Clock – Have you ever wondered who invented the clock and when this ingenious device was created? If you’ve ever pondered these questions, you’re in for an enlightening discussion today.
In this article, we’ll uncover the brilliant mind behind the invention of the clock and the fascinating history of when it came into existence.
There was a time when people wore clocks not just for practicality but also as a fashion statement. Clocks have been instrumental in helping us keep track of time from anywhere.
While wristwatches and smartwatches have become more common, understanding the origins of the clock is still significant. Join us as we dive into the intriguing world of clock invention and history!
What Does the Clock Mean?
Let’s begin by exploring the meaning of a clock, or in simpler terms, what a watch is all about. A watch is a special piece of technology that helps us know the exact time, no matter where we are in the world. It’s like a little timekeeper that we carry with us.
In today’s world, there are many different types of watches that we use every day. Some common ones include:
- Quartz Watch
- Mechanical Watch
- Dress Watch
- Diving Watch
- Chronograph Watch
And there are even more types out there that people like you and me use regularly.
But regardless of the type of watch, they all serve one primary purpose – to tell us the time. So, no matter which watch you choose, its main job is to help you keep track of time.
Who Invented the First Clock?
Now that you know what a watch is, let’s delve into the fascinating history of who invented the very first watch.
The clocks we use to keep track of time are essential in our lives. So, it’s important to learn about the ingenious inventor behind this remarkable device.
Meet Peter Henlein, the person credited with inventing the world’s first watch. He’s the one who brought the concept of timekeeping through a portable device into existence.
Although most of us today rely on our mobile phones to check the time, there was a time when clocks were one of the primary ways to know what time it was. As times have changed, so have we, adapting to the advancements in technology.
Nowadays, we don’t need to glance at a clock to check the time. We can easily find out the specific time by looking at our mobile phones, computers, televisions, and more.
So, in this discussion, you’ve learned about the brilliant inventor who gave us the first watch: Peter Henlein.
Peter Heinlein and the Invention of the Clock
In our previous discussion, we discovered what a watch is and learned that it was Peter Heinlein who first invented it. Now, let’s dive deeper into the fascinating story of Peter Heinlein and the invention of clocks.
The clock made its debut back in 1505, thanks to the brilliant mind of Peter Heinlein. However, you might have heard that clocks were invented in 1577. Well, that’s not quite accurate. Peter Heinlein was the true pioneer, creating the first clock in 1505.
So, why do some people believe clocks were invented in 1577? Here’s the explanation: In 1577, Switzerland made a significant advancement by inventing the first clock with minute divisions. This innovation led to the misconception that clocks were first invented in 1577.
But here’s another interesting tidbit: people didn’t start using clocks widely until around 1650. That’s when they realized that this remarkable device called a clock could help them precisely tell the time, and it marked the beginning of widespread clock usage.
History of Clock Invention
Today, we’re about to embark on an exciting journey into the history of clock invention. While we know who invented the clock and what it’s called, there’s so much more to discover about the fascinating past of this timekeeping device.
Every invention has a unique story behind it, and the clock is no exception. Take, for instance, the watch invented by Peter Heinlein – it has a rich history that led to its creation. So, why not delve into the history of clock invention?
If we go back in time, we’ll find various kinds of clocks, like water clocks and sundials. Each of these clocks had a distinct purpose. Unlike modern wall clocks, these ancient timekeepers showed hours, minutes, and seconds in different ways, making the past world of timekeeping truly intriguing.
Also Read, What is POCO? All About Poco Company
How to see the time in the sun clock?
Let’s explore a special kind of clock called a Sundial. Just like how we use mobile phones or watches to check the time today, people in 1500 BC used the Sundial for the same purpose. It might sound a bit puzzling at first, but once you understand how it works, you’ll be amazed. So, let’s uncover the secret of telling time with a Sundial.
Here’s how it’s done:
- First, you’d stick a simple rod into the ground in your backyard.
- Next, you’d draw a circle around the rod and divide it into several equal parts.
- Then, by observing the sunlight falling on those divided parts, you could figure out what time it was.
Back then, a day wasn’t divided into 24 hours like it is today. Instead, it was divided into eight watches. But Sundials could only tell the time when the sun was up. If, for some reason, the sun didn’t shine in the sky, they couldn’t tell the time. And at night, when there was no sunlight, telling time was impossible.
Interestingly, while we call it a Sundial today, people in 1500 AD referred to this specific type of clock as the ‘Dial of Ahaz.’
How to see the time in the water clock?
In our previous discussion, we explored sundials that relied on sunlight to tell time. Now, let’s dive into the world of water clocks. These unique timekeepers were used around 1600 BC.
During this time, water clocks were quite popular in places like Babylon and Egypt. Interestingly, some historians even believe that the first use of water clocks dates back to around 4000 BC.
Also Read, Itel Company – All About Itel Company
When was the clock invented?
As we learned earlier, the clock was first invented by Peter Heinlein. But you might be wondering, when did this groundbreaking invention take place?
Well, here’s the answer: clocks were invented in 1505. When Peter Heinlein created this remarkable timekeeping device, it marked a significant moment in history. People soon became accustomed to using wristwatches for timekeeping.
If we take a glimpse into history, we can see that since 1650, people have been relying on wristwatches to keep track of time. From then until now, clocks have remained an essential tool for telling time.
Who invented the pendulum clock and when?
Let’s delve into the intriguing world of the pendulum clock. When you hear its name, you might wonder what kind of clock it is and how it tells time. Well, this remarkable clock was actually invented back in 1511.
The first spring-operated clock of its kind was created by a man from Germany. However, when it was initially invented, it had some issues with keeping accurate time. In other words, it couldn’t tell time precisely.
To address this challenge, a special kind of clock was later developed in Switzerland around 1584. This clock was a type of mechanical watch, and it introduced the concept of minute divisions, making it much more accurate in telling time.
Importance of clock invention
From our previous discussions, we’ve learned about the inventors of clocks, including the pendulum clock. Now, let’s explore why the invention of clocks is so important.
Clocks are incredibly vital technology for us. They allow us to keep track of time, from the swiftly passing hours and minutes to the ticking seconds.
Understanding the importance of clock invention is essential because it’s thanks to these inventions that we can know the time accurately. Without clocks, we’d be in the dark about what time it is.
Before clocks, people had different ways to estimate time, but it wasn’t precise. With clocks, we can now know the exact time, which is crucial for our daily lives.
Unknown information about the watch
Prepare to be amazed as we uncover some intriguing secrets about clocks! While we’ve already learned about the inventor of the clock, there’s so much more to discover about these timekeepers. Here are some lesser-known facts that will surely pique your interest:
- Clocks were first invented in 1524.
- The brilliant inventor behind the clock is Peter Hennepin.
- There’s a clock in France, dating back to 1360, that’s still ticking today.
- Clocks started using batteries for the first time in 1906.
- Throughout history, different types of clocks have been used.
- In the pages of history, we find intriguing names like water clocks, star clocks, sun clocks, sand clocks, and wall clocks.
- China introduced a unique clock called the ‘Momghari’.
I hope you find these unknown facts fascinating! They shed light on many remarkable aspects of clocks. Which of these facts do you find the most intriguing? Please share your thoughts in the comments below.
Who Invented the Clock?
How Does the Biological Clock Tick?
How to Make a Clock?
Is Death Clock Accurate?
How Does the Biological Clock Tick?
Our last word on watches
Hello, my friends! In today’s chat, we talked about the inventor of the clock and shared some interesting facts about watches that you might not have known. If you’ve been paying close attention to today’s article, you’ve probably discovered some new insights about your watch.
If you want to be the first to uncover more hidden gems about various topics, make sure to visit our website regularly. And if you enjoyed reading this article, please don’t hesitate to leave a comment. Thank you for taking the time to join us once again!


Hello! My name is Ms. Williamson and I teach Music. This is my first year at PS 49, and it is a great school with wonderful teachers and curious and smart students! I have a doctorate in music from the CUNY Graduate Center and I will be finishing my Master's in music education from Lehman College this fall. I taught at Lehman College for about a decade, but I am happy to have transitioned to K-12 music education to continue my music teaching career.
Other than music and teaching, I enjoy playing softball, hiking, cooking, and film.


