text:
Huntington not approaching Deadline with urgency
CINCINNATI -- The 2013 Trade Deadline is a big one for the Pirates, as they try to acquire pieces that could help them to their first winning season in 20 years and their first playoff appearance since 1992.
Bur for any teams that think they can use the Pirates' lack of success in the last two decades against them, Pittsburgh general manager Neal Huntington has a message: "Don't bother."
"We as a group posture with the best of them, and part of posturing is gamesmanship," Huntington said. "I would say maybe those that don't know me all that well might throw that out there with the hopes that maybe that does have an impact. But those that know I think pretty well know that it won't have an effect."
With the July 31 non-waiver Trade Deadline closing in, the Pirates have not been playing their best baseball, dropping seven of their last 10 games entering Sunday. The offense, which has been middle of the pack much of the season, has had a particularly tough stretch, scoring three runs or fewer in six of those defeats.
But as Huntington and his staff look to fill their needs, he said it's important to look at the whole body of work -- both as a team and with individual players -- and not be swayed by the hot and cold streaks that are a part of the game.
Along the same lines, Huntington said the organization likes what it already has in place, and various players aren't performing to their career averages. That will hopefully change, he said, and that factors into how decisions are made.
"As we look at our offense, we don't really have a guy that's well above his career norms, [and] we have a few guys that are below," Huntington said. "Does it mean we don't look? No. But does it mean we have a sense of desperation? It absolutely does not mean we have a sense of desperation."
As trade talks increase and the Deadline nears, Huntington said he knows exactly what players he wants, and by most indications the club will pick up a bat if it makes a move. And if the Pirates have to surrender valuable pieces in order to compete for a division title, then so be it.
"We're willing to stretch where it's appropriate, and we recognize we're going to have to give up probably more than we want to," Huntington said. "But that's where we are at this point in time. We just can't be foolish about it."


text:
Summary: Arrestin (or S-antigen), N-terminal domain
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Arrestin Edit Wikipedia article
|S-antigen; retina and pineal gland (arrestin)
Crystallographic structure of the bovine arrestin-S.[1]
|Alt. symbols
|NCBI gene
|Other data
|Chr. 2 q37.1
|arrestin beta 1
|Alt. symbols
|ARR1, arrestin-2
|NCBI gene
|Other data
|Chr. 11 q13
|arrestin beta 2
|Alt. symbols
|ARR2, arrestin-3
|NCBI gene
|Other data
|Chr. 17 p13
|arrestin 3, retinal (X-arrestin)
|Alt. symbols
|ARRX, arrestin-4
|NCBI gene
|Other data
|Chr. X q
Arrestins (abbreviated Arr) are a small family of proteins important for regulating signal transduction at G protein-coupled receptors.[2][3] Arrestins were first discovered as a part of a conserved two-step mechanism for regulating the activity of G protein-coupled receptors (GPCRs) in the visual rhodopsin system by Hermann Kühn, Scott Hall, and Ursula Wilden[4] and in the β-adrenergic system by Martin J. Lohse and co-workers.[5][6]
In response to a stimulus, GPCRs activate heterotrimeric G proteins. In order to turn off this response, or adapt to a persistent stimulus, active receptors need to be desensitized. The first step in desensitization is phosphorylation of the receptor by a class of serine/threonine kinases called G protein coupled receptor kinases (GRKs). GRK phosphorylation specifically prepares the activated receptor for arrestin binding. Arrestin binding to the receptor blocks further G protein-mediated signaling and targets receptors for internalization, and redirects signaling to alternative G protein-independent pathways, such as β-arrestin signaling.[7][8][9][10][6] In addition to GPCRs, arrestins bind to other classes of cell surface receptors and a variety of other signaling proteins.[11]
Mammals express four arrestin subtypes and each arrestin subtype is known by multiple aliases. The systematic arrestin name (1-4) plus the most widely used aliases for each arrestin subtype are listed in bold below:
- Arrestin-1 was originally identified as the S-antigen (SAG) causing uveitis (autoimmune eye disease), then independently described as a 48 kDa protein that binds light-activated phosphorylated rhodopsin before it became clear that both are one and the same. It was later renamed visual arrestin, but when another cone-specific visual subtype was cloned the term rod arrestin was coined. This also turned out to be a misnomer: arrestin-1 expresses at comparable very high levels in both rod and cone photoreceptor cells.
- Arrestin-2 was the first non-visual arrestin cloned. It was first named β-arrestin simply because between two GPCRs available in purified form at the time, rhodopsin and β2-adrenergic receptor, it showed preference for the latter.
- Arrestin-3. The second non-visual arrestin cloned was first termed β-arrestin-2 (retroactively changing the name of β-arrestin into β-arrestin-1), even though by that time it was clear that non-visual arrestins interact with hundreds of different GPCRs, not just with β2-adrenergic receptor. Systematic names, arrestin-2 and arrestin-3, respectively, were proposed soon after that.
- Arrestin-4 was cloned by two groups and termed cone arrestin, after photoreceptor type that expresses it, and X-arrestin, after the chromosome where its gene resides. In the HUGO database its gene is called arrestin-3.
