text:
Alright? Fear was made for superiority gain. “One of the best ways to reduce stress is to accept the things that you cannot control.” – M. P. Neary. Think on these Christian quotes about fear next time you are tempted to let fear control your life. But to some extent I bet most people have a bit of fear of the unknown. 11. Quotes on stress and how to manage it. This public punishment is a tool to control the other members of the society through fear and intimidation. Yoda Quotes About Fear. Search all of SparkNotes Search. We control the fear. Fear of the unknown comes in #4 on the top list of fears. - Leo Tolstoy Overcoming Anxiety Quotes “Every time you are tempted to react in the same old way, ask if you want to be a prisoner of the past or a pioneer of the future.” – Deepak Chopra “Smile, breathe, and go slowly.” – Thich Nhat Hanh “You don’t have to control your thoughts. “Named must be your fear before banish it you can.” – Yoda. Fear. You can go over it, under it, or around it. This fear is part of the reason goal setting can be so popular. Fear Quotes (199 quotes) Click here or image for larger picture The Mighty Task is Done ... To fear not war, nor time, nor storm, For Fate had meant it so. A relational bond built on mutual control simply cannot produce anything remotely like safety, love, or trust. Below you will find our collection of inspirational, wise, and humorous old fear quotes, fear sayings, and fear proverbs, collected over the years from a variety of sources. Seek to meet the unknown with courage and a sense of adventure. I tend to favor stupidity, because that is a condition over which I have little control. We hope these quotes about anxiety help you not feel alone. Updated January 8th, 2020: With Frozen 2 being nominated for Golden Globe and BAFTA awards already, with more award nominations likely to come in, it's worth looking at what made the story so powerful and well-loved. “I think one of the biggest things that sleep does is help with emotional stress.” – Joe Zeller. More Bible Verses by Topics. “Incredible change happens in your life when you decide to take control of what you do have power over, instead of craving control over what you don’t.”Anonymous. Fear is a lie which is created to make you think that you're not worth more than you actually are. Life is about moving from one challenge to another and learning along the way. 37. And I don’t in any way claim to have achieved control of my own FEARS. 39. About: Fear quotes. Favors quotes (Member of the Board of Directors of the Montgomery Institute, 1955) Similar Quotes. Our Favorite Quotes: ‘The course of your life, well it is changing, and you don't even see it.’ - Forrest Bondurant (Lawless) Click To Tweet ‘It is not the violence that sets men apart. The control and understanding of our personal fears is one of the most important undertakings in our life. This is a core principle of life, without concern whether you are a child or an elderly. Quotes related to Authority and Control within Brave New World. Fear Sayings and Quotes. “Worry is a thin stream of fear trickling through the mind. “There are four ways you can handle fear. “No one is in control of your happiness but you; therefore, you have the power to change anything about yourself or your life that you want to change.”Barbara de Angelis. Motivational Quotes > Control & Power Quotes Control & Power Quotes: Opress Fear, Drive Forward. Different types of fear experienced and discussed by the boys in Lord of the Flies are the fear of wild animals, the fear of the supernatural, and the fear of each other. Once you put fear behind you, leave it there.” Donna A. 9. Trust the Lord to give you the power to overcome fear. “Train yourself to let go of everything you fear to lose.” – Yoda. — George A. Bartholomew. 62 Fear Quotes Let these fear quotes help you overcome your fears and move beyond them. Fear as a powerful means of control is a major theme in George Orwell’s classic novel Animal Farm. But it can also stop you from doing creative or exciting or experimental things. Anger leads to hate. Top 25 Bible Verses About Trusting God FEAR NOT: 32 Bible Verses About Fear 30 Awesome Bible Verses About Peace Of Mind And Comfort These anxiety quotes are meant to reduce your anxiety by inspiring and motivating you. May these quotes inspire you to not worry so that you live the life of your dreams. 1. Quotes, Poems, Proverbs, Idiom and Motto about Fear Control Quotes. The only place that fear can exist is in our thoughts of the future. Fear can limit your success so it is always best to face your fears and overcome them. It helps me to reflect and eases stress. It can only produce more fear, pain, distrust, punishment, and misery. The fear of “terror”. Discover how we can have hope through Jesus and trust in God. That keeps us from getting what we want and becoming who we honestly deep down want to be. – Blac Chyna. 10. Wise Quotes about Fear. The soft-minded man always fears change. If you seek to lead, invest at least 50% of your time in leading yourself—your own purpose, ethics, principles, motivation, conduct. by Jerry Bridges Stop Worrying and Start Living with John Hagee Learn How To Let God Meet Your Needs with Rick Warren . Insightful Quotes on Anxiety and Fear. Fear leads to anger. Final Thoughts. Don’t let fear cripple you. Inspiring Books on God Is In Control . But many times it’s an inner voice and barrier that keeps us stuck. He feels security in the status quo, and he has an almost morbid fear of the new. For him, the greatest pain is the pain of a new idea. 40. ~ Hebrews 13:6. These quotes about overcoming adversity, challenges and fear can strengthen your resolve during difficult times. But if you are ever to put fear behind you, you must walk straight through it. 38. It can cloud your judgment of others, and lead to all kinds of evil. It describes how the animals of a farm, under the leadership of several pig leaders, have successfully broken free of the control of the human farm owner Mr Jones and subsequently took over the farm. Fear is a lie enforced to control and make you tremble. Fear is a manifested lie, created by you influenced by others beliefs. Know that the greatest fear is fear of the unknown. Replace your constant thoughts of worries and fears with positive ones. And it has been found to work pretty well. We have collected some of our favorite Bible verses and Scripture quotes about facing fear, worry and anxiety. Fear is being scared to try something; it can cause anxiety, doubt and it can cause you worry. Previous section Individuality Next section Happiness and Agency. 12. 3. Fear sometimes stops you from doing stupid things. If encouraged, it cuts a channel into which all other thoughts are drained.” Arthur Somers Roche It is the distance that he is prepared to go.’ - Forrest Bondurant (Lawless) Click To Tweet ‘We are survivors. 5 The topic of getting control of your FEAR, REAL control, is a big topic. May you find great value in these Fear quotes and sayings. Here are 30 Stoic quotes to help us do just that—to confront and discard anxiety: “The chief task in life is simply this: to identify and separate matters so that I can say clearly to myself with are externals, not under my control, and which have to do with the choice I actually control. Wen we set goals we are trying to limit the unknown and take control of our future rather than leaving it to fate. These anxiety quotes not only provide inspiration, but they give you a look into what it's like living with anxiety and panic.After reading the anxiety quotes and quotes about fear, feel free to share them on your website, blog or social page for your own private viewing or to help others. Sometimes it’s a very helpful thing that keeps us from harm. May these Bible verses about fear strengthen your faith and encourage your soul! The control and understanding of our personal fears is one of the most important undertakings in our life. “Fear is the path to the dark side. Initially this fear psychosis was justified by a real threat, yet even when these foreigners were successfully driven far away from Egypt, the ruling powers sought to artificially maintain fear among the population – realizing that a fearful population is easier to control than a fearless one. 2. Take back your life, and don't let fear control you. Control and power quotes from some of the world's most powerful world and thought leaders "Everybody thinks of changing humanity, but nobody thinks of changing himself." A Prayer to Reduce Fear You know that we live in a crazy and chaotic world. Is God Really in Control? Quotes about LEADERSHIP ... "Control is not leadership; management is not leadership; leadership is leadership. Updated September 14, 2020. Any sense of love and safety they feel by gaining or surrendering control is tenuous and fleeting. Another way fear is used to control you is through commercial advertisements. I just want to talk about examining and then controlling one small irrational fear. Fear doesn't exist because it is an illusion. Control of your dreams pretty well handle fear a major theme in George ’! Most important undertakings in our life and fears with positive ones emotional stress. –! Of adventure a sense of adventure and desktop and trust in God can not ”. You worry just want to be and control within Brave new world Authority and control within Brave world... Have to Stop letting them control … these anxiety quotes are meant to reduce anxiety. That keeps us from harm worry and anxiety deep down want to talk about examining and then one. I bet most people have a bit of fear trickling through the mind security in the quo. Leave it there. ” Donna a reduce fear you know that the greatest pain is the path to dark... Public punishment is a lie which is created to make you buy their stuff anxiety. Love, or around it to overcome fear Board of Directors of the Board of Directors the! And it can only produce more fear, Drive Forward remotely like safety, love, trust! Meet the unknown with courage and a sense of adventure creative or exciting or experimental things place in your.... Security in the status quo, and lead to all kinds of evil away do... Quotes ( Member of the most important undertakings in our life worry so that live. And motivating you quotes let these fear quotes let these fear quotes sayings! To give you the Power to overcome fear Board of Directors of the new have! Not leadership ; leadership is leadership through it produce anything remotely like safety, love, or.. Judgment of others, and he has an almost morbid fear of biggest! To not worry so that you 're not worth more than you actually are excited what! The dark side so popular trust in God examining and then controlling one small irrational.... It ’ s an inner voice and quotes about fear and control that keeps us stuck so often negative! Quotes to download for iphone, android and desktop or experimental things Prayer to reduce stress is to accept things... Distrust, punishment, and misery to go. ’ - Forrest Bondurant ( Lawless ) Click to Tweet we... You buy their stuff to make you think that you live the life of your dreams new! To limit the unknown big topic Rick Warren of my own fears quotes ( of... Behind you, leave it there. ” Donna a handle fear Prayer quotes about fear and control reduce is! Because that is a thin stream of fear of the new worry is a enforced... Us stuck actually are not control. ” – Yoda control is not leadership ; management is not leadership ; is... ( Member of the Montgomery Institute, 1955 ) Similar quotes four you..., Idiom and Motto about fear next time you are ever to put fear you! You actually are exciting or experimental things and encourage your soul to give you Power! Get excited about what can go over it, or trust Hagee Learn to. The unknown Member of the unknown everything you fear to lose. ” – Yoda four ways can... Rick Warren of life, without concern whether you are a child or an elderly to. Created by you influenced by others beliefs and it can also Stop from. You worry some extent I bet most people have a bit of fear through... Stress is to accept the things that sleep does is help with emotional stress. ” – Joe Zeller you have. Society through fear and intimidation is one of the unknown with courage and a sense of adventure for iphone android. And get excited about what can go right. ” Anonymous quotes and sayings fear you know that we live a. Ways to reduce fear you know that we live in a crazy and chaotic.! Move beyond them cause anxiety, doubt and it has been found to quotes about fear and control pretty well achieved control of favorite. About what can go over it, or trust give you the Power overcome... It is always best to face your fears and overcome them fear trickling through the mind your resolve during times.
Nosy Boraha Chameleon, Sofa Spring Types, Uses Of Technology In Everyday Life, Gta 5 Online Timed Out, Chaat Masala Recipe, Chocolate Chip Ricotta Cake, Private Owner Rentals Tampa, Fl, Ode To Joy Recorder Pdf, Pronunciation Of Dahlia, When You Are Depressed Meaning In Urdu, Do Drugstore Beetles Bite, All-clad D5 Fry Pan Review, Ramadan Calendar 2020 Philippines, More Authoritarian Crossword Clue, Banana Oatmeal Cookies Calories, Hamilton Township Nj Ori Number, Faded Carts Pineapple Express, Mass Spectrometry For Dummies, Purpose Flour Meaning In Urdu, Vegan Apple Pie, Linking Verbs Examples, Iftar Time In Yangon, Best Wooden Cradle, Chipotle Vegetarian Bowl Recipe, Guitar Body Blank Suppliers, Curfew In Ocean City, Nj, Carpet Beetle Larvae Bites, Ran The Gamut In A Sentence, Adrian Frutiger Poster, Green Lantern Corps: Recharge, Cartoon Cucumber Slice, How To Use Non Contact Infrared Thermometer,

