text:
nafiche 123
How Does the Executive Email List
Marketing is an area of knowledge that every designer needs to have more or less. In addition to throwing out specific business goals and strategic design, there executive email list are many ways to play in the interactive form of operational activities: one-shot, sensory recognition, 360-degree panorama, simulation effects, etc. Therefore, Laohe has organized some interesting executive email list activities and expressions, and described them in combination with [features + scenes]. Help everyone match the appropriate creative gameplay when doing operational activities.
How does the operation work? These 7 creative interactions give you the answer 1. Sensory recognition Use the senses of the human body (finger, mouth, etc.) to executive email list start the activity. After the system recognizes the user's sensory instructions, the next activity process can be triggered. Such as: fingerprint entry. For example, Jeep's White Day event requires users to enter fingerprints to select the theme of the event, and enter fingerprints in executive email list the event to complete the agreement, which has a sense of Valentine's Day ritual. How does the operation work? These 7 creative interactions give you the answer Voice input: For example, Tencent Philanthropy's
English Translator requires users to read a paragraph of English during the activity to understand the triggers and difficulties of poor children in learning, executive email list so as to initiate donation activities. How does the operation work? These 7 creative interactions give you the answer Blowing air: Another example is Xiaomi's challenge "blowing" strength executive email list activity, which needs to be used to blow air into the [mobile phone microphone], and the fan on the page will rotate according to the size of the air. Very interesting and very test of lung capacity. How does the operation work.
hjkk
We have reached the time of year where the winter coats have come out, the holiday treats are on the kitchen counter, and the poinsettias are all the rage. As the most wonderful time of the year is upon us, that also means that various teams in the NFL are in a position to clinch playoff spots whether as a wildcard or by way of securing a division title. It has felt like a foregone conclusion for a while that the Dallas Cowboys would be winning the NFC East in 2021, and while they gave us a bit of a scare in November, the waters have stabilized and it seems that hats and t-shirts are but a moment away. Since the team won in Washington there has been some confusion as to when exactly that moment would arrive. Originally it appeared as if the Cowboys only needed to defeat the New York Giants and pick up a Washington loss in Week 15 in order to wrap up the NFC East, but early discussions around the football cognoscenti suggested that this might not be the case and that a few other things would be necessary Leighton Vander Esch Jersey. The NFL releases playoff-clinching scenarios later in the week, but on Wednesday their own television network was discussing the Cowboys and put scenarios on the screen. According to NFL Network the Cowboys can lock up the division with a win and Washington loss OR tie this week. Courtesy of NFL Network. Again, this runs counter to what many people have been saying all week long as the general assumption has been that a larger number of dominoes have to fall in the right direction for the Cowboys to win the NFC East, but NFL Network clearly feels confident that this is not the case. Where the roadblock has seemed to be for people is that wins from Dallas and Washington would put the Cowboys at 10-4 with a perfect 4-0 record in the division, but the Eagles would be 7-7 with a 1-2 record in it Devin Harper Jersey. Theoretically there then could be a world where Dallas and Philadelphia both finished the season 10-7 with a 4-2 record in division which is why it didn't seem like Dallas could lock things up this week with these two things alone and that some strength-of-schedule pieces might need to fall into place as well. To state the obvious, the simpler that things are the better, but above all the Cowboys need to make sure that they continue to win their games and do their part. Let's hope that continues on Sunday afternoon. Update: 3:00pm ETAs fate would have it the NFL did release the playoff-clinching scenarios for Week 15 shortly after this post originally went out. Washington losing to Philadelphia would in fact help the Cowboys' odds of winning the division this week, but they would also need to have every strength-of-victory tiebreaker over Philadelphia. Ultimately we are rooting for the Cowboys primarily and the Eagles as a secondary thing https://www.prodallasstore.com/Ben_Dinucci_Jersey-68. And while the Cowboys can clinch a playoff berth with a New Orleans loss it should be noted that the Saints are visiting the Tampa Bay Buccaneers this week and our hope remains that Dallas can surpass Tampa in the overall NFC hierarchy which means we need a Saints win. It's about the long game.
https://www.prodallasstore.com/Demarcus_Lawrence_Jersey-38
https://www.prodallasstore.com/Tyron_Smith_Jersey-31
How Do New Qatar Phone Number List
Reduce Content Executive Email List Production
Building A Data Indicator Category Email List


Why I Decided to Be the First Openly Transgender Woman to Compete in Miss Montana USA The platform let me share a very important message.
10 Transgender People Share What They Wish They Knew Before Transitioning"It's the best thing I ever did for myself."
I Transitioned While Working for the Army, and I Wasn't a DisruptionTrans people in uniform aren't burdens.
Your Well-Intentioned 'I Don't See Gender' Comment Makes Me Feel InvisibleI want you to see—and accept—me.
What Transgender Women Need to Know About Their Risk of Prostate CancerYour risk may be related to your transition.
This Transgender Woman Documented Her Transition Through Emotional IllustrationsShe captured her experiences in a series of comics.
Mack Beggs, a Transgender Boy, Just Won a Girls' Wrestling Championship in TexasBeggs should be allowed to compete with fellow boys.
Donald Trump's Administration Just Reversed Key Transgender Bathroom Guidelines This can have a drastic impact on trans students.


text:
» Fr. Clint Farabaugh – Archdiocese of Los Angeles
Fr. Clint Farabaugh – Archdiocese of Los Angeles
On Behalf of Horowitz Law | Sep 1, 2020 | Abuser Profiles
Father Clint Farabaugh (Precious Blood)
Archdiocese of Los Angeles
1956-1969: Unknown
1970-1990: St. Agnes Catholic Church, Los Angeles, CA
Summary of Abuse Allegations against Father Clint Farabaugh:
Father Clint Farabaugh was ordained a religious order priest of the Society of the Precious Blood in 1955, who served in multiple parishes in the Archdiocese of Los Angeles. According to media reports, he was accused of child sexual abuse from 1973 to 1976 at St. Agnes Catholic Church in Los Angeles. He died in 1990.
In 2004, his name appeared on the Archdiocese of Los Angeles' report of clergy credibly accused of sex abuse of minors.
The Archdiocese of Los Angeles released Father Farabaugh's and other personnel files of clergy who were subject of the 2007 global settlement.
Horowitz Law is a law firm representing victims and survivors of sexual abuse by Catholic priests and other clergy in the Archdiocese of Los Angeles. If you need a lawyer because you were sexually abused by a priest or other Catholic clergy in California State, contact our office today. Although many years have passed, those abused by Catholic clergy in the Archdiocese of Los Angeles now have legal options, but filing deadlines will apply so do not delay in reaching out to us. Our lawyers have decades of experience representing survivors of clergy sexual abuse in Los Angeles and nationwide. We can help.

redpajama_set_name: RedPajamaCommonCrawl


Are you screening all your volunteers? If not, you could be compromising the safety of your church staff, your other volunteers, and the people your ministry serves. Even in small ministries where everyone knows everyone, or where other safety nets have been put in place, screening is an important step.
In their whitepaper, To Screen or Not to Screen?, Verified Volunteers outlines 4 key misconceptions about background screening. These 4 misconceptions lead ministries to mistakenly avoid screening some or all volunteers and staff. Unfortunately, as also explained in the whitepaper, this can be a costly mistake.
When you read the whitepaper, you'll discover whether or not your ministry is avoiding volunteer screening because of one of the 4 misconceptions, and how to respond.
Ministries should not feel immune to attracting a volunteer that may not have the right heart or motives. In fact, a person with ill-intent (to steal, or to work with a vulnerable population, etc.) may volunteer at your church expecting that a ministry will trust everyone.
By making it your ministry policy to screen everyone, and by making that policy clear and prominent on your website or volunteer communications, you'll send a strong message to anyone who may have ill-intent, and may discourage them from applying in the first place. Plus, sharing this policy will instill more trust in your ministry among other members and visitors.
Additionally, by making it a policy to screen all your volunteers, you don't have to single out the person who joins your ministry that nobody knows that well yet. You also don't run the risk of letting someone fall through the cracks just because they are well-known, or perhaps are related to someone who is well known in your ministry.
Background screening does not replace the need for discernment; instead it's a tool you can use in your process of discerning. Sometimes you may discern someone is not right for a particular role in your ministry before you even consider background screening them. Other times, you may do a routine background screen, only to discover there is something in a volunteer's history that will require you to discern if it will affect his ability to serve in a particular role.
Read the whitepaper to learn more about the need for background screening.
To get started today, contact Servant Keeper here. Or click here to learn more about Verified Volunteers.
Get Started Now. Sign Up From Within Your Servant Keeper Version 8!
Did you know, you can sign up for Verified Volunteers right from your Servant Keeper Version 8?
Step 2: Select Integrate with Verified Volunteers.
Step 3: Select Sign Up for Verified Volunteers.


