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Caleb Chase
Characters » Caleb Chase
Registry of the Evolved Database
File #18 Apr 2010 22:38
Name Caleb Chase Aliases
Status Unregistered Evolved Ability Electrokinesis
Gender Male Race/Eth. Caucasian
Birthdate Unknown Age 17
Height 6'1" Build Slim
Eyes Blue Hair Dark Brown
Residence Moves
Employment None
Parents Faith and Scott Chase Siblings Older Brother
Marital Status Single Children None
First Seen Last Seen
Profile About six foot, one inch tall, weighs about one hundred and forty eight pounds, dark brown hair, brown eyes, Caucasian, thin runners build, wears dark colours.
Martin Johnson
Caleb was born at his parents (Liam and Darla Harris) apartment in Littleton, Colorado on the 31st of October 1993. The first year of his life was a normal, happy one up until the 4th of November 1994 when a neighbour found him crying in his crib, his parents dead in their bedroom, a burglary gone wrong. The police were called but never found their attacker and Caleb was put into care. All things considered Caleb had a pretty happy childhood, he lived in a care home until he was six when he was adopted by Faith and Scott Chase. Growing up he developed an interest in music and freestyle fighting (Faith taught freestyle fighting at their local community centre and Scott was a music teacher), as he grew older he began to focus more on vocals then just general music. He was an average student at school and got good enough grades to keep his parents happy. Shortly after Caleb turned 13 his parents moved them to Los Angeles, where Scott had got a new job teaching at an arts school. Caleb also joined this school and got involved in a school band as the lead singer and joined the cheerleading squad, he also began performing with his band at various school events such as school dances.
At age 14 Caleb's abilities surfaced, one day he had stayed late afterschool to work on some homework in the computer lab, he was working on his English homework which was not his best subject, he got frustrated and discharged several blast of electricity, short-circuiting the power in the school, shocked and afraid he ran home. When his parents got home from work that day, they found Caleb on his bed in tears refusing to say anything, no matter what they said he never told them about his ability. Not long after this the explosion in New York occurred, both him, his brother and parents were shocked by the tragedy. On June 15th, 2007 the of Evolved Registry came into place, making Caleb even more frightened of his abilities. Three years later just after his 17th birthday and he was being plagued by constant nightmares of being discovered as an evolved human. He was terrified of seeing that look in peoples eyes, as if was bad or wrong in some way, and their hate, he'd also heard of groups against the Evolved, so was terrified about what may happen if he got registered. His parents could find no way to help him and believed he was suffering from depression and wanted him to see a doctor, desperate Caleb turned to his brother for help and told him about his ability, shocked he knew that if Caleb stayed, he'd be taken to the doctor and they would find out and he'd be registered, so he withdrew what money he had and gave it to him along with his jacket, before telling Caleb to go on the run. He's now been on the run for about three months, he's pretty much run out of the money his brother gave him and has been stealing in order to get by. He hasn't been paying much attention to where he's been going and has recently found himself in the New York area.
Caleb had a tenancy to rely on his brother for support when he was frightened or unsure of what to do. The one thing he enjoys above everything else is singing. He has a fear of spiders (they creep him out) and HATES being known as his brother's little brother ( Just because he's the quiet one doesn't mean he doesn't want his own identity). He likes Vampire movies, hates Musicals, is into punk rock, likes the colour red, the Twilight saga irritates him, but he enjoyed the Darren Shan books, has made it clear that if he'd been given the choice he wouldn't have been christened Catholic, for the life of him he cannot understand the appeal of football, he can be very sarcastic, he uses text-speak but hates people who answer everything with lol or kk, he finds Dizzy Rascal very annoying, gets annoyed at himself when he accentually sings along with Lady Gaga songs, and loves the rain.
Caleb's ability allows his to generate and control electricity from his body. He has limited control on which form it takes though he tends to favour a bolt (they're easiest for him to control), but the strength of the current is random at the moment, but when frightened or angry he tends to create his strongest discharge. He mainly focuses the energy with his hands but can release it from any part of his body. His main weakness is water, using his powers when wet can cause him to lose his immunity to it. He farthest distance the electricity can travel is about twelve metres, though he has put little practice into using his power his has some control over his aim, but if something causes him to lose focus, it can go wildly out of control. When he overexerts himself his ability can backfire, the discharge acting like a tazer and knocking him out (how long he's knocked out for depends on how much he overexerts himself by).
Currently due to his limited control for now his power will be mainly destructive, he'd probably freak out and use it if someone working with the registry tried to apprehend him, which would be a tazer blast, which as with electric shocks could kill, a blast aimed at a car could cause it to explode, some point down the line when he learned some control he can do more useful things, like running some electrical appliances which at this point he just destroy.
evolvedunregistered


Is Infinova A US Or Chinese Company?
I've hear of it being referenced as a Chinese company, but their website says they are US based in New Jersey and they list offices in various places around the world with Hong Kong as one of them. Is it a joint venture?
Infinova is a Chinese / American company. They trade on the Shenzhen China stock market, see Infinova's stock quote. Their market capitalization is $800 million. 2013 revenue is ~$153 million, including their Chinese operations and March.
Infinova acquired March Networks in 2011. March continues to market under its own brand, not Infinova's.
Infinova is a US based surveillance products manufacturer having multiple factories including US and China, and the product reliability and support is not a doubt, they have various critical infrastructure projects to their name which are all of national security importance in various countries.


The sleeve is that tiny bit on the left side of the picture. I do intend to finish the garment soon, maybe even in time for the gold medal ceremony on Sunday. The pieces have been sent off to Matt for seaming so I can add the collar while knitting the sleeves. (Yes, Matt does all of my finishing). I think he's seaming right now, actually....seriously.
What lured me away from the beautiful Yelena? Why.......Mountain Colors' new yarn called Twizzle (scroll down to see the specs on it). It's 85% merino wool and 15% silk, and the silk part is one ply, making the finished yarn look really interesting. There's 250 yards in a skein and it works up around 4-5 stitches per inch and it's $22 per skein. One hank would make a lovely scarf, a pair of mittens, or a stunning hat. At this gauge, there's tons of options as far as other sweater projects, too (one of my favorites would be Cabin Fever's "Take It From The Top", a great top-down sweater with no seaming required).
Of course, the color sensibility is incredible, as it's dyed by the great folks from Mountain Colors. Wanna see some options?
I'm using the Meadow colourway, and it's just lovely knitted up. This is one yarn that's way WAY prettier in the knitted fabric than in the hank, as the silk strand stands out in the hank but it blends right into the knitted fabric. And it is 85% merino and 15% silk, so you KNOW it's a soft, SOFT piece of knitting.
If you're interested in any of these little goodies, just slip me an e-mail or use our new toll-free line (866-939-BEAR) and we'll get stuff in the mail to you right away!
I'm off to go knit....have a great weekend and enjoy the last weekend in February and the last one before the Lenten season arrives.
That's the finished back, the finished left side, and the start of the right side. All that will soon remain is the sleeves, then it's off to Matt for seaming. I'll add the quickie collar after that and claim my place on the podium.
I'm enjoying the textured part of the pattern, but I'm itching to get back to the colorwork portion of our program, which begins after just 14" of body are completed (I'm pushin' 12" right now). HOORAY!
That's 14 skeins of saving grace, courtesy of the fantastic folks at Lamb's Ear Farm in Tacoma, WA. THANKS, ROXI...you saved my project! I only needed five, but since it was a discontinued color, I cleaned her out completely (partially in case I want to make any matching accessories and partially to be nice and not leave her with odd skeins of a discontinued shade). I also received a nice little package from the sweet lady at kidsknits.com with a partial, unlabeled skein out of her stash. I had called last Sunday in terror of not finding enough to finish and she was SURE what she had in her personal stash was the same shade...sure enough, it was! KNITTERS ARE AMAZING PEOPLE!
There's been some random poo-pooing of the idea of 4,000+ people all joining in on the Knitting Olympics, particularly with some of the more snarky bloggers out there. One specific person asked those who are participating to distinguish what we're doing from the behaviour of sheep (who tend to be mindless and follow in packs). Also, said blogger challenged participants to think about what they're gaining from the knit along, and why it should be an interesting thing to be a part of.
Rekindling my love for colourwork, particularly stranding (versus weaving, a la Philosopher's Wool). As I've mentioned here, I haven't done this type of knitting since early 2001, and I'm thoroughly enojoying it. So much so that I may do another Dale official design, but I'm also looking at something from SandnesGarn (we're ramping up stock in yarn from this company).
A rekindled love of traditional knitting and designs. While I knew that I liked texture and color knitting, I almost never make specific projects like this, due to the need for shop models. I need to do more traditional things more often.
I've actually committed to making something for myself. HOORAY! They're no small projects, but it's important that I wear my own handknits....and I have two, after 36 years of knitting (both made in the past six months, too).
And with that, I'm off to go work on my sweater (or should that be sweaters, plural)!


