Ohio Valley Wrestling Television Recap Episode 714

From Jimmie Daniel:

This is the recap for Ohio Valley Wrestling TV Episode 714 to air in Louisville on Saturday 4/27. As always the show can also be seen at http://www.ovwrestling.com/tv/714. OUR OVW Announce Team this week is Dean "San Juan" Hill?, ?Anchorman" Gilbert Corsey, and ?Rocky Mountain Mouth" Michael Titus. OUR OVW Ring Announcer is Terry Boddie. Gilbert says that seven OVW superstars were attacked by the Coalition last week.

Speaking of which, the Coalition (One-half of OUR OVW Tag Team Champions "The Washington Generals" Jason Wayne, "Squad Alpha" Jack Black & Joe Coleman, "Squad Bravo" Shiloh Jonze & Raul Lamotta, and the Spanish Moss Guy) come out to the ring without Crimson (the other half of the tag team champs). Wayne commandeers the mic and says that OVW has been attacked and that the mission of the Coalition is to rid OVW of all evildoers so that red-blooded fans can have a group that they can truly be proud of! They are working around the clock to complete this mission-OVW Operation Freedom! They unleashed Shock and Brawl last week which removed Alex Silva, Sam Shaw, "Smooth" Johnny Spade, and James "Moose" Thomas. This brings out OUR OVW Director of Operations Michael (not PS) Hayes comes out appearing to be quite agitated even before having mic problems. Wayne reminds Hayes that he can't touch the Coalition or even throw them out of the building, as Hayes gets all up in their faces. Wayne also mentions that Crimson is in a diplomatic meeting with the OVW Board of Directors. Hayes can't take the Coalition on by himself but does have "people" and brings out OUR OVW TV Champion Rockstar Spud followed by Tony Gunn, "Triple R Superstar" Randy Royal, and "White Kryptonite" Eddie Diamond (all four also were attacked last week). Wayne reminds Hayes that he still has Hayes outnumbered 6 to 4 but then Hayes brings out "Welsh Colossus" Rob Terry! Wayne says it's still 6 on 5 but then Jay Bradley comes out! Bradley says he might not like Hayes' "people" but the Coalition stuck their noses in his business last week by attacking Spade and Moose, so he's going to make a statement on the Coalition tonight! So we have a 12-man tag match in the main event.

Match #1: Lovely Lylah vs OUR OVW Ladies Champion Trina
Lylah is a brunette about the same size and build as Epiphany, whom Trina defeated last week to win the title. Titus refers to Epiphany as a "bohemoth" (?). Trina gets all offensive with clotheslines and slams, then finishes Lylah with a full nelson slam to wrap up her first title defense.

Match #2: "The Great" Cliff Compton vs "Best Rudy Ever" Rudy Switchblade
Compton shows off his tumbling skills ala Matt Dillinger. Dean is happy that Rudy has broken away from "Mr. Pec-tacular" Jesse Godderz. Rudy tries to lock a Boston crab but Compton kicks him away. Rudy stomps Compton's fingers then goes for a tenpunch but Compton rakes his face. Compton slings Rudy across then legdrops him for 2 before draping him across the top rope and coming off with a forearm, cutting him a flip onto the mat. Compton chinbreakers Rudy for 2 then locks him into a sleeper, taking him down to the mat. Rudy appears to chew his way free and goes for the crab again but Compton again kicks him away. Rudy snaps Compton on the top rope as Coleman and Black run out and attack Rudy for the DQ. Jonze and Lamotta follow but Bradley, Royal (with a 2x4), et al; come out ot clear the ring. Hayes returns and declares that there will be no more of this (run-in attacks) and the 12-man tag is still on. Compton stands in front of the Coalition with the mic and says they are looking to draft the man...and the man is Cliff Compton! However the Coalition decides that Compton is not the man and proceeds to beat him down until the group in the ring chases them away.

