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Full sound effects list for Drawing and Handwriting Collection:Drawing_and_Handwriting_Collection_Metadata
This library has a unique selection of drawing and handwriting sounds, recorded and edited with the utmost care in a recording booth, with a perfect acoustic treatment, for dry and clean sounds.
Includes 1040 files 24Bit/96kHz, containing more than 6000 sounds from 26 different tools, which makes the most comprehensive drawing and handwriting library ever !
Each tool includes short sounds ( letters and punctuations with speed variations : fast and slow ), medium ( words ), long ( sentences ) and a part dedicated to drawing, allowing endless possibilities. For even more precision, some tools have been recorded on several materials like Paper ( in books and on desks ), Papyrus, Canvas, etc.
Tools used :
● Ball Pen ● Correction Fluid Pen ● Bamboo Reed Pen ● Chalk & Chalkboard Eraser ● Charcoal Stick with Paper Stump and Kneaded Rubber Eraser ● Dip Pen ● Finger on Fogged Glass ● Fountain Pen ● Graphics Tablet ● Markers / Felt Pens ( Broad and Fine Point ) ● Paint Brush ● Pencil with Eraser, Sharpener and Electric Sharpener ● Quill Pen ● Sand ● Scratch Art ● Stone ( Thin & Thick Chisel ) ● Wax Crayon ● Whiteboard Marker ( Broad and Fine Point ) with Whiteboard Eraser.
Includes embedded Soundminer metadata.


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Faculty members are encouraged to apply for the Carolina for the Kids Research Grant Award made possible through generous support from Carolina for the Kids. Two awards of $40,000 are available to early career and established investigators pursuing pediatric research.
Carolina for the Kids (CFTK), a UNC student-led organization, raises funds through donations and events, including their annual dance marathon. In addition to their primary mission of providing emotional, medical, and financial support for the patients and families served by UNC Children's Hospital, CFTK supports a Research Grant Program. This program prioritizes clinical/translational research projects focused on children's health.
We are excited to announce extension of the deadline for the Carolina for the Kids Faculty Investigator Award. This mechanism supports early career and established faculty investigators. Projects primarily or wholly based at UNC are prioritized. More information can be found below:
- Anticipated awards: Up to 2.
- Projected Maximum Award Amount: $40,000.
- Eligibility: There are 3 categories for the CFTK Faculty Investigator Award:
- Early career faculty investigators who have not previously competed successfully for an NIH-supported research project, specifically Assistant Professors or Instructors who are generating preliminary data for an extramural grant application.
- Established faculty investigators with a track record of NIH funding and scholarly productivity in need of bridge funding (investigator salary support is not covered). Investigators who have submitted an NIH grant that received positive reviews but was not funded are eligible. The application must include the review summary statement, responses to noted weaknesses, and plan for resubmission.
- Established faculty investigators who are expanding or redirecting research activities toward a new extramural funding opportunity.
- Requirements: Applications must present a clear research proposal and a plan for subsequent extramural funding. It is expected that an extramural grant application will be submitted within 6 months of the completion of the CFTK Research proposal.
The application deadline is Monday, December 16, 2019 at midnight.
Visit http://childrensresearch.unc.edu/grants for more information.

subset: commoncrawl


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Since David Grant laid Silloth golf course out in 1892 over the linksland west of the docks it has been a key tourist attraction. Over the years the course has evolved, with contributions from two great classic designers Dr Alister MacKenzie and Willie Park Junior.
A number of blind holes still remain, architecturally-incorrect in the modern era, but a source of uncertainty, surprise and occasional delight to successive generations of members and visitors. Some of the original sandy wastes remain as heroic hazards, but the course is mostly clad in mature dune flora that is ideal for presenting the great challenge of links golf. Three holes are typical.
The elevated tee on the par 3 Ninth looks down on a small island green with a steep fall to the right, protected to the front and side by an array of deep bunkers that demand an accurate shot from anything between a wedge and three iron, depending on the wind.
This event is held over 2 days – the best score from either day will count.
The competition format is Pairs better ball stableford played off 75% handicap. The winners from each event are invited to the competition week on the Costa del Sol in November 2019 or February 2020, which includes a 3 night stay including Breakfast, return flights, all transfers and 3 competitive rounds of golf.
You must be a member of The Golf Guide Tour Membership to win the trip to Spain and have a current CONGU handicap to win any of the top three prizes.
To protect the integrity of our events and in line with the recommendations on England Golf, we do notify all home clubs of the players away day scores and we have adopted a general play rule which will see handicap adjustments for all pairs scoring 42 points or above. For further information, please see our T&C's.
Due to the increased popularity of the events, a non-refundable £15 deposit per person is required to secure your place. Any cancellations made within 7 days of the event will be liable for full payment.
Contact email@example.com for payment options.
If you play in 4 or more Golf Guide Tour Events in 2019, you will automatically enter the Race to Fancourt. The Top 10 pairs on the leaderboard, after the last event at Notts Hollinwell will then be invited to the UK final – the winners on the day will receive a 7 day trip to Fancourt, South Africa courtesy of Chaka Travel.


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|Fire Danger: CATASTROPHIC (delete)
This page has been tagged as a candidate for deletion during Forest Fire Week and will be huffed after seven days.
If you love it, fix it up or move it to your userspace. Just be sure to list the redirect on QVFD.
This Page Hates you. You will be hated by one person every second you're on this page.
Hate' is one of the few little joys in life which is still not even taxed, or made way more cheaply by slave labor in Chinese sweat-shops.
A "Brief" History Of The Origins of Hate[edit]
Once upon a time deep in the gayest forest, beyond the nectar nest, past the gumdrop men, and down in sweet pit there lived a kind old bitch who grew the most delicious candied carrots that ever could be grown. Well one day Finkle the Rabbit and his friends sniffed out the succulent scent of these delicious orange delicacies, and helped themselves to their fill of candied carrots.
Late in the day when the Gnome, Gnomey G. Gnomestein returned from town from a long day of shopping for women's undergarments for purposes he would rather not discuss, he was dismayed to find his carrot patch decimated. 'Oh me oh my! Who would eat all my candied carrots that took a whole season to grow?!? Ah, Woe is me.'
'Woe is you is right, you selfish motherfucker. Damn straight we got our eat on with your carrots, how you like me now bitch?' Yelled Finkle the Rabbit, a regular rotten young rigger of a rabbit. Then they gave Gnomey the middle digit and ran off. Gnomey did not know what do do, he had never had anyone steal from him before, as he was quite generous, and being called selfish stunned him.
And since the anger grew in him and he could not catch the rabbits to punish them, his sadness turned to anger, and retribution thwarted, his anger turned into a new feeling; murderous rage. Not only had they stolen from him, they had taunted, humiliated and snickered at him, then ran away like cowards. This caused the core of his being to light up like a white hot poker, in a way he had not way to describe. In his rantings to relieve himself of the anger (As Gnomes should never be angry - unless you have a Gareth close by, as they are known to be the Underpants Gnomes greates enemy) he screamed gibberish of which one word was hate.
Hate was the word he and the world would from now on use.
He then went inside and tuned up his crossbow with the poison bolts, hoping soon to skewer a young rabbit in the face.
To be continued...
But wait! There's more to come...[edit]
Bogus pseudo-scientist's and alternative spiritual guru's predict, in the future hate technology will advance to the point where we will be able to power automobiles, lawnmowers and vibrators with the sheer power of hatred. Sith Lords will be paid handsomely to sit in power plants and just think about that guy who AWP'ed him on Counterstrike.
In addition, we will be using the worlds surplus hate to export to help feed the Martian-masses on Mars. Actually I meant grapes, but I am not strong in the area of speling. Or in fruit-lore or astrology. Or in anythin', for that matter. hate is a strong word you frickin frickers AHAHAHAHAHAHAHAHA


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After a bit of shopping at Macy's, Britney changes tops before heading back to her Beverly Hills home. Probably also bought a leash and soap for what's his name. January 13, 2008.
Britney screams to the paparazzi (in a British accent): "******* OVER IT! GET OUT OF MY ******** FACE!" Yep, great influence on her… =(
Source: WENN.com, splashnewsonline.com, x17online.com, hollywood.tv