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An incredible chance to work with dancers from the New Adventures company to create an original piece of choreography in response to our current show on tour and perform it for an audience. This opportunity is usually delivered in partnership with the theatres we tour to or with established groups that we have led other projects with prior to this experience.
Our curtain raisers primarily give young aspiring dancers the opportunity to work with our world-renowned company through the exploration and development of their technical and creative skills. Resulting in the creation of a short piece, as a response to the themes and movement discovered in the work, they then performance on stage before the show.
As part of our current tour of Matthew Bourne's Swan Lake we have delivered three curtain raisers involving over 60 young dancers on the main stage at Sadler's Wells (London), Birmingham Hippodrome and Mayflower Theatre (Southampton). We regularly work with Sadler's Wells Associate Schools to give this opportunity to young, aspiring dancers in Islington and in 2018 and 2019 it was proudly supported by team Archie. In 2019 we celebrated 10 years of Curtain Raisers at Birmingham Hippodrome.
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domain: artistic


Marijohn Wilkin: 07/14/1920 to 10/28/2006
Some called her “The Den Mother of Music Row,” but Marijohn Wilkin was one of the best pack members herself. In the film Tootsie’s Orchid Lounge: Where The Music Began, she sits there between Willie Nelson and Kris Kristofferson, reminiscing about the years when their generation of songwriters came to Nashville and raised everyone’s idea of what a Music Row song might turn out to be. She cranks up some rhythm, clapping until the two of them reach the speed to back her as she sings the endlessly covered recovery song she wrote with Kris, “One Day At A Time”.
And that was not even the best-known song in Wilkin’s provocative, substantial song catalogue. In 1959, the year after this Texan moved to Nashville to play piano at a bar in Printer’s Alley, she co-wrote two songs that would hit the charts the same day — Stonewall Jackson’s incessantly catchy “Waterloo” and, yes, that indelible saga “Long Black Veil”, a song so telling in story detail that it was often mistaken for an ancient folk tome, all the more so by those who first heard it by Joan Baez or The Band rather than Lefty Frizzell, who had the original, spookifying hit.
Marijohn Wilkin songs were grabbed up by the rock ‘n’ roll world, as well as country — “Cut Across Shorty” (Eddie Cochran, Rod Stewart) and “I Just Don’t Understand” (the Beatles) for two.
Wilkin joined the likes of Mel Tillis and John D. Loudermilk as a key member of the Cedarwood Music writers stable, and was a pioneer as a top-level woman writer and music publisher in very male-dominant Nashville (she discovered and signed Kristofferson, for instance). All the while, she remained a much-in-demand studio backup singer, sometimes joining the fabled Jordanaires, sometimes as leader of her own group, frequently seen on the Bobby Lord television show. She recorded several relatively obscure country LPs of her own for major labels before establishing a more successful performing career in gospel.
Wilkins’ songwriting took hold in the ’50s when her guitar-slinger son Bucky (later of surf rockers Randy & the Daytonas of “G.T.O.” fame), began appearing on the “Ozark Jubilee” national TV series out of Missouri; she began providing songs for the show. Acknowledged struggles with depression and alcoholism may have complicated her personal life and her health, but it never sidelined the grit and gifts of a singular talent.
Kristofferson noted, when news came of her passing on October 28 at age 86, “Marijohn embodied the spirit of the way of life to which I was to commit myself some 40 years ago….She was a tough, intelligent, and funny woman making it in a man’s world. She taught me more in the first couple of years I was in Nashville about the heart and soul of the Nashville music world than I could ever have learned on my own.”


TRENTON — In its first and only meeting this month, the state Senate this afternoon is scheduled to vote on raising the state's minimum wage.
The upper house will consider two pieces of legislation on the raise.
One is a bill (S3) that would increase the minimum wage from $7.25 to $8.50 and tie future automatic increases to inflation. The Assembly passed it six months ago, though they'll have to take the legislation up again when they meet Monday because it has changed slightly since then.
The other is a resolution that would ask voters to write an increase, including the annual cost of living adjustments, into the state constitution. The Senate is taking that up in the event that Gov. Chris Christie vetoes the bill.
To get the constitutional amendment before voters next November, both the Senate and Assembly need to pass it once this year and again next year, or cobble together a three-fifths majority — which they’re not expected to get.
The Senate is also taking up more than two dozen other bills, including one (S2) that would penalize towns that refuse state recommendations on sharing services, and a measure (S1434) that would require toll booth screens to show E-ZPass users how much they're paying.
The session is scheduled to begin at 2 p.m.


Skip to comments.Frank Rich Is Wrong: Hate Didnít Kill Kennedy, But It Is Killing Civil Discourse in America
Posted on 11/22/2011 3:28:24 PM PST by jazusamo
Today marks the 48th anniversary of the assassination of President John F. Kennedy. The slain presidents wife, his successor, and the liberal media blamed the murder on Dallas climate of hate. That smear cast a pall on the innocent citizens of that city for decades. I know, because I grew up in the shadow of Big D and in the shadow of Kennedys killing. For decades after Nov. 22, 1963, you could go anywhere in the country, tell anyone you were from Dallas, and if you spent enough time with that person, Kennedys assassination would inevitably come up.
Frank Rich chose to mark the 48th anniversary by smearing Dallas, again, and by extension conservatives of the present. Its a column which should get him ridiculed and fired; no one who is so irresponsible with the hard facts of life has any place in the commentariat.The title gives Richs game away. Its What Killed JFK? not Who Killed JFK? as it should be. A what is much easier to abstract, isolate, and attack than a who who had inconvenient opinions and motivations, and a madness to move.
The cold, hard fact of that day in Dallas is this: Whether Kennedy was killed by a lone gunman or by a conspiracy that included others, Dallas climate had nothing to do with it. Dallas was the scene of the crime but wasnt responsible for it. Lee Harvey Oswald was not a mainstream Dallas man. He would not have been a Tea Partier. Lee Harvey Oswald was a communist. He had defected to the Soviet Union, become disillusioned, and returned. He had tried to travel to Cuba and failed. If hate was Oswalds motive in Kennedys killing, the hate lived in the chest of a man who had failed at life, had rejected the freedoms of his country, and used bullets to write himself into the history books. Lee Harvey Oswald was an America-hating leftist.
Or, alternatively, Kennedy was killed by a conspiracy to stop his Vietnam policy or whatever the Oliver Stones of the world think. You make the call. Either way, Dallas is not collectively guilty of Kennedys death anymore than Washington DC is collectively guilty of Lincolns.
To the extent that his politics are relevant today, Lee Harvey Oswald belongs to the same ideological strain that later gave us Pentagon bomber Bill Ayers. That same strain of politics can be traced through a certain church in Chicago, right to the camps in Oakland, Los Angeles and Wall Street. People who subscribe to this strain of thought blame others for their feelings of powerlessness. They reject American freedom and damn America. They accept some violence as a legitimate political tactic. They despise America and want to bring her down to create a moment in which they can rearrange power to their benefit.
But Im less interested in them at the moment than I am interested in Frank Rich. His column shows that in all the decades since Kennedys murder, the left has never really changed. They blamed Dallas for Kennedys death then, and they blame Sarah Palin and conservatives for the senseless shooting in Tucson this year. The facts of the story change, but the smear stays the same. Frank Rich blames hate for both, but the only hate on display is his own. It blinds him to the fact that Oswald was a man very much of the left, and that the Tucson shooter had no discernible ideology at all. But men of the left such as Rich prefer to assign collective guilt on their political enemies. Without pushing that collective guilt on others, their own lives have no meaning. They cannot convince themselves of their own superiority without an inferior other to hate. And collective guilt is a useful tool to intimidate. There is a reason that Saul Alinsky has found such a receptive audience among the left. Theyre fueled by hate; Alinsky gave them the means of channeling that hate toward useful (to the haters) ends.
Frank Richs hatefulness is killing civil discourse in America. It dishonestly condemned an entire city for generations and turns an innocent campaign map into a murder map. It replaces individual responsibility with collective guilt, and turns what should be a unifying national tragedy into corrosive partisan crossfire.
That's stating the obvious, ain't it? But it would be the NYT that lets a theater critic become a political "pundit".
Frank Rich Is Wrong
I ‘m so bored with the left and their “hate” chatter. They sound like a bunch on junior high school girls.
I’d like to apologize to the junior high school girls for the previous post.
You are demeaning junior high school girls. The left doesn’t even rise to that level...when my daughters were in middle school they were MUCH more responsible.
He’s not only quick, he’s correct. :-)
Frank Rich has never been right about anything...including his positive review of “Follies” way back when...
I agree, and I was speaking of fkabuckeyesrule.
Texan LBJ was his VP. LHO just happened to live in Texas, his activities were such he could’ve lived anywhere and acted as he did.
Yep. There’s been speculation about LBJ being involved and I confess that thought came to mind when Kennedy was assassinated. I have no idea but LBJ was a crook in my view.
Dallas and its citizens were no more responsible for the JFK assassination than LA was for RFK, Miami was for Mayor Cermak, Washington was for Lincoln or Garfield or Buffalo was for McKinley. It serves a purpose for nasty rotund liberals like Frank Rich to target entire groups with hate - they are the true haters. The Dallas police were incompetent, JFK should never have been riding in an open convertible and wearing a stiff neck brace, the Secret Service should not have been out drinking the night before. But none of this was the cause of the assassination - the real cause was a misfit Communist who dreamed of foul glory. Deniers of Oswald’s role in the assassination have never been able to explain just why he killed Officer Tippitt, other than to escape apprehension for the JFK murder.
Same thing happened to Laramie, Wyoming. Because two meth heads thought a gay panic defense would be a good idea, a good town was smeared.
Wait Frank Rich IS wrong! The Rolling Stones said Kennedy was killed “by yooou and meeee...”
LBJ killed Kennedy....according to Jackie!! I’m with Jackie.
LBJ killed Kennedy....according to Jackie!! I’m with Jackie.
Oswald WAS a communist - he was NEVER a typical Dallas conservative. He was an OWS, Bill Ayers type. Period. Liberals were and are the haters...
Yep...I knew that. Thanks
Yes, he was, and this has been known by everyone (except Frank Rich, apparently) for nearly 50 years.
This is a very good column and Dallas is worthy of being publicly defended, but it is a shame the column was inspired by a floating turd like Rich. He simply should never be taken seriously.
The case connecting Oswald to Officer Tippets murder is also flawed.The only witness first claimed to see two men at the murder scene and only changed her mind after a visit by the FBI.Several other witness’s claimed to see two Cuban looking men running from the scene.Also Officer Tippets mistress had just informed him that morning of her pregnancy and that her husband was “gunning for him”.The ballistics were also wrong and Oswald passed the parafin test.probably just the normal BS in any murder investigation but it goes to show the enduring mystery of this case.


