggregates, 1.7-fold inhibition at 20 µM and ∼2-fold at 40 µM was observed (Figure 1B). Thus, we observed a significant dose-dependent inhibitory effect on both htt72Q-GFP and Het-s-GFP aggregates.
Percentage of cells with aggregates was analyzed after transient treatment with different concentrations of compounds. Aggregation counting was done for three independent transformants for each treatment. Error bars represent standard errors of the mean of triplicates. To assess the significance between treated and untreated samples, t-test was performed (* depicts p value<0.01). Validation of the effect of 20 µM curcumin on htt72Q-GFP by C) sucrose density gradient (0% to 70%) and D) centrifugation assay. 'Sup' represents the supernatant fraction. For both assays, cell lysate was normalized for total protein and processed. DMSO was used as control (0 µM) and blots were probed with anti-GFP antibody.
The inhibitory effect of curcumin treatment on htt72Q-GFP aggregation was validated by sedimentation profile of htt72Q-GFP aggregates on sucrose step-gradient. Cells over expressing htt72Q-GFP were transiently (8 hours) treated with curcumin, lysed and loaded on sucrose gradient. In absence of curcumin, higher molecular weight htt72Q-GFP aggregates penetrated deeper into the higher fractions of sucrose gradient. In cells treated with 20 µM curcumin, higher molecular weight aggregates decreased significantly (fractions 4–6) and lower molecular weight aggregates increased (fractions 2 and 3) (Figure 1C). Centrifugation assay also showed a clear decrease in the pellet fraction, which again validates the inhibition of aggregation after curcumin treatment (Figure 1D).
We also analyzed the effect of three other known antioxidants on htt72Q-GFP and Het-s- GFP aggregation. Morin showed a significant dose-dependent decrease (2-fold at 150 µM and 4-fold at 300 µM) and α-tocopherol showed ∼2-fold decrease but at much higher dosage (400 µM) in htt72Q-GFP aggregates. Ascorbic acid did not show any effect on htt72Q-GFP aggregates (Figure 1A). No significant effect of morin, α-tocopherol and ascorbic acid on Het-s aggregation was observed (Figure 1B).
Curcumin downregulates Vps36, a component of the ESCRT-II complex
As curcumin exhibited an appreciable inhibition of appearance of both Q-rich and non Q-rich aggregates, we were curious to decipher the mechanism of action of curcumin. To identify the cellular target of curcumin, we utilized the information provided by the chemogenomics profiling fitness database (http://fitdb.stanford.edu/fitdb.cgi) that lists heterozygous or homozygous deletion mutants with increased sensitivity to compounds [24]. We examined htt72Q-GFP aggregation in eight homozygous yeast deletion strains (cc2Δ, ypk1Δ, atx1Δ, vps36Δ, sip3Δ, pho86Δ, vam7Δ and fet3Δ) shown to exhibit the maximum growth defect in the presence of curcumin. The growth defect in these deletion strains was confirmed in the presence of curcumin (data not shown). Out of eight, seven strains showed aggregation similar to BY4741. The vps36Δ strain showed a significant decrease in the percentage of cells with htt72Q-GFP aggregates (Figure 2A). We confirmed that this decrease in aggregation is not due to growth inhibition as no appreciable decrease in growth rate was observed between BY4741 and vps36Δ. To analyze the effect of Vps36 on htt72Q-GFP aggregation in another yeast strain background, deletion of VPS36 was recreated in the VL2 strain and confirmed by PCR (data not shown). A similar decrease in aggregation was observed in this strain and validated by a shift towards lower fractions on sucrose density gradient (Figure 2B) and a significant decrease in pellet fraction (Figure 2C).
A) htt72Q-GFP aggregation was quantified in BY4741 and nine deletion strains by calculating percentage of cells with aggregates for each strain. Three independent transformants were analyzed for each strain. Only vps36Δ showed a significant decrease in aggregation. Error bars represent standard errors of the mean for triplicates. The significant difference in aggregation between BY4741 and vps36Δ was calculated by t-test (* depicts p value<0.05). The inhibitory effect due to VPS36 deletion was validated by B) sucrose density gradient and C) centrifugation analysis in the VL2 background. Cells expressing htt72Q-GFP were lysed, normalized for total protein and processed. Blots were probed with anti-GFP antibody. In centrifugation assay, β-actin was used as loading control.
VPS36 is a component of the ESCRT-II complex and encodes Vacuolar Protein Sorting protein 36. To validate if the inhibiton of aggregation after curcumin treatment is through Vps36, the effect of curcumin on expression levels of Vps36 was analyzed. A dose and time-dependent decrease in mRNA levels of Vps36 was observed by real time PCR. VL2 strain was treated with curcumin for 16 hours, a 1.5-fold and >4-fold decrease in levels of Vps36 mRNA was observed for 20 µM and 40 µM, respectively (Figure 3A). The time-dependent effect was monitored at 20 µM curcumin after 17, 24 and 40 hours of treatment. A significant decrease in Vps36 mRNA levels at 17 hours and further decrease at 24 hours was observed. However, after 40 hours, the levels of Vps36 mRNA increased a little compared to the untreated sample (Figure 3B). A moderate decrease in the protein levels of Vps36 was also observed after curcumin treatment (Figure 3C) by probing for TAP-tagged Vps36 in BY4741 strain background. The levels of Vps4, which is involved in disassembly of ESCRT–III complex, showed no change after curcumin treatment (Figure 3A and 3D). Deletion of vps4 did not show any change in percentage of cells with aggregation compared to BY4741 (Figure 2A). Hence, curcumin significantly downregulates Vps36 levels in yeast.
A) mRNA levels of Vps36 and Vps4 after 16 hours of curcumin treatment (20 µM and 40 µM) in the VL2 strain was quantified by real time PCR using SYBR green. B) Time-dependent effect of 20 µM curcumin on mRNA levels of Vps36 was determined at 17 hours, 24 hours and 40 hours in the VL2 strain. The genes were considered to be upregulated if the fold change was above 1 and downregulated if below 1. The untreated sample was normalized to 1. Each bar represents the standard error of mean of triplicates. Protein levels of C) Vps36 and D) Vps4 in respective TAP-tagged strains were determined after curcumin treatment (20 µM and 40 µM) by immunoblotting with anti-GFP antibody. The intensity of Vps36 and Vps4 (untreated and treated) protein levels was quantified by densitometer and normalized with β-actin. Error bars represent standard errors of the mean of triplicates.
Curcumin destabilizes Q-rich aggregates pre-formed in yeast
As curcumin is known to destabilize pre-formed Aβ fibrils [25], we asked if curcumin also acts on pre-formed htt72Q-GFP aggregates. Cells with htt72Q-GFP were grown in inducing media for 48 hours, analyzed for aggregates and lysed. Cell lysate containing the pre-formed aggregates was treated in vitro with 100 µM curcumin at 37°C for 16 hours and analyzed by sedimentation profiling. The aggregates from untreated lysate penetrated into higher fractions of sucrose gradient, which diminished considerably after treatment (Figure 4A). The aggregates appeared more concentrated in supernatant and lower fractions of sucrose gradient. This shows that curcumin destabilizes htt72Q-GFP aggregates that are pre-formed in yeast.
A) htt72Q-GFP aggregates were pre-formed by inducing its expression in the VL2 strain. Cell lysate treated with 100 µM curcumin was subjected to sucrose density gradient and fractions were resolved on SDS-PAGE. The blot was probed using anti-GFP antibody. B) Weak [PSI+] strain was treated with 1 mM and 10 mM of curcumin. The curing of yeast prion was observed by plating on rich media (YPD) by change in color from light pink (uncured) to red (cured). The cells near the disc were picked and restreaked on media lacking curcumin. 10 mM guanidine hydrochloride was used as a positive control and DMSO was used as a negative control.
The effect of curcumin was also analyzed on the endogenous yeast prion. A dose-dependent effect of curcumin on weak [PSI+] was observed on rich media plates as an increase in red coloration of colonies around the discs soaked with increasing concentration of curcumin (Figure 4B). These red colonies were picked and restreaked on rich media lacking curcumin, which propagated as red color [psi−] colonies as shown in figure 4B. The control discs soaked in DMSO did not cause any color change. No effect of curcumin was visible on strong [PSI+] strain (data not shown).
Emerging evidence suggest a neuroprotective role of curcumin in Alzheimer's disease and several clinical trials have been initiated to examine the effect of curcumin in AD patients. Contrary to this, curcumin has been shown to increase the aggregation of mutant huntingtin and also enhance toxicity associated in PC12 cells by augmenting the proteasomal dysfunction [19]. Impairment of proteasomal machinery is implicated in other amyloid disorders including AD and HD [26]–[28], therefore, if curcumin enhances a proteasomal defect, a similar increase in aggregation is expected on treatment for other amyloid proteins. Though Aβ peptide and mutant huntingtin protein form similar cross β-sheet structures, the major difference lies in their sequence. While Aβ lacks glutamine repeats, huntingtin protein is glutamine rich. This intrigued us and we investigated aggregation of mutant huntingtin with expanded glutamine repeats and Het-s, a non Q-rich fungal prion protein, after curcumin treatment in yeast. In accordance with a protective effect of curcumin for neurodegenerative disorders, we demonstrate an inhibitory effect of curcumin on both Q-rich and non Q-rich protein aggregation in yeast and describe the likely mechanisms of inhibition.