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Varicocele Treatment
Normally, oxygenated blood flows to the testicles via an artery, and deoxygenated blood flows out via a network of small veins that drain into another vein, and is eventually carried back to the heart. During this process, backflow to the testicles is prevented by a series of one-way valves in the vein. In some individuals, however, these valves do not work well. As a result, the blood flows in reverse and causes "back pressure" to stretch and enlarge the network of small veins around the testes, forming a varicocele.
What is a varicocele?
How did I get a varicocele?
What are the symptoms of a varicocele?
How is a varicocele diagnosed?
Do I need to be treated?
What are the avaliable treatments?
How is the embolization procedure performed?
How well does embolization work?
Are there any complications associated with varicocele embolization?
How do I know which treatment will be best for me?
Varicocele Embolization
A varicocele, pronounced var'e-ko-seel, is a network of dilated blood vessels, or varicose veins, in the scrotum. For unknown reasons, varicoceles usually occur in the left testes. Varicoceles are a relatively common condition that tend to occur in young men, usually during the second or third decade of life. This condition affects approximately 15 to 20% of the general male population and up to 40% of infertile males.
Normally, oxygenated blood flows to the testicles via an artery, and deoxygenated blood flows out via a network of small veins that drain into another vein, and is eventually carried back to the heart. During this process, backflow to the testicles is prevented by a series of one-way valves in the vein. In some individuals, however, these valves do not work well. As a result, the blood flows in reverse and causes "back pressure" to stretch and enlarge the network of small veins around the testes, forming a varicocele.
Many times a varicocele is silent and does not cause symptoms. However, some varicoceles cause a dull or aching pain especially when the person has been in upright position for a long time. Heavy lifting may also cause pressure build up in the varicocele.
In some individuals, a varicocele may cause decreased fertility or infertility. As many as 40% of men with decreased fertility have a varicocele. A commonly accepted theory is that the varicocele raises the testicular temperature and adversely affects the sperm count and quality. More than half of men with decreased fertility will have improvement in the sperm count and quality after treatment of the varicocele.
In some men, varicoceles can cause shrinking (atrophy) of the testicles. In many cases, when the varicocele is treated on the affected side, the testicle may return to normal size.
It is best to catch a varicocele before it can cause major problems, such as infertility. Self-exam of the scrotum is the best way to diagnose a varicocele early. A varicocele can feel like a "bag of worms", and is usually found in the left testicle. The majority of varicoceles are detected by a doctor during a health checkup.
In many cases, the varicoceles cause no symptoms and do not need to be fixed. However, if there is associated pain, decreased fertility, or testicular shrinking, treatment may help. All adolescents with varicoceles should be treated to avoid future infertility.
What are the available treatments?
Varicoceles may be treated surgically by a urologist (varicocelectomy) or by a minimally invasive method (varicocele embolization) by an Interventional Radiologist.
Embolization requires no stitches or general anesthesia and only a 1/4 of an inch incision. Nearly all the patients can be treated on an outpatient basis and may return to normal activities in two to three days. Surgical treatment requires an incision and may require several days or even weeks to return to full activities. Studies have shown that embolization and surgery are equally effective.
Regardless of the treatment, the varicocele may recur and may require repeat treatment. If the varicocele has been previously treated with surgery, embolization is still an option. If recurrence occurs after the embolization, embolization can generally be repeated. If a repeat embolization fails, surgery can still be performed.
Varicocele embolization is usually performed on an outpatient basis under sedation and local anesthesia. A small catheter (tube) is inserted into a leg vein near the hip or neck vein through a tiny skin incision. This tube is placed into the varicocele vein under X-ray guidance. Small amounts of X-ray dye (contrast) are injected to confirm the position of the catheter. Then tiny coils made of stainless steel or platinum, balloons, or other materials are inserted in the vein to block it and stop the backflow, or pressure, in the varicocele. Blood can still exit the testicle through other normal pathways. Once it is confirmed that there is no flow in the affected vein, the catheter is removed.
There is a 90% success rate with embolization, and of those with success, about 10% may experience late recurrence. These results are the same as those achieved with more invasive surgical techniques. Varicocele embolization has been performed for over 25 years and has an excellent long-term safety record. Its safety and effectiveness has been shown in very large trials.
As with any treatment, there are potential complications associated with this procedure. Minor complications such as bruising at the entry site, mild backache, or nausea (rare) may occur. Complications associated with surgery such as hydrocele (collection of fluid in the testes), infection, or loss of testicle are exceedingly rare with an embolization procedure.
Embolization does not affect sexual function. Sexual activity may be resumed the day after the embolization. However, since it takes sperm about three months to mature, improvement in fertility may take three months or longer.
How do I know which treatment will be the best for me?
The best treatment for a varicocele depends on whether or not you have had prior treatment for a varicocele. You should discuss your treatment options with your physician. Some questions to ask:
Is varicocele embolization an option for me?
What are the risks and benefits of the treatment plan prescribed for me?
How do I pay for varicocele embolization?
The cost is similar to surgery. Most insurance companies pay for the procedure. However, coverage depends on the particular insurance company and should be discussed with them.
http://www.varicoceles.com/treatment.htm
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Senate moving forward with anti-discrimination bill
On behalf of John A. Klassen, P.A. | Nov 15, 2013 | Employment Discrimination
No matter a person's age, gender and sexual orientation, residents in Minnesota seek to obtain a career that they not only feel comfortable in but are also where they are treated appropriately. When a worker experiences employment discrimination, the event could seriously impact them. A person's characteristics could lead to wrongful termination or cause an employee to quit in order to escape the workplace discrimination.
It was recently reported that the United States Senate passed a bill that would prohibit workplace discrimination based on sexual orientation and gender identity. With a vote of 61-30, the legislation would impact employers that have at least 15 employees. This legislation will bring various viewpoints and issues to the forefront, and those supporting the bill believe that it will send a strong message of bipartisan support for the LGBT community. The legislation now goes to the United States House of Representatives.
Anti-discrimination laws not only seek to prevent discrimination in the workplace but they also seek to protect certain groups while also encouraging them to stand up for their rights. When an employee believes that they are being discriminated against, it is important that they seek out options and understand their rights. They could file a claim for employment discrimination or wrongful termination.
Dealing with employment discrimination is a difficult reality to accept. This makes it especially important for those affected by these issues to know their options. This can help them plan their route to better their situation and file a claim if needed.
Source: Minnesota Public Radio, "Employment Non-Discrimination Act Passes First Senate Hurdle," Eric Krupke, Nov. 4, 2013
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Home » Products » Rhododendrons » Species Rhododendrons » Rhododendron stewartianum
Rhododendron stewartianum
Item: SSTEW
3 litre 5 litre 7.5 litre
White, yellow, pink or red bell shaped flowers often flushed a different colour at the margins or on the reverse. Flowering early, anytime from February to April. The flower colour is very variable and this plant is rare in cultivation. With an upright habit, it has peeling fawn bark. Height 120cm in 10 years.
Named after L.B. Stewart (1876-1934), a former Curator of the Royal Botanic Garden in Edinburgh.
Recommended for early flowers.
Easy to grow.
Ideal position: sheltered woodland.
Habit: open.
Group: Species Rhododendron.
Subsection: Thomsonia.
Introduction date: pre 1950 (1919).
Species distribution: SE Tibet, NW Yunnan, NE and E Upper Burma, Assam.
Approximate altitude: 3,000 to 4,500m.
Ideal soil: pH 4.5 to 6.0
RHS Hardiness Rating: H5.
How we usually propagate this plant: Seed.
Species Rhododendrons often have wonderful foliage, but are fairly specialist and are best grown by more experienced gardeners.
These are the plants which were discovered by plant collectors, growing in the wild in the Himalayas and other mountain regions of the world. Being species they do not have the 'hybrid vigour' of named varieties, but they often do have great character and interest in flower and foliage. We pride ourselves in one of the best ranges of rhododendron species in the country, and we try to propagate these from recognised good forms. These may be identified by the original plant collector's seed number, (eg R. denudatum EGM 294) or by a clonal name given to a selected plant (eg R. degronianum 'Ho Emma'). Many new species rhododendrons have been introduced in the last 25 years, and many are well worth growing for their foliage alone!
Rhododendrons like moist acidic soil, with good drainage, and plenty of organic matter such as leaf-mould and added ericaceous compost. Species should be given the best planting positions, which are neither too wet nor too dry. Yellow varieties need especially good drainage. For a guide to plant spacing, use the height we give in 10 years as a guide to the distance between each plant. Plant no deeper than the top of the rootball, and dig in plenty of good ericaceous compost around the sides. Most species require very little fertilizer and half a teaspoon of slow release feed is sufficient for a 3 litre plant, rising to a tablespoonful for a mature plant. Those in the taliensia and neriiflora subsections are particularly salt-sensitive, and should only be fed with a mulch. Most species in this section are not troubled by deer and rabbits.
Please note: It can take a number of years before some species start to flower, but often you can enjoy some lovely foliage while you are waiting. Flower colour of species can vary considerably from one clone to the next. eg R. campanulatum can flower from white to pink or deep lilac, and R. arboreum flowers from red to pink to white depending upon the elevation collected. Typically, species are not recommended for growing in pots, as it is too difficult to provide the necessary care that they need.