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BY LEE ZIMMERMAN
Retro has come to mean any number of things in today’s genre-obsessed mindset. It’s not enough for a band to tag itself as simply roots-related; instead, it becomes mandatory to identify exactly which roots are being referenced. So when a band like The Dustbowl Revival comes along, a group that seems to take its cues from a smorgasbord of past precedents, it’s bound to throw the purists for a loop. This, their sophomore set, includes a number of weathered standards that stretch back a century or more, as well as several songs dating from the ‘20s, ‘30s and the prewar period in general.
That’s not to insinuate that Carry Me Home is merely a rehash or a history lesson; rather, this L.A.-based collective adds imagination and instrumental enhancements that actually affirm the original intents. The revered gospel hymn “Swing Low” begins with hushed harmonies and grows gradually into a rousing spiritual celebration. “John The Revelator” sheds its somber overtones in favor of raucous revelry. The Civil War lament “Soldier’s Joy” is transformed from a weary lament into a spontaneous foot-stomping, hand-clapping hoedown. Other tracks follow suit, flush with the sound of doo-wop, Dixieland, whimsy and ragtime. Ultimately, The Dustbowl Revival stay true to their name, and the results achieve something extremely rare, a sound that taps tradition while paying no heed to parameters. Praise be—this is one hell of a hallelujah.
DOWNLOAD: “Swing Load,” “Soldier’s Joy,” “John the Revelator”


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Austin Mahone is doing everything to win Camila Cabello back
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domain: celebrity


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Are there too many crime dramas on TV?
BBC1 controller Danny Cohen has criticised the number of crime dramas on TV.
He also said the BBC ran the risk of having too many” male detectives on screen.
Cohen said the number of male-led crime shows had fuelled his decision to axe the Rome-based series Zen earlier this year after just three episodes.
He said he was hoping to “broaden the range” of shows commissioned for BBC1.