The molecular mechanism of action of curcumin is complex and multiple molecular targets have been proposed by several independent studies [29]. Curcumin has been shown to have a therapeutic effect on AD by reducing oxidative damage [30], decreasing β-amyloid formation by inhibiting GSK-3β-mediated presenilin-1 levels [31] and Wnt/β-catenin signaling pathway activation [32] and also inhibiting trafficking and maturation of Amyloid Precursor Protein (APP) into Aβ peptide [33]. We scored aggregation in eight homozygous deletion strains hypersensitive to curcumin and only deletion of VPS36 caused significant inhibition of formation of aggregates of mutant huntingtin. Vps36, a component of the ESCRT-II complex, appeared to be a functional target of curcumin as it was downregulated in a dose and time-dependent manner. Vps36 is involved in trafficking soluble and integral membrane proteins from the trans-golgi network to the perivacuolar region and finally to the vacuole [34]. As misfolded proteins including mutant huntingtin are known to localize in the perivacuolar region [35], we propose that in vivo deletion or downregulation of Vps36 caused by curcumin treatment prevents recruitment of misfolded protein to the perivacuolar compartment and thus inhibits formation of visible large aggregates. The importance of protein trafficking pathways in aggregation of amyloid proteins has been demonstrated previously. Several genes from endocytic pathway and vacuolar protein sorting are known to affect aggregation of amyloid proteins including mutant huntingtin [36] and prion proteins [37]. In compliance with previous work, our work further strengthens that protein trafficking pathways can be exploited for developing small molecule inhibitors of amyloid disorders.
Curcumin has been shown to destabilize Aβ fibrils but disassembly of mutant huntingtin by curcumin has not been described earlier. In vitro, disruption or remodelling of mutant huntingtin aggregates pre-formed in yeast clearly supports anti-aggregation potential of curcumin. Furthermore, our findings are supported by a very recent report that shows a clear decrease in number of aggregates in the striatum of knock-in HD mouse model [38]. Curcumin is known to cross the blood-brain barrier but bioavailibity is still poor. Hence, analogs of curcumin or combination of small molecules that increase the bioavailability of the active molecule need to be evaluated.
Morin, a polyphenol, present in red wine, has been suggested to have potential for developing therapies for AD and tauopathies by inhibiting GSK-3β [39], [40]. Recently, it has been reported to inhibit amyloid formation of Islet Amyloid Polypeptide (IAPP) [41]. We show that morin is an effective inhibitor of mutant huntingtin aggregates. Morin treatment also led to slight inhibition of non-Q rich aggregates. Further work is required to understand the mechanism of action of morin.
The key findings of our study are that curcumin is a more potent inhibitor of both Q-rich and non Q-rich aggregates than morin and α-tocopherol. Furthermore, it inhibits mutant huntingtin aggregation by acting through protein trafficking pathways and also destabilizes pre-formed aggregates. Based on our data and previous studies, curcumin is a promising compound for development of preventives and therapeutics for both Q-rich and non Q-rich amyloid disorders.
Supporting Information
Figure S1.
Microscopic image of cells showing the effect of curcumin on htt72Q-GFP aggregates in yeast.
We thank Prof. Susan Liebman, Dr. Rakesh Sharma and Dr. Veronique Dinand for carefully evaluating our work and giving useful suggestions and Kavita for helpful comments on the manuscript. We thank Prof. Nirmal Kumar Ganguly for the support and encouragement during this study.
Author Contributions
Conceived and designed the experiments: MV VT. Performed the experiments: MV AS SN. Analyzed the data: MV AS SN RK VT. Wrote the paper: MV SN VT. Critically reviewed the paper: RK. Performed initial aggregation scoring for Htt and het-s: AKB.
- 1. Westermark P (2005) Aspects on human amyloid forms and their fibril polypeptides. FEBS J 272: 5942–5949.
- 2. Shastry BS (2003) Neurodegenerative disorders of protein aggregation. Neurochem Int 43: 1–7.
- 3. Nelson R, Eisenberg D (2006) Structural models of amyloid-like fibrils. Adv Protein Chem 73: 235–282.
- 4. Willingham S, Outeiro TF, DeVit MJ, Lindquist SL, Muchowski PJ (2003) Yeast genes that enhance the toxicity of a mutant huntingtin fragment or α-synuclein. Science 302: 1769–1772.
- 5. Zabrocki P, Pellens K, Vanhelmont T, Vandebroek T, Griffioen G, et al. (2005) Characterization of α-synuclein aggregation and synergistic toxicity with protein tau in yeast. FEBS J 272: 1386–1400.
- 6. Boone C, Bussey H, Andrews BJ (2007) Exploring genetic interactions and networks with yeast. Nat Rev Genet 8: 437–449.
- 7. Treusch S, Hamamichi S, Goodman JL, Matlack KE, Chung CY, et al. (2011) Functional links between Aβ toxicity, endocytic trafficking, and Alzheimer's disease risk factors in yeast. Science 334: 1241–1245.
- 8. Sherman MY, Muchowski PJ (2003) Yeast Models as Tools to Study Neurodegenerative Disorders. NeuroMolecular Medicine 4: 133–146.
- 9. Shkundina IS, Ter-Avanesyan MD (2007) Prions. Biochemistry (Mosc) 72: 1519–1536.
- 10. Taneja V, Maddelein ML, Talarek N, Saupe SJ, Liebman SW (2007) A non-Q/N-rich prion domain of a foreign prion, [Het-s], can propagate as a prion in yeast. Mol Cell 27: 67–77.
- 11. Roberts BE, Duennwald ML, Wang H, Chung H, Lopreiato NP (2009) A synergistic small-molecule combination directly eradicates diverse prion strain structures. Nat chem Biol 5: 936–946.
- 12. Sarkar S, Perlstein EO, Imarisio S, Pineau S, Cordenier A (2007) Small molecules enhance autophagy and reduce toxicity in Huntington's disease models. Nat Chem Biol 3: 331–338.
- 13. Yang F, Lim GP, Begum AN, Ubeda OJ, Simmons MR (2005) Curcumin inhibits formation of amyloid beta oligomers and fibrils, binds plaques, and reduces amyloid in vivo. J Biol Chem 280: 5892–6901.
- 14. Lim GP, Chu T, Yang F, Beech W, Frautschy SA (2001) The curry spice curcumin reduces oxidative damage and amyloid pathology in an Alzheimer transgenic mouse. J Neurosci 21: 8370–8377.
- 15. Garcia-Alloza M, Borrelli LA, Rozkalne A, Hyman BT, Bacskai BJ (2007) Curcumin labels amyloid pathology in vivo, disrupts existing plaques, and partially restores distorted neurites in an Alzheimer mouse model. J Neurochem 102: 1095–1104.
- 16. Ahmad B, Lapidus L (2012) Curcumin prevents aggregation in α-synuclein by increasing reconfiguration rate. J Biol Chem 287: 9193–9199.
- 17. Pandey N, Strider J, Nolan WC, Yan SX, Galvin JE (2008) Curcumin inhibits aggregation of alpha-synuclein. Acta Neuropathol 115: 479–489.
- 18. Hafner-Bratkovic I, Gaspersic J, Smid LM, Bresjanac M, Jerala R (2008) Curcumin binds to the alpha-helical intermediate and to the amyloid form of prion protein - a new mechanism for the inhibition of PrP(Sc) accumulation. J Neurochem 104: 1553–1564.
- 19. Dikshit P, Goswami A, Mishra A, Nukina N, Jana NR (2006) Curcumin enhances the polyglutamine-expanded truncated N- terminal huntingtin-induced cell death by promoting proteasomal malfunction. Biochemical and Biophysical Research Communications 342: 1323–1328.
- 20. Baudin A, Ozier-Kalogeropoulos O, Denouel A, Lacroute F, Cullin C (1993) Simple and efficient method for direct gene deletion in Saccharomyces cerevisiae. Nucleic Acids Res 21: 3329–3330.
- 21. Gietz RD, Woods RA (2002) Transformation of yeast by lithium acetate/single-stranded carrier DNA/polyethylene glycol method. Methods in enzymology 350: 87–96.
- 22. Yılmaz R, Akça O, Baloglu MC, Öz MT, Avni H, et al. (2012) Optimization of yeast (Saccharomyces cerevisiae) RNA isolation method for real-time quantitative PCR and microarray analysis. African Journal of Biotechnology 11: 1046–1053.
- 23. Inge-Vechtomov SG, Tikhodeev ON, Karpova TS (1988) Selective systems for obtaining recessive ribosomal suppressors in yeast Saccharomyces cerevisiae. Genetika 24: 1159–1165.
- 24. Giaever G, Flaherty P, Kumm J, Proctor M, Nislow C, et al. (2004) Chemogenomic profiling: identifying the functional interactions of small molecules in yeast. Proc Natl Acad Sci USA 101: 793–798.
- 25. Ono K, Hasegawa K, Naiki H, Yamada M (2004) Curcumin has potent anti-amyloidogenic effects for Alzheimer's beta-amyloid fibrils in vitro. J Neurosci Res 75: 742–750.
- 26. Upadhya SC, Hegde AN (2007) Role of the ubiquitin proteasome system in Alzheimer's disease. BMC Biochemistry 8: S1–S12.
- 27. Davies JE, Sarkar S, Rubinsztein DC (2007) The ubiquitin proteasome system in Huntington's disease and the spinocerebellar ataxias. BMC Biochemistry 8: S1–S2.
- 28. Keller JN, Hanni KB, Markesbery WR (2000) Impaired Proteasome Function in Alzheimer's disease. J Neurochem 75: 436–439.
- 29. Lin JK (2007) Molecular Targets of Curcumin. Adv Exp Med Biol 595: 227–43.
- 30. Lim GP, Chu T, Yang F, Beech W, Frautschy SA, et al. (2001) The Curry Spice Curcumin Reduces Oxidative Damage and Amyloid Pathology in an Alzheimer Transgenic Mouse. J Neurosci 21: 8370–8377.