Fish and other vertebrates appear to have only three arrestins: no equivalent of arrestin-2, which is the most abundant non-visual subtype in mammals, was cloned so far. The proto-chordate C. intestinalis (sea squirt) has only one arrestin, which serves as visual in its mobile larva with highly developed eyes, and becomes generic non-visual in the blind sessile adult. Conserved positions of multiple introns in its gene and those of our arrestin subtypes suggest that they all evolved from this ancestral arrestin.[12] Lower invertebrates, such as roundworm C. elegans, also have only one arrestin. Insects have arr1 and arr2, originally termed "visual arrestins†because they are expressed in photoreceptors, and one non-visual subtype (kurtz in Drosophila). Later arr1 and arr2 were found to play an important role in olfactory neurons and renamed "sensoryâ€. Fungi have distant arrestin relatives involved in pH sensing.
Tissue distribution
One or more arrestin is expressed in virtually every eukaryotic cell. In mammals, arrestin-1 and arrestin-4 are largely confined to photoreceptors, whereas arrestin-2 and arrestin-3 are ubiquitous. Neurons have the highest expression level of both non-visual subtypes. In neuronal precursors both are expressed at comparable levels, whereas in mature neurons arrestin-2 is present at 10-20 fold higher levels than arrestin-3.
Arrestins block GPCR coupling to G proteins in two ways. First, arrestin binding to the cytoplasmic face of the receptor occludes the binding site for heterotrimeric G-protein, preventing its activation (desensitization).[13] Second, arrestin links the receptor to elements of the internalization machinery, clathrin and clathrin adaptor AP2, which promotes receptor internalization via coated pits and subsequent transport to internal compartments, called endosomes. Subsequently, the receptor could be either directed to degradation compartments (lysosomes) or recycled back to the plasma membrane where it can again signal. The strength of arrestin-receptor interaction plays a role in this choice: tighter complexes tend to increase the probability of receptor degradation (Class B), whereas more transient complexes favor recycling (Class A), although this "rule†is far from absolute.[2]
Arrestins are elongated molecules, in which several intra-molecular interactions hold the relative orientation of the two domains. In unstimulated cell arrestins are localized in the cytoplasm in this basal "inactive†conformation. Active phosphorylated GPCRs recruit arrestin to the plasma membrane. Receptor binding induces a global conformational change that involves the movement of the two arrestin domains and the release of its C-terminal tail that contains clathrin and AP2 binding sites. Increased accessibility of these sites in receptor-bound arrestin targets the arrestin-receptor complex to the coated pit. Arrestins also bind microtubules (part of the cellular "skeletonâ€), where they assume yet another conformation, different from both free and receptor-bound form. Microtubule-bound arrestins recruit certain proteins to the cytoskeleton, which affects their activity and/or redirects it to microtubule-associated proteins.
Arrestins shuttle between cell nucleus and cytoplasm. Their nuclear functions are not fully understood, but it was shown that all four mammalian arrestin subtypes remove some of their partners, such as protein kinase JNK3 or the ubiquitin ligase Mdm2, from the nucleus. Arrestins also modify gene expression by enhancing transcription of certain genes.
- ^ a b PDB: 1CF1; Hirsch JA, Schubert C, Gurevich VV, Sigler PB (April 1999). "The 2.8 A crystal structure of visual arrestin: a model for arrestin's regulation". Cell. 97 (2): 257–69. doi:10.1016/S0092-8674(00)80735-7. PMID 10219246.
- ^ a b Moore CA, Milano SK, Benovic JL (2007). "Regulation of receptor trafficking by GRKs and arrestins". Annual Review of Physiology. 69: 451–82. doi:10.1146/annurev.physiol.69.022405.154712. PMID 17037978.
- ^ Lefkowitz RJ, Shenoy SK (April 2005). "Transduction of receptor signals by beta-arrestins". Science. 308 (5721): 512–7. doi:10.1126/science.1109237. PMID 15845844.
- ^ Wilden U, Hall SW, Kühn H (March 1986). "Phosphodiesterase activation by photoexcited rhodopsin is quenched when rhodopsin is phosphorylated and binds the intrinsic 48-kDa protein of rod outer segments". Proceedings of the National Academy of Sciences of the United States of America. 83 (5): 1174–8. doi:10.1073/pnas.83.5.1174. PMC 323037. PMID 3006038.
- ^ Lohse MJ, Benovic JL, Codina J, Caron MG, Lefkowitz RJ (June 1990). "beta-Arrestin: a protein that regulates beta-adrenergic receptor function". Science. 248 (4962): 1547–50. doi:10.1126/science.2163110. PMID 2163110.
- ^ a b Gurevich VV, Gurevich EV (June 2006). "The structural basis of arrestin-mediated regulation of G-protein-coupled receptors". Pharmacology & Therapeutics. 110 (3): 465–502. doi:10.1016/j.pharmthera.2005.09.008. PMC 2562282. PMID 16460808.