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Zcchc11 Uridylates Mature miRNAs to Enhance Neonatal IGF-1 Expression, Growth, and Survival
The Zcchc11 enzyme is implicated in microRNA (miRNA) regulation. It can uridylate let-7 precursors to decrease quantities of the mature miRNA in embryonic stem cell lines, suggested to mediate stem cell maintenance. It can uridylate mature miR-26 to relieve silencing activity without impacting miRNA content in cancer cell lines, suggested to mediate cytokine and growth factor expression. Broader roles of Zcchc11 in shaping or remodeling the miRNome or in directing biological or physiological processes remain entirely speculative. We generated Zcchc11-deficient mice to address these knowledge gaps. Zcchc11 deficiency had no impact on embryogenesis or fetal development, but it significantly decreased survival and growth immediately following birth, indicating a role for this enzyme in early postnatal fitness. Deep sequencing of small RNAs from neonatal livers revealed roles of this enzyme in miRNA sequence diversity. Zcchc11 deficiency diminished the lengths and terminal uridine frequencies for diverse mature miRNAs, but it had no influence on the quantities of any miRNAs. The expression of IGF-1, a liver-derived protein essential to early growth and survival, was enhanced by Zcchc11 expression in vitro, and miRNA silencing of IGF-1 was alleviated by uridylation events observed to be Zcchc11-dependent in the neonatal liver. In neonatal mice, Zcchc11 deficiency significantly decreased IGF-1 mRNA in the liver and IGF-1 protein in the blood. We conclude that the Zcchc11-mediated terminal uridylation of mature miRNAs is pervasive and physiologically significant, especially important in the neonatal period for fostering IGF-1 expression and enhancing postnatal growth and survival. We propose that the miRNA 3′ terminus is a regulatory node upon which multiple enzymes converge to direct silencing activity and tune gene expression.
Published in the journal:
. PLoS Genet 8(11): e32767. doi:10.1371/journal.pgen.1003105
Category: Research Article
doi: 10.1371/journal.pgen.1003105
The Zcchc11 enzyme is implicated in microRNA (miRNA) regulation. It can uridylate let-7 precursors to decrease quantities of the mature miRNA in embryonic stem cell lines, suggested to mediate stem cell maintenance. It can uridylate mature miR-26 to relieve silencing activity without impacting miRNA content in cancer cell lines, suggested to mediate cytokine and growth factor expression. Broader roles of Zcchc11 in shaping or remodeling the miRNome or in directing biological or physiological processes remain entirely speculative. We generated Zcchc11-deficient mice to address these knowledge gaps. Zcchc11 deficiency had no impact on embryogenesis or fetal development, but it significantly decreased survival and growth immediately following birth, indicating a role for this enzyme in early postnatal fitness. Deep sequencing of small RNAs from neonatal livers revealed roles of this enzyme in miRNA sequence diversity. Zcchc11 deficiency diminished the lengths and terminal uridine frequencies for diverse mature miRNAs, but it had no influence on the quantities of any miRNAs. The expression of IGF-1, a liver-derived protein essential to early growth and survival, was enhanced by Zcchc11 expression in vitro, and miRNA silencing of IGF-1 was alleviated by uridylation events observed to be Zcchc11-dependent in the neonatal liver. In neonatal mice, Zcchc11 deficiency significantly decreased IGF-1 mRNA in the liver and IGF-1 protein in the blood. We conclude that the Zcchc11-mediated terminal uridylation of mature miRNAs is pervasive and physiologically significant, especially important in the neonatal period for fostering IGF-1 expression and enhancing postnatal growth and survival. We propose that the miRNA 3′ terminus is a regulatory node upon which multiple enzymes converge to direct silencing activity and tune gene expression.
Non-canonical poly(A) polymerases (PAPs) comprise a family of enzymes highly conserved across Eukaryota and capable of catalyzing the template-independent transfer of uridines and adenines onto single-stranded RNA substrates [1], [2]. Several non-canonical PAPs, including the uridyltransferase Zcchc11 (PAPD3/TUT4), can mediate 3′ terminal nucleotide additions to mature miRNA [3], [4], [5]. The uridylation or adenylation of mature miRNAs does not impact miRNA quantity, but instead limits miRNA silencing of select, targeted transcripts [3], [5]. By other means, Zcchc11 can regulate quantities of mature miRNA. In mouse embryonic stem cell lines, Zcchc11 recognizes complexes of Lin28 and pre-let-7 and adds an oligouridine tail to the 3′ terminus of the pre-miRNA, preventing maturation and/or enhancing degradation of the precursor [6], [7]. Knockdown of Zcchc11 or Lin28 in stem cell lines increases mature let-7 and decreases pluripotency markers [6], [8], [9]. Both of these models propose that uridylation by Zcchc11 circumvents miRNA-mediated transcript silencing, but they invoke disparate mechanisms. While not mutually exclusive, they have never been concurrently examined, and each has been demonstrated only in reductionist cell line systems focusing on small subsets of miRNAs. The degree to which miRNA quantity and/or sequence diversity may be remodeled by Zcchc11 (or any non-canonical PAP) and the roles of Zcchc11 in integrated biological systems remain speculative and represent major knowledge gaps.
Zcchc11 enhances the growth and survival of young mice
We derived a line of mutant mice from embryonic stem cells carrying a gene-trap insertion in the fourth intron of the 31 exon Zcchc11 gene [10]. This mutation (Figure S1A) was upstream of all known protein domains and effectively ablated Zcchc11 expression (Figure 1A and Figure S1B). Because Zcchc11 is necessary to limit let-7 in embryonic stem cell lines [6], [7], we anticipated that its loss might be incompatible with development and viability in utero. Surprisingly, there was no evidence of decreased fitness through gestation, with offspring from heterozygous parents born in Hardy-Weinberg equilibrium (Figure 1B) and displaying normal morphology and weights (Figure 1C). Furthermore, we observed no increase in let-7 content in Zcchc11-deficient embryonic stem cells compared to embryonic stem cells that were wild type or heterozygous for Zcchc11 (Figure 1D). Thus, Zcchc11-deficient embryonic stem cells were not disadvantaged, and Zcchc11 is dispensable for embryonic stem cell maintenance.
By post-partum day 8, we observed approximately 50% mortality in the Zcchc11-deficient mice (Figure 1B). While initially similar in size, Zcchc11-deficient pups grew more slowly than wild type littermates in the first week (Figure 1C). Most organs were proportionately affected, suggesting systemic effects (Figure 1E). Early bodyweight differences were sustained for months (Figure S1C), but otherwise those mutants surviving beyond the perinatal period displayed no defects in lifespan or gross or histologic morphology (Figure S1D). In contrast to the more restricted tissue expression observed in adult mice [3], Zcchc11 expression was found to be nearly ubiquitous in the first days after birth with protein levels in all organs examined except the thymus decreasing over time (Figure 1F). These findings highlight the neonatal period as a time when Zcchc11 is fundamental to mouse growth and development.
Zcchc11 does not affect mature miRNA quantities
To address the predominant functions for Zcchc11 in miRNA biology in vivo, we used deep sequencing of small RNAs to simultaneously determine mature miRNA quantity and end-modification in an unbiased and comprehensive fashion. We focused our deep sequencing efforts on the liver because it has a relatively homogenous population of cells, Zcchc11 is strongly expressed in this tissue in young mice, and there was precedent for miRNA terminal modifications in the liver [4]. Libraries of small RNAs were constructed from 3 different paired sets of 8-day-old livers from Zcchc11+/+ or Zcchc11−/− sex- and littermate-matched mice. More than 85 million sequences were obtained, which exhibited a total of >75% alignment to miRBase (Table S1).
Since Zcchc11-mediated uridylation of let-7 precursors in embryonic stem cells diminishes mature let-7 abundance [6], [7], we expected to observe increased quantities of these and perhaps other miRNAs in the Zcchc11-deficient livers. Instead, all detectable miRNAs exhibited a strong correlation in quantity between wild type and Zcchc11-deficient mice (Figure 2A). There were no significant differences due to genotype in the content of any mature miRNA in the liver. Cross-method validation using qRT-PCR analyses of representative miRNAs of interest confirmed that levels of let-7a, let-7b, let-7c, miR-122, miR-139, and miR-379 were equivalent (Figure 2B). A third independent method, northern blotting, also confirmed no increase in let-7a due to Zcchc11 deficiency (Figure 2C). Consistent with this observation, there was no aberrant expression of core miRNA machinery, including Drosha, Dicer, and Argonaute in Zcchc11-deficient livers (Figure 2D). Because mature miRNA levels were unchanged, we considered that Lin28 proteins might be absent from these tissues. While Lin28a was undetectable, Lin28b was present in young mouse livers and was unaffected by Zcchc11 deficiency (Figure 2E). This may be relevant, since Lin28a is more specifically tied to Zcchc11 regulation of let-7, relating to cytoplasmic localization [11]. Altogether, the present data suggest that the high level of Zcchc11 expression in the young liver does not influence mature miRNA abundance, including let-7 family members.
Zcchc11 mediates mature miRNA lengths and terminal uridine frequencies
In addition to precursor modification, Zcchc11 family members are capable of uridylating or adenylating the 3′ termini of mature miRNAs [3], [4], [5], [12]_ENREF_13. While the general pattern of small RNA read lengths from our deep sequence libraries was similar between genotypes, with sequence lengths of 21–23 nucleotides predominating, there were significantly fewer 23 nucleotide-long sequences in the livers of the Zcchc11-deficient mice (Figure 3A). To identify potential enzymatic additions by Zcchc11, aligned sequences were interrogated at the position 1 nucleotide beyond the 3′ terminal residue listed in miRBase [13], [14]. Potential uridylation and adenylation events, included if present at levels of 1 or more sequence per 1,000 reads, were identified for many miRNA species in the livers of wild type mice (Figure S2). Some of these highly modified species, such as miR-26b and miR-122, match those identified previously [4],[5], while others represent novel modification targets. We compared the levels of terminal adenines and uridines in mutant mice for each of the miRNAs that were so modified in the livers of wild type mice. A waterfall plot depicting the changes in terminal adenines between the livers of wild type and Zcchc11-deficient mice revealed a balanced distribution with a mean centered around 0 (Figure 3B–3C). Conversely, the distribution of terminal uridines was significantly skewed, with most of the sequences bearing terminal uridines occurring less frequently in the absence of Zcchc11, suggesting that miRNA uridylation was broadly decreased in Zcchc11-deficient livers (Figure 3B–3C). The expression of other non-canonical PAPs, including PAPD5, GLD-2, and Zcchc6, were unchanged in the livers of Zcchc11 deficient mice (Figure 3D–3E).
Terminal uridines that are 3′ of the expected mature miRNA sequence and dependent on Zcchc11 most likely represent enzymatic additions, but they could also arise from alternative processing of the pre-miRNA. To complement the above analyses, we analyzed miRNAs with terminal uridines that were not genomically encoded and therefore could only result from enzymatic addition, referred to as unambiguous uridylation events. For miRNAs observed in every library from both genotypes, 179 different species showed evidence of unambiguous uridine additions in all 3 wild type libraries, whereas only 118 did so across mutant libraries (p<0.001, χ2 test). This analysis supports the conclusions of the more comprehensive analyses above (Figure 3), together indicating definitively that Zcchc11 deficiency decreases the terminal uridylation of mature miRNAs. These results provide the first compelling evidence, to our knowledge, that Zcchc11 plays a specific and essential role in the length and uridylation of a broad swath of mature miRNAs in vivo.
Zcchc11 uridyltransferase activity contributes to IGF-1 expression
Of the miRNAs ending in uridine more frequently in wild type livers compared to mutants, many were predicted to target IGF-1 (Figure 3B), a growth factor which is liver-derived and essential to early growth and survival in mammals [15], [16]. The IGF-1 3′-UTR is highly polymorphic [17]. We found that an approximately 6.5 kb 3′-UTR was predominant in 8 day old mouse livers (Figure 4A). We cloned this isoform from the livers of C57BL/6 mice and incorporated it into a reporter plasmid to assess the effect of Zcchc11 on the IGF-1 3′-UTR. Addition of this UTR significantly decreased reporter expression vs. the coding region alone (Figure 4B), as would be expected for a long 3′-UTR that likely contains many negative regulatory elements. To test the effect of Zcchc11 expression on the IGF-1 3′-UTR, this reporter was co-transfected into cells along with enhanced GFP (EGFP, control), wild type Zcchc11, or Zcchc11 mutants lacking enzymatic activity. Overexpression of wild type Zcchc11 significantly increased levels of the IGF-1 3′-UTR reporter (Figure 4C), indicating that Zcchc11 facilitates IGF-1 expression through its 3′-UTR. Importantly, a catalytically null mutant Zcchc11, in which 2 aspartic acid residues necessary for uridyltransferase activity were changed to alanines [3], was significantly less capable of amplifying the IGF-1 reporter (Figure 4C). Moreover, an N-terminal deletion mutant of Zcchc11 lacking the C-terminal half of the protein and devoid of the uridyltransferase domain, PAP-associated domains, and RNA-binding zinc knuckles was completely incapable of altering IGF-1 expression (Figure 4C). Thus, Zcchc11 can enhance IGF-1 expression through a uridyltransferase-dependent mechanism.
MicroRNA silencing of IGF-1 is inhibited by terminal uridine addition
Of the multiple miRNAs which had terminal uridines that required Zcchc11 in our deep sequencing datasets and were predicted to target the 3′ UTR of IGF-1 (Figure 3B), we examined the ability of 4 (miR-126-5p, miR-194-2-3p, miR-379 and Let-7d) to suppress IGF-1 expression. Cells were co-transfected with the IGF-1 3′-UTR luciferase reporter construct along with either miRNA mimetics or a control non-targeting sequence. MiR-126-5p, miR-194-2-3p, and miR-379, but not Let-7d, significantly silenced the IGF-1 reporter (Figure 5A). We next assessed the influence of terminal uridine additions on the silencing activity of these miRNAs by comparing the effects on the IGF-1 reporter of unmodified miRNA mimetics to those with 2 uridines added onto the 3′ end. The uridylation of miR-126-5p or miR-379 significantly diminished IGF-1 silencing by these miRNAs, while uridylation of miR-194-2-3p had no effect (Figure 5B). These data demonstrate that uridylation of specific miRNA species may influence silencing. Interestingly, varying the length of the terminal uridine tail, to reflect the different forms observed for each of these miRNAs in our deep sequencing datasets, had minimal impact for both miR-126-5p and miR-379 (Figure 5C–5D), demonstrating that even a single uridine is sufficient to mitigate silencing by these miRNAs. Terminal uridylation did not completely eliminate silencing effects, suggesting that these end modifications provide tuning ability rather than a binary on-off switch. The effects of adding uridine(s) to the 3′ terminus were modest in comparison to the effects of altering bases in the seed region of the 5′ terminus, which completely eliminated repression of the IGF-1 3′-UTR reporter (Figure 5E), indicating that the effects described here reflect a scaling of canonical miRNA activity. Interestingly, when 2 miRNAs targeting the IGF-1 3′-UTR were simultaneously co-transfected, silencing was minimally influenced if only 1 of the 2 was uridylated, but it was very effectively attenuated when both were uridylated (Figure 5F). These data indicate that uridylation events have cumulative effects across the set of miRNAs targeting a given 3′-UTR. The combination of such effects provides a wide dynamic range over which expression can be tuned.
IGF-1 expression is compromised by Zcchc11 deficiency in vivo
The above results, demonstrating that Zcchc11 contributes to the uridylation of miRNAs which target IGF-1 and that miRNA uridylation relieves silencing to enhance IGF-1 expression, suggested the possibility that the decreased size and survival of Zcchc11-deificient mice may be associated with decreased expression of IGF-1 in vivo. Supporting this hypothesis, Zcchc11 deficiency reduced hepatic IGF-1 expression to approximately half of wild type levels (Figure 6A). To differentiate regulation of the IGF-1 transcript in the liver from upstream signals, we examined STAT5 phosphorylation in the liver and growth hormone (GH) in the blood. Neither was affected by Zcchc11 deficiency (Figure 6B–6C), suggesting a local hepatocyte role for this enzyme in regulating IGF-1 mRNA. To test whether IGF-1 expression was selectively enhanced or whether many diverse growth factors were dependent upon Zcchc11 in neonatal mouse livers, we performed a PCR array for mouse growth factor transcripts. Only IGF-1 was strongly expressed and diminished by Zcchc11 deficiency in these livers (Figure 6D). The impact of Zcchc11 deficiency on IGF-1 was comparable to its impact on IL-6, which was previously demonstrated to depend on Zcchc11 [3]. These data reveal that Zcchc11 effects are transcript-specific rather than transcriptome-wide, and that IGF-1 is a particular target of Zcchc11 regulation. We also measured the expression of histone H3 in these livers, since this protein contributes to cell proliferation and is enhanced by Zcchc11 in some but not other cell lines [18], . There was no effect of Zcchc11 deficiency on histone H3 content in the young mouse liver (Figure 6E). Reflecting the changes in liver transcript, Zcchc11 deficiency reduced circulating IGF-1 concentrations to about half of wild type levels (Figure 6F), suggesting that diminished IGF-1 could contribute to systemic phenotypes. We conclude that Zcchc11 is essential to facilitating IGF-1 expression during neonatal periods.
The present communication reports, to our knowledge, the first studies of Zcchc11 in vivo. We find that Zcchc11 is widely expressed across multiple tissues shortly after birth and that in neonatal mice Zcchc11 deficiency results in a failure to thrive, associated with diminished IGF-1 expression. Mice with a complete IGF-1 deficiency have perinatal lethality and decreased growth rates [15], [16] consistent with, but more severe than, the phenotypes observed in the Zcchc11-deficient mice. Like the Zcchc11-deficient mice, genetic engineering that reduces but does not eliminate IGF-1 signaling causes proportionally decreased growth [20], [21]. Zcchc11 deficiency results in decreased uridylation of miRNAs in the liver, including miRNAs that target the IGF-1 3′-UTR. Gene expression tied to this 3′-UTR is enhanced by the uridylation of miRNAs or the increased expression of Zcchc11. Altogether, we interpret these results as supporting a model in which the uridylation of miRNAs by Zcchc11 in the neonatal liver is essential for optimal IGF-1 expression and its promotion of growth and survival through the early postnatal period. However, Zcchc11 is a large and multifunctional protein, and we recognize that the abilities of Zcchc11 to uridylate other substrates [19] and to exert uridylation-independent activities [18] may additionally contribute to the complex phenotypes of Zcchc11-deficient mice.
The decreased growth rate of Zcchc11-deficient mice is complementary to the increased growth rate observed in Lin28a-overexpressing transgenic mice [22]. Knockdown of Lin28 and Zcchc11 in cell lines results in similar phenotypes, and these proteins physically interact [6], [7], [8]. These similarities support the concept that Zcchc11 and Lin28 are involved in overlapping pathways in vivo. However, the suggestion that Zcchc11-Lin28 interactions may be essential for embryonic stem cell maintenance [6], [7], [8] is not supported by our observation that Zcchc11 deficiency does not impact growth or survival during embryogenesis. Like Zcchc11, Lin28 proteins are particularly expressed in the tissues of young mice [23]. It will be of great interest to learn whether mice with deficiencies in Lin28a, Lin28b or both have phenotypes involving perinatal lethality and decreased growth, as observed with the Zcchc11-deficient mice.
Untemplated uridines and adenines on mature miRNAs are consistent findings in deep sequencing analyses [5], [24], but the mechanisms and significance of such terminal additions have been difficult to discern. Previous in vitro studies had suggested that Zcchc11 is one of several enzymes capable of end-modifying mature miRNAs and that miRNA sequence variety might regulate transcript expression [3], [12]. The only other mouse model of PAP mutation, mice deficient in PAPD4/GLD-2, has no reported growth or survival phenotype [4], [25]. Along with our data that other PAPs were expressed in the neonatal livers of the Zcchc11-deficient mice, these findings conclusively demonstrate that the different PAPs have unique and non-overlapping roles in vivo. Unlike GLD-2, Zcchc11 is critical for thriving through the neonatal period, likely due in part to its ability to enhance hepatic IGF-1 expression.
In embryonic stem cell lines, Zcchc11 knockdown increases let-7 levels, due to Zcchc11-mediated uridylation of precursors [6], [7]. The Zcchc11-deficient mice allowed the examination of miRNA regulation in primary cells of living animals, and they revealed that Zcchc11 is not an essential determinant of mature let-7 or any mature miRNA quantity in the neonatal liver. Furthermore, insertional mutagenesis of Zcchc11 did not increase let-7 quantities in primary embryonic stem cells derived from these mice. The relationships among these terminal uridyltransferases (Zcchc11 and Zcchc6), Lin28 proteins (a and b), and let-7 miRNAs in embryonic stem cells are complex and dynamic [26], [27]. The present data show that Zcchc11 is not an absolute requirement for stem cell maintenance or low levels of let-7. There may be other conditions in which precursor uridylation by Zcchc11 is essential to regulating let-7, such as perhaps early embryogenesis when Lin28a is especially active. This mouse model will serve as a useful resource for determining if and when this uridyltransferase enzyme may influence miRNA biogenesis or content.
In contrast to the unchanged abundance of miRNAs in the liver, mature miRNA lengths and sequences were altered by Zcchc11 deficiency. Mature miRNAs in the liver were longer and more likely to end in uridine, including untemplated uridines, when Zcchc11 was present. Thus, our data show that Zcchc11 functions to uridylate mature miRNAs in vivo.
In addition to providing unprecedented evidence of an enzyme actively uridylating the 3′ terminus of miRNAs in vivo, these mice yield new insights into the scope of Zcchc11 modification of the miRNome. Rather than targeting only one individual miRNA, as has been previously documented for Zcchc11 and other PAPs [3], [4], [5], we show here that Zcchc11 targets the 3′ terminus of multiple miRNAs. This broad substrate repertoire dramatically increases the potential targeting power of Zcchc11. Importantly, most of the end-modifications observed varied by a small number of terminal nucleotides, and we observed that even a single uridine addition was sufficient to alleviate silencing activity. Such mono-uridylation by Zcchc11 appears to distinguish the effect of Zcchc11 on mature miRNAs from that described for pre-miRNAs, which is processive and results in a string of uridines being added [6], [28]. Our data further expand our understanding of the molecular implications of miRNA uridylation by demonstrating that coordination of miRNA uridylation events across a 3′-UTR have combinatorial effects. The ability to adjust the silencing activity of many miRNAs targeting one transcript provides a wide dynamic range for enhancing gene expression. The exonuclease Nibbler was recently identified as capable of shortening miRNAs by removing terminal nucleotides [29], [30]. Such enzymes may counter-balance the nucleotidyltransferase activities of PAPs like Zcchc11. The abundance and remarkable stability of miRNAs suggest that mechanisms regulating miRNA activity are crucial, but they are only beginning to be elucidated [31].
We propose that the miRNA 3′ terminus functions as a critical regulatory node that is remodeled by diverse enzymes to adjust miRNA silencing and tune gene expression. The present results support this nascent paradigm by demonstrating essential in vivo roles of Zcchc11 in miRNome remodeling and postnatal development. Zcchc11 mediates mature miRNA uridylation, facilitates hepatic IGF-1 expression, and enhances growth and survival through the neonatal period.
Materials and Methods
Zcchc11-deficient mouse model
A mouse embryonic stem (ES) cell line (RRR277) containing a gene-trap insertion in the Zcchc11 gene was obtained from BayGenomics at the Mutant Mouse Regional Resource Center at University of California-Davis [10]. C57BL/6 blastocysts were microinjected with mutant ES cells to create chimeric mice that were subsequently backcrossed onto a C57BL/6 genetic background for at least 10 generations. The gene-trap genomic insertion site was located within intron 4 of Zcchc11, generating a fusion protein containing the first 314 amino acids of Zcchc11 joined in frame with the β-galactosidase reporter. All known conserved protein motifs and domains in Zcchc11 are downstream of this site. The mutant allele was detected by genomic PCR using the primers listed in Table S2. All murine studies were performed under approval of the Boston University School of Medicine IACUC.
Embryonic stem cell derivation
Eight-cell stage mouse embryos were collected in M2 medium (Millipore) from superovulated Zcchc11+/+, Zcchc11+/−, or Zcchc11−/− females mated with Zcchc11+/+ or Zcchc11+/− males. Embryos were cultured to the early blastocyst stage in KSOM (Millipore) supplemented with 2i (1 µM PD0325901 and 3 µM CHIR99021 (Cayman Chemical)), followed by 48 hours of culture in Neurobasal medium supplemented with N2, B27 (Invitrogen) 2i and Leukemia Inhibitory Factor (LIF, Millipore) at 37°C, under 5% CO2. The resulting expanded blastocysts were cultured on laminin (Sigma, 10 µg/ml) coated tissue culture plastic in N2B27+2i+LIF until the blastocysts had attached and outgrowths were visible (3–4 days). These ES outgrowths were recovered by mouth pipette, disaggregated to single cells with 0.25% Trypsin (Invitrogen) and plated on laminin-coated tissue culture plastic to establish embryonic stem cell lines. Cell line genotype was determined by amplifying wild type and mutant products of Zcchc11 alleles.
Cell line transfections
H1299 cells were plated at 2.5×106 cells/well in 6-well plates and transfected with 0.5 µg reporter construct, 0.25 µg phRLTK control reporter (Promega) and 200 nM miRNA mimetic using 4 µl/well Lipofectamine 2000 (Invitrogen). EGFP or Zcchc11 constructs were transfected at 3 µg/well. Luciferase was measured using the Dual Luciferase Reporter Assay System (Promega). Mimetics were duplexed siRNA (Dharmacon); sequences are presented in Table S2.
RNA and protein assays
Liver growth factors were measured by PCR Array (SA Biosciences) using 1 µg RNA pooled from 4 Zcchc11+/+ or 4 Zcchc11−/− mice. IGF-1 and 18S rRNA qRT-PCR was performed using the TaqMan RNA-to-Ct kit (Applied Biosystems) with primers and probes shown in Table S2. Small RNAs were reverse transcribed using the TaqMan miRNA assay system (Applied Biosystems). Northern blot analysis was performed on 15 µg of total RNA electrophoresed through a 1% agarose-formaldehyde gel and immobilized on a BrightStar-Plus nylon membrane. For probe creation, IGF-1 cDNA (Open Biosystems) was digested out of a pCMV-Sport6 vector using XbaI and SalI restriction enzymes (NEB). GAPDH probes were purchased (SA Biosciences). Antibodies were obtained from Cell Signaling Technologies except goat anti-Zcchc11 (ProSci), Rabbit anti-Goat (R&D), Rabbit anti-GLD-2 (Abgent), and Rabbit anti-PAPD5 (Genetex). Whole blood was collected from the hepatic vein of 10-week old mice or by cardiac puncture from 8-day-old litters of Zcchc11+/− breeding pairs; serum was separated and components were measured using mouse IGF-1 and GH ELISA Kits (R&D Systems).
Cloning and plasmid construction
All Zcchc11 overexpression studies were performed using the same plasmid backbone as the control Enhanced GFP (pEGFP-N, Clontech). Creation of the Zcchc11 and DADA mutant plasmids has been previously described [3]. The N-terminal region of Zcchc11 was PCR amplified from the Zcchc11 plasmids using Phusion High Fidelity DNA Polymerase (NEB) with the primers indicated in Table S2. The resulting product was ligated between NotI and BsrGI sites in the full length Zcchc11 plasmid. The full-length IGF-1 3′ UTR (Accession # NM_001111274.1) was amplified from a cDNA library of whole liver RNA from 8 day-old C57BL/6 mice with Herculase II DNA polymerase (Agilent) using primers shown in Table S2. The resulting band was ligated between SacI and MluI restriction sites into the pMir-Report expression vector (Ambion). All plasmid constructs were sequenced.
Small RNA cloning and deep sequencing
Livers from 8 day-old mice were stored in RNA later (Qiagen). Half of each liver was homogenized in BioPure RNA isolation reagent (BiooScientific) with 0.5 mm zirconium oxide beads using a bullet blender (Next Advance). RNA <30 nt long was purified from phenol-chloroform extracted RNA using a FlashPAGE fractionator (Ambion). Small RNA library creation was performed using an adapted Illumina small RNA sample prep v1.5.0. Briefly, small RNA samples were adaptor ligated with one of four different 3′ adaptors using T4 RNA Ligase 2 (NEB) to allow multiplex sequencing of Zcchc11+/+ and Zcchc11−/− samples. A conserved 5′ adaptor was added using truncated T4 RNA Ligase 2. Samples were gel extracted on a 10% TBE-Urea gel to remove adaptor only ligation products. cDNA was created using SuperScript III Reverse Transcriptase (Invitrogen) then PCR amplified with GoTaq DNA Polymerase (Promega). Adaptor and primer sequences are shown in Table S2. The resulting library was sequenced on an Illumina Genome Analyzer IIx. In total, three libraries were created each containing RNA from two Zcchc11+/+ and two Zcchc11−/− sex matched littermates. Libraries were uploaded to the NCBI Sequence Reads Archive (Accession Number: SRA059070).
Analysis of deep sequencing data
All library analyses were performed using the Genomic Workbench software platform (CLC Biosystems). First, sequences were sorted by adaptor barcode and perfectly matched adaptor sequences were trimmed while ambiguous/unrecognizable adaptor sequences were discarded. The samples were then grouped, counted and aligned to v16.0 of miRBase [13], [14] allowing no more than 2 internal mismatches and no more than 5 at the 3′ end of the sequence. For identification of sequence modifications the libraries were aligned to the mouse genome annotated with v9.0 of the mouse database from the UCSC genome browser. SNP detection was performed using the neighborhood quality score algorithm [32] to identify sequence variants occurring at greater than one per 1,000 sequences. Full genome alignment was used to empower the use of quality scores (average quality score of 15, minimum central quality of 20, with a window length of 5) for SNP detection. SNP position alignment data was exported for further analysis and adenylation/uridylation was defined as A or T variants occurring at the position one nucleotide beyond the published 3′ terminal end of the miRNA. Unambiguous uridylation events were defined as substitutions of a non-genomic U for any other nucleotide at the 3′ terminal end of miRNA.
Supporting Information
1. RisslandOS, MikulasovaA, NorburyCJ (2007) Efficient RNA polyuridylation by noncanonical poly(A) polymerases. Mol Cell Biol 27: 3612–3624.
2. KwakJE, WickensM (2007) A family of poly(U) polymerases. RNA 13: 860–867.
3. JonesMR, QuintonLJ, BlahnaMT, NeilsonJR, FuS, et al. (2009) Zcchc11-dependent uridylation of microRNA directs cytokine expression. Nat Cell Biol 11: 1157–1163.
4. KatohT, SakaguchiY, MiyauchiK, SuzukiT, KashiwabaraS, et al. (2009) Selective stabilization of mammalian microRNAs by 3′ adenylation mediated by the cytoplasmic poly(A) polymerase GLD-2. Gene Dev 23: 433–438.
5. BurroughsAM, AndoY, de HoonMJ, TomaruY, NishibuT, et al. (2010) A comprehensive survey of 3′ animal miRNA modification events and a possible role for 3′ adenylation in modulating miRNA targeting effectiveness. Genome Res 20: 1398–1410.
6. HeoI, JooC, KimYK, HaM, YoonMJ, et al. (2009) TUT4 in concert with Lin28 suppresses microRNA biogenesis through pre-microRNA uridylation. Cell 138: 696–708.
7. HaganJP, PiskounovaE, GregoryRI (2009) Lin28 recruits the TUTase Zcchc11 to inhibit let-7 maturation in mouse embryonic stem cells. Nat Struct Mol Biol 16: 1021–1025.
8. HeoI, JooC, ChoJ, HaM, HanJ, et al. (2008) Lin28 mediates the terminal uridylation of let-7 precursor MicroRNA. Mol Cell 32: 276–284.
9. ViswanathanSR, DaleyGQ, GregoryRI (2008) Selective Blockade of MicroRNA Processing by Lin28. Science 320: 97–100.
10. StrykeD, KawamotoM, HuangCC, JohnsSJ, KingLA, et al. (2003) BayGenomics: a resource of insertional mutations in mouse embryonic stem cells. Nucleic Acids Res 31: 278–281.
11. PiskounovaE, PolytarchouC, ThorntonJE, LaPierreRJ, PothoulakisC, et al. (2011) Lin28A and Lin28B inhibit let-7 microRNA biogenesis by distinct mechanisms. Cell 147: 1066–1079.
12. WymanSK, KnoufEC, ParkinRK, FritzBR, LinDW, et al. (2011) Post-transcriptional generation of miRNA variants by multiple nucleotidyl transferases contributes to miRNA transcriptome complexity. Genome Res 21: 1450–1461.
13. Griffiths-JonesS, SainiHK, van DongenS, EnrightAJ (2008) miRBase: tools for microRNA genomics. Nucleic Acids Res 36: D154–158.
14. KozomaraA, Griffiths-JonesS (2011) miRBase: integrating microRNA annotation and deep-sequencing data. Nucleic Acids Res 39: D152–157.
15. LiuJ-P, BakerJ, PerkinsAS, RobertsonEJ, EfstratiadisA (1993) Mice carrying null mutations of the genes encoding insulin-like growth factor I (Igf-1) and type 1 IGF receptor (Igf1r). Cell 75: 59–72.
16. BakerJ, LiuJP, RobertsonEJ, EfstratiadisA (1993) Role of insulin-like growth factors in embryonic and postnatal growth. Cell 75: 73–82.
17. TemmermanL, SlonimskyE, RosenthalN (2010) Class 2 IGF-1 isoforms are dispensable for viability, growth and maintenance of IGF-1 serum levels. Growth Horm IGF Res 20: 255–263.
18. BlahnaMT, JonesMR, QuintonLJ, MatsuuraKY, MizgerdJP (2011) Terminal uridyltransferase enzyme Zcchc11 promotes cell proliferation independent of its uridyltransferase activity. J Biol Chem 286: 42381–42389.
19. SchmidtMJ, WestS, NorburyCJ (2011) The human cytoplasmic RNA terminal U-transferase ZCCHC11 targets histone mRNAs for degradation. RNA 17: 39–44.
20. HolzenbergerM, LeneuveP, HamardG, DucosB, PerinL, et al. (2000) A targeted partial invalidation of the insulin-like growth factor I receptor gene in mice causes a postnatal growth deficit. Endocrinology 141: 2557–2566.
21. LemboG, RockmanHA, HunterJJ, SteinmetzH, KochWJ, et al. (1996) Elevated blood pressure and enhanced myocardial contractility in mice with severe IGF-1 deficiency. J Clin Invest 98: 2648–2655.
22. ZhuH, ShahS, Shyh-ChangN, ShinodaG, EinhornWS, et al. (2010) Lin28a transgenic mice manifest size and puberty phenotypes identified in human genetic association studies. Nat Genet 42: 626–630.
23. YokoyamaS, HashimotoM, ShimizuH, Ueno-KudohH, UchibeK, et al. (2008) Dynamic gene expression of Lin-28 during embryonic development in mouse and chicken. Gene Expr Patterns 8: 155–160.
24. LandgrafP, RusuM, SheridanR, SewerA, IovinoN, et al. (2007) A mammalian microRNA expression atlas based on small RNA library sequencing. Cell 129: 1401–1414.
25. NakanishiT, KumagaiS, KimuraM, WatanabeH, SakuraiT, et al. (2007) Disruption of mouse poly(A) polymerase mGLD-2 does not alter polyadenylation status in oocytes and somatic cells. Biochem Biophys Res Commun 364: 14–19.
26. MeltonC, JudsonRL, BlellochR (2010) Opposing microRNA families regulate self-renewal in mouse embryonic stem cells. Nature 463: 621–626.
27. ThorntonJE, ChangHM, PiskounovaE, GregoryRI (2012) Lin28-mediated control of let-7 microRNA expression by alternative TUTases Zcchc11 (TUT4) and Zcchc6 (TUT7). RNA 18: 1875–1885.
28. YeomKH, HeoI, LeeJ, HohngS, KimVN, et al. (2011) Single-molecule approach to immunoprecipitated protein complexes: insights into miRNA uridylation. EMBO Rep 12: 690–696.
29. HanBW, HungJH, WengZ, ZamorePD, AmeresSL (2011) The 3′-to-5′ exoribonuclease Nibbler shapes the 3′ ends of microRNAs bound to Drosophila Argonaute1. Curr Biol 21: 1878–1887.
30. LiuN, AbeM, SabinLR, HendriksGJ, NaqviAS, et al. (2011) The exoribonuclease Nibbler controls 3′ end processing of microRNAs in Drosophila. Curr Biol 21: 1888–1893.
31. KimYK, HeoI, KimVN (2010) Modifications of small RNAs and their associated proteins. Cell 143: 703–709.
32. BrockmanW, AlvarezP, YoungS, GarberM, GiannoukosG, et al. (2008) Quality scores and SNP detection in sequencing-by-synthesis systems. Genome Res 18: 763–770.
ŠtítkyGenetika Reprodukční medicína
Článek vyšel v časopise
PLOS Genetics
2012 Číslo 11
Nejčtenější v tomto čísle
Tomuto tématu se dále věnují…
- Zcchc11 Uridylates Mature miRNAs to Enhance Neonatal IGF-1 Expression, Growth, and Survival
- Mechanisms Employed by to Prevent Ribonucleotide Incorporation into Genomic DNA by Pol V
- Tissue-Specific Regulation of Chromatin Insulator Function
- Inference of Population Splits and Mixtures from Genome-Wide Allele Frequency Data
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text: The dangerous disconnect between the exciting and engaging content your customers genuinely want and the hard-sell content companies have traditionally been trained to deliver means many campaigns are dead in the water. How can you make sure your messaging to customers ends up top of mind — and not top of the heap? The post Engage Your Audience With Engaging (And Curated) Content appeared first on Mobile Presence.