domain: law


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Inflammation and apoptosis play critical roles in the acute progression of ischemic injury pathology. Emerging evidence indicates that vagus nerve stimulation (VNS) following focal cerebral ischemia and reperfusion (I/R) may be neuroprotective by limiting infarct size. However, the underlying molecular mechanisms remain unclear. In this study, we investigated whether the protective effects of VNS in acute cerebral I/R injury were associated with anti-inflammatory and anti-apoptotic processes. Male Sprague-Dawley (SD) rats underwent VNS at 30 min after focal cerebral I/R surgery. Twenty-four h after reperfusion, neurological deficit scores, infarct volume, and neuronal apoptosis were evaluated. In addition, the levels of pro-inflammatory cytokines were detected using enzyme-linked immune sorbent assay (ELISA), and immunofluorescence staining for the endogenous “cholinergic anti-inflammatory pathway” was also performed. The protein expression of a7 nicotinic acetylcholine receptor (a7nAchR), phosphorylated Akt (p-Akt), and cleaved caspase 3 in ischemic penumbra were determined with Western blot analysis. I/R rats treated with VNS (I/R+VNS) had significantly better neurological deficit scores, reduced cerebral infarct volume, and decreased number of TdT mediated dUTP nick end labeling (TUNEL) positive cells. Furthermore, in the ischemic penumbra of the I/R+VNS group, the levels of pro-inflammatory cytokines and cleaved caspase 3 protein were significantly decreased, and the levels of a7nAchR and phosphorylated Akt were significantly increased relative to the I/R alone group. These results indicate that VNS is neuroprotective in acute cerebral I/R injury by suppressing inflammation and apoptosis via activation of cholinergic and a7nAchR/Akt pathways.
Citation: Jiang Y, Li L, Liu B, Zhang Y, Chen Q, Li C (2014) Vagus Nerve Stimulation Attenuates Cerebral Ischemia and Reperfusion Injury via Endogenous Cholinergic Pathway in Rat. PLoS ONE 9(7): e102342. https://doi.org/10.1371/journal.pone.0102342
Editor: Yvette Tache, University of California, Los Angeles, United States of America
Received: March 18, 2014; Accepted: June 16, 2014; Published: July 18, 2014
Copyright: © 2014 Jiang et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Data Availability: The authors confirm that all data underlying the findings are fully available without restriction. All relevant data are within the paper and its Supporting Information files.
Funding: This work was supported by the National Nature and Science Foundation of China (Grant NO. 81271306). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Competing interests: The authors have declared that no competing interests exist.
Acute cerebral ischemia triggered by interruption of blood flow can cause rapid activation of a variety of detrimental cellular processes, including excitotoxicity, oxidative and nitrosative stress, cortical spreading depolarization, inflammation, necrosis, and apoptosis –. It is known that revascularization of occluded blood vessels is the most effective treatment for patients with acute ischemic stroke . However, reperfusion may cause secondary injury via mitochondrial dysfunction, excessive release of glutamate, and overproduction of pro-inflammatory mediators and reactive oxygen species (ROS). These factors directly influence the prognosis of stroke patients , and controlling excessive inflammatory response is an important therapeutic challenge.
Since its approval for clinical use by the Food and Drug Administration (FDA) in 1997, vagus nerve stimulation (VNS) has been a safe and effective treatment for refractory partial epilepsy seizures – and resistant depression . Its therapeutic potential in other applications, including pain , obesity , cognitive impairment , and anxiety  have been explored as well. Outside the CNS, VNS has been reported to have an anti-inflammatory effect . In rat cardiomyocytes under hypoxia conditions, VNS activates the anti-apoptotic process involving increased phosphorylation of Akt via upregulation of acetylcholine (Ach) release . Emerging evidence demonstrated that a brief VNS initiated 30 min after both transient and permanent cerebral ischemia significantly improved neurological function deficits and reduced infarct volume in I/R rats . However,the molecular mechanisms underlying VNS-mediated neuroprotection are still unknown.
In this study, we evaluated the neuroprotective effects of VNS in an animal model of acute cerebral I/R. We assessed neurological deficit scores, infarct volume, and neuronal apoptosis. In addition, we measured the level of pro-inflammation cytokines, activation of the cholinergic anti-inflammatory pathway, and the a7nAchR/Akt signaling pathway involved in preventing neuron death under acute cerebral I/R conditions.
Materials and Methods
The experimental protocols were performed in strict accordance with the Guidelines for the Care and Use of Laboratory Animals approved by the Institutional Ethics Committee of Chongqing Medical University (Permit No. SCXK (Chongqing) 2007-0001) and the State Science and Technology Commission of China. Animal experiments were performed at the Laboratory Animal Management Committee of Chongqing Medical University. Male Sprague-Dawley (SD) rats (250–350 g, n = 158) were obtained from Experimental Animals Center of Chongqing Medical University and housed at 20–25°C and 60% humidity with a 12 h light/dark cycle, and free access to food and water. Animals were randomly assigned to one of three groups (n = 8 rats/group): sham+VNS group; I/R group; and I/R+VNS group. There was no significant difference in weight among the groups.
The focal cerebral ischemia and reperfusion model
The focal cerebral ischemia model was established according to the intraluminal occlusion technique as previously described by Koizumi et al . First, animals were anesthetized with 10% chloral hydrate (350 mg/Kg). After a midline neck incision with the animal in supine position, the right common carotid artery (CCA) and internal carotid artery (ICA) were sequentially exposed from adjacent nerves and tissue. With the right external carotid artery (ECA) ligated, microaneurysm clips were placed at both ICA and ECA, a small incision was made on the ECA stump near the carotid bifurcation, and a nylon filament coated with silicone (diameter = 0.31–0.32 mm) was inserted into the right internal carotid artery about 9–10 mm. The animals were then placed into a stereotaxic frame, and a laser doppler flowmeter probe (Peri Flux system 5000; Perimed, Stockholm, Sweden) monitored changes in cerebral blood flow (CBF) in the right middle cerebral artery region in order to confirm successful middle cerebral artery occlusion (MCAO). When the nylon filament was inserted approximately 18–22 mm, a silk suture was then tightened around the ECA stump and nylon filament. Reperfusion was achieved after removal of the nylon filament 2 h after occlusion. The standard I/R model was defined as a decrease in cortical CBF to 70–80% of baseline during the first 30 min and >70% flow recovery within the initial 10 min of reperfusion. Animals that did not meet these requirements or those without neurological deficits were excluded from the study. Throughout the duration of the experiment, animals were anesthetized and body temperature was maintained at 37±0.5°C with a heating pad. The caudal ventral artery of the tail (coccygeus medial artery, CVA) was exposed, and 24 G catheters (Becton Dickinson and Company, Franklin Lakes, NJ, USA) were inserted and connected to a Datex AS3 physiological monitoring instrument (Communications Specialties, Inc., Ronkonkoma, NY, USA) through heparin-filled pressure transducers and sampled for blood gas analysis. Invasive blood pressure (BP) monitoring occurred at five time points: baseline (BS), before VNS (BVNS) (0–30 min after MCA occlusion), during VNS (DVNS) (30–90 min after MCAO), after VNS and before reperfusion (AVNS), and after reperfusion (AR); and heart rate (HR) was measured at the same time points during the duration of the experiment. Blood gases were measured at three points: BVNS, DVNS, and AR (ABL700, Radiometer, Bronshoi, Denmark).
Electrical stimulation of right cervical VN
Animals received VNS 30 min after MCAO with a Grass Model S48 stimulator (Grass Technologies, Warwick, RI, USA). VNS consisted of 30 s, 20 Hz trains of 0.5 mA, 0.5 ms pulses delivered every 5 min for a total of 60 min . The stimulating electrodes were self-constructed, as previously described , and were composed of two polyethylene coated curved silver wires held 1.5 mm apart by a solid bar. Following a ventral midline incision made on the neck, muscles were retracted and the right carotid sheath was exposed. The right cervical VN was carefully dissected from the carotid sheath, and the exposed wires inside of the curve of the stimulating electrode were placed on the nerve. Electrodes were then sutured to the sternocleidomastoid muscle and wrapped around the right cervical nerve. Identical procedures were performed in the I/R+VNS and sham+VNS group with the exception of the occlusion in the sham+VNS group (Fig.1). Two rats died during the stimulation process because of cardiac arrest (I/R+VNS group), and one (I/R group) died due to the suffocation.
I/R and I/R+VNS groups underwent transient MCAO surgery. In the I/R+VNS and sham+VNS group, VNS was initiated at 30 min after occlusion and repeated every 5 min for 1 h. At 120 min, I/R and I/R+VNS groups underwent reperfusion. During the experiment, the mean CVA, HR, and blood gas were measured at the designated time points. Laser doppler flowmetry monitored the changes of right cerebral middle artery blood flow, and temperature was maintained at approximately 37°C. Neurological deficit scores assessment was performed at 3 and 24 h after reperfusion.
Evaluation of neurological function scores
Neurological function of the rats (n = 8 rats/group) was evaluated 3 and 24 h after surgery according to the criteria of a 5-point rating scale: 0, no deficit; 1, failure to extend the left forepaw; 2, decreased grip strength of left forepaw; 3. circling to left after pulling the tail; 4, spontaneous circling .
Cerebral infarct volume measurement
At 24 h after assessment of neurological deficit scores, rats (n = 8 for each group) were deeply anesthetized and sacrificed, and fresh brains were rapidly removed and frozen at −20°C for 20 min. The brains were coronally sectioned into 2- mm thick sections with a stainless steel mold, and sections were stained in a 2% 2,3,5-triphenyltetrazolium chloride (TTC, Sigma-Aldrich, St. Louis, MO, USA) solution for 30 min at 37°C in the dark, and fixed in 4% paraformaldehyde (PFA) in 0.1 M PB. Stained slices were photographed with a digital camera and analyzed with Image J software (NIH Image, Bethesda, MD, USA).The infarct volume was calculated as described previously . The percentage of infarct volume was calculated as the (normal hemisphere volume minus non-infarct volume of infarct side) over the normal hemisphere volume times 100%.
DNA fragmentation, a marker of apoptosis, was measured using TdT mediated dUTP nick end labeling (TUNEL) staining with an In Situ Cell Death Detection Kit® (Roche, Basel, Switzerland), as previously described . At 24 h after reperfusion, rats (n = 10 for each group) were first anesthetized with 10% chloral hydrate (350 mg/Kg) and serially transcardially perfused with 150 ml phosphate-buffered saline (PBS) and 150 ml 4% paraformaldehyde until all limbs became stiff. The brains were removed, post-fixed in 4% paraformaldehyde for 24 h, and then embedded in paraffin for slicing 5 µm sections. Briefly, the sections were post-fixed in ethanol-acetic acid (2∶1), rinsed, incubated with 1% proteinase K (in 50 mM Tris/5 mM EDTA buffer) for 15 min, rinsed, incubated in 3% H2O2, permeabilized with 0.5% Triton X-100, and rinsed again. Subsequently, sections were incubated in the TUNEL mixture for 1 h at 37°C, rinsed, and visualized using a converter-POD with 0.03% 3,3′-diaminobenzidine, counterstained with hematoxylin/eosin (HE). Five different random high-power fields (400X magnification) in peri-infarct region were counted for each condition using a light microscope, and TUNEL-positive apoptotic cells appeared as brown nuclear or cytoplasmic staining. The numbers of TUNEL positive cells from three slices per brain were averaged. Cell counting was performed by a pathologist blinded to the experiment condition.
Enzyme-linked immune sorbent assay