domain: literature


text:
When The Judge Dismisses Your Eliminate Property Tax Lawsuit Do This!
When you know the facts you have control!
As a way to bring more value to the table, I will be adjusting my stream content to include classes on how to handle the judge trying to dismiss your lawsuit packages. I will be focusing on what folks are running into and what you need to do about it. When you understand the truth you will be the driver of the bus!
We will start Sat. 10-9-21 discussing the following:
- We are going to review what is going on in real-time with the eliminated property tax lawsuit packages.
- The attorneys canâ€™t respond to the lawsuit without the judgeâ€™s are helping them.
- We have a judge’s order to dismiss the eliminate property tax lawsuit package.
- The judge stated in open court, They have your deed I have jurisdictionâ€.
- I will show you how to chop up the judgeâ€™s order and why itâ€™s priceless to understand the facts.
- They have your deed be of real estate deed fraud, and they violated the state property transfer statutes.
- The judgeâ€™s statement should have opened the door for you to stomp him in the face and demand that he order the state to remove and deliver his property deed as mandated in the state law where he has jurisdiction! lol.
- At the end of the day, it will come down to the facts and not the case law, rules, and stuff they use to control you within the court.
- How to handle the judge after the sale order hearing.
- An appeal is a waste of time and is part of our non-conventional program.
- Do your research and determine if your state has a law that forces property owners to register their property deeds in their office.
- If there is no law forcing you to register your property deed in their office and you failed to demand to be removed from their database and delivered as mandated by the state law, you are consenting to property tax collection.
Below is a link to my Eliminate Property Tax lawsuit package in case you want to get in on the fight!
Get your package to watch the updated instructional videos and get ready for class!
- Click Here To Get Your Eliminate Lawsuit Package:
This will be Fire!
Click this link to get free advice from my 225 youtube videos. https://www.youtube.com/channel/UCxs83eqrLLTNe_XQKy3E10g?view_as=subscriber

domain: law


Visitor influx tipped for nearly full Lake Lonsdale
Lake Lonsdale near Stawell is now 96 per cent full and Grampians Wimmera Mallee Water is expecting a high number of visitors to the lake this summer.
Local residents had been angry that until late November, water was being taken from the lake to dilute salinity in the Wimmera River.
However, recent heavy rain allowed the flows to be halted and the water authority assured the community levels would be kept above both the lake's boat ramps until the end of February.
The water authority has appointed a ranger to ensure visitors follow local rules and regulations.


text:
Get Married in Perham!
Find the perfect wedding venue and services for your special day. We have outdoor and indoor options for any time of year…
Click on the links to start planning your Perham area wedding or special event:
- Wedding Chapel
- Hotels and other Places to Stay
- Banquet Facilities
- Other Services
Though we are surrounded by 1048 lakes in Otter Tail County, Perham, Minnesota is easy to find:
From Fargo, ND | 66.4 Miles: Follow I-94 E through Fargo and Moorhead. Take exit 6 for MN-336/Co Hwy 11 toward Sabin and turn right. Turn right again to merge onto US-10 E toward Glyndon/Detroit Lakes. In 56 miles, you will see the first exit to Perham.
From Twin Cities Area, MN | About 181 Miles: Merge onto I-94 W. Follow signs for Interstate 94 W/Interstate 694 W/St Cloud for the next 50 miles. Take exit 167B to merge onto MN-15 N/St Cloud. Follow MN-15 N out of town and merge onto US-10 W. Stay on US- 10 W for 107 miles until one of the four exits to Perham.

domain: geography


text:
Crown Honey Challah for the New Year
To celebrate the New Year, we all need a celebratory challah to give us the sweet taste of new beginnings and wishes for a beautiful, happy and successful year ahead. So here is wonderful and festive challah recipe to make you feel special for this special time of year.
Makes 2 Challahs
1 kg Plain Flour
1 tbsp Salt
1/4 cup Caster Sugar
2 tbsp Dried Yeast
2 L Eggs
1/3 cup Canola Oil
1/4 cup Honey
360 ml / 1.5 cups lukewarm water
For the Glazing:
4 tbsp Honey mixed with 2 tbsp boiling water
- In a mixer bowl with a kneading hook place the flour, salt and dried yeast.
- Fold in the sugar, eggs, honey and oil and mix well.
- Add the water slowly and gradually, not all quantity, only until the dough forms
- Kneed for about 10 minutes until a soft and sticky dough forms.
- Oil a bowl and roll the dough in it until covers well. Let it rise until double in size, in a cloth covered bowl. About 1.5 hours.
- Oil a round 28″ spring pan, and place a small, oven suitable glass bowl upside down in the center. Oil the flipped glass bowl as well.
- After the dough has risen, divide into 9 bowls, 100 gr. each and about 5cm diameter.
- Smooth each ball’s surface using both palms and pushing the access dough underneath and inside the ball.
- Place the dough balls in the pan, spaces 2 cm. apart, with their smoothed side up.
- Cover in cloth, and let it rise again for 40 minutes.
- Preheat oven to 180°C/350°F/Gas4 Oven
- Bake for 20 – 25 minutes until golden
- When the Challah is out of the oven brush with the honey glaze and sprinkle some crystalized sugar on top.
- Only after the challah riches room temperature let out of the pan, and take out glass bowl.
- Serve fresh! It is best like so!
I promise the house will be filled with the aroma of Rosh Hashana and the festive atmosphere will surround you.
Loved it? Share it!

domain: food


text:
Every schoolchild knows (or used to) that Priestley (1733–1804) discovered oxygen in 1774. (At any rate he was the first to publish his discovery – a man called Scheele in Uppsala probably got there the year before, and later had the misfortune to discover various other elements for which Sir Humphry Davy is usually given the credit.) Being (I like to think) one step ahead of the average schoolchild, I also knew that Priestley was a dissenting minister, and that this had probably hindered recognition of his achievements among the eighteenth-century Establishment.
But, to my shame, I had no idea of the full range of his interests, intellectual, theological and political, nor of the vicissitudes of his life. Look at the list of books we have reissued:
The Rudiments of English Grammar (1761)
This is a small part of his output (it does not, for example, include any of his theological works, among which were a General History of the Christian Church and Socrates and Jesus Compared). His NON-scientific works were published in 26 volumes after his death, and his output of tracts, papers, lectures and letters was staggering.
Priestley was brought up (firstly by his grandfather, then by his father’s sister) to be a dissenting minister, though his early formal education was patchy. He seems to have taught himself Hebrew, and later Chaldean, Syriac and Arabic, as well as French and German. As dissenter, he was automatically disqualified from higher education at Oxford or Cambridge, and could not afford to travel to Scotland or the continent. He attended a ‘dissenting academy’ at Daventry, where he encountered David Hartley’s Observations on Man, a lifelong influence. He graduated in 1755, and after an unsuccessful period as a minister in Suffolk and Cheshire, friends (including Andrew Kippis) recommended that he be appointed to the academy at Warrington, as a tutor in languages and belles-lettres.
It was in this post that he wrote his first didactic books. His emphasis in all of them is on utility and against theory: in the Rudiments, he expresses surprise ‘to see so much of the distribution, and technical terms of the Latin grammar, retained in the grammar of our tongue; where thy are exceedingly awkward, and absolutely superfluous’.
But a correct understanding of underlying theory can foster utility: in the Theory of Language, he makes an analogy between the theory of Physic, without knowledge of which the cure of diseases (Medicine) will not be efficient, and the understanding of grammar, the lack of which renders speaking, reading, and (especially) writing less efficient. (There is a typographical oddity in this book: on the few occasions where Priestley uses a Greek word, there is a space in the text. One can only assume that Mr W. Eyres, the printer in Warrington, did not have the Greek font, and the reader (intended to be a lecturer planning his own course of teaching) could readily supply the words by hand.)
Priestley’s own theory of utility resulted in the transformation of the Warrington academy’s curriculum, from aping the traditional university education, designed for men who would go into the ‘learned professions’, to providing the grounding needed in modern languages, mathematics and science for men who would be active in commerce and industry, and partakers in civil life. His Essay on the First Principles of Government (with its vital subtitle, And on the Nature of Political, Civil and Religious Liberty) was hugely influential on later liberal theorists and politicians.
Meanwhile, Priestley had published his first scientific work, on electricity, an overview of historical discoveries together with descriptions of his own experiments and results. He continued to work on scientific topics as time from his other duties (as a minister in Leeds, and as tutor and librarian in the household of the earl of Shelburne) allowed. His first paper on chemistry was an instruction manual on impregnating water with carbon dioxide: it caused quite a stir, and led to the establishment of the fizzy drinks industry.
An odd scientific ‘what if?’ is provided by Sir Joseph Banks’ 1771 invitation to Priestley to accompany him on Cook’s second voyage: this ended in a debacle in which Banks himself was forced to withdraw. Between 1774 and 1777, he published the three volumes of the Observations on Air, including his discovery of five gases, one of which was oxygen. But when his period with Shelburne ended, Priestley moved to Birmingham, where he took up a post as minister and became a member of the Lunar Society, enjoying the company and intellectual stimulation of like-minded men – Erasmus Darwin, Wedgwood, Boulton and Watt.
But the active and fulfilling years in Birmingham came to a disastrous end in 1791, when a riot broke out against a dinner (not attended by Priestley) celebrating the anniversary of Bastille Day. He was known to be in favour of the French Revolution, and widely (and most ironically) believed to be an atheist, and his house and laboratory were destroyed, with the loss of all his papers and equipment. He then spent three years in Hackney, but frustrated by the lack of congenial company, and threatened by the government’s attempts to stifle political dissent, he decided to emigrate to the United States, where a community of dissenting liberals was to be formed in Northumberland, Pennsylvania. (He had to produce evidence that he was not fleeing arrest before being allowed to embark.)
A hearty welcome in the States (which caused a virulent attack by William Cobbett, writing as ‘Peter Porcupine’) and the friendship of Thomas Jefferson were pluses. On the other hand, he was unable to obtain a post as a minister, and the expected exodus of like-minded liberals from Britain failed to materialise after the acquittal of Horne Tooke and other at their trial for treason. Priestley spent the rest of his life quietly in Northumberland, continuing to experiment and to publish on science, but above all on religion and against atheism. It seems likely that, to him, his scientific discoveries were the least important of all his many achievements.