In the back, "Diamond Steel" Ryan Howe is warming up as Heidi Lovelace comes over to talk. She asks about the gifts that Howe has allegedly been sending Taeler Hendrix but Howe brushes off the question, saying he doesn't care about that but is caring about getting his hands on Doug Williams and Dylan Bostic tonight. Taeler interrupts and calls Heidi "psychotic" and tells Heidi that Howe belongs to her! Bostic comes over and grabs Taeler, who refers to Bostic as an "overgrown Ken doll" as she is being dragged away by Bostic.
Camera pans over to Timmy Danger reading a magazine while Diamond is lying in the arms of his favorite girl, Epiphany. Diamond apologizes to her for costing her the ladies title last week but she says not to worry about it since to her, no goal is more important than him! Bradley walks up and sees this and becomes indignant, reminding Diamond that they are going to war tonight. He tells Diamond to come with him but tells Danger and Epiphany to stay behind. They go over to where Royal, Gunn, and Spud are standing. Spud tells Bradley he doesn't exactly trust Bradley and is keeping both eyes on him. Bradley suggests Spud keep his eyes on his pot of gold, which sets off some sniping among the group particularly Royal reminding Spud that he wants a shot at the TV title. Terry comes up to emphasize to the others that they all need to work together.

Match #3: Dylan "Freakin'" Bostic & Doug Williams vs "Diamond Steel" Ryan Howe & OUR OVW Champion Jamin Olivencia
Titus calls Williams the "Guiding Light of OVW". Howe plays us some riffs before Jamin comes out. Howe fires up on Williams a bit before tagging in Jamin, who also gets some action in before missing a splash. Bostic comes in but is greeted with a dropkick and Howe tagging back in. Howe hits a Thesz press on Bostic and peppers him with rights. Williams tags in and whips Howe into a Bostic kick to the back. Williams suplexes Howe then chokes him in the ropes, which begins an extended period of Howe being isolated while ref Josh Ashcraft keeps Jamin from coming in illegally. Williams kicks Howe in the groinular region and Jamin runs in with a full head of steam and attacks Williams. The two scuffle out of the ring and through the curtain as Ashcraft calls for the bell in what appeared to be a countout. Howe and Bostic are duking it out in the ring when Taeler comes into the ring and gets between the two. Taeler tells the guys to stop fighting over her then asks Howe why he got her the gifts. Bostic chimes in that everyone knows it was Howe! An angry Howe takes the mic and says it was not him, adding that he realizes that Taeler is hot but girls like her are a dime a dozen (not sure if hot redheads are a dime a dozen but whatever)! Howe wonders aloud if Bostic bought her the gifts to try to take her mind off fantasizing about Howe. Taeler starts to cry and no one has a Kleenex :( Heidi comes out and says the mysterious gift-giver was her!!! Taeler is stunned.

Back from break Dean, Gilbert, and Titus seem stunned as well. Gilbert plugs a house show in Elizabethtown, KY that Compton may make if the Coalition didn't beat him up too bad, lol.

Match #4: Gunn & Royal & Diamond & Terry & Spud & Bradley vs Wayne & Black & Lamotta & Jonze & Coleman & Spanish Moss Guy
Opponents rush the ring and attack the Coalition but then we go to break. Back from break, Jonze drags Diamond over to the corner and tags Spanish Moss Guy. Diamond is able to overcome the moss and tag in Gunn, who flapjacks Jonze. Lamotta runs in and neckbreakers Gunn but Royal comes in to give Lamotta a running knee. Lamotta rolls out and Coleman lariats Royal but here comes Spud! Coleman throws Spud into the wrong corner for some choking in the ropes followed by Wayne and Black taking turns beating on him. Spud gets away and hits a delayed Thesz press on Black then Bradley comes in to give Black a running boot. Wayne attacks Bradley from behind to stop all that but then Terry comes in. Terry splashes Wayne in the corner and prepares to whip him into Bradley, who has the Boomstick ready to go. Black runs in and hits Bradley with a foreign object for the DQ.
Coalition brings out the steel rods and its beatdown time! Switchblade and The Mobile Homers (Ted McNaler & Adam Revolver) run out to help but soon feel the wrath as well. Jonze and Lamotta arm themselves and wait at the entrance as the Baxter brothers, Nick Dumeyer, and Elvis Pridemore all come through the curtain and get ambushed. In the ring after hitting Terry upside the head with the belt, Wayne takes the mic and says OVW is going to have to bring more to the table if they want to defeat the Coalition. Wayne then lines up the troops and leads the Coalition pledge as the show goes off.