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Genius 11-Year Old Entrepreneur in NYC Selling 5 Minutes of Emotional Advice for $2
Ciro Ortiz, a sixth-grader from New York City, has found business success helping stressed-out New York subway-goers. For just $2, passerbyers in need of some advice or encouragement can stop and have a 5-minute consultation with him. And so far, the idea is a very profitable one!
How he came up with the idea
Ciro, who was a victim of bullying in the past, says he was sitting around watching TV one day when he came up with the idea to be a counselor - despite his young age. He says he figured there were a lot of people like him that could use some help, so he decided to do something about it.
He told his parents, "I think I'm wise enough to give good advice!" And they agreed to let him test out his idea.
How he works it
Because he's young ang still in school, Ciro is only able to work for two hours every Sunday (usually 12noon to 2pm or 2pm to 4pm). During these times, he goes to the Bedford L-train subway platform in Brooklyn, sets up his table and sign which reads "Emotional Advice For $2", and he waits for people to approach.
When they approach him, he listens to their problems regarding work, relationships, and other general issues in life. On average, he makes about $50 a week - quite a bit of money for an 11-year old.
He says that his first day out on the platform was nerve-wrecking, but he quickly got over it because it was an instant hit. Many passerbyers were immediately interested in his services. He told UpWorthy.com, "I didn't know if people were going to stare or laugh at me... [but they] saw that I was taking it seriously."
Now, his clients include men, women, and even police officers.
Ciro is not greedy. He strongly believes in helping the community, and so he donates all his profits to helping kids at his school who can't afford to buy snacks or lunch.
He says his friends don't quite get it, and that they don't really understand what he's doing or why. "But that's ok," he says.
He just cares about helping people. "Everyone needs help sometimes," he says. "You can't get through life without help."
What a huge inspiration he is for all entrepreneurs - both young and old alike!
Watch the video below:


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La estación de Seraing es una estación de tren belga situada en Seraing, en la provincia de Lieja, región Valona.

Pertenece a las líneas  y  de S-Trein Lieja.

Situación ferroviaria
La estación se encuentra en la línea 125 (Aguesses-Flémalle).

Historia

Intermodalidad

Véase también

 S-Trein Lieja

Referencias

Estaciones de ferrocarril de Bélgica
Lieja

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From traditional to gourmet to low-fat and sugar-free, this section has everything you need for delicious food the entire week of Passover. You will love these recipes so much, you might just find that you use them throughout the year!
While all of the ingredients in the Passover recipes are kosher for Passover, each community has its own customs as to what to use or not use on Passover. Please also note that any processed food must have a reliable "Kosher for Passover" certification.


This is such a great dessert for fall and it's SO simple to make! We used these six inch tart dishes and got two servings, but you could use traditional ramekins and it would make four individual servings. This Easy Cranberry Apple Crisp is best served warm with a scoop of a vegan So Delicious Dairy Free Almond Milk Vanilla Ice Cream. Yum!
There are only nine ingredients in this dish. It begins with apples and cranberries combined with sugar and a small amount of flour to help thicken.
The topping consists of quick-cooking oats, flour, brown sugar, melted vegan margarine (such as Earth Balance) and chopped pecans.
You'll want to place these crisps onto a lined baking sheet because there WILL be some bubbling over. It's inevitable. Once baked, you'll want to let these cool slightly before serving. That filling is very, VERY hot.
Serve with a scoop of vegan So Delicious Dairy Free Almond Milk Vanilla Ice Cream and you have an easy, festive dessert.
In a bowl, combine the apples, cranberries, sugar and flour. Set aside, stirring occasionally.
In another bowl, combine the oats, flour, sugar, melted vegan margarine and chopped pecans. Be sure the mixture is coated with the margarine and resembles coarse clumps.
Spoon the cranberry mixture into individual ramekins or baking dishes.
Crumble the topping mixture over the cranberry mixture.
If you are using the individual ramekins, some bubbling over is usually invevitable. Place them on a lined baking sheet to catch any drippings.
You can also use a larger baking dish to make this recipe (less chance of bubbling over).
Allow to cool for 15 minutes before serving as that sugar is very, very hot.
Serve with vegan vanilla ice cream.


Use creativity to decorate things up. You can make use of inexpensive linen that could be adorned with fabric colors to create an amazing design.
As for the return gits, think of something innovative. You can pack the return gifts in a colorful goodie bag. The kids will love it!
Make the ceilings flooded with colors. Balloons and myriad of streamers will come to your rescue in this context.
Cut the sandwiches with big cookie cutters, which will give the sandwiches their unique shape. The party will get more interesting.
Ask your child and his friends about the theme they would like to have in the party. Decorate your rooms in the same way and tell all the kids to come in dresses that match the themes.
With these amazing ideas you are all set to organize a party that will not only set the kids top the fun mode but the adults will love them too. But make sure you do not include anything that pose dangerous for them such as sharp objects that are within their reach.
Yoga for Constipation: 4 Asanas to Help You Out!


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Classic Hollywood #66 – Rudolph Valentino Goes To Court In Costume
Rudolph Valentino Is Not Acting, He's Actually In Court – 1925
Rodolfo Alfonso Raffaello Pierre Filibert Guglielmi di Valentina d'Antonguella – aka Rudoplh Valentino, one of the world's biggest film stars in 1925.
As big as a film star Valentino was it would not prevent him from being compelled to show up in court against his wishes to answer a speeding violation. His crime: going 38 in a 20 mile per hour zone in Santa Monica.
The news caption reads:
Valentino in Court in Screen Costume – Fined $50
Rudolph Valentino, failing in an attempt to have a representative answer speeding charges in court asked to have court held at his studio pleading business pressure. Justice Marchetti became angered demanded Valentino's appearance and fined him $50. Photo of "The Sheik" in the costume of his latest screen vehicle – 9-11-25 (photo Wide World)
Valentino was not being a prima donna asking the court to come to the studio. Shutting down production for one day of the film he was starring in, "The Eagle" would cost $10,000. More importantly the people who could least afford it, all the extras involved in the filming, would have lost a days wages
On September 8 Justice Marchetti said, "I am sorry that anyone should lose money or be inconvenienced, but the court can show no partiality. Before the law a famous actor is in the same situation as anyone else. The dignity of the law would be compromised, the courts would be made a laughing stock, were I to set up legal machinery in a studio."
Previously on September 2, Valentino sent a member of the Automobile Club to appear at court as his representative. Justice Marchetti was not pleased by the failure of Valentino to show up.
When Valentino showed up on Friday, September 11, 1925 at Noon, he testified that the officer who ticketed him was mistaken. When Justice Marchetti asked how fast Valentino was going, he replied, "35 to 40 kilometers per hour, it's a French car and speed is not shown in miles per hour."
"What is the equivalent in miles?" asked the justice. Vaelntino took out a piece of paper and began trying to figure out the answer. After a minute Valentino said he did not know.
Why don't you put a modern speedometer on your car?" Justice Marchetti wanted to know.
Valentino answered "I can't find one that will fit the hole in the instrument board. But I will have one soon."
Valentino paid the $50 fine for speeding, pledged not to jay-walk, install a new speedometer and drive more carefully in the future. Before he left the court Valentino was asked by the court to be a witness for Donald Nutting, 22 and Mary Virginia Angell, 19 who were waiting to be married. Valentino happily complied and signed their marriage certificate.
Valentino left the court, posing patiently for photographers and then hurried back to his studio declaring "wild horses shall not drag me to court again."
They wouldn't.
Within a year Valentino was dead at the age of 31. He died in New York City on August 21, 1926 after developing peritonitis and pleuritis due to complications of an operation for gastric ulcers.
Old New York In Postcards #10 - Restaurants
If Star Wars Had Been A Silent Film
Classic Hollywood #28 - Norma Talmadge
This entry was posted in Classic Hollywood, Movies, Photography and tagged 1920s, Entertainment, Los Angeles, News - Press Photo, Rudolph Valentino on December 15, 2017 by B.P..
← Yankee Stadium As You've Never Seen It – 1928 Old New York In Photos #82 – Central Park Mall c. 1870 →
3 thoughts on "Classic Hollywood #66 – Rudolph Valentino Goes To Court In Costume"
Marketa October 22, 2019 at 9:27 am
Very nice and well written article, showing Rodolfo' s humanity – while taking part in that wedding.
Kevin December 19, 2017 at 10:25 pm
This has to be the silliest newspaper photo/article I've ever seen.
B.P. Post author December 20, 2017 at 4:22 pm
Not if comparing it to any article about any Kardashian.