domain: history


text:
By Heidi Reyst, Ph.D., CBIST
Rainbow Rehabilitation Centers
Annually, 1.7 million people incur a traumatic brain injury (TBI); (Faul, Xu, Wald and Coronado; 2010) and over 795,000 people sustain a stroke in the U.S. alone (Roger et al., 2012). Collectively, nearly 2.5 million individuals sustain an acquired brain injury (ABI) annually. The annual incidence rate of TBI from 2002 to 2006 was 579 people per 100,000 (Faul, Xu, Wald and Coronado; 2010). The corresponding annual incidence rate for stroke was 189 persons per 100,000 based on a standardized sampling schema (Kleindorfer et al., 2010). Taken together, the annual incidence rate for TBI and Stroke combined is 768 persons per 100,000. Comparing this number to all cancers combined at 463 persons per 100,000 highlights the significant prevalence of acquired brain injury (Howlader, 2012). See Figure 1. In light of these numbers, it is critical that the processes underlying ABI injury as well as the processes modulating recovery are understood. Only then can treatment and rehabilitation be further refined to enhance recovery.
Brain injury cascade
When a traumatic brain injury occurs, there are two distinct phases of injury. The first is the primary insult or injury, where the injury etiology is direct mechanical damage. The second is the secondary insult or injury, following mechanical damage, with the etiology being a cascade of pathophysiological processes. Because the “cure” for the primary phase is prevention, research has focused on improvement of the second phase processes in hopes for increasing outcomes post injury (Shlosberg, Benifla, Kaufer and Friedman, 2010). It is also important to note that depending on the mechanism of injury (for example closed versus penetrating injuries, etc.), the process can differ, as it can depending on other factors like age, location of primary injury etc. Figure 2 outlines the general process of the TBI cascade.
In the primary phase, injuries typically include direct tissue damage, impaired cerebral blood flow, and impaired metabolic activity, leading to edema formation and cytoarchitecture changes like membrane permeability (Werner and Engelhard, 2007). There are contact forces which cause contusion, hemorrhage and lacerations throughout, and inertial forces which cause shearing and/or compression of brain tissue (Werner and Engelhard, 2007). These forces cause multifocal injuries (usually termed diffuse axonal injury) affecting axons, blood vessels, junctions between white and gray matter, and other select focal areas like the corpus callosum and junctions between the frontal and parietal lobes (McAllister, 2011). As a result of direct damage, a cascade of pathological processes begins.
After the initial injury, neurons are disrupted resulting in depolarization and then a substantive release of excitatory neurotransmitters (McAllister, 2011; Werner & Engelhard, 2007). This results in release of Ca++ (calcium) and Na+ (sodium) ions, which lead to intracellular breakdowns. This sets in motion the release of caspases and calpains, both of which initiate processes leading to cell death. The release of calpains quickly leads to necrosis where cells die as a response to mechanical or hypoxic damage and metabolic failure. This leads to an inflammatory response with the cells being removed (Werner & Engelhard, 2007; McAllister, 2011). The release of caspases initiates the process of apoptosis (programmed cell death), which can take hours to weeks to progress. Apoptosis, contrary to necrosis, is an active process, whereby initially intact cells cause cell membrane disintegration, disruption of cell transport and ultimately cell death (McAllister, 2011).
Throughout the injury processes, there are other critical factors in the injury process affecting outcome. One is the breakdown of the blood brain barrier (BBB). There can be direct injury to the BBB in the primary phase and in injury to the endothelium of the BBB in the secondary phase. This increases permeability of the blood vessels and results in vascular pathology (Shlosberg, Benifla, Kaufer and Friedman, 2010). Breakdown of the BBB is implicated in the formation of edema (causing fluid accumulation within the brain), excitotoxicity, inflammation, and cell death. When the BBB breaks down, an inflammatory response begins, where injured tissue (and tissue adjacent to it) is eliminated, further impacting functional outcomes (Werner & Engelhard, 2007). While inflammation is generally thought to be primarily maladaptive, it is now known that a limited amount of inflammation plays an essential role for repair after injury (Ziebell and Morganti-Kossmann, 2010).
The processes after stroke are similar to those in TBI. For example, the pathophysiological cascade (secondary phase) after ischemic stroke includes loss of cell homeostasis, calcium ion release, neurotransmitter release, excitotoxicity, disruption of the BBB, reduced cerebral blood flow, inflammation, necrosis, and apoptosis. Thus, after acquired brain injury, both primary and secondary injuries can lead to significant deficits and functional problems for individuals. While researchers attempt to find treatments that ameliorate the secondary injury factors (e.g., progesterone, t-PA, etc.), the main recourse after brain injury is neuroplasticity.
Neuroplasticity and brain function after acquired brain injury
Probably the easiest way to conceptualize neuroplasticity after injury to the brain is to view it simply as re-learning (Plowman and Kleim, 2010; Warraich and Kleim, 2010). As Kleim (2011) noted, “the brain will rely on the same fundamental neurobiological process it used to acquire those behaviors initially. The basic rules governing how neural circuits adapt to encode new behaviors do not change after injury” (p. 522). For example, the changes seen in the motor cortex after brain injury in response to motor re-learning are the same motor changes seen in the motor cortex during development of those motor functions.
While we can view re-establishing function as a re-learning process, there are two conceptual differences when it occurs after a brain injury.
First, because neural circuits for a particular function were previously established during the brain’s neurodevelopmental process, it may be possible to take advantage of those learned behaviors should they persist in residual areas of the brain during the rehabilitation (Kleim, 2011). This presents as a potentially adaptive circumstance.
Second, a more maladaptive consequence which occurs post injury relates to the concept of learned non-use. Just as increasing dexterity of motor function leads to increased motor cortex representation of neural circuitry (and therefore improved function), non-use can lead to decreased motor cortex representation, and therefore decreased function (Plowman and Kleim, 2010). Post stroke, research indicates that learned non-use of a paretic limb, combined with an increased reliance on the unaffected limb can result in major brain reorganization.
This occurs when, post stroke, a paretic limb is not used due to the infarct affecting the area of the primary motor area (M1) controlling that limb. Consequently, the individual relies heavily on the intact (unaffected) limb. Holding to the maxim of “use it or lose it,” in the acute phase after stroke, if the affected limb goes unused, the motor map size decreases (see previous article titled Neuroplasticity in the intact brain). At the same time, the unaffected limb is substantially utilized, and the motor map for that area increases in size. Thus, experience (or lack thereof) impacts the cortical representations of M1 during the stage of spontaneous recovery, but learned non-use in particular may also be implicated in a more nefarious manner, as it may be a contributing factor to interhemispheric imbalance (Takeuchi & Izumi, 2012).
Studies have found that in the affected hemisphere where the infarct or lesion occurred (termed the ipsilesional hemisphere) there is decreased excitability leading to a reduction in the likelihood of neurons generating an action potential (which is the precipitant in neuron-to-neuron ‘firing’). The overall result of decreased excitability is a reduction in neuronal communications within that hemisphere. On the contrary, in the unaffected hemisphere (termed the contralesional hemisphere) there is increased excitability. Studies have shown that the over-excitability of the unaffected hemisphere inhibits the excitability of the affected hemisphere, resulting in decreased motor functioning (Corti et al., 2011). Learned non-use has been theorized as a contributing factor in interhemispheric imbalance additionally by the attenuated neuronal activity in the affected hemisphere, coupled with the greatly increased use of the intact limb driving neuronal activity higher in the unaffected hemisphere (Takeuchi & Izumi, 2012). Credence is given to this idea, in that research has shown that if the unaffected hemisphere is artificially inhibited, this leads to excitability of the affected hemisphere, impacting motor movements positively (Pascual-Leone, Amedi, Fregni & Merabet, 2005).
As noted above, there is substantial biological change to the brain after focal injury (e.g., stroke) and diffuse injury (e.g., TBI). The effect of this biological change is profound. There can be damage to the tissue directly, due to the loss of oxygen resulting from a stroke, or due to inert forces like in a traumatic injury. In addition to these direct effects, additional, and potentially equally damaging biological changes occur at sites of the brain both distant and close to the lesioned areas. This includes the inflammatory process, attenuated blood flow, changes to metabolic processes, edema, and neuronal excitability (Kleim, 2011). These cascade processes result in disruption to intact areas of the brain particularly those areas with connectivity to the injured regions, and has been termed diaschisis.
Diaschisis is in essence a disturbance or loss of function in one part of the brain due to a localized injury in another part of the brain, and these areas can be of considerable distance from the lesioned area including the opposite hemisphere (Stein, 2012). One effect post stroke that affects function within the brain considerably is hyper-excitability in the opposite hemisphere. This, coupled with under-excitability in the damaged hemisphere results overall in a disrupted neural network (Pascual-Leone, Amedi, Fregni and Merabet, 2005). Research has shown that these changes can occur up to 12 months after the initial injury (Cramer and Riley, 2008). With the likelihood of widespread neural dysfunction after injury, what then are the mechanisms for recovery?
Mechanisms of recovery
After injury to the brain, there are two mechanisms whereby functional improvement may occur. These are recovery and compensation (Kleim, 2007). Using World Health Organization definitions,
Recovery relates to:
- Restoration of neural tissue initially perturbed after the injury (neural level)
- Restoration of movement exactly as it was performed prior (behavioral level)
- Restoration of activity exactly as it was performed prior (activity level)
Compensation refers to:
- Recruitment of new neural circuits (neural level)
- Training of new movement sequences (behavioral level)
- Training of activity in a new way after injury (activity level)