There's a gluten-free explosion days, but how much of it is real and how much of it is hype? Ellie demystifies the gluten issue once and for all with the help of her stepbrother and yoga instructor David Wilder, who has celiac disease. In this episode, Ellie also underscores just how many foods are naturally gluten-free, with recipes that will satisfy everyone.


text:
Home > Programmes > MSc Investment & Wealth Management > Our Community > Faculty Profiles
World-class finance faculty
School faculty members are specialists in their field. They have international research reputations, consult for global corporations, advise government and international agencies, sit on the boards of mature companies as well as new ventures, and are frequently asked by the media for academic insight on a wide variety of topics.
Imperial College Business School has a tradition of research excellence in quantitative finance. Our faculty has international research reputations, consult for global corporations and advise financial firms.
James Sefton
Academic Programme Director MSc Investment & Wealth Management and MSc Finance & Accounting, Chair in Economics and Professor of Economics
Professor Sefton works both in academia and industry; he is a Professor of Economics at Imperial, and a Senior Quantitative Analyst at UBS Investment Bank. As an academic, he participates in the current UK pension debate, as a financial analyst he specialises in understanding asset pricing anomalies and equity investment strategies. James qualified first as an Information Engineer, before studying for a PhD in systems theory at Cambridge University. His career as an economist began at the Department of Applied Economics, Cambridge University, and then at the National Institute for Economic and Social Research. He has published widely in areas as varied as computable general equilibrium modelling, national accounting, portfolio management and econometrics. In 2001 he was appointed to a Chair of Economics at Imperial College and became an Executive Director at UBS.
Read Professor Sefton's profile
Emiliano Pagnotta
Assistant Professor of Finance
Dr Pagnotta's research interests lie at the intersection of market microstructure, asset pricing, and the industrial organisation of financial markets. His recent studies examine the effects of speed and trading fragmentation on asset prices and social welfare; the effect of central clearing reforms on prices and liquidity; the transmission of information in financial markets; and the consequences of new regulations on market quality and performance. Dr Pagnotta holds a BA in Economics from the University of Buenos Aires, an MA in Economics from Universidad de San Andrés, Argentina, and his PhD from the Economics Department at Northwestern University.
Read Dr Pagnotta's profile
Lara Cathcart
Academic Programme Director MSc Finance and MSc Risk Management & Financial Engineering, and Associate Professor of Finance
Professor Cathcart holds a Master's degree and PhD in Finance from Birkbeck College, University of London. She specialises in the study of credit risk, derivative pricing and fixed income products. Her work has appeared in finance journals such as Journal of Money Credit and Banking, Journal of Banking and Finance, and Quantitative Finance and in practitioner publications such as Risk and Professional Investor. Professor Cathcart is also an associate editor for the European Journal of Finance, and has consulted for several investment banks and HM Treasury.
Read an interview with Dr Lara Cathcart about MSc Finance.
Read Professor Cathcart's profile
Walter Distaso
Professor of Financial Econometrics
Professor Distaso holds a PhD from the University of York. His research interests are in the area of estimation, specification testing and prediction of financial volatility in continuous time models; analysing macroeconomic and financial time series using long memory models; identifying the macroeconomic determinants of stock-market volatility; studying the dependence of multivariate financial time series using copulas; evaluating competing trading strategies; and analysing the features and the effects of market microstructure noise.
Read Professor Distaso's profile
Professor of Financial Economics
Professor Miles is an Economic Advisor to the Bank of England and to the UK Debt Management Office. Between May 2009 and September 2015 Professor Miles was a member of the Monetary Policy Committee at the Bank of England. His experience also includes roles as Chief UK Economist and Managing Director at Morgan Stanley, Board member and Non Executive Director at The Financial Services Authority, London, and Chief UK Economist at Merrill Lynch, London. His current research focuses on policy issues connected with financial stability, the housing market and the setting of monetary policy. He is involved with the co-ordination between monetary policy and financial stability. One strand of research which reflects this is on the use of macro-prudential policy tools and, specifically, the setting of bank capital requirements. Future work will focus on how liquidity requirements and the setting of monetary policy interacts with capital requirements.
Read Professor Miles' profile
Cláudia Custódio
Associate Professor of Finance
Since completing her PhD at the London School of Economics, Dr Custódio spent time working at the W. P. Carey School of Business, Arizona State University, and NOVA School of Business and Economics. Dr Custódio is a research associate of the Centre for Economic Policy Research (CEPR), the European Corporate Governance Institute (ECGI), and the Financial Markets Group (FMG). Her focus is Corporate Finance and her work has been published several times in academic journals such as the Journal of Finance, the Journal of Financial Economics and the Review of Financial Studies.
Read Dr Custódio's profile
Katrin Tinn
Dr Tinn holds a BSc in Economics from Tallinn Technical University, a BA in Art from Estonian Academy of Art, a MSc in Economics from University College London and a PhD in Economics from London School of Economics. Her research focuses on applied theory and her research interests include financial economics, rational expectations, economic growth, technological innovation, information imperfections in financial markets, the relationship between equity markets and aggregate economy, trading incentives of financial institutions, asset market anomalies, international finance and trade, and the role of imperfect information in elections. Her research has been published in the American Economic Review, the top peer-reviewed journal in Economics.
Read Dr Tinn's profile
Andrea Buraschi
Chair in Finance
Professor Buraschi's research interests are in the fields of Financial Economics, Asset Pricing and Derivatives, and Financial Econometrics. He earned his PhD from The University of Chicago specialising in Financial Economics and Econometrics. Professor Buraschi's work has been published in journals including The Journal of Finance, The Journal of Financial Economics, Review of Financial Studies, Journal of Derivatives, European Financial Management and The Journal of Banking and Finance.
Read Professor Buraschi's profile
Department of Finance faculty
Further information about the Department of Finance's faculty and their research areas is available on the Department's webpages.
CFA University Affiliation Program
Compare our Finance Master's programmes
Self-assessment Maths test
Women in Finance


text:
Q: Displaced ViewTransition not triggered in QML So I have a ListView and ListModel to which I'm adding objects dynamically. I want a displaced animation to happen to when a new object is added, but from what I can see, only the add transition is triggered and the displaced transition is never triggered. Based on the tutorial, this works:
  Rectangle {
        anchors.fill: parent
        ListView {
          width: 240; height: 320
          model: ListModel {
              id: model
          }

          Component {
              id: del
              Row {
                  height: 20
                  spacing: 20
                  Text { text: name }
                  Text { text: age }
              }
          }

          delegate: del

          add: Transition {
              NumberAnimation { property: "opacity"; from: 0; to: 1.0; duration: 1000 }
          }

          displaced: Transition {
              NumberAnimation { properties: "x,y"; duration: 1000; easing.type: Easing.OutBounce }
          }

          focus: true
          Keys.onSpacePressed: model.insert(0, { "name": "Item " + model.count, "age":21})
        }
    }

But this only triggers the add transition.
        Rectangle {
            height: 500
            width: 0.90 * parent.width
            anchors {
                top: parent
                topMargin: 30
                left: parent.left
                leftMargin: 45
            }
            ListView {
                anchors.fill: parent
                model: notificationModel
                delegate: notificationDelegate
                spacing: 30

                add: Transition {
                    NumberAnimation { property: "opacity"; from: 0; to: 1; duration: 1000 }
                }
                displaced: Transition {
                    NumberAnimation { properties: "x,y"; duration: 1000; easing.type: Easing.OutBounce }
                }
            }
        }

        ListModel {
            id: notificationModel
            Component.onCompleted: {
                    notificationModel.append({"name": "Tony"})
                }
        }

        Timer {
            interval: 5000; running: true; repeat: true
            onTriggered: notificationModel.append({"name": "Stark"})
        }

        Component {
            id: notificationDelegate
            Row {
                spacing: 20
                Text { text: name; color: "white" }
            }
        }

Any idea why this happens? Thanks!