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By NATARIO McKENZIE
Tribune Business Reporter
A senior Baha Mar executive said yesterday the mega resort is running at 50 per cent occupancy with more than 2,000 Bahamians being currently employed.
Robert Sands, Baha Mar's senior vice president of government and external affairs said the SLS Lux remains on track for its opening during the first week of November, with the Rosewood to follow in the first quarter of 2018.
"Group bookings continue to get interest and expand as we look forward and our occupancy continues to grow. We are encouraged by business levels today. Employment is over now at 2,000 Bahamians. Hopefully we'll get to the 5,500 figure by full opening next year. Our occupancy is still round 40-50 per cent remains steady," said Mr Sands.
"We just recently opened the current art exhibit which is an area we are showcasing artists and exhibits. We're quite happy about John Cox the curator. We have a space where we will showcase on an ongoing basis over 8,500 pieces of art so we're very happy about that," Mr Sands added.
Baha Mar is expected to generate more than $65 million in direct taxation to the Bahamas annually and over $100 million in combined direct, indirect and induced tax revenues
Under its original developer Sarkis Izmirlian, the $4.2 billion project was scheduled to open in December 2014. After construction completion deadlines were missed, Mr Izmirlian filed for Chapter 11 bankruptcy protection in the US in June 2015. The former government vigorously opposed this process, saying it threatened the Bahamas' sovereignty, and instead petitioned the Supreme Court to place Baha Mar into liquidation. Mr Izmirlian ultimately lost control of the mega resort after being defeated in the US and Bahamian courts, and Chow Tai Took Enterprises (CTFE), the conglomerate formed by the late billionaire, Cheng Yu Tung, was revealed as the new owner last year. CTFE is pushing for a full opening by April 2018.
Baha Mar also includes a 300-room SLS resort, a 200-room Rosewood Baha Mar property, and the 694-room Melia Nassau Beach, which has been open for three years and operates as an adults-only, all-inclusive.
Sickened 3 years, 2 months ago
Have they ever said how many rooms are actually opened at this point? The last I heard was 200 rooms but that was a while ago. I recently heard that all of the rooms (both sides) of the main hotel were open, but I don't know for sure. This 50% figure is not great, but it may be worse if there is only a few hundred rooms available.
alfalfa 3 years, 2 months ago
Visited Bahamar over the weekend and I doubt their story of 50% occupancy, period. You can count the number of tourists easily, and the large majority of people about were Bahamians, like me, looking around. I wonder how long before they start charging for valet, and prohibiting locals from using their pool facilities.
BahamasForBahamians 3 years, 2 months ago
The hotel is closed remember...
This government is going to find a buy.. remember?
turtle777 3 years, 2 months ago
It is damaging to underestimate the understanding of the Bahamian people, and of even greater importance, the understanding of international lendors and financial rating agencies watching Baha Mar so closely, to state "..50% occupancy..". What was meant was '..50% of available rooms..'. If Baha Mar's operator actually meant "50%", then roughly 1,200 of the planned rooms are occupied. If so, great! Well on the way to that magic 65% of all available rooms occupancy all hotels must reach to break even.
And please: Baha Mar's management should not exclude separately branded sections of the hotel so that "50%" seems more believable. It is not. We all know there were between 2,200 to 2,400 rooms originally planned. (Depends what news release one refers to.)
Baha Mar can ill afford for further red flags to be waved by the world's financial observers.
Please, for honesty's sake, how many rooms in Baha Mar, regardless of brand, are actually available and how many occupied?
A simple question gentlemen.
Tom Rickards Windemere
turtle777 3 years, 2 months ago
I would like to clarify my post on August 15th.
I wrote: "What was meant was '..50% of available rooms..'."
I should have written:. "What the management meant was 'We hope to eventually have 50% of all available rooms occupied, including all our hotel brands at Baha Mar.', or similar.
As I previously wrote, Baha Mar must reach occupancy rates of about 65%, including all brands, to reach sustained profitability.