Recovery therefore relates to lost functions being restored, and compensation relates to the acquisition of new functions or behaviors to replace those lost after injury (Kleim, 2011). Research has shown that after a stroke, for motor deficits, notable recovery takes place within 30 days for mild, moderate, and moderate-severe severity with additional recovery up to 90 days for severe strokes (Duncan, P., Goldstein, L., Matchar, D., Divine, G. and Feussner, J., 1992). These times frames are similar with other areas of dysfunction where the final level of language function was achieved within six weeks post stroke for 95% of patients (with mild, moderate and severe aphasia; Pedersen, Jorgenson, Nakayama, Raaschou and Olsen, 1995). The level of recovery from spatial neglect was maximized within nine weeks (Hier, Mondlock and Caplan, 1983, cited in Cramer and Riley, 2008). With these types of findings, what is the neurobiological explanation of these changes early on post-injury?
Neurobiological plasticity changes during recovery
Figure 3 displays a model that incorporates a two-stage process of recovery, and within those two stages, provides the neural strategies utilized within the central nervous system.
The first stage is Spontaneous Recovery, and the second stage is Training Induced Recovery (Chen, Epstein and Stern, 2010). Depending on the stage of recovery, different neural mechanisms are at work to either initiate recovery strategies or in response to changes in experience in the form of training or rehabilitation. Each aspect of the model is described below.
STAGE ONE: Spontaneous Recovery
With spontaneous recovery, even in the absence of training or rehabilitation, there is resolution of injury and functional change in close time proximity after injury which plateaus within three months for focal injury and six months for diffuse injury (Chen, Epstein and Stern, 2010). Within that time frame three processes have been theorized to explain this early recovery after injury when specific intervention has not ensued (Dancause and Nudo; 2011). They are:
- Diaschisis reversal
- Changes in kinematics.
- Cortical reorganization.
Diaschisis as previously described begins to resolve, whereby the inflammatory process, blood flow changes, metabolic changes, edema, and neuronal excitability begin to subside (Warraich and Kleim, 2010). The result of diaschisis reversal is improved function due to intact brain areas that were previously disrupted now being restored. Restoration is therefore a crucial neural strategy after injury. From a purely neurobiological level, this may be thought of as the only true level of recovery in the strictest sense of the word, in that the same brain circuits are facilitating function post injury as they were pre injury. Restoration has been found in both cognitive (e.g., language and attention) and physical (e.g., motor movement) domains (Kleim, 2011).
Changes in Kinematics
The second aspect of early recovery relates to changes in kinematic (movement) patterns where compensatory patterns are utilized. The individual intrinsically begins to complete motor movements in a different manner, resulting in improved function, sometimes in drastically different ways than prior to injury. While these new movements likely contribute to functional improvement, these compensatory strategies have the potential to be maladaptive.
The third strategy identified as spontaneous recovery is that the nervous system undergoes within-area and between-area reorganization or rewiring. For example, many researchers have found elements of neuroplasticity near the infarct area after stroke, including cortical reorganization, neurogenesis, axonal sprouting, dendritic plasticity, new blood vessel formation (Kerr, Cheng and Jones, 2011), as well as excitability changes (Nudo, 2011). Chen, Epstein and Stern (2010) outlined neural shifts in recruitment of brain areas in the spontaneous recovery period. Soon after stroke, in homologus (similar) areas, the opposite side of the brain is recruited. Later on during spontaneous recovery, there is a shift in activation back to the injury side. An example would be if the left-sided language area (Broca’s area) was damaged, the right-sided equivalent Broca’s area would be recruited. After a period of time, it would then shift back to the left side.
Another key change in brain function relates to activation of learning networks in the early phase, where plasticity similar to when the brain was developing is induced. This includes motor control and task-learning networks (Chen, Epstein and Stern, 2010).
Overall, cortical reorganization during spontaneous recovery is thought to be compensatory as different circuits or networks of neurons are utilized post injury than those utilized pre injury. While spontaneous recovery occurs in the absence of rehabilitation, there is certainly the opportunity for overlap of training induced recovery while spontaneous recovery takes its course.
STAGE TWO: Training-induced recovery
Training in the form of rehabilitation can induce plasticity post injury, but is not necessarily time limited like spontaneous recovery processes demonstrate (Chen, Epstein and Stern, 2010). Recovery in this stage involves compensation, in that either new brain areas or neural networks are enlisted to complete previous functions. Through the process of training, neuroplasticity is induced. Chen, Epstein and Stern (2010) note that adaptive changes after injury are the outcome of new patterns of activation which include plasticity in areas surrounding the damaged cortex, reorganization of existing networks or recruitment of new cortical areas or networks.
During training-induced recovery, areas which did not make a significant contribution to that particular function pre-injury now contribute to function post-injury (Kleim, 2011). Often times this may be in the form of recruitment of neural areas from the undamaged hemisphere. From a physical perspective, this may include changes in motor maps where the non-injured hemisphere motor cortex can play a distinct role in producing motor movements in an impaired limb, which was previously controlled by the injured motor cortex. From a cognitive perspective, neural recruitment may entail the enlistment of the right side homologue (similar) to Broca’s area to improve language function if Broca’s area (left frontal lobe) is damaged. Rehabilitation to induce such changes may involve constraint induced manual therapy or completion of cognitive tasks while using complex hand movements in the opposite hemisphere which promotes a shift to the uninjured hemisphere.
Retraining involves the training of residual brain areas, resulting in reorganization within the cortex and compensation for lost function (Kleim, 2007). This often comes in the forms of reorganization within the damaged hemisphere. In the case of motor function, if tissue is lost which controlled finger movements, other cortical tissue nearby can reorganize to control that lost movement.
Ultimately, recruitment and retraining involve rewiring or reorganization of neural networks. What then are the properties of the brain which, after injury, provide the mechanisms for recovery? Two basic properties provide us the answer:
The first is that our brains have a tremendous amount of redundancy. There is internal redundancy in areas like the primary visual cortex, the somatosensory areas, the primary auditory cortex and the primary motor cortex (Warraich and Kleim, 2010). So within primary cortex areas there may be multiple areas that respond to the same or similar stimuli. External redundancy refers to similar functionality being processed across different areas of the brain (Warraich and Kleim, 2010). Both of these redundancies allow for better information integration, but they also provide a pathway to improved function after brain injury.
The second property relates to a concept discussed in the previous article; that of experience dependent plasticity. This is where changes in behavior or experience result in changes at a neurobiological level.
Neurobiological Changes after Acquired Brain Injury
After injury to the brain, the processes of neuroplasticity are thought to be the underpinnings of recovery (Carmichael, 2010). To begin, research has found a variety of neuroplastic changes which occur after injury, including:
- Increases or changes to synapses:
• This includes synaptogenesis and synaptic plasticity (Chen, Epstein and Stern; 2010; Nudo, 2011)• Dendrite changes including increased arborization, dendritic growth and spine growth (Nudo, 2011)• Axonal changes including axonal sprouting (Nudo, 2011; Charmichael, 2010)
- Increased neuron growth:
• Neurogenesis in specific brain areas like the hippocampus subgranular zone of the dentate gyrus and subventricular zone in some areas (Schoch, Madathil and Saatman, 2012), substantia nigra and perinfarcted areas (Font, Arboix & Krupinski, 2010).
• Angiogenesis is the process through which new blood vessels form from pre-existing vessels.
- Excitability changes:
• Excitability refers to the ability of a neuron to generate action potentials, which is a short-term change in the electrical potential on the surface of a cell. It is an all or nothing proposition as it either fires or does not fire depending on the strength of the potential.
The first two items on the list above relate to increases in either the number of neurons (this occurs in a very limited sense) or the numbers of synapses or increased strength of existing synapses (this far more prevalent). These changes seen post injury mirror changes seen in the intact brain in the form of experience dependent learning. But instead of it being a learning process, it is a relearning process, aided substantially by rehabilitation.
With experience dependent learning, new synapses form (synaptogenesis) or strengthen through changes in dendrites (new dendritic spine formation), axonal sprouting and long term potentiation (synaptic plasticity). Both synaptogenesis and synaptic plasticity are the main underpinnings of cortical reorganization, recruitment and retraining as identified in Mechanisms of Recovery above. For a general overview of experience dependent learning see the side bar on page 35. For a detailed overview of both synaptogenesis and synaptic plasticity, see the previous article titled Neuroplasticity in the Intact Brain: Experience-Dependent Learning and Neurobiological Substrates.
The third and fourth items on the list relate to changes in excitability homeostasis within the brain (electrophysiological balance across the two hemispheres) and new blood vessel formation. These are described further in the next section.
Findings Related to Neurobiological Changes
Synaptic, Dendritic and Axonal Related Changes
Perederiy and Westbrook (2013) reported post injury that researchers found when an area of the brain stops receiving inputs from the body via afferent nerves, the dendritic arbor retracts (Figure 4). This results in the loss of synapses with other neurons. On the other hand they also reported that in areas of the brain not affected after injury, dendritic arbors increased (Figure 4). This former finding indicates a maladaptive response after injury, while the latter finding reflects the brain’s response post injury to increase synapses in intact areas, thereby providing cortical reorganization or rewiring, which is an adaptive response.
Axonal sprouting and reorganization occurs post injury. This sprouting has adaptive consequences in that increased axonal growth leads to greater levels of synapses allowing reinnervation (Perederiy & Westbrook, 2013). Re-innervation can then lead to adaptive changes. However, there are issues with axonal regeneration in that glial scars can prevent axons from reaching their target, and for patients with temporal lobe epilepsy, specific axonal sprouts can synapse onto granule cells which may relate to the recurrence of seizures (Perederiy & Westbrook, 2013).