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(-) Remove <label class='research-domain' title='Diagnostics, Therapies, Applied Medical Technology and Public Health'>LS7 (12)</label> filter LS7 (12)
(-) Remove Denmark (5) filter Denmark (5)
Displaying 1 - 10 of 23. Show 10 | 20 results per page.
Project acronym BEAT
Project The functional interaction of EGFR and beta-catenin signalling in colorectal cancer: Genetics, mechanisms, and therapeutic potential.
Researcher (PI) Andrea BERTOTTI
Host Institution (HI) UNIVERSITA DEGLI STUDI DI TORINO
Call Details Consolidator Grant (CoG), LS7, ERC-2016-COG
Summary Monoclonal antibodies against the EGF receptor (EGFR) provide substantive benefit to colorectal cancer (CRC) patients. However, no genetic lesions that robustly predict 'addiction' to the EGFR pathway have been yet identified. Further, even in tumours that regress after EGFR blockade, subsets of drug-tolerant cells often linger and foster 'minimal residual disease' (MRD), which portends tumour relapse. Our preliminary evidence suggests that reliance on EGFR activity, as opposed to MRD persistence, could be assisted by genetically-based variations in transcription factor partnerships and activities, gene expression outputs, and biological fates controlled by the WNT/beta-catenin pathway. On such premises, BEAT (Beta-catenin and EGFR Abrogation Therapy) will elucidate the mechanisms of EGFR dependency, and escape from it, with the goal to identify biomarkers for more efficient clinical management of CRC and develop new therapies for MRD eradication. A multidisciplinary approach will be pursued spanning from integrative gene regulation analyses to functional genomics in vitro, pharmacological experiments in vivo, and clinical investigation, to address whether: (i) specific genetic alterations of the WNT pathway affect anti-EGFR sensitivity; (ii) combined neutralisation of EGFR and WNT signals fuels MRD deterioration; (iii) data from analysis of this synergy can lead to the discovery of clinically meaningful biomarkers with predictive and prognostic significance. This proposal capitalises on a unique proprietary platform for high-content studies based on a large biobank of viable CRC samples, which ensures strong analytical power and unprecedented biological flexibility. By providing fresh insight into the mechanisms whereby WNT/beta-catenin signalling differentially sustains EGFR dependency or drug tolerance, the project is expected to put forward an innovative reinterpretation of CRC molecular bases and advance the rational application of more effective therapies.
Monoclonal antibodies against the EGF receptor (EGFR) provide substantive benefit to colorectal cancer (CRC) patients. However, no genetic lesions that robustly predict 'addiction' to the EGFR pathway have been yet identified. Further, even in tumours that regress after EGFR blockade, subsets of drug-tolerant cells often linger and foster 'minimal residual disease' (MRD), which portends tumour relapse. Our preliminary evidence suggests that reliance on EGFR activity, as opposed to MRD persistence, could be assisted by genetically-based variations in transcription factor partnerships and activities, gene expression outputs, and biological fates controlled by the WNT/beta-catenin pathway. On such premises, BEAT (Beta-catenin and EGFR Abrogation Therapy) will elucidate the mechanisms of EGFR dependency, and escape from it, with the goal to identify biomarkers for more efficient clinical management of CRC and develop new therapies for MRD eradication. A multidisciplinary approach will be pursued spanning from integrative gene regulation analyses to functional genomics in vitro, pharmacological experiments in vivo, and clinical investigation, to address whether: (i) specific genetic alterations of the WNT pathway affect anti-EGFR sensitivity; (ii) combined neutralisation of EGFR and WNT signals fuels MRD deterioration; (iii) data from analysis of this synergy can lead to the discovery of clinically meaningful biomarkers with predictive and prognostic significance. This proposal capitalises on a unique proprietary platform for high-content studies based on a large biobank of viable CRC samples, which ensures strong analytical power and unprecedented biological flexibility. By providing fresh insight into the mechanisms whereby WNT/beta-catenin signalling differentially sustains EGFR dependency or drug tolerance, the project is expected to put forward an innovative reinterpretation of CRC molecular bases and advance the rational application of more effective therapies.
Project acronym BONEPHAGY
Project Defining the role of the FGF – autophagy axis in bone physiology
Researcher (PI) Carmine SETTEMBRE
Host Institution (HI) FONDAZIONE TELETHON
Call Details Starting Grant (StG), LS4, ERC-2016-STG
Summary Autophagy is a fundamental cellular catabolic process deputed to the degradation and recycling of a variety of intracellular materials. Autophagy plays a significant role in multiple human physio-pathological processes and is now emerging as a critical regulator of skeletal development and homeostasis. We have discovered that during postnatal development in mice, the growth factor FGF18 induces autophagy in the chondrocyte cells of the growth plate to regulate the secretion of type II collagen, a major component of cartilaginous extracellular matrix. The FGF signaling pathways play crucial roles during skeletal development and maintenance and are deregulated in many skeletal disorders. Hence our findings may offer the unique opportunity to uncover new molecular mechanisms through which FGF pathways regulate skeletal development and maintenance and to identify new targets for the treatment of FGF-related skeletal disorders. In this grant application we propose to study the role played by the different FGF ligands and receptors on autophagy regulation and to investigate the physiological relevance of these findings in the context of skeletal growth, homeostasis and maintenance. We will also investigate the intracellular machinery that links FGF signalling pathways to the regulation of autophagy. In addition, we generated preliminary data showing an impairment of autophagy in chondrocyte models of Achondroplasia (ACH) and Thanathoporic dysplasia, two skeletal disorders caused by mutations in FGFR3. We propose to study the role of autophagy in the pathogenesis of FGFR3-related dwarfisms and explore the pharmacological modulation of autophagy as new therapeutic approach for achondroplasia. This application, which combines cell biology, mouse genetics and pharmacological approaches, has the potential to shed light on new mechanisms involved in organismal development and homeostasis, which could be targeted to treat bone and cartilage diseases.
Autophagy is a fundamental cellular catabolic process deputed to the degradation and recycling of a variety of intracellular materials. Autophagy plays a significant role in multiple human physio-pathological processes and is now emerging as a critical regulator of skeletal development and homeostasis. We have discovered that during postnatal development in mice, the growth factor FGF18 induces autophagy in the chondrocyte cells of the growth plate to regulate the secretion of type II collagen, a major component of cartilaginous extracellular matrix. The FGF signaling pathways play crucial roles during skeletal development and maintenance and are deregulated in many skeletal disorders. Hence our findings may offer the unique opportunity to uncover new molecular mechanisms through which FGF pathways regulate skeletal development and maintenance and to identify new targets for the treatment of FGF-related skeletal disorders. In this grant application we propose to study the role played by the different FGF ligands and receptors on autophagy regulation and to investigate the physiological relevance of these findings in the context of skeletal growth, homeostasis and maintenance. We will also investigate the intracellular machinery that links FGF signalling pathways to the regulation of autophagy. In addition, we generated preliminary data showing an impairment of autophagy in chondrocyte models of Achondroplasia (ACH) and Thanathoporic dysplasia, two skeletal disorders caused by mutations in FGFR3. We propose to study the role of autophagy in the pathogenesis of FGFR3-related dwarfisms and explore the pharmacological modulation of autophagy as new therapeutic approach for achondroplasia. This application, which combines cell biology, mouse genetics and pharmacological approaches, has the potential to shed light on new mechanisms involved in organismal development and homeostasis, which could be targeted to treat bone and cartilage diseases.
Project acronym CARDIOEPIGEN
Project Epigenetics and microRNAs in Myocardial Function and Disease
Researcher (PI) Gianluigi Condorelli
Host Institution (HI) HUMANITAS MIRASOLE SPA
Call Details Advanced Grant (AdG), LS4, ERC-2011-ADG_20110310
Summary Heart failure (HF) is the ultimate outcome of many cardiovascular diseases. Re-expression of fetal genes in the adult heart contributes to development of HF. Two mechanisms involved in the control of gene expression are epigenetics and microRNAs (miRs). We propose a project on epigenetic and miR-mediated mechanisms leading to HF. Epigenetics refers to heritable modification of DNA and histones that does not modify the genetic code. Depending on the type of modification and on the site affected, these chemical changes up- or down-regulate transcription of specific genes. Despite it being a major player in gene regulation, epigenetics has been only partly investigated in HF. miRs are regulatory RNAs that target mRNAs for inhibition. Dysregulation of the cardiac miR signature occurs in HF. miR expression may itself be under epigenetic control, constituting a miR-epigenetic regulatory network. To our knowledge, this possibility has not been studied yet. Our specific hypothesis is that the profile of DNA/histone methylation and the cross-talk between epigenetic enzymes and miRs have fundamental roles in defining the characteristics of cells during cardiac development and that the dysregulation of these processes determines the deleterious nature of the stressed heart's gene programme. We will test this first through a genome-wide study of DNA/histone methylation to generate maps of the main methylation modifications occurring in the genome of cardiac cells treated with a pro-hypertrophy regulator and of a HF model. We will then investigate the role of epigenetic enzymes deemed important in HF, through the generation and study of knockout mice models. Finally, we will test the possible therapeutic potential of modulating epigenetic genes. We hope to further understand the pathological mechanisms leading to HF and to generate data instrumental to the development of diagnostic and therapeutic strategies for this disease.
Heart failure (HF) is the ultimate outcome of many cardiovascular diseases. Re-expression of fetal genes in the adult heart contributes to development of HF. Two mechanisms involved in the control of gene expression are epigenetics and microRNAs (miRs). We propose a project on epigenetic and miR-mediated mechanisms leading to HF. Epigenetics refers to heritable modification of DNA and histones that does not modify the genetic code. Depending on the type of modification and on the site affected, these chemical changes up- or down-regulate transcription of specific genes. Despite it being a major player in gene regulation, epigenetics has been only partly investigated in HF. miRs are regulatory RNAs that target mRNAs for inhibition. Dysregulation of the cardiac miR signature occurs in HF. miR expression may itself be under epigenetic control, constituting a miR-epigenetic regulatory network. To our knowledge, this possibility has not been studied yet. Our specific hypothesis is that the profile of DNA/histone methylation and the cross-talk between epigenetic enzymes and miRs have fundamental roles in defining the characteristics of cells during cardiac development and that the dysregulation of these processes determines the deleterious nature of the stressed heart's gene programme. We will test this first through a genome-wide study of DNA/histone methylation to generate maps of the main methylation modifications occurring in the genome of cardiac cells treated with a pro-hypertrophy regulator and of a HF model. We will then investigate the role of epigenetic enzymes deemed important in HF, through the generation and study of knockout mice models. Finally, we will test the possible therapeutic potential of modulating epigenetic genes. We hope to further understand the pathological mechanisms leading to HF and to generate data instrumental to the development of diagnostic and therapeutic strategies for this disease.
Project acronym CHILDGROWTH2CANCER
Project Childhood body size, growth and pubertal timing and the risk of cancer in adulthood
Researcher (PI) Jennifer Lyn Baker
Host Institution (HI) REGION HOVEDSTADEN
Call Details Starting Grant (StG), LS7, ERC-2011-StG_20101109