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Big Baller Brand co-founder Alan Foster countersued LaVar Ball for fraudulent concealment and breach of contract, accusing him of embezzling millions of dollars from the company, according to The Blast.
Per the report, Foster has accused LaVar of embezzling more than $2.5 million from the family-owned companies "to fund his own extravagant lifestyle."
"In early 2016, in furtherance of LaVar's intense desire to share in, or rise above, the glory and spotlight of his sons, LaVar approached Alan and asked for his business guidance on how to monopolize and gain fortune and fame from the names and likenesses of his three sons," the lawsuit says, via The Blast. "In response, Alan suggested that the two men brand the 'Ball' family name in order to create basketball and entertainment-related businesses. LaVar loved Alan's idea and wanted to make sure that he was the biggest star in the family, notwithstanding the fact that he was broke, had no savings, poor credit and zero business acumen."
Per the report, Foster alleges that LaVar used the money to upgrade their home and purchase new cars.
The Ball family cut ties with Foster in March after $1.5 million allegedly went missing from Lonzo's personal and business accounts, which prompted them to sue the former family friend for fraud. The FBI reportedly opened an investigation into Foster, too, over the Ball family's claims.
Foster previously owned 16.3 percent of the Big Baller Brand. He was convicted in 2002 of running a fraudulent stock scheme that yielded nearly $4 million, and served more than five years in prison. He has also pleaded guilty to mail fraud and money laundering, and spent five more months in prison for violating his probation.
The Ball family denied Foster's allegations in a statement on Friday, and vowed to continue their initial lawsuit against him.
"Alan Foster's claims are not only unfounded and devoid of any truth, but are an egregious attempt to turn the attention away from the millions of dollars that he embezzled from the Ball Family and the Ball Family Business," the family said in a statement, via ESPN's Ramona Shelburne. "Not only will LaVar Ball and his family continue to vigorously pursue their civil action against Foster seeking civil damages, but will also continue to cooperate with law enforcement in order to seek justice for his egregious actions.
"Alan Foster is a convicted felon and is currently being investigated by the FBI. He has served seven years in jail for fraud and has a deep criminal past defrauding those who have placed their trust in him. The Ball family are all united in relentlessly pursuing Foster for his grave injustices, and will always fight to protect the respected Ball family name, despite Foster's futile attempt to defile it."
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Alma Pond
Alma Pond is an artificial impoundment located on the headwaters of Honeoye Creek in south-central Allegany County. A permanent earthen dike was built near the site of a beaver dam and existing pond, probably in the 1940s. Sometime later a concrete spillway was added to control the water level.
By increasing the size of the original beaver pond, one can imagine that the pond covers many old stumps and logs. It is perfect for snagging anglers' lines but also perfect habitat for largemouth bass and crappie. The summer fishery consists of largemouth bass and assorted panfish. Ice fishing targets mostly assorted panfish with an occasional northern pike being caught. There are also numerous carp and ******* in the pond.
Largemouth Bass: Largemouth bass are common in Alma Pond. Fish of all sizes are present indicating a balanced population. Bass up to 20 inches and 5 pounds are taken annually. Despite being a very shallow pond, aquatic vegetation is lacking due to the lack of transparency of the water. This is generally caused by algae blooms and turbidity due to the feeding activity of the bullhead and carp. Surface plugs, crank baits and live bait offer the best chance for success.
Panfish: Panfish include black crappie, bluegill, pumpkinseed and yellow perch. Live baits, such as worms and minnows, work the best. These fish tend to have average to slow growth rates as they are generally sight feeders. Feeding is hampered by both the turbidity of the pond as well as low fertility. However, large black crappies (18 inches) are occasionally taken.
Carp and Bullhead: Carp and brown bullhead are abundant in Alma Pond. Both are easy to catch as they rely on smell and taste to find their food. Live bait such as worms work for both, while carp also can be taken with corn or dough balls.
Ice Fishing:
Ice fishing is permitted on Alma Pond.
Alma Pond is not affiliated with AmericanTowns Media