- ^ Smith JS, Lefkowitz RJ, Rajagopal S (January 2018). "Biased signalling: from simple switches to allosteric microprocessors". Nature Reviews. Drug Discovery. doi:10.1038/nrd.2017.229. PMC 5936084. PMID 29302067.
- ^ Cahill TJ, Thomsen AR, Tarrasch JT, Plouffe B, Nguyen AH, Yang F, et al. (February 2017). "Distinct conformations of GPCR-β-arrestin complexes mediate desensitization, signaling, and endocytosis". Proceedings of the National Academy of Sciences of the United States of America. doi:10.1073/pnas.1701529114. PMC 5347553. PMID 28223524.
- ^ Kumari P, Srivastava A, Banerjee R, Ghosh E, Gupta P, Ranjan R, Chen X, Gupta B, Gupta C, Jaiman D, Shukla AK (November 2016). "Functional competence of a partially engaged GPCR-β-arrestin complex". Nature Communications. 7: 13416. doi:10.1038/ncomms13416. PMC 5105198. PMID 27827372.
- ^ Kumari P, Srivastava A, Ghosh E, Ranjan R, Dogra S, Yadav PN, Shukla AK (April 2017). "Core engagement with β-arrestin is dispensable for agonist-induced vasopressin receptor endocytosis and ERK activation". Molecular Biology of the Cell. 28 (8): 1003–10. doi:10.1091/mbc.E16-12-0818. PMC 5391177. PMID 28228552.
- ^ Gurevich VV, Gurevich EV (February 2004). "The molecular acrobatics of arrestin activation". Trends in Pharmacological Sciences. 25 (2): 105–11. doi:10.1016/j.tips.2003.12.008. PMID 15102497.
- ^ Gurevich EV, Gurevich VV (2006). "Arrestins: ubiquitous regulators of cellular signaling pathways". Genome Biology. 7 (9): 236. doi:10.1186/gb-2006-7-9-236. PMC 1794542. PMID 17020596.
- ^ Kang Y, Zhou XE, Gao X, He Y, Liu W, Ishchenko A, et al. (July 2015). "Crystal structure of rhodopsin bound to arrestin by femtosecond X-ray laser". Nature. 523 (7562): 561–7. doi:10.1038/nature14656. PMC 4521999. PMID 26200343.
- ^ Han M, Gurevich VV, Vishnivetskiy SA, Sigler PB, Schubert C (September 2001). "Crystal structure of beta-arrestin at 1.9 A: possible mechanism of receptor binding and membrane Translocation". Structure. 9 (9): 869–80. doi:10.1016/S0969-2126(01)00644-X. PMID 11566136.
External links
- Arrestin at the US National Library of Medicine Medical Subject Headings (MeSH)
This page is based on a Wikipedia article. The text is available under the Creative Commons Attribution/Share-Alike License.
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Arrestin (or S-antigen), N-terminal domain Provide feedback
Ig-like beta-sandwich fold. Scop reports duplication with C-terminal domain.
Literature references
Palczewski K; , Protein Sci 1994;3:1355-1361.: Structure and functions of arrestins. PUBMED:7833798 EPMC:7833798
Granzin J, Wilden U, Choe HW, Labahn J, Krafft B, Buldt G; , Nature 1998;391:918-921.: X-ray crystal structure of arrestin from bovine rod outer segments. PUBMED:9495348 EPMC:9495348
Hirsch JA, Schubert C, Gurevich VV, Sigler PB; , Cell 1999;97:257-269.: The 2.8 A crystal structure of visual arrestin: a model for arrestin's regulation. PUBMED:10219246 EPMC:10219246
Internal database links
|Arrestin_C Bul1_N LDB19 Rgp1 Spo0M Vps26
|Similarity to PfamA using HHSearch:
|Arrestin_C Vps26 Spo0M LDB19
External database links
This tab holds annotation information from the InterPro database.
InterPro entry IPR011021
G protein-coupled receptors are a large family of signalling molecules that respond to a wide variety of extracellular stimuli. The receptors relay the information encoded by the ligand through the activation of heterotrimeric G proteins and intracellular effector molecules. To ensure the appropriate regulation of the signalling cascade, it is vital to properly inactivate the receptor. This inactivation is achieved, in part, by the binding of a soluble protein, arrestin, which uncouples the receptor from the downstream G protein after the receptors are phosphorylated by G protein-coupled receptor kinases. In addition to the inactivation of G protein-coupled receptors, arrestins have also been implicated in the endocytosis of receptors and cross talk with other signalling pathways. Arrestin (retinal S-antigen) is a major protein of the retinal rod outer segments. It interacts with photo-activated phosphorylated rhodopsin, inhibiting or 'arresting' its ability to interact with transducin [PUBMED:15335861]. The protein binds calcium, and shows similarity in its C terminus to alpha-transducin and other purine nucleotide-binding proteins. In mammals, arrestin is associated with autoimmune uveitis.