Rats (n = 15 for each group) were sacrificed 24 h after neurological functional assessment, and the right ischemic penumbra cortices (n = 5 for each group/time) were isolated and rinsed with ice-cold physiological saline for enzyme-linked immune sorbent assay (ELISA) and immunoblotting. Using ELISA, the concentrations of TNF-a, IL-1β, and IL-6 in ischemic cortex tissue homogenates were measured according to the manufacturer's instructions (R&D systems, Minneapolis, MN, USA). The experiments were performed in triplicate.
Double immunofluorescence staining for microglia and a7nAchR
Rats (n = 8 for each group) were anesthetized 24 h after surgery and serially transcardially perfused with 150 ml PBS and 150 ml 4% paraformaldehyde in 0.1 mol/L PBS (pH 7.4). Brains were post-fixed in the same fixative overnight and infiltrated with 30% sucrose at 4°C. Frozen brains were sliced into 10 µm thick coronal sections, permeabilized with 0.4% TritonX-100 for 10 min, blocked in 10% normal donkey serum for 30 min, and incubated with primary antibodies (rabbit anti-a7nAchR, 1∶500, Abcam, Cambridge, UK and goat anti-Iba-1, 1∶500, Novus Biologicals, Littleton, CO, USA) for 16 h at 4°C. The next day, sections were rewarmed at 37°C for 1 h, washed with PBS for 15 min, incubated with secondary antibodies (AMCA-conjugated AffiniPure Donkey Anti-Rabbit IgG 1∶200 and FITC-conjugated AffiniPure Donkey Anti-Goat IgG;1∶200, Sheng Gong,Shanghai,China) for 1.5 h at 37°C, and washed for 30 min with PBS. Sections were observed and images were captured using a Laser Scanning Confocal Microscope (LEICA TCS SP2,Wetzlar, Germany).
As previously described, protein samples were generated from frozen cortex homogenized with lysis buffer . Equal amounts of protein were loaded onto either 10% or 12% sodium dodecy1 sulfate-polyacrylamide gel electrophoresis gels (SDS-PAGE) and electrophoretically transferred onto nitrocellulose membranes. Membranes were blocked with Tris-buffered saline+0.1% Tween-2 (TTBS) plus 50 g/L nonfat milk for 2 h and then incubated with a rabbit anti-p-Akt antibody (1∶1000; Cell Signaling Technology, Beverley, MA, USA), a rabbit anti-a7nAchR antibody (1∶1000, Abcam) a mouse anti-caspase-3 antibody (1∶1000; Cell Signaling Technology), and a mouse anti-β-actin (1∶5000; Sigma) at 4°C overnight. The membranes were washed for 15 min in TBST and incubated with HRP-conjugated secondary antibodies for 2 h at 37°C. The bands were visualized using an enhanced chemiluminescence reagent kit (GE Healthcare, Chalfont St. Giles, UK), detected on X-ray film, and analyzed with the Image J (National Institutes of Health, Bethesda, MD, USA). Results were expressed as the ratio of target protein OD over β-actin OD.
All experimental data, except for neurological scores, were expressed as mean±standard error of the mean (SEM) and compared using a one-way analysis of variance (ANOVA) with a post hoc Tukey multiple-comparison test. The neurological scores were analyzed with Kruskal-Wallis test. P-value of less than 0.05 was considered statistically significant. All statistical analyses were carried out using SPSS, Version 17.0 (Chicago, IL, USA).
As shown in Fig. 2, the mean CVA pressure in the baseline period was 90.5±6.3 mmHg in the sham+VNS group, 87.3±5.7 mmHg in the I/R group, and 88.7±5.1 mmHg in the I/R+VNS group. There were no significant changes in mean CVA pressure during the MCAO. In the sham+VNS and I/R+VNS groups, the BP decreased relative to baseline by 81.2±14.7 and 78.7±15.1 mmHg, respectively, during the 30 s stimulation period. After VNS, mean arterial pressure rapidly recovered near to baseline level.
Changes in tail arterial pressure are shown for the three groups during the experiment. The time points are as follows: baseline (BS), after occlusion but before stimulation (BVNS), during the stimulation (DVNS), after stimulation but before reperfusion (AVNS), and after reperfusion (AR). * p<0.05 relative to the time point (BVNS). #p<0.05 relative to the time point (AVNS).
There was no significant difference in HR during baseline between the I/R+VNS group and other groups (p>0.05). HR in the I/R+VNS group decreased dramatically during the 30 s electrical stimulation, approximately 265±27 beats per minute (bpm), and HR returned immediately to normal range upon cessation of the stimulation. A similar change in HR was observed in the sham+VNS group (Fig.3). In all three groups, arterial blood gases(PH, PO2, and pCO2) remained within the normal range during the experimental period (Table.1).
HR is plotted for the same time points as in Fig. 2. HR and BP immediately fell during each pulse train and recovered to baseline values upon cessation of the stimulation in I/R+VNS and sham+VNS groups. * p<0.05 in comparison to the time point (BVNS). #p<0.05 in comparison to the time point (AVNS).
Monitoring of region cerebral blood flow
As shown in Fig. 4, CBF of the right middle cerebral artery region was decreased by 70–80% of baseline after occlusion and returned to pre-ischemic level when the filament was removed in both I/R and I/R+VNS groups. Although there was a small increase in the I/R+VNS group relative to the I/R group during the stimulation, it was not statistical difference (p>0.05), suggesting that VNS had no significant effect on the changes of CBF in I/R rat.
Neurological deficit scores
Neurologic deficit scores were acquired at 3 h and 24 h after occlusion in the I/R and I/R+VNS groups. The scores of the I/R+VNS group were significantly lower than the I/R group at 24 h but not 3 h (Fig. 5, p<0.05), suggesting that VNS reversed neurological deficits 24 h after ischemia.
Measurement of infarct volume
In order to determine the extent of brain damage 24 h following reperfusion, TTC staining was performed. As shown in Fig. 6, the infarct volume was significantly smaller in the I/R+VNS group relative to I/R group. The percentage of infarct volume of the contralateral hemisphere in the I/R+VNS treatment group was 25.4±6.3% and 44.1±8.0% for the I/R group (p<0.05). Therefore, VNS reduced the infarct volume 24 h after reperfusion.
TTC staining in the three groups at the level of bregma 0.4mm. A: sham+VNS group, B: I/R group, and C: I/R+VNS group. D. Histograms show that the relative percentage of infarct volume 24 h after acute I/R. Red area is the healthy tissue, and the white area is the infarct tissue. *p<0.05 with relative to the I/R group, #p<0.05 relative to sham+VNS group.
The number of TUNEL-positive cells in the per-infarct area of the right cortex in the I/R+VNS group was significantly less than that in the I/R group (Fig. 7). Quantitative analysis showed that VNS suppressed apoptotic responses, which may partly explain the neuroprotective effect of VNS in ischemic brain injury.
Representative photomicrographs of neuron apoptosis in right ischemic penumbra cortex 24(magnification 400×). A: sham+VNS group, B: I/R group, C: I/R+VNS group. D: Quantitative analysis of the number of TUNEL-positive cells in the ischemic penumbra. Data are expressed as mean ±SEM; *P<0.05 vs I/R group, #p<0.05 vs sham+VNS group, scar = 100 µm.
Effect of VNS on the inflammatory cytokines
To determine the anti-inflammatory response following transient VNS in rats with I/R injury, we measured the levels of pro-inflammatory cytokines (TNF-a, IL-1β, IL-6) in the ischemic penumbra cortex 24 h after reperfusion. As expected, the levels of TNF-a, IL-1β,IL-6 were significantly decreased in the I/R+VNS group compared with the I/R group(p<0.05, Fig. 8). This clearly showed that VNS modulated the expression of inflammatory cytokines in brain under ischemic conditions.
The concentrations of TNF-a, IL-1β, and IL-6 of the peri-infarct region were measured by ELISA. A: TNF-a, B: IL-1β, C: IL-6 at 24 h reperfusion in the peri-infarct region. Data are presented as mean±SEM (n = 15 per group); *P<0.05 vs I/R group, #p<0.05 vs sham+VNS group.
Expression of a7nAchR on microglia following ischemia-reperfusion
Under normal conditions, microglia have highly motile branches that persistently survey the CNS to detect aberrations from homeostasis. In response to brain injury, microglia reduce the complexity of their shape by shortening their branches and rapidly move to injury sites to express chemokines and growth factors. As shown in Fig. 9, microglia were activated rapidly with morphological changes consistent with brain injury in both the I/R and I/R+VNS groups. There was no significant difference between the sham and sham+VNS groups. The expression of a7nAchR on microglia in the ischemic penumbra was significantly elevated in the I/R+VNS group compared with the I/R group. These findings suggest that VNS may modulate inflammatory responses induced by I/R injury in brain via activating a7nAchR on microglia.
The expression of a7nAchR was reduced following I/R and increased by VNS. Underwent ischemic insults, the morphology of the microglial cell changed. A: Staining for a7nAchR in red, B: Staining (microglia) Iba-1 in green, C: merge of A and B. scare bar = 75 µm.
Western blot analysis
As shown in Fig. 10, protein expression of a7nAchR was significantly decreased in the I/R group relative to the sham+VNS group, and this downregulation was inhibited by VNS (P<0.05). We found that the expression of a7nAchR in brain could be regulated by VNS treatment after I/R in rats, suggesting that the neuroprotective effect induced by VNS may be partly due to the up-regulation of a7nAchR expression. To further investigate the anti-apoptotic mechanism of VNS on cerebral I/R, we also measured the protein expression of phosphorylated Akt and cleaved caspase 3 in ischemic penumbra cortex 24 h after reperfusion. Relative to the I/R group, the level of phosphorylated Akt (p-Akt) was significantly upregulated and the level of cleaved caspase-3 was noticeably decreased in I/R+VNS group (p<0.05, Fig.9). Thus, VNS may exert anti-apoptotic effect via activation a7nAchR/Akt signaling pathway in brain following cerebral I/R.
Western blot showing the differential protein expression of a7nAchR, P-Akt, and cleaved caspase-3 24 h following reperfusion in the ischemic penumbra of rats among the three groups. β-actin is a loading control, showing equal loading of protein. A: sham+VNS group; B: I/R group; C: I/R+VNS group. (A) The density of a-7nAchR, (B) p-Akt, and (C) cleaved caspase 3 protein expression normalized to β-actin protein expression. *P<0.05 relative to the I/R group, #p<0.05 relative to the sham+VNS group, n = 8/group.
In this study, we found that a brief repetitive VNS could improve neurological deficit scores, attenuate cerebral infarct volume, and decrease neuronal apoptosis 24 h after reperfusion. Importantly, the neuroprotective effect is independent of any alterations in CBF .
Previously, it was shown that VNS could improve neurological scores and reduce infarct volume by nearly 50% 24 h after transient MCA occlusion in a rat model of I/R injury , suggesting a neuroprotective role of VNS in acute cerebral ischemia. Interestingly, it had been demonstrated that the neuroprotection induced by VNS could be maintained up to three weeks after the ischemic event . Here, at 24 h after ischemia, neurologic deficit scores, ischemic infarct volume, and the number of TUNEL positive cells were decreased in the I/R+VNS group relative to the I/R group, consistent with another study . It is our supposition, based on our and other studies, that VNS-associated neuroprotection in acute ischemic stroke is due to inhibition of inflammatory and apoptotic processes.
Recently, direct electrical stimulation of the peripheral VN in the liver of endotoxemia rats was found to inhibit TNF-a synthesis, attenuate peak serum TNF-a levels, and prevent the development of shock . Similarly, vagotomized mice with experimental pancreatitis exhibited significantly worse tissue damage relative to mice with intact VNS. The severity of the pacreatitis was significantly decreased after administration of GST-21 and a7nAchR receptor agonists . In this study, we found that VNS decreased the level of pro-inflammatory cytokines (TNF-a, IL-1β, and IL-6) 24 h after reperfusion in the ischemic penumbra.
The cellular and molecular mechanisms for anti-inflammation are partly attributable to acetylcholine (Ach), a neurotransmitter mainly released from VN endings. Activation of a7nAChR by Ach on macrophages suppresses the release of pro-inflammatory cytokines in peripheral circulation, thereby preventing tissue damage via the inflammation reflex of the VN. Although it had identified that VNS was effective due to recruitment of the cholinergic anti-inflammatory signaling pathway in the periphery system , there was little evidence available regarding its link to neuro-inflammatory modulation in the central nervous system (CNS).
The signals triggered by VNS elicit the endogenous cholinergic anti-inflammatory pathway by activating a7nAchR. These receptors are commonly expressed in brain, including neurons,glia, and endothelial cells; and activation of these receptors can enhance neuronal resistance to ischemic or other types of insults. This is the so-called “cholinergic anti-inflammatory pathway,” and it represents a physiological mechanism whereby the brain can interact with the innate immune system to control inflammatory response .
