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[–]akatookey[tookey] (NA) -12 points-11 points ago
Or rather, the posting of personal information isn't allowed (by reddit rules themselves) and Destiny's blog post does just that!
[–]Clam- 2 points3 points ago
How about freedom of speech? Or even better, listening to community? Because I'm pretty sure that majority of this subreddit would like to know what's going on with and Destiny explained everything about it pretty damn well - at least what happened to him.
[–]akatookey[tookey] (NA) 0 points1 point ago
Where is freedom of speech guaranteed for subreddits? Or even better, listen to the rules!
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For a cool $1000, you can buy the Sonos Bundle 150 and wirelessly play music from a single remote control in two separate rooms in your house. On the other hand, for about $100 or less if you've already got the right equipment, you can get the same functionality from your iPhone or iPod touch. Let's take a closer look at how to use the iTunes Remote application for the iPhone 2.0 with inexpensive equipment you may already have to remote control music playback wirelessly in any room in your home.
The Sonos homepage describes its popular but expensive product thusly:
To start playing music, just grab the full-color wireless Controller and simply pick a room, pick a song and hit play. With the Controller in hand you'll have instant access to your entire music collection....
When you're done here, any iPhone or iPod touch will do exactly the same thing, in addition to all that email, calendar, internet, and mapping functionality that's made them so popular already—and for hundreds of dollars less. You can play music in any room individually, or in several rooms with the music playback synced between rooms.
The special sauce in this setup is a feature of Apple's AirPort Express wireless routers called AirTunes, which streams iTunes music wirelessly over your home network to any room in your house. AirTunes isn't new by any means, but with the advent of the new Remote app for the iPhone and iPod touch running 2.0 software, its usefulness has increased dramatically; it's become a Sonos killer.
What You'll Need
I'm going to price out the cheapest (or nearly cheapest) version of this setup, including the price of the iPhone or iPod touch. If you already have any of the necessary equipment, the price drops significantly.
1. iPhone or iPod touch: $199 (8GB iPhone minus wireless costs) or $299 (8GB touch)
2. Linksys WRT54GL Wireless Router: $50 (not the only supported router; see below)
3. Headphone-to-RCA Cable: $2 (I'm estimating, but you can get these things cheap at your local RadioShack.)
4. Apple AirPort Express: $100
Grand Total: $351 (iPhone) or $451 (iPod touch)
Cutting Costs
I actually had all of these things on hand, so it didn't cost me a dime. If you've already got an iPhone or iPod touch, the price drops to a meager $151 for the router, headphone-to-RCA cord, and AirPort Express router.
The Linksys WRT54GL router is not required, but it's inexpensive and it's what I'm using. It's likely you've already got a basic wireless router on your home network, and as long as you can set it up as a Wireless Distribution System (WDS), you probably won't need to buy a new router. The Apple AirPort Extreme ($180) is the easiest to set up with an AirPort Express, naturally. In my setup below, I used the much cheaper, much cooler WRT54GL running the free, open-source Tomato router firmware (which I showed you how to install here). The previously mentioned DD-WRT firmware supports WDS as well. If your current router supports WDS, you can shave an extra $50 off the setup price.
Because it's made specifically to extend iTunes wirelessly, the $100 AirPort Express wireless router is the one must-have piece of equipment—no substitutions here. You'll need one for every additional set of speakers you want to add to your set wireless remote control setup. (Of course you can find them cheaper on Craigslist or eBay.)
The added bonus to all of this is that we're setting up the AirPort Express as a wireless network bridge. That means that not only will it give you the very cool music functionality—it'll also extend the range of your wireless network by boosting your signal in the room you've got it installed. It'll still show up as one Wi-Fi network to all of your wireless devices, so you don't have to do anything special to take advantage of it once you've set it up.
Gather Your Setup Information
Before you get started tweaking settings, let's write down a few important bits of information to make things easier on us down the road. You may find this information in varying places depending on your base router, but the information you need to gather is the same.
First, head to the Basic Network settings page (Tomato link) on your router and find the section Wireless section. Copy your Wireless MAC address, which should look something like XX:00:X0:0X:00:XX. Also write down your SSID and Channel, and take note of your B/G mode.
Next, plug your AirPort Express into a power outlet and connect it to your router with an Ethernet cable. (I'm setting up the AirPort Express on a Mac, but it should work similarly on a Windows PC.) Open the AirPort Utility, and after a few seconds it should scan and recognize your AirPort Express on your network. Once it does, click on the Express in the AirPort Utility sidebar and write down the AirPort ID (which is really just the MAC address).
Now that you've got all that, you're ready for the heavy lifting.
Set Up Your Base Router
This setup should work with any router that supports WDS—check your router's manual and/or administration interface to find out if it does. If you want to follow along exactly with me, I'm using the open-source Tomato firmware (if you don't have it installed on a supported device, here's how).
Return to the Basic Network settings page (Tomato link). The first thing you need to do is change your Wireless Mode to Access Point + WDS.
Next head down to the Security section and change your wireless security type to WEP if it's not what you're using already. Set a passphrase and generate your keys (or just let Tomato randomly choose a secure option for you). Copy down your first key—you'll need it later to set up the AirPort Express and to connect other devices to your wireless network (including your iPhone or iPod touch).
(NOTE: WEP security was an unfortunate concession; I normally recommend the more secure WPA2 Personal, but I had trouble getting the AirPort Express to connect correctly as a wireless bridge using WPA2 security. WEP 128, on the other hand, worked fine.)
Finally, move down to the WDS section and enter the MAC address of your AirPort Express (the AirPort ID we wrote down earlier). Make sure the drop-down is set to Link With. Once you've finished all these steps, hit Save at the bottom of the page. Your router will update your settings, and you're ready to set up the AirPort Express.
Set Up Your AirPort Express Router
Start up the AirPort Utility, again with the AirPort Express plugged into your main router with an Ethernet cord. Click the AirPort Express name in the sidebar. This time, click the Manual Setup button. We'll be making a lot of changes in the AirPort Express setup to get it working as a wireless bridge (and iTunes extender), so make sure you've got the information we gathered above on hand.
First, click the Base Station tab and give your AirPort Express a name (this is the name that will show up in iTunes and on your iPhone remote). I chose Living Room, because that's where my AirPort Express will be. Next, set a password for the AirPort Express. This password isn't actually important for our setup as far as I can tell, but it's unavoidable. Make it anything you want.
Now head to the Wireless tab and change the Wireless Mode drop-down to Participate in a WDS network. Set the network name to the SSID, the Radio Mode to the wireless B/G mode, and the channel to match the broadcast channel of your base router as you wrote them down above. Set your wireless security to WEP 128 bit, and enter the key you generated above.
Now click on the WDS tab, where you should select WDS remote in the WDS Mode drop-down and paste your base router's MAC address (the one we wrote down above) in the text box labeled WDS Main.
Next click on the Internet tab at the top of the AirPort Utility. You shouldn't have to do much here, but make sure that you're connecting using WDS (you shouldn't have a choice at this point), set Configure IPv4 to "Using DHCP," and set Connection Sharing to Off (Bridge Mode).
At this point, you've got just one more thing left to do. Go to the Music tab and tick the checkbox next to Enable AirTunes. If you want to, set a speaker password (I wouldn't unless you've got a good reason to).
Once you've done all that, click the Update button. The AirPort Utility will update your AirPort Express with all your new settings and your AirPort Express will restart. If everything went as planned, your AirPort Express is now set up as a wireless bridge for your base router, and you're ready to stream your music wirelessly to any room in your house. (Hint: Your router will glow amber until it's working, at which point it'll glow green. If it's flashing amber, that means there was a problem.)
Hook Up the AirPort Express to Your Stereo
Unplug your AirPort Express from the router and the power outlet and move it to wherever you plan on setting it up (mine's behind my TV). Plug it in, and plug the headphone-to-RCA converter into it and your stereo. If you have a fancier stereo than I do, the AirPort Express supports digital signals, so the right kind of S/PDIF cord would work as well.
Enable AirTunes in iTunes
The next to last thing you need to do is open up the iTunes preferences and tell your computer to look for remote speakers with iTunes. You'll find this checkbox in the Advanced tab of the iTunes preferences.
Once this is done, you've already got wireless streaming set up in iTunes. When it's working, you should see a drop-down in the bottom right corner of iTunes where you can choose which speaker set you want playing or choose multiple speakers.
Finally, it's time to set up our iPhone or iPod touch as remotes.
Install and Set Up Remote on Your iPhone or iPod touch
After all the sweat you've put in so far, this step is dead simple. We've already covered how to set up the Remote App on your iPhone, so I won't go into all the details here.
Once Remote is set up and running on your iPhone or iPod touch, you can play back and remotely control your entire iTunes library from anywhere in your house you've got an AirPort Express set up. To toggle your speakers, just hit Settings in the Remote app and toggle the speakers on or off.
How Does It Work?
After a short time, I can tell you nothing feels better on an afternoon of household chores than walking around your home to a unified soundtrack in every room. I've only got one AirPort Express with AirTunes set up on my network, but you could easily add more rooms and speakers at just $100 or so a pop. If I'm just going to be hanging out in the living room, I'll turn off the computer speakers and just play from there. Likewise, the music stays at my computer when that's where I am.
The iPhone Remote app also works with the Apple TV, but I haven't tried it with this setup. If you have—or you've done multi-room remote control with your iPhone or iPod touch and AirTunes—share your experience in the comments. If you're looking for a similarly cheap wireless solution, check out Gizmodo's review of the EOS Wireless iPod Dock and Speaker System.
Now if only the music followed me based on proximity to wireless nodes and transferred to my iPod headphones when I left my wireless network. A boy can dream, can't he?
Adam Pash is a senior editor for Lifehacker who wants nothing more than to be bathed uniformly in music no matter what room of his apartment he's in. His special feature Hack Attack appears every Tuesday on Lifehacker. Subscribe to the Hack Attack RSS feed to get new installments in your newsreader.
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Saturday, December 8, 2007
Persistence Pays (And So Does Sloth)
Orange County Bird of the Week: The Roseate Spoonbill
There is a fundamental difference between the way bird photographers operate, and the way birders operate. Photographers seek out big, pretty birds in nice, pretty settings. Birders seek out anything with wings. Birders can spend hours looking into thick, shadowy foliage for that special warbler; photographers won't bother because (1) birds are great, but actually looking for birds is boring, and (2) even if that bird is in there, it'll make a crappy shot.
Birders flit from spot to spot in search of some rarity rumored to have been seen there 15 minutes earlier, while photographers plant themselves, like sequoias, in scenic locations, waiting for the birds to compose themselves into a perfect shot. This can take weeks.
I know this because Glenn is a photographer who happens to be deeply into birds, and I'm a birder who occasionally takes photos so Glenn won't think I'm making stuff up when I see something he doesn't.
But when the Roseate Spoonbill first showed up in the Santa Ana River in Orange on Thursday, we both knew we had to see it. It had everything both birdheads and photographers could want: It's a rarity. It would be a lifer for both of us. It's big, pink, and pretty. And it's here.
Since I work at home of Fridays, I set off first thing Friday morning to find it: I knew I was in the right place because of the large number of people with spotting scopes and binoculars pacing up and down the bike path. But after several hours, no one had seen it, and I gave up. After all, I was supposed to be at home working.
Today, both of us headed back to Orange, chasing reports that it had been seen downriver late Friday afternoon. Someone told us it had actually been seen a few minutes earlier UP the river, so we returned to our car and followed a caravan of birders to the intersection of Lakeview and Riverdale. There, we learned that the darned thing had been spotted napping nearby earlier, but had just taken off.
Nevertheless, we slogged up the path, Glenn hauling his usual ton of photo gear, hoping the Spoonbill would return. Several people decided to cross the river to see if it was foraging on the channel on the other side. We started heading back to the car. Sigh. This is precisely the sort of birding that photographers hate.
I debated crossing the river to see what was there, but I knew Glenn didn't want to drag his gear all the way back up the path and across the berm spanning the river. We agreed that I'd go and wave back to him if I saw anything.
Just as I turned to go, something big and pink flew up from the channel: the Spoonbill! Glenn immediately started shooting away—and it circled around and landed in the river, just in front of us!
And I realized that we had totally lucked out: had we given up and left a moment sooner, we would have missed it. Had we persisted and crossed the river with the other birders, we also would have missed that great close-up view of him. We only got to see it because we were slothful and indecisive—too indecisive to even give up.
It's a rare moment when one's vices become virtues—and we plan to enjoy it.
1 comment:
Birdfreak said...
Sometimes luck is what it takes! :-)
Good birding to you!
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Listen to everyone, then make up your own mind
Ben Silbermann, cofounder of Pinterest
I am writing a book called Winning Isn't Normal. Check it out.
Related Posts:
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Lewis LaLanne aka Nerd #2 59 pts
"Wisdom comes from multiple perspectives." Gregory Bateson
That's one of my favorite quotes and your post and what you expressed as a learning here reminded me of it. It''ll be very cool to see the story of how these multiple perspectives led you to your 1.3M.
I also completely agree with you on the stand point of how making tough "ass on the line" decisions help you become a more resourceful, confident and capable individual.
mlinsey 7 pts
I think this is a great post. The only thing I would add is to look for patterns in the kind of people who give certain kinds of advice, and make your first decision about what kind of person you want to be.
mechanical_fish explained this point far better than I ever could, so I'm going to just copy his comment (probably one of the greatest comments in HN history) right here. (original link: http://news.ycombinator.com/item?id=469940)
mechanical_fish writes:
This guy has gone to the zoo and interviewed all the animals. The tiger says that the secret to success is to live alone, be well disguised, have sharp claws and know how to stalk. The snail says that the secret is to live inside a solid shell, stay small, hide under dead trees and move slowly around at night. The parrot says that success lies in eating fruit, being alert, packing light, moving fast by air when necessary, and always sticking by your friends.
His conclusion: These animals are giving contradictory advice! And that's because they're all "outliers".
But both of these points are subtly misleading. Yes, the advice is contradictory, but that's only a problem if you imagine that the animal kingdom is like a giant arena in which all the world's animals battle for the Animal Best Practices championship [1], after which all the losing animals will go extinct and the entire world will adopt the winning ways of the One True Best Animal. But, in fact, there are a hell of a lot of different ways to be a successful animal, and they coexist nicely. Indeed, they form an ecosystem in which all animals require other, much different animals to exist.
And it's insane to regard the tiger and the parrot and the snail as "outliers". Sure, they're unique, just as snowflakes are unique. But, in fact, there are a lot of different kinds of cats and birds and mollusks, not just these three. Indeed, there are creatures that employ some cat strategies and some bird strategies (lions: be a sharp-eyed predator with claws, but live in communal packs). The only way to argue that tigers and parrots and snails are "outliers" is to ignore the existence of all the other creatures in the world, the ones that bridge the gaps in animal-design space and that ultimately relate every known animal to every other known animal.
So, yes, it's insane to try to follow all the advice on the Internet simultaneously. But that doesn't mean it's insane to listen to 37signals advice, or Godin's advice, or some other company's advice. You just have to figure out which part of the animal kingdom you're in, and seek out the best practices which apply to creatures like you. If you want to be a stalker, you could do worse than to ask the tiger for some advice.
jonkrop 7 pts
So true, and too often learned the hard way.
A related point: whenever someone gives me advice, I always ask "What's your reasoning for that?" Very often someone's advice is just a prescription: "If I were you, I'd do this." I think there's almost no value in that. Even if the advisor is very smart or accomplished, it's probably a bad idea to just blindly do what they say, for a bunch of reasons. But reasoning is useful; you can examine it, test it, and use it to inform your own decision.
jasonshen 45 pts moderator
jonkrop For sure, reasoning is really important. A lot of times the reasoning is based on hypotheses about the real world or generalizations: "In my experience, VC's do pose a signaling risk for startups" which is hard to prove or disprove, so you still have to go with your gut.
MtnEvan 12 pts
I forgot where I saw it, but it went something like:
"Don't seek advice. Seek information."
Conversation from Twitter
karldotter @karldotter 06 Jul
I cross-reference advice just like books in the library, nice post by @JasonShen on distilling feedback with your gut http://t.co/yXAHavza
CatherinewithaC @CatherinewithaC 06 Jul
@karldotter @JasonShen Small world, I know Jason!
BacktrackFire @BacktrackFire 05 Jul
@HNTweets Una NUEVA comunidad de investigadores, estudiantes y entusiastas de la Seguridad Informática. http://t.co/cUy3G2cG
1. [...] Listen to Everyone, Then Make Up Your Own Mind (Ridejoy Fundraising Lessons) (jasonshen.com) [...]