Arrestins comprise a family of closely-related proteins that includes beta-arrestin-1 and -2, which regulate the function of beta-adrenergic receptors by binding to their phosphorylated forms, impairing their capacity to activate G(S) proteins; Cone photoreceptors C-arrestin (arrestin-X) [PUBMED:7720881], which could bind to phosphorylated red/green opsins; and Drosophila phosrestins I and II, which undergo light-induced phosphorylation, and probably play a role in photoreceptor transduction [PUBMED:8452755, PUBMED:1517224, PUBMED:2158671].
The crystal structure of bovine retinal arrestin comprises two domains of antiparallel beta-sheets connected through a hinge region and one short alpha-helix on the back of the amino-terminal fold [PUBMED:9495348]. The binding region for phosphorylated light-activated rhodopsin is located at the N-terminal domain, as indicated by the docking of the photoreceptor to the three-dimensional structure of arrestin.
The N-terminal domain consists of an immunoglobulin-like beta-sandwich structure and is found in arrestin and related proteins. For example, thioredoxin-interacting protein (TXNIP) matches the arrestin N domain [PUBMED:18664266, PUBMED:23519408].
Domain organisation
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Pfam Clan
This family is a member of clan Arrestin_N-like (CL0135), which has the following description:
The families in this clan are involved in vacuolar protein trafficking, G protein signal termination and sporulation. The Arrestin N terminal domain has an Ig-like beta sandwich fold which binds to receptors and impairs their capacity to active G proteins [1]. Arrestins have also been implicated in the endocytosis of receptors and cross talk with other signalling pathways [2].
The clan contains the following 6 members:Arrestin_C Arrestin_N Bul1_N LDB19 Spo0M Vps26
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|Finn RD , Griffiths-Jones SR
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|141.30 aa
|Average identity of full alignment:
|18 %
|Average coverage of the sequence by the domain:
|29.96 %
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There are 4 interactions for this family. More...
We determine these interactions using iPfam, which considers the interactions between residues in three-dimensional protein structures and maps those interactions back to Pfam families. You can find more information about the iPfam algorithm in the journal article that accompanies the website.
For those sequences which have a structure in the Protein DataBank, we use the mapping between UniProt, PDB and Pfam coordinate systems from the PDBe group, to allow us to map Pfam domains onto UniProt sequences and three-dimensional protein structures. The table below shows the structures on which the Arrestin_N domain has been found. There are 65 instances of this domain found in the PDB. Note that there may be multiple copies of the domain in a single PDB structure, since many structures contain multiple copies of the same protein sequence.
Loading structure mapping...

subset: commoncrawl


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Patent Trolls vs. Progress
Microsoft announced this week that it's paying America Online $1.1 billion in cash for 800 of its patents. This comes just nine months after Apple, Microsoft and others beat out Google and Intel for control of Nortel Networks' 6,000 patents, paying a then astounding $4.5 billion in cash. And in August of last year, Google announced a deal for Motorola Mobility along with their 24,000 patents for $12.5 billion. What's going on here?
It goes back to March 2006, when BlackBerry phone maker RIM agreed to pay a whopping $612.5 million to settle a mobile email patent infringement case with patent-holding company NTP. This comes to $6 for each BlackBerry ever sold. So-called patent trolls, those that own patents but don't sell products or services, are a pain in the side of those that do.


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Auto Publishers Price Starting at
*Based on model year EPA mileage ratings. Use for comparison purposes only. Your atual mileage will vary, depending on how you drive and maintain your vehicle, driving conditions, battery pack age/condition (hybrid only) and other factors.VIEW OUR INVENTORY
Multiple model configurations to suit all needs; ample available V8 power with improved V6 and EcoDiesel V6; increased fuel efficiency; user-friendly cabins; Ram-Box bed-side storage
For 2017, the Ram 1500 features a few changes. Among them, the Ram 1500 Rebel adds several standard features, like Uconnect 8.4, remote start, and rear park assist with rearview camera. Elsewhere, the Ram 1500 Sport adds remote start and an alarm system, the Laramie Longhorn adds LED bed lighting, Keyless Go, SmartBeam headlights, and rain-sensing wipers, and the Big Horn adds automatic temperature control. The Ram Outdoorsman trim has been discontinued, as has the 6-speed automatic transmission, leaving only the 8-speed automatic to transfer power in the 1500 series. Across the entire 1500 range, a 5-micron cabin air filter is standard.


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Nice Way To Keep Students Awake.
Today, we didn't even touch the clock. You know it seemed to us a stale idea. And honestly speaking, none of us had the energy to think of a new and improved one. Plus, we had to submit an ass-ignment today and nobody had done it, so the fear of hearing an acerbic lecture and the threat of solving an unwanted quiz discouraged us to even go near the darn clock. We were hoping to get our exam papers back. But we weren't lucky enough and we had to study and complete the darn-ish chapter :/
When around 1 pm, 90% of the class dozed off and 10% had actually started snoring, our CEO proffy asked us to take out a piece of paper. "QUIZZZZZZ????" was the first thought that striked our sleepy minds and made us more indisposed and lugubrious. Nobody was in the "mood" of a quiz. After looking at our distorted faces, he said, "It's kind of a game". He then asked us to open our books, jump to the blukh-blah case study, form groups of 2, nominate ourselves as Manager and make our other friend as our Assistant and....