A: The displaced transition is triggered when an item in the list is forced to move because another item is added/removed/etc. The working example works because a single item gets inserted at the beginning of the list causing the remaining items to be displaced.
With the current code you are showing, the problem is that you are using the append function instead of insert. Append adds items to the bottom of the list, so no items are getting displaced.
Before you edited your question, you had a different problem. You were using insert to add items to the beginning of the list, but every time you added one, you were clearing the entire list and rebuilding it. So again, nothing was getting displaced because the entire list was getting recreated every time.

redpajama_set_name: RedPajamaStackExchange


Eat a Cranberry Day takes place on November 23, 2019. The fruit of cranberries is a berry that is larger than the leaves of the plant; it is initially white, but turns a deep red when fully ripe. It is edible, with an acidic taste that can overwhelm its sweetness.
Cranberries are a major commercial crop in certain American states and Canadian provinces. Most cranberries are processed into products such as juice, sauce, jam, and sweetened dried cranberries, with the remainder sold fresh to consumers. Cranberry sauce is regarded as an indispensable part of traditional American and Canadian Thanksgiving menus and some European winter festivals.


Swimming, watching/collecting movies, reading books, playing mini golf, playing Wii, and being with his family.
The dentist, thunder and other loud noises.
If you would like to nominate someone as a #FriendofFRAXA, simply email a photo accompanied with age, location, and a few of his or hers interests and challenges to brianne@fraxa.org.
We welcome all who have been touched by Fragile X, including friends, grandparents, siblings, professionals and companions alike.


text:
HomePreviewsMonster Hunter World to have Milla Jovovich movie event for some reason
Monster Hunter World to have Milla Jovovich movie event for some reason
November 26, 2020 admin Previews 0
Good news fans of Milla Jovovich! For what appears to be no reason in particular, a digital character bearing her voice and likeness is getting two events added to Monster Hunter World. I'm not sure why they'd pick her, considering how she starred in a series of awful films based on Capcom's Resident Evil movies, but they must really like her. It's certainly that and not the fact that she's married to the guy that made all that garbage. It's almost as if they're advertising something else. Some kind of new Milla Jovovich movie related to Monster Hunter. Let me do a quick Google search. Oh, a trailer! What is this?
I should not have watched the trailer. The event in Monster Hunter World, known as the Artemis "Monster Hunter" Movie Quest, is billed as a special collaboration. I like how they put Monster Hunter in quotes there since that's an apt way to describe whatever the upcoming movie is supposed to be. This crossover contains two single-player quests where players can control Artemis as she shoots a Black Diablos in the face with some kind of stupid rocket launcher or something.
Related Article: Yoshi's Woolly World (Wii U) Review
Both parts of the quest will be available for an entire year and can be undertaken starting December 3 at 4 PM PST. The first part sees Artemis hunting the aforementioned Black Diablos, while the second puts her up against a Rathalos. The former will reward players with an armor set while the latter has a layered armor set. This will be perfect for the people that want to parade Milla Jovovich around during online Monster Hunter World hunts for the purpose of hatefully reminding fans that the movie does, in fact, exist. Anyway, the movie is going to come out and almost everyone is going to hate it because it was written and directed by Paul W.S. Anderson. I am not going to watch it and you can't make me.
Continue Reading >>> Source link
Jovovich
Secret Wars TPB to serve as 'primer' to lead fans into the big event series
The Flash Monster S3E5 (TV) Review
Turok: Dinosaur Hunter (N64) Retro Review


Gibbons was the representative for Florida's 11th congressional district and was a Democrat. He served from 1993 to 1996.
He was previously the representative for Florida's 7th congressional district as a Democrat from 1973 to 1992; the representative for Florida's 6th congressional district as a Democrat from 1967 to 1972; and the representative for Florida's 10th congressional district as a Democrat from 1963 to 1966.
I live in Florida's 11th congressional district.
I want to urge Gibbons to take an action on a bill.
Look for a contact form on Rep. Sam Gibbons's website to express your opinion.
Head over to Rep. Sam Gibbons's website. If you are having a problem with a government agency, look for a contact link for casework to submit a request for help. Otherwise, look for a phone number on that website to call his office if you have a question.
You are currently on the website GovTrack.us, which has no affiliation with Gibbons and is not a government website. Choose from the options above to find the right way to contact Gibbons.
Gibbons is shown as a purple triangle ▲ in our ideology-leadership chart below. Each dot was a member of the House of Representatives in 1996 positioned according to our liberal–conservative ideology score (left to right) and our leadership score (leaders are toward the top).
The chart is based on the bills Gibbons sponsored and cosponsored from Jan 3, 1991 to Oct 3, 1996. See full analysis methodology.
H.R. 5060 (103rd): To provide for the continuation of certain fee collections for the expenses of the Securities and Exchange Commission for fiscal year 1995.
H.R. 3981 (99th): A bill to extend until December 19, 1985, the application of certain tobacco excise taxes.
From Jan 1963 to Sep 1996, Gibbons missed 1,636 of 15,207 roll call votes, which is 10.8%. This is much worse than the median of 2.7% among the lifetime records of representatives serving in Sep 1996. The chart below reports missed votes over time.


Network operators are being forced to add capacity to meet the tremendous growth in network demand from video services (e.g. YouTube), file sharing, and software updates. Josh Adelson of Peerapp explained to me at the TelcoTV trade show that inserting smart video storage and distribution services (transparent caching) into DSL networks can dramatically reduce the capacity needs on the network. Without video caching, network operators will have excessive cost and complexity of adding capacity or provide a poor quality of service resulting in higher support costs or customer churn. The solution is to add transparent caching servers that can automatically identify and store popular video content. Transparent caching helps to reduce network capacity load, minimizes the capacity need (and cost) for Internet transit links, and increases customer satisfaction (higher video quality levels). Transparent caching automatically identifies popular content and stores the content as close to the subscriber as possible. The PeerApp Ultraband Transparent cache can be inserted almost anywhere within the IP portion of a DSL network. When caches are placed close to the edge, the network capacity savings increases because the transport is reduced over larger parts of the network. Transparent caching is simple to install and additional caching servers can be installed as the need increases (easily scalable).


Here I am with non-existing my baby bump. The place everything started. I am in Adana where is south of Turkey, also is my hometown.
Adana is the 6th biggest city in Turkey. It's best known for the very famous food called "Adana Kebab". Which is why I call the land of kebab. I think my hometown is the hilarious city in Turkey. Because the weather is too hot, people of this city do crazy things. Like there was this guy who opened fire to the sky to punish God because It was too hot. Crazy, right?! Have you ever heard something like this before?!
I missed Adana so much mostly because my family lives there but also for these incredible street food carts. Whenever in the city you go, you find something to eat from the streets. And they are the yummiest foods. And I miraculously lose weight whenever I go to Adana if I stay more than 10 days. I still don't know how that happens all the time. Of course, I'm not complaining. You eat the most delicious food and still lose weight?!
I bought a couple of dresses larger than what my size usually is so I can skip all these buying maternity clothes. I already love to wear oversize clothes, so I can still wear my extra large clothes after babies.


We're excited to announce the 2011 class of Google Policy Fellows, and we're expecting great things from the 16 students selected for the fourth summer of the Google Policy Fellowship. Our host organizations selected the 2011 fellows from over 900 impressive submissions – nearly double the number of applications from 2010. The 2011 class includes undergrads and graduate students from 15 schools, studying computer science, economics, information policy, intellectual property, international affairs, law, library sciences, and public policy.
Congratulations to the 2011 Google Policy Fellows!
The 2011 Fellows will spend 10 weeks this summer at our host organizations in Washington, D.C., San Francisco, Toronto, and Ottawa working on Internet and technology policy issues including free expression, privacy, security, and intellectual property.
Thank you to everyone who applied. Each year brings more and more outstanding applicants, and we hope everyone will stay engaged, involved, and consider applying again for future programs. Please sign up here to receive program announcements, and visit google.com/policyfellowship for more information.
Grats! Enjoy the summer it is a great ride.
Great. I salute Google for doing the good work.