- 31. Xiong Z, Hongmei Z, Lu S, Yu L (2011) Curcumin mediates presenilin-1 activity to reduce β-amyloid production in a model of Alzheimer's Disease. Pharmacol Rep 63: 1101–1108.
- 32. Zhang X, Yin WK, Shi XD, Li Y (2011) Curcumin activates Wnt/β-catenin signaling pathway through inhibiting the activity of GSK-3β in APPswe transfected SY5Y cells. Eur J Pharm Sci 42: 540–546.
- 33. Zhang C, Browne A, Child D, Tanzi RE (2010) Curcumin decreases amyloid-beta peptide levels by attenuating the maturation of amyloid-beta precursor protein. J Biol Chem 285: 28472–28480.
- 34. Raymond CK, Howald-Stevenson I, Vater CA, Stevens TH (1992) Morphological classification of the yeast vacuolar protein sorting mutants: evidence for a prevacuolar compartment in class E vps mutants. Mol Biol Cell 3: 1389–402.
- 35. Kaganovich D, Kopito R, Frydman J (2006) Misfolded proteins partition between two distinct quality control compartments. Biochemical and Biophysical Research Communications 342: 1323–1328.
- 36. Meriin AB, Zhang X, Alexandrov IM, Salnikova AB, Ter-Avanesian MD, et al. (2007) Endocytosis machinery is involved in aggregation of proteins with expanded polyglutamine domains. FASEB J 8: 1915–1925.
- 37. Mathur V, Taneja V, Sun Y, Liebman SW (2010) Analyzing the birth and propagation of two distinct prions, [PSI+] and [Het-s]y, in yeast. Mol Biol Cell 21: 1449–1461.
- 38. Hickey MA, Zhu C, Medvedeva V, Lerner RP, Patassini S, et al. (2012) Improvement of neuropathology and transcriptional deficits in CAG 140 knock-in mice supports a beneficial effect of dietary curcumin in Huntington's disease. Mol Neurodegener 7–12.
- 39. Jagota S, Rajadas J (2012) Effect of phenolic compounds against Aβ aggregation and Aβ- induced toxicity in transgenic C. elegans. Neurochem Res 37: 40–48.
- 40. Gong EJ, Park HR, Kim ME, Piao S, Lee E, et al. (2011) Morin attenuates tau hyperphosphorylation by inhibiting GSK3β. Neurobiol Dis 4: 223–230.
- 41. Noor H, Cao P, Raleigh DP (2012) Morin hydrate inhibits amyloid formation by islet amyloid polypeptide and disaggregates amyloid fibers. Protein Sci 21: 373–382.


text:
| 20 February 2013
COPENHAGEN, Denmark: Napatech, the global leader in intelligent network adapters, today provided details on their exhibition at the Mobile World Congress in Barcelona, Spain, February 25 – 28. Napatech will debut tunneling protocol and onboard PTP support, as well as demonstrate 100G throughput and the DeepFlow Telecom probe with its partner, Qosmos. These features and demos will showcase how the power of Napatech adapters can address the monitoring and analysis needs of the telecom industry.
The proliferation of smart mobile devices has led to increasing speeds and exponential growth in data traffic. Carriers must react quickly and adapt effectively in order to assure service performance for their customers. As Ethernet and IP networks are highly dynamic, telecom equipment vendors need scalable solutions that can monitor and analyze high-speed mobile networks in real-time.
Napatech will debut two new features that will address these issues. New tunneling protocol support extracts information from GTP and IP-in-IP tunnels to allow efficient analysis of applications and services used on mobile networks. Napatech adapters perform flow identification and intelligent distribution to multiple server CPU cores based on the contents of the tunnels, rather than on the tunnel itself. This enables Napatech telecom equipment vendors and their customers to accelerate their mobile data analysis application. Napatech's existing features can also identify and distribute IP fragments that often result when tunneling in mobile networks.
Napatech will also debut onboard PTP support on 1G and 10G adapters, which have the advantage of being able to plug directly into the PTP network. These highly anticipated products make time synchronization implementation easier for OEM venders and end-users. The nanosecond precision time-stamping capabilities can precisely measure jitter and delay in mobile networks.
"Tunneling and onboard PTP support are powerful features for telecom equipment vendors who need to build mobile network monitoring products," stated Erik Norup, President and CMO, Napatech. "With these new features, we can off-load and accelerate data analysis, allowing our customers to focus on optimizing the processing resources in their standard servers. This is critical to carriers providing superior service at an affordable cost."
These new features will be revealed at Napatech's exhibition booth with several demos. One will present 100G throughput with zero packet loss using Napatech adapters in a Dell PowerEdge R720. A joint demo with vendor Qosmos will demonstrate how a high performance Deep Packet Inspection (DPI) analysis solution can be provided using a standard server, Napatech adapters and Qosmos software.
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building a small journal 327.
hey im going to be building a small journal 327. i dont know much about the small journals. i have only worked with std. 350 journal 327. so heres some things that i would like to find out. 1) what is the actual size differance between the std. 350 journal and a small journal 327? 2)also kinda dumb one but are the connecting rod journals als smaller? 3) if anyon knows where to getsmll journal splayed main caps that would be great. or if anyone knows if theres a way to make std sized splayed caps work with the small journal that wuld be awsome too. thanx. i will also post pics. of the build when we start it also.
LOL, you sure are stubborn. Despite what everyone tells you, you gotta do it your way. I'm kinda the same way so I guess I understand- I just hate to see you waste all that money on a 327 when a 350 is the way to go.
With that being said run the longest rods you can while keeping the oil ring out of the wrist pin. And in your very limited class you won't see enough of a gain running small journals to justify the cost. If you're going to build the wrong displacement atleast build the right journal size.
well with that big said the stock cranks in the early 327 blocks like i have are forged from the factory rather then cast like in the later 327 and 350 so they are alot stronger and more cost efficiant then spendig $400 or $500 on a new forge crank. w do have 5 other 350 blocks laying around that we will be building at the end of the season also so not all is waisted lol. weonly have 2 races let and we are'nt in the points race anyway. but theowner of the car is stuck on using the 327. im just the mechanic lol. which i can see the theory behind it. the350 we ran didnt spin up verry fast. and from personal dyno testing experiance a 327 spins up aot faster and you can mak elativly the same hp with more torque for the same price. i still say heck wth it just build a 383 stroker and pray that we dont get engine tear down tech'ed. lmao
oh and i will take your advise with the connecting rod thing... will that make much of a differance as far as the fact that we are '0' decking the block?
The 327 is a fine motor and a small journal has less bearing speed which may or may not be of interest to an engineer. What I would like to know is how someone with only 23 years can possibly expect to have such a wealth of experience. I have air in tires twice that old and gasoline in float bowels and my people don,t know as much as the young fella. LOL.
I know enough to know that this guy in an amateur class would be better of spending more time and money on his heads, carb, pistons, rods, crank, or ignition than worrying about journal size. the difference between small and medium journals is a nonissue when you're so short on cash you have to use stock cranks. If he's not going over 500hp he'd be money and power ahead forgetting about journal sizes and some magic 3.25" crank and go with a 4bolt high nickel 350 with a forged crank, off the shelf rods, and boxed pistons.
One of the things us engineers have to do is determine where money is best spent... And in these basic builds journal size is pretty far down the list- Right below valve material selection.
Even a 23 year old pup could figure that one out.
And, if you want to learn more, do as my grandpa said, "steal with your eyes," or my dad, "pick up a book."
well for one im not talking about bearing speed im referin to the fact of quickness from 1000 rpm to 6000 rpm. a shorter stroke means more revolutions per min. and times have changed lmao. a match built 327 and 350 the 327 will have a faster 0-60 time. i have spent alot of time and money on school to pick old timers brains that grew up around this stuff. so ya i know alt more then most 24 yr old punks lol. this is what i enjoy doing and i dont plan on stoping but any info is helpfull im always up or learning more. the bearing speed is helpful due to the knowledge of knowing that can extend bearing and crank life and temps will be lower, for ability of spinning higher rpm.
but till no one has answered my questions abut the size differance. and other questins posted.
and as someone once told me hp s only a calculated number created by torque it's all about the torque. more torque then hp is always better then more hp. and the shorter the stroke and the bigger the bore the better off you are and the more the torque you can make quicker.
w aready have the heads as good as we can get without porting and polishing because w cant port and polish eather. its realy restricted class. thats why its such a challange buildng a quick car.runing a 1/4 mile circle track is a whole different animal then going in a straight 1/4 mile drag race. in that case i would agree with running a 350. but what it costs to make a 350 move as quick as a 327 is alot more and for the most part is not legal for us to do. oh and a update on the blown engine from the last race therear end locked up in the front straight andhe ws at about 6000 rpm and i think because we are runing a manual trans. it stoped he motor too fast and send a rod thru the pan. and that motor was fast. but also illegal with vortec heads and higher compression. and i have got all te specs. for that motor and what is going in to the 327 and for a cheaper cost i will be making 20hp more and almost 100ft lbs of torque more. and the 327 will be completely legal as to where the old 350 wasnt. again thank you guys for your input. it has been helpful. and has challanged my thinking i always love a good challange. oh and the only reason im wondering so much about the journal sizes because im trying to figure out what to do for splayed caps. way stronger then using a std 4 bolt. and my heads and intake are already set up same with our carb.
oh also we are only using the 327 because we got it for free we have 6 other 010 350 blocks which are high nickel blocks but we are saving those for off seaon builds for next season. we are just testing the short stroke theory on a short track. because if a 60 yr old man is runing away from the pack with a 327 then theres got to be something to it. and next season we will have 2 cars on the track. this season has just been a test season so to speak. but heres what we will be runing let me know what you think. 4.060 bore, 3.25 stroke, 51.4cc chamber, .030 gasket, '0' deck clearance with eather flat top pistons maybe dome if we cant shave the heads down enough to get the 51.4cc chamber. 496 camel hump heads(origonaly 64cc heads), we can only use back dump manifolds so we are using up swept back dump stock manifold, with an edelbrock air gap dual plane intake. we are using the dual plane because we cant have single plane and has tobe oem equivelent intake. and thats the best we could find that was oem rated. and fially we have a willy's 500cfm 2 barrel carb. due to regulations we cant run 4 barrel under certain wheel base.