Summary The goal of the proposed research is to examine how the independent and combined effects of childhood adiposity (assessed by body mass index [BMI]; kg/m2) height, change in BMI and height, and pubertal timing from the ages of 7 to 13 years are associated with the risk of cancer incidence in adulthood. Greater body size (adipose tissue and different types of lean tissue) reflecting past or ongoing growth may increase the risk of cancer in individuals as greater numbers of proliferating cells increase the risk that mutations leading to the subsequent development of cancer occur. As childhood is a period of growth, it is plausible that it is of particular relevance for the early establishment of the risk of cancer. Data from the Copenhagen School Health Records Register, which is based on a population of schoolchildren born between 1930-1983 and contains computerised weight and height measurements on >350.000 boys and girls in the capital city of Denmark, as well as data from other cohorts will be used. Survival analysis techniques and the newly developed Dynamic Path Analysis model will be used to examine how body size (BMI and height) at each age from 7 to 13 years as well as change in body size during this period is associated with the risk of multiple forms of cancer in adulthood with a simultaneous exploration of the effects of birth weight and pubertal timing. Additionally, potential effects of childhood and adult health and social circumstances will be investigated in sub-cohorts with this information available. Results from this research will demonstrate if childhood is a critical period for the establishment of the risk for cancer in adulthood and will lead into mechanistic explorations of the associations at the biological level, investigations into associations between childhood body size and mortality and contribute to developing improved definitions of childhood overweight and obesity that are based upon long-term health outcomes.
The goal of the proposed research is to examine how the independent and combined effects of childhood adiposity (assessed by body mass index [BMI]; kg/m2) height, change in BMI and height, and pubertal timing from the ages of 7 to 13 years are associated with the risk of cancer incidence in adulthood. Greater body size (adipose tissue and different types of lean tissue) reflecting past or ongoing growth may increase the risk of cancer in individuals as greater numbers of proliferating cells increase the risk that mutations leading to the subsequent development of cancer occur. As childhood is a period of growth, it is plausible that it is of particular relevance for the early establishment of the risk of cancer. Data from the Copenhagen School Health Records Register, which is based on a population of schoolchildren born between 1930-1983 and contains computerised weight and height measurements on >350.000 boys and girls in the capital city of Denmark, as well as data from other cohorts will be used. Survival analysis techniques and the newly developed Dynamic Path Analysis model will be used to examine how body size (BMI and height) at each age from 7 to 13 years as well as change in body size during this period is associated with the risk of multiple forms of cancer in adulthood with a simultaneous exploration of the effects of birth weight and pubertal timing. Additionally, potential effects of childhood and adult health and social circumstances will be investigated in sub-cohorts with this information available. Results from this research will demonstrate if childhood is a critical period for the establishment of the risk for cancer in adulthood and will lead into mechanistic explorations of the associations at the biological level, investigations into associations between childhood body size and mortality and contribute to developing improved definitions of childhood overweight and obesity that are based upon long-term health outcomes.
Project acronym ContraNPM1AML
Project Dissecting to hit the therapeutic targets in nucleophosmin (NPM1)-mutated acute myeloid leukemia
Researcher (PI) Maria Paola MARTELLI
Host Institution (HI) UNIVERSITA DEGLI STUDI DI PERUGIA
Summary Acute myeloid leukemia (AML) is a group of hematologic malignancies which, due to their molecular and clinical heterogeneity, have been traditionally difficult to classify and treat. Recently, next-generation, whole-genome sequencing has uncovered several recurrent somatic mutations that better define the landscape of AML genomics. Despite these advances in deciphering AML molecular subsets, there have been no concurrent improvements in AML therapy which still relies on the 'antracycline+cytarabine' scheme. Hereto, only about 40-50% of adult young patients are cured whilst most of the elderly succumb to their disease. Therefore, new therapeutic approaches which would take advantage of the new discoveries are clearly needed. In the past years, we discovered and characterized nucleophosmin (NPM1) mutations as the most frequent genetic alteration (about 30%) in AML, and today NPM1-mutated AML is a new entity in the WHO classification of myeloid neoplasms. However, mechanisms of leukemogenesis and a specific therapy for this leukemia are missing. Here, I aim to unravel the complex network of molecular interactions that take place in this distinct genetic subtype, and find their vulnerabilities to identify new targets for therapy. To address this issue, I will avail of relevant pre-clinical models developed in our laboratories and propose two complementary strategies: 1) a screening-based approach, focused either on the target, by analyzing synthetic lethal interactions through CRISPR-based genome-wide interference, or on the drug, by high-throughput chemical libraries screenings; 2) a hypothesis-driven approach, based on our recent gained novel insights on the role of specific intracellular pathways/genes in NPM1-mutated AML and on pharmacological studies with 'old' drugs, which we have revisited in the specific AML genetic context. I expect our discoveries will lead to find novel therapeutic approaches and make clinical trials available to patients as soon as possible.
Acute myeloid leukemia (AML) is a group of hematologic malignancies which, due to their molecular and clinical heterogeneity, have been traditionally difficult to classify and treat. Recently, next-generation, whole-genome sequencing has uncovered several recurrent somatic mutations that better define the landscape of AML genomics. Despite these advances in deciphering AML molecular subsets, there have been no concurrent improvements in AML therapy which still relies on the 'antracycline+cytarabine' scheme. Hereto, only about 40-50% of adult young patients are cured whilst most of the elderly succumb to their disease. Therefore, new therapeutic approaches which would take advantage of the new discoveries are clearly needed. In the past years, we discovered and characterized nucleophosmin (NPM1) mutations as the most frequent genetic alteration (about 30%) in AML, and today NPM1-mutated AML is a new entity in the WHO classification of myeloid neoplasms. However, mechanisms of leukemogenesis and a specific therapy for this leukemia are missing. Here, I aim to unravel the complex network of molecular interactions that take place in this distinct genetic subtype, and find their vulnerabilities to identify new targets for therapy. To address this issue, I will avail of relevant pre-clinical models developed in our laboratories and propose two complementary strategies: 1) a screening-based approach, focused either on the target, by analyzing synthetic lethal interactions through CRISPR-based genome-wide interference, or on the drug, by high-throughput chemical libraries screenings; 2) a hypothesis-driven approach, based on our recent gained novel insights on the role of specific intracellular pathways/genes in NPM1-mutated AML and on pharmacological studies with 'old' drugs, which we have revisited in the specific AML genetic context. I expect our discoveries will lead to find novel therapeutic approaches and make clinical trials available to patients as soon as possible.
Project acronym DissectPcG
Project Dissecting the Function of Multiple Polycomb Group Complexes in Establishing Transcriptional Identity
Researcher (PI) Diego PASINI
Host Institution (HI) UNIVERSITA DEGLI STUDI DI MILANO
Summary The activities of the Polycomb group (PcG) of repressive chromatin modifiers are required to maintain correct transcriptional identity during development and differentiation. These activities are altered in a variety of tumours by gain- or loss-of-function mutations, whose mechanistic aspects still remain unclear. PcGs can be classified in two major repressive complexes (PRC1 and PRC2) with common pathways but distinct biochemical activities. PRC1 catalyses histone H2A ubiquitination of lysine 119, and PRC2 tri-methylation of histone H3 lysine 27. However, PRC1 has a more heterogeneous composition than PRC2, with six mutually exclusive PCGF subunits (PCGF1–6) essential for assembling distinct PRC1 complexes that differ in subunit composition but share the same catalytic core. While up to six different PRC1 forms can co-exist in a given cell, the molecular mechanisms regulating their activities and their relative contributions to general PRC1 function in any tissue/cell type remain largely unknown. In line with this biochemical heterogeneity, PRC1 retains broader biological functions than PRC2. Critically, however, no molecular analysis has yet been published that dissects the contribution of each PRC1 complex in regulating transcriptional identity. We will take advantage of newly developed reagents and unpublished genetic models to target each of the six Pcgf genes in either embryonic stem cells or mouse adult tissues. This will systematically dissect the contributions of the different PRC1 complexes to chromatin profiles, gene expression programs, and cellular phenotypes during stem cell self-renewal, differentiation and adult tissue homeostasis. Overall, this will elucidate some of the fundamental mechanisms underlying the establishment and maintenance of cellular identity and will allow us to further determine the molecular links between PcG deregulation and cancer development in a tissue- and/or cell type–specific manner.
The activities of the Polycomb group (PcG) of repressive chromatin modifiers are required to maintain correct transcriptional identity during development and differentiation. These activities are altered in a variety of tumours by gain- or loss-of-function mutations, whose mechanistic aspects still remain unclear. PcGs can be classified in two major repressive complexes (PRC1 and PRC2) with common pathways but distinct biochemical activities. PRC1 catalyses histone H2A ubiquitination of lysine 119, and PRC2 tri-methylation of histone H3 lysine 27. However, PRC1 has a more heterogeneous composition than PRC2, with six mutually exclusive PCGF subunits (PCGF1–6) essential for assembling distinct PRC1 complexes that differ in subunit composition but share the same catalytic core. While up to six different PRC1 forms can co-exist in a given cell, the molecular mechanisms regulating their activities and their relative contributions to general PRC1 function in any tissue/cell type remain largely unknown. In line with this biochemical heterogeneity, PRC1 retains broader biological functions than PRC2. Critically, however, no molecular analysis has yet been published that dissects the contribution of each PRC1 complex in regulating transcriptional identity. We will take advantage of newly developed reagents and unpublished genetic models to target each of the six Pcgf genes in either embryonic stem cells or mouse adult tissues. This will systematically dissect the contributions of the different PRC1 complexes to chromatin profiles, gene expression programs, and cellular phenotypes during stem cell self-renewal, differentiation and adult tissue homeostasis. Overall, this will elucidate some of the fundamental mechanisms underlying the establishment and maintenance of cellular identity and will allow us to further determine the molecular links between PcG deregulation and cancer development in a tissue- and/or cell type–specific manner.
Project acronym DNAMET
Project "DNA methylation, hydroxymethylation and cancer"
Researcher (PI) Kristian Helin
Host Institution (HI) KOBENHAVNS UNIVERSITET
Summary "DNA methylation patterns are frequently perturbed in human diseases such as imprinting disorders and cancer. In cancer increased aberrant DNA methylation is believed to work as a silencing mechanism for tumor suppressor genes such as INK4A, RB1 and MLH1. The high frequency of abnormal DNA methylation found in cancer might be due to the inactivation of a proofreading and/or fidelity system regulating the correct patterns of DNA methylation. Currently we have very limited knowledge about such mechanisms. In this research proposal, we will focus on elucidating the biological function of a novel protein family, which catalyzes the conversion of 5-methyl-cytosine (5-mC) to 5-hydroxymethyl cytosine (5-hmC). By catalyzing this reaction the TET proteins most likely work as DNA demethylases, and they might therefore have a role in regulating DNA methylation fidelity. Interestingly, accumulated data has in the last 2 years shown that TET2 is one of the most frequently mutated genes in various hematological cancers. We propose to investigate the molecular mechanisms by which TET2 regulates normal hematopoiesis, how its inactivation leads to hematopoietic malignancies and how the protein contributes to the regulation of DNA methylation patterns and transcription. Furthermore, we propose several experimental approaches for identifying proteins required for the recruitment of TET proteins to target genes and to analyze their role in the regulation of DNA methylation patterns and in cancer. Finally, we will investigate the potential functional role of 5-hmC and explore the potential mechanisms by which this modification could be erased. We expect to provide new insights into the biology of DNA methylation, hydroxymethylation and contribute to unravel the roles of TET proteins in normal physiology and cancer."