text:
Four Duval County Public Schools will Receive Solar Electric Emergency Shelter Power Systems
Thursday, January 13th, 2011, 11:31am
Four Duval County Public Schools have recently been selected to receive solar electric emergency shelter power systems as part of the SunSmart Schools E-Shelter (Emergency Shelter) program.
The selected schools are LaVilla School of the Arts, Abess Park Elementary, Arlington Middle and Chets Creek Elementary.
UNF English Department Holds Auditions for Shakespeare-in-the-Park Production
The University of North Florida's Department of English will hold auditions for the April Shakespeare-in-the-Park production of "The Tempest," from 6:30 to 9:30 p.m. Monday, Jan. 17; Thursday, Jan. 20; and Friday Jan. 21; in the Andrew A. Robinson Jr. Theater, Building 14A. Auditions are open to members of the University and Jacksonville communities.
UNF Sophomore First Student Published in National Literary Magazine
Alexandra Marshall, a sophomore in the School of Nursing at the University of North Florida, was recently published in The Collegiate Scholar, an online national publication produced by The National Society of Collegiate Scholars (NSCS). She is the first UNF student to be selected for publication in the national literary magazine.
Cultural Center Art and Essay Contest
Duval County Public Schools (DCPS) recently partnered with the Amity Turkish Cultural Center for their 2nd annual art and essay contest for middle and high school students. The contest aims to promote awareness, understanding and positive interactions among different cultures and communities. This year's theme was "Empathy: Walking in Another's Shoes."
Duval County Schools Acceleration Programs Recruitment Events
High School Acceleration Programs are available in every Duval County public high school to provide advanced educational opportunities to students throughout the county. Students are urged to review the program offerings and attend one or more information session or open house to learn more about enrollment and how the programs can better prepare students for post-secondary education.
During the presentation portion of the monthly meeting of the Duval County School Board, Superintendent Ed Pratt-Dannals and Board members recognized a community partner, a school and a business partner for their outstanding accomplishments and contributions to Duval County Public Schools:
Episcopal High School Opens Two New Academic Halls
Monday, January 10th, 2011, 1:43pm
Episcopal High School has completed the first phase of its campus master plan expansion project by opening the school's two new $4 million academic halls. Coinciding with the Christian holiday Epiphany, a dedication ceremony for Parks and Lastinger Halls was held today complete with a student procession, choral performances and tours of the new facilities.


Two idols, Kazanari Tsubasa and Amō Kanade, collectively known as Zwei Wing, battle against an alien race known as Noise using armour known as Symphogear, which uses the power of music to counteract the Noise's destructive capability. However, Kanade sacrifices herself to protect a girl named Hibiki Tachibana, who ends up with a piece of Kanade's Symphogear relic, Gungnir, embedded in her chest.
Two years later, Hibiki awakens the power of the Gungnir relic inside her body, gaining the same Symphogear armor that Kanade had. Using the power of song, Hibiki and her fellow Symphogear wielders must fight to protect the innocent and defeat those who would use the Noise for evil.
There are 2 queer characters listed for this show; 2 are dead.
If you like Symphogear you may also like these shows.
While the anime is very popular, it's got poor queer rep.


Newbury, MA – Harold E. Pingree, age 83, longtime Newbury resident, died peacefully at Port Healthcare Center in Newburyport early Tuesday morning, May 22, 2018. He was the beloved husband of Carlene J. (White) Pingree, who died April 7, 2015.
Peabody MA – Carl L. Jones Sr….
William C. ("Bill") Byrne, Jr.
Susan Carol Brown of West Yarmouth past away Thursday 5/17/2018 . She was a loving devoted mother,grandmother, and great grandmother.Google her for more info.


If your complexion is dull and spotted because of acne breakouts, you can refresh it with acne treatment. We offer several acne treatments and when you talk to our skin specialist, the best treatment for your unique condition may be recommended. You may have tried many over-the-counter creams and ointments to little effect, but they are intended for the general public so the active ingredient may be so slight, it is not effective. We will give you prescription acne medication that is suitable for your type of acne and skin type.
Here at FamWell MD, we are proud to offer a number of avenues to address your acne. Some of these include the Fotona Laser, Thermi RF, Isolaz, Carbossi, CORE CO2, facials, and Obagi Skin Care, as well as PRP therapy and chemical peels; below are some in-depth looks into these lattermost two.
PRP therapy is an acne treatment that uses the healing power of your own blood. With this route, a small sample of your blood is drawn and spun to separate the platelet-rich plasma within. This substance, rich with healing growth factors, is implemented into an injectable serum and reintroduced beneath your skin to prompt a flood of regeneration. This can make a notable dent in your acne.
Chemical peels are available in many blends and strengths to tackle various intensities of acne. For this process, a qualified professional applies a special blend of chemical components to your face and leaves them on for a period of time, after which the peel is removed and a new layer of healthy skin is revealed.
To learn more about what each acne treatment may be able to do for you, we warmly invite you to reach out and make an appointment with FamWell MD! At our convenient locations in Jacksonville, our caring and dedicated team of professionals will be pleased to explain our options in full and help you decide which one would be best for you. Contact us today to set up your consultation – we look forward to speaking with you!


The adidas adiZero ClimaCool Tempaia II tennis shoe features a durable and lightweight microfiber SPRINTSKIN upper that provides stability and comfort. adiTUFF on the medial toe to protect from abrasions during athletic movement. Forefoot SPRINTWEB construction adds maximum stability during extreme cut movements. External dual-density SprintFrame construction ensures maximum heel support while preventing pronation. An OrthoLite sockliner improves not only the comfort, but the moisture management properties of the Tempaia II as well. It's paired with an anatomically pre-molded EVA inlay for enhanced fit. The adiPRENE insert delivers comfort and shock absorption. adiPRENE+ insert aids forefoot propulsion efficiency. TORSION SYSTEM for a unique transition from heel to toe. A low-profile, hardcourt adiWEAR outsole gives the best durability in high wear areas, no matter what direction you're moving. miCoach compatible. Wt. 10.2 oz.


text:
Games With Real Cash Economy
Do you wish you could download all your favorite PS3 and Xbox 360 games on the internet? You know when you're playing a game and you think "ok, I'll just play this for a while before bedtime" and the next time you look up its already dawn? Yeah that is Skyrim. While the story isn't that great in my opinion (You are the chosen hero called the "Dragonborn," out to save the world from the apocalypse at the scaly hands of an all powerful dragon named Alduin and his flying reptilian brothers), what makes Skyrim ps3 work is the gameplay. The nonlinear open world gameplay of the previous Elder Scrolls games is still intact, and the elements that worked from the previous game, Oblivion, are brought back (I.e. the players actions will greatly affect the way NPCs react to you, and NPCs have their own schedules). And it's that freedom that makes Skyrim so fun, you can really be the hero, the villain or whatever you want. Everything you do or don't do will affect the world in some way, shape or form, not matter how small.
I'll admit, I haven't ever played a CD Project game. Among their released titles, include The Witcher and its sequel, which are said to be some of the finest games ever made… for the PC only. You can't use Remote Play on your mobile device's cellular data network. A high-speed Wi-Fi® network is required. Great list! Everyone of these games are awesome! KoA is a great under the radar game, excellent combat that satisfies the button mashing tendencies. Fallout and Elder Scrolls are great and I can't wait till Fallout 4 and ES Online. An internet search for www racing games will also reveal an exceptional off road experience among Xbox 360 racing games: the MX vs. ATV Unleashed. This unique racer brings monster trucks, trophy trucks and motorcycles together on one race track and adds a few airplanes and helicopters above for a racing experience that will dazzle any player at first try.
The second generation of video game consoles is also described as the era of programmable ROM cartridges. Programmable cartridges led to software oriented video game designs. In the earlier generation, video games had the same pong game, but in different variations. This generation, however, had different types of games produced on different consoles. This led to the first known console wars. Atari 2600, Magnavox Odyssey and Intellivision all started producing different types of video games. Notable video games of this generation include; Pacman and Space Invaders. One entertaining activity available online is gaming. Both children and grown-ups engage in relaxing and brain-stimulating games. Quake is rated as number four and was created in 1996. It was one of the best 3D animated games of its time. It allowed users to use a range of weapons and involved a simple aim and shoot game play.
Tags: economy games
Previous How To Upload Videos To GoDaddy Website
Next Best Strategy Browser Games In 2018
An interview with FromSoftware's Hidetaka Miyazaki