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Saturday, August 02, 2008
TWQ: Vacation Problems
As it's the time of year when a lot go on vacation, this TWQ (The Weekend Question) is themed to find the things we dread.
What problems don't you like to face while going on vacation? List as many as you wish.
My answers are:
1: All the trouble getting on and off an aircraft. It takes longer than the flight nowadays.
2: The drive by holiday reps to sell optional excursions, making the vacation cost far higher.
3: When on a coach tour, we are told we can't stay too long in a really interesting place as he wants to take us to an interesting carpet place where his brother wants to sell us some.
4: The fact that when we get home, we are more exhausted than when we left... and it's supposed to be a restful vacation!
Now it's over to you...
celadon2 said...
Not exactly a problem but seeing as I over see the packing for the whole family, and husband has no idea what I've packed until we unpack - for me it has to be packing!
We do our own thing on holidays, so no reps, no coaches,but then you have the discussions about what you want to do and where you want to go!
Sol said...
Packing.. For the same reason as Celadon... husband has no clue what he's got.
The one vacation we can take we are going to his parent's house. His dad has a list of things to do.. you know, like build a shed and such. Yes, we still refer to it as a vacation.
If we go on the motorcycle.. my behind gets sore. If we go in the car or plane, I get tired of sitting. That's the worst. Sitting!
Michele sent me .. and heck, It was interesting to feel like I was coming to someone's blog and complaining..
I do hope you have a wonderful weekend!
panthergirl said...
- The entire ordeal of air travel. It is just not fun anymore. I have sat in too many airports for hours on end, or had flights cancelled and had to go to another airport while my car was in long-term parking at the first one.
- Unpacking and doing laundry. Yuck.
Otherwise, I really do love to travel and go to new places... I wish I could just wiggle my nose and be there!
Here by way of Michele today...
Better Safe Than Sorry said...
i agree with yours but i also hate when you take the kids to some amusement park, pay a huge admission price just to get in the door and then have to wait hours and hours in lineups to ride the rides, to use the rest rooms, to buy something as simply as an ice cream cone. and charging $3 for a bottle of water after paying $50 head to get in, grrrrrrrrrrr.
Lahdeedah said...
Driving there.
Trying to keep three children occupied indoors in a place with no television or their normal toys when it rains.
The fact that this year we're not doing a vacation.
Jon the Intergalactic Gladiator said...
For some reason, either my wife or I always get pulled out of the line at the airport for the extra security check. Fun fun.
Empress Bee (of the High Sea) said...
oh i hate to fly, hate everything about it!
and i don't like packing up when it is time to get off the cruise ship either! i want to stay longer!
(sorry you can't comment capt. are you using internet explorer? that is giving people lots of trouble lately. try firefox??? or email me?)
smiles, bee
The Mistress of the Dark said...
Driving through Philly to get to Atlantic City.
Hotel workers in the US that don't speak ENGLISH!
R. Sherman said...
Greetings via Michele.
We do a lot of hiking vacations. In no particular order:
1. Idiot tourists who cannot follow the rules in National Parks re: wildlife, trails, etc.
2. Too many bugs.
3. Loud people in motels.
4. Driving through Kansas on I-70 to Colorado, a journey which sucks the soul from your very being.
Linda said...
My biggest problem is not being able to afford a vacation to begin with! Everything after that is cake!
HollyGL said...
1. Definitely the nightmare of security before boarding the plane.
2. Other travellers who apparently don't understand the meaning of "common courtesy".
3. Like Linda said, the sheer cost of a vacation anymore - with gas prices, etc... really makes the whole idea of travel a bit of a bummer. :(
Fab said...
I still have a month before I go on vacation. My boyfriend and I are planning a trip to Croatia, to the seaside...
1. delays with trains are terrible things
2. having a belt that makes the alarms go off at the airport checkpoint and being approached like a criminal
3. hotel rooms that smell funky
4. tourist centres that are usually all the way on the other side of the city's train station, a foreign city where the city map is available at the tourist centres cause it is so damn convenient (thank god for internet!)
Titania Starlight said...
I try to keep vacations simple but that is just wishful thinking on my part.
* Long layovers when flying. Good thing that I like to read.
* When driving, I hate going through large cities. I really and truly hate
bad drivers on a large scale. Give me the countryside any day!
*Getting lost. I have only done this a few times. Actually I did it all in one town. At least a dozen times! This town is so bad to get around that each place of business has a map of where you are at! Good to see I am not the only one that thinks this town is a maze.
I enjoy these weekend questions. :o)
Jean-Luc Picard said...
I share so many of the things that irritate you.
Panthergirl, airtravel is an ordeal, as you say, no longer a pleasure.
Jon, you must have a suspicious face.
Bee, I will try Firefox. I recently put it in to see the new Beta Facebook pages. If it fails, I'll let you know via Facebook.
Holly, gas prices have forced the cost of vacations up.
You've all given great answers.
Jason Todd said...
Jelly fish, I hate jelly fish
PI said...
We don't fly so that makes life easier but I dread getting lost en route, traffic, narrow lanes and a disappointment at the other end. Usually we are lucky (lots of previous research helps)
Michele says hi.
The Real Mother Hen said...
Ohhh I don't like the PACKING bit! Absolutely hate it.
And I also don't like to face with so much dirty laundry (from the travel) when I got home.
Jane said...
I hate the packing and the airport hassles. You are exhausted by the time you get where you are going. It makes you not want to bother!!! BUT, we do...go figure!
Thanks for the well wishes for my birthday!
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Saturday, June 24, 2006
Book review: Gibraltar Sun by Michael McCollum
As a child the first set of books I read for fun were those in the Black Stallion series by Walter Farley. Next I worked through the Hardy Boys and Tom Swift books. The Tom Swift books transitioned me into Science Fiction, and for close to ten years almost all of the books I read for fun were Science Fiction.
Around the time I was twelve or thirteen I realized there was a treasure of science fiction books up in the attic. As a teenager and young man my father had collected science fiction books and magazines. He had boxes of books from the 1940s, 1950s, and 1960s. He also had a fairly complete collection of Astounding, which later become Analog. Often I would come home from school, go up into the attic, and read a book during the afternoon.
As an adult, later as a husband, and especially as a parent I've not been able to keep up that pace. I still greatly enjoy science fiction, but I tend to read one or two books a month.
Recently I read Gibraltar Sun by Michael McCollum. Gibraltar Sun is the second in a trilogy. Most stories have the hero struggling against overwhelming odds. Sometimes the hero is outnumbered two to one, or five to one, or greater. In the Gibraltar series humanity is outnumbered about a million to one. The Broa has conquered every alien race they meet. Earth has learned of the Broa and survives as an independent race only because the Broa don't yet know about Earth.
Gibraltar Earth (the first book) sets the stage as humans learn about the Broa. While out exploring another solar system a human space ship rescues the lone survivor of a space battle. Humanity finds out there is a huge civilization of a million solar systems, and this civilization is run by the Broa.
Gibraltar Sun is the story of how humanity decides to fight the Broa. The first half of the book is mostly focused on the various factions on Earth that are pushing for different responses. Some want to hide. Some want to fight. A few want to contact the Broa and surrender. Our heroes are not willing to be slaves, or hope to hide forever. They recognize they can't win in a straight head on war, so they decide to see if they can trigger rebellions and help the thousands of races who are slaves to the Broa break their chains.
The second half of the book is about our heroes sneaking back into Broa space to do some scouting. Before taking a step in their war on the Broa humans need to find out exactly where the Broa systems are located. There is great excitement as negotiate with a conquered race.
I enjoy Michael McCullum's world building. The two Gibraltar books paint an interesting universe. Michael does a good job of making the Broa universe seem real.
This is a fun book. I read it in one sitting. A lot happens, but there is so much more hinted at, that I wonder how Michael McCollum will be able to wrap up everything.
If you like classic space opera, then I think you'll enjoy Gibraltar Sun.
You buy Gibraltar Sun through Amazon. But I encourage you to order directly from Michael McCullum. Most authors go through a publishing company. The publishing company gives a fraction of the sales for a book to the author. Michael McCullum is self publishing. He has created Sci Fi - Arizona, Inc. His sales may be less, but he gets all the profit when he sells directly to the reader. You can order from here. Michael makes the book available in both eletronic form, and in hardcopy.
Technorati tags: , , ,
Anonymous said...
I agree with your review of both Gibralter books. Enjoyed readin' your post.
Henry Cate said...
You might be interested in knowing that Michael McCollum has finished the conclusion.
I knew he had been working on it, and when I just checked now, I was pleased to learn it is available! I'll order it tomorrow.
r2lf.nga.s said...
Muy interesante, yo lo traduje al español GIBRALTAR EARTH, para quien lo desee descargar aqui, dejo mi aporte, ya que no lo encontre en español
Oja la sea de ayuda!!!
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Robert V. Clutter Jeffrey A. Modisett
Indianapolis, Indiana Attorney General of Indiana
Kathryn Janeway
Deputy Attorney General
Indianapolis, Indiana
CHARLES BURKE, )
Appellant (Defendant Below ), )
v. ) Cause No. 49S00-9808-CR-478
STATE OF INDIANA, )
Appellee (Plaintiff Below ). )
The Honorable Nancy Broyles
Cause No. 49G04-9705-CF-070920
November 19, 1999
SHEPARD, Chief Justice.
Appellant Charles Burke contends that a jury wrongly convicted him of murder inasmuch as the evidence showed he killed in sudden heat, making the crime voluntary manslaughter instead. We conclude there was ample evidence that Burke had time to contemplate his actions and therefore affirm.
Burke and Margaret Allison lived together for nine years until the relationship went south and she asked him to move out of the house. As they began to disengage, Burke lived for a while in a trailer parked in the back yard and then at the residence of his aunt. He still tended to hang around Allison's house, hoping to re-ignite the relationship.
At about 4 p.m. on May 13, 1997, Burke called Allison to ask if he could come pick up some belongings. She said another time would be better. When Burke called again, a male voice answered. Burke decided to go to the house.
Upon arrival, he encountered the source of the male voice on the telephone: Michael Minardo, Allison's new boyfriend. At twenty-three, he was half Allison's age. Allison told Burke she had been dating Minardo for several months, and was pregnant by him. Though Burke remained in the house for a few moments, he readily became “vicious” and “wild.” (R. at 126-27.)
Burke went out on the front porch. Next-door neighbor Terry Johnson saw Burke and invited him over. As the two men sat talking and drinking beer on Johnson's front porch, an angry Burke declared, “I'm going to kill both them [m-fs].” (R. at 99, 115.) He pulled a small gun from his pocket and asked Johnson if he thought it would kill somebody. Johnson replied it would, but said it “wasn't worth ruining his life over” and tried to talk Burke into giving him the gun. (R. at 101.)
Burke was not much of a drinker, but on this occasion he left to buy more beer and then returned. About fifteen minutes later, he went over to Allison's house, entered, stood for a time watching Allison and Minardo, and then demanded some of his belongings. Minardo helped Burke carry the items to his car.
Burke spent another twenty minutes talking with Johnson on his porch and then re-entered Allison's house. Minardo was asleep on the bed that Burke and Allison had long shared. Burke had a brief conversation in the living room with Minardo's mother, who had been present throughout the events. He then entered the kitchen, where Allison was playing solitaire. She asked him to leave, and matters began to escalate.
Working his way out of the house, Burke nodded in the direction of the sleeping Minardo and said to Allison, “Is this what you want?” (R. at 136-37.) Allison said it was. Burke took out his gun and shot Minardo in the head.
The charge against Burke was murder, but he contends he committed only voluntary manslaughter, a killing “while acting under sudden heat.” Ind. Code Ann. § 35-42-1-3-(a) (West 1998). “Sudden heat” is defined as “anger, rage, sudden resentment or terror sufficient to obscure the reason of an ordinary man”; it prevents deliberation and premeditation, excludes malice and renders a person incapable of cool reflection. Utley v. State, 491 N.E.2d 200, 202 (Ind. 1986).
When the evidence in a case suggests the presence of sudden heat, the State must disprove its existence beyond a reasonable doubt to obtain a conviction for murder. Finch v. State, 510 N.E.2d 673, 675 (Ind. 1987); Holland v. State, 454 N.E.2d 409 (Ind. 1983).
We conclude the State presented evidence adequate to warrant the jury's verdict. Burke announced his intent to kill Minardo some thirty or forty minutes before he shot him. In the meantime, he drank beer and talked with Johnson, made a trip to purchase more beer, carried his belongings to the car with Minardo's help, stood in Allison's home watching the two targets of his ire, chatted with Minardo's mother, and so on.
This was adequate evidence of time for deliberation. The jury could reasonably have rejected the claim of sudden heat and found Burke guilty of murder.
We affirm.
Dickson, Sullivan, and Boehm, JJ., concur.
Text Box
Converted from WP6.1 by the Access Indiana Information Network
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'I realised Sylvia knew about Assia's pregnancy - it might have offered a further explanation of her suicide'
In a heart-breaking new twist in the story of the lives and deaths of Ted Hughes and Sylvia Plath, Elizabeth Sigmund recalls a moment of terrible realisation
In 1963, the poet Sylvia Plath, distraught at the break-up of her marriage to Ted Hughes, committed suicide. Six years later, Hughes faced more tragedy when his mistress Assia Wevill - who had lured him away from Plath - killed herself and their four-year-old daughter Shura. Elizabeth Sigmund, a close friend of Sylvia Plath, prompted by the Guardian's account of Wevill's death (Saturday Review, 10/4/99) recalls the aftermath of Plath's suicide and the terrible events surrounding the death of Assia and Shura.
In March 1963, I went with my young daughter, Meg, to visit Sylvia Plath's small children in the flat in Fitzroy Road, Primrose Hill, where their mother had killed herself weeks earlier. I had been told that Ted Hughes's aunt, Hilda, was looking after the children, four-year-old Frieda and one-year-old Nicholas. Before gassing herself, Sylvia had left food and drink for her children and made sure they were safe in their bedroom.
When Meg and I arrived we found that Frieda and Nicholas were being cared for by a young nanny, who told me that Assia Wevill had ordered Hilda out of the flat, and had moved in herself. I learnt that Assia and Ted were out, and when I asked where they were the nanny said "She's having an operation and will be back soon."
The "operation" was an abortion, and when they returned to the flat Ted came into the kitchen and handed me a copy of The Bell Jar, which had been recently published and was dedicated to me. He looked distraught and said "At night I hear the wolves howling in Regent's Park, it seems appropriate".
I realised that Sylvia would have known of Assia's pregnancy, and that the thought of Assia giving birth to Ted's child might have offered a further explanation of Sylvia's final ability to face the future. To add to this, the Third Programme - as it was then - had broadcast Ted's play, The Difficulties of a Bridegroom, a few days before Sylvia's death. This play, which bears no relation to his book of short stories under that title, published in 1995, was based on a dream which Ted told to friends, in which a young man, driving to London, ran over and killed a hare; he took the hare to a butcher, who gave him money which he spent on red roses to give to his mistress.
The second part of the play details the obsession, mixed with fear, that the man feels for his mistress's body. It must have been agonising for Sylvia to hear this, and to realise that their circle of literary friends would have been listening, as anything new by Ted was an important event. The public humiliation and loss of dignity must have been unbearable for Sylvia.
Her last letter to me, written only days before her death, was full of plans for the future, looking forward to taking part in The Critics on the radio and hosting a poetry session in a London theatre, and of her longing to return to Court Green, their country house in Devon which she had left when Ted's affair with Assia had become unbearable, "in time for my daffodils, thank God you will be there". She said, "Ted comes to visit, and I can't help longing for lost Edens". The last few days turned all that hope into despair.
Immediately after Sylvia's death, I and my husband and three children were asked by Ted to live at Court Green, as he couldn't face going back there, and wanted to sell the house. Later he changed his mind, and moved back to bring up the children there, with the help of his sister, Olwyn. We moved into a cottage in the village, and were in daily contact with Ted and his family. I heard no further mention of Assia until 1967, when she came to live at Court Green with Shura, the child she had subsequently had with Ted, who was then two years old.
I saw Assia walking about the village looking lost and miserable. She had aged and put on weight, and Ted told everyone she was dyeing her hair, as she was going quite grey by then. Hughes's children with Plath, Frieda and Nick, used to bring Shura to see us, and she would climb on my knee. She was a silent and sad child, and we never saw Ted give any indication that she was his daughter. He was so proud of Frieda and Nick, and the contrast must have been acutely painful to Assia.