Yeah, can you guess what he asked us to do? He said, "I want you all to write your names on the paper and count all the E's in the case study and write that number on the sheet, and submit it to me!!!!!" With the speed of light, every team joined their heads in finding out the E's in the case, beacuse he tricked us by saying, "Whoever is going to submit me their answer first will get 2 marks". The kind of 'duffer' class we have, everybody wanted to grab those 2 numbers. It was fun - people started counting loudly, some were striking out E's so their count was the perfect, and the others were admonishing those few who were counting loudly. =D It was a mess and a whole lot of fun too =D
After the proffy made sure all of us were completely awake and all charged up, he then calmly burdened us with another very berry long ass-ignment =(
Cheerio folks =(
PS: I scored 20/20 in QMDM, Alhamdolillah =D Yayyy =D


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After flaunting some of the most impressive capital ratios in last week's Dodd-Frank stress test results, BB&T (NYSE:TFC) shareholders were stunned to discover that the Federal Reserve "objected" to certain parts of the bank's capital plan.
Thursday evening, the Federal Reserve released the second part of the annual banking stress test results, which examined the largest U.S. banks' ability to make capital distributions and maintain certain capital levels during an economic downturn. Although the Fed did not object to the Winston Salem, NC-based bank's continuation of its increased dividend from the first quarter of 2013, the bank recently disclosed that it re-evaluated its process related to calculating risk-weighted assets because of regulatory guidance. The change in methodology was not reflected in the Fed's numbers, prompting the objection and necessary revision.
Should we speak up?
CEO Kelly King has already issued a statement reiterating BB&T's financial strength and commitment to returning capital to shareholders. Although King and his management team have carried a solid reputation during recent years, investors may begin to question the company's handling of the situation. Despite announcing the RWA calculation change prior to the release of the Dodd-Frank stress test results, in its own press release on the same day, BB&T did not highlight the increased probability of receiving an "objection" during the Fed's Comprehensive Capital Analysis and Review (CCAR). While it may be likely that BB&T did not have any knowledge that would lead it to believe the change would result in an "objection," investors may wonder if management should have been more proactive in highlighting the change and its potential impact.
Impact to capital ratios
Despite posting an impressive actual Tier 1 common ratio of 9.5% in Q3 in 2012, and a more impressive ratio of 9.4% under the severely adverse scenario last week, BB&T's Tier 1 common ratio shrunk to a minimum of 7.76% under its "objected" planned capital action.


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Now that the Android 4.0 SDK is available, we'll have tons of hackers tearing up the latest release searching for even more goodies hidden within the code. You could spend your time installing the emulator and playing with it yourself or you could just turn to Android engineer Dan Morrill for a quick cheat-sheet that he shared on Google+.
Here are some of Dan's favorite new Android 4.0 features not covered in the launch demo:
- Updated Settings: We've seriously revamped the Settings screen organization. Items are arranged much better now, and it's easier and usually requires fewer actions to find what you're looking for.
- Disabling Apps: ICS adds the ability to disable an app outright. Don't like an app that came preinstalled? Disable it! Its resources never run and its launcher icon is gone until you re-enable it. (This doesn't free up any space — it can't, since pre-installed apps are included in the read-only system storage. But it does put them "out of sight, out of mind").
- Camera Controls: The camera controls have been redesigned and are easier to find and mess around with.
- Improved Download Manager: It looks better and is easier to find and use and to see and clear any downloads you might have.
- Support for Encryption for Phones: Honeycomb added full-device encryption, but ICS brings it to phones.
- Audio Effects: There's a new audio effects API. Nuff said, really. 🙂
Find any other cool Android 4.0 features that haven't been widely reported? Just send us a tip or leave a comment and we can update our list.
« SIM-free UK Galaxy Nexus coming early Nov. for £515, says retailer Andy Rubin doesn't believe in tablet-specific apps »


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Singer-Songwriter Bonnie Raitt Plays Not My Job
This segment was originally broadcast on Sept. 6, 2012.
Back in the early 1970s, a young woman at Radcliffe College faced a choice: Stay in school and get her degree, or drop out and become a legendary blues singer and guitarist. It's pretty clear Bonnie Raitt made the right choice.
We've invited Raitt to play a game called, "I'm sorry, did you say BONNIE Raitt?" Bonnie Raitt is a multiple award-winning, legendary musician. Change one little letter in her name and you get Donnie Raitt, who worked at the Des Moines, Iowa, Metro Waste Authority for 31 years. (It's amazing what you find sometimes just by mistyping your search terms into Google.) We'll ask Bonnie Raitt three questions about Donnie Raitt.
Bonnie Raitt is one of those very rare women in music. She's had a long and acclaimed career. She's lasted decades, and she's never had to appear with a skimpy dress and a python draped around her neck.
CARL KASELL: At least not in public.
SAGAL: The great blues woman appeared on our show last year, along with Tom Bodett, Paula Poundstone and Jessi Klein, as well as guest scorekeeper Bill Kurtis. And we asked her what it was like being on the road after so many years.