THOUGHTS: Somebody dared to oppose the Coalition this week, whoda thunk it? Trina had no wardrobe issues this week plus she had the distinction of scoring the only pinfall. Compton/Switchblade and the 4-man tag were pretty good for the action part. And yes, Trent Van Drisse called Heidi as the gift-giver several weeks ago so kudos to him! Epiphany sure seemed happy with Diamond. They should do like Glee and start naming couples (for example, Finn + Rachel="Finchel" and Brittany + Santana= "Brittana?. Not sure what Taeler + Heidi would be). So we get like a six minute beatdown after the main. I kept waiting for the fans to start throwing garbage into the ring. I think this is where I picked up OVW about this time last year with Jo-V-W running over everyone and everything. Maybe this time next year the Baxter, Dumeyer, and Pridemore will be doing a Four Horseman gimmick, I can't wait! Anyway, this still was a slight improvement over the past couple of weeks so I'll give it a "just a hair above the middle" thumbs in the middle.

Source: http://www.gwhnews.com/2013/04/ohio-valley-wrestling-television-recap_28.html

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Air Pollution Linked To Hardening Of The Arteries

Fried and fatty foods aren't the only things bad for your arteries -- a new study suggests the air you breathe could play a role, too.

Prolonged exposure to air pollution could be linked to heart attacks and strokes by speeding the hardening of the arteries -- a condition known as atherosclerosis that is linked with heart disease, according to new research.

The study showed a link between higher concentrations of particulate air pollution and faster thickening of the inner two layers of the carotid artery, as well as a link between slowed progression of atherosclerosis with decreasing air pollution.

The findings are published in the journal PLOS Medicine, and are based on data from 5,362 people ages 45 to 84 who came from six U.S. metro areas that were part of the Multi-Ethnic Study of Atherosclerosis (MESA Air). Over three years, researchers estimated home air pollution levels of all the study participants, as well as their blood vessel health.

On average, the study participants all experienced an average increase in carotid artery thickness of 14 micrometers each year. However, people who lived in more polluted areas experienced faster thickening, compared with those breathing cleaner air.

"Linking these findings with other results from the same population suggests that persons living in a more polluted part of town may have a 2 percent higher risk of stroke as compared to people in a less polluted part of the same metropolitan area," Sara Adar, an assistant epidemiology professor at the University of Michigan School of Public Health, said in a statement.

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Source: http://www.huffingtonpost.com/2013/04/26/air-pollution-atherosclerosis-hardening-arteries_n_3157353.html

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Clenching right fist may give better grip on memory

Apr. 24, 2013 ? Clenching your right hand may help form a stronger memory of an event or action, and clenching your left may help you recollect the memory later, according to research published April 24 in the open access journal PLOS ONE by Ruth Propper and colleagues from Montclair State University.

Participants in the research study were split into groups and asked to first memorize, and later recall words from a list of 72 words. There were 4 groups who clenched their hands; One group clenched their right fist for about 90 seconds immediately prior to memorizing the list and then did the same immediately prior to recollecting the words. Another group clenched their left hand prior to both memorizing and recollecting. Two other groups clenched one hand prior to memorizing (either the left or right hand) and the opposite hand prior to recollecting. A control group did not clench their fists at any point.

The group that clenched their right fist when memorizing the list and then clenched the left when recollecting the words performed better than all the other hand clenching groups. This group also did better than the group that did not clench their fists at all, though this difference was not statistically 'significant'.

"The findings suggest that some simple body movements -- by temporarily changing the way the brain functions- can improve memory. Future research will examine whether hand clenching can also improve other forms of cognition, for example verbal or spatial abilities," says Ruth Propper, lead scientist on the study.

The authors clarify that further work is needed to test whether their results with word lists also extend to memories of visual stimuli like remembering a face, or spatial tasks, such as remembering where keys were placed. Based on previous work, the authors suggest that this effect of hand-clenching on memory may be because clenching a fist activates specific brain regions that are also associated with memory formation.

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Journal Reference:

1. Ruth E. Propper, Sean E. McGraw, Tad T. Bruny?, Michael Weiss. Getting a Grip on Memory: Unilateral Hand Clenching Alters Episodic Recall. PLoS ONE, 2013; 8 (4): e62474 DOI: 10.1371/journal.pone.0062474

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

Source: http://feeds.sciencedaily.com/~r/sciencedaily/~3/_QYBoZyfE3E/130424185159.htm

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Suppressing protein may stem Alzheimer's disease process

Public release date: 25-Apr-2013
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Contact: Jules Asher
NIMHpress@nih.gov
301-443-4536
NIH/National Institute of Mental Health

Runaway regulator clogs removal of toxic debris -- NIH funded study

Scientists funded by the National Institutes of Health have discovered a potential strategy for developing treatments to stem the disease process in Alzheimer's disease. It's based on unclogging removal of toxic debris that accumulates in patients' brains, by blocking activity of a little-known regulator protein called CD33.