text:
Comparing the Responses of Osseous Versus Soft-Tissue Metastases of Renal Cell Carcinoma to Receptor Tyrosine Kinase Inhibitors and Immunotherapy
Authors: Tai, Katherine Yuxia | El Abiad, Jad M.b | Morris, Carol D.b | Markowski, Mark Christopherc | Levin, Adam S.b; *
Affiliations: [a] The Johns Hopkins School of Medicine, Baltimore, MD 21287, USA | [b] Department of Orthopaedic Surgery, The Johns Hopkins University, Baltimore, MD 21287, USA | [c] The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University, Baltimore, MD 21231, USA
Correspondence: [*] Correspondence to: Adam S. Levin, MD, Department of Orthopaedic Surgery, The Johns Hopkins University, 601 North Caroline Street, Baltimore, MD 21287, USA. Tel.: +1 410 502 2698; Fax: +1 410 614 1451; E-mail: [email protected].
Keywords: Biologic agents, metastasis, neoplasms, complex and mixed, neoplasms, connective and soft tissue, renal cell carcinoma
Checkpoint inhibitors and receptor tyrosine kinase inhibitors (RTKIs) have changed the standard of care for metastatic renal cell carcinoma (mRCC). Anecdotal evidence suggests these therapies may be less effective for treating bone than soft-tissue metastases.
We performed a retrospective review evaluating the relative clinical responses in soft-tissue and bone metastases in patients undergoing therapy using RTKIs and anti-programmed death-1 (PD-1) agents for mRCC.
Of the 2,212 patients in our institutional cancer registry with renal cell carcinoma (1997–2017), 68 (82 disease courses) were identified with measurable bone and soft-tissue metastases treated with RTKIs and/or PD-1s. Extent of metastasis was quantified at the time of therapy initiation (baseline) and at 3 months, 6 months, and 1 year. Changes in disease status were categorized as complete response, partial response, stable, mixed, or progression of disease according to RECIST v1.1 and MD Anderson criteria. These categories were further organized into "response to treatment" or "evidence of progression" to generate a generalized linear effects model with soft-tissue response as the independent variable and bone response as the dependent variable. Alpha = 0.05.
Soft-tissue response correlated with bone response at 3 months (76 disease courses, p = 0.005) and 6 months (48 disease courses, p = 0.017). Of the patients with controlled soft-tissue disease, only 14 (19%) and 15 (32%) had progression in bone at 3 and 6 months, respectively.
Contrary to anecdotal reports, osseous metastases do not appear to respond worse than soft-tissue metastases to treatment with these agents.
Renal cell carcinoma (RCC) represents approximately 3.8% of all newly diagnosed malignancies in the United States, and approximately 20%–30% of patients with metastatic RCC (mRCC) ultimately develop osseous metastases. [1] The prognosis associated with distant metastatic disease is poor at baseline, with a 5-year survival rate of 8%–12%, [2] but patients with osseous metastases often have a worse prognosis. Additionally, the prevalence of osseous metastases among patients with RCC has increased, likely because of improvements in imaging modalities and advances in systemic therapeutic options.
Since the approval of vascular endothelial growth factor (VEGF)/receptor tyrosine kinase inhibitor (RTKI) sunitinib in 2006, [3] the National Comprehensive Cancer Network Clinical Practice Guidelines in Oncology recommend VEGF/RTKI therapy as first-line treatment for mRCC. [4] Since approval, RTKI therapies have rapidly become more common, being used as first-line treatment in 70%–90% of cases of mRCC. [2] In 2018, the options for first-line treatment shifted again with the approval of immunotherapy agents (nivolumab plus ipilimumab), which showed superior overall survival and objective response rates compared with sunitinib. [5] Currently, biologic agents (RTKI and immunotherapy agents) are used routinely in the treatment of metastatic disease, including for patients with bone metastases. [6]
Although these agents have improved disease progression outcomes and patient survival, osseous metastases remain a marker of poor prognosis for patients with mRCC. In 2011, Abel et al. [7] identified bone metastases as a significant predictor of shorter survival among patients receiving sunitinib for mRCC. In 2014, McKay et al. [8] drew a similar conclusion from data on more than 2,700 patients receiving sorafenib, sunitinib, and/or axitinib. In 2011, Beuselinck et al. [6] studied 233 patients receiving first-line sunitinib and found that median progression-free survival and overall survival were shorter in patients with bone metastases than in those without. [6] However, anecdotal evidence suggests that the response to these agents is greater in soft-tissue metastases than in bone. A divergent response may improve the patient's overall prognosis for survival without concomitant stabilization of osseous disease. Thus, patients may be at higher risk for progression of osseous metastatic disease, leading to more skeletal-related adverse events, such as fractures, spinal cord compression, bone pain, and hypercalcemia. These complications are likely to compromise quality of life and may affect overall survival. Lack of efficacy in osseous metastases is of particular concern in radioresistant tumors, for which few options exist other than targeted therapy.
This suggestion of a dichotomy between osseous and soft-tissue metastatic response to targeted therapy has not been proven. To our knowledge, no comprehensive study has directly compared the efficacy of biologic agents between the sites of metastatic involvement, partly because of the difficulty in quantifying bone metastases. The Response Evaluation Criteria in Solid Tumors, version 1.1, (RECIST 1.1) criteria classify bone metastases as unmeasurable unless a soft-tissue component is present. [9] In this study, we aim to address this gap in knowledge by evaluating the relative clinical responses in soft-tissue and osseous sites of disease in patients undergoing therapy using RTKIs and anti-programmed death-1 (PD-1) agents for mRCC.
This study was approved by our institutional review board (IRB00170728), and patients were identified via the cancer registry at the Cancer Center database at the Sidney Kimmel Comprehensive Cancer Center at The Johns Hopkins University). A waiver of the requirement for signed consent for this study was granted by our institutional review board because of the nature of the inquiry and its anonymized data reviewed. All 2,212 patients treated for RCC by The Johns Hopkins University Departments of Orthopaedic Surgery, Oncology, and Radiation Oncology between January 1997 and December 2017 were considered for inclusion. We included adults (18 years or older) with metastatic bone and soft-tissue involvement from RCC treated with RTKI (sunitinib, pazopanib, cabozantinib, axitinib, sorafenib, and/or lenvatinib) and/or PD-1 inhibitors (nivolumab, pembrolizumab, atezolizumab, durvalumab, and/or avelumab). We excluded patients with bone or soft-tissue lesions secondary to primary neoplastic processes or metastases from another primary malignancy. We also excluded those who underwent radiation or surgery for metastatic lesions before or during RTKI or PD-1 treatment (only the site that received radiation or surgery was excluded from evaluation). Overall, 218 patients met the inclusion criteria, of whom 68 patients had both identifiable bone and soft-tissue metastatic disease, and 150 had bone or soft-tissue metastases but not both. We included only the 68 patients with both bone and soft-tissue metastatic disease in our study (Fig. 1).
Inclusion and exclusion criteria applied to renal cell carcinoma (RCC) patient database. Adequate documentation (doc) refers to measurable metastases documented at baseline and at one or more follow-up time points. (mRCC, metastatic renal cell carcinoma; PD-1, programmed death-1; pts, patients; RTKI, receptor tyrosine kinase inhibitors).
Medical records were reviewed for patient characteristics, treatment course, and disease progress. Imaging, pathology test results, and clinical reports were used to confirm the presence of metastases, as well as the treatment modalities used, their duration, and dosing. The dimensions of target soft-tissue and bone metastatic lesions were collected from radiographic imaging studies at baseline (when treatment was initiated) and at least one other time point (3 months, 6 months, and/or 1 year after treatment initiation). Lesions were measured independently by at least two researchers. Most imaging consisted of computed tomography scans, although bone scan images and magnetic resonance imaging studies were also referenced.
Our study is isolated to lesion changes after the first course RTKI or PD-1 therapy. Of the 68 qualified patients, 14 received both RTKI and anti-PD-1 therapy at different times. In such cases, we analyzed both the first course of RKTI and the first course of anti-PD-1 therapy.
We used the RECIST 1.1 [9] criteria to assess soft-tissue metastases and the MD Anderson (MDA) criteria [10] to assess bone metastases, because the RECIST 1.1 criteria classify bone metastases as unmeasurable disease unless a soft-tissue component is present (Table 1). In accordance with RECIST 1.1 criteria, soft-tissue metastases were measured in one dimension, with a cutoff of 1 cm in the longest dimension. The exception to this was lymph nodes, for which the cutoff was 1.5 cm in the shortest dimension. Furthermore, only the two largest lymph nodes present at baseline were considered target lesions and followed. For the MDA criteria, measurement of two perpendicular dimensions was required with a cutoff of 1 cm in the longest dimension. The dimensions were summed when considering disease change over time.
MD Anderson and RECIST criteria applied for assessing bone and soft-tissue metastases, respectively
Parameter MD Anderson Criteria RECIST Criteria
Size threshold None specified (applied cut-off of 1 cm in longest diameter) 1 cm in longest diameter (1.5 cm for lymph node in short diameter)
Required measurements Sum of two perpendicular dimensions Longest diameter (short diameter for lymph node)
Complete response Complete resolution Complete resolution
Progression of disease ≥25% increase ≥20% increase
Partial response ≥30% decrease ≥50% decrease
RECIST, Response Evaluation Criteria in Solid Tumors, version 1.1.
At each time point, the sizes of individual osseous or soft-tissue target lesions were aggregated and compared with baseline. The percentage change from baseline was categorized as complete response, partial response, stable, progression of disease, or mixed response. The thresholds for these categorizations often varied between bone and soft-tissue in accordance with the criteria against which they were measured.
Target lesions had to resolve completely to be categorized as having complete response for either bone or soft-tissue. For partial response, MDA criteria require the cumulative size of bone metastases to reach a 50% or greater reduction in size, whereas RECIST criteria define partial response as a 30% reduction in overall soft-tissue lesion size. For progression of disease, bone metastases must grow by 25% or more, and soft-tissue metastases must grow by at least 20%. [9, 10] Stable disease in bone or soft-tissue lesions thus represents the range between partial response and progression of disease. Mixed response was further defined as partial or complete response with new measurable metastatic lesions.
If a lesion was unmeasurable at a particular time point, that lesion was excluded from the calculation for that time point. Similarly, target lesions treated with surgery or radiation were excluded from analyses after their local treatment.
After establishing the disease status, we used a generalized linear mixed effects model to determine significance. Bone metastasis response was used as the independent variable, and soft-tissue metastasis response, time point, and their interaction were the dependent variables. For all assessments, significance was considered at p < 0.05.
Patient and disease characteristics
Of the 68 patients, 14 were treated with both RTKI and anti-PD-1 therapy; therefore, we analyzed 82 total disease courses (Table 2). Of these, 63% represented treatment by RKTI and 37% by anti-PD-1 therapy. Regarding histologic subtypes, most cases were the clear cell subtype (74%). Other subtypes included papillary carcinoma (6%) and sarcomatoid carcinoma (4%), with the remainder consisting of various combinations of subtypes.
Characteristics of 82 disease courses (in 68 patients) with metastatic spread to both bone and soft-tissue, treated with RTKI and/or PD-1, 1997–2017
Characteristic N (%)
Female sex 18 (22)
Anti-PD-1 30 (37)
RTKI 52 (63)
Never 29 (35)
Unknown 27 (33)
Former 21 (26)
Current 5 (6)
Clear cell 50 (74)
Not available 6 (9)
Sarcomatoid 4 (6)
Papillary 3 (4)
Chromophobe 2 (3)
Clear cell and papillary features 2 (3)
Clear cell with sarcomatoid features 1 (1)
Unique lesions
Soft-tissue† 4.7±2.6*
Bone‡ 2.8±2.7*
Anti-PD-1, anti-programmed death-1; RTKI, receptor tyrosine kinase inhibitor. *Data presented as mean±standard deviation. †A total of 389 unique soft-tissue lesions were recorded. ‡A total of 229 unique osseous lesions were recorded.