BONNIE RAITT: It's really fun. It's as close to running away with the circus as you can get. And, you know, you don't have to do as many chores as you do when you're at home.
SAGAL: That's true.
SAGAL: Has the lifestyle on tour changed? Has the quality of groupies improved, for example?
RAITT: Oh, that's so funny.
RAITT: You know, I'll tell you what's changed is the internet has made maintaining those relationships at home much more fun and compassionate because, you know, you can do Skype calls. It's cheaper. You can be in whatever clothes or no clothes you want.
RAITT: It makes those calls a lot more - those calls to home a lot more fun. And that's a big change, you know, from the first.
SAGAL: Right.
RAITT: It's fun partying when you're young but as you get older, it takes its toll.
SAGAL: So, in the 70s, partying with groupies, now, naked skyping.
SAGAL: And you feel this is an improvement.
RAITT: Yes, with groupies.
SAGAL: With groupies, of course.
RAITT: The ones you're monogamous with.
SAGAL: Yeah, I understand. We were really curious and interested in your upbringing because you became - some people say you're the greatest female blues guitarist ever. But you did not grow up in that environment. You grew up a Quaker of all things. Is that right?
RAITT: Well, yeah, but that brought me into the counterculture. Early on, I went to the summer camps when my dad would be touring in his Broadway shows.
SAGAL: I should say that your father, of course, for those who don't know, was the amazing and immortal John Raitt, who created...
RAITT: Oh, thank you very much. He's the star of "Oklahoma" and "Carousel." But, you know, I'm a kid of my times and the folk music craze was taking over when I was 9 or 10, and Joan Baez was on the cover of Time magazine and Peter, Paul and Mary, and Bob Dylan.
They all - you know, I was ripe as a pre-teen for idolizing my counselors at camp, all of whom were exactly imitating every folkie in Greenwich Village. And I was trying so hard to get that sallow hollow-cheek look and it just wasn't working on my little round freckled face.
RAITT: So, yeah, I mean I came in through it through folk music. It was just a hobby, never expected to do it. You know, I was a cheap opening act. I didn't need a band. I could play - opened for James Taylor. I did a little ballads; I did a little modern stuff.
And I thought it was a cool way to make some extra money during college. But the last thing I was expecting was to be offered a record deal at 20. I told the college people I'd be back in a year and I guess that didn't work out.
SAGAL: You know, I was just there. They're still hurt.
RAITT: You know they gave me the Harvard Arts Medal a few years ago, even though I only went two years. It was great.
PAULA POUNDSTONE: Wow.
SAGAL: It is generally true that the coolest people dropped out.
RAITT: Oh.
SAGAL: You, Peter Seger, Bill Gates, Zuckerberg, Mark Zuckerberg. That's the thing to do.
POUNDSTONE: Wow.
RAITT: There you go. I'm going to go do it again. They said I could come back and audit classes and finish whenever this wasn't working out.
SAGAL: You see. When you were going back and forth from Radcliffe to Harvard to blues clubs, was that weird to make the transition? Did you have to stop outside before you went into the blues club and muss up your hair?
RAITT: No, you know we all had that soulful beatnik kind of long hair thing going on in the late 60s and early 70s. And that end of the business that's more rootsy in America - they call it Americana music.
SAGAL: Yeah.
RAITT: We're the kind of artists that get a chance to age gracefully in this business. We don't sell as many records but here I am at 62, still with a career. And if I was dancing around in my underwear when I was in my 20s, I don't know if it'd still be doing that.
POUNDSTONE: Boy, apparently I made the right choice as well.
RAITT: Paula, we have found...
SAGAL: I know. If you'll forgive me, thinking about these young singers, particularly these female singers and performers are so carefully packaged these days. And I'm wondering when you started out, when you were signed to that record deal, did the record company execs say OK, we want you to do this, we want you to dress like this?
RAITT: Oh, I told them - well, first of all, Warner Brothers was a small label. They had Randy Newman and Ry Cooder and they said, fine, you know, we'll pay for your records and the other kind of non-commercial artists we have like Randy and Ry, we'll pay for them with Black Sabbath and Deep Purple. And that was the philosophy was the big money makers would pay for the more artsy projects.
But those days of not paying attention to how your image - with all the social media I think - I just want to say on behalf of Lady Gaga and Taylor, and, you know, even Norah Jones doing so well, and Adele, they're incredibly poised and mature in the way that they're approaching their career.
I'm really, really impressed with this crop of - especially with the crop of women singers I just mentioned, but there's a lot of guys. Even if they're being managed, they seem to be very self-aware. There's a lot more sophistication.
TOM BODETT: If I can back up, Bonnie. You said that Black Sabbath and Deep Purple helped basically pay for Bonnie Raitt and James Taylor. So we can thank "Smoke on the Water," for like "Love me like a Man," is that what you're saying?
RAITT: Exactly.
BODETT: Oh man.
RAITT: You know, Katy Perry helps pay of all those Americana acts that don't shave, men and women.
SAGAL: Is that a genre, the non-shaving music?
RAITT: Yeah, I think hairiness is making a big comeback.