"DNA methylation patterns are frequently perturbed in human diseases such as imprinting disorders and cancer. In cancer increased aberrant DNA methylation is believed to work as a silencing mechanism for tumor suppressor genes such as INK4A, RB1 and MLH1. The high frequency of abnormal DNA methylation found in cancer might be due to the inactivation of a proofreading and/or fidelity system regulating the correct patterns of DNA methylation. Currently we have very limited knowledge about such mechanisms. In this research proposal, we will focus on elucidating the biological function of a novel protein family, which catalyzes the conversion of 5-methyl-cytosine (5-mC) to 5-hydroxymethyl cytosine (5-hmC). By catalyzing this reaction the TET proteins most likely work as DNA demethylases, and they might therefore have a role in regulating DNA methylation fidelity. Interestingly, accumulated data has in the last 2 years shown that TET2 is one of the most frequently mutated genes in various hematological cancers. We propose to investigate the molecular mechanisms by which TET2 regulates normal hematopoiesis, how its inactivation leads to hematopoietic malignancies and how the protein contributes to the regulation of DNA methylation patterns and transcription. Furthermore, we propose several experimental approaches for identifying proteins required for the recruitment of TET proteins to target genes and to analyze their role in the regulation of DNA methylation patterns and in cancer. Finally, we will investigate the potential functional role of 5-hmC and explore the potential mechanisms by which this modification could be erased. We expect to provide new insights into the biology of DNA methylation, hydroxymethylation and contribute to unravel the roles of TET proteins in normal physiology and cancer."
Project acronym ENVNANO
Project Environmental Effects and Risk Evaluation of Engineered Nanoparticles
Researcher (PI) Anders Baun
Host Institution (HI) DANMARKS TEKNISKE UNIVERSITET
Summary The objective of the project Environmental Effects and Risk Evaluation of Engineered Nanoparticles (EnvNano) is to elucidate the particle specific properties that govern the ecotoxicological effects of engineered nanoparticles and in this way shift the paradigm for environmental risk assessment of nanomaterials. While current activities in the emerging field of nano-ecotoxicology and environmental risk assessment of nanomaterials are based on the assumption that the methodologies developed for chemicals can be adapted to be applicable for nanomaterials, EnvNano has a completely different starting point: The behaviour of nanoparticles in suspension is fundamentally different from that of chemicals in on solution. Therefore, all modifications of existing techniques that do not take this fact into account are bound to have a limited sphere of application or in the worst case to be invalid. By replacing the assumption of dissolved chemicals with a particle behaviour assumption, the traditional risk assessment paradigm will be so seriously impaired that a shift of paradigm will be needed. EnvNano is based on the following hypotheses: 1. The ecotoxicity and bioaccumulation of engineered nanoparticles will be a function of specific physical and chemical characteristics of the nanoparticles; 2. The environmental hazards of engineered nanoparticles cannot be derived from hazard identifications of the material in other forms; 3. Existing regulatory risk assessment procedures for chemicals will not be appropriate to assess the behaviour and potential harmful effects of engineered nanoparticles on the environment. These research hypotheses will be addressed in the four interacting research topics of EnvNano: Particle Characterization, Ecotoxicty, Bioaccumulation, and Framework for Risk Evaluation of Nanoparticles aimed to form the foundation for a movement from coefficient-based to kinetic-based environmental nanotoxicology and risk assessment.
The objective of the project Environmental Effects and Risk Evaluation of Engineered Nanoparticles (EnvNano) is to elucidate the particle specific properties that govern the ecotoxicological effects of engineered nanoparticles and in this way shift the paradigm for environmental risk assessment of nanomaterials. While current activities in the emerging field of nano-ecotoxicology and environmental risk assessment of nanomaterials are based on the assumption that the methodologies developed for chemicals can be adapted to be applicable for nanomaterials, EnvNano has a completely different starting point: The behaviour of nanoparticles in suspension is fundamentally different from that of chemicals in on solution. Therefore, all modifications of existing techniques that do not take this fact into account are bound to have a limited sphere of application or in the worst case to be invalid. By replacing the assumption of dissolved chemicals with a particle behaviour assumption, the traditional risk assessment paradigm will be so seriously impaired that a shift of paradigm will be needed. EnvNano is based on the following hypotheses: 1. The ecotoxicity and bioaccumulation of engineered nanoparticles will be a function of specific physical and chemical characteristics of the nanoparticles; 2. The environmental hazards of engineered nanoparticles cannot be derived from hazard identifications of the material in other forms; 3. Existing regulatory risk assessment procedures for chemicals will not be appropriate to assess the behaviour and potential harmful effects of engineered nanoparticles on the environment. These research hypotheses will be addressed in the four interacting research topics of EnvNano: Particle Characterization, Ecotoxicty, Bioaccumulation, and Framework for Risk Evaluation of Nanoparticles aimed to form the foundation for a movement from coefficient-based to kinetic-based environmental nanotoxicology and risk assessment.
Project acronym ERMITO
Project Molecular Anatomy and Pathophysiology of the endoplasmic reticulum-mitochondria interface
Researcher (PI) Luca Scorrano
Host Institution (HI) UNIVERSITA DEGLI STUDI DI PADOVA
Summary Organelles are not randomly organized in the cytoplasm of the cell, but often are orderly arranged in mutual relationships that depend on physical, protein bounds. Understanding the molecular nature of the tethers that regulate relative position and juxtaposition of the organelles is one of the main quests of cell biology, given their functional importance. For example, the juxtaposition between mitochondria and endoplasmic reticulum (ER) has been suggested by us and others to crucially impact on Ca2+ signalling and apoptosis. We recently identified the first structural ER-mitochondrial tether in mitofusin 2 (Mfn2), a pro-fusion mitochondria-shaping protein. A fraction of Mfn2 is also located on the ER regulating its morphology, and acting in trans to tether it to mitochondria. The tethering function of Mfn2 impacts on the transmission of Ca2+ signals between the two organelles and is regulated by the oncosuppressor trichoplein/mitostatin. Mfn2 is likely only one of the tethers, as others exist in yeast. Furthermore, the dynamicity of the ER-mitochondria contact is known, but remains poorly understood. Therefore, a clear picture of the anatomy and pathophsyiology of ER-mitochondrial connection is far from being reached. Here we hypothesize that ER-mitochondrial contacts are crucial specialized hubs of cellular signalling whose architecture is modulated by cellular cues, impacting on integrated signalling cascades and ultimately affecting cellular function. To address this hypothesis we wish to setup a research project that aims at (i) increasing our knowledge on the molecular nature of tethers and modulators of ER-mitochondrial tethers in mammalian cells; (ii) clarifying how mitochondrial and ER function are controlled by the tethering; (iii) addressing how juxtaposition influences complex cellular responses including autophagy and cell death; (iv) elucidating the role of tethering in vivo by generating animal models with defined ER-mitochondrial distance.
Organelles are not randomly organized in the cytoplasm of the cell, but often are orderly arranged in mutual relationships that depend on physical, protein bounds. Understanding the molecular nature of the tethers that regulate relative position and juxtaposition of the organelles is one of the main quests of cell biology, given their functional importance. For example, the juxtaposition between mitochondria and endoplasmic reticulum (ER) has been suggested by us and others to crucially impact on Ca2+ signalling and apoptosis. We recently identified the first structural ER-mitochondrial tether in mitofusin 2 (Mfn2), a pro-fusion mitochondria-shaping protein. A fraction of Mfn2 is also located on the ER regulating its morphology, and acting in trans to tether it to mitochondria. The tethering function of Mfn2 impacts on the transmission of Ca2+ signals between the two organelles and is regulated by the oncosuppressor trichoplein/mitostatin. Mfn2 is likely only one of the tethers, as others exist in yeast. Furthermore, the dynamicity of the ER-mitochondria contact is known, but remains poorly understood. Therefore, a clear picture of the anatomy and pathophsyiology of ER-mitochondrial connection is far from being reached. Here we hypothesize that ER-mitochondrial contacts are crucial specialized hubs of cellular signalling whose architecture is modulated by cellular cues, impacting on integrated signalling cascades and ultimately affecting cellular function. To address this hypothesis we wish to setup a research project that aims at (i) increasing our knowledge on the molecular nature of tethers and modulators of ER-mitochondrial tethers in mammalian cells; (ii) clarifying how mitochondrial and ER function are controlled by the tethering; (iii) addressing how juxtaposition influences complex cellular responses including autophagy and cell death; (iv) elucidating the role of tethering in vivo by generating animal models with defined ER-mitochondrial distance.
Project acronym FAST
Project Investigating new therapeutic approaches to Friedreich's Ataxia
Researcher (PI) Roberto Testi
Host Institution (HI) UNIVERSITA DEGLI STUDI DI ROMA TOR VERGATA
Summary Friedreich's Ataxia (FRDA) is a devastating degenerative disease with no specific therapy. It is passed by autosomal recessive inheritance and affects 1:30,000 individuals in Caucasian populations. Symptoms appear in the first decade of life and include progressive and unremitting lack of movement coordination, leading to complete inability, and dilated cardiomyopathy leading to congestive heart failure, the most common cause of premature death. FRDA is due to the insufficient transcription of the gene coding for the mitochondrial protein frataxin. Reduced cellular levels of frataxin cause impaired mitochondrial function and increased sensitivity to oxidative stress, leading to accelerated cell death in critical tissues. Severity of the disease critically depends on residual frataxin levels. Therapeutic efforts are mostly focused on increasing cellular frataxin . We found that frataxin is normally degraded by the ubiquitin-proteasome system. We identified the lysine responsible for the ubiquitination of frataxin and, by computational screening followed by experimental validation, we identified and validated a series of small molecules, called ubiquitin-competing molecules (UCM), that prevent frataxin ubiquitination and induce frataxin accumulation in cells derived from FRDA patients. Moreover, treatment with UCM partially rescues aconitase and ATP production defects in cells derived from FRDA patients. Our goal is two fold: 1) submit a set of leads we already identified, as well as their new and more complex derivatives, to preclinical testing in FRDA mice 2) identify the E3 ligase that is responsible for frataxin ubiquitination, and investigate the possibility to use it as a druggable target for small molecules to prevent frataxin degradation.
Friedreich's Ataxia (FRDA) is a devastating degenerative disease with no specific therapy. It is passed by autosomal recessive inheritance and affects 1:30,000 individuals in Caucasian populations. Symptoms appear in the first decade of life and include progressive and unremitting lack of movement coordination, leading to complete inability, and dilated cardiomyopathy leading to congestive heart failure, the most common cause of premature death. FRDA is due to the insufficient transcription of the gene coding for the mitochondrial protein frataxin. Reduced cellular levels of frataxin cause impaired mitochondrial function and increased sensitivity to oxidative stress, leading to accelerated cell death in critical tissues. Severity of the disease critically depends on residual frataxin levels. Therapeutic efforts are mostly focused on increasing cellular frataxin . We found that frataxin is normally degraded by the ubiquitin-proteasome system. We identified the lysine responsible for the ubiquitination of frataxin and, by computational screening followed by experimental validation, we identified and validated a series of small molecules, called ubiquitin-competing molecules (UCM), that prevent frataxin ubiquitination and induce frataxin accumulation in cells derived from FRDA patients. Moreover, treatment with UCM partially rescues aconitase and ATP production defects in cells derived from FRDA patients. Our goal is two fold: 1) submit a set of leads we already identified, as well as their new and more complex derivatives, to preclinical testing in FRDA mice 2) identify the E3 ligase that is responsible for frataxin ubiquitination, and investigate the possibility to use it as a druggable target for small molecules to prevent frataxin degradation.