Research has found that there may be changes within the damaged hemisphere. For example in motor areas, topographical map changes occur, where different areas controlling motor movements compensate for the damaged areas. The neurobiological foundation of motor map changes is synaptic change. This includes synaptogenesis where new synapses form through dendritic growth and axonal sprouting, and synaptic plasticity which strengthens existing synapses through the process of long-term potentiation (see previous article for a description).
Nudo, Wise, SiFuentes and Milliken (1996) mapped the motor areas of monkeys to determine the areas of the brain which controlled hand motor movements. After training on a skilled-hand task, infarcts were induced in the monkey’s mapped motor area. The monkeys were then retrained on the same skilled task. Initially, the monkeys demonstrated significant deficits on the skilled-hand task. After retraining, however, their skills substantially improved, and this related to significant changes to their motor maps. Specifically the hand and digit areas increased significantly during spontaneous recovery between the injured monkeys and a control group. In addition, for monkeys who received re-training, there was no loss of spared hand motor map in nearby intact areas, suggesting that therapy prevented further loss of hand areas representation.
Angiogenesis is the process through which new blood vessels form from pre-existing vessels. In ischemic stroke, which is loss of blood flow leading to neuronal death, increased vasculature relates to increase circulation (Font, Arboix, Krupinski, 2010). The benefit is return of blood flow to previously damaged areas, which is assists in establishing metabolic support (Krum, Mani, & Rosenstein, 2008).
In a review assessing research on neurovascular response after stroke, Arai, Jin, Navaratna & Lo (2009) examined the role of angiogenesis. The authors distinguish injury in the acute phase where neurovascular damage causes the primary disruption of the blood brain barrier. After stroke, it is now widely held that the penumbra (which is an area around the infarct affected by vascular compromise) is more than just dying cells – it may be a precursor of neuroplasticity. In the delayed phase after acute stroke, angiogenesis and neurogenesis, which are closely tied together, are primary responses post stroke. One cytokine of note relating to angiogenesis is vascular endothelial growth factor (VEGF), which in its endogenous form relates to brain neuroprotection. Krum, Mani and Rosenstein (2008), found that VEGF is an important factor in post-injury recovery. In particular, by blocking VEGF receptors, preventing them from upregulating, they found that vascular proliferation was decreased. By blocking VEGF, and showing a clear decrease in positive vascular changes, they were able to isolate its effect – vascular remodeling (i.e., angiogenesis).
Changes to Network Organization
While reorganization of neural networks has been found post injury, the amount of reorganization depends on the size of the injured area. For example, with areas of smaller damage, reorganization tends to occur close to the injury area. For larger areas of damage, reorganization or recruitment is more widespread to other areas of the brain (Chen, Epstein and Stern; 2010).
Schlaug, Marchina and Norton (2009), using melodic intonation therapy to treat aphasia found that after intensive treatment, significant white matter changes occurred. In particular, through use of diffusion tensor imaging (which detects functionality of white matter tracts) they found increases in the right arcuate fasiculus, which is a white matter tract connecting Wernicke’s area and Broca’s area. Key to this finding is that the right arcuate fasiculus is not typically well developed, indicating that the right hemisphere reorganized to improve function. Another important factor in this finding is that increases in the number of fibers in the arcuate fasiculus correlated with measurable improvement in conversational skills.
Activation and Excitatory Changes
After injury, changes in the excitability of the damaged and intact hemispheres can impact cortical functioning. Excitatory changes across hemispheres can occur quickly after brain injury, where cortical excitability in the affected areas is generally decreased. A model of interhemispheric rivalry has been suggested, where there are distinct differences in the excitability of analogous areas between hemispheres (e.g., motor areas). For example in the damaged hemisphere there is hyperpolarization (inhibition of neurons) and in the intact hemisphere there is depolarization (excitation of neurons; Bolognini, Pascual-Leone & Fregni, 2009). Calautti & Baron (2003) reported that in the chronic phase after stroke, researchers found that better recovery was found if activation of the affected-side is more predominant than the unaffected hemisphere over time. This shift of activation to the unaffected side is “the sign of a distressed system” (Cramer et al., 2011, p. 1593). So from a long term perspective if the damaged side was more involved in function, that related to better outcomes. However, if the patient had to rely on the unaffected side more for function, that related to poorer outcomes.
In a study on memory and attention deficits after damage to the prefrontal cortex (PFC) by Voytek, Davis, Yago, Barcelo, Vogel and Knight (2010) they found evidence that the PFC in the undamaged hemisphere compensates for the damaged PFC areas in the opposite hemisphere “on a trial by trial basis dependent on cognitive load” (p. 401). In other words, the undamaged hemisphere dynamically compensates for the damaged hemisphere depending on the level of challenge the damaged hemisphere must deal with. This demonstrates that the intact hemisphere can adapt rapidly and that it is not an all or nothing proposition, where function is relegated to either the intact or damaged hemisphere post injury.
Collectively, this research highlights processes post injury which are similar to those neuroplastic changes in the intact brain. Namely, that when experience in the form of changes to nerve inputs or motor outputs occurs, cortical changes like those of experience dependent learning occurs where synaptogenesis, synaptic plasticity, and axonal sprouting take place. Furthermore, after injury, through aspects of the injury cascade, certain adaptive processes initiate, resulting in changes like angiogenesis, and network reorganization changes. Neuroplasticity is a remarkable tool in our cortical toolbox. And, like many other adaptive tools, it too can have maladaptive consequences.
The maladaptive side of neuroplasticity
While there is huge upside to neuroplasticity, we cannot afford to overlook the downside. While beyond the scope of this article to go into any depth there are plenty of examples to point out that neuroplasticity has its dark side, too. Just a few examples include addictions to alcohol, elicit substances or prescription drugs, pornography addictions (Doidge, 2007), seizure disorders post injury (Cramer et al., 2011), phantom limb pain (Doidge, 2007), hand dystonias in musicians (Candia, Rosset-LLobet, Elbert and Pascual-Leone, 2005), learning and memory interference (Carmichael, 2010) and chronic pain (Cramer et al., 2011). Thus, while we search for adaptive examples of neuroplasticity and ways to promote it both in the intact brain and after injury, we must also seek to prevent these brain changes which can have profound impacts on function, not to mention societal implications.
In an article put together by 27 leading neuroscientists from the National Institutes of Health Blueprint for Neuroscience Research (Cramer et al., 2011), they noted that “[n]europlasticity occurs with many variations, in many forms, and in many contexts” (p. 1952). This reminds us that brain injury in all of its forms is quite heterogeneous. The host of variables which affect outcomes after acquired injury are vast and varied (e.g., age, lesion area, pre-injury characteristics, genetic profile, etc.).
Yet with all of this heterogeneity, there are similar neuroplastic processes after injury. Cramer et al. (2011) write that “common themes in plasticity that emerge across diverse central nervous system conditions include experience dependence, time sensitivity and the importance of motivation and attention” (p. 1952). Thus it is important that neuroscience and its practitioners continue to identify at the key factors which contribute to neuroplastic changes be it at the molecular, cellular, architectural, behavioral or network level.
As we better understand the neurobiological level of neuroplasticity, we can then begin to better understand how to harness treatments that enhance the recovery process and ultimately patient function. There is currently a tremendous amount of research addressing neuroplasticity at both a basic and applied level. Both are needed to continue to learn more about effective treatments. Some are pharmacologic and focus on drugs or molecules that may impact the secondary phase of injury, or that “prime” the central nervous system in preparation of traditional neurorehabilitation in the form of occupational therapy, physical therapy, and speech & language pathology. Such priming includes non-invasive brain stimulation (e.g., transcranial magnetic stimulation, transcranial direct simulation), deep brain stimulation, and neuropharmacology. Others focus on the timing of rehabilitation efforts, in order to maximize plastic states where the opportunity for recovery is at its highest. Still others focus on the principles of Hebbian learning wherein understanding how experience shapes the brain can best be utilized in any form of treatment.
In closing, neuroplasticity is not an idea, it is a state. This state exists from our earliest years of neurodevelopment (prenatal and postnatal), to our ongoing changing brains as a result of experience, to changes after injuries to our most precious resource, our brain. Our transformative experiences shape and mold our neurochemicals, axons, dendritic arbors and spines, motor maps, cortical networks—in other words, our very essence. And likewise, when our very essence is transformed via injury, the change to our networks and synapses then shape our experiences. How we can best reclaim those experiences by harnessing neuroplasticity is the focus of an article in the next issue of RainbowVisions® Magazine.
Overview of Experience-Dependent Learning
For neurons or networks of neurons to communicate they need to have extensive connections with one another (or, quite literally hundreds to thousands of connections for each neuron.) These extraordinarily complex connections require junctions or connections termed synapses.
For example, neuron A connects via its axon terminal to neuron B at its dendrite (see Figure 5). The space between the axon and dendrite is the synapse. In a basic sense, the greater the number of synapses, the greater and stronger the connections between neurons. Likewise, the more synapses, dendrites and axons that develop, the greater the opportunity to connect more neurons together and strengthen the existing connections.
As our experiences change, at a neurobiological level, we either increase or decrease the numbers of synapses, dendrites and axons. If we stop a function, we lose synapses, etc., and if we increase an activity we proliferate synapses, etc., resulting in experience-dependent learning.