Now talking about the pluses and minuses of that advantage reguarding engines, the bottom line is that these different stroke lengths will cause a 327 vs a 350 to reach peak hp at a different rpm. Im building a 327 myself and Ive looked at the difference between the two quite a bit. In order to take advantage of the 327's shorter stroke, its a good ide to have a lighter car and suitable gears. The 350 will have better low end grunt which is good for a heavier car and quick holeshots, whereas a 327 will have a natural willingness to pull hard in the upper rpms.
Splayed caps? Unless you are going with some kind of forced induction or nitrous you shouldnt need them. As I recall 2 bolt mains should be fine up to about 450-500 hp. You would be much better off spending that money on lightweight pistons, aftermarket rods and a good balancing job. Doing those things will do more to beef up the bottom end than adding splayed caps because it removes stress from the rods and crank. The better you do it the less stress there will be.
But theres more. Lightening up and ballancing the bottom end will not only strenghten the motor, but it will give you more power, adding splayed caps will not..
Last edited by 65smallblock; 01-06-2009 at 12:48 AM.
that was great advise thanx. now on our track we usually stay in around 6000 to 7000 rpm. now a 327 would tend to spin up allot quicker to the higher rpm out of a corner then a 350 would which the track we are racing on has sharp corners and long follow thru with short straights. and our 350 engines just didn't seem to have the top end response to catch the leader. he is running a small journal 327. could his quickness out of the corners have to do with the fact of the 327 better top end ability? we were able to stay on him everywhere else but if he had a open track coming out f a corner he would just run away quick and there would be no catching up. our cars are limited to how light we can be and our car is at the limit.
One thing I like to point out is the fact that a longer stroke is not the only way to make torque. Everyone seems so hung up on the stroke thing thesedays. Gears can create torque! Different intakes and carburetors can too. But additionaly a 350 can also be made to rev.. Then you have power to weight ratios that open a whole nother can of worms. The reason the other guy is smoking you out of the turns is because his ride is well configured to do it. The motor is the heart and soul of a race car, but without EVERYTHING working in harmony you aint gonna win!
Basically what Im trying to say is that having a 350 is NOT a handicap against a 327. 350's can be made to rock and rev to! You just need to set up that car so it is pulling hard at the right time. And when it comes to engines, knowledge is power..
with that being said thats why i started this post, so i can get some good insite. as far as our car set up for the most part all the cars are the same. only difference is tire stagger camber cater and engine build. as far as our chassis set up with tire stagger and camber caster we got the car hooked up it sticks on the track anywhere you put it and it runs hard. but he just seems to power out of the corners alot faster then us. we were also running a 350 out of a modified race car and he was still running away. and our engine was built with more power. given we were able to pace him just couldnt catch him. he comes ot of corners like theres no tommorow. we could pace the rest. but when he came out of corner's he would walk away a Lil more .
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Big Cat in Salem
On February 21, 2013 while traveling northbound on Rt. 85 in Salem at about 12:30 p.m. we saw a big cat about 3 feet tall to top of body plus a long neck of about 6 to 8 inches, with a cheetah-like face. It was white with brownish-orange patches. It was on the west side …
Mountain Lion Salem CT
a very young mountain lion ran in front of my car on route 11 in salem today.
What the $%$*! was that?
Today, Sept 3, 2011, I was heading out to run some errands. We live on the boarder of Salem and Colchester, CT. I was headed toward route 354, a main road that connects the 2 towns, when I saw what I thought was a deer crossing the road. I slowed down and thats when my …
Salem CT – crossed in front of my truck
Was driving out of my yard on july 6, had to stop to let it cross in front of my truck 10 ft from me. I know what I saw, not a bobcat, was definitely a mountain lion, kept seeing strange tracks in topsoil I had recently spread. No doubt.
Cougar or Mtn lion in Salem, CT
6/27 9:30 am cougar or young mtn lion crossed Rt 2 in Salem, Ct All beige, body w/o tail 30 in long, long tail. Height 2 ft. Any other sightings?


text:
4l60E servo cover question
I recently put in the larger corvette servo piston in my truck and two days later its puking fluid and the case is chipped. It is chipped from the bottom of one of the two small reliefs in the servo boss (to access the snap ring) diagonally outward. I am missing less than 1/4" of the actual snap ring groove.
I must have not fully seated the snap ring because the cover cocked sideways and popped it loose.
Do you think I could stab the servo assembly one more time and re seat the snap ring and it would still seal ok with the small chunk missing? Is that servo cover O-ring under full line pressure?
It does have high Pr.
Inspect all the Servo seals 2/4 & Cover & reinstall, it should hold. Probably wasn't seated properly.
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Zero 88 Betapak 3 DMX Installation
Zero 88 Betapak 3 Power Pack Hardwired DMX - new features include: MCB protection as standard, isolated DMX input, 12 programmable backup memories, 3 programmable 99-step sequences with adjustable times, auto DMX termination when loop-through plug is removed, auto frequency tracking, lock and reset functions, temperature monitoring and progressive overheat shutdown.
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Be The Expert: Receive Weekly How-To Tips & Specials
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Joshua Horton
|Southold, Long Island, New York
|Died in Southold, Long Island, New York
|Immediate Family:
Son of Barnabas Horton and Mary Horton
|Managed by:
|Ken Jon Schonberg
|Last Updated:
Matching family tree profiles for Joshua Horton
Immediate Family
About Joshua Horton
Abstract of New York Wills, vol. I, 1665-1707
Will of Barnabas Horton: "To fourth son Joshua, he leaves his home, land and meadows, orchards and Commons of pasture and 1/2 of lands at Accabauk and meadows at Oyster Ponds."
- Horton genealogy; or, Chronicles of the descendants of Barnabas Horton, of Southold, L. I., 1640 by Horton, Geo. F. (George Firman)
- https://archive.org/details/hortongenealogyo00hort
- https://archive.org/stream/hortongenealogyo00hort#page/9/mode/1up
- I. BARNABAS HORTON, son of Joseph Horton, born in Mousely, Leicestershire, England, 13 July (old style), 1600. Emigrated to America in the ship "Swallow," Captain Jeremy Horton, master and owner, in 1635 to '38, landed at Hampton, Massachusetts, came to New Haven in 1640; his wife, MARY, and two children, Joseph and Benjamin, with him. He settled permanently on the east end of Long Island, now Southold, Suffolk County, New York, in October, 1640.
- Children, all born in Southold, except Joseph and Benjamin, who were born in England :
- 1. Joseph, born about 1632; married Jane Budd, daughter of John Budd I.
- 2. Benjamin, born about 1634; married Anna Budd, sister of Jane.
- 3. Caleb, born about 1640; married Abigail Hallock.
- 4. Joshua, born about 1643; married Mary Tuthill.
- 5. Jonathan, born about 1648; married Bethia Wells.
- 6. Hannah, married Barnabas Terrill.
- 7. Sarah, married Joseph Conklin.
- 8. Mary, married Joseph Budd, son of John Budd.
- 9. Mercy, married Christopher Youngs.
- 10. Abigail, married Charles Booth.
- Second Generation. - Joseph I.
- .... etc.
- https://archive.org/stream/hortongenealogyo00hort#page/11/mode/1up
- Second Generation. - Joshua I.
- IV. JOSHUA, son of Barnabas Horton I., born at Southold, L. I., in 1643; married, about 1667, MARY TUTHILL. In 1673, '76, '78 and '95 he deeds land to various persons. In 1676 he is one of the patentees of Southold, and has six males and five females in his family. He is a Lieutenant in 1693. (See "Moore's Indexes of Southold," p. 88.) He died in Southold, 1729. His wife died 2 January, 1718.
- Children, all born in Southold :
- 1. Joshua, ensign, born 1669.
- 2. Joseph, born 1671 ; married.
- 3. Sarah, born 1673; married Richard Terry, son of Richard I.
- 4. Mary, born ; married 2 January, 1 70S, Zaccheus Goldsmith.
- 5. Bethia, born ; married in Jan., 1716, Ichabod Hallock. She died 1753.
- 6. Keziah or Zerniah, married Israel Cose.
- 7. Ephraim, born 1786; married, in 1707, Martha Vail.
- .... etc.
- The refugees of 1776 from Long Island to Connecticut by Mather, Frederic Gregory
- https://archive.org/details/refugeesof1776fr00mathuoft
- https://archive.org/stream/refugeesof1776fr00mathuoft#page/405/mode/1up
- HORTON - The ancestor of this name, on L. I. was Barnabas1, who was b. at Mowsley, Leicestershire, Eng., about 1600. (Moore's "Index," p. 22) He was one of the original settlers at Southold; and one of the 12 who constituted the Church of Rev. John Youngs, in 1640. He d. July 13, 1680, aged 80. (Tombstone at Southold) The house which he erected at Southold was known as the "Old Castle." His son, Capt. Jonathan2, built the West part of the house a few years later. (Griffin's "Journal," p. 229. See Page 406) Moore (pp. 22-24, 88-92) has been pains-taking in regard to this Family ; but later, and more accurate, information is found in the Horton Gen. (G. F. Horton, Phila., 1876), which is followed, below. "The Early Hortons, of Westchester Co., N. Y.," may be found in the N. Y. Gen'l and Biog'l Rec., Jan. and Apr., 1905.