On Christmas Eve, 1967, Ted came to invite us to Court Green for sherry. He said that Assia was very depressed, as she had made a special Russian Christmas cake, and no one was coming to eat it with them. We reluctantly went with Ted, and found Assia standing in the kitchen, in the shadows, looking profoundly unhappy. We felt very sorry for her, and anxious about her state of mind, despite the fact that she had always regarded us as "enemies", as we loved Sylvia and were appalled at her death. We stayed for a very short time, and several weeks later I met Olwyn Hughes, Ted Hughes' sister, in the village; she told me Assia had gone back to London, and that she had been making Ted's life a misery.
In March 1969, Assia dragged a bed into the kitchen of her Clapham flat, dissolved sleeping tablets in a glass of water and gave the drink to her daughter before draining the rest herself. Then she turned on the gas stove and got into bed with the child.
I didn't hear of Assia and Shura's death until many months later, and I still feel acute grief at the thought of that child's life. Fay Weldon, who worked with Assia at an advertising agency, has told me of the suffering that she saw Assia going through after she returned to London, as people blamed her for Sylvia's suicide, and turned their backs on her, and how Ted, although already preparing to marry Carol Orchard, was making vague promises of setting up house with Assia and Shura.
The dedication to Assia and Shura of Ted's Crow poems demonstrates the anguish he was suffering after their death. He talked to me, a year before their publication in 1970, of an image he had, of a man sitting in the desert, holding a loaded gun with only one bullet. There is a black bird sitting in a nearby tree, and the man cannot decide whether to shoot the bird or himself.
There are many biographies of Ted and Sylvia, but barely a mention of the life and death of Shura. She was a child who was conceived in a doom-laden relationship, lived a life of confusion, with a deeply depressed mother, and died what must have been a terrible death. The more one learns of these events, the more the whole thing assumes the proportions of a Greek tragedy.
The life that Sylvia and Ted had decided upon at Court Green, of working poets, not to be seduced by the lure of literary London, bringing up their children, growing vegetables and keeping bees, was only a dream for Sylvia, as it turned out. She had shown me round the house and garden when we first met, and told me of their plans to have five children, to write, to cook, to be part of a rural community, and to shun publicity.
She believed that Ted was committed to this plan, and the discovery that he was having an affair with a woman who was married to another poet (David Wevill), was not the least bit interested in living a rural idyll, and was the exact opposite of Sylvia in personality, appearance and ambitions, felt like a complete betrayal of everything that her marriage had meant. She felt that she had been thrown out of Eden, and could find no resting place.
Her decision to go back to London in the autumn of 1962 was an attempt to recapture her earlier ambition to be a brilliant literary figure, with "a salon". With the reality of two small children, a fearsomely bitter winter, frozen water pipes, the onset of 'flu and the increasing knowledge that Ted was not coming back to her, came despair and a return of the depression which she dreaded. She was presented with the impossibility of going on. The fact that she left a legacy of brilliant poetry, which came out of that despair, is an extraordinary irony, as the fame and recognition she craved in those last months only came after her death. After Assia's death, Ted resumed the life he had planned with Sylvia, but with his second wife, Carol.
Nick and Frieda have had to bear the weight of their mother's death, the subsequent miseries of jealous women fighting for Ted's affection, and their half-sister's death, balanced by their very real love and pride in their father, and gratitude for the kindness of Carol, their step-mother. I saw the suffering endured by Sylvia, her mother and children, and Ted's mother. Now, learning in the Guardian of that of Assia's relations, who cannot bear to see her and Shura's death dismissed as a footnote to the Plath/Hughes tragedy, I feel as if there is no end to the heart-breaking echoes, as Sylvia wrote in her poem, "Words":
After whose stroke the wood rings,
And the echoes!
Echoes travelling
Off from the centre like horses.
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Advertisement weblogs careymm
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Fractions and Decimals on a Number Line: A Study Guide Pin Me
Learn about Fractions and Decimals on a Number Line
written by: Sylvia Cini • edited by: Amanda Grove • updated: 1/9/2012
A number line is a simple visual aid used for comparing numbers. Usually, we use number lines to show whole numbers, but we can also show decimals and fractions on a number line. Use this study guide to learn more about whole numbers, fractions and decimals on a number line.
• slide 1 of 9
Whole Numbers
Whole numbers, also called integers or counting numbers, are the numbers we use to show complete quantities. Whole numbers are written without a decimal or fraction. For example:
• I read one book this summer.
• There are five cats in my Grandma’s house.
• I would like to buy 19 camel saddles.
• I am in debt. I have -$10 because I spent $10 more than I had available.
• slide 2 of 9
Fractions are numbers used to express a part of a whole. Fractions are written as a ratio of the number of parts to the whole. The parts are always of equal value.
• I ate ½ of the pizza. (The pizza was divided into two equal parts. I ate one of those two parts.)
• Only ¾ of the class went on the field trip. (If the class were divided into four equal groups, three out of four groups went on the trip.)
• I wasn’t going to buy a whole pineapple, so I ordered 1/3 of a pineapple.
• slide 3 of 9
Decimals are used just like fractions—to show a part of a whole. Decimals are written using the same symbols as whole numbers but are distinguished by a dividing period, called a decimal point. The decimal places, those to the right of the period, also have place value just like whole numbers.
• .1 is one tenth. Another way of talking about 1 out of 10 parts.
• .15 is one tenth and five hundredths—or 15 out of 100 parts.
• The movie is 1.5 hours long. (One complete hour and five out of ten parts of an hour. )
• I spend $4.56 on a birthday card for my Uncle Tom. (Four whole dollars and 56 out of 100 parts of a dollar--56 pennies.)
• slide 4 of 9
Number Line
A number line is constructed of one long horizontal line and several vertical lines. The vertical lines, sometimes called ticks or marks, are used to divide the number line into equal sections. (i.e., equal parts) Labels on the ticks tell you what each one means.Number Line In this number line, there are three negative and three positive integers. (i.e., -3, -2, -1, 1, 2, 3) Between each number there is an unlabeled tick. Since they are halfway between one number and the next, we can deduce that these unlabeled marks represent half values. (i.e., 1/2 or .5)
On a number line, fractions and decimals are represented the same way--as parts of a whole. Fractions and decimals of equal value will be shown the same way. (e.g., 1/4 will look the same was .25)
• slide 5 of 9
Example 1
Number Line -1 Look at the red dot on the number line above. It falls exactly on the line marked "-1." This is a negative integer so we know that we are talking about a negative value. In this case, having 1 unit less than zero. (Since the graph is not labeled with a title this number could represent many things: a test score, money owed, yards in a football game.)
• slide 6 of 9
Example 2
Number Line .5 The graph (above) has a red dot on an unmarked tick halfway between 0 and 1. Since we know that every other line has a value of one unit, we can deduce that every tick has a value of one half. To find the value of the dot you can reference the line before or ahead of the indicated mark.
• 0 plus one half is one half (i.e., 1/2 or .5) or
• 1 minus one half is one half
• slide 7 of 9
Example 3
Number Line 2.25 Since the dot is not on a tick we will only be able to estimate the value of the dot. This one is a bit tricky so let's take it one step at a time.
1. Identify the ticks closest to the dot. The dot is between 2 and 2.5. You can see that the whole number 2 has already been passed, so the value of the dot is 2 plus an unknown fraction. Steps 2 and 3 will help you find the value of this part.
2. Estimate the position of the dot. The dot is halfway between 2 and 2.5.
3. Figure out the value of 1/2 of 1/2, .5 of .5. Multiply the fractions/decimals to find the value of the dot's position. (1/4 or .25) Alternately, use another visual aid to help you figure this out. Draw a circle. Divide the circle in half and divide the circle in half again. The value of one section is--one quarter!
4. Add the value of this fraction/decimal with the whole number value of the dot. (2 + .25 or 2 + 1/4)
The sum is 2.25 or 2 1/4
• slide 8 of 9
Practice Problems
Can you figure out the value of the green dots for each of these graphs? (The answer key is after the Resources)Number Line b Number Line c Number Line a Number Line d
• slide 9 of 9
Here are some links to help you learn about fractions and decimals on a number line.
• Learning Wave: Number Line (http://www.learningwave.com/chapters/integers/numline.html)
• Maths Dictionary For Kids (http://www.amathsdictionaryforkids.com/dictionary.html)
• Helping With Math: Number Lines (http://www.helpingwithmath.com/resources/oth_number_lines.htm)
• Fun Brain: Number Line Game (http://www.funbrain.com/linejump/index.html)
• Math Is Fun: Number Line (http://www.mathsisfun.com/number-line.html)
Photo Credit
"Number Line Series" by Sylvia Cini. Creative Commons.
Answers to Practice Problems:
• -1.5 or -1 1/2
• -2.75 or -2 3/4
• -.25 or -1/4
• 1.75 or 1 3/4
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When the bizarre story of Notre Dame football star Manti Te’o and his imaginary girlfriend broke earlier this month, one word shot to prominence with blinding speed: “catfish.”
“Catfish” is the name of a 2010 documentary about an online romance that turned out to be predicated on a fictitious identity. The makers of the movie developed a spinoff reality show for MTV, also called “Catfish,” devoted to the same theme of duplicity in virtual relationships. Te’o’s story fit the “Catfish” narrative: He fell for a girl he never met based on a trumped-up social media presence, before her tragic “death” from leukemia. He had been “catfished.”
“Catfish” is only the latest in a long line of shorthand terms, often derived from literary or cinematic allusions, to designate the deceptive psychological games that people play. Such shorthand can take a whole complex pattern of behavior and boil it down into a pithy linguistic packet, but it can also help us get a handle on seemingly inexplicable personal dynamics by evoking a juicy, compelling narrative. In the case of “catfishing,” it’s a narrative tailor-made for the age of Twitter and Facebook.
After the sports blog Deadspin revealed that the supposed girlfriend, Lennay Kekua, was a hoax, Notre Dame athletic director Jack Swarbrick attempted to explain Te’o’s victimization by pointing to the documentary and MTV series “and the sort of associated things you’ll find online and otherwise about ‘catfish’ or ‘catfishing.’” He described “catfishing” as a scam “perpetrated with shocking frequency,” admitting that he had learned the term from a recent episode of “Dr. Phil.”
Before the documentary was released, Urban Dictionary entries for “catfish” included various negative metaphorical uses, typically referring to an ugly person or “bottom-feeder” of some sort. But after the film’s debut, a new definition emerged: “someone who pretends to be someone they’re not using Facebook or other social media to create false identities, particularly to pursue deceptive online romances,” as a July 22, 2010, entry puts it. The following year, an entry for “catfished” illustrated how the new word could be used as a verb (a usage that the MTV show has sought to capitalize on).
But why “catfish” in the first place? At the end of the movie, the husband of the scam’s perpetrator is interviewed and spins an anecdote about how live codfish were shipped from Alaska to China in vats. In order to keep the cod’s flesh from getting mushy, someone came up with the idea of putting catfish in the vats to “keep the cod agile.” He further explained that “there are those people who are catfish in life”: “They keep you guessing, they keep you thinking, they keep you fresh.”
The tale of the catfish and the cod has all the hallmarks of apocryphal folklore, and indeed it has been floating around in one form or another for at least a century. It was used as a kind of Christian parable (referring to the Atlantic rather than the Pacific fishing trade) in Henry W. Nevinson’s 1913 “Essays in Rebellion” and again in Charles Marriott’s novel “The Catfish” published later the same year.
In those days, the catfish story served a moralistic purpose, but it had nothing to do with matters of the heart. Even then, though, there were romantic frauds—and a need to name them. A full-page New York Times Magazine article in 1910 told of “poor George Osborne,” a Connecticut bachelor who had been deceived for many years into thinking that he was writing love letters to his sweetheart, when in fact it was an elaborate ploy by his neighbor to bilk him.
The headline of the article, “Wooed a ‘Marjorie Daw’ for Fourteen Long Years,” alluded to an 1869 short story by Thomas Bailey Aldrich, in which an exchange of letters between two friends leads to one of them inventing the titular character. His correspondent falls for young Marjorie Daw and seeks her out, until (in the last line of the story) she is revealed to be a fabrication. Aldrich’s work was celebrated at the time and inspired such writers as O. Henry to make their own short stories with dramatic twist endings.
Literature has provided metaphorical models for human deceit at least since Homer and Virgil described the treachery of the “Trojan horse.” The tall tales associated with Baron Münchhausen, a fictionalized version of a real 18th-century German nobleman, prompted the British physician Richard Asher in 1951 to dub the condition of feigning illness in order to draw sympathy “Munchausen syndrome.”Continued...
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Brides of Dracula
The Brides of Dracula are characters in Bram Stoker's 1897 novel Dracula. They are three seductive female vampire "sisters" who reside with Count Dracula in his castle in Transylvania, where they entrance male humans with their beauty and charm, and then proceed to feed upon them. Dracula provides them with victims to devour, mainly infants and children.
Like Dracula, they are the living dead, repulsed by religious objects. In chapter three of the novel, two are described as dark haired and the other as blond, though some film adaptations depict them as a blonde, a brunette and a redhead.
In the novel the three vampire women are not individually named. Collectively, they are known as the 'sisters', and are at one point described as the "weird sisters".[1]
Although the three vampire women in Dracula are popularly referred to as the "Brides of Dracula", they are never referred to as such in the novel, instead referred to as the 'sisters'; whether they are married to Dracula or not is never mentioned, nor are they described as having any other relation to him. Though it is mentioned by the sisters that Dracula does not love, nor has he ever loved them, the count himself claims he once loved them in the past.[2] The two dark-haired women, however, are described by Jonathan Harker to have "high aquiline noses, like the Count's". It has been suggested from this that it may have been Stoker's intent that these two are Dracula's daughters, extending the sexuality metaphor of vampirism to incest.[3] Despite their words, the sisters have oddly never attempted to leave the castle and follow Dracula's orders without question. Likewise Dracula, while angered at them disobeying trying to feed on Jonathan, shows he does care somewhat for them by giving them something to eat in the form of the contents of the "wiggling bag" and honors his promise to give them Harker when he leaves.
As vampires, the sisters are powerful in their own right; their beauty and playful charm belie lethal, predatory interiors. Their beauty and flirtatious manner appears to be their greatest power when it comes to bewitching their victims into a trance-like state. Harker and Van Helsing are both attracted to, and yet repulsed by them. They can seemingly appear out of nowhere and are inhumanly strong as shown when they kill Helsing's horses. Though they live in fear of Dracula, the blond vampire can be seen defying him when she demands to feed upon Harker. The blond vampire is described by one of the brunettes as, "The First" and she is depicted as the leader of the three and Dracula's favourite. This may suggest that the blonde is in fact Dracula's wife, and may be the mother of the two dark-haired women if they are indeed his daughters. Or it may be that she is the most recent addition to his women-folk, and the brunettes are simply training her in how to prey upon humans.
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Sometime near the beginning of the novel, Harker encounters them when he wanders the castle during Dracula's absence and enters a luxurious salon where the sisters are kept. As it's nightfall when he does this, the sisters are awake and roaming the castle. More than delighted that fresh prey has entered their domain, they proceed to seduce him. Harker tries to resist their seduction and is saved by Dracula, who drives them back, chastising them for trying to feed on Harker when he wasn't done with him, though he promises to give Harker to them after his business deal is concluded and gives then a "wiggling bag" (highly presumed by Harker to be a child) to appease them. Dracula makes good on his word and leaves Harker to the sisters when he heads for England, but Harker manages to escape the castle before they can drain him, though he is badly traumatized by the encounter.
The sisters aren't seen again till near the end of the novel as the protagonists approach Castle Dracula in pursuit of the vampire. The sisters suddenly appear at a camp consisting of Van Helsing and Mina Harker. Sensing that Mina is bitten and nearly a vampire, they beckon the latter to join them, referring to her as their "sister". However, thanks to the holy symbols placed around her, Mina keeps her sense of self and is repulsed by them, though does feel the urge to heed their calls. Van Helsing manages to keep them at bay, but the sisters persist in trying to take Mina. In the middle of this, they manage to kill and feed on their horses. The sisters are forced to flee when the sun rises. Van Helsing subsequently goes to Dracula's castle and, after locating their tombs, destroys them by staking and decapitating them.
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In other media
Commonly all three brides appear in film adaptations of the novel, though some adaptations show fewer than three, such as the 1995 spoof Dracula: Dead and Loving It, in which two appear, and Dracula (1958) and Drakula İstanbul'da, where a single bride appears. They are typically depicted as enchantingly beautiful young women, coquettish and seductive in manner, often appearing to men like succubi in the night, dressed in flowing silk nightgowns and behaving in a wild and sexually aggressive manner.