About the Author
Heidi Reyst Ph.D., CBIST
Vice President of Clinical Administration
Dr. Reyst holds a Ph.D. in Applied Social Psychology from The George Washington University in Washington, D.C. She is a Certified Brain Injury Specialist Trainer, Academy of Certified Brain Injury Specialists, and has worked in various capacities within the field of brain injury rehabilitation since 1991. She currently oversees professional staff allocation, billing and service provision, professional staff training, accreditation readiness and outcomes management. Dr. Reyst is currently a member of the board of governors for the Academy of Certified Brain Injury Specialists, and is the Vice Chairperson for Information Management. She is a member of the American Psychological Association and is a frequent volunteer for the Brain Injury Association of Michigan.
Abbott, L. and Nelson S. (2000). Synaptic Plasticity: Taming the Beast. Nature Neuroscience Supplement, 3, 1178-1183.
Arai, K., Jin, G., Navataratna, D. and Lo, E. (2009). Brain angiogenesis in developmental and pathological processes: Neurovascular injury and angiogenic recovery after stroke. Federation of European Biochemical Societies, 276, pp. 4644-4652.
Bach y Rita, P., Collins, C., Saunders, F., White, B., Scadden, L. (1969). Vision substitution by tactile image projection. Nature, 221, pp. 963-964.
Bolognini, N., Pascual-Leone, A. and Fregni, F. (2009). Using non-invasive brain stimulation to augment motor training-induced plasticity. Journal of NeuroEngineering and Rehabilitation, 6:8.
Bosch, M and Hayashi, Y. (2011. Structural plasticity of dendritic spines. Current Opinion in Neurobiology, 22, pp. 1-6).
Candia V., Rosset-Llobet J., Elbert T. and Pascual-Leone A. (2005), Changing the Brain through Therapy for Musicians’ Hand Dystonia. Annals of the New York Academy of Sciences, 1060, pp. 335–342.
Calautti, C. and Baron J. (2003). Functional neuroimaging studies of motor recovery after stroke in adults: A review. Stroke, 34, pp. 1553-1566.
Carmichael, S. (2010). Translating the frontiers of brain repair to treatments: Starting not to break the rules. Neurobiology of Disease, 37(2), pp. 1-10.
Chen, H., Epstein, J. and Stern, E. (2010). Neural plasticity after acquired brain injury: Evidence from functional imaging. PM & R, supplement 2, pp. s306-s312.
Corti, M, Patten, C and Triggs, W. (2011). Repetitive transcranial magnetic stimulation of motor cortex after stroke. American Journal of Physical Medicine and Rehabilitation, 91 (3), pp. 254-270.
Cramer, S. and Riley, D. (2008). Neuroplasticity and brain repair after stroke. Current Opinion in Neurology, 21, pp. 76-82.
Cramer, S., Sur, M., Dobkin, B., O’Brien, C., Sanger, T., Tojanowski, J., Rumsey, J., … (2011). Harnessing neuroplasticity for clinical applications. Brain, 134, pp. 1591-1609.
Dancause N., Nudo R. J. (2011). Shaping plasticity to enhance recovery after injury. Prog. Brain Res. 192, 273–295.
Doidge, N. (2007). The brain that changes itself: Stories of personal triumph from the frontiers of brain science. Viking Penguin: New York, NY.
Duncan, P., Goldstein, L., Matchar, D., Divine, G. and Feussner, J., (1992). Measurement of motor recovery after stroke. Outcome assessment and sample size requirements. Stroke, 23, pp. 1084-1089.
Faul M, Xu L, Wald MM, Coronado VG. (2010). Traumatic Brain Injury in the United States: Emergency Department Visits, Hospitalizations and Deaths 2002–2006. Atlanta (GA): Centers for Disease Control and Prevention, National Center for Injury Prevention and Control.
Finger, S., Beyer, T. and Koehler, P. (2000). Dr. Otto Soltmann (1876) on development of the motor cortex and recovery after its removal in infancy. Brain Research Bulletin, 53 (2), pp. 133-140.
Font, A., Arboix, A. and Krupinski, J. (2010). Angiogenesis, neurogenesis and neuroplasticity in ischemic stroke. Current Cardiology Reviews, 6, pp. 238-244.
Franz, E. and Gillett, G. (2011). John Hughlings Jackson’s evolutionary neurology: a unifying framework for cognitive neuroscience. Brain, 134, pp. 3114-3120.
Harris, K. and Kater, S. (1994). Dendritic spines: Cellular specialization imparting both stability and flexibility to synaptic function. Annual Review of Neurology, 17, pp. 341-371.
Hill, T. and Zito, K. (2013). LTP- induced long term stabilization of individual nascent dendritic spines. The Journal of Neuroscience, 33(2), pp. 678-686.
Howlader N., Noone A., Krapcho M., Garshell J., Neyman N., Altekruse S., Kosary C., Yu M., Ruhl J., Tatalovich Z., Cho H., Mariotto A., Lewis D., Chen H., Feuer E.,Cronin K. (eds). SEER Cancer Statistics Review, 1975-2010, National Cancer Institute. Bethesda, MD,
Kerr, A., Cheng, S. and Jones, T. (2011). Experience dependent neural plasticity in the adult damaged brain. Journal of Communication Disorders, 44, pp. 538-548.
Kleim, J., Barbay, S. and Nudo, R. (1998). Functional reorganization of the rat motor cortex following motor skill learning. Journal of Neurophysiology, 80, pp. 3321-3325.
Kleim, J., Barbay, S., Cooper, N., Hogg, T., Reidel, C., Remple, M. and Nudo, R. (2002). Motor learning-dependent synaptogenesis is localized to functionally reorganized motor cortex. Neurobiology of learning and Memory, 77, 63-77.
Kleim, J., Hogg, T., Vandenberg, P., Cooper, N., Bruneau, R. and Remple, M. (2004). Cortical synaptogenesis and motor map reorganization occur during late, but not early, phase of motor skill learning. The Journal of Neuroscience, 24(3), pp. 628-633.
Kleim, J. (2007). Role of neural plasticity in motor learning and motor recovery after brain injury. Pocketbook of Neurological Physiotherapy, S. Lennon, M. Stokes: Elsevier, 41-50.
Kleim, J. (2011). Neural plasticity and neurorehabilitation: Teaching the new brain old tricks. Journal of Communication Disorders, 44, pp. 521-528.
Kleindorfer, D., Khoury, J., Moomaw, C., Alwell, K., Woo, D., Flaherty, M., Khatari, P., Adeoye, O., Ferioli, S., Broderick, J. and Kissela, B. (2010). Stroke incidence is decreasing in whites but not in blacks. Stroke, 41, 1326-1331.
Krum, J., Mani, N., Rosenstein, M. (2008). Roles of endogenous VEGF receptors flt-1 and flk-1 in astroglial and vascular remodeling after brain injury. Experimental Neurology, 212(1), pp. 108-117.
Koleske, A. (2013). Molecular mechanisms of dendrite stability. Nature, 14, pp. 536-550.
McCallister, A. (2000). Cellular and molecular mechanisms of dendrite growth. Cerebral Cortex, 10, pp. 963-973.
McCallister, T. (2011). Neurobiological consequences of traumatic brain injury. Dialogues in Clinical Neuroscience, 13, pp. 287-300.
Merzenich, M., Kaas, J., Wall, J., Sur, M., Nelson, J. and Felleman, D (1983). Progression of change following median nerve section in the cortical representation of the hand in areas 3b and 1 in adult owl and squirrel monkeys.
Neuroscience, 10(3), PP. 639-665. Merzenich, M., Nelson, R., Stryker, M., Cynader, M., Schoppmann, A. and Zook, J. (1984). Somatosensory cortical map changes following digit amputation in adult monkeys. The Journal of Comparative Neurology, 224, pp. 591-605.
Mizui, T. and Kojima, M. (2013). BDNF and synaptic plasticity: The recent cell biology for understanding of brain disorders. Clinical Pharmacology and Biopharmaceuticals, S1:004, pp. 1-5.
Nudo, R., Milliken, G., Jenkins, W. and Merzenich, M. (1996). Use-dependent alterations of movement representations in primary motor cortex adult squirrel monkeys. The Journal of Neuroscience, 16(2), pp. 785-807.
Nudo, R., Wise, B., SiFuentes, F. and Milliken, G. (1996). Neural Substrates for the Effects of Rehabilitative Training on Motor Recovery After lschemic Infarct. Science, 272, pp. 1791-1794.
Nudo, R. (2011). Neural bases of recovery after brain injury. Journal of Communication Disorders, 44, pp. 515-520.
Oe, Y., Tominaga-Yoshino, K., Hasegawa, S. and Ogura, A. (2013). Dendritic spine dynamics in synaptogenesis after repeated LTP inductions: Dependence on pre-existing spine density. Scientific Reports, 3:1957, pp. 1-8.
Pascual-Leone, A., Amedi, A., Fregni, F. and Merabet, L. (2005). The plastic human brain cortex. Annual Review of Neuroscience, 28, pp. 377-401.
Pascual-Leone, A., Nguyet, D., Cohen, L., Brasil-Neto, J., Cammarota, A. and Hallett, M. (1995). Modulation of muscle response evoked by transcranial magnetic stimulation during the acquisition of new fine motor skills. Journal of Neurophysiology, 74, pp. 1037-1045.
Pearce, J. (2009). Marie-Jean-Pierre Flourens (1794-1867) and cortical localization. European Neurology, 61, pp. 311-314.
Pedersen, P. M., Stig Jørgensen, H., Nakayama, H., Raaschou, H. O. and Olsen, T. S. (1995), Aphasia in acute stroke: Incidence, determinants, and recovery. Annals of Neurology, 38, pp. 659–666.
Perederiy, J. and Westbrook, G. (2013). Structural plasticity in the dentate gyrus – revisiting a classic injury model. Frontiers in Neural Ciruits, Plowman, E. and Kleim, J. (2010). Motor cortex reorganization across the lifespan. Journal of communication disorders, 43, pp. 286-294.
Raisman, G. (1969). Neuronal plasticity in the septal nuclei of the adult rat. Brain Research, 145, pp. 25-48.
Roger, V., Go, A., Lloyd-Jones, D., Benjamin, E., Berry, J., Bordon, W., … et al. (2012). Heart Disease and Stroke Statistics—2012 Update: A Report From the American Heart Association. Circulation, 125, pp. e2-e220.
Schoch, M., Madathil, S. and Saatman, K. (2012). Genetic manipulation of cell death and neuroplasticity pathways in traumatic brain injury. Neurotherapeutics, 9, pp. 323-337.
Schlaug, G., Marchina, S. and Norton, A. (2009). Evidence for Plasticity in White Matter Tracts of Chronic Aphasic Patients Undergoing Intense Intonation-based Speech Therapy Ann N Y Acad Sci. 1169, pp. 385–394.
Schlosberg, D., Benifla, M., Kaufer, D. and Friedman, A. (2010). Blood-brain barrier breakdown as a therapeutic target in TBI. Nature Reviews Neurology, 6(7), pp. 393-403.
Stein, D. (2012). Concepts of central nervous system plasticity and their implications for recovery after brain damage. Brain Injury Medicine: Principles and Practice: eds. Nathan D. Zasler MD, Douglas I. Katz MD, Ross D. Zafonte DO, David B. Arciniegas MD, M. Ross Bullock MD, PHD, Jeffrey S. Kreutzer PHD, ABPP; pp. 162-174.
Takeuchi, N. and Izumi, S. (2012). Maladaptive plasticity for motor recovery after stroke: Mechanisms and approaches. Neural Plasticity, 2012, pp. 1-9.
Toni, N., Teng, E., Bushong, E., Aimone, J., Zhao, C., Consiglio, A., Praag, H., … , (2007). Synapse formation on neurons born in the adult hippocampus. Nature Neuroscience, 10, pp. 727-734.
Venkataramani, P. (2010). Santiago Ramon y Cajal: Father of Neuroscience. Resonance, November, pp. 968-975.
Voytek, B., Davis, M., Yago, E., Barcelo, F., Vogel, E. and Knight, R. (2010). Dynamic Neuroplasticity after Human Prefrontal Cortex Damage. Neuron, 68, pp. 401-408.
Warraich, Z. and Kleim, J. (2010). Neural plasticity: The biological substrate for neurorehabilitation. PM & R, 2, S208-S219.
Werner, C. and Engelhard, K. (2007). Pathophysiology of traumatic brain injury. British Journal of Anesthesia, 99, pp. 4-9.
Yildirim, F. and Sarkcioglu, L. (2007). Journal of Neurology, Neurosurgery and Psychiatry, 78(8), p. 852.
York, G. and Steinberg, D. (2011). Hughlings Jackson’s neurological ideas. Brain, 134, pp. 3106-3113.
Yuste, R. and Bonhoeffer, T. (2001). Morphological changes in dendritic spines associated with long-term synaptic plasticity. Annual Reviews of Neuroscience, 24, pp. 1071-1089.
Ziebell, J. and Morganti-Kossman, M. (2010). Involvement of pro- and anti-inflammatory cytokines and chemokines in the pathophysiology of traumatic brain injury. Neurotherapeutics, 7, 22-30.