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GHOST's TOBIAS FORGE Opens Up On Lawsuit Filed Against Him From Ex-Band Members
September 26, 2019 October 14, 2019 Reeder
In an interview with Colorado Springs Independent, GHOST mastermind Tobias Forge spoke about the lawsuit filed against him by four former members of the band.
When asked if he thinks his former bandmates would have been less vindictive if he had given names to his Nameless Ghouls, Forge responded: "You mean, if I'd given them names instead of making them completely anonymous? Probably, I guess. It's hard to say. Because with most people that are drawn to the performance stage, you do so with a certain inclination to be seen and appreciated.
"So maybe if our positions were reversed, I would have felt the same way. Until seven or eight years ago, I really wanted to be famous, so my idea of being in a band was definitely different from what it turned out to be.
"I've been in charge and working on this full-time, nonstop, for 10 years," he continued. "Other people in GHOST would work a few hours every day, and then, during the four months between tours when I was making a record, they weren't really doing anything that had to do with GHOST.
"And since I was representing the band at all of the meetings, I was getting pats on the back and feeling like what I was doing was good. Whereas, if you had nothing to do with the day-to-day stuff, you maybe didn't get the pat on the back that you needed in order to feel fulfilled in life.
"So, you know, maybe if they had gotten their name on there, and could at least be recognized in the street, maybe that would have changed things. But on the other hand, I've played with others who didn't give a sh*t about that happening."
Forge, who founded the group eight years ago, was sued by the four ex-members in April 2017. Forge was sued by ex-members in April 2017 who accused the singer of cheating them out of their rightful share of the profits from the band's album releases and world tours.
The musicians have since appealed the ruling, and the case has now been referred to the Göta court of appeal in Jönköping, where it will be heard in March 2020.
The lawsuit, which was filed in the district court of Linköping, where GHOST was originally based, claimed that a partnership agreement existed between Forge and the four former members, all of whom performed anonymously in the band as Nameless Ghouls.
Forge said that "no legal partnership" ever existed between him and the other members and that they were paid a fixed salary to perform as his backing band.
The trial in Linköping District Court lasted for six days, and at 11 a.m. on October 17, a 108-page decision was released dismissing the case. The four former GHOST members were also ordered to pay Forge's legal fees.
Forge claimed more than two million kronor (approximately $225,000) in legal costs, but the district court was of the opinion that 1.3 million kronor ($146,000) was more reasonable.
ghost tobias forge
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Blake Fry named MCC's executive director of communication and marketing
Lisa KalellNovember 5, 2019
Dr. Blake Fry
Blake Fry, Ed.D., has been named Metropolitan Community College's new executive director of district communication and marketing. The MCC Board of Trustees approved his appointment Oct. 25.
Fry most recently served as president of the Lee's Summit Chamber of Commerce, where he led the development of a new strategic plan and the renewal of the organization's five-star accreditation from the U.S. Chamber of Commerce. Fry had previously served as president of the Hudson Area Chamber of Commerce and Tourism Bureau in Wisconsin.
With more than 20 years of higher education experience, Fry has served in a variety of roles, including director of communications and external relations and special assistant to the chancellor at the University of Wisconsin-River Falls. As the senior communications officer, he led marketing, media and government relations, and community engagement. Fry also has experience in student affairs at the University of Central Oklahoma and Avila University.
Fry has served on and chaired the boards for several national and regional professional, economic development and civic organizations. In 2013 he received the Distinguished Service Award from the National Association of Presidential Assistants in Higher Education.
He earned his doctorate of education in higher education from Oklahoma State University in 2008. Fry's research focused on the interrelationship between co-curricular leadership experiences and cognitive development.
He also holds a bachelor's degree in political science from Wichita State University and master's degrees from Avila University and the University of Missouri-Kansas City.
Tags: Blake Fry