- Barnabas1, b. July 13 (O. S.), 1600, came to Hampton, Mass., in 1635-1638; to New Haven and to Southold, in 1640, with his wife Mary and sons, Joseph2 and Benjamin2. His other sons were : Caleb2 , Lt. Joshua2 and Capt. Jonathan2. His dau., Sarah2, m. William1 Salmon. (See Salmon)
- Joseph2, b. about 1632-1635; m. Jane Budd; removed to Rye, N. Y. Moore states that he m. Abigail, dau. of John Vail. (See Vail)
- Benjamin2, b. about 1634-1637; m. Anna Budd; removed to Rye, about 1665, where he d. s. p. Nov. 3, 1690.
- Caleb2, b. in 1640; m. Abigail, dau. of Peter1 Hallock (See Hallock); d. Oct. 3, 1702. His son, Jonathan3, b. in 1668; m. Bethia Conklin. He had a son, Jonathan4, b. in 1694, m. Elizabeth Goldsmith.
- Lt. Joshua2, b. about 1643; m. Mary Tuthill; d. in 1729. Among his children were: Ens. Joshua3; and Ephraim3. Ens. Joshua3, b. in 1669; m. (1) Elizabeth, dau. of Simon Grover, (2) Wid. Mary Gillam; d. about 1744. Ephraim3, b. in 1686; m. Martha Vail. His son, Joseph4, b. in 1708; perhaps m. Deliverance Reeves.
- https://archive.org/stream/refugeesof1776fr00mathuoft#page/406/mode/1up
- Capt. Jonathan 2, b. Feb. 23, 1648; m. Bethia, dau. of William1 Wells; d. Feb. 23, 1707. Among his children were: William3, b. in 1677, m. Christina Youngs; Jonathan3, b. Dec. 23, 1783, m. Mary Tuthill, and was the father of Rev. Azariah4, who was Missionary to the L. I. Indians, 1741-1750; and Dea. James3, b. in 1694, m. Anna Goldsmith, d. May 16, 1762. He was the father of Rev. Ezra4, who m. Mary, dau. of Robert Hempstead. (See Hempstead) He kept a valuable Diary.
- HORTON BARNABAS4 .... etc.
- .... etc.
- Horton family year-book Vol. 5
- https://archive.org/details/hortonfamilyyear05hort
- https://archive.org/stream/hortonfamilyyear05hort#page/11/mode/1up
- 1 BARNABAS HORTON1 of Southold, Long Island, New York, was born in 1600, at Mowsley, Leicestershire, England, and died July 13, 1680, at Southold, L. I. He married, in 1622, Ann Smith, of Stanion, Northamptonshire, England. She died before the family came to America. Barnabas Horton married (2d) Mary ---- , who survived him. He emigrated to America prior to 1640, and settled at Hampton, New Hampshire. As early as 1651 he removed to Southold, and resided there until his death. He held many public offices. He was Deputy to the General Court of the New Haven Colony in 1654, 1656, 1658, 1659 and 1661. In 1663 and 1664 he was a Commissioner for Southold.
- Children :
- 2 i Joseph Horton, m. Jane Budd.
- ii Benjamin Horton, m. Anna Budd.
- iii Hannah Horton, m. Barnabas Trevale (or Terrill).
- iv Sarah Horton, m. Joseph Conklin.
- v Mary Horton, m. Joseph Budd.
- vi Caleb Horton, m. Abigail Hallock.
- vii Joshua Horton, m. Mary Tuthill.
- viii Jonathan Horton, m. Bethia Wells.
- ix Mercy Horton, m. Christopher Youngs.
- 2 LIEUTENANT JOSEPH HORTON2 (Barnabas1), son .... etc.
- Abstracts of wills on file in the Surrogate's office: City of New York Vol. I by William Smith Pelletreau, New York (County). Surrogate's Court ....
- https://archive.org/details/abstractswillso03kellgoog
- https://archive.org/stream/abstractswillso03kellgoog#page/n128/mode/1up
- Pg.110
- Page 417.— BARNABAS HORTON, Southold. "I Barnahas Horton of Southold, finding many distempers daily growing upon me." Leaves to eldest son Joseph 10 sheep, to what he formerly had as his full portion. To second son Benjamin, 10 sheep, to what he formerly had, as his full portion. To eldest daughter Hannah Trevalle, 10 sheep as her full portion. To Joseph
- https://archive.org/stream/abstractswillso03kellgoog#page/n129/mode/1up
- Pg.111
- Conckling, son of my daughter, Sarah Conckling, 5 sheep. To my 3d daughter Mary Budd, 5 sheep. To my third son, Caleb 1 horse and 1/2 of all my right in Accabauk to what he hath in possession at Corchaug for his full portion. To my fourth son Joshua, all my house, land, and meadows, orchards, and Commons of pasture which was mine and is now in his possession, and 1/2 of my meadow and upland within the bounds of Accabauk, and all my meadow at Oyster Ponds. To my fifth son Jonathan, all my dwelling house, barn, home lots and meadow and all the rest of the real estate, except that the new house shall be for the use of Mary, my wife, during her life, and she is to have the third bushel of all grain, and he is "to winter and summer for her four cows." To youngest daughter Mercy Youngs 4 cows and bed and bed clothes. Makes wife Mary executor.
- Dated May 10, 1680. Witnesses, Jonas Holdsworth, Richard Benjamin. Proved at Court of Sessions held in Southampton March 4, and confirmed November 18, 1681.
- Inventory. Land and Housing £200, 7 oxen, £30, 5 cows, £12, 16 horse kind, £24, 90 sheep, £35. Total amount £405. Taken by John Corwin, John Carey, Benjamin Youngs.
- (Pg.11 in The Horton Genealogy says JOSHUA HORTON married MARY TUTHILL)
- Family History Compiled by Lucy Henderson Horton ... By Mrs. Lucy Henderson Horton
- https://books.google.com/books?id=hWtVAAAAMAAJ&pg=PA272&lpg=PA272&dq=JOSHUA+HORTON+1643&source=bl&ots=Hq4uihcgJl&sig=ndevd6MjE8Wr34zR8Br6uQ2w13g&hl=en&sa=X&ei=98ShVeTDAdDqoAT28orgBQ&ved=0CCwQ6AEwAzgU#v=onepage&q=JOSHUA%20HORTON%201643&f=false
- Pg.272
- In Dictionary of United States History by Jameson on Page 377 the statement is made that "the English settled the eastern portion of Long Island, N. Y., in 1640:"
- 1. Barnabas Horton; born in Mousley, Leicestershire, England, died at Southold, Long Island, New York, in 1680 (see page 9 of Horton Genealogy). The tombstone which marks his grave at his old home also proves this.
- 2. Joshua; son of Barnabas Horton, was born at Southold, L. I., in 1643; married, 1667, Mary Furthell. She died in 1729 (see page 11 Horton Genealogy).
- 3. Joshua Horton; Ensign, was son of Joshua Horton and his wife, Mary Furthell. He was born at Southold, L. I., in 1669. He married first, Elizabeth Glover, second, a widow, Mary Gillam. He died in 1744 (see page 170, Horton Genealogy).
- Pg.273
- 4. Ephriam Horton, son of Ensign Joshua Horton; married Martha Vail.
- 5. Joseph Horton, son of Ephraim Horton and his wife, Martha Vail; was born at Southold, 1708.
- 6. Joshua Horton, son of Joseph Horton; was born 1730 (see page 170, Horton Genealogy).
- (We think that this is Joshua Horton, the explorer, who came to what is now Tennessee in 1766 with Col. James Smith, of Pennsylvania, and Uriah Stone, for whom Stones river was named, and Wm. Baker and a negro servant. They named Cumberland mountains and Cumberland river in honor of the Duke of Comberland.
- .... etc.
- Joshua Horton
- Birth: 1643 Southold, Suffolk County, New York, USA
- Death: unknown
- Family links:
- Parents:
- Barnabas Horton (1600 - 1680)
- Mary Langdon Horton (1611 - 1670)
- Spouse:
- Mary Tuthill Horton
- Children:
- Ephraim Horton (1686 - 1733)*
- Siblings:
- Mary Horton Budd (____ - 1688)*
- Benjamin Horton**
- Joseph Horton (1625 - 1699)**
- Joshua Horton (1643 - ____)
- Jonathan Horton (1648 - 1707)*
- *Calculated relationship
- **Half-sibling
- Burial: Unknown
- Find A Grave Memorial# 45182806
- From: http://www.findagrave.com/cgi-bin/fg.cgi?page=gr&GRid=45182806
- Barnabas Horton
- Early Southold, Long Island Settler
- ....etc.
- Which wife was the mom to which kids is not absolute, as the death date of the first, and marriage date of the second wife, are not certain.
- Hortons in America makes some serious errors in the spouses of children of Barnabas Horton. I present the information below from Hortons in America, along with notes I have made. .... etc
- BARNABAS HORTON, born in Mowsley, Leicestershire, England (old style). In 1622 he married Anne Smith of Stanion of Northamptonshire, England. She died, and he married Mary Langton. He emigrated to America in the ship Swallow, Captain Jeremy Horton, master and owner, in 1635 to 1638, landed at Hampton, Mass., where he owned a plot of ground.(*) He came to New Haven, 1640, with his wife, Mary, and two children, Joseph and Benjamin. He settled permanently on the east end of Long Island, now Southold, Suffolk County, N. Y., in October, 1640.
- Children of first wife, Anne Smith:
- 1. Joseph, born 1625; married Jane Budd, daughter of John Budd I.
- [This is Jane-2 Budd, dau of the first John Budd, md Katherine Brown. She is sister of the Long Island Pioneer John-2 Budd, who married Mary Horton. nmt]
- 2. Benjamin, born 1627; married Anna Budd, sister of Jane.