After an ischemic insult, resident microglia and astrocytes activate the CNS immune response, produce pro-inflammatory cytokines, and upregulate the production of reactive oxygen species (ROS) by NADPH oxidase (detrimental for stroke outcome). TNF-a and IL-1β in brain tissue are primarily produced by microglia and other immune cells  that rapidly respond to local injury. In recent studies, growing evidence has shown that activation of a7nAchR expressed on microglia is neuroprotective and an integral party in the fight against various brain injuries. In addition, microglia a7nAchR activation may afford neuronal protection against ischemic injury in vitro models of oxygen and glucose deprivation . Wang et. al  found that although VNS inhibited cytokine release in wild type littermates, it had no effect on the prevention of TNF-a release in a7nAchR knockout mice. Immunofluorescence staining for a7nAchR and microglia cells partly overlapped, suggesting that VNS suppression of pro-inflammatory cytokines production was in part due to activation of a7nAchR expressed on microglia cells.
The PI3K/Akt signaling pathway plays a crucial role during cellular development, function, and survival . Akt is considered to be cytoprotective through intrinsic mechanisms during cell injury , and p-Akt can activate downstream caspases, which is associated with the release of cytochrome, the activation of caspase 9, and activation of caspase 3. Previous reports had shown that the hepatic protective effect of nicotine was associated with a suppression in peripheral inflammation via activation of the vagal cholinergic pathway, increased expression of the anti-inflammatory protein heme oxygenase-1,and downstream activation of Akt . In acute myocardial ischemia, vagal nerve stimulation increased Hypoxia-inducible factor-1 alpha (HIF-1a) expression and reduced infarct size . Krafft PR et al.  demonstrated that that a7nAchR activation decreased neuronal cell death by increasing p-Akt and decreasing cleaved caspase 3 expression in a mouse model of intracerebral hemorrhage. Interestingly, nicotine via activation of the α7nAChR receptor in the pro-survive pathway is neuroprotective in PC12 cells . In order to assess the anti-apoptotic mechanism of VNS in acute cerebral I/R models, we evaluated protein expression of a7nAchR, p-Akt, and caspase 3 at 24 h after ischemic stroke.
From our study, we observed that the protein level of both a7nAchR and p-Akt was significantly higher in the I/R+VNS group than the I/R group and that the expression of cleaved caspase-3 was significantly less in the I/R+VNS group. Thus, the protective effect provided by VNS in ischemic brain tissue may be partly due to increased expression of a7nAchR and p-Akt and decreased activation of proapoptotic caspase. Similar findings were demonstrated in a rat model of subarachnoid hemorrhage following a7nAchR stimulation . Taken together, these data suggested that activation of the endogenous cholinergic pathway led to anti-inflammation and prevention of apoptosis partly by activation of a7nAchR expressed on microglial cell and a7nAchR/Akt pathway in brain, respectively. Therefore, activation of a7nAchR, either electrically with VNS or pharmacologically, could be a novel therapeutic method for early intervention in preventing secondary injury in acute ischemic stroke.
However, there are several limitations of our study. We only used an acute cerebral I/R model and did not confirm our findings at later time points in a chronic cerebral I/R model. To date, there is a little evidence available to suggest that neuroplastic processes could be enhanced by VNS in the rat brain during the recovery phase following stroke  and if it might be an effective therapy to restore motor function clinically. Interestingly, some studies have found that acute VNS increased the expression in cortex and hippocampus of rat of brain-derived neurotrophic factor and fibroblast growth factor in the hippocampus and cortex of rat, both beneficial for enhancing neurogenesis and functional recovery . In addition, our methods for the assessment of neurological deficit score were not ideal and could be improved upon in subsequent studies.
We showed that VNS could modulate the inflammatory responses in a rat model of acute cerebral I/R injury by activation of a7nAchR expressed on microglia. Furthermore, the a7nAchR/Akt pathway may be involved in the anti-apoptotic processes induced by VNS. Although there are also other mechanisms responsible for VNS-associated neuroprotection after ischemic stroke, the “endogenous cholinergic pathway” likely plays an important role in brain in response to ischemic insults.
Conceived and designed the experiments: YJ LLL CQL. Performed the experiments: YJ CQL. Analyzed the data: YJ CQL. Contributed reagents/materials/analysis tools: BL YHZ QC. Contributed to the writing of the manuscript: YJ CQL.
- 1. Brouns R, De Deyn PP (2009) The complexity of neurobiological processes in acute ischemic stroke. Clin Neurol Neurosurg 111: 483–495.
- 2. Wang Q, Tang XN, Yenari MA (2007) The inflammatory response in stroke. J Neuroimmunol 184: 53–68.
- 3. Wang JY, Shen J, Gao Q, Ye ZG, Yang SY, et al. (2008) Ischemic postconditioning protects against global cerebral ischemia/reperfusion-induced injury in rats. Stroke 39: 983–990.
- 4. Fu SH, Zhang HF, Yang ZB, Li TB, Liu B, et al. (2014) Alda-1 reduces cerebral ischemia/reperfusion injury in rat through clearance of reactive aldehydes. Naunyn Schmiedebergs Arch Pharmacol 387: 87–94.
- 5. You SJ, Kang HC, Kim HD, Ko TS, Kim DS, et al. (2007) Vagus nerve stimulation in intractable childhood epilepsy: a Korean multicenter experience. J Korean Med Sci 22: 442–445.
- 6. Morris GL 3rd, Gloss D, Buchhalter J, Mack KJ, Nickels K, et al. (2013) Evidence-based guideline update: vagus nerve stimulation for the treatment of epilepsy: report of the guideline development subcommittee of the american academy of neurology. Epilepsy Curr 13: 297–303.
- 7. Conway CR, Sheline YI, Chibnall JT, Bucholz RD, Price JL, et al. (2012) Brain blood-flow change with acute vagus nerve stimulation in treatment-refractory major depressive disorder. Brain Stimul 5: 163–171.
- 8. Borckardt JJ, Kozel FA, Anderson B, Walker A, George MS (2005) Vagus nerve stimulation affects pain perception in depressed adults. Pain Res Manag 10: 9–14.
- 9. Burneo JG, Faught E, Knowlton R, Morawetz R, Kuzniecky R (2002) Weight loss associated with vagus nerve stimulation. Neurology 59: 463–464.
- 10. Boon P, Moors I, De Herdt V, Vonck K (2006) Vagus nerve stimulation and cognition. Seizure 15: 259–263.
- 11. Fanselow MS (2013) Fear and anxiety take a double hit from vagal nerve stimulation. Biol Psychiatry 73: 1043–1044.
- 12. Calvillo L, Vanoli E, Andreoli E, Besana A, Omodeo E, et al. (2011) Vagal stimulation, through its nicotinic action, limits infarct size and the inflammatory response to myocardial ischemia and reperfusion. J Cardiovasc Pharmacol 58: 500–507.
- 13. Kakinuma Y, Ando M, Kuwabara M, Katare RG, Okudela K, et al. (2005) Acetylcholine from vagal stimulation protects cardiomyocytes against ischemia and hypoxia involving additive non-hypoxic induction of HIF-1alpha. FEBS Lett 579: 2111–2118.
- 14. Sun Z, Baker W, Hiraki T, Greenberg JH (2012) The effect of right vagus nerve stimulation on focal cerebral ischemia: an experimental study in the rat. Brain Stimul 5: 1–10.
- 15. Belayev L, Alonso OF, Busto R, Zhao W, Ginsberg MD (1996) Middle cerebral artery occlusion in the rat by intraluminal suture. Neurological and pathological evaluation of an improved model. Stroke 27: 1616–1622.
- 16. Ilknur Ay, Jie Lu, Hakan Ay, Sorensen AG (2009) Vagus nerve stimulation reduces infarct size in rat focal cerebral ischemia. Neuroscience Letters 459: 147–151.
- 17. Smith DC, Modglin AA, Roosevelt RW, Neese SL, Jensen RA, et al. (2005) Electrical stimulation of the vagus nerve enhances cognitive and motor recovery following moderate fluid percussion injury in the rat. J. Neurotrauma 22: 1485–150.
- 18. Schäbitz WR, Weber J, Takano K, Sandage BW, Locke KW, et al. (1996) The effects of prolonged treatment with citicoline in temporary experimental focal ischemia. J Neurol Sci 138: 21–25.
- 19. Kong Y, Rogers MR, Qin X (2013) Effective neuroprotection by ischemic postconditioning is associated with a decreased expression of RGMa and inflammation mediators in ischemic rats. Neurochem Res 38: 815–825.
- 20. Wang Q, Li X, Chen Y, Wang F, Yang Q, et al. (2011) Activation of epsilon protein kinase C-mediated anti-apoptosis is involved in rapid tolerance induced by electroacupuncture pretreatment through cannabinoid receptor type 1. Stroke 42: 389–396.
- 21. Furmaga H, Carreno FR, Frazer A (2012) Vagal nerve stimulation rapidly activates brain-derived neurotrophic factor receptor TrkB in rat brain. PLoS One 7: e34844.
- 22. Ay I, Sorensen AG, Ay H (2011) Vagus nerve stimulation reduces infarct size in rat focal cerebral ischemia: An unlikely role for cerebral blood flow. Brain Research 1392: 110–115.
- 23. Hiraki T, Baker W, Greenberg JH (2012) Effect of Vagus Nerve Stimulation During Transient Focal Cerebral Ischemia on Chronic Outcome in Rats. Journal of Neuroscience Research 90: 887–894.
- 24. Mravec B (2010) The role of the vagus nerve in stroke. Auton Neurosci 158: 8–12.
- 25. Rosas-Ballina M, Ochani M, Parrish WR, Ochani K, Harris YT, et al. (2008) Splenic nerve is required for cholinergic antiinflammatory pathway control of TNF in endotoxemia. PNAS 31: 11008–11013.
- 26. van Westerloo DJ, Giebelen IA, Florquin S, Bruno MJ, Larosa GJ, et al. (2006) The vagus nerve and nicotinic receptors modulate experimental pancreatitis severity in mice. Gastroenterology 130: 1822–30.
- 27. Borovikova LV, Ivanova S, Zhang M, Yang H, Botchkina GI, et al. (2000) Vagus nerve stimulation attenuates the systemic inflammatory response to endotoxin. Nature 405: 458–462.
- 28. Tracey KJ (2007) Physiology and immunology of the cholinergic antiinflammatory pathway. J Clin Invest 117: 289–96.
- 29. Gregersen R, Lambertsen K, Finsen B (2000) Microglia and Macrophages are the major source of tumor necrosis factor in permanent middle cerebral artery occlusion in mice. J Cereb Blood Flow and Metab 20: 53–65.
- 30. Parada E, Egea J, Buendia I, Negredo P, Cunha AC, et al. (2013) The Microglial a7-acetylcholine nicotinic receptor is a key element in promoting neuroprotection by Inducing Heme Oxygenase-1 via nuclear factor erythroid-2-related factor. Antioxid Redox Signal 19: 1135–1148.
- 31. Wang H, Yu M, Ochani M, Amella CA, Tanovic M, et al. (2003) Nicotinic acetylcholine receptor alpha7 subunit is an essential regulator of inflammation. Nature 421: 384–388.
- 32. Zhang L, Qu Y, Tang J, Chen D, Fu X, et al. (2010) PI3K/Akt signaling pathway is required for neuroprotection of thalidomide on hypoxic–ischemic cortical neurons in vitro. Brain Research 1357: 157–165.
- 33. Chong ZZ, Li F, Maiese K (2005) Activating Akt and the brain's resources to drive cellular survival and prevent inflammatory injury. Histol Histopathol 20: 299–315.
- 34. Park J, Kang JW, Lee SM (2013) Activation of the cholinergic anti-inflammatory pathway by nicotine attenuates hepatic ischemia/reperfusion injury via heme oxygenase-1 induction. Eur J Pharmacol 707: 61–70.
- 35. Kakinuma Y, Tsuda M, Okazaki K, Akiyama T, Arikawa M, et al. (2013) Heart-specific overexpression of choline acetyltransferase gene protects murine heart against ischemia through hypoxia-inducible factor-1α-related defense mechanisms. J Am Heart Assoc 2: e004887.
- 36. Krafft PR, Altay O, Rolland WB, Duris K, Lekic T, et al. (2012) a7 nicotinic acetylcholine receptor agonism confers neuroprotection through GSK-3β inhibition in a mouse model of intracerebral hemorrhage. Stroke 43: 844–850.
- 37. Marrero MB, Bencherif M (2009) Convergence of alpha 7 nicotinic acetylcholine receptor-activated pathways for anti-apoptosis and anti-inflammation: central role for JAK2 activation of STAT3 and NF-kappaB. Brain Res 23 1256: 1–7.
- 38. Duris K, Manaenko A, Suzuki H, Rolland WB, Krafft PR, et al. (2011) a7 nicotinic acetylcholine receptor agonist PNU-282987 attenuates early brain injury in a perforation model of subarachnoid hemorrhage in rats. Stroke 42: 3530–3536.
- 39. Khodaparast N, Hays SA, Sloan AM, Hulsey DR, Ruiz A, et al. (2013) Vagus nerve stimulation during rehabilitative training improves forelimb strength following ischemic stroke. Neurobiol Dis 60: 80–88.
- 40. Murphy TH, Corbett D (2009) Plasticity during stroke recovery: from synapse to behaviour. Nat Rev Neurosci 10: 861–872.