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Pediatricians issue new guidelines for depression screening for teens
By Melanie Dadourian | Fox News
The American Academy of Pediatrics issued new guidelines that recommend yearly depression screening for all teenagers between the ages of 12 and 21. The report cites that about 50 percent of adolescents with depression are diagnosed before reaching adulthood and as many as 2 in 3 depressed teens don't get any help or care.
"It's a huge problem," Dr. Rachel Zuckerbrot, who helped write the guidelines, told NPR.
The psychiatrist and associate professor at Columbia University further explained the new guidelines were created to help primary care clinicians "in the identification and initial management of adolescents with depression in an era of great clinical need and shortage of mental health specialists."
SEASONAL AFFECTIVE DISORDER IN KIDS
According to the Centers for Disease Control and Prevention, depression can lead to suicide, which is the second-leading cause of death for children aged 10 to 24, behind unintentional injury.
These guidelines were developed for primary care doctors who may be in a position to help teenagers who show signs of depression in their practice settings.
Zuckerbrot said pediatricians are encouraged to perform the depression screenings during regular visits, sports physicals or other office visits.
Zuckerbrot added, "It's an opportunity for the adolescent to answer questions about themselves privately."
'BIG BROTHER' CONTESTANT'S DAUGHTER DEAD IN APPARENT SUICIDE AMID RECENT STRING OF TEEN DEATHS IN OHIO TOWN
The report by the American Academy of Pediatrics (AAP) said, "Each of these ordinary developmental stages and experiences put young people at a greater risk for impulsive and sometimes violent action, particularly for adolescents with a history of aggressive and violent behaviors, suicide attempts or depression."
The AAP urged parents with depressed teens to keep away from firearms, saying "adolescent suicide risk is strongly associated with firearm availability."


Our First Annual Chili Cook Off was a success!
After tabulating all the votes for the wide range of chilis (that were anonymously numbered so no cheating!) the winner was our very own June Stevens- chef and baker extraordinaire!
Her white chicken chili won her the coveted Chili Cook Off Spoon. She has generously shared her recipe if you want to make it at home.
Saute the chicken breast in a little oil and butter. I season my chicken with a mixture called Sweet Heat Chipotle Magic, which I got at a craft fair. It's from Hot Squeeze, an Atlanta Company.
Heat the oil and butter in a large saucepan over medium-heat. Slowly cook and stir the onion until tender.
Mix in garlic, jalepeno, green chile peppers, cumin, oregano, and cayenne. Continue to cook and stir the mixture until tender, about 3 minutes. Mix in the chicken broth, chicken and white beans. Simmer, stirring occasionally for 20-30 minutes. Stir in cheese until melted. Serve warm.