SAGAL: Oh, I like to listen to adult hairy contemporary. You know that's my taste.
RAITT: That is so great.
SAGAL: Well, Bonnie Raitt, we are delighted to have you with us. We've asked you here to play a game that this time we're calling?
BILL KURTIS: I'm sorry, did you say Bonnie Raitt?
SAGAL: You, Bonnie Raitt, are a multiple award winning legendary musician. Change one little letter and you get Donnie Raitt, who worked at the Des Moines Iowa Metro Waste Authority for many years.
RAITT: Oh my god.
SAGAL: It's amazing.
RAITT: I should have looked him up. We were just close to there.
SAGAL: I know. It's amazing what you will find when you do a typo when you Google search.
SAGAL: So we actually called up the Des Moines Iowa Metro Waste Authority and found out a little bit about Donnie Raitt, and we're going to as you, Bonnie Raitt, about him, Donnie Raitt.
RAITT: That is so fantastic.
RAITT: I was trying to figure out what you might ask me.
SAGAL: That's what we're going to do. So, if you get two right you win a prize for one of our listeners. Bill Kurtis, who is Bonnie Raitt playing for?
KURTIS: Peter Jacoby from Woodbury, Connecticut.
SAGAL: Here we go, first question. Donnie Raitt worked for the Metro Waste Authority for 31 years, a long and fulfilling career. What's the MWA's stated policy on disposing of old medication? It is A: Quote, "mix with items such as kitty litter or coffee grounds and double bag them"? B: Quote, "dispose of them immediately on their expiration date, unless you have Vicodin, which, trust us, is always fun"?
SAGAL: Or C: Quote, "pour them out into a big bowl and create a fun party grab-bag game"?
RAITT: Oh, I love that third one. But my 20s are over, so I'm going with number one.
SAGAL: The kitty litter. Yes, you're right, yes, kitty litter.
RAITT: And what if you don't have a cat or you don't drink coffee?
SAGAL: Well, buy a cat who drinks coffee.
SAGAL: The next question, Donnie Raitt retired from the Metro Waste Authority in 2008. Until then, what was his specialty? A: Waste tasting?
SAGAL: B: Shaming of people who don't recycle? Or C: Composting?
RAITT: Oh boy, I'd have to say the third one.
SAGAL: The composting. You would be right, yes.
SAGAL: He was the working foreman.
SAGAL: Donnie Raitt was, at the composting center.
RAITT: I'm a big composter. I'm so glad to hear somebody in my family, there's not that many Raitts around. I'm very proud. Maybe I'll call him up.
SAGAL: You should.
RAITT: We'll talk about kitty litter and composting, coffee grounds.
BODETT: Skype him, you know.
SAGAL: Yeah.
SAGAL: It could be after 31 years of working in the waste that could be the biggest thrill of his life. Last question...
RAITT: Exactly, especially if I'm wearing what I'm wearing - well almost wearing right now.
JESSI KLEIN: Bonnie.
BODETT: You tease.
SAGAL: Last question. Donnie Raitt used to joke with his coworkers that he was really what? A: A killer robot from the future? B: Elvis? Or C: Bonnie Raitt's cousin?
RAITT: Oh, I think C, but I might be sounding too puffed up.
SAGAL: No, it is in fact true.
POUNDSTONE: All right.
SAGAL: That he, being one letter away from you, used to claim that he was your...
RAITT: I bet you we have DNA strands that are connected. There's not that many Raitts.
SAGAL: It's possible. It's possible. But he apparently is not related to you. By the way, we were told - we wanted to talk to Donnie, but were told he doesn't use the phone much.
RAITT: Oh boy.
SAGAL: So we talked to his former colleagues about him.
RAITT: Oh.
SAGAL: By the way, but we did find out from them that he is a fan. So there you are.
RAITT: Oh, I'm so glad that you told me about him. That's fantastic.
SAGAL: Isn't it exciting? Bill, how did Bonnie Raitt do on our quiz?
KURTIS: Bonnie's perfect. Three in a row.
RAITT: Oh.
POUNDSTONE: All right.
RAITT: You are so sweet.
KURTIS: And Peter Jacoby will love you for it.
RAITT: I love you, Bill.
SAGAL: Bonnie Raitt's newest album is "Slipstream." It's terrific. Pick it up now. Bonnie Raitt, thank you so much for joining us on WAIT WAIT...DON'T TELL ME!
(SOUNDBITE OF MUSIC) Transcript provided by NPR, Copyright NPR.


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With summer upon us, the minds of some pranksters and water battlers will inevitably turn to water balloons and the havoc they can wreak. Photographer Edward Horsford's series of high-speed photos, however, invite us to see these water weapons in a different light, capturing the water the moment after the balloon has popped, but before the water has entirely lost its shape.
Horsford built his own trigger to snag these photos at just the right moment. Many of these photos are shot in the dark, with the flash focusing our attention on the water and hands. The results are certainly a technical achieve, but they're also incredibly playful, and you can see a real sense of fun in the various shots he devises. There are many more of these balloon photos, as well as Horsford's stunning macro and nature photos, at his website.