domain: literature


text:
At the end of the day, you just need help!
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domain: economics


Daily Science News on Fox News Read about the latest and breaking news from the world of science. From biology to physics see the science news with Fox now.
Chinese researchers claim planned space telescope will surpass NASA’s Hubble: Report
on 10 Ottobre 2023 at 21:53
China’s space agency plans to launch the Xuntian space telescope in 2024 and says it will have higher optical capabilities than NASA’s Hubble Space Telescope.


text:
Anyone who has ever driven to Emergency, or visited loved ones in hospital, is familiar with the often exorbitant parking rates found near healthcare facilities. Now, there may be a cure.
The Ontario government has just announced a new policy they say will lower expenses for 900,000 patients and visitors, including 135,000 seniors.
As of today, there’s a three-year freeze on Ontario hospital parking rates, and beginning October 1, 2016, any hospital charging more than $10 a day to park will have to provide five-, 10- and 30-day passes that are:
– Discounted by 50 per cent off their daily rate,
– Transferable between patients and caregivers
– Equipped with in-and-out privileges throughout a 24-hour period
– Good for one year from the date of purchase.
“Parking fees should never be a barrier for patients when they go to the hospital,” said Health Minister Dr. Eric Hoskins in a press release. “With today’s announcement, we are providing relief from the high cost of parking at some hospitals in Ontario. By making parking more affordable for patients and their loved ones who visit the hospital often, we are helping to reduce the burden of parking fees and putting patients first.”
The release also says that last fall the ministry consulted with “a number of hospitals and the Ontario Hospital Association in regards to parking fee changes.”
However, the OHA released a statement today opposing the changes.
“For the past ten years, government has actively encouraged hospitals to generate revenue to help fund hospital operations. Revenue generated from parking fees is always used for patient care, towards the purchase of capital equipment and projects, infrastructure, clinical research, and day-to-day operations such as facility maintenance,” the statement reads. “The decision to cut revenues could not come at a worse time.”
This new policy, which fulfills a 2014 provincial election promise, will affect an estimated 36 hospitals that charge more than $10 a day. Toronto Western Hospital, for instance, charges $4.50 per half-hour or a $25 daily maximum, while elsewhere in the province, 45 hospitals offer free parking and 54 charge $10 or less per day.
The push to reduce or eliminate hospital parking fees is not new, nor is it restricted to Ontario. In 2011, a Canadian Medical Association Journal editorial called for free hospital parking across the country, dubbing them “user fees” and arguing they hurt health care.
“Some patients (who have often waited several weeks to see a doctor) try to end a consultation abruptly when they realize that they will have to pay for an additional hour for parking,” Dr. Rajendra Kale wrote. “This is parking-centred health care, which is not compatible with patient-centred health care.”
In 2013, CBC Marketplace reported that the cost of parking was causing Canadians to miss hospital appointments and increasing their stress.
“Parking fees are a penalty for having a disease. It seems like an unfair tax on my patients,” cancer specialist Dr. Bob Winston told Marketplace co-host Erica Johnson. “My patients have a lot of stress from the get-go, and with the addition of more stress with regards to the parking is sort of salt in the wound.”
Hospital parking was made free in Scotland in 2008 and there’s a current push to do the same in England, specifically to assist patients (and their caregivers and visitors) who must go to the hospital frequently, are gravely ill or are there for an extended stay.
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text:
The Paris headboard is a modern but simple looking fabric headboard sullplied with fixing struts and bolts.
This item is brand new, unused and in its orginal packaging.
•Clean and striking design
•a stylish fabric in a dark chestnut colour
•Padded for extra comfort
The headboard featured in the picture is for illustrative purposes only, as the headboard I am selling is somewhat darker than the one in the picture.
If you would like further information please PM me.
This item can not be posted and must be collected from my home and payment is cash on collection.

domain: design


AFP reports that Cypriot Foreign Minister Ioanis Kasoulides did not name the country, but did say missiles tests would be carried out this week in the Mediterranean.
Cyprus on Monday said a “friendly country” would be conducting missile tests in the Mediterranean this week, French news agency AFP reported, adding that the country carrying out the tests is not taking part in any potential military action against the regime of Syrian President Bashar Assad.
The report comes a week after Israel and the U.S. carried out a missile test in the Mediterranean Sea, amid rising tensions in the region over the crisis in Syria.
The Arrow III missile defense system was tested with a “sparrow” missile, which simulates a ballistic missile, and is launched from a plane, during the exercise.
The exercise was carried out from an Israel Air Force base in central Israel, the Defense Ministry said in the statement.
Russia’s defense ministry on Monday reprimanded Israel’s local military attache over last week’s missile test.
Cypriot Foreign Minister Ioanis Kasoulides told state radio a “friendly country” would carry out the tests from Monday to Saturday in the eastern Mediterranean. He did not name the country.
Meanwhile, AFP also reported that Cypriot Defense Minister Fotis Fotiou said on Monday the island was preparing to serve as a safe haven for those fleeing war-torn Syria.
“If Cyprus was not a safe destination it would not have chosen by other countries to evacuate their nationals here,” Fotiou told reporters, according to AFP.
“We have been assured that Cyprus will not be used as a launch pad for any operation or attack [against Syria], neither is it a target, that has been made clear,” Fotiou reportedly said.
View original HAARETZ publication at: http://www.haaretz.com/news/diplomacy-defense/1.546173