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A business failure does not have to be the end of the story. Almost always overlooked by accountants and financial planners, there is a tax payback benefit provided by the IRS to business owners who have experienced a failed business venture. Past Due Payroll Tax Audit Section 1244 of the Internal Revenue Code allows failed business owners to turn owed payroll tax around to become an ordinary loss, offsetting income for a set period of time following the business loss.
At Thinking Outside The Box, Inc., we have the tax law understanding to find solutions like this that can be used to turn an otherwise disappointing situation around to the benefit of our clients. Located in Naperville, Illinois, our law firm represents clients throughout the Chicago metropolitan area. Contact ustoday.
Developing A Plan To Make The IRS Pay You For Your Business Failure
Often struggling businesses do not pay their payroll tax withholding and instead use the payroll taxes to pay other bills. Technically, this money belongs to the employees and it is a serious offense when these taxes are not paid.
Under these circumstances, it is often advantageous for the company to shut down and reconstitute as a new company the next day. When this happens, the past-due payroll taxes must be paid. However, once the old company is closed the employer's portion of the tax goes away; this reduces the total tax liability by approximately 25 percent.
Then Section 1244 of the Tax Code allows payment of the unpaid payroll taxes for the closed company. Each dollar paid to satisfy the payroll taxes then generates a dollar of ordinary losses.
The payroll tax is assessed to the owner of the company. This means that every time the owner pays on that tax debt personally, an ordinary loss is created under Section 1244. This offsets any type of dividends, interest or wages of the owner or his family. The owner can use the ordinary loss to reduce his taxes for the next few years until it is used up.
Basically, the IRS gives you a significant tax deduction (ordinary loss) for paying your taxes after the business is closed.