Although missing from the silent film Nosferatu, the Brides made silent appearances in the 1931 film Dracula and the Spanish language version of Drácula. (The latter film, shot simultaneously on the same sets at night with a separate cast and crew, depicts the brides as more obviously sexual than in the more chaste English-language version.)
The three brides are present but silent in the Jack Palance television adaptation although shown as a bit more ravenous as they attack Harker on sight. Dracula saves Harker from them the first time. But Harker is later caught while trying to escape the castle and thrown into their chambers. Upon awakening, Harker finds the brides waiting for him, they corner him easily and feed on him with no Dracula to stop them. Harker is later shown having died from this and became a ravenous vampire himself.
They had lines in the 1977 BBC production entitled Count Dracula. Dracula is a bit less antagonistic to them in this version, talking to them sternly yet gently and almost playfully.
In Francis Ford Coppola's 1992 film Bram Stoker's Dracula, the brides were played by Monica Bellucci, Michaela Bercu and Florina Kendrick. They lure Jonathan Harker to a secluded bedchamber in Dracula's castle before sexually abusing him in an erotic frenzy. When Dracula voyages to England to seduce Mina, Harker is given to The Brides. They keep him prisoner, draining just enough of his blood to keep him in an anaemic stupor. He eventually escapes them (a deleted scene shows Harker managing to bypass them by using a makeshift cross), and they are not seen again until a confrontation with Van Helsing in the Carpathian mountains, after which he beheads them. Bellucci, Bercu and Kendrick's dialogue was entirely in Romanian, and Kendrick reportedly helped her co-stars to speak her native tongue correctly.
While the Brides usually remain nameless, they are called Marishka, Aleera, and Verona (played by actresses Josie Maran, Elena Anaya and Silvia Colloca, respectively) in the 2004 film Van Helsing. For the first time, the Brides are more than brief background, becoming important minions of Dracula and powerful combatants. In Van Helsing, both Dracula and his Brides have the ability to transform into large winged monsters.
The concept was also present in the 1987 horror comedy The Monster Squad, where Dracula has abducted three young women (Mary Albee, Joan-Carrol Baron, and Julie Merrill) and turns them into his vampire brides.
In Dracula 2000, the Brides are composed of Dracula victims he bites upon his awakening and journeying to New Orleans. They include Solina (Jennifer Esposito), a thief who was part of a group mistaking his coffin for a treasure chest. Dracula seduces and bites her during the plane ride along with the rest of group. Valerie Sharpe (Jeri Ryan), a news reporter covering the plane crash that was carrying his coffin. Dracula awakens, kills her camera man before turning her. and Lucy Westerman (Colleen Fitzpatrick), Mary's roommate whom Dracula meets while tracking her, she's seduced and turned during sex with Dracula. The three help Dracula capture Mary but are killed during the final confrontation. Valeria by a stake, Solina and Lucy by decapitation.
The Brides also appeared in the Buffy The Vampire Slayer in the season 5 premier "Buffy vs. Dracula". They were referred to as "The Three Sisters." As Buffy fights Dracula, the Brides work to "distract" Giles from coming to her aid. They are credited as "Vampire Girls" and played by Marita Schaub, Leslee Jean Matta, and Jennifer Slimko.
They appear in Dracula, the musical where they sing Forever Young and have intricate and elaborate flying sequences.
They also appear in the French Canadian musical Dracula - Entre l'amour et la mort played by Rita Tabbakh, Elyzabeth Diaga, Brigitte Marchand, and Casiopée.
They also appear in the 2002 Italian adaption of Dracula (Known as Dracula's Curse in foreign markets), Like the 1992 version they speak in their native tongue and play up their supernatural nature by being able to fly and phase through objects.
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In literature
In Fangland, author John Marks re-imagines the Brides of Dracula as Greek brothers.
In the alternate history novel Anno Dracula, Dracula becomes dominant in Britain and eventually weds Queen Victoria, becoming Prince consort and Lord Protector. Despite being married to Victoria he keeps his retinue of brides, who despise the now-powerless and chained Victoria. It is mentioned that one of the brides is Barbara of Celje.
In the first sequel, The Bloody Red Baron, the Brides of Dracula are mentioned as including Mata Hari, Lady Marikova (from the novel The House of Dracula by Ronald Chetwynd-Hayes), Lola-Lola (from the film The Blue Angel), Sadie Thompson, Lemora, and the Baron Meinster (from the film The Brides of Dracula).
In the beginning of the second sequel, Dracula Cha Cha Cha, a list of Dracula's official brides is given. They are: Elisabeta of Transylvania (from Bram Stoker's Dracula), 1448–1462; Ilona Szilagy (Vlad III's real-life second wife), 1466–1476; Marguerite Chopin of Courtempierre (from Vampyr), 1709–1711; Queen Victoria, 1886–1888; and Sari Gábor, 1948-1949. The plot surrounds Dracula's engagement to Princess Asa Vajda (from Black Sunday).
Chelsea Quinn Yarbro has written a trilogy called Sisters of the Night, with each book featuring the story of one of brides: Kelene: The Angry Angel (1998), Fenice: The Soul of an Angel (1999) and Zhameni: The Angel of Death (unpublished).[4]
In The Diaries of the Family Dracul by Jeanne Kalogridis, the Brides are imagined as Zsuzsanna Tsepesh, a descendant of Vlad Dracul (believed in the novels to be his niece); Dunya, a Transylvanian servant of Vlad's mortal descendants, and Elisabeth Bathory, the notorious Hungarian noblewoman who murdered hundreds of her servants and bathed in their blood.
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In comic books
A number of brides are seen in the Marvel Comics series, The Tomb of Dracula ranging from victims long since turned from ancient times to recent ones of modern day. Likewise in the follow up series Dracula Lives, a two part story in particular called The Pit of Death in which the protagonist is thrown into the titular pit where many of Dracula's brides are kept, among them his blind wife.
The Brides are seen in the DC Comics mini series, Victorian Undead II: Sherlock Holmes vs Dracula. Led by Lucy Westenra, they attack the heroes when they come to search their lair.
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1. ^ Dracula, pg 47 "I dared not wait to see him return, for I feared to see those weird sisters",pg 244 "He come on moonlight rays as elemental dust, as again Jonathan saw those sisters in the castle of Dracula pg 377 "Then I braced myself again to my horrid task, and found by wrenching away tomb tops one other of the sisters, the other dark one. I dared not pause to look on her as I had on her sister, lest once more I should begin to be enthrall. But I go on searching until, presently, I find in a high great tomb as if made to one much beloved that other fair sister which, like Jonathan I had seen to gather herself out of the atoms of the mist. She was so fair to look on, so radiantly beautiful, so exquisitely voluptuous, that the very instinct of man in me, which calls some of my sex to love and to protect one of hers, made my head whirl with new emotion."
2. ^ Dracula, pg 38
3. ^ Jan B. Gordon's "The Transparency of Dracula", in Bram Stoker's Dracula: Sucking Through the Century, 1897-1997, edited by Carol Margaret Davison.
4. ^ http://www.chelseaquinnyarbro.net/biblio_alpha.html
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Last modified on 4 May 2013, at 11:32
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Saban: Nothing has changed for Alabama after romp
TUSCALOOSA, Ala. (AP) -- Alabama coach Nick Saban is quick to deliver a reality check when the latest opponent can't.
The No. 2 Crimson Tide's restocked defense came up with big plays, accomplished its primary goal of containing quarterback Denard Robinson. The unit also looked similarly formidable to last year's group in Saturday night's opening win over No. 8 Michigan.
Enter Saban, who wants to ensure reporters and players alike know that the perception outside the football building is all that's changed.
''Everyone thought we were too young, too inexperienced, couldn't handle success,'' Saban said Monday. ''Everybody was saying all those things about our team. Now, people are saying something different. But my question is what's different? Nothing.
''We're still young, we're still inexperienced. We've still got things to work on. It's going to be all about the maturity that the team has to be able to focus on what they need to do to correct the deficits that we have.''
Convincing the team might be easier than fans who watched the dominant performance.
The defending national champions looked every bit the part of a contender in that 41-14 romp after facing an offseason of questions starting with a defense replacing four high NFL draft picks and eight starters. Experience, not talent, was the question.
The main charge was to contain Michigan's Robinson. Alabama accomplished that mission except for one long ball apiece yielded by the starting cornerbacks, Dee Milliner and Deion Belue.
The Wolverines still managed just 269 yards, 115 on those two plays.
The next day, Saban brought the Tide back to earth ahead of Saturday's visit from Western Kentucky.
''He told us that that was just the first game, so don't get all hyped up about that because we've got a lot more games to come and we've got a lot more improvement to do,'' linebacker C.J. Mosley said.
Milliner fell down on a 44-yarder from Robinson and Belue, a junior college transfer, gave up a 71-yarder in the first half.
Saban noted that wasn't all on the cornerbacks. Both those plays came on double moves from the receiver, which left an instant longer for the defensive front to pressure Robinson. One came on a blitz that couldn't reach him in time.
Even if Western Kentucky can't make Alabama pay on plays like that, a visit to No. 10 Arkansas and quarterback Tyler Wilson comes next.
''There's a lot of things we need to fix, there's a lot of things they did well'' Saban said. ''They played hard, they were physical. They did a good job of stopping the run, which was the goal in the game.
''The goal of the game was not to let the quarterback run the ball. He didn't have very many opportunities to run it. Even on his zone option reads we were sort of making it so he was going to hand the ball off and make somebody else beat us. We did a good job of executing the game plan.''
Building a 31-0 lead allowed Alabama to get some youngsters from the latest highly rated recruiting class to get onto the field. That includes players who could be relied on to provide depth such as Belue's backup Geno Smith, No. 2 linebacker Denzel Devall and safety Landon Collins.
Alabama had to replace three first-round draft picks and early second-rounder Courtney Upshaw from a defense that led the nation in all the major statistical categories.
The Tide's defense featured a number of sophomores thrust into bigger roles - including safeties Ha Ha Clinton-Dix and Vinnie Sunseri and linebackers Xzavier Dickson and Adrian Hubbard. Saban's mixed reviews certainly applied. For instance, Sunseri perfectly read an option play to stuff a third-down run in the third quarter but also jumped offsides on a blitz.
Center Barrett Jones has seen the group develop leading up to the season, and wasn't surprised with the initial result.
''We felt very confident with our defense,'' Jones said. ''It didn't feel too much different out there. They got us the ball in good field position. They did a lot of great things out there. Got a lot of stops, lot of three-and-outs, turnovers. We were very pleased with them. We couldn't have asked for much more from them.''
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Friday, June 04, 2004
Kevin and Me
Most days, I’m pretty much on the same
wavelength as Kevin Drum (Washington Monthly’s Political Animal) when it comes to political discourse. Any disagreements I might have with Kevin's opinions are usually more semantic in nature than anything else, even though Kevin certainly tacks a wee bit to the right of me.
Today, though, we depart in opinion.
Kevin has compiled a short and fairly accurate analysis of the current issues with oil supplies. He specifically looks at the situation from the demand side (where any such discussion should start), and compares historic demand for oil with capacity to produce it. What was a bit of an eye opener for me was his demand / capacity graph. Looking at the graph from a historic perspective, it's clear as a bell that the West is heading for some rough waters. In Kevin's analysis, you should enjoy your $2.25 gas, because it looks like prices will (long term) be headed increasingly upward. He even takes a pretty good swing at why demand has become so skewed - and it isn't all the fault of the West.
On these issues we agree. And I'll give Kevin this - he tries to look at all sides of the Rubik's cube. Our departure in opinion is on solutions.
There are two ways to stabilize the situation: suck more oil out of the ground, and/or decrease demand.
Kevin posits that there are five key actions that could positively impact the demand/capacity imbalance:
The five key actions that Kevin lists are basically the same actions that the energy lobby supports, in one manner or another. What these actions, as a group, fail to do is bring what every consumer and business person everywhere needs more than lower prices: price predictability. I believe that it's not so much the high price that drives us nuts (although when I filled up this morning, watching the wheels spin on the gas pump meter was certainly on my mind), but the unpredictability of gasoline prices for our vehicles and natural gas / fuel oil to heat our homes in the winter.
The bottom line is that there is a finite supply of oil at present and predicted consumption rates (20 years? 50? 100?). At some point in time, as a species, we're going to have to decide to bite the bullet. I know that there's no political will to bite any friggin’ bullet, but I'd like to offer a reasonable start at a long term solution that at least brings predictability to the consumer, doesn't mortgage our energy future, doesn't rape the environment in our collective last gasp for more oil, eliminates a major flash point in world politics, and positions us, as a species, for the future.
The quickest and most reasonable way to solve energy problems in the long run is to adopt a sensible application of consumer energy taxes and tax credits - a carrot and stick approach to solving the energy problems once and for all. One (a tax) won't work without the other (tax credits). Here's my "non-economist" view of how it works:
1. Raise the tax on consumer energy products (gasoline, natural gas, fuel oil, etc.), and make the tax a variable tax - in other words, as the market price for oil increases, the tax rate decreases. Vice-versa, as the market price for oil decreases, the tax rate increases. Effectively, then, the price of finished oil products to the consumer is stabilized, regardless of market or seasonal fluctuations. A portion of the tax could be utilized for R&D on alternative energy sources - for example, fuel cell technology that is actually, and economically, scalable.
2. Offer significant tax credits for use / purchase of non-fossil fuel alternative energy sources.
3. Offer credits for purchase of hybrid / alternative energy vehicles.
4. Offer significant tax credits for fuel conservation purchases - I'll give you an example - let's say I have a 15 year old central air system in my house. Now, I know inherently that if I replaced the system with current technology, I'd probably save a significant amount of energy dollars over the course of a year. But the initial outlay is so high that I'm willing to limp along with the old unit until it gives up the ghost. Now, if I had the ability to write off say, an amount equal to the differential in energy costs for a year, now that would be some incentive to change out my old power hog, and to buy the most energy efficient unit possible.
That's a starting point, anyway. It's fair, reasonably equitable, reduces demand, and rewards both efficiency and development of alternative energy sources. (Sidebar: Can you imagine what kind of impact the investment of $200 billion in alternative energy research would have in actually bringing some of these technologies to market. $200 billion is what we've expended in Iraq, to date.)
But, but, but. The above isn't my biggest point of departure with Kevin Drum. The following paragraph at the end of his posting is what tweaked me:
Liberals can help too. How about a deal that trades ANWR drilling for higher CAFE standards, for example? Sounds horrible, doesn't it? But it might be a politically feasible trade, and in the end the benefit from higher mileage cars probably vastly outweighs the negatives of another pipeline in Alaska. Consider it food for thought.
What Kevin views as a "trade", I view as abject capitulation. CAFE (auto fuel efficiency standards) for ANWR is not a tradeoff -- it's an environmental Faustian bargain.
I'm no longer willing to concede the need for raping ANWR or any other scrap of the planet in our increasingly urgent quest for the last drop of oil. We long ago reached a point of diminishing returns in what we get for both money invested in oil exploration / drilling -- and the vulnerability this quest brings to the environment around us has become unacceptable. Again, it's way past time to quit whistling past the energy graveyard. We've reached a critical convergence of world politics, energy politics, and environmental politics, and someone in a powerful position needs to stand up at a podium and say so.
I believe President Gore would have done just that. George Bush would drink a gallon of Texas Light crude before he would admit there's a big problem that needs more than a bandaid solution. And I don't think John Kerry will take any significant steps in that direction, either, at least not without a clear mandate to do so and at least one (cough, cough...Democratic Party) house of congress behind him.
Yeah, I know, I'm a goddam pollyanna. Perhaps Kevin is more of a realist than myself, and that's OK, too. What I do know is that even if we, as a species, decided to make the commitment to change today, the upside of being forced into the future probably wouldn't be realized in my lifetime.
But we've gotta start somewhere. The discussion has to start somewhere, sometime, and and that sometime needs to be sooner than later.
Why not now?
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Fun with Purple
OK, the movie Purple: Organized Crime in aSmallTown, has come and gone leaving behind renewed interest in Clare’s gangster past.
I wrote a column a few weeks ago about Meyer Lansky, who was called “the chairman of the board” of organized crime inAmericaand his partnership with long time Clare resident Sam Garfield. Yes, Clare had a big time gangster operating here [at least some of the time] but no, he wasn’t a Purple. In fact Clare’s organized crime involvement came years after the Purple Gang had faded away.
The Purple Gang, however, sounds romantic while money laundering through oil leases is a snoozer.The result is an attempt to connect two separate historical happenings [The Purples & Clares gangsters] that were years apart to make a better story.