"Too much CD33 activity appears to promote late-onset Alzheimer's by preventing support cells from clearing out toxic plaques, key risk factors for the disease," explained Rudolph Tanzi, Ph.D., of Massachusetts General Hospital and Harvard University, a grantee of the NIH's National Institute of Mental Health (NIMH) and National Institute on Aging (NIA). "Future medications that impede CD33 activity in the brain might help prevent or treat the disorder."

Tanzi and colleagues report on their findings April 25, 2013 in the journal Neuron.

"These results reveal a previously unknown, potentially powerful mechanism for protecting neurons from damaging toxicity and inflammation," said NIMH Director Thomas R. Insel, M.D. "Given increasing evidence of overlap between brain disorders at the molecular level, understanding such workings in Alzheimer's disease may also provide insights into other mental disorders."

Variation in the CD33 gene turned up as one of four prime suspects in the largest genome-wide dragnet of Alzheimer's-affected families, reported by Tanzi and colleagues in 2008. The gene was known to make a protein that regulates the immune system, but its function in the brain remained elusive. To discover how it might contribute to Alzheimer's, the researchers brought to bear human genetics, biochemistry and human brain tissue, mouse and cell-based experiments.

They found over-expression of CD33 in support cells, called microglia, in postmortem brains from patients who had late-onset Alzheimer's disease, the most common form of the illness. The more CD33 protein on the cell surface of microglia, the more beta-amyloid protein and plaques damaging debris had accumulated in their brains. Moreover, the researchers discovered that brains of people who inherited a version of the CD33 gene that protected them from Alzheimer's conspicuously showed reduced amounts of CD33 on the surface of microglia and less beta-amyloid.

Brain levels of beta-amyloid and plaques were also markedly reduced in mice engineered to under-express or lack CD33. Microglia cells in these animals were more efficient at clearing out the debris, which the researchers traced to levels of CD33 on the cell surface.

Evidence also suggested that CD33 works in league with another Alzheimer's risk gene in microglia to regulate inflammation in the brain.

The study results and those of a recent rat study that replicated many features of the human illness add support to the prevailing theory that accumulation of beta-amyloid plaques are hallmarks of Alzheimer's pathology. They come at a time of ferment in the field, spurred by other recent contradictory evidence suggesting that these presumed culprits might instead play a protective role.

Since increased CD33 activity in microglia impaired beta-amyloid clearance in late onset Alzheimer's, Tanzi and colleagues are now searching for agents that can cross the blood-brain barrier and block it.

###

Reference

Alzheimer's disease risk gene CD33 inhibits microglial uptake of amyoid beta. Griciuc A, Serrano-Pozo A, Parrado AR, Lesinski AN, Asselin CN, Mullin K, Hooli B, Choi SH, Hyman BT, Tanzi RE. Neuron, April 25, 2013.

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AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.

Public release date: 25-Apr-2013
[ | E-mail | Share ]

Contact: Jules Asher
NIMHpress@nih.gov
301-443-4536
NIH/National Institute of Mental Health

Runaway regulator clogs removal of toxic debris -- NIH funded study

Scientists funded by the National Institutes of Health have discovered a potential strategy for developing treatments to stem the disease process in Alzheimer's disease. It's based on unclogging removal of toxic debris that accumulates in patients' brains, by blocking activity of a little-known regulator protein called CD33.

"Too much CD33 activity appears to promote late-onset Alzheimer's by preventing support cells from clearing out toxic plaques, key risk factors for the disease," explained Rudolph Tanzi, Ph.D., of Massachusetts General Hospital and Harvard University, a grantee of the NIH's National Institute of Mental Health (NIMH) and National Institute on Aging (NIA). "Future medications that impede CD33 activity in the brain might help prevent or treat the disorder."

Tanzi and colleagues report on their findings April 25, 2013 in the journal Neuron.