At the 3-month point, 76 disease courses were tracked. Six disease courses were unmeasurable at 3 months because either bone or soft-tissue metastases had not developed. At 6 months, there were 34 evaluable patients (48 disease courses), and at 12 months there were 26 evaluable patients (22 disease courses). At 6 months, the most common reason for attrition was progression of disease (71%), followed by death (15%), progression and adverse effects (9%), and loss to follow-up (6%). At 12 months, the most common reason for attrition was also progression of disease (69%), followed by death (15%), progression and adverse effects (8%), adverse effects alone (4%), and loss to follow-up (4%).
Each disease course included a mean (±standard deviation) of 4.7±2.6 evaluable soft-tissue lesions, resulting in a total of 398 unique soft-tissue lesions. The most common sites for soft-tissue lesions were the lung (33% of total lesions), lymph nodes (28%), and liver (15%). A total of 229 unique osseous lesions were identified and followed. For osseous metastases, each disease course included a mean of 2.8±2.7 unique lesions, with the most common sites of metastases being the pelvis (35% of total osseous lesions), vertebrae (29%), and ribs (19%).
Disease response
The disease response of osseous and soft-tissue metastatic burden was followed at three time points. Figure 2 provides a descriptive view of the response for bone and soft-tissue analyses, but no statistical analyses comparing bone and soft-tissue categorically were conducted.
Renal cell carcinoma soft-tissue and bone metastasis response to receptor tyrosine kinase inhibitors or programmed death-1 therapy at (A) 3 months, (B) 6 months, and (C) 12 months after initial treatment classified by Response Evaluation Criteria in Solid Tumors, version 1.1, and MD Anderson criteria, respectively, and compared with baseline measurements. (CR, complete response; Diff, difference; PD, progression of disease; PR, partial response).
For bone metastases, stable disease was the most common response, representing 67% at 3 months, 50% at 6 months, and 68% at 12 months. When comparing osseous sites of metastases with soft-tissue sites, the proportion with stable disease was 26% greater at 3 months in the osseous sites. Conversely, a 16% greater proportion of soft-tissue metastases had progression of disease at 3 months compared with osseous metastases. However, a 13% greater proportion of soft-tissue metastatic lesions also exhibited a partial response to therapy compared with osseous metastatic lesions.
The numbers of disease courses in each of the five disease status categories were inadequate to power the model and thus were reclassified as response to treatment (partial response, complete response, or stable) or evidence of progression (progression of disease or mixed) (Fig. 2). At 3 months, 34 of 42 patients with soft-tissue response also had bone response, and 8 had bone progression. Similarly, at 6 months, 13 of 19 patients with soft-tissue response also had bone response, and 6 had bone progression. At 6 months, 29 patients had soft-tissue progression, of whom 20 also had bone progression, and 9 had bone response. Similarly, at 12 months, 9 of the 11 patients with soft-tissue response also had bone response, and 2 had bone progression.
Results of tests of association
We found a positive association between soft-tissue metastasis response and bone response at 3 months (p = 0.005). The model indicates that if a patient has evidence of progression in soft-tissue metastases, the odds of that patient also having progression in bone are 18 times greater than having response in bone. We also found a positive association at 6 months (p = 0.017), with the model indicating that if a patient has evidence of progression in soft-tissue metastases, the odds of that patient also having progression in bone are 10 times greater than having response in bone (Fig. 3). No significant association between soft-tissue response and bone response was found at 12 months (p = 0.772).
Generalized linear model indicates that soft-tissue response correlates with bone metastasis response at (A) 3 months and (B) 6 months (*p < 0.05) but not at (C) 12 months. Graphs show the proportion of response (R) and evidence of progression (EP) of disease in bone if a patient has R or EP in soft-tissue (x-axis).
The poorer prognosis associated with osseous metastatic disease reported in previous studies raised the possibility that bone metastases may respond differently than soft-tissue metastases to RTKIs. Anecdotal reports also indicate that bone metastases may not respond as well to these biologic agents. The results we report herein indicate that, at least early in the disease course (<6 months), bone metastases do not respond significantly differently than soft-tissue metastases to RTKI and immunotherapy agents. Contrary to anecdotal suggestion, patients with soft-tissue metastases that respond to therapy are likely to have bone metastases that respond similarly. However, a sizeable proportion of patients with controlled soft-tissue metastases did show progression in bone (19% at 3 months and 32% at 6 months). Also, among patients whose soft-tissue metastases were not controlled, approximately one-third had disease control in bone (38% at 3 months and 31% at 6 months). Although bone metastases may not necessarily have an inferior response to treatment compared with soft-tissue metastases, they often respond differently.
This observation is further supported by the finding that a greater proportion of soft-tissue metastases had response and progression than did bone metastases. Similarly, a greater proportion of bone metastases remained stable than did soft-tissue metastases. These results may reflect the different measurement criteria between the sites of metastasis, although the dichotomous findings raise questions about why the presence of bone metastases remains an independent predictor of overall survival in patients with mRCC treated with these agents.
While our study examines a similar patient population to those of Beuselinck et al. [6] and Zolnierek et al., [11] we attempted to examine response on an individual patient level to better control for confounding factors within the patient population. We included only patients who had both bone and soft-tissue metastases and compared each patient's response in bone metastases with their response in soft-tissue metastases. This represents a novel method of analyzing this patient population compared with previous studies that aggregated patient data and performed categorical analyses, which may be skewed by outliers and confounding variables.
Additionally, Beuselinck et al. [6] and Zolnierek et al. [11] relied solely on the RECIST 1.1 criteria. Because these criteria allow only the soft-tissue extension of osseous lesions to be used as measurable disease, most osseous lesions become unmeasurable. We are concerned that this does not allow for the most accurate tracking of bone metastasis response; thus, we opted to use the MDA criteria to track progression of bone metastases.
Beuselinck et al. [6] suggested that the underlying mechanism may involve osteoclast activation in the presence of malignant cells that liberate cytokines, such as transforming growth factor-beta (TGF-β), insulin-like growth factor, and fibroblast growth factor, that further stimulate other malignant cells, similar to the vicious cycle of lytic bone metastases proposed by Mundy. [12] We recognize the interplay between TGF-β, for example, and T-cell immunity, and a means of overcoming such an increase in TGF-β may be critical to improving the efficacy of checkpoint inhibition. [13] We did not evaluate the potentially confounding role of antiresorptive therapy in patients with osseous metastatic disease. Although antiresorptive therapy has not been shown to influence overall survival in patients with mRCC, its effect on skeletal-related events and ability to decrease the osteoclast-mediated release of TGF-β are clearly described. [14]
Similarly, we are currently evaluating whether the soft-tissue and osseous lesions in this patient population respond differently from those lesions in patients with only bone or soft-tissue lesions, but not both. An understanding of differences in barriers of defense to the spread of disease could lead to identification of better predictors of and treatments for RCC. [15]
Although we analyzed a large cohort of patients with RCC, our study has several limitations, largely because of patient population size and strict inclusion criteria. To limit confounding patient-related and tumor-related factors, we evaluated only patients who had both bone and soft-tissue metastases to compare lesion progression within individual patients. We also did not include lesions treated with radiotherapy. Furthermore, because of attrition over time, the number of eligible patients declined. As a result of the limited patient population, we had insufficient statistical power to analyze drug classes (RTKI and PD-1) individually. Similarly, the study was underpowered to evaluate a more granular response pattern (e.g., complete vs. partial response). A more detailed evaluation of therapy classes or response gradation would likely require a multi-institutional analysis. Another limitation concerns our use of both the RECIST 1.1 and MDA criteria, which specify different cut-offs for evaluating disease progression. Thus, our results rely on the relative clinical validity of each of these criteria.
Bone and soft-tissue metastatic lesions responded similarly to targeted therapy in patients with mRCC who had both bone and soft-tissue metastases. Our study provides a foundation for further investigation into the role of targeted therapy for bone metastases in mRCC.
Katherine Yuxi Tai: Acquisition, analysis, interpretation of data, drafting the work, final approval, agreement to be held accountable for the work
Jad M. El Abiad: Acquisition, analysis, interpretation of data, drafting the work, final approval, agreement to be held accountable for the work
Carol D. Morris: Interpretation of data, drafting the work, final approval, agreement to be held accountable for the work
Mark Christopher Markowski: Interpretation of data, drafting the work, final approval, agreement to be held accountable for the work
Adam S. Levin: Acquisition, analysis, interpretation of data, drafting the work, final approval, agreement to be held accountable for the work
The authors have no conflict of interest to report.
The authors would like to thank Gayane Yenokyan, PhD from The Johns Hopkins Bloomberg School of Public Health for her assistance with this manuscript.
Jemal A , Siegel R , Ward E , Hao Y , Xu J , Murray T , Thun MJ . Cancer statistics, 2008. CA Cancer J Clin. 2008;58(2):71–96.
Pal S , Gong J , Mhatre SK , Lin SW , Surinach A , Ogale S , Vohra R , Wallen H , George D . Real-world treatment patterns and adverse events in metastatic renal cell carcinoma from a large US claims database. BMC Cancer. 2019;19(1):548.
Verhagen PC . Re: Sunitinib versus interferon alfa in metastatic renal-cell carcinoma. Eur Urol. 2007;51(5):1444.
National Comprehensive Cancer Network. NCCN Clincial Practice Guidelines in Oncology (NCCN Guidelines): Kidney Cancer, version 4.2018. Available at https://www2.tri-kobe.org/nccn/guideline/urological/english/kidney.pdf Accessed on Aug 13. 2019.
Motzer RJ , Tannir NM , McDermott DF , Aren Frontera O , Melichar B , Choueiri TK , Plimack ER , Barthelemy P , Porta C , George S et al. Nivolumab plus Ipilimumab versus Sunitinib in Advanced Renal-Cell Carcinoma. N Engl J Med. 2018;378(14):1277–90.
Beuselinck B , Oudard S , Rixe O , Wolter P , Blesius A , Ayllon J , Elaidi R , Schoffski P , Barrascout E , Morel A et al. Negative impact of bone metastasis on outcome in clear-cell renal cell carcinoma treated with sunitinib. Ann Oncol. 2011;22(4):794–800.
Abel EJ , Culp SH , Tannir NM , Tamboli P , Matin SF , Wood CG . Early primary tumor size reduction is an independent predictor of improved overall survival in metastatic renal cell carcinoma patients treated with sunitinib. Eur Urol. 2011;60(6):1273–9.
McKay RR , Lin X , Perkins JJ , Heng DY , Simantov R , Choueiri TK . Prognostic significance of bone metastases and bisphosphonate therapy in patients with renal cell carcinoma. Eur Urol. 2014;66(3):502–9.
Eisenhauer EA , Therasse P , Bogaerts J , Schwartz LH , Sargent D , Ford R , Dancey J , Arbuck S , Gwyther S , Mooney M et al. New response evaluation criteria in solid tumours: revised RECIST guideline (version 1. 1). Eur J Cancer. 2009;45(2):228–47.
Costelloe CM , Chuang HH , Madewell JE , Ueno NT . Cancer Response Criteria and Bone Metastases: RECIST 1. 1, MDA and PERCIST. J Cancer. 2010;1, 80–92.
Zolnierek J , Nurzynski P , Langiewicz P , Oborska S , Wasko-Grabowska A , Kuszatal E , Obrocka B , Szczylik C . Efficacy of targeted therapy in patients with renal cell carcinoma with pre-existing or new bone metastases. J Cancer Res Clin Oncol. 2010;136(3):371–8.
Mundy GR . Mechanisms of bone metastasis. Cancer. 1997;80(8):1546–56.
Ungefroren H . Blockade of TGF-beta signaling: a potential target for cancer immunotherapy? Expert Opin Ther Targets. 2019;23(8):679–93.
Beuselinck B , Wolter P , Karadimou A , Elaidi R , Dumez H , Rogiers A , Van Cann T , Willems L , Body JJ , Berkers J et al. Concomitant oral tyrosine kinase inhibitors and bisphosphonates in advanced renal cell carcinoma with bone metastases. Br J Cancer. 2012;107(10):1665–71.
Massague J , Obenauf AC . Metastatic colonization by circulating tumour cells. Nature. 2016;529(7586):298–306.
如果您在出版方面需要帮助或有任何建, 件至: [email protected].nl