Current as of January 14, 2020
The F-15E Strike Eagle is a dual-role fighter designed to perform air-to-air and air-to-ground missions. An array of avionics and electronics systems enables the F-15E to fight at low altitude, day or night, and in all weather.
The aircraft uses two crew members, a pilot and a weapon systems officer (WSO). Previous models of the F-15 were assigned air-to-air roles; the "E" model is a dual-role fighter. It has the capability to fight its way to a target over long ranges, destroy enemy ground positions, and fight its way out.
The aircraft's navigation system uses a laser gyro and a Global Positioning System to continuously monitor the aircraft's position and provide information to the central computer and other systems, including a digital moving map in both cockpits.
The F-15E can have one of two RADARs, the APG-70 Mechanically Scanned Array or the APG-82 Active Electronically Scanned Array. The radar systems allow aircrew to detect air and ground targets from long ranges. One feature of this system is that after generating high resolution maps of a target area, the crew freezes the air-to-ground map then goes back to air-to-air mode to clear for air threats. During the air-to-surface weapon delivery, the pilot is capable of detecting, targeting and engaging air-to-air targets while the WSO finds the ground target and manages systems to precisely guide the weapon(s) to impact.
The low-altitude navigation and targeting infrared for night (LANTIRN) system allows the aircraft to fly at low altitudes, day or night, in any weather conditions, and attack ground targets with a variety of precision-guided and unguided weapons. The system consists of two pods mounted externally on the aircraft, a navigation pod and a target pod.
The navigation pod contains terrain-following RADAR which allows the pilot to safely fly at a very low altitude following cues displayed on a heads up display. This system can be coupled to the aircraft's autopilot enabling a nearly "hands-off" terrain following capability.
The targeting pod contains a laser designator and a tracking system capable of marking enemies at long ranges. Once tracking has been started, targeting information is automatically handed off to GPS-aided or laser-guided bombs. The LANTIRN or SNIPER targeting pod gives the F-15E unequaled accuracy in weapons delivery day or night.
The most important addition to the F-15E is the rear cockpit and the weapon systems officer. On four screens, this officer can display information from the radar, electronic warfare, or infrared sensors, monitor aircraft systems, weapons status, possible threats, select targets, and use an electronic "moving map" to navigate. Two hand controls are used to select new displays and to refine targeting information. Displays can be moved from one screen to another, chosen from a "menu" of display options.
In addition to three similar screens in the front seat, the pilot has a transparent glass heads up display (HUD) at eye level and a Joint Helmet Mounted Cueing System (JHMCS) that displays vital flight and tactical information. The pilot doesn't need to look down into the cockpit, for example, to check weapon status or aircraft parameters. At night, the HUD is even more important because it can display a video picture similar to a daylight view of the world generated by the forward-looking infrared sensor.
The F-15E is powered by two Pratt & Whitney F100-PW-220 or 229 engines that incorporate advanced digital technology for improved performance. For example, with a digital electronic engine control system, F-15E pilots can accelerate from idle power to maximum afterburner in less than four seconds, a 40 percent improvement over the previous engine control system. Faster engine acceleration means quicker takeoffs and crisper response while maneuvering. The F100-PW-220 engines can produce 50,000 pounds of thrust (25,000 each) and the F100-PW-229 engines 58,000 pounds of thrust (29,000 each).
Each of the low-drag conformal fuel tanks mounted to the F-15E's fuselage can carry 750 gallons of fuel. These fuel tanks also hold weapons on short pylons rather than conventional weapon racks, reducing drag and further extending the range of the Strike Eagle.
Combat load-outs can include nearly any air-to-ground weapon in the Air Force inventory as well as any array of air-to-air missiles and a 20mm gun loaded with over 500 rounds.
The F-15's superior maneuverability and acceleration are achieved through its high engine thrust-to-weight ratio and low-wing loading. It was the first U.S. operational aircraft whose engines' thrust exceeded the plane's loaded weight, permitting it to accelerate even while in vertical climb. Low-wing loading (the ratio of aircraft weight to its wing area) is a vital factor in maneuverability and, combined with the high thrust-to-weight ratio, enables the aircraft to turn tightly without losing airspeed.
The first flight of the F-15A was made in July 1972. In November 1974, the first Eagle was delivered to the 58th Tactical Fighter Training Wing at Luke Air Force Base, Ariz., where training began in both F-15A and B aircraft. In January 1976, the first F-15 destined for a combat squadron was delivered to the 1st Tactical Fighter Wing at Langley AFB, Va.
The single-seat F-15C and two-seat F-15D models entered the Air Force inventory in 1979 and were first delivered to Kadena Air Base, Japan. These models were equipped with production Eagle package improvements, including 2,000 pounds of additional internal fuel, provisions for carrying exterior conformal fuel tanks, and increased maximum takeoff weight of 68,000 pounds.
The first production model of the F-15E was delivered to the 405th Tactical Training Wing, Luke AFB, Ariz., in April 1988.
Primary function: Air-to-ground attack aircraft
Builder: McDonnell Douglas Corp.
Power plant: Two Pratt & Whitney F100-PW-220 or 229 turbofan engines with afterburners
Thrust: 25,000 - 29,000 pounds each engine
Wingspan: 42.8 feet (13 meters)
Length: 63.8 feet (19.44 meters)
Height: 18.5 feet (5.6 meters)
Speed: Mach 2.5 plus
Maximum takeoff weight: 81,000 pounds (36,450 kilograms)
Service ceiling: 50,000 feet (15,000 meters)
Combat ceiling: 35,000 feet (10,500 meters)
Range: 2,400 miles (3,840 kilometers) ferry range with conformal fuel tanks and three external fuel tanks
Armament: One 20mm multibarrel gun mounted internally with 500 rounds of ammunition. Up to eight air-to-air missiles including AIM-9M/X Sidewinders and AIM-120 AMRAAMs. Almost any air-to-surface weapon in the Air Force inventory from 250 lb class to 5,000 lb class conventional and nuclear.
Crew: Pilot and weapon systems officer
Unit cost: $31.1 million (fiscal 98 constant dollars)
Date deployed: April 1988
Inventory: Approximately 217


text:
Today’s episode is another reality check. Caring too much about what others think will be the main factor of your downfall. At the end of the day, it’s just you. Don’t care about their opinions… They’re not YOU.
Episode 117 Time Stamps:
(3:30) Why you should read
(4:50) We have a human need to be accepted and loved
(5:33) The evils of social media
(6:26) We have it made easy in this day and age)
(7:48) Convenience has made us emotionally soft!
(9:00) Caring too much about what other people think...
(9:10) Not going as hard, because it makes others feel uncomfortable
(10:58) Failure within team communication, to avoid being "that guy"
(11:43) Indecisive of future plans, to avoid upsetting parents/coaches/others
(12:33) Muting your own voice to avoid conflict
(12:50) Accept things that you don't agree with, to avoid upsetting people
(13:58) People don't really care about your decisions/actions
(14:30) You just might be making them look bad...
(15:00) Everyone else actually cares about what YOU think (a little too much)
(15:08) People are waiting for a LEADER!
(16:02) What is your outcome?
(17:10) You will remain very average (continuing to care what other people think)
(17:46) Evolving into a "hater"
(19:36) Taking out your frustrations out on everything
(20:34) If I cared too much about what others thought about my podcast, where would I be now?
(22:10) Your respect. Your trust.
Today's blog post can be found here: Episode #117 Blog
Need a Sports Results Coach?: SRC Program
As always, if you're diggin' the podcast, please subscribe and rate the show!
Blog posts for ALL podcast episodes can be found here: IMNOTYOU.COM/PODCAST
Thanks for listening to another IMNOTYOU Sports Motivation Podcast!

domain: psychology


text:
The active ingredients of traditional Chinese medicine extracts such as turmeric may help eliminate the new coronavirus The novel coronavirus pneumonia (COVID-19) has evolved into a global pandemic. Worldwide, the situation of the new crown epidemic continues to escalate, and the prolonged soaring e
The Washington State University research team has developed a drug delivery system that uses curcumin, the main ingredient in the spice turmeric, which can successfully inhibit bone cancer cells while promoting the growth of healthy bone cells. Osteosarcoma is currently the second most prevalent cau
As the largest consumer market for turmeric, the United States imports millions of pounds of turmeric raw materials all over the world every year. A large part of them are used in fragrance products and dietary supplements. However, as the market continues to heat up, more and more new turmeric prod
Boosts Immunity: Curcumin has a huge therapeutic value and boosting immunity is one of the most important properties of curcumin."5 to 8 times stronger than vitamin E and stronger than vitamin C, this antioxidant breakthrough may help boost your immunity, maintain normal cholesterol levels, and put
8 Proven Health Benefits of Turmeric Extract Curcumin What 're Turmeric ExtractTurmeric extract is a turmeric plant Curcuma longa L. Dry root rhizome extract, the main biological activity is curcumin and ginger flavonoids, with a variety of effects. Turmeric extract has been widely used as a natural
The study of Hawaiian herbal medicine is being restored at the University of Hawaii at Manoa. Professors there are bringing back Laau lapaau, an ancient Hawaiian practice that uses island plants and herbs to treat various ailments. The Hawaiian word for health (ola) also means life.

domain: medical