The Purple Gang was a short lived outfit. It came to prominence inDetroitabout 1927 and by 1932 had virtually disappeared. The Purples were unique in that they were the only Jewish gang to dominate an entire city. In other places the Irish, Jewish, and Sicilian gangs either fought each other [Capone vs. O’Bannon, St. Valentines Day massacre] or combined in alliances like Meyer Lansky and Luck Luciano inNew York.
The Purples were a creation of Prohibition. They were largely a family operation. Ray Bernstein was the founder. When he was convicted of murder and went to prison his son Abe took over. The Bernstein’s, Abe, Ray, Joey, and Izzy were the core of the gang. Other family’s, the Kewell’s and Fleisher’s made up the balance. Compared to Capone and his organization the Purples were remarkably small.
The Purples were extraordinarily violent. They were predatory and went after other gangs, and even their own members. In 1931 a group of three Purples had broken away and formed what was called The Little Jewish Navy. They ran liquor across the Detroit River in small boats. Lured to an apartment by the Purples, the three were murdered in what came to be called The Collingwood Massacre. This was the last straw and the State ofMichiganand City ofDetroitcops came down on them hard. When they got through, most of the Purples were in prison and the gang was a shadow of its former self.
With the Purples vulnerable, Joe Zirilli and the Italians decided to take over their territory. After killing a few Purples, they succeeded. By 1932 the Purple Gang as a meaningful force inDetroitcrime was gone.
While all of this was going on inDetroit, Meyer Lansky was operating a gambling operation out ofManhattan. He wasn’t a Purple and he wasn’t in the liquor business. He was partnered up with Lucky Luciano, not the Bernstein’s.
It wasn’t until 1964, 33 years after the Purples ended that Meyer
Lansky came to Clare and joined Sam Garfield in the oil business.Garfield’s money probably came from his association withLas Vegasmobster, Moe Dalitz. Even though they knew each other fromDetroit, they were connected withClevelandandOhiomobs rather thanDetroit. Certainly not with thugs like the Purples.
Now there’s a website that claims that after prohibition gangsters “took over the Doherty Hotel.” They didn’t. A.J. Doherty likes to let people think that because it makes a more romantic story for the hotel. But no, gangsters never took over anything in Clare, let alone the Doherty Hotel.
And no,Livingstonkilling Isaiah Leebove didn’t have anything to do with the Purples or organized crime. These were just two shady oil guys, one of whom was nuts and a drunk. If the shooting hadn’t taken place in the Doherty Hotel Bar in front of people it wouldn’t have been noticed. Now it’s part of our folklore.
So, Clare did have a connection with organized crime on its very highest levels, but that was 33 years after the Purples and Prohibition. Did any of these people know each other back then?
Probably. One of the Bernstein’s worked for Sam Garfield at Mammoth Producing, his oil company. But mainly they operated in different cities and in different criminal businesses. Lansky/Luciano [of Murder Incorporated fame] inNew Yorkgambling, and the Purples inDetroitsmuggling liquor.Garfield was in basketball gambling and various semi-legal enterprises inOhio. He was also an investor in the Havana Hilton.
I know that Forrest Meek, who died two weeks ago, was researching a book he was going to call Purple Crude which would be about organized crime and the oil business. He never finished his research but I’m presuming a great deal of his work found its way into the documentary film many of you saw. I wish he’d finished the book. I’d have been first in line to buy it.
So, even if the connections are tenuous, and the facts a little shaky, the Purple Gang in Clare makes a great story and should provide us with years of entertainment. Thanks to Forrest Meek and moviemaker Ben Tigner for adding a little color and fun to our history.
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Reply to a comment
Reply to this comment
valandingham1 writes:
Why did this Horse Owner not Dispose of the Horses before it could cause damage to the Bold Eagles and possibly other Wild Life in the Area?
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Navigational Differences Between Men and Women
Are there any differences in the abilities of men and women to navigate?
Anyone who has sat in the front of a car with someone of the opposite sex is likely to have an opinion on this subject, although to be honest it is not something that I had given a huge amount of thought to before I was asked live on national radio. Men and women have been signing up for my courses in roughly equal numbers since, so I do not think I offended too many people in my answer. Although I am still a long way from having any final or definitive answers to this question, I have certainly taken more of an interest since.
Looking for answers to this in history is fraught with problems. There are sexist biases in most earlier cultures and the record itself is often biased towards the male perspective, ‘the powerful role of women, moreover, has been virtually ignored’. We find this bias woven into the world around some cultures. The Innuit see the steady east-southeast wind as male, but the temperamental west-northwest wind as female. The Gwi of the Kalahari know a male rain that is hard and driving, it ‘shouts loudly’ and comes from thunderstorms. There is also a female rain which is steadier, ‘speaks softly and is gentle’.
The roles of men and women have tended to favour men’s opportunities to improve their navigational ability, but not universally as Colonel Dodge noticed when observing the Native Americans in the 19th century,
‘The older women have a vast amount of outdoor work, hunting up stray ponies, etc., particularly in winter, when it is too cold for her lord and master to be out, or when he is probably losing the stray animals at the gaming-table.’
Some cultures have also recognized that the people who are chosen to do the navigating may not be the best ones to pass on that knowledge. In the Australian outback Lindsay discovered that the men made poor teachers and the ‘best of all instructors is an Aboriginal woman who has taught the art to many children in her time.’ This may be the reason that in some Pacific myths navigation is the gift of women.
The relationship between sex, our place in the universe and our journeys in it has long been an imperfect one and although always changing the modern age has obviously not ironed out all biases. In the late sixties S. Jocelyn Bell Burnell worked to help discover the strange and ‘phenomenal objects’ in the universe that are now known as pulsars,
It remains a contentious area. Even if we appreciate that opportunities in the workplace should be equal, it does not mean that the two sexes are equal in all innate abilities. Men do, on average, run faster and have a reputation for being more aggressive. Women have a better sense of smell and a reputation for being able to do more than one thing at a time. The world is a much more interesting place because of the differences and fairer one for not deciding everything on the basis of irrelevant ones.
Part of the challenge is that we live in a society that recognizes male and female strengths and abilities more fairly, if not perfectly, than has historically been the case, but we are interested in an ability that may have been shaped prior to such developments. Even if there was no genetic difference at one stage of human development that does not rule out the possibility that sociological and anthropological conditions introduced them. If a woman’s genes were more likely to be passed on by her physical appearance than her hunting and foraging ability then those are the genes that would be favoured and vice versa. That may not represent the world we live in now, but it may be the one that our genes have all sprung from. So are there any differences?
‘Whenever a sexual difference has been found, most spatial tests on humans, of whatever age, have shown males to be more adept than females.’
This quote by the scientist, Robin Baker, who led research into human navigational ability, seems fairly conclusive. As ever it is not quite so simple. Baker discovered that although men often performed better than women in the tests it was not necessarily due to any inherent ability, but because of their reading of external cues, which may have been due to experience. In one experiment the women’s ability to orientate themselves actually deteriorated after a blindfold was taken off. Women were relying on intuition more than the men who were improving their ability to find direction by using external clues like the sun and the wind. Conversely, women proved more effective at navigating in situations where external clues could not be used. They were better able to orientate themselves at the end of short journeys as a blindfolded passenger for example.
If, as Baker suggests, these differences are due to natural selection then it can be traced back through primitive behaviour to monkeys. The male traits being consistent with the ‘solitary long-distance exploration’ that is more prevalent in males of tribes across the world as well as primates like the Japanese Macaque.
This is where my reading of the situation diverges from Baker’s and the probably the scientific community as a whole. I should emphasise that I have not conducted any rigorous scientific experiments to date.
When I fell in love with the subject of natural navigation it was because it addressed a desire in me to reconcile a scientific, pragmatic view of the world with something more fundamental, perhaps even primeval and certainly holistic. Science can explain why a wind blows, but I doubt that it will ever properly explain the desire I sometimes have to go for a walk on a windy day. My research into and experience of the subject has always needed to veer between the scientific to the experiential. I think for this reason I have a different theory as to differences in navigational ability between men and women in this area.
The first thing I should say is that I believe a lot of the differences in ability between individuals can be accounted for in a non-gender-specific way. The individual attributes, aptitudes and characters, of men and women overlap so thoroughly that any attempt to isolate individual traits will have very widespread exceptions. If I describe an aggressive muscular mathematician with facial hair and a body-odour problem, then female readers may rush to disown them, but they cannot do so with total authority.
A key difference between individuals is what is sometimes referred to as ‘left brain’ or ‘right brain’ thinking or an analytical versus intuitive approach. I think this may help to understand not just the difference between some men and women in this area, but individuals generally and may possibly hold the key to navigating more effectively and at the very least enjoying the process more. This is how.
I do believe that most people have a bias towards either objective analytical thought (left-brain) or intuitive holistic subjective thought (right-brain). I do also believe that there is a slight bias towards left-brain thinking in men and right-brain thinking in women. Natural navigation tends to favour those that do not hold onto one type of thinking too religiously. My experience in the field has proven, to my own satisfaction, that both approaches have severe limitations and that a full and accurate picture can best be built up by trying to improve your weaker side. Let’s look at an example.
A test that I have conducted with dozens of men and women is to ask them to look at a photograph of a country house, taken in low light, and then ask in which direction the picture is taken. There are numerous rational logical clues including a low sun on the left side of the picture. There are also some holistic clues that can only be spotted by thinking beyond the physical, these include the orientation of the garden and the fact that there are a lot of lights on in the house.
Men and women have faired equally well in this task, but the approach is subtly different. Men favour the physical clues, women favour the holistic. I made one discovery by accident, because the large laminated photos were quite expensive to produce I only had five printed. This meant when teaching a group of twenty it was necessary to form teams. I did this by convenience, grouping people according to where they were sat in the room. This meant that there have been some all-male teams, some all-female teams and some mixed groups.
Something that I began to notice is that the all-male teams were quite regularly getting it confidently right or wrong and the all-female teams were getting it hesitantly right and wrong, but slightly more were getting it right than the all-male teams. The mixed teams often managed to get it confidently right.
The all-male teams saw the low sun and focused on this, making the fair assumption that it was the start or end of the day. The objective analytic clues to back this up were a lot more difficult, including tree shape and faint stars. The men were therefore getting divided in their ability to work out whether it was dawn or dusk, but settled on one.
The all-female teams also saw the sun and made a similar assessment but then tended to jump to a more holistic view that took into account human behaviour. There is a large garden in the photograph foreground and all the lights in the house were on. The holistic assessment often went along the lines of: most people like to have a south-facing garden and nobody turns all the lights on in a house at dawn.
The mixed teams often used the holistic view to back up observations of a more analytical nature. The shape of the trees and other clues do fit a north-facing pattern quite readily when you have the idea about the lights or the garden to work with.
This is only anecdotal, there is no academically valid data that I have accumulated, only what I have observed – this is mainly because at the time of these observations I am being paid to teach, not research. It would also be fair to say that many individuals and groups have gone against this model, but if I was to bet on a team confidently solving the puzzle then it would be a mixed team.
The lesson for all of us if there is one in this is that it is very helpful in natural navigation, and probably other natural challenges, to understand whether we have a left or right-brain bias and to not let that dictate our every thought. Nature reveals clues in equal measure to an objective analytical approach and a subjective holistic one, if we charge ahead with only one of these we are likely to miss half the picture.
Back to Library
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| 61
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Health knowledge made personal
Ron Unger Patient Expert
According to what has been called the medical model, people who have been diagnosed with "schizophrenia" and with "psychosis" in general, have a brain disease or chemical imbalance. Past life experience such as trauma, according to that model, has nothing to do with why... Full Bio
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http://www.wellsphere.com/ron-unger/134421/bookmarks
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08 March 2011
Drilling in Gulf is dangerous and unmanageable
Marilyn Clark, a Magdalen Islander studying at Memorial University, argues that oil and gas exploration in the Gulf of St. Lawrence is unmanageable and dangerous in the current regulatory context.
She writes in the Montreal Gazette:
What will governance look like with four offshore regulators in less than 500 kilometres of water? If we believe that Quebec and Newfoundland will cooperate to prioritize citizens, we are kidding ourselves. They have already sliced moving water down the middle to conduct their environmental assessments.
The lack of a harmonized approach for a single body of water will permit pollution without political accountability; the citizens of one province will have no way of holding the governments of other provinces responsible.
Why is the government gambling with the assets of my region, while the renewable resources of southwest Nova Scotia and British Columbia are protected? The Gulf only fully flushes itself out once a year. If drill cuttings, waste water and chronic spills are the new ingredients of our Gulf, we will be importing our lobster from the Caribbean and our crab from Asia. How can I be expected to invest in my region when I know that the offshore regulatory framework is so flawed that oil companies monitor themselves?
- srbp -
No comments:
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In our busy lives, we see people on a daily basis or every couple of days for a short time and we move on.
Many times it is about the same time of day and in the same place. We check in with them, perhaps talking about common interests, the weather, what we did or what we are going to do. Pretty simple.
But there are those people who have a "joie de vivre" about them and they make your encounter with them just a bit more special. So here are some people I see on a regular basis on my "dawn patrols" who bring a smile and good feeling with them as they start the day. These three people are part of the greater Monterey "dawn patrol." They get an early morning start to their day's events and are usually seen with a smile, which is passed on to others.
Pete is a surfer, surfboard entrepreneur, blogger and retired educator who I see maybe three to five days a week walking the streets of Monterey in the early morning. Whether it be foggy, sunny or wet, Pete is usually on the streets by 7 a.m., dressed in his green coordinated workout wear.
Pete was a world class Rugby player, legendary high school football coach and currently is a retired gentleman of leisure, who dabbles in what he wants to dabble in. When we talk, it is usually about surfing-related events, activities, people or our travels. When we go on to our separate ways, I have a good feeling of connection and it appears that we both like what we are doing, if only we could lose a few pounds that retirement has bestowed upon us.
Solomon is a joy to see in the morning, as he is always in the "up position." He knows more people in Monterey, does more in the Monterey community being involved in all types of events, and goes the extra distance in supporting individuals in need.
I have termed every Friday "Happy Solomon Day" as that is the day he works at the Sports Center and it brings a smile to all who enter. I see Solomon walking the recreation trail with his wife, Kathy, as well as running into him in many different places from Big Sur, walking in Pacific Grove to patrolling the aisles of Costco. Saying "good morning" and talking with Solomon is like a breath of fresh air. He is always in a good mood and it is passed on to others.
Bucky does his "dawn patrol" usually at Asilomar Beach, but can also be seen at Carmel parked on Scenic and the Dunes parking lot in Pebble Beach checking out the surf conditions. Bucky defies the aging process by going out in big wave conditions, where younger surfers, just sit and watch.
Bucky's day job is in the golf industry, and he can pick and choose his work schedule depending on the surf. Bucky has a fluid "old school" style of surfing, yet he is right there when it comes to positioning on a wave. There is a flow in his movements on a wave that define surfing grace, style and knowledge.
Bucky and I share a love of reading papers, while we check the surf, as we wait for the tide to change. I pass on my San Francisco Chronicle to him and if he is out surfing, I will stick it on his windshield under the wipers.
Surfers can be a moody lot, especially when there is no surf. Bucky is a bright spot as he is always in a good mood, whether the surf is up or down. I have seen him even get a smile out of several of the perennial sourpuss younger surfers. As an older surfer, Bucky is given a lot of respect not so much for his age, but for his surfing ability, knowledge and experience. A day in the water, or a go out with Bucky, is a great "feel good" session because of the positive friendly "vibes" he has.
So if you have people in your life who make your day better with a great start, let them know how you appreciate seeing them.
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| 541
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The EFF and NSA will square off in court yet again
Comments Threshold
RE: Good Luck EFF
By Don Tonino on 9/19/2008 9:50:55 AM , Rating: 2
Usually that is done with the knowledge and authorization of the judicial system, so there's a check to what the government is rightfully allowed to monitor. True, there have been many cases of illegal wirings and taps, but as far as I've heard illegal was the word defining it.
I do welcome any useful informations on any systematic monitoring going on though, as I readily admit not knowing much about that (and being willing to get to know more)
Anyway, if something is perceived (or it actually is) wrong or illegal, it doesn't make it any better if it's done somewhere else by someone else. If EU countries were to have the same activities going on, to me they would be equally wrong in doing that.