"These results reveal a previously unknown, potentially powerful mechanism for protecting neurons from damaging toxicity and inflammation," said NIMH Director Thomas R. Insel, M.D. "Given increasing evidence of overlap between brain disorders at the molecular level, understanding such workings in Alzheimer's disease may also provide insights into other mental disorders."

Variation in the CD33 gene turned up as one of four prime suspects in the largest genome-wide dragnet of Alzheimer's-affected families, reported by Tanzi and colleagues in 2008. The gene was known to make a protein that regulates the immune system, but its function in the brain remained elusive. To discover how it might contribute to Alzheimer's, the researchers brought to bear human genetics, biochemistry and human brain tissue, mouse and cell-based experiments.

They found over-expression of CD33 in support cells, called microglia, in postmortem brains from patients who had late-onset Alzheimer's disease, the most common form of the illness. The more CD33 protein on the cell surface of microglia, the more beta-amyloid protein and plaques damaging debris had accumulated in their brains. Moreover, the researchers discovered that brains of people who inherited a version of the CD33 gene that protected them from Alzheimer's conspicuously showed reduced amounts of CD33 on the surface of microglia and less beta-amyloid.

Brain levels of beta-amyloid and plaques were also markedly reduced in mice engineered to under-express or lack CD33. Microglia cells in these animals were more efficient at clearing out the debris, which the researchers traced to levels of CD33 on the cell surface.

Evidence also suggested that CD33 works in league with another Alzheimer's risk gene in microglia to regulate inflammation in the brain.

The study results and those of a recent rat study that replicated many features of the human illness add support to the prevailing theory that accumulation of beta-amyloid plaques are hallmarks of Alzheimer's pathology. They come at a time of ferment in the field, spurred by other recent contradictory evidence suggesting that these presumed culprits might instead play a protective role.

Since increased CD33 activity in microglia impaired beta-amyloid clearance in late onset Alzheimer's, Tanzi and colleagues are now searching for agents that can cross the blood-brain barrier and block it.

###

Reference

Alzheimer's disease risk gene CD33 inhibits microglial uptake of amyoid beta. Griciuc A, Serrano-Pozo A, Parrado AR, Lesinski AN, Asselin CN, Mullin K, Hooli B, Choi SH, Hyman BT, Tanzi RE. Neuron, April 25, 2013.

---

[ | E-mail | Share ]

?

AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.

Source: http://www.eurekalert.org/pub_releases/2013-04/niom-spm042313.php

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Pain and Gain Review: A Roided-Out Crime Movie

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Animal study finds deep brain stimulation reduces binge eating behavior

Thursday, April 25, 2013

Stimulating a region of the brain known to be involved in reward decreases binge eating behavior in mice, according to a study published in the April 24 issue of The Journal of Neuroscience. The findings add to a growing body of evidence supporting the role of the brain?s reward system in driving the consumption of palatable food. It could one day pave the way for more effective and lasting treatments for obesity.

The numbers of people worldwide living with obesity continues to climb. Recent studies suggest that the consumption of high calorie foods activates regions of the brain associated with reward. As a result, scientists are increasingly interested in understanding how changes taking place in the brain may be responsible for driving individuals to consume more calories than needed.

In the current study, Tracy Bale, PhD, and colleagues at the University of Pennsylvania set out to see if activating the nucleus accumbens ? a region of the brain involved in the promotion of motivational behaviors ? would alter binge-eating behavior in mice. The researchers used a technique called deep-brain stimulation (DBS) to directly deliver electrical impulses to the nucleus accumbens of mice that regularly binged on their food (ate 25 percent of their daily caloric intake within one hour). While mice that did not receive DBS showed little change in their eating habits, DBS significantly lessened the others? interest in binging on high fat food.

?Little is currently known about the neurobiological mechanisms of binge eating, and there are few effective treatments,? explained Paul Kenny, PhD, who studies addiction at the Scripps Research Institute and was not involved in this particular study. ?This study provides insights into the mechanisms that play a role in binge eating,? he added.

Bale?s group also tested the long-term effects of DBS on obese mice that were given unlimited access to high-fat food. After four days of continuous DBS, the obese mice consumed fewer calories and their body weight dropped.

?Overall, these studies indicate that activity in the reward centers of the brain may be a critical component driving individuals to overeat despite known negative health consequences,? Bale said. ?These results are very exciting as they provide our best evidence yet that we might be able to modify specific behaviors linked with body weight changes and obesity,? she added.