High-Speed Photography [Edward Horsford via My Modern Metropolitan]


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EPITAPH SIGNS SHY KIDx NEW ALBUM 5/14
Epitaph Records is proud to announce the signing of Shy Kidx, the Italian electronic dance music sensation who's first EP Orion is set to hit streets on May 14th, 2013. Recently featured in Alternative Press' 2013 100 Band's You Need To Know issue, Shy Kidx is a talented artist on the cutting edge of electronica and he is about to take his unique brand of EDM sound Stateside as one of the most compelling artists of the year.
To get an early look at Shy Kidx and his music go to BeatPort here:
Cutting his teeth as a teenager playing in punk bands, Shy Kidx has since crafted a unique sound influenced by a slew electronica pioneers such as the Bloody Beetroots and Skrillex. With the Orion EP, Shy Kidx delivers a unique brand of EDM that not only draws fans to the dance floor from around the world, but from all realms of music by redefining what is considered "punk."
"To me the attitude in electronica and punk rock are the same even if there are no lyrics in the music because they both come from the underground," he explains. "There's a definite relationship between those two worlds because neither one is doing what we're traditionally supposed to be doing with music--and that's what drew me to both genres in the first place."
From the carefully controlled chaos of title track "Orion" to the shimmering pop gem "Majestic 12," this EP shows the incredible sonic range that Shy Kidx has been able to achieve. Songs like "Final Warning" do the speaking for him via hypnotic synthesizers, syncopated drums and Earth-shaking grooves that are a far cry from the typical drum and bass soundtrack you'll hear at dance clubs.
"I bring my laptop with me on the road even when I'm not touring so all of these songs were written in different parts of the world which I think gives them their own character, explains Shy Kidx, a fact that he will put to the test when he realizes another dream this summer by bringing his upbeat dance party to the Vans Warped Tour.
Shy Kidx continues, "The most amazing part about electronic music to me is that it's so international and it just seems to keep growing; it's like there's a community all over the world and we're all working toward the same goal."
For more information exciting news about upcoming tours stay tuned to:
Shy Kidx On Warped Tour 2013 EDM Stage:
WED 6/19 Chula Vista, CA (San Diego) Cricket Wireless Amphitheatre
THU 6/20 Pomona, CA Pomona Fairplex
FRI 6/21 Pomona, CA Pomona Fairplex
SAT 6/22 San Francisco, CA Shoreline Amphitheatre
SUN 6/23 Ventura, CA Seaside Park
WED 6/26 Las Cruces, NM N.M.S.U. Practice Field
THU 6/27 Phoenix, AZ Salt River Fields
FRI 6/28 Las Vegas, NV Silverton Casino Parking Lot
SAT 6/29 Salt Lake City, UT Utah State Fairplex
SUN /30 Denver, CO Sports Authority Field at Mile High
WED 7/3 Noblesville, IN (Indianapolis) Klipsch Music Center
FRI 7/5 Toronto, ON Molson Canadian Amphitheatre
SAT 7/6 Darien Center, NY (Buffalo) Darien Center PNC
SUN 7/7 Holmdel, NJ PNC Bank Arts Center
TUE 7/9 Virginia Beach, VA Farm Bureau Live
WED 7/10 Columbia, MD (Washington, D.C.) Merriweather Post Pavilion
THU 7/11 Mansfield, MA (Boston) Comcast Center
FRI 7/12 Camden, NJ (Philadelphia, PA) Susquehanna Bank Center
SAT 7/13 Uniondale/ Wantagh, NY Nassau Veterans Memorial Coliseum
SUN 7/14 Hartford, CT The Comcast Theatre
TUE 7/16 Scranton, PA Toyota Pavilion
WED 7/17 Burgettstown, PA (Pittsburgh) First Niagara Pavilion
THU 7/18 Cuyahoga Falls, OH (Cleveland) Blossom Music Center
FRI 7/19 Auburn Hills, MI (Detroit) The Palace of Auburn Hills
SAT 7/20 Tinley Park, IL (Chicago) First Midwest Bank Amphitheater
SUN 7/21 Shakopee, MN (Minneapolis) Canterbury Park
TUE 7/23 Bonner Springs, KS (Kansas City) Sandstone Amphitheater
WED 7/24 Maryland Heights, MO (St. Louis) Verizon Wireless Amphitheater
THU 7/25 Atlanta, GA Aaron's Amphitheatre at Lakewood
FRI 7/26 St. Petersburg, FL (Tampa) Vinoy Park
SAT 7/27 West Palm Beach, FL (Miami) Cruzan Amphitheatre
SUN 7/28 Orlando, FL Central Florida Fairgrounds
MON 7/29 Charlotte, NC Charlotte Verizon Wireless Amphitheatre
TUE 7/30 Cincinnati, OH Riverbend Music Center
WED 7/31 Milwaukee, WI Marcus Amphitheatre
FRI 8/2 Dallas, TX Gexa Energy Pavilion
SAT 8/3 San Antonio, TX AT&T Center
SUN 8/4 Houston, TX Reliant Park - Main St. Lot


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