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'I will live': Mum-of-six determined to defy the odds
AFTER months of pain and receiving very few answers, mother of six Pippa Edwards was hit with the devastating news: she had just weeks to live.
Pippa's been diagnosed with an aggressive and rare form of stomach cancer. But as far as Pippa's concerned, she's in it for the long haul.
She said she's determined to see her children grow up.
"I'm in for the fight of my life," Pippa said.
"I said to the doctors, no I'm not accepting that. Miracles happen all the time in medicine. I believe I will live."
It all began in January when Pippa was working full time with the business she owns with husband Michael - Lite Moves Furniture Removals.
She was fit and running up to 10km a day when she was struck down with digestive issues.
Doctors told her she had irritable bowel syndrome but as the months wore on, the stomach pains worsened.
When she was correctly diagnosed in August the cancer had already spread.
"It's shocking and it's disappointing. I'd been seeing doctors for seven months," she said.
"Then to be told you only have weeks to live - it's a shock."
Pippa has since been referred to palliative care and, after spending some time recovering in Sydney, her health is finally at a stage where she can undergo chemotherapy.
She will receive the treatment for 12 weeks and hopes after that she will undergo a relatively new surgery in Sydney.
Pippa and Michael are determined to find treatments to prolong her life, and have set up a GoFundMe page.
In less than two weeks, the local family have already raised $14,000.
Pippa's situation has hit home for many people who have left messages of hope on the fundraising page.
"As another mum I wish you strength in recovery, because I dare say your babies are at the forefront of your mind. You've got this," wrote Sarah Cavanagh.
"My heart aches for this young mum. Having recently done treatment for cancer, my heart is full of support and love for her and family. If we can alleviate some stress, blessed be," wrote Kay Hehir.
Lalaland Moonee Beach will be holding a fundraiser for Pippa and her family on Saturday, October 5. Everyone is invited to bring the kids for a play anytime between 5.30pm-8.30pm, and all proceeds will be donated to the family.