Future clinical trials will need to explore the effectiveness of DBS in reducing obesity in people before researchers know whether or not DBS presents a viable treatment option for the millions worldwide living with obesity. However, as noted by lead study author Casey Halpern, MD, a neurosurgeon at the University of Pennsylvania, DBS targeting other areas of the brain is currently used to treat Parkinson?s disease, and is being tested in clinical trials for the treatment of depression, obsessive-compulsive disorder, and addiction.

?Once replicated in human clinical trials, DBS could rapidly become a treatment for people with obesity due to the extensive groundwork already established in other disease areas,? Halpern said.

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Society for Neuroscience: http://www.sfn.org

Thanks to Society for Neuroscience for this article.

This press release was posted to serve as a topic for discussion. Please comment below. We try our best to only post press releases that are associated with peer reviewed scientific literature. Critical discussions of the research are appreciated. If you need help finding a link to the original article, please contact us on twitter or via e-mail.

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Source: http://www.labspaces.net/127893/Animal_study_finds_deep_brain_stimulation_reduces_binge_eating_behavior

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Payback: Greek govt to launch legal battle for new WWII reparations ...

Greece has officially declared it will seek reparations from Germany dating back to the Nazi occupation during World War II, which could amount to over ?100 billion, likely putting further strain on relations between the two Eurozone countries.

"We will exhaust every means available to arrive at a settlement," Greek Foreign Minister Dimitris Avramopoulos told parliament in Athens on Wednesday. "One can't compare the times, but also one cannot erase the memories."

A Greek Finance Ministry report leaked to local media earlier this month showed that Greece believes that Berlin owes it ?162 billion ? ?108 billion for infrastructure damage during the occupation between 1941 and the end of the war, and ?54 billion as compensation for an interest-free loan Germany took from the country to support its war effort.

If paid in full, the sum would nearly empty the national currency and gold reserves of Germany (?185 billion as of last month), though this would still not be enough to cover Greece?s national debt (over ?350 billion).

Demands for such a reparation scheme have been voiced intermittently by Greek politicians over the past 60 years, but have gained renewed energy amid the recent financial crisis, in which the country has been subjected to tough austerity measures in exchange for largely German-backed loans.

The latest campaign is driven by radical Socialist opposition leader Alexis Tsipras, and is supported by 4 out of 5 Greeks, according to polls.

It remains unlikely that Germany will part with the money voluntarily.

?Instead of misleading the people in Greece [about the possibility of reparations] it would be better to show them the road to reform,? German Finance Minister Wolfgang Sch?uble said when the numbers in question first surfaced several weeks ago. ?The issue was settled a long time ago. Paying reparations is out of the question.?

In his speech, Avramopoulos said the ?Greek people suffered, went hungry and were looted like no other country,? and few contest that alongside the Soviet Union, Poland and parts of the Balkans, Greece was the hardest-hit of the invaded countries during World War II.

Still, the legal avenues open to the Greek government seem limited.

In the aftermath of the war, Greece was awarded provisional reparations amounting to a present-day value of about $2.5 billion.

Later, the 1953 London Debt Agreement ? in which around half of Germany?s external debt was written off ? stipulated that Greece would demand no further reparations until the unification of Germany. When the two German republics finally reunified in 1990, Greece conceded that it had no further claims.

In 1960, Germany also compensated Greeks who suffered under the Nazis.

While anti-German protests ? including some that portray Chancellor Angela Merkel as a mustachioed Nazi ? have become a staple of Greek political life, and set off what the media has labeled a ?new Cold War? between the countries.

The demand for reparations is apparently not just about a thirst for retribution, or even necessarily a chance to retake money from Germany: as numerous historians in both countries have pointed out, the London Debt Agreement was made because Germany couldn?t pay its debts without crippling its future. Forgiving these debts set the scene for Germany?s ?economic miracle? in the following decade.

Similarly, Greece?s current debts are about one-and-a-half times its Gross Domestic Product. Media commentators in Athens have repeatedly pointed to the historic parallels, and say that it is now Germany?s chance to allow Greece a better future, instead of suffocating it with obligations it can never repay.

Source: http://rt.com/news/greece-wwii-reparations-germany-339/

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