Facing Your IP Address Reveal?
Just Your IP Address Reveal?
Just Your Internet protocol address Reveal?
Who is not going to love the main Web? IPsec VPN supplies risk-free online towards management and business marketing networks just for out of the way and even mobile owners, office places of work in addition to internet business spouses….


Having Hard Time With Your Android's Wi-Fi ?
You might already be worried about your friends coming to you for asking your Wi-Fi's password. When you disclose your password (because you think he's just a friend so why not to…), they can come to you to have their Android phone fixed to receive your network's signal (even you don't know whether the problem is in the phone, your router or something else). Today, you are going to learn about the most common Wi-Fi problems boasted by an Android device.
1. Network Never Gets Scanned!
There are mainly two reasons for your phone not being able to scan a network. If you want to connect to a Ad-Hoc network, you need to reconfigure your phone. As a side note, most of the networks are not Ad-Hoc in nature so just forget this. Likewise, any hidden network won't be shown and for the same, you misunderstand that a Wi-Fi network is not being scanned. For solving the Ad-Hoc problem, you need to root your phone (which is not recommended) and patch the wpa_supplicant file on your phone so that the system becomes compatible with Ad-Hocs.
The easiest way to solve the 'hidden network' thing would be to ask your mate not to make the network hidden. Other than this, you should ask your friend to enter everything from SSID to Password correctly on your phone by using the 'Add Network' option and the hidden network won't be hidden anymore.
If you are facing this problem, you are probably one who doesn't have a decent battery and have kept your phone in battery saving mode at its best. Your phone gets disconnected from Wi-Fi whenever it goes to sleep because the Wi-Fi also gets turned off to save some juice. To solve this problem, head to your phone's settings and go for advanced Wi-Fi options and do this!
However, remember that you might need to lose extra juice for remaining connected all the time.
Note: If you use third party juice savers like Battery Doctor and Du Battery Saver, you might need to check the settings of those apps, too.
3. Obtaining IP Address Forever!
Let's not move deep inside how this problem occurs (maybe this is an Android bug so let Google take care of it).
The very first step to have this annoying problem fixed would be to restart your device. Secondly, you can restart the Wi-Fi router to see if that helps. There are a lot shouting that resetting your phone solves the problem but that's not the right solution. Instead, you can install Wi-Fi Fixer (this app resets your Wi-Fi system files just like on Windows) and be hopeful. Last but not the least, you can go for a static IP address usage if you know the IP address being broadcast by the router. If nothing helps, you may buy a new phone.
4. Unable to Connect to Internet Via Wi-Fi?
Though the Wi-Fi symbol is filled, you might not be able to use the Internet. This mainly happens when the router is on a coffee break or something has gone wrong with the DNS settings. Just use another device such as your PC to see if the router is working. Likewise, you can also try your luck with the IP address or the gateway.
To sum up, be advised that there are quite a lot of Android Wi-Fi problems, which can arise without any music and you will be nothing but finding solutions to the problem you are facing. You just need to opt a 'hit and trail' drill and probably, the problem will be solved. But in fact, almost all the solutions mentioned above should work. And yeah, keep solving all these Android's Wi-Fi problems!