- [This Benjamin married, first, Ann/Anna (____) Tooker/Tucker (sister of Christopher Youngs wife), former wife of John Youngs (see Torrey and Southold Town Records). Torrey assigns her no identity. She was the second wife of John Tooker/Tucker]
- The McLaurin "Descendants of Barnabas Horton", 1990, indicates the proof for her identity as Ann-2, daughter of John-1 Budd, comes from an undated document where she and her brother John-2 Budd wrap up details from their father's estate. He gives no location for this document. I haven't found it in Southold records, perhaps it is in Rye records.
- Benjamin's second wife was Mary Mapham. He apparently had no children by either wife, as his will provided for siblings, and mentions no children or grandchildren.
- Children of second wife, Mary Langton:
- 3. Caleb, born 1640; married Abigail Hallock.
- Caleb's first wife, and probable mother of all of his children, is unknown. Even her first name eluded being recorded in any documents located so far. She is likely mother to all of Caleb's children, except possibly the youngest, Phebe.
- There was a recorded marriage for a Caleb Horton to an Abigail Horton in 1697, but there were more than one Caleb Horton in 1697 to assign this marriage to. (In fact, McLaurin assigns the marriage to a nephew of Caleb-2.) Caleb married last, Esther, probably: (Crafford) [Wedge] [Homan] Horton. She is his wife referred to in his will. She is likely the Esther Homan, widow, as shown in the 1698 census. A Esther Horton witnessed the will of the daughter of Esther Homan (Deliverance Whitehair) in 1699.
- 4. Joshua, born 1643; married Mary Tuthill.
- [McLaurin presents data from a Wheeler genealogy which convincingly shows Joshua's wife was Mary Wheeler. Joshua was referred to as "brother" by a brother of Mary Wheeler in the distribution of a Wheeler matriarch's estate in Southampton. ]
- 5. Jonathan, born 1648; married Bethia Wells.
- [This couple identified in Ancestors of American Presidents, pg 18, for President Harrison.]
- 6. Hannah, married Barnabas Terrill.
- No, there was no Barnabas Terrill. The will of Barnabas gave: "to Hannah Tevalle 10 sheep as her full portion.". Hannah married 1) Thomas Hildreth abt 1648 2) Jonas Bower abt 1659 and 3) Thomas Trevally abt 1673. (See McLaurin, "Descendants of Barnabas Horton,", 1995, and/or: Hoff, NYGBR 123:210, 1992 "Additions & Corrrections", to NYGBR 120:74 (article about Peter Hildreth): Identity of Hannah, wife of Thomas Hildreth, Jonas Bower, and Thomas Trevally.
- 7. Sarah, married Joseph Conklin.
- [She married first, William Salmon (See TAG 21:246-253 for a very interesting review of the Horseneck lawsuit whereby family relationships were determined by many documents relative to this lawsuit that lasted for years. She had two children by William. She then married John Conklin, December 02, 1657. nmt]
- [The persistent reports that the first John Budd SR had a son named Joseph Budd who married a Sarah Horton appear to be a complete sham. Sarah Horton, daughter of Barnabas, is comfortably with two husbands during her life, completely documented in the Horse Neck lawsuit documents. If she did "squeeze" in this marriage, she had no issue, as the various documents re the "orphans" in the lawsuits would have named them somewhere along the way. There is no Joseph in John Budd, SR's will of 1669. (there is in John Budd JR's will.) Sarah's son, Joseph Conklin, is referred to in Barnabas Horton's will of 1680. John Conklin outlived Sarah Horton, his wife. There is no such marriage in Torrey. This Joseph Budd appears to be a ghost and the Sarah so often cited for his wife likely not the daughter of Barnabas, or the whole marriage is just a complete sham. nmt]
- For another interesting article on this branch of the family, see: Gale Ion Harris, TAG 1996:235-241 - Sarah (Salmon) (Edwards) Curtis of LI and Conn.
- 8. Mary, married Joseph Budd, son of John Budd.
- [Mary married JOHN-2 Budd, not Joseph. Mary was referred to as Mary Budd in Barnabas' will, so she definitely married a Budd. Torrey says Mary Horton married JOHN Budd, Jr. (1620-1684), son of John and Katherine (Brown) Budd. John Budd, Jr.'s will refers to wife Mary. I find no Joseph Budd that could be a possible match in the Budd tree. nmt]
- 9. Mercy, married Christopher Youngs.
- [Mercy md first John Youngs, son of Cpt Joseph (who was brother of Rev John), abt 1675/6 and had four children with him. She md second, Christopher Youngs Bet. 1689 - 1698, and had no children with him. See Youngs Genealogy, by Selah Youngs.] She is in the 1698 census with Christopher and her children, but he was their step-father (and first cousin to their natural father), not their father.
- 10. Abigail, married Charles Booth.
- The daughter Abigail is from Horton's in America and is not a daughter. She was Abigail Mapham, daughter of John and Mary (Hampton) Mapham. Her mother, Mary, was a wife of Benjamin-2 Horton. Her name as the widow "Mary Horton" led early researchers to believe she was Mary (Langton) Horton, probably leading to that misidentification of Abigail as a daughter of Barnabas. See McLaurin and NYGBR 38:322.
- .... etc.
- Resources
- Hortons in America - White, Adaline H., (1929). Below average scholarship, all assertions should be challenged - be very careful in using this error-prone genealogy. It is in genealogylibrary.com
- "Descendants of Barnabas Horton" by Banks McLaurin, Jr. (1990). The scholarship of this Horton genealogy is of higher scholarship than Hortons in America, correcting many errors in HIA. It also contains transcripts and photo-copies of many Horton documents (wills and other documents.) However, it is not without its errors and its presentation is sometimes confusing as it presents photo-copies of submitted lineages that conflict with other info elsewhere in the book.
- NYGBR 102:69-??, 1971 - Documentary Evidence of the Life and Labors of Barnabas Horton. Explores English ancestry and early years of Barnabas. Lists documents and records in which Barnabas is found. A "must-have" for Horton descendants.
- Edward Hart - Descendants and Allied Families, Horton Section, pp 144-147. Short sketch in a "all my ancestors" type book, but above average scholarship, more reliable than HIA.
- Torrey, "New England Marriages Before 1700"
- From: http://ntgen.tripod.com/bw/hort_index.html
- (NOT ABLE TO FIND READABLE McLaurin Jr., Banks, Descendants of Barnabas Horton of Southold, Vol. 1, revised 1995)
- Barnabas (1600-1680)
- The heritage of Barnabas Horton has been carried on through the generations from Southold to Salem. Exactly when he left England and on what ship he traveled has never been proven. What is known is that he was a man of unquestionable character and great faith, which is shown on his Tablestone and in his will. He became a freeman in Hartford before arriving in Southold where he served as a constable and then as a Deputy to the General Court in 1663 and 1664. As a founding father of the Town and of the church he was active in the affairs of both, and of the colony. It is said that he agreed to maintain the lane to the dock, which allowed him to have lots on either side of Horton's Lane. In 1640 he received a land grant which included the land on which the Horton's Point Lighthouse now sits.
- BARNABAS1 HORTON1 was born July 13, 1600 in Mowsley, Leicestershire, England, and died July 13, 1680 in Southold, Suffolk County, Ny2where he is buried in the Old Burying Ground of the First Presbyterian Church. He married (1) ANNE SMITH3. She was born Abt. 1602, and died Abt. 1630. He married (2) MARY LANGTON3Abt. 1631 in England. She was born Abt. 1611 in England, and died Aft. 1698.
- Children of BARNABAS HORTON and ANNE SMITH are:
- i. JOSEPH2 HORTON4,5, b. Abt. 1625; d. Bef. June 12, 1696, Rye, Ny; m. JANE BUDD6, Abt. 1645; b. Abt. 1627; d. Aft. June 12, 1696.
- ii. BENJAMIN HORTON6, b. September 1627; Baptism: England d. November 03, 1690; m. (1) ANNA BUDD6, February 22, 1658/59, Southold, Suffolk County, Ny; b. Abt. 1629; d. Bef. 1686; m. (2) MARY HAMPTON6, 1686.
- iii. ANNE HORTON, b. October 04, 1629. Baptism: England
- Children of BARNABAS HORTON and MARY LANGTON are:
- iv. HANNAH2 HORTON7, b. Abt. 1632; d. Aft. 1698; m. (1) THOMAS HILDRETH7, 1648; b. Abt. 1611; d. 1657, Southampton, Suffolk County, Ny; m. (2) JONAS BOWER7, Abt. 1659; b. Abt. 1630; d. May 29, 1671, Southampton, Suffolk County, Ny8; m. (3) THOMAS TREVELLY9, 1673;b. 1630; d. 1687.
- v. SARAH HORTON10, b. Abt. 1634; m. (1) WILLIAM SALMON10, Bef. 1657; m. (2) CAPTAIN JOHN CONKLIN/CONCKYLNE11, December 02, 165712; b. 1631, Nottingham, Northamptonsire, England; d. April 06, 1694, Southold, Suffolk County, Ny13.
- vi. MARY HORTON14, b. Abt. 1635; d. Aft. 1684; m. JOHN BUDD14, Abt. 1652; b. Abt. 1631; d. November 05, 1684.
- vii. CALEB HORTON22, b. Abt. 1640, Southold, Suffolk County, NY; d. October 03, 1702; m. (1) <UNNAMED>23, Abt. 1665; m. (2) ESTHER24, April 26, 1699; b. 1648; d. November 28, 1740.
- viii. JOSHUA HORTON15, b. Abt. 1643; d. June 17, 1729, Southold, Suffolk County, Ny; m. MARY WHEELER15, Abt. 1667, Southold, Suffolk County, Ny; b. Abt. 1650; d. November 24, 1732, Southold, Suffolk County, Ny.