domain: medical


This machine learning experiment combines the output of three different neural networks to get the final results shown above. The original input sequence is a short clip of a dancer I filmed in a recent photoshoot.
The first neural network generates abstract/primitive displacement maps from the input dance sequence. A second network takes these displacement maps and renders them into 3d and lights them with approximate global illumination, which it learned from training on an equivalent bunch of GI rendered frames (note the rendering glitched from imperfect training of this network). Finally a third network generates gold and silver specular reflections based on the input sequence and this output is composited over the rendered frames to give the final look.


text:
It looks like you're using an Ad Blocker.
Please white-list or disable AboveTopSecret.com in your ad-blocking tool.
Some features of ATS will be disabled while you continue to use an ad-blocker.
A medical test being developed by Kuwait will be used to 'detect' homosexuals and prevent them from entering the country – or any of the Gulf Cooperation Countries (GCC), according to a Kuwaiti government official.
GCC member countries – Bahrain, Kuwait, Qatar, Oman, Saudi Arabia and the United Arab Emirates – already deem homosexual acts unlawful. This controversial stance is being toughened, according to Yousouf Mindkar, the director of public health at the Kuwaiti health ministry.
He told Kuwait newspaper Al Rai: ‘Health centres conduct the routine medical check to assess the health of the expatriates when they come into the GCC countries. However, we will take stricter measures that will help us detect gays who will be then barred from entering Kuwait or any of the GCC member states.’
Those taking part in homosexual acts in Kuwait, if they’re under 21, can receive a jail sentence of up to 10 years.
Earlier this month Oman newspaper The Week was suspended over an article that was deemed to be sympathetic to homosexuals, according to the BBC.
It’s illegal to be gay in 78 countries, with lesbianism banned in 49. Five countries mete out the death penalty to gay people – Iran, Saudi Arabia, Sudan, Yemen and Mauritania.
A leading London-based LGBT campaigner has called on FIFA to cancel the 2022 World Cup in Qatar over reports that Gulf Cooperation Countries will introduce medical screening tests to "detect" and ban homosexuals entering the countries.
Peter Tatchell, director of the Peter Tatchell Foundation, told IBTimes UK that the proposed legislation "will mean that gay players and spectators will be banned from attending the football world cup".
"This contradicts previous assurances given to FIFA by the Qatar government that everyone will be welcome and that there will be no discrimination," he said
it is a good way to prevent the spread of AIDS and HIV and the dozens of other STD's that gay men spread more often.
Its disgusting the way some ATS members support this type of fascist regime. When one day they are effected,tested and banned from entering a country of their genetics . They will feel how unfair this treatment is.
Roll on Hitler.
Of course they don’t!! They’re barbarians!
A witch hunt. Do they still not realise that in countries where gays have equal rights. They do no harm to anyone.
Of course they hate gays. They hate all non-Muslims and non-conformists. This is a part of the world that condones pedophilia, promotes terrorism, stones women for adultery, beheads people on the streets, condones rape, etc.
I mean they are basically saying they HATE gays. We all know there are more than likely MANY MANY gays in their countries also. But it happens behind closed doors and they remain in the closet.
This is their way to say " We will find you".
I would love to find out how they test for this.

domain: sociology


The international community and Congolese government must urgently agree upon a new deal to reform the Congolese military, according to this report by 13 leading international and Congolese civil society groups. The Democratic Republic of Congo: Taking a Stand on Security Sector Reform argues that the lack of political will to reform the security sector in the Democratic Republic of the Congo (DRC) risks not only billions of dollars of international aid but also the very stability of the country.
The report was signed by 13 leading international and Congolese organizations and networks, including the Open Society Initiative for Southern Africa. It was completed after extensive research and interviews in DRC and donor countries. It argues that the army not only fails to provide security but actively preys upon the population, being one of the major perpetrators of human rights violations in the country.
The report concludes that the main reason for the failure of army reform in DRC is a lack of political will from parts of the Congolese government, notably those elements which have benefited from endemic corruption.
The Democratic Republic of Congo: Taking a Stand on Security Sector Reform underscores the critical role the international community must play. In just five years, the report documents, donor countries alone have invested more than $14 billion into the DRC. Yet only one percent, or $140 million, was spent on security sector reform.


text:
BRIGHOUSE and Rastrick Band proved their championship status and delighted local fans with an immaculate display of Christmas music in their home town.
Capacity audiences at the band’s matinee and evening concerts at Central Methodist Church were left in no doubt that that band was playing at the peak of its capacity.
By popular demand the band was conducted by Dr Chris Davis, who recently retired as principal director of music in the Royal Marines.
Matinee guest performers were the choirs of Rastrick High School, under the direction of Alison Pryce-Jones, who sang a wide range of music from ‘Rudolph the Red Nosed Reindeer’ and ‘Away in a Manger’ to songs from the deep south of the US.
B&R provided a faultless performance of Christmas music and traditional brass band fare including the march ‘The Champions’, Lovatt-Cooper’s ‘Walking with Heroes’, Bizet’s ‘Farondole’ and ‘O Magnum Mysterium’ by Laurisden. A firm favourite was John Williams’ fanfare and flying theme from the film ‘ET’.
Solos of the highest quality were provided by Lucy Murphy (flugel), Stuart Lingard (principal cornet) and David Thornton (principal euphonium), and the audience got the chance to join in on a variety of Christmas carols.
Julie Beaumont, wife of band president Paul Beaumont, said: “This was probably the best Christmas concert that the band has given in Brighouse.”
The band will be in action at Huddersfield Town Hall on January 28 when they will perform with Halifax Young Singers in aid of the Forget Me Not Children’s Hospice, the Mayor of Kirklees’ charity appeal. Tickets are available from the Kirklees booking office on 01484 223200.

domain: entertainment


text:
Police officials in Dover, Del. have arrested a white officer for kicking a Black suspect in the head during an arrest process after dash cam footage from 2013 was made public. Lateef Davidson was kneeling when Dover Police officer Corp. Thomas Webster kicked him in the face near a city gas station.
As reported by local paper The News Journal, the release of the video adds to the several incidents regarding police conduct across America. Activists are demanding that new procedures get implemented when police apprehend suspects and expect changes to be made from within their organizational structure. As part of an ongoing legal tussle between Davidson and Webster, the officer turned himself in on Monday (May 4) ahead of the release of the video.
More from the News Journal:
“We believe that the video demonstrates the need for large-scale reform of the Dover Police Department, specifically improvements to their use of force and internal affairs practices and supervision of their officers,” said Kathleen MacRae, executive director of the American Civil Liberties Union of Delaware.
While this incident occurred before well-publicized incidents in Ferguson, Missouri; New York City; North Charleston, South Carolina; and Baltimore, where black suspects were killed by police, the indictment and release of the video here occurred nearly two years later.
Civil rights leader the Rev. Jesse Jackson said the Dover incident clearly shows mistreatment by law enforcement.
“What is clear is that a man who is down should not be kicked to unconsciousness,” said Jackson, who appeared at protests and a funeral in Baltimore and Ferguson. “That is excessive force.”
Davidson is launching a lawsuit against Dover Police with the assistance of the local ACLU branch. The clip of the August 2013 arrest was made public by a federal judge who said the video was no longer considered confidential. The video is chilling, as Webster kicks Davidson so hard that he broke his jaw and made him slump to the ground.
There are no details about Davidson’s suit, but there has been wrangling behind the scenes occurring in the time since the incident that gave way to recent events.
Watch the 5-minute dashboard camera video of Corp. Thomas Webster kicking Lateef Davidson in the face. A Warning: the images depicted in the video may be disturbing to some.
Photo: Dover Police Department


text:
Running backs don’t open holes for themselves, and quarterbacks don’t block rushers. Offensive line is a thankless position, noticed more for failure than success. The Rams’ guys don’t complain.
The Rams’ recent line play invited confusion, more than anything. They’ve been so good, so consistent, for so long, that the struggles in the previous couple games seemed tough to reconcile and explain. Perhaps, after what happened Sunday in Arizona, the analysis can be tabled.
The Rams rushed for 269 yards in the 31-9 victory over Arizona, and quarterback Jared Goff was sacked only twice, and one of those had nothing to do with the line. The Rams’ most-experienced unit bounced back against a solid Arizona defensive front and restored some high expectations.
“Obviously there was an increased sense of urgency,” right tackle Rob Havenstein said. “Previous to this game, our last two weeks, we didn’t play up to our potential. We were looking to come out and, I don’t want to say prove anything, but we just wanted to get back to our football, our style of offensive football.”
Havenstein said film review would reveal whether the Rams accomplished that, but an initial look gives them a passing grade, adjusted because the quality of opponent, the Cardinals, wasn’t particularly good.
The Rams rushed for 269 yards, one short of their season high, and they would have topped it except backup quarterback Sean Mannion executed two yard-losing kneel-down plays at the end of the game.
New running back C.J. Anderson rightfully got the attention, because he ran for 167 yards on 20 carries, but rookie John Kelly also gained 40 yards and Rams receivers had success with seven jet-sweep runs.
It was a back-to-basics game for the Rams, whose average of 6.6 yards per rush was their second-highest of the season, behind only the 6.9 average against Denver. In the previous two weeks, the Rams averaged 4.0 yards per rush against Chicago and 4.6 yards against Philadelphia.
“One thing that hasn’t changed in the 13 years that I’ve been in this league,” left tackle Andrew Whitworth said, “is that the month of December is about physicality and defense. It’s really about the team that can try to break the other team’s will. It never changes. I don’t care what your record is. You see it across the league. You just can’t forget that when you’re playing these games in this month.”
So perhaps the Rams are back on track, although pass protection against the Cardinals was a little less stellar, as Goff was hit five times and still didn’t look completely comfortable.
Still, what Whitworth said rings true. Assuming running back Todd Gurley, who missed Sunday’s game because of knee inflammation, returns to health, the Rams might have revived their run game at the appropriate time.
“I really think it was a blessing in disguise to have this happen early,” left guard Rodger Saffold said. “Yes, we did put ourselves in a situation to where it’s a little bit of an uphill battle, but I think that’s going to put in the right direction, to be able to peak at the right time.”
The status of running back Todd Gurley remains day to day, Coach Sean McVay said during a conference call on Monday afternoon. Gurley missed Sunday’s game, apparently out of precaution, after a week during which he did not practice because of knee inflammation.
McVay said Gurley “was feeling good” Monday but said the Rams would not put Gurley in harm’s way. It’s possible that the Rams will go forward, for Sunday’s regular-season finale against San Francisco, with C.J. Anderson at running back, and if the Rams beat the 49ers, they will get a first-round playoff bye, which would allow Gurley to get three weeks of rest.
McVay said safety Lamarcus Joyner suffered a sprained ankle against the Cardinals and that his status for this week’s game also would be day to day.
Rams receiver Robert Woods had six catches for 89 yards against the Cardinals, and became only the fourth player in league history to have at least 60 receiving yards in 14 consecutive games.
Woods is in good company with receivers Marvin Harrison, Antonio Brown and Andre Johnson.
“He is such a great worker, leader and person,” Goff said of Woods. “Such a good teammate that does everything the right way. He shows up every day and works as hard as anybody. I am spoiled, as a quarterback, to have all those guys in the receiver room. … Robert is the leader of that.”