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| 5,539
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Year of Publication
1. sRAGE Induces Human Monocyte Survival and Differentiation
The receptor for advanced glycation end products (RAGE) is produced either as a transmembrane or soluble form (sRAGE). Substantial evidence supports a role for RAGE and its ligands in disease. sRAGE is reported to be a competitive, negative regulator of membrane RAGE activation, inhibiting ligand binding. However, some reports indicate that sRAGE is associated with inflammatory disease. We sought to define the biological function of sRAGE on inflammatory cell recruitment, survival, and differentiation in vivo and in vitro. To test the in vivo impact of sRAGE, the recombinant protein was intratracheally administered to mice, which demonstrated monocyte- and neutrophil-mediated lung inflammation. We also observed that sRAGE induced human monocyte and neutrophil migration in vitro. Human monocytes treated with sRAGE produced proinflammatory cytokines and chemokines. Our data demonstrated that sRAGE directly bound human monocytes and monocyte-derived macrophages. Binding of sRAGE to monocytes promoted their survival and differentiation to macrophages. Furthermore, sRAGE binding to cells increased during maturation, which was similar in freshly isolated mouse monocytes compared with mature tissue macrophages. Because sRAGE activated cell survival and differentiation, we examined intracellular pathways that were activated by sRAGE. In primary human monocytes and macrophages, sRAGE treatment activated Akt, Erk, and NF-κB, and their activation appeared to be critical for cell survival and differentiation. Our data suggest a novel role for sRAGE in monocyte- and neutrophil-mediated inflammation and mononuclear phagocyte survival and differentiation.
PMCID: PMC3671884 PMID: 20574008
2. Organ-derived coatings on electrospun nanofibers as ex vivo microenvironments
Biomaterials 2010;32(2):538-546.
Idiopathic pulmonary fibrosis (IPF) is an interstitial lung disease characterized by irreversible scarring. Collagen deposition, myofibroblast expansion, and the development of fibroblastic foci are the hallmark pathological events. The origin and mechanism of recruitment of myofibroblasts, the key cell contributing to these events, is unknown. We hypothesize that the fibrotic lung microenvironment causes differentiation of arriving bone marrow-derived cells into myofibroblasts. Therefore, a method of isolating the effects of fibrotic microenvironment components on various cell types was developed. Electrospun nanofibers were coated with lung extracts from fibrotic or nonfibrotic mice and used to determine effects on bone marrow cells from naïve mice. Varying moduli nanofibers were also employed to determine matrix stiffness effects on these cells. At structured time points, bone marrow cell morphology was recorded and changes in fibrotic gene expression determined by real-time PCR. Cells plated on extracts isolated from fibrotic murine lungs secreted larger amounts of extracellular matrix, adopted a fibroblastic morphology, and exhibited increased myofibroblast gene expression after 8 and 14 days; cells plated on extracts from nonfibrotic lungs did not. Similar results were observed when the nanofiber modulus was increased. This ex vivo system appears to recapitulate the three-dimensional fibrotic lung microenvironment.
PMCID: PMC3671867 PMID: 20875916
Fibrosis; ECM; Electrospinning; Polycaprolactone; Fibroblast; Three-dimensional cell culture
3. Chronic Restraint Stress Upregulates Erythropoiesis through Glucocorticoid Stimulation
PLoS ONE 2013;8(10):e77935.
In response to elevated glucocorticoid levels, erythroid progenitors rapidly expand to produce large numbers of young erythrocytes. Previous work demonstrates hematopoietic changes in rodents exposed to various physical and psychological stressors, however, the effects of chronic psychological stress on erythropoiesis has not be delineated. We employed laboratory, clinical and genomic analyses of a murine model of chronic restraint stress (RST) to examine the influence of psychological stress on erythropoiesis. Mice exposed to RST demonstrated markers of early erythroid expansion involving the glucocorticoid receptor. In addition, these RST-exposed mice had increased numbers of circulating reticulocytes and increased erythropoiesis in primary and secondary erythroid tissues. Mice also showed increases in erythroid progenitor populations and elevated expression of the erythroid transcription factor KLF1 in these cells. Together this work reports some of the first evidence of psychological stress affecting erythroid homeostasis through glucocorticoid stimulation.
PMCID: PMC3799740 PMID: 24205034
4. Stabilization of HIF-2α induces sVEGFR-1 production from tumor-associated macrophages and decreases tumor growth in a murine melanoma model1
Macrophage secretion of VEGF in response to hypoxia contributes to tumor growth and angiogenesis. In addition to VEGF, hypoxic macrophages stimulated with GM-CSF secrete high levels of a soluble form of the VEGF receptor (sVEGFR-1), which neutralizes VEGF and inhibits its biological activity. Using mice with a monocyte/macrophage-selective deletion of HIF-1α or HIF-2α, we recently demonstrated that the anti-tumor response to GM-CSF was dependent on HIF-2α-driven sVEGFR-1 production by tumor-associated macrophages, while HIF-1α specifically regulated VEGF production. We therefore hypothesized that chemical stabilization of HIF-2α using an inhibitor of prolyl hydroxylase 3 (PHD3; an upstream inhibitor of HIF-2α activation) would increase sVEGFR-1 production from GM-CSF-stimulated macrophages. Treatment of macrophages with the PHD3 inhibitor AKB-6899 stabilized HIF-2α and increased sVEGFR-1 production from GM-CSF-treated macrophages, with no effect on HIF-1α accumulation or VEGF production. Treatment of B16F10 melanoma-bearing mice with GM-CSF and AKB-6899 significantly reduced tumor growth compared to either drug alone. Increased levels of sVEGFR-1 mRNA, but not VEGF mRNA, were detected within the tumors of GM-CSF- and AKB-6899-treated mice, correlating with decreased tumor vascularity. Finally, the anti-tumor and anti-angiogenic effects of AKB-6899 were abrogated when mice were simultaneously treated with a sVEGFR-1 neutralizing antibody. These results demonstrate that AKB-6899 decreases tumor growth and angiogenesis in response to GM-CSF by increasing sVEGFR-1 production from tumor-associated macrophages. Specific activation of HIF-2α can therefore decrease tumor growth and angiogenesis.
PMCID: PMC3436995 PMID: 22869907
5. In Vivo Monitoring of pH, Redox Status, and Glutathione Using L-Band EPR for Assessment of Therapeutic Effectiveness in Solid Tumors
Magnetic Resonance in Medicine 2011;67(6):1827-1836.
Approach for in vivo real-time assessment of tumor tissue extracellular pH (pHe), redox, and intracellular glutathione based on L-band EPR spectroscopy using dual function pH and redox nitroxide probe and disulfide nitroxide biradical, is described. These parameters were monitored in PyMT mice bearing breast cancer tumors during treatment with granulocyte macrophage colony-stimulating factor. It was observed that tumor pHe is about 0.4 pH units lower than that in normal mammary gland tissue. Treatment with granulocyte macrophage colony-stimulating factor decreased the value of pHe by 0.3 units compared with PBS control treatment. Tumor tissue reducing capacity and intracellular glutathione were elevated compared with normal mammary gland tissue. Granulocyte macrophage colony-stimulating factor treatment resulted in a decrease of the tumor tissue reducing capacity and intracellular glutathione content. In addition to spectroscopic studies, pHe mapping was performed using recently proposed variable frequency proton–electron double-resonance imaging. The pH mapping superimposed with MRI image supports probe localization in mammary gland/tumor tissue, shows high heterogeneity of tumor tissue pHe and a difference of about 0.4 pH units between average pHe values in tumor and normal mammary gland. In summary, the developed multifunctional approach allows for in vivo, noninvasive pHe, extracellular redox, and intracellular glutathione content monitoring during investigation of various therapeutic strategies for solid tumors. Magn Reson Med 000:000–000, 2011.
PMCID: PMC3305854 PMID: 22113626
solid tumors; bitroxides; glutathione; redox status; pH; L-Band EPR; PyMT mice; mammary gland; in vivo
6. The Role of the NADPH Oxidase Complex, p38 MAPK, and Akt in Regulating Human Monocyte/Macrophage Survival
M-CSF induces PI 3-kinase activation, resulting in reactive oxygen species (ROS) production. Previously, we reported that ROS mediate macrophage colony-stimulating factor (M-CSF)–induced extracellular regulated kinase (Erk) activation and monocyte survival. In this work, we hypothesized that M-CSF–stimulated ROS products modulated Akt1 and p38 activation. Furthermore, we sought to clarify the source of these ROS and the role of ROS and Akt in monocyte/macrophage survival. Macrophages from p47phox−/− mice, lacking a key component of the NADPH oxidase complex required for ROS generation, had reduced cell survival and Akt1 and p38 mitogen-activated protein kinase (MAPK) phosphorylation compared with wild-type macrophages in response to M-CSF stimulation, but had no difference in M-CSF–stimulated Erk. To understand how ROS affected monocyte survival and signaling, we observed that NAC and DPI decreased cell survival and Akt1 and p38 MAPK phosphorylation. Using bone marrow–derived macrophages from mice expressing constitutively activated Akt1 (Myr-Akt1) or transfecting Myr-Akt1 constructs into human peripheral monocytes, we concluded that Akt is a positive regulator of monocyte survival. Moreover, the p38 MAPK inhibitor, SB203580, inhibited p38 activity and M-CSF–induced monocyte survival. These findings demonstrate that ROS generated from the NADPH oxidase complex contribute to monocyte/macrophage survival induced by M-CSF via regulation of Akt and p38 MAPK.
PMCID: PMC1899309 PMID: 16931806
Akt; macrophage/monocyte; p47phox; p38 MAP; ROS
7. Program in pharmacogenomics at the Ohio State University Medical Center
Pharmacogenomics 2012;13(7):751-756.
Established in 2002, the Ohio State University Medical Center Program in Pharmacogenomics, lead by Wolfgang Sadee, is comprised of nearly 50 members dedicated to the discovery, investigation and translation of genetic biomarkers with the primary goal of advancing personalized healthcare. This article describes the research teams, bioinformatics infrastructure, supporting laboratories and Centers for Personalized Healthcare and for Clinical and Translational Science, current molecular genetic studies, translational and clinical pharmacogenomic studies, examples of biomarkers under development, and the future directions of the program.
PMCID: PMC3650730 PMID: 22594506
8. Pulmonary Fibrosis Inducer, Bleomycin, Causes Redox-Sensitive Activation of Phospholipase D and Cytotoxicity Through Formation of Bioactive Lipid Signal Mediator, Phosphatidic Acid, in Lung Microvascular Endothelial Cells
The mechanisms of lung microvascular complications and pulmonary hypertension known to be associated with idiopathic pulmonary fibrosis (IPF), a debilitating lung disease, are not known. Therefore, we investigated whether bleomycin, the widely used experimental IPF inducer, would be capable of activating phospholipase D (PLD) and generating the bioactive lipid signal-mediator phosphatidic acid (PA) in our established bovine lung microvascular endothelial cell (BLMVEC) model. Our results revealed that bleomycin induced the activation of PLD and generation of PA in a dose-dependent (5, 10, and 100 μg) and time-dependent (2-12 hours) fashion that were significantly attenuated by the PLD-specific inhibitor, 5-fluoro-2-indolyl des-chlorohalopemide (FIPI). PLD activation and PA generation induced by bleomycin (5 μg) were significantly attenuated by the thiol protectant (N-acetyl-L-cysteine), antioxidants, and iron chelators suggesting the role of reactive oxygen species (ROS), lipid peroxidation, and iron therein. Furthermore, our study demonstrated the formation of ROS and loss of glutathione (GSH) in cells following bleomycin treatment, confirming oxidative stress as a key player in the bleomycin-induced PLD activation and PA generation in ECs. More noticeably, PLD activation and PA generation were observed to happen upstream of bleomycin-induced cytotoxicity in BLMVECs, which was protected by FIPI. This was also supported by our current findings that exposure of cells to exogenous PA led to internalization of PA and cytotoxicity in BLMVECs. For the first time, this study revealed novel mechanism of the bleomycin-induced redox-sensitive activation of PLD that led to the generation of PA, which was capable of inducing lung EC cytotoxicity, thus suggesting possible bioactive lipid-signaling mechanism/mechanisms of microvascular disorders encountered in IPF.
PMCID: PMC3503147 PMID: 21131602
bioactive lipid signaling; interstitial pulmonary fibrosis; lung microvascular endothelial cell; oxidative stress; phosphatidic acid; phospholipase D; thiol redox
9. Transcription Factor ets-2 Plays an Important Role in the Pathogenesis of Pulmonary Fibrosis
Ets-2 is a ubiquitous transcription factor activated after phosphorylation at threonine-72. Previous studies highlighted the importance of phosphorylated ets-2 in lung inflammation and extracellular matrix remodeling, two pathways involved in pulmonary fibrosis. We hypothesized that phosphorylated ets-2 played an important role in pulmonary fibrosis, and we sought to determine the role of ets-2 in its pathogenesis. We challenged ets-2 (A72/A72) transgenic mice (harboring a mutated form of ets-2 at phosphorylation site threonine-72) and ets-2 (wild-type/wild-type [WT/WT]) control mice with sequential intraperitoneal injections of bleomycin, followed by quantitative measurements of lung fibrosis and inflammation and primary cell in vitro assays. Concentrations of phosphorylated ets-2 were detected via the single and dual immunohistochemical staining of murine lungs and lung sections from patients with idiopathic pulmonary fibrosis. Ets-2 (A72/A72) mice were protected from bleomycin-induced pulmonary fibrosis, compared with ets-2 (WT/WT) mice. This protection was characterized by decreased lung pathological abnormalities and the fibrotic gene expression of Type I collagen, Type III collagen, α–smooth muscle actin, and connective tissue growth factor. Immunohistochemical staining of lung sections from bleomycin-treated ets-2 (WT/WT) mice and from patients with idiopathic pulmonary fibrosis demonstrated increased staining of phosphorylated ets-2 that colocalized with Type I collagen expression and to fibroblastic foci. Lastly, primary lung fibroblasts from ets-2 (A72/A72) mice exhibited decreased expression of Type I collagen in response to stimulation with TGF-β, compared with fibroblasts from ets-2 (WT/WT) mice. These data indicate the importance of phosphorylated ets-2 in the pathogenesis of pulmonary fibrosis through the expression of Type I collagen and (myo)fibroblast activation.
PMCID: PMC3262682 PMID: 21562315
ets-2; Type I collagen; pulmonary fibrosis; bleomycin; fibroblast
10. The distribution of immunomodulatory cells in the lungs of patients with idiopathic pulmonary fibrosis
Modern Pathology 2011;25(3):416-433.
We have characterized the immune system involvement in the disease processes of idiopathic pulmonary fibrosis in novel ways. To do so, we analyzed lung tissue from 21 cases of idiopathic pulmonary fibrosis and 21 (non-fibrotic, non-cancerous) controls for immune cell and inflammation-related markers. The immunohistochemical analysis of the tissue was grouped by patterns of severity in disease pathology. There were significantly greater numbers of CD68+ and CD80+ cells, and significantly fewer CD3+, CD4+, and CD45RO+ cells in areas of relatively (histologically) normal lung in biopsies from idiopathic pulmonary fibrosis patients compared to controls. In zones of active disease, characterized by epithelial cell regeneration and fibrosis, there were significantly more cells expressing CD4, CD8, CD20, CD68, CD80, CCR6, S100, IL-17, tumor necrosis factor-α, and retinoic acid-related orphan receptors compared to histologically normal lung areas from idiopathic pulmonary fibrosis patients. Inflammation was implicated in these active regions by the cells that expressed retinoid orphan receptor-α, -β, and -γ, CCR6, and IL-17. The regenerating epithelial cells predominantly expressed these pro-inflammatory molecules, as evidenced by co-expression analyses with epithelial cytokeratins. Macrophages in pseudo-alveoli and CD3+ T cells in the fibrotic interstitium also expressed IL-17. Co-expression of IL-17 with retinoid orphan receptors, and epithelial cytoskeletal proteins, CD68, and CD3 in epithelial cells, macrophages, and T-cells, respectively, confirmed the production of IL-17 by these cell types. There was little staining for Foxp3, CD56, or CD34 in any idiopathic pulmonary fibrosis lung regions. The fibrotic regions had fewer immune cells overall. In summary, our study shows participation of innate and adaptive mononuclear cells in active-disease regions of idiopathic pulmonary fibrosis lung, where the regenerating epithelial cells appear to propagate inflammation. The regenerative mechanisms become skewed to ultimately result in lethal, fibrotic restriction of lung function.