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Culture Trip stands with
Black Lives Matter
St. Stanislaus Kostka Church in Pulaski Park was founded in 1867 as the first Polish parish in Chicago and is the "Mother Church" of all other Polish churches in the Archdiocese of Chicago.
The cornerstone of this church was laid in 1914 and, like many Polish Cathedrals, the architectural firm of Worthmann and Steinbach modeled its design on Rome's St. Peter's Basilica.
St. Hedwig's was completed in 1901 at a cost of $160,000. The church was designed by Adolphus Druiding, who also designed St. John Cantius in West Town. The interior was refurbished in 2008 after a fire.
Founded in 1894, the first Mass took place at St. Hyacinth in 1921. Another work by Worthmann and Steinbach, it was designated a minor basilica by Pope John Paul II in 2003.
Completed in 1912, this church has stained-glass windows imported from Poland. Also designed by Worthmann and Steinbach, Holy Innocents was one of a number of churches built within the old "Polish Downtown," which centered on the Polish Triangle at Division, Ashland, and Milwaukee Avenues.
Holy Trinity was founded in 1872 to relieve overcrowding at St. Stanislaus Kostka, but a feud between the two parishes meant Holy Trinity was not recognized canonically until the Vatican sent an Apostolic Delegate to resolve the issue 20 years later. In 2006, the parish hosted Polish Prime Minister Jaroslaw Kaczynski for Mass during a visit to Chicago.
The growth of Chicago's Polish community necessitated the priest at St. Stanislaus Kostka to begin plans for a new church in 1893, and by 1898, St. John Cantius Church was completed. In 2013, the interior underwent restoration to return it to its original splendor.
St. Mary of Częstochowa was founded as a Polish parish in 1895, and has since grown to accommodate a large Hispanic population, today offering Mass in English, Polish, and Spanish. Al Capone's sister Mafalda was married at the church in 1930.


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For some time now, I've wanted to draw up a list of journals that publish articles about legal translation and legal interpreting or more generally about language and law. So here it is!
Tag Archives: language and law
Conference – Legal translation & legal linguistics, Poznań, Poland
The Institute of Linguistics at Adam Mickiewicz University is to hold the Eighth Conference on Legal Translation and Legal Linguistics. The aim is to provide a forum for discussion in those scientific fields where linguistic and legal interests converge, and to facilitate integration between linguists, computer scientists and lawyers from all around the world.
The conference will be held over 3 days, from 28th June to 30th June (Friday-Sunday) 2013 in Poznań, Poland. Papers are invited on the following topics:
Reporting from Brussels – Translation Studies Days, part 2
Following Part 1, this post will discuss the second of the five studies on translation and related matters recently published by the Directorate-General Translation of the European Commission, presented at the Translation Studies Days held in Brussels on 20 & 21 September 2012.
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Conference – Forensic Linguistics, Oporto, Portugal
The Faculty of Arts/Faculty of Law of the University of Porto (Porto, Portugal) will host the 3rd European Conference of the International Association of Forensic Linguists on the theme of Forensic Linguistics: Bridging the Gap(s) between Language and the Law.
The conference, which is organised jointly by the two Faculties, aims to bridge the gap(s) between language and the law by sharing the latest research in the field of forensic linguistics/language and the law, and will be held from 15 to 18 October 2012.


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Ferry Service Campaign Kicks Off in Kitsap
Aboard the Spirit, a ferry capable of hauling up to 100 people without their cars, a loose group of about a dozen passenger-only ferry supporters launched a campaign Monday to see more trips from Kitsap to Seattle.
Richard Hayes, executive director of Kitsap Transit, explained the details and answered a few questions from the group — called Fast Ferries Now — about the plan to use sales tax money to begin ferry runs to Seattle from Bremerton, Kingston, Port Orchard and Southworth.
Hayes said the measure was a way to create economic development locally by bringing commuters to Kitsap County, some of whom would eventually opt to plant their businesses here rather than continue commuting.
It was much the same message he gave earlier in the day to Kitsap County commissioners, who unanimously endorsed a resolution supporting the Feb. 6 ballot measure that would help fund the venture.
"You have to make an investment in infrastructure to bring business here," said Commissioner Josh Brown. "I think this is great opportunity for Kitsap County to leap ahead into the future."
Should voters say "yes," sales taxes would increase 3 cents on a $10 purchase in the county. In return, 10 round trips on weekdays from Bremerton would begin by mid-year, from Kingston by the end of the year, from Port Orchard in 2009 and Southworth in 2011.
Hayes called the possible economic impact the "Bellevue Effect." He said the Eastern King County community grew with a significant number of high-income residents. Some of them eventually tired of the commute to Seattle and planted their businesses in Bellevue instead, creating a bustling business community of its own.
Hayes said it's possible just such a scenario could occur here years into the future if Seattle commuters have a new place to launch from. "We think this is probably the soundest long-term economic development program that at least the transit system can help with, and it's the long-term way to get the better jobs and housing balance," Hayes said.
The measure had plenty of opponents Monday morning.
Carl Palmer of unincorporated Bremerton argued that encouraging commuters to move here would have unforeseen costs. "Three-tenths of 1 percent is not the cost. The cost is increasing the pressures here in Kitsap County on infrastructures that currently are being neglected, arguably by some," he said.
Vivian Henderson said the price tag for the new service was too expensive. "The cost, in my opinion, is too high proportionately to the number of people who will benefit from it. I also believe that these costs are just the beginning," she said.
Henderson also cautioned Hayes against using the "Bellevue Effect" argument, saying many residents don't want to see Kitsap become like Bellevue and that the idea could turn off potential supporters. "It certainly made the hair on the back of my neck stand up," she said.
Commissioner Chris Endresen agreed with Henderson on that point, but disagreed with Henderson's contention that Washington State Ferries could continue to meet the commuter need in Kitsap County. "Washington State Ferries has not been responsive to Kitsap County in the 20 years I've been involved in local government," Endresen said.
"We have been asking for better service and a third boat on the Bremerton run for over 10 years and it hasn't happened. In fact they cut service," she continued. "I don't believe that the ferry system is ready to reinvent itself and it needs to. But I don't think that we need to be held hostage while they're not being responsive. This is a way for us to take control of our own destiny."
Ballots for the Feb. 6 election will be mailed by the county next week.