- (THE REFERENCE 15 FOR THIS IS Descendants of Barnabas Horton of Southold, Vol. 1, revised 1995 BUT IN THE ABOVE LISTING IT IS STATED THAT McLaurin SAYS IT WAS DATA FROM THE WHEELER GENEALOGY, WHICH LISTS JOSIAH HORTON - C.POMEROY)
- ix. CAPTAIN JONATHAN HORTON16, b. February 23, 1647/48, Southold, Suffolk County, Ny; d. February 23, 1706/07, Southold, Suffolk County, Ny17; where he is buried with his father in the Old Burying Ground; m. BETHIAH WELLS18, Abt. 1672, Southold, Suffolk County, Ny; b. Abt. 1653, Southold, Suffolk County, Ny; d. April 14, 1773, Southold, Suffolk County, Ny19. and is buried in the Old Burying Ground
- x. MERCY HORTON20, b. Bet. 1650 - 1655; d. Aft. 1698; m. (1) JOHN YOUNGS20, Abt. 1675; b. March 23, 1634/35; d. Bef. 1689; m. (2) CHRISTOPHER YOUNGS, JR.21, Bet. 1689 - 1698; b. Abt. 1653; d. December 1698.
- Endnotes
- 1. .... etc.
- 15. McLaurin Jr., Banks, Descendants of Barnabas Horton of Southold, Vol. 1, revised 1995, pg. 237.
- http://longislandgenealogy.com/barnabas/barna001.htm
- Links
- http://www.longislandsurnames.com/getperson.php?personID=I22982&tree=Conklinother
- http://brookhavensouthhaven.org/hamletpeople/tng/getperson.php?personID=I4127&tree=hamlet
- The Genealogical and Encyclopedic History of the Wheeler Family in America by Albert Gallatin Wheeler
- https://archive.org/stream/genealogicaland00genegoog#page/n631/mode/1up
- Pg.593
- 10328. THOMAS WHEELER, son of Thomas (10327). Died Dec. 1656. Married Alice --- --- . He lived at New Haven, Conn. The widow rem. to Southampton, L. I., with her children, and married there Josiah Stanborough as his 2d wife.
- Children:
- 10329. THOMAS WHEELER, born April 21, 1652.
- One of the daughters married Josiah Horton, of Southold, L. I., and the other married Francis Sayre, of Southampton, L. I.
Joshua Horton's Timeline
January 2, 1643
Southold, Long Island, New York
Age 25
Southold, Long Island, Province of New York
Age 27
Age 29
Age 35
Age 42
Southold, Suffolk County, Province of New York
Age 43
Age 46
Southold, Suffolk, NY
June 17, 1729
Age 86
Southold, Long Island, New York


text:
What is it about Alfa Romeo?
Their cars make so little sense outside of Rome and Southern California.
And you need a Southern California-sized wallet to take care of them too.
Let's see...first there's the rust issues. Then there is the poor reliability. Engine problems. Electrical gremlins. Then there is the expensive and hard to find parts. By the time you find one without all those potential problems, it's no longer fun or affordable, which was supposed to be the whole point of them (well, at least the fun part).
Yet despite that, they have a devoted following. They have racing history. They are part of the whole Italian car culture that also spawned Ferrari. They look awesome, thanks to Pininfarina (who also styled Ferrari). And they're supposedly fun to drive.
Like many others, I just like them.
This being a '79 GT, it's probably a simple four-cylinder model with a manual transmission.
It's also in terrible shape.
This car has just about every strike against it, especially as far as an Alfa goes. It looks like it's been sitting outside in New England for ages. It has poor paint, lopsided turn signals and missing trim and pieces everywhere. Worse, it has no windshield. There seems to be a blue tarp on the ground that may have covered the windshield. But given New England's tumultuous weather systems, blue tarp is no match for rain, sleet, snow, dust, wind, humidity, you name it. I imagine the interior is a damp, moldy mess.
Despite the physical ailments, the seller states the car is a special edition that ran recently. That's good news, because a crippled engine underneath this cosmetic nightmare is an absolute deal-breaker. The seller mentions the wheels are desirable, so perhaps they sense the car is at the point of just parting out and they are close to giving in.
There is no mention of rust.
I'm split on the worthiness of this one. The seller wants $1,200 or best offer, which is a good start. But given the cost of at least a windshield for a vintage 1979 Alfa and the most rudimentary engine tuneup at a local mechanic who knows what they are doing (if you can find one), you'd be looking at investing at least double or triple what you paid for it, assuming it's in the range of what the buyer wants. On the other hand, it would be a shame to part it out or let it rot into the ground. The car appears to be whole and may not need too much if you don't plan on a full restoration. This is probably a good deal if you can get it for under $1,000. Like, in the range of $500-$800.
Alfa Romeo's legacy in the U.S. is mixed. There will always be the beloved Spyder. But then there is this GT, the value of which has really never recovered, perhaps except for the GTV6. And then there are their sedans, the Milano and the 164, which are much more practical and dare I say better looking, but worth even less.
So unless you're in Rome or California and you find an immaculate one, the rest of us have to sort through the good and bad of these old Alfa cars. As long as they are acquired for cheap, they start to make some sense.
Find it here on Craigslist in Warren, Rhode Island.


text:
Domestic magnate stand up for her company in the controversy with JC Penney and Macy's.
Martha Stewart, the doyenne of American domestic life who once ended up in jail after lying about a stock trade, was back in court on Tuesday in a high-profile case that is as much about her public image as it is a seemingly arcane contract dispute.
Stewart is defending her firm in a complex fight involving two of America's biggest and most famous department stores – Macy's and its rival JC Penney.
The case revolves around the issue of whether Penney's 2011 deal with Stewart violates a pre-existing deal to sell many of Stewart's goods through Macy's. Macy's says they have exclusive rights to the products that are branded with Stewart's well-known name.
Meanwhile Stewart's company insists that it is allowed to pursue other deals and the Macy's agreement covers only specific goods and brands.
But, as with all things Stewart, the trial has become as much about the drama of her reputation and personality as much as the more obscure parts of American contract law. Some court testimony has portrayed Stewart as abandoning Macy's CEO Terry Lundgren – a close personal friend – so she could enrich her troubled company.
During testimony last week, Lundgren described how he hung up the phone on Stewart after she told him about the Penney deal. Such allegations only reinforce Stewart's reputation as a ruthless businesswoman which is often at odds with the buying public perception of her as their favourite homemaker whose goods sell in their millions across the nation.
Lundgren hasn't spoken to her since putting the phone down on her, and in court last week even appeared choked up at times. "I was completely shocked and blown away," he testified. "It was so far from anything I could imagine." Stewart was asked about the phone call and said in court that she was shocked at Lundgren's reaction. "I was quite taken aback by his response. When he hung up on me I was kind of flabbergasted," she said.
But, displaying her now infamously imperious temperament, Stewart engaged in various testy exchanges with Macy's lawyer Ted Grossman. Grossman asked her at the start if she was comfortable in the witness box, to which she replied with a withering: "As comfortable as could be."
Dressed in a beige outfit and cream blouse, Stewart also showed a perhaps unfortunate knack for not quite realizing how ordinary Americans live in a country still recovering tepidly from the Great Recession. When asked by Grossman if it was likely that a customer might buy one set of equipment, like a Stewart-branded casserole dish or set of knives and forks, in one store and then walk into a different store and buy them again, Stewart replied: "They might have two houses! They might have two kitchens!"
The two repeatedly sparred over how Stewart interpreted her firm's obligations to Macy's and whether or not they clashed over a desire to do a major deal with Penney. Grossman pressed her on her commitment to Macy's and a timeline of when she started talking to Penney and working on designs for them. "We thought, and I hope rightly so, we were absolutely allowed to do such a thing," Stewart said.
Macy's has sued the media and merchandising company Stewart founded alleging she breached their contract when she signed a deal with Penney to open shops at most of its stores this spring. Macy's, which has sold Martha Stewart products including towels and pots since 2007, is trying to block Penney from selling those products.
The case is a high-risk effort for almost everyone involved. For Stewart any legal disaster could easily hurt her brand and her image which has survived the earlier travails over allegations of insider trading that saw her go to jail.
The latest legal trouble also comes at a time when her business is struggling to fatten merchandising revenue as it tries to offset declines in its broadcast and publishing divisions. Martha Stewart Living Omnimedia is in its fifth straight year of losses. In 2012, the firm posted revenue of $197.6m, down nearly 11% from the previous year. Losses jumped to $56m from $15.5m the year before and its share price is down more than 90% from $36 in February 2005 – when Stewart was about to emerge from jail.
Penney has its own troubles too. The giant retailer is in the middle of a turnaround plan that is struggling in the face of big losses and sales declines for four straight quarters. The deal with Stewart, which included a roll-out of mini-shops inside its stores, had been planning to use the Martha Stewart brand as a core part of its revival.
Finally, Macy's is keen to protect an area of its own business that has been a success. Sales for the Martha Stewart brand at Macy's rose 8% last year, double the sales increase for the entire company. In a possible personal olive branch to Macy's Stewart told the court that she was a huge fan of the store. "I love Macy's," she said. "I have shopped at Macy's since I was a young child." But at the same time she heaped praise on Penney chief executive Ron Johnson. "He is a visionary," she said. "He had the foresight to re-imagine the American department store."
guardian.co.uk © Guardian News & Media Limited 2010
Published via the Guardian News Feed plugin for WordPress.