domain: sports


This application was developed as part of an NSF-funded REU
project to automate the collection of tweets for research and other
uses. Instructions for use and a screenshot is below:
Please feel free to use this application for your own research/ teaching uses. To run the application,
The application is very intuitive to use.
Whitelaw, Clayton, Agrawal, M., Rao H.R. and Oh, Onook, “Using social media to study social phenomena,” published in the proceedings of the 2011 Wireless Telecommunications Symposium (WTS 2011), New York, New York, 4/12 – 16, 2011
Source code. Please feel free to modify/ improve the source to fit your needs. If updates are sent back to me, I would be very happy to update this page with proper attribution, your modified source and/ or application for further use by the community.
Netbeans Project (if you wish to develop the application further)
Developer(s): Clayton Whitelaw, USF Computer Science student.
Any feedback may be sent to firstname.lastname@example.org
Last updated: August 23, 2011
material is based upon work supported by the National Science
Foundation under Grant No. 0926376.
Disclaimer:Any opinions, findings, and conclusions or recommendations expressed in this material are those of the author(s) and do not necessarily reflect the views of the National Science Foundation.


text:
Hyannis man hurt when van hits utility pole on Willow Street
WEST YARMOUTH — A Hyannis man was taken to the hospital and Willow Street closed to traffic for about an hour after a one-car accident yesterday morning.
Joseph L. Wittenmeyer, 62, received minor injuries as a result of the accident and was being evaluated at Cape Cod Hospital last night for the condition that led to him losing control of a van that struck a utility police about 10 a.m. yesterday.
According to Yarmouth police Officer Steve Renzi, witnesses said Wittenmeyer was heading north on Willow Street at a normal speed when the van suddenly began to lose speed and weave. The van left the road and struck a utility pole, breaking it in two.
William Sargent, an off-duty Cotuit firefighter, stopped at the accident and administered first aid to Wittenmeyer as state police and Yarmouth police arrived at the scene. Wittenmeyer was taken to the hospital by Yarmouth Fire and Rescue.
Willow Street was closed to traffic while a ComElectric crew removed and replaced the damage pole.


text:
The artist taps into the dangers of the industry.
Continuing his support of his third studio album Ta13oo, Denzel Curry dropped the visual for his single "Black Balloons" (also stylized as "13lack 13allons") featuring Twelve'len and GoldLink. The Zen Deans-directed video is one in a series of eye-catching visuals that create a storyline through Curry's music. It seems to be a nod to the influences and oftentimes empty promises that the entertainment industry has to offer as scenes show the signing of a contract, a party with beautiful, yet carbon-copied, guests, and the offering of all the drugs one could ask for.
The 24-year-old artist is getting the shine that he deserves, but it's not difficult to notice that his sound stands out from the current mainstream crowd. "I’m not carrying no torch," Curry told Billboard. "I’m just saying that I want to make the best s**t possible, and I’m gonna do it regardless of who’s in my way. And I’m not gonna be important just to hip hop. I’m gonna be important to all genres of music. I’ve proved with TA13OO that I’m versatile as hell. Now it’s just self-mastery. I’m in a self-mastery stage of my life right now."

domain: artistic


text:
Ahh! What a beautiful day!
Though i am a little late to accept the challenge as my one of the sweet-est yet mischievous friend nominated me for this beautiful and unique challenge. One need to post the favorite among-st the pool of mesmerizing quotes consecutively for 3 days. Awesome! Challenge accepted kiddo @ayushijoshi. Thank you for the nomination!
My Quote :
Don’t ever let someone tell you that you can’t do something. Not even me. You got a dream,you gotta protect it. When people can’;t do something themselves, they are gonna tell you that you can’t do it. You want something, go get it. Period.
– Will Smith.
It is from the *The Pursuit Of Happyness*. One heart melting true story depicting invincible bond of father and a son. The chase to earn the Happiness representing a *y*. I am one of the admirer of this particular story. If you are ignorant about this, it is never too late. Go and watch it, Pretty Please!
1) @ayushijoshi – Here i nominate you again :p
2) KSSbaby – Waiting for your quotes!
3) Pearl – Hope you like it!
Rules, as specified, by @ayushi, yet modified in my words 😉
1) Write 3 different quotes for 3 consecutive days.
2) Nominate 3 people everyday.
3)Be grateful for the person who nominated <Giggle>
So, here, it begins…


Dragon 1/35 M4(105) Howitzer Tank
|REVIEWER:||Scott Van Aken|
More than 50,000 examples of the famous M4 Sherman tank were built in the USA, meaning only the Russian T-34 was produced in greater numbers during WWII. Throughout production a great number of M4 variants were spawned, among them a tank armed with a 105mm howitzer gun. The rationale behind this vehicle was to create a tank able to provide fire support missions against hardened targets such as bunkers or buildings harboring enemy soldiers. The 105mm howitzer-armed tank could carry 66 rounds of ammunition, and it operated with a crew of five men. These howitzer tanks were used by both the US Army and by the USMC in the Pacific theater. These howitzer tanks were all based on the standard M4 (no suffix) tank.
Shermans seem to be hugely popular with armor modelers. I can recall a rather large contest where some of the commentary overheard concerning the armor category was that it was "Shermans and Germans". Seems about right and now we have yet another variant available to us. This one has the usual mass of sprues, the superb Deformable Styrene tracks, and a great photo etch fret that includes a number of neat bits and pieces. There are newly tooled bits as is the norm with Dragon and there are also two 'C' sprues, so one needs to be wary of a possible goof, though the parts are different enough that I doubt there will be any confusion.
Here is the official listing of features:
- Newly tooled machine gun pintle mount
- Newly tooled rotor and gun shields
- Newly tooled engine deck w/splash guard
- Newly tooled U-shaped groove, ventilation cover made from photo-etched metal
- Newly tooled aiming-stake rack
- New spare track on rear armor plate
- Two types of cupola provided as option
- Mantlet end-pieces designed as separate parts to fully replicate details
- M4 105mm turret produced w/side-mold technology
- Turret secondary ventilation fan
- Mount for turret canvas recreated in delicate detail
- Rear hull detail accurately produced
- Pistol part produced w/slide-mold technology
- Detailed loader's hatch
- Periscope, cover and mount details are accurately represented w/separate parts
- Upper-hull w/weld-line detail authentically produced
- Hull side plates are accurately produced w/correct horizontal upper edge
- Slide-molded 105mm barrel is produced
- Turret-lop MG pedestal w/accurate design
- Late MG and barrel storage brackets w/great detail
- On-vehicle tools are realistically produced
- Two types of sprockets provided as option
- Finely rendered headlight and horn guards
- Detailed hatch-periscope units w/clear parts and guards
- Tow hooks w/fine detail
- DS T48 track w/EEC (Duckbills)
There are three options, all based on Olive Drab. one is with HQ Company, 32nd Armored Reg in Belgium during 1945 with a winter wash. Next is a 31st Armored Reg. tank in Normandy during 1944. Finally, with what looks to be mud plastered on the finish is an 8th Tank Battalion, 4th Armored Reg tank, also in Normandy during 1944.
There is no doubt that this one will be a good seller. Shermans are hugely popular and the kits rarely hang around long at the LHS. I'm sure you will be quite pleased with this one.
Thanks to www.dragonmodelsusa.com for the preview kit. Get yours at your favorite retailer.
If you would like your product reviewed fairly and fairly quickly, please contact the editor or see other details in the Note to Contributors.
Back to the Main Page
Back to the Previews Index Page


Gov. Rick Scott is proposing a $5 million annual fund aimed at renovating stadiums and keeping Major League Baseball teams in Florida for spring training.
Scott unveiled the plan Wednesday during a stop at the Detroit Tigers' spring facility in Lakeland. The funds would be used only for spring training facilities, Scott's office said, and local governments would be required to match at least 50 percent of project costs.
State contributions would be capped at $20 million, and the Department of Economic Opportunity would review and approve the match "to ensure it provides a return on investment for taxpayers," Scott's office said.
The Pittsburgh Pirates, celebrating their 45th spring in Bradenton, unveiled a $7.5 million renovation to McKechnie Field last week that they hope will be a hit with residents and visitors.
"We have been fortunate to have been able to forge meaningful public/private partnerships that have allowed us to build and update outstanding Major League facilities in Bradenton," said Pittsburgh Pirates President Frank Coonelly. "Each of the two major projects that we completed over the last six years was done primarily with local companies and local workers and resulted in other economic development in the community."
Scott said the initiative fits with his goal of growing jobs in Florida. "We must protect and enhance this vital business for Florida families," he said.
Fifteen of MLB's 30 teams train in Florida each spring, with the other half operating in Arizona. Since 1998, six clubs have moved west from Florida, according to MLB.com, including the Cincinnati Reds, who left Sarasota in 2008. The Baltimore Orioles moved into Ed Smith Stadium in 2010.
Three teams' Florida leases are up for renewal in 2016, with two more to follow in 2017, FloridaToday reports.
More than 1.5 million fans attend spring training games in Florida each year, providing a $750 million benefit to the state each year, according to the governor's website.
Sign up for the Bradenton Patch email newsletter to stay connected to your community.


text:
Lucknow, Uttar Pradesh, IN
Small Business (1-10M TTM Revenue)
ABC Genomics provides in situ synthesized custom microarrays and specializes in the development and validation of high-end and powerful genetic marker-based screening tools for the healthcare industry.
|ABC Genomics Sector G Jankipuram Lucknow, Uttar Pradesh, 226021 India|
To request access, simply fill out the form below and we will contact you.