PMCID: PMC3270219 PMID: 22037258
Idiopathic pulmonary fibrosis; co-expression analysis; immunohistochemistry; inflammation; IL-17; retinoic acid-related orphan receptors; usual interstitial pneumonia
11. HIF-2α regulates GM-CSF-derived sVEGFR-1 production from macrophages and inhibits tumor growth and angiogenesis1
Macrophage secretion of VEGF in response to the hypoxic tumor microenvironment contributes to tumor growth, angiogenesis, and metastasis. We have recently demonstrated that macrophages stimulated with GM-CSF at low O2 secrete high levels of a soluble form of the VEGF receptor (sVEGFR-1), which neutralizes VEGF and inhibits its biological activity. Using siRNA targeting to deplete HIF-1α or HIF-2α in murine macrophages, we found that macrophage production of sVEGFR-1 in response to low O2 was dependent on HIF-2α, while HIF-1α specifically regulated VEGF production. In our current report, we evaluated the growth of B16F10 malignant melanoma in mice with a monocyte/macrophage-selective deletion of HIF-1α or HIF-2α (HIF-1αflox/flox-or HIF-2αflox/+/LysMcre mice). GM-CSF treatment increased intra-tumoral VEGF and sVEGFR-1 in control mice, an effect that was associated with a decrease in microvessel density. GM-CSF treatment of HIF-1αflox/flox/LysMcre mice induced sVEGFR-1 but not VEGF, resulting in an overall greater reduction in tumor growth and angiogenesis compared to control mice. In addition, real-time PCR for melanoma-specific genes revealed a significantly reduced presence of lung micrometastases in HIF-1αflox/flox/LysMcre mice treated with GM-CSF. Conversely, GM-CSF treatment induced VEGF but not sVEGFR-1 in HIF-2αflox/+/LysMcre mice, and correspondingly, GM-CSF did not decrease tumor growth, angiogenesis, or lung metastasis in these mice. This study reveals opposing roles for the HIFs in the regulation of angiogenesis by tumor-associated macrophages, and suggests that administration of GM-CSF might be an effective means of inducing sVEGFR-1 and inhibiting tumor growth and angiogenesis in patients with melanoma.
PMCID: PMC3150377 PMID: 21765015
12. Towards a “4I” approach to personalized healthcare
Personalized healthcare holds the promise of ensuring that every patient receives optimal wellness promotion and clinical care based upon his or her unique and multi-factorial phenotype, informed by the most up-to-date and contextually relevant science. However, achieving this vision requires the management, analysis, and delivery of complex data, information, and knowledge. While there are well-established frameworks that serve to inform the pursuit of basic science, clinical, and translational research in support of the operationalization of the personalized healthcare paradigm, equivalent constructs that may enable biomedical informatics innovation and practice aligned with such objectives are noticeably sparse. In response to this gap in knowledge, we propose such a framework for the advancement of biomedical informatics in order to address the fundamental information needs of the personalized healthcare domain. This framework, which we refer to as a “4I” approach, emphasizes the pursuit of research and practice that is information-centric, integrative, interactive, and innovative.
PMCID: PMC3560982 PMID: 23369359
Individualized Medicine; Informatics; Organization & Administration
13. Mesenchymal Stem Cells for Cardiac Regeneration: Translation to Bedside Reality
Stem Cells International 2012;2012:646038.
Cardiovascular disease (CVD) is the leading cause of death worldwide. According to the World Health Organization (WHO), an estimate of 17.3 million people died from CVDs in 2008 and by 2030, the number of deaths is estimated to reach almost 23.6 million. Despite the development of a variety of treatment options, heart failure management has failed to inhibit myocardial scar formation and replace the lost cardiomyocyte mass with new functional contractile cells. This shortage is complicated by the limited ability of the heart for self-regeneration. Accordingly, novel management approaches have been introduced into the field of cardiovascular research, leading to the evolution of gene- and cell-based therapies. Stem cell-based therapy (aka, cardiomyoplasty) is a rapidly growing alternative for regenerating the damaged myocardium and attenuating ischemic heart disease. However, the optimal cell type to achieve this goal has not been established yet, even after a decade of cardiovascular stem cell research. Mesenchymal stem cells (MSCs) in particular have been extensively investigated as a potential therapeutic approach for cardiac regeneration, due to their distinctive characteristics. In this paper, we focus on the therapeutic applications of MSCs and their transition from the experimental benchside to the clinical bedside.
PMCID: PMC3382381 PMID: 22754578
14. Thrombospondin-1–Deficient Mice Are Not Protected from Bleomycin-Induced Pulmonary Fibrosis
Thrombospondin-1 (TSP-1) is an extracellular protein critical to normal lung homeostasis, and is reported to activate latent transforming growth factor-β (TGF-β). Because active TGF-β is causally involved in lung fibrosis after bleomycin challenge, alterations in TSP-1 may be relevant to pulmonary fibrosis. We sought to determine the effects of TSP-1 deficiency on the susceptibility to bleomycin-induced pulmonary fibrosis in a murine model. Age-matched and sex-matched C57BL/6 wild-type (WT) and TSP-1–deficient mice were treated twice weekly for 4 weeks with intraperitoneal bleomycin (0.035 U/g) or PBS, and were allowed to rest 1 week before being killed. Their lungs were inflated with PBS, fixed in formalin, paraffin-embedded, and sectioned. A certified veterinary pathologist blindly scored each slide for inflammation and fibrosis. Lungs were homogenized to obtain RNA and protein for the real-time RT-PCR analysis of connective tissue growth factor (CTGF) and collagen I, and for Western blotting to detect phospho-Smad2, or total Smad2/3, respectively. In response to bleomycin treatment, measures of fibrosis and inflammation, along with CTGF and collagen I mRNA concentrations, were increased in TSP-1–deficient mice compared with WT mice. Notably, Smad 2/3 signaling was of equal strength in WT and TSP-1 knockout mice treated with bleomycin, suggesting that TSP-1 is not required for the activation of TGF-β. These results demonstrate that TSP-1 deficiency does not protect mice from systemic bleomycin challenge, and that TSP-1 deficiency is associated with increased expression of lung collagen and CTGF.
PMCID: PMC3095927 PMID: 20581099
TSP-1; pulmonary fibrosis; TGF-β; bleomycin
15. Identifying Common Genes and Networks in Multi-Organ Fibrosis
Fibroproliferative diseases of organs are poorly understood and generally lack effective anti-fibrotic treatments. Our goal was to identify the key regulatory factors in pathologic fibrosis, common between organ-based fibrotic disease. We analyzed 9 microarray datasets publicly available in the GEO datasets from lung, heart, liver and kidney fibrotic disease tissue (489 microarrays total, disease and control). We identified a set of 90 genes differentially expressed in at least five microarray datasets. We used IPA and DAVID analysis to identify gene networks and their molecular functions. A mutual information based network work activity analysis showed that a connective tissue disorders network was the most active for all types of fibrosis included in this analysis. Conclusion: Our analysis indicates that despite different disease manifestation, organ fibrosis share a specific set of genes suggesting the potential for a common origin.
PMCID: PMC3392050 PMID: 22779061
16. Glucose variability and mortality in patients with sepsis*
Critical care medicine 2008;36(8):2316-2321.
Treatment and prevention of hyperglycemia has been advocated for subjects with sepsis. Glucose variability, rather than the glucose level, has also been shown to be an important factor associated with in-hospital mortality, in general, critically ill patients. Our objective was to determine the association between glucose variability and hospital mortality in septic patients and the expression of glucose variability that best reflects this risk.
Retrospective, single-center cohort study.
Academic, tertiary care hospital.
Adult subjects hospitalized for >1 day, with a diagnosis of sepsis were included.
Glucose variability was calculated for all subjects as the average and standard deviation of glucose, the mean amplitude of glycemic excursions, and the glycemic lability index. Hospital mortality was the primary outcome variable. Logistic regression was used to determine the odds of hospital death in relation to measures of glucose variability after adjustment for important covariates.
Main results
Of the methods used to measure glucose variability, the glycemic lability index had the best discrimination for mortality (area under the curve = 0.67, p < 0.001). After adjustment for confounders, including the number of organ failures and the occurrence of hypoglycemia, there was a significant interaction between glycemic lability index and average glucose level, and the odds of hospital mortality. Higher glycemic lability index was not independently associated with mortality among subjects with average glucose levels above the median for the cohort. However, subjects with increased glycemic lability index, but lower average glucose values had almost five-fold increased odds of hospital mortality (odds ratio = 4.73, 95% confidence interval = 2.6 – 8.7) compared with those with lower glycemic lability index.
Glucose variability is independently associated with hospital mortality in septic patients. Strategies to reduce glucose variability should be studied to determine whether they improve the outcomes of septic patients.
PMCID: PMC3176449 PMID: 18596625
sepsis; hyperglycemia; insulin therapy; mortality
17. An In Silico Modeling Approach to Understanding the Dynamics of Sarcoidosis
PLoS ONE 2011;6(5):e19544.
Sarcoidosis is a polygenic disease with diverse phenotypic presentations characterized by an abnormal antigen-mediated Th1 type immune response. At present, progress towards understanding sarcoidosis disease mechanisms and the development of novel treatments is limited by constraints attendant to conducting human research in a rare disease in the absence of relevant animal models. We sought to develop a computational model to enhance our understanding of the pathological mechanisms of and predict potential treatments of sarcoidosis.
Based upon the literature, we developed a computational model of known interactions between essential immune cells (antigen-presenting macrophages, effector and regulatory T cells) and cytokine mediators (IL-2, TNFα, IFNγ) of granulomatous inflammation during sarcoidosis. The dynamics of these interactions are described by a set of ordinary differential equations. The model predicts bistable switching behavior which is consistent with normal (self-limited) and “sarcoidosis-like” (sustained) activation of the inflammatory components of the system following a single antigen challenge. By perturbing the influence of model components using inhibitors of the cytokine mediators, distinct clinically relevant disease phenotypes were represented. Finally, the model was shown to be useful for pre-clinical testing of therapies based upon molecular targets and dose-effect relationships.
Our work illustrates a dynamic computer simulation of granulomatous inflammation scenarios that is useful for the investigation of disease mechanisms and for pre-clinical therapeutic testing. In lieu of relevant in vitro or animal surrogates, our model may provide for the screening of potential therapies for specific sarcoidosis disease phenotypes in advance of expensive clinical trials.
PMCID: PMC3103504 PMID: 21637752
18. Thrombospondin-1 Contributes to Mortality in Murine Sepsis through Effects on Innate Immunity
PLoS ONE 2011;6(5):e19654.
Thrombospondin-1 (TSP-1) is involved in many biological processes, including immune and tissue injury response, but its role in sepsis is unknown. Cell surface expression of TSP-1 on platelets is increased in sepsis and could activate the anti-inflammatory cytokine transforming growth factor beta (TGFβ1) affecting outcome. Because of these observations we sought to determine the importance of TSP-1 in sepsis.
Methodology/Principal Findings
We performed studies on TSP-1 null and wild type (WT) C57BL/6J mice to determine the importance of TSP-1 in sepsis. We utilized the cecal ligation puncture (CLP) and intraperitoneal E.coli injection (IP E.coli) models of peritoneal sepsis. Additionally, bone-marrow-derived macrophages (BMMs) were used to determine phagocytic activity. TSP-1−/− animals experienced lower mortality than WT mice after CLP. Tissue and peritoneal lavage TGFβ1 levels were unchanged between animals of each genotype. In addition, there is no difference between the levels of major innate cytokines between the two groups of animals. PLF from WT mice contained a greater bacterial load than TSP-1−/− mice after CLP. The survival advantage for TSP-1−/− animals persisted when IP E.coli injections were performed. TSP-1−/− BMMs had increased phagocytic capacity compared to WT.
TSP-1 deficiency was protective in two murine models of peritoneal sepsis, independent of TGFβ1 activation. Our studies suggest TSP-1 expression is associated with decreased phagocytosis and possibly bacterial clearance, leading to increased peritoneal inflammation and mortality in WT mice. These data support the contention that TSP-1 should be more fully explored in the human condition.
PMCID: PMC3090410 PMID: 21573017
19. Reciprocal regulation of activating and inhibitory Fcγ receptors by TLR7/8 activation: Implications for tumor immunotherapy
Activation of Toll-like Receptors (TLR) 7 and 8 by engineered agonists has been shown to aid in combating viruses and tumors. Here, we wished to test the effect of TLR7/8 activation on monocyte Fcγ receptor (FcγR) function, as they are critical mediators of antibody therapy.
Experimental Design
The effect of the TLR7/8 agonist R-848 on cytokine production and antibody-dependent cellular cytotoxicity (ADCC) by human peripheral blood monocytes (PBM) was tested. Affymetrix microarrays were done to examine genomewide transcriptional responses of monocytes to R-848, and Western blots were done to measure protein levels of FcγR. Murine bone marrow-derived macrophages (BMM) from wild-type and knockout mice were examined to determine the downstream pathway involved with regulating FcγR expression. The efficacy of R-848 as an adjuvant for antibody therapy was tested using a CT26-HER2/neu solid tumor model.
Overnight incubation with R-848 increased FcγR-mediated cytokine production and ADCC in human PBM. Expression of FcγRI, FcγRIIa and the common γ-subunit was increased. Surprisingly, expression of the inhibitory FcγRIIb was almost completely abolished. In BMM, this required TLR7 and MyD88, as R-848 did not increase expression of the γ-subunit in TLR7−/− nor MyD88−/− cells. In a mouse solid tumor model, R-848 treatment superadditively enhanced the effects of antitumor antibody.
These results demonstrate an as-yet undiscovered regulatory and functional link between the TLR7/8 and FcγR pathways. This suggests that TLR7/8 agonists may be especially beneficial during antibody therapy.
PMCID: PMC2848878 PMID: 20332325
Toll-like receptor; Fc-gamma receptor; immunotherapy; antibody; tumor
20. Social disruption induces lung inflammation
Brain, behavior, and immunity 2009;24(3):394-402.
Social disruption (SDR) is a well-characterized mouse stressor that causes changes in immune cell reactivity in response to inflammatory stimuli. In this study, we found that SDR in the absence of an immune challenge induced pulmonary inflammation and increased pulmonary myeloperoxidase activity. The percentage of neutrophils within the lungs increased 2-fold after social disruption. Monocyte accumulation in the lungs was also significantly increased. In addition, SDR increased the percentage of neutrophils that expressed CD11b, indicating that more neutrophils were in an activated state. In the lungs, we observed an increased level of the inflammatory cytokine, IL-1β, as well as higher levels of KC/CXCL1, MIP2/CXCL2, and MCP-1/CCL2, which are chemokines responsible for neutrophil and monocyte recruitment. Furthermore, social disruption led to increased lung expression of the adhesion molecules P-selectin, E-selectin, and ICAM-1, which localize and recruit immune cells. These data support previous findings of an inflammatory environment induced by SDR. We demonstrate that this effect also occurs in the pulmonary milieu and in the absence of an inflammatory stimulus.
PMCID: PMC2826531 PMID: 19903521
Innate immunity; social stress; psychoneuroimmunology; lung; inflammation; Social disruption (SDR)
21. Asc-Dependent and Independent Mechanisms Contribute to Restriction of Legionella Pneumophila Infection in Murine Macrophages
The apoptosis-associated speck-like protein containing a caspase recruitment domain (Asc) is an adaptor molecule that mediates inflammatory and apoptotic signals. Legionella pneumophila is an intracellular bacterium and the causative agent of Legionnaire's pneumonia. L. pneumophila is able to cause pneumonia in immuno-compromised humans but not in most inbred mice. Murine macrophages that lack the ability to activate caspase-1, such as caspase-1−/− and Nlrc4−/− allow L. pneumophila infection. This permissiveness is attributed mainly to the lack of active caspase-1 and the absence of its down stream substrates such as caspase-7. However, the role of Asc in control of L. pneumophila infection in mice is unclear. Here we show that caspase-1 is moderately activated in Asc−/− macrophages and that this limited activation is required and sufficient to restrict L. pneumophila growth. Moreover, Asc-independent activation of caspase-1 requires bacterial flagellin and is mainly detected in cellular extracts but not in culture supernatants. We also demonstrate that the depletion of Asc from permissive macrophages enhances bacterial growth by promoting L. pneumophila-mediated activation of the NF-κB pathway and decreasing caspase-3 activation. Taken together, our data demonstrate that L. pneumophila infection in murine macrophages is controlled by several mechanisms: Asc-independent activation of caspase-1 and Asc-dependent regulation of NF-κB and caspase-3 activation.
PMCID: PMC3112328 PMID: 21713115
inflammasome; caspase-1; Legionella pneumophila; Asc
22. Personalized healthcare in clotting disorders
Personalized medicine 2010;7(1):65-73.