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What should I do to get a Biaks HealthCare Vending Machine to my office?
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on Monday, 28 October 2019.
Posted in Archives, Conservation, History Centre
Quite often I come across interesting things as I go about my business in the strong rooms at the WSHC. Today was no exception when I discovered this rather odd-looking book. On first glance it appears that someone has rather hurriedly wedged a large book into a small bag but on closer inspection I discovered I was looking at a medieval chemise binding.
The binding contains an Act and Memoranda Book for the Tailors' Guild of Salisbury including byelaws, admissions of freemen and apprenticeship indentures, dating from 1444-1838 and gives us a wealth of information regarding their organisation and activities.
It is big and extremely heavy and has a particularly large piece of leather skirting along the tail edge (lower edge). It has visible sewing stitches along the edges and two metal clasps on the foredge (front edge) that attach to corresponding slits in the cover. The book dates from 1444 so is most likely an original medieval binding, although more recent sewing repairs are visible around the edges. The text block pages are made from parchment and contain varying manuscripts, some with illuminations.
Above: Examples of parchment pages from the book
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on Tuesday, 01 October 2019.
Posted in History Centre, Traditions and Folklore, Wiltshire People, Wiltshire Places
Do you love reading and history?
Our latest venture might just suit you down to the ground!
Our reading group is based at the History Centre on the 1st and 3rd Monday of every month, 2-3.30pm, free entry. It's a chance for anyone who is at a loose end to come along and listen to extracts of books from our Local Studies Library on a wide range of topics, take a look at a range of documents from the Archives and photographs from our Local Studies Collection, not to mention tea/coffee, biscuits and a chat at the end!
Feel free to join in with any memories or comments you may have, or just enjoy the friendly atmosphere with others and the chance to take a look at the many fascinating and little seen items from our vast range of collections.
Topics we've covered so far have been as wide-ranging as Royal Forests, the Workhouse, the Fair, Ironworks, Education, Cinema, 1950s Chippenham, Washday, Harris' of Calne and Alfred Williams. The extracts mostly cover Wiltshire places but we also find out about the origin of the subjects to add context, covered by our general reference (Heritage) collection held at the library. The group also suggest topics of interest for us to cover in future sessions, which is proving to be very successful and interesting to date.
You'll be amazed by what there is to discover and uncover; we've found out about sea eagle bones which were purported to have been used in medieval bird hawking; the common labourer who was writing to tell others of the plight of his follow workers in the 18th century, the pioneer of the modern-day cinema, based in Salisbury, and much more!
We are a small, friendly group at the moment who would love to expand; please feel free to drop in and join us sometime soon; no appointment or booking necessary. A copy of our leaflet with further information can be found here.
Comments from attendees include "Brings back memories I'd forgotten I had"; "It's lovely to hear other people's ideas and learn new things"; "Brings up questions and new things to think about"…
We look forward to meeting you!
Julie DavisReading Group Leader and County Local Studies Librarian
on Tuesday, 30 July 2019.
Posted in Archives, History Centre
One of the many joys of our archive is how it encompasses not only the county's history – its people and places – but also world events as witnessed and experienced by Wiltshire folk through the centuries.
Each year I am in the privileged position of being able to take young historians on an archival journey round the world thanks to the extensive collections held by Wiltshire and Swindon Archive. These youngsters come to the Wiltshire and Swindon History Centre for work experience and for a week they get to explore the archive and local studies collections, as well as learn about the work of the conservators, archaeologists, civil registration certificates team and business support staff.
During five weeks of work placements – this year we took 14 students from six schools –the archives have transported us through time and space. We have crossed continents and centuries, catching a glimpse of the ordinary and extraordinary lives of people from another time.
As Education Officer at the History Centre there are types of documents that I frequently use because they make great classroom resources – maps, photographs, diaries, personal letters, school log books. And then there are the topics for which we have excellent collections – Tudors, Victorians, canals and railways, the First and Second World Wars and the Cold War.
But with the arrival of work experience students I have the opportunity to explore the archives at a more leisurely pace and in broader terms – and I am always finding new things to look at or seeing familiar documents in a different way. A good example is Siegfried Sassoon's February 1933 letter predicting war. This year was the third time I produced the document for students and it was as they were practicing their transcribing skills I finally made out a word that had been eluding me all this time – 'entente'. It was so obvious that I'm slightly embarrassed to admit that I had not worked it out sooner.
Although we often begin by digging out documents related to topics being studied at GCSE and A-Level, the challenge is to find the more unusual and quirky among them that don't always see the light of day but which take us on wonderfully unexpected journeys.
One of the quirkiest set we produced this year concerned the gift of an elephant to Queen Charlotte (wife of George III) in 1794. Three letters (WSA 9/34/42) contain hints and allegations of an East India Company man, who acted as an intermediary in delivering the elephant, claiming back the cost of the animal despite it being a gift.
The East India Company is well documented across a number of significant collections within the Wiltshire and Swindon Archive, including archives from Wilton House, the Earls of Radnor (Longford Castle), the Seymour family (Dukes of Somerset), politician Walter Hume Long and the Money-Kyrle family.
But I was not expecting to find any further reference to elephants… Yet in the Lacock archive, among documents belonging to the Davenport family, is a cache of letters, invoices, receipts and company accounts detailing goods being shipped – including elephants' teeth! (WSA 2664/3/2B/125 & 139 and WSA 2664/3/2D/79 et al.)
on Tuesday, 04 June 2019.
Posted in History Centre
Hello! I'm Louise a long serving volunteer at the History Centre in Chippenham. I have worked on and off in a voluntary capacity since 2005. I first discovered the Wiltshire Buildings Record (WBR) when it was located within the Wiltshire Record Office at Trowbridge. Dorothy Treasure, who is responsible for the day to day running of the charity, recognised my real passion for old houses and recruited me to her keen band of volunteers. Over the years my contribution has varied due to the needs of my family but I have always been encouraged to continue. Dorothy is also our Principal Building Historian; she is a real expert in her field and I feel very fortunate to be able to work with her.
Volunteers at the History Centre come from all walks of life and work the hours of their choosing. In my case I had worked as an HR professional prior to having a family rather late. Some volunteers are still in paid employment and join us when they can. This is the case with some of our committee members. Some volunteers work with the WBR for a while in order to gain experience to advance their careers in the heritage sector. What we all have in common is an interest in our country's heritage and a wish to rub shoulders with like-minded people and those working in professional roles. There are four strands to my voluntary work - documentary research into the history of individual buildings, building recording, data entry into the Historic Environment Record (HER) and committee work.
Typically I begin the week with the Archaeology Service, entering data from the WBR archive records onto the HER database. With 18,000 buildings records to work through, I think I've gained a job for life! Tom, the HER Manager is always nearby to guide me through the more complex aspects of the system. I am one of four volunteers he manages each week. We all do different things based on our interests and skill sets. I love the challenge of locating buildings particularly when building names have changed, buildings have been altered and only sketchy address details are given!
Tom the HER Manager and I at the History Centre and Martin one of the archaeologists in action at Avebury (photo taken by Terry Waldron)
Working alongside the Archaeology Service has given me a real insight into the challenging work the team undertakes, the county of Wiltshire not only has an important World Heritage Site, Stonehenge and Avebury, but also many other important historic assets to protect. I always enjoy listening to the office banter, the team are a lively and adventurous bunch. The team even has its own Morris dancer!
On a Tuesday, I work with Dorothy and spend my time researching the history of individual buildings. It is a day when I am able to catch up with other office-based volunteers over coffee or lunch. As a charity we need to generate an income and we do this mainly through commission work for individual house owners. Each report we produce includes a comprehensive recording of a building and some documentary history. Documentary research is my main area of expertise, built up over a number of years. It did help studying for an Undergraduate Advanced Diploma in Local History from Oxford University. All the study was done via the internet which was fantastic. The Archives team has always provided me with great support when I needed it, along with the WBR.
Studying maps in the Archive room to locate a particular cottage in the village of Netheravon. The building I am looking at is identified by No.90 on the 1790 Enclosure Award map for the parish
on Tuesday, 16 April 2019.
Posted in Archives, History Centre
Here at the History Centre we continue to acquire new collections to add to our archives. In this way we ensure our collections reflect as many aspects of Wiltshire life as possible, which helps us to engage with a wide diversity of research interests. So with this in mind, here is an introduction to some of the new collections we've received since the start of the year.
The Women's Institute of Little Somerford have donated a significant collection of committee minute books, attendance registers and programmes dating back as far as 1941 (collection reference number 2587A). The minutes alone tell us much about the activities undertaken and the groups' decision-making processes. In addition, the programmes show the diversity of lectures, demonstrations and competitions the group has undertaken. The collection joins over 200 other WI groups who have deposited material with us. This year marks the centenary of the foundation of Wiltshire's Women's Institutes with events planned all over the county.
We have also received a welcome addition to our considerable collection of tithe maps. This 1838 map covers the tithing of Widhill, part of the parish of Cricklade St Sampson, where much of the land is owned either by the Earl of Radnor or by Lord Redesdale. The accompanying apportionment document details both the occupiers and the use for each parcel of land, as well as the value of produce sent as tithe. These maps continue to prove a popular source of local, family and social history.
From the Wiltshire Scout Council comes a collection of logbooks kept by Peggy Shore Baily, the former Akela of the Westbury Leigh Cub Scouts. The collection (reference 4450) spans the years 1932 to 2007, and includes logbooks and scrapbooks, plus several of her personal photograph albums. Also, accompanying scrapbooks compiled by the First Aldbourne (Dabchick) Cub Pack and Winterslow Scout Group from 2007. This is just one of many scout and guide collections we house at the History Centre.
Another of our new personal collections is an addition to the papers of the Mackay and Tucker families of Holt and Trowbridge (reference 3840). This new accrual concerns Lucy Tucker Mackay, and includes a collection of her beautiful sketchbooks. Lucy was a gifted watercolourist who sketched studies of flora and fauna, as well as hundreds of views both of Wiltshire and from her extensive travels across Europe and further afield. Similarly, her photograph albums detail her many travels, most notably visits to her son Edward who was stationed in India with the British Army between the late 1920s and the late 1940s. This was a key time in the relationship between Britain and India, and the albums document the British Army and their families in their leisure time.
We have recently received several very different farming collections. From Box we have a set of haulage account books from Ashley Farm (reference 2324A), covering 1909 to 1964. These detail the transportation of livestock and other goods to and from market, and includes the details of the names and addresses of farmers across Wiltshire, Somerset and Gloucestershire. The volumes are packed with details of goods and charges, and are an aid to the identification of farming families across Wiltshire and beyond.
We have also acquired sale particulars for numerous farms located at Braydon, Brinkworth, Cricklade, Potterns and Pinkney. This collection (reference 831J) dates from 1962 and 1963. Each sale particular describes the homestead, farming buildings and any standing features, plus use and acreage for the agricultural land, as well as any locally given names for parcels of land.
From Donhead St Mary we have the papers of the Bridge Farm Trust (reference 3833A), a communal farming enterprise established in 1975. The farm's ethos combined environmental awareness with sensitive commercial dairy farming. The project also purchased a nearby farmhouse which served as a guest house and centre for the Community. Also of a farming nature, we have received a certificate presented by the Chippenham Agricultural Association to a Charles Sully, marking 29 years' service to the Case family at Cleverton Manor Farm (reference 831H). The certificate was originally accompanied by a reward of £2, a considerable windfall at the time. This leaves us wondering whether similar certificates for agricultural long-service are out there somewhere.
on Monday, 18 March 2019.
Posted in Archaeology, History Centre
Do you have an interest in archaeology? Would you like to know what has been found in your local area, or want to know more about how people lived in Wiltshire in the past? If so, then you might be interested to access our new website that allows you to research the finds, buildings, sites and monuments that exist on the county Historic Environment Record (HER).
The Historic Environment Record (HER) is a fantastic resource that holds information on all the currently known archaeology for Wiltshire and Swindon. This includes everything from Palaeolithic flint tools that are half a million years old to World War I practice trenches created only a hundred years ago – as well as everything in between! Using the HER can be fun and helps to guide your research, as it can tell you about the character and date of archaeological sites/finds as well as how they have been investigated and where you can find more (such as in journals, books and reports).
The new website allows people to easily search the archaeology of Wiltshire and presents data on both a map and dynamic database. To have a go, click to visit the HER homepage
The new website is easier to use than our previous one and allows you to search by the following themes:• Unique identifier number – so you can find records you've accessed before…• Keyword – to find particular find/site types – such as castles or axeheads!• Site name – for place names you know like your parish church or famous sites like Stonehenge!• Period – so you can see all Roman artefacts or all prehistoric archaeology we know about…• Grid reference – if you know exactly where you want to research - whether rural or urban!
You can also browse by navigating the interactive map – which can show both Ordnance Survey mapping or aerial photography. You can pan and zoom using the tools and the grid reference of your location handily shows at the top in case you need it!


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Hey guys. I'm new here but I heard you might be nice enough to take a look at my build and help me with an appropriate power supply. I'm thinking of overclocking a little (and at most 4.6GHz which should be around 1.35v).
NZXT Manta Mini ITX Case for PC - Black by NZXT (£108.97)
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I thought of this 600 W power supply from EVGA:
EVGA 600 W 80+ PC Power Supply Unit - White by EVGA (£48.95)
I don't know if it's enough or even good for my build but tell me what you think.
Any help would be appreciated!


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