text: alright, im trying to trade/sell my specialized big hit 1 downhill/jumping bike. its worth about $1200 but depending on what your willing to trade or pay im more than willing to drop the price. bike is in awesome condition. and is a great bike for anybody whos looking to get into jumping or downhill. anyone have anything? im looking for an access port, up/down pipes, exhaust, vf39, sti tmic, headlights, grill, front lip/splitter, or anyhting you think might be worth around the same price, let me know thanks! im located in slc utah and AM willing to ship, and my car is an 03 WRX wagon.


text:
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American DJ AC3PDMX5
5' Professional DMX Light Cable 3-Pin XLR
Product Description for the American DJ AC3PDMX5
5 foot 3-pin DMX cable to hook up lights to controllers, or to connect dimmer packs together.
- Nominal Characteristic Impedence: 110 Ohms
- Nominal Capacitance Conductor to Conductor @ 1KHz: 12.8 pF/f t
- Nominal Cap Cond. To Other Cond. & Shield @ 1KH z: 23 pF/ft
- Nominal Velocity of Propagation: 66%
- Nominal Delay: 1.6 Nanoseconds per foot
- Nominal Conductor DC Resistance @ 20 degrees C: 24 Ohms/1000 ft
- Nominal Outer Shield D C Resistance @ 20 degrees C: 3.4 Ohms/ 1000 ft
- Nominal Attenuation (dB/100 ft): 0.6 (@ 1 MH z) dB/100 ft
- Maximum Recommended Current: 2.1 A mps per conductor @ 25 degree C
|American DJ
|Dimensions (WxHxD)


text:
Walk in the steps of the Liverpool pop stars on this two-hour tour of Beatles-related spots. Hear about their first U.S. trip, with stops at the Ed Sullivan Theater, Carnegie Hall and the Plaza Hotel, where the band hid from shrieking fans, and visit other associated locales, such as the Dakota and the Lennon memorial at Strawberry Fields. Location disclosed with ticket purchase.
|Event website:
To improve this listing email: firstname.lastname@example.com


text: Today, I would like to take you to Geneva. A gorgeous city located in the french part of Switzerland. One word that comes to my mind when I think about Geneva is Cozy. The city is very memorable for its gigantic fountain, lake Geneva, chocolate, motor show and expensive shops. It is the second biggest city in Switzerland, but it felt quite small to me. The first thing you need to know before coming to Switzerland is how expensive everything is. Therefore, if you plan to visit this beautiful country bear this major point in mind. But, don't let the prices scare you away from coming to Switzerland, it's worth it.Geneva deserves a full day of a walking tour. So, wear comfortable shoes! Don't forget to take a stop at a chocolate shop to try out the famous Swiss chocolate. Transportation in Geneva is the best I've ever used. I loved taking tram rides everywhere I went. Every bus, train, and tram that I went on was very clean and reliable The peace and slow pace of this city were very inspiring to me. I found Switzerland to be a very laid-back country, which I think is great. Switzerland should be on top of your list if you're looking for a calm place where you can reflect back on your life, get a higher education or write a novel. In my opinion, the best time to come to Geneva is in the summer or during a motor show. Every march, Geneva hosts a very popular motor show. If you want to see the show, you will need to buy a ticket earlier than the actual show through their website. I bought my ticket a month in advance. If you will get a chance to see the show, definitely take it. It was really awesome. What remained in my memory is how crowded it was and good-looking future cars that I've seen.See the Lake Geneva, wander around the town, visit Musee des Arts, stop by a local park and enjoy the clean Swiss air. If you are coming to Switzerland in the winter, then skiing is a must. If you will want to go on a nice dinner, don't worry, there are many options to choose from. I dined at the Cafe du Centre and really liked the atmosphere and food. My favorite part of visiting Geneva was walking along the lake during the sunset. For me, dusk is the prettiest time of the day and Geneva looks charming at such time. It is a very comfortable city. After five days that I spent there, I felt very familiar with the city and actually didn't want to leave. I made many wonderful memories in Switzerland, and I hope you will get a chance to come and make many memories there too! Follow me on BLOGLOVIN', TWITTER, FACEBOOK, TUMBLR, GOOGLE +


text:
Philippine Veterans Bank joins BancNet
BancNet recently welcomed the Philippine Veterans Bank as the newest member of its network.
By joining BancNet, ATM cardholders of Veterans Bank will benefit from BancNet services particularly debit shopping or payment using the ATM card and easy payment of bills in more than 2,000 BancNet ATMs nationwide.
The Philippine Veterans Bank is a private commercial bank with 60 branches nationwide, providing a wide array of services for individuals and public & private corporations. PVB offers ATM/payroll services, corporate & retail loans, investment & trust services. It also serves as a government depository bank as a nation's grateful response to its owners, the Filipino World War II veterans.
Signing the agreement are (from left) BancNet executive vice president and chief operations officer Aristeo P. Zafra, Jr., president Francisco M. Caparros, Jr., chairman Ricardo R. Chua, Philippine Veterans Bank president and chief executive officer Ricardo A. Balbido, Jr., executive vice president Jesus Vicente O. Garcia and senior vice president Camille Maricelle Canullas.


text:
10am-6pm Monday-Friday
open til 10pm show nights
We now have over 130,000 live concert pictures from concerts at The Rave/Eagles Club for you to enjoy.
The Rave does not advise purchasing tickets from craigslist, ebay, ticket resellers such as StubHub or TicketsNow, scalpers, street vendors, or other private parties, and cannot guarantee the validity and subsequent admission on such tickets. Many of these tickets are counterfeit/duplicate and will not get you into the show. The Rave strongly suggests you purchase tickets only from TheRave.com, eTix.com and official band websites.


text:
From the Cutting Room Floor
Every few weeks, the Young Artists Showcase builds up such a store of wonderful performances that we just can't find time to put into our Wednesday night hour. This week, host Bob Sherman has gathered up some beautiful odds and ends that didn't fit into previous shows.
We catch up with YAS piano alumni Tanya Bannister and Sara Daneshpour, get encores from saxophonist Ashu and cellist Narek Haknazaryan, and Brian Yeubin Lin adds a bonus from our Sydney Piano Competition studio session: the devilishly difficult Islamey Fantasy by Mily Balakirev.
Program details:
Schumann: Abegg Variations
-- Tanya Bannister, piano.
Liszt: Gnomenreigen
-- Sara Daneshpour, piano.
Chopin: Grand Polonaise Brilliante, Op 22
-- Claire Huangci, piano.
Ennio Morricone: Cinema Paradiso, main theme
Piazzolla: Libertango
-- Ashu, saxophone; Kyuang-Hao Huang, piano.
Rostrapovich: Humoresque
-- Narek Haknazaryan, cello; Noreen Polera, piano.
Tchaikovsky: Original Theme and Variation, Op 19/6
-- Mikhail Berestnev, piano.
Balakirev: Islamey Fantasy
-- Brian Yuebin Lin, piano.


text:
Honor Scholars program at Mount Ida College
The Honor Scholars program at Mount Ida College offers you the opportunity to customize your academic experience even more than our signature degree programs already do. Designed for highly motivated students with demonstrated academic potential, the program offers you an academic, social and cultural experience that encourages independent and interdisciplinary study and research.
Gain a competitive edge for the job market or graduate school
While others merely focus on tasks or data, as an Honor Scholar, you'll learn to see the big picture – across disciplines or areas of study. While others use only logic or strategy, you'll harness all of your senses and talents to create solutions with greater potential. Your honors faculty mentor guides your academic adventures, on campus and off, by teaching you how to leverage all of your knowledge and skills to solve problems.
In addition to your degree program classwork and internships, you will have the chance to work one-on-one with a faculty mentor and complete honors projects of interest to you. Your honors advisor can provide opportunities to take part in honors research, go on field trips and attend professional conferences. Everything you do as an Honors Scholar helps build important career skills, such as critical thinking and leadership. Our goal is simply to help you discover untapped strengths and uncover your best self.
Additional Honor Scholars benefits
Learn more about the criteria and requirements of our program and enjoy many benefits and leadership opportunities as an Honors Scholars student:
- Attend honors field trips, programs and events
- Attend an annual honors reception with Mount Ida's president, members of the Board of Trustees, faculty and administrators
- Attend national and regional honors conferences
Mount Ida recognizes your additional academic work with a special Honors Scholars designation on your official college transcript and at graduation.
Of course, you'll remain eligible for other honors, including the Dean's List, Latin honors (magna cum laude, for example) and honor society membership.


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Leapin' leprechauns, it's Guinness records day
LONDON (Reuters) - Irish leprechauns, tea-sipping Britons, Australian ABBA impersonators and the oldest yoga teacher on the planet were just some of the people setting world records on Thursday.
More than 300,000 people around the world took part in the seventh annual Guinness World Records Day, in which a number of records have already been confirmed.
They included the largest cream tea party (334 participants) in Essex, England; the largest gathering of people dressed as leprechauns (262 participants) in Dublin; the oldest yoga teacher (91 years old) and the largest hula hoop workout (221 children) both in Florida.
Jane Malyon from The English Cream Tea Company, who hosted the Essex cream tea party, said the record combined her passion for quality time with her love of British tradition.
"Strangers became friends over scones, cream, jam and tea - and the atmosphere was as special as this amazing Guinness World Record," Malyon said in a statement from Guinness.
In keeping with the national theme, 262 members of the public in Dublin got into leprechaun costume to break the record previously set in the United States.
"We believe that a record for leprechauns belongs to its native soil and we're really pleased to bring it back to Ireland," Derek Mooney from Ireland's RTE Radio One said.
To mark the special day, 91-year-old Bernice Mary Bates was officially recognized as the oldest yoga teacher at the Mainlands Retirement Community Center in Pinellas Park, Florida.
Nearby, 221 school children from Longleaf Elementary School in New Port Richey, Florida were involved in setting the largest hula hoop workout record. Continued...