In terms of managing thrombotic disorders, genotype-based individualized patient care emerged as early as 1994 when the association of factor V Leiden (G1691A), and later, prothrombin (G20210A), with thrombotic phenotypes were discovered. Since then, genetic tests for specific thrombophilic SNPs have been routinely incorporated into daily practices in both thrombotic risk assessment and clinical decision-making with respect to prophylactic anti-thrombotic therapy. Recently, the area of pharmacogenomics in major anti-thrombotic drugs, such as warfarin and clopidogrel, has been the principal driver for personalized therapy based on one’s own individual characteristics.
PMCID: PMC2824443 PMID: 20174595
anticoagulant; antiplatelet; clopidogrel; clotting; pharmacogenomics; SNP; warfarin
23. microRNA 133B targets prosurvival molecules MCL-1 and BCL2L2 in lung cancer
Lung cancer is the most frequent cause of cancer-related death in this country for men and women. MicroRNAs (miRNAs) are a family of small non-coding RNAs (approximately 21–25 nt long) capable of targeting genes for either degradation of mRNA or inhibition of translation. We identified aberrant expression of 41 miRNAs in lung tumor versus uninvolved tissue. MiR-133B had the lowest expression of miRNA in lung tumor tissue (28 fold reduction) compared to adjacent uninvolved tissue. We identified two members of the BCL-2 family of pro-survival molecules (MCL-1 and BCL2L2 (BCLw)) as predicted targets of miR-133B. Selective over-expression of miR-133B in adenocarcinoma (H2009) cell lines resulted in reduced expression of both MCL-1 and BCL2L2. We then confirmed that miR-133B directly targets the 3’UTRs of both MCL-1 and BCL2L2. Lastly, over-expression of miR-133B induced apoptosis following gemcitabine exposure in these tumor cells. To our knowledge, this represents the first observation of decreased expression of miR-133B in lung cancer and that it functionally targets members of the BCL-2 family.
PMCID: PMC2824514 PMID: 19654003
microRNA; apoptosis; lung cancer; chemotherapy; BCL2; MCL-1
24. Trityl-based EPR probe with enhanced sensitivity to oxygen
Free radical biology & medicine 2009;47(5):654-658.
An asymmetric derivative of triarylmethyl radical, TAM-H, containing one aldehyde and two carboxyl groups was synthesized. The electron paramagnetic resonance, EPR, spectrum of TAM-H is characterized by a doublet of narrow lines with linewidth of 105 mG in anoxic conditions and hyperfine interaction constant 245 mG. The partial overlap of the components of the doublet results in enhanced sensitivity of the spectral amplitudes ratio to oxygen compared with oxygen-induced linewidth broadening of a single line. Application of the TAM-H probe allows for EPR measurements in an extended range of oxygen pressures from atmospheric to 1 mmHg whereas the EPR spectrum linewidth of the popular TAM-based oxygen sensor, Oxo63, is practically insensitive to oxygen partial pressures below 20 mmHg. Enhanced sensitivity of TAM-H probe relative to Oxo63 was demonstrated in detection of oxygen consumption by Met-1 cancer cells. The TAM-H probe allowed prolonged measurements of oxygen depletion during the hypoxia stage and down to true anoxia (≤ 1.5 mmHg).
PMCID: PMC2739013 PMID: 19523513
trityl; TAM; oximetry; water soluble oxygen probes; EPR; electron paramagnetic resonance
25. MicroRNAs in the Pathogenesis of Lung Cancer
Lung cancer is the leading cause of cancer related deaths in the United States. It is estimated that in 2008 there were 215,000 new diagnoses of lung cancer and 163, 000 deaths. Despite emerging technologies for potential early diagnosis and discovery of novel targeted therapies, the overall five year survival remains a disappointing 15%. Explanations for the poor survival include late presentation of disease, a lack of markers for early detection and both phenotypic and genotypic heterogeneity within patients of similar histological classification. In order to further understand this heterogeneity and thus complexity of lung cancer, investigators have applied various technologies including high throughput analysis of both the genome and proteome. Such approaches have been successful in identifying signatures that may clarify molecular differences in tumors, identify new targets and improve prognostication. In the last decade, investigators have identified a new mode of gene regulation in the form of non-coding RNAs termed microRNAs (miRNAs or miRs). First determined to be of importance in larval development, microRNAs are ~19–22 nucleotide single stranded RNAs that regulate genes by either inducing mRNA degradation or inhibiting translation. MiRNAs have been implicated in several cellular processes including apoptosis, development, proliferation and differentiation. By regulating hundreds of genes simultaneously, miRNAs have the capacity for regulation of biological networks. Global alterations in miRNA expression in both solid organ and haematological malignancies suggest their importance in the pathogenesis of disease. To date, both in vivo and in vitro studies in lung cancer demonstrate a dysregulation of miRNA expression. Furthermore, investigators are beginning to identify individual targets and pathways of miRNAs relevant to lung tumorigenesis. Thus, miRNAs may identify critical targets and be important in the pathogenesis of lung cancer.
PMCID: PMC2723999 PMID: 19474765
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Journal of Creation Volume 16Issue 2 Cover
Journal of Creation 16(2):13–15
August 2002
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C4 photosynthesis—evolution or design?
Life depends on photosynthesis, where plants take carbon dioxide from the atmosphere and ‘fix’ it into high-energy sugars using light as the energy source. Two basic forms of photosynthesis have been discovered. In one, the first compound made from CO2 is a three-carbon compound, so this is called C3 photosynthesis. In the other, the first compound is a four-carbon compound, so it is called C4 photosynthesis.1 Most plants are C3; about 15% of species have the C4 system. Examples of C3 plants include wheat, rice, potatoes and cabbage. C4 plants include maize, sugar cane, sorghum and succulents—mainly tropical/arid environment species.
C4 and C3 plants differ in their leaf anatomy and where photosynthesis occurs. C3 plants have chloroplasts throughout the internal (‘mesophyll’) leaf cells, and there are air spaces around the cells to allow ready diffusion of CO2 into them. In C4 plants, the photosynthetic cells cluster around the vascular bundles (leaf veins) and there are no air spaces around the photosynthetic cells. The photosynthetic cells are called bundle sheath cells because they form a tight sheath around the vascular bundles.
Diagram 1
The Calvin-Benson Cycle of photosynthesis. Each turn of the cycle produces a molecule of phosphoglyceraldehyde ‘PGAL’, (containing 3 carbon atoms). This is transported from the chloroplast to make glucose and fructose, which in turn condense to form sucrose.
C3 and C4 plants share the same light-harvesting systems, as well as the same enzyme cycle for incorporating the carbon into sugars—the Calvin-Benson cycle. The first enzyme in this cycle, nicknamed ‘Rubisco’, makes up 25% of the protein in leaves, which makes it the most abundant protein on Earth. Rubisco takes CO2 and adds it to a 5-carbon sugar, making two 3-carbon sugar molecules.
C4 plants have extra enzymes operating in the leaf. These incorporate the CO2 (actually bicarbonate, HCO3) into a 4-carbon compound (usually malate), which the mesophyll cells transport into the bundle sheath cells via many tiny tubes called plasmodesmata. Here another enzyme releases the CO2 for Rubisco to fix into sugars in the same manner as in C3 plants. The bundle sheath cells have specialized thickened cell walls and they have no air spaces around them, so the CO2 cannot escape and it becomes concentrated to at least 10 times that of normal outside air. This accounts for one of the major differences between C3 and C4 plants: in the short term, C3 plants increase their rate of photosynthesis in response to increased atmospheric levels of CO2, but C4 plants don’t.
C3 and C4 plants also differ in that C3 plants exhibit ‘photorespiration’, where they lose some of the CO2 fixed into 3-carbon sugar, whereas C4 plants don’t. This happens because O2 competes for the active site on Rubisco to which CO2 binds. While Rubisco has a much greater affinity for CO2, the partial pressure of O2 in air is 700 times greater than that of CO2. Oxygen drives the release of CO2 with the production of the energy-depleted forms of energy-carrier molecules (ADP and NADP).
This seems to be a safety mechanism to avoid damage to the photosynthesis system at low CO2 levels. If there is inadequate CO2 to fix the energy harvested by the chlorophyll system, then oxygen radicals form and these damage the light harvesting system. Photorespiration maintains a supply of ADP and NADP to accept the energy generated by the light-harvesting system.
C4 plants concentrate their CO2, thus suppressing photorespiration. Also, since the supply of CO2 is maintained, even at low concentrations, there is always a sink for the energy from the light harvesting, so damage to the photosystems is avoided. So there is no need for photorespiration.
Why two methods of fixing CO2?
Why do C3 plants tend to be temperate in their adaptation and C4 plants tropical/arid? The rate of photorespiration rises rapidly with temperature, so it becomes a much more serious problem, in terms of its ‘inefficiency’ (loss of fixed carbon), in the tropics. On the other hand, the C4 system has energy costs: each CO2 fixed into malate needs one NADPH and one ATP for the complete cycle. So the relative advantages seem to be due to the trade-off between photorespiration in C3 plants and the extra costs of carbon fixation in C4 plants. With increasing temperatures, the cost of photorespiration becomes greater than the extra cost of the C4 system, which is met by the increased sunlight energy anyway, so the latter prevails.
C4 plants also do well in arid environments. In this situation the plant closes its stomata (leaf pores) to conserve water. This also reduces the amount of CO2 entering the leaf and raises the leaf temperature. The enzyme that fixes CO2 in C4 plants has a much greater affinity for CO2 than Rubisco, which does the job alone in C3 plants. So C4 plants are still able to supply plenty of CO2 to the Rubisco in the photosynthetic cells, whereas a C3 plant would have trouble.2
The origins of the C4 system
Some 8,000 to 10,000 species of plants in 18 families, including both monocots (which includes grasses) and dicots (roughly, ‘broad-leaved’ plants), have the C4 system. C4 metabolism has even been found in a single-celled marine diatom.3
Many flowering plant families have both C3 and C4 species. Some species are intermediate, showing both C3 and C4 characteristics. In the Atriplex genus, some species are C3, while others are C4, and C3 and C4 species have been hybridized.4 Wood and Cavanaugh have reviewed the genus Flaveria, which has species of C3, C4 and intermediate type, many of which hybridize.5
The distribution of C4 species does not form any pattern that could relate to any reasonable evolutionary phylogeny.
The distribution of C4 species does not form any pattern that could relate to any reasonable evolutionary phylogeny. Consequently, evolutionists have proposed that C4 photosynthesis has arisen independently at least 30 times—a classic case of ‘polyphyletic evolution’.
However, C4 chemistry involves several complex enzyme systems and the chemistry is remarkably consistent across the spectrum (there are three types of enzyme used to release the CO2 from the organic acid that transports the CO2, otherwise the chemistry is similar).
To believe that C4 chemistry arose once by natural processes would require super ‘faith’ for the evolutionist. But to propose that such a system with its new complex coded genetic information arose separately some 30 times by mutations and natural selection, and that these processes arrived at essentially the same solution, stretches credulity to breaking point. This would be an extreme example of ‘convergent evolution’—even more than the supposed polyphyletic origin of the eye in general and the compound eye in particular.6
Some species that exhibit both C3 and C4 forms are even able to switch from one to the other during development. This suggests that maybe the C4 chemistry is latent in C3 plants, or is suppressed by some means. In the marine diatom mentioned above, C4 metabolism seems to be facultative.3
Wood and Cavanaugh5 concluded from their baraminological study of Flaveria that the C4 photosynthetic pathway arose from plants that were originally C3, and this probably happened post-Flood. These authors propose that the genetic information for C4-mode photosynthesis was present in the original created kinds, but latent and has become activated since.
Surprise: C3 plants have the C4 system!
Diagram 2
Diagrammatic representation of the Hatch-Slack system of CO2 capture and fixation that operates in the roots and stems of C3 plants, which were thought to lack this capacity entirely. (Xylem and phloem are actually in vascular bundles together; not separated as in the diagram.)
Now Hibberd and Quick have shown that tobacco and celery, two classical C3 plants, contain virtually all the C4 characteristics, not in their leaves, but in their roots, stems and petioles.7 They showed that CO2 respired in the roots is fixed into malate by the same enzyme that fixes CO2 in the leaves of C4 plants. The malate moves in the xylem stream up the plant where it transfers into bundle sheath cells surrounding the vascular bundles in the stems and petioles. Here all three decarboxylation (CO2-releasing) enzymes identified in the three sub-types of the C4 system are present in elevated levels. They release the CO2 so that Rubisco can use it in the Calvin cycle. The chemistry is apparently identical to the C4 system. These plants differ from C4 plants only in the site of synthesis of the malate (roots in C3 plants versus leaf mesophyll cells in C4 plants) and its transfer to the bundle sheath cells. Even the anatomy of the bundle sheath cells in the stems and petioles is similar.
This makes for a very efficient system for retrieving respired carbon from the roots. Indeed, CO2 may even enter the roots from the soil, where the level of CO2 is usually quite high due to the activity of heterotrophic micro-organisms. This would reduce the CO2 concentration in the soil, which would be beneficial to the aerobic organisms living there. What wonderful design for an efficient ecology!
Hibberd and Quick point out that since so much of the C4 system is already present in the C3 plants, ‘fewer modifications are needed for C4 photosynthesis to evolve’. Indeed, are we talking about the origin of new complex, coded genetic information at all, or are we looking at adaptation based on existing genetic information—as proposed by the creationists Wood and Cavanaugh?
It now seems that the genes for C4 enzymes and anatomy are selectively expressed in the roots, stems and petioles of C3 plants, but are suppressed in the leaves. C4 plants differ in having these genes expressed in the leaves as well. If the suppression in the leaves of C3 plants were due to the synthesis of proteins that interact with promoter sequences, for example, it may even be possible to see mutations in the genes for these proteins that result in the expression of C3–C4 or C4 photosynthesis. Or there might be some designed means of switching on this adaptation genetically so that it is inherited once switched on—something like Wood’s Altruistic Genetic Elements (AGEs)?5
These developments underline just how cleverly the original plants were created—with built-in latent capacity for adaptation to a wide range of environments. It will be interesting to see the details fleshed out.
1. The basic details of C4 photosynthesis were elucidated by Australian scientists in the 1960s. See Hatch, M.D. and Slack, C.R., Photosynthesis by sugarcane leaves, Biochem. J. 101:103–111, 1966. Return to Text.
2. A variation on the C4 theme is seen in CAM (crassulacean acid metabolism) plants. Typically succulent desert plants, they open their stomata at night to fix CO2, storing the fixed form in vacuoles (reservoirs within cells), then release the CO2 for photosynthesis during the day when the stomata shut. In this manner they conserve water very efficiently. Return to Text.
3. Reinfelder, J.R., Kraepiel, A.M.L. and More, F.M.M., Unicellular C4 photosynthesis in a marine diatom, Nature 407:996–999, 2000. Return to Text.
4. Sengbusch, P. v., Influence of different parameters on the efficiency of the CO2-uptake—C3-and a C4-plant, <www.biologie.>, accessed 15 March 2002. Return to Text.
5. Wood, T.C. and Cavanaugh, D.P., A baraminological analysis of subtribe Flaverinae (Asteraceae: Helenieae) and the origin of biological complexity, Origins (GRI) 52:7–27, 2001. Return to Text.
6. Oakley, T.H. and Cunningham, C.W., Molecular phylogenetic evidence for the independent evolutionary origin of an arthropod compound eye, Proc. Nat. Acad. Sci. USA 99(3):1426–1430, 2002. Their abstract says, ‘These results illustrate exactly why arthropod compound eye evolution has remained controversial, because one of two seemingly very unlikely evolutionary histories must be true. Either compound eyes with detailed similarities evolved multiple times in different arthropod groups or compound eyes have been lost in a seemingly inordinate number of arthropod lineages.’ Return to Text.
7. Hibberd, J.M. and Quick, W.P., Characteristics of C4 photosynthesis in stems and petioles of C3 flowering plants. Nature 415:451–453, 2002. Return to Text.
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Kmart's 'Ship My Pants' ad goes viral
NEW YORK — If Kmart has proven anything, it's the transcendental power of potty humor. But at any rate, the mass merchandise retailer has garnered significant attention with its "Ship My Pants" ad, which has received close to 7.4 million views on YouTube and coverage in news outlets nationwide.
The ad is for a service the chain offers whereby customers who can't find what they're looking for in the store can order it online and have it shipped to them.
It's part of parent company Sears Holdings' omnichannel investments, which chairman and CEO Edward Lampert touted in the company's fourth quarter 2012 earnings call in February. Also in February, Sears Holdings launched Mygofer Express, allowing customers to pick up items ordered through Mygofer at Sears' flagship store in Chicago.
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