Click on Original image (3.7 MB) to check the image in bigger size.
I'm already disappointed. You know why?
Because my stupid old laptop will interfere with me watching this presumably beautiful, awesome anime gold.
Okay, new wallpaper. Even with the text, it's still too adorable to resist!
I think CLAMP is determined to give everyone toothaches from all the sweetness in this show, fine by me!
SOOO ADORABLE! *—-*! I fell in love with the picture definetly! Kobato looks so cute. And Fujimotooo *O* Chiho & Chise lookes adorable too!
i can't wait for october 6th! did i mentioned it?
Speaking of wallpaper, i hope we see a clean version of this image pretty soon.
OMG IT'S GORGEOUS!!! *_____* …. It's Seriously perfect!
Thank You for Sharing it!!!
I haven't tried the manga yet, but of course I have high expectations for it since it's clamp!
There's a collection of characters from Chobits, Angelic Layer and the old fortune-telling woman from xxxHolic. Wish has been hinted at being apart of the story, though the manga hasn't covered much details about that yet.
Are yu going to upload new Kobato drops D=?
And I squee when I see Chii-chan!
These pictures are heightening my expectations of needing this anime to start soon… ;_; oh gawd, i can't wait~!!!
Kobato. pic. is so cute!


The car accident had been a blessing in many ways because Rey would have suffered a slow, painful, and agonizing death to multiple organ failure due to Cystic Fibrosis. Rey was killed on impact. However, Junior was more than likely a carrier of the gene but did not suffer from CF at all. He was healthy, smart, and compassionate and helped his family care for his brother and sister. No one expected death to touch him. It was a grave loss all around and the feelings associated with both brothers' passing were difficult, conflicting, and confusing. The family really had very little support to offer a grieving mother, a desperate older sister, a father that pushed his own feelings down, and a little young girl that was very confused by it all and dealing with the fact that she had the same disease that would have ultimately killed her brother Rey.
It is because of this very fact we have created a new foundation called the Appreciate Every Breath Foundation. Our efforts with this foundation is to solicit the donation of time by counseling and mental health professionals to members of the foundation, who are patients suffering from Cystic Fibrosis. The foundation will also be extending benefits to caregivers, family, and friends of those affected by Cystic Fibrosis. We are looking to build a network of qualified mental health professionals that are willing to donate one hour per week to the cause for one year. Once we have established a wide list of counselors that register with us, we will begin opening the doors to patients and their families for private counseling sessions.
All patients, family members, and friends will be allowed access to a private Discord Server where they can interact and help each other. Our counselors will lurk about in that server to offer counsel and help as needed during their availability as some counselors will want to do more than just one hour. We will also hold group sessions and provide monthly support groups for patients themselves, spouses/partners of patients, as well as family members and friends of patients with Cystic Fibrosis.
Once a year our foundation will also participate in the annual "Adding Tomorrows" initiative with the Cystic Fibrosis Foundation to raise funds for Cystic Fibrosis research in an effort to bring us one step closer to a cure — a cure that will help thousands of affected families throughout the world. It is our sincere hope that all our friends and family help us launch this effort. If you or anyone you know would like to participate in a Great Strides Walk, Xtreme Hike, Cycle for Life or any other "Adding Tomorrows" fundraiser or if you are or someone you know is a mental health professional that may wish to donate your services, please let us know. Email us directly at donate@aebfoundation.org.
The Last Prophecy Gaming, Inc.


Home / News / PS3 update 4.82 out & should you update? NO!
The cat (worried about a new webkit exploit that leaked for the PS3) has only been out of the bag for a couple days now and Sony already pushing a new FW updated after a year later. Like normal, this firmware does not bring anything new to the system other than patching exploits, just like Sony says in the picture below.
So just like predicted by several people on twitter, this update will most likely patch one or more exploits that will probably be used for the announced 4.81 Hack by team PS3Xploit and proof-of-concept-wise used for this IDPS dumper too.
Thank you, idiot who leaked PS3 webkit exploit, Sony has now fixed it and put out a new PS3 firmware 4.82. This is why we can't have nice things.
Now nothing has been confirmed or denied yet whether there is anything more patched than the WebKit entry point BUT if you are looking forward to finally hacking/downgrading your PS3 the general rule applies… DO NOT UPDATE… ever, unless told to.
2) We have ran into a few issues concerning 300x and 4xxx consoles as far as writing to flash with lv0.2. These models will most likely require another exploit to take full advantage of CFW features like older consoles, and may not have full support upon release. These models may need the community to build upon our current work….this is not fully worked out yet and may be resolved. no promise on release date, but x-mas is a good goal for now.
So it seems the drama in the PS3 scene can and will never end but at least this quick update shows that Sony still cares about their PS3 system although it has reached their end-of-life cycle already!
Have a great day & stay tuned!
Previous Review: Perception for Switch with Dev Interview!
Next Kansas City Comic Con!


text:
Is Jordyn Woods Deliberately Hanging out with Khloe Kardashian's Exes?
Christina Montford
Friends, the drama in the Kardashian world never ceases. They do, after all, have a whole season of Keeping up with the Kardashians to fill.
It seems like at least one of them is always going through relationship issues. And since Kim Kardashian is happily married, Kendall Jenner is always off modeling, and Kourtney Kardashian is pretty much over men in general, the torch has to be carried by Khloe Kardashian and Kylie Jenner.
A post shared by Khloé (@khloekardashian) on Jul 22, 2019 at 5:43am PDT
Khloe's love life
Khloe has had a rough go of it when it comes to love. Throughout her younger years on KUWTK, we saw men cheat on her and treat her poorly. But then, she met basketball player Lamar Odom and it was love at first sight. The two wasted no time getting engaged and married.
On their show, Khloe & Lamar, everything seemed to be going well with the pair, but underneath it all, Odom struggled with drug addiction. The relationship ended when Odom's addiction got the best of him, causing him to cheat on Khloe and overdose in a brothel in Las Vegas.
Later, she began dating Tristan Thompson. The two also seemed to be in love. Together, they welcomed their first child, True Thompson, into the world. Unfortunately, just as Khloe was about to give birth, pictures of Thompson with other women hit the internet.
Khloe was eventually able to forgive Thompson for the sake of keeping their family together.
Bali 10.2018 #FBF
What happened with Thompson and Jordyn Woods?
Everyone who watches KUWTK knew that Kylie and Jordyn Woods were best friends. They even lived together. But, apparently, one night Woods was seen kissing Thompson at an afterparty.
This ended, not only Thompson and Khloe's relationship but Woods and Kylie's friendship as well.
What other man has Woods been hanging out with?
Before she met Thompson, Khloe dated basketball player James Harden. Woods was recently seen getting cozy with Harden at a bar.
"Khloe Kardashian is truly confused as to why Jordyn Woods was hanging out with James," a source close to the family told HollywoodLife. "Khloe feels Jordyn is hanging out with her exes deliberately to get a reaction out of her and truly doesn't care about her or her family's feelings. She does not believe she accidentally ran into him at all. To Khloe, this was not a coincidence. It's really disheartening and she wishes she would stop. She honestly thought after Tristan, she would never be seen with a Kardashian ex ever again and feels this is really a low blow and not cool."
don't worry bout fittin in when you're custom made ✨
A post shared by HEIR JORDYN (@jordynwoods) on Jul 23, 2019 at 7:05pm PDT
For Khloe, the first instance of betrayal was enough. But now hanging out with another one of her former flames is just too much.
"She just doesn't understand why Jordyn is doing this still and wishes she'd find someone not connected to the family to go hang out with," the source continued. "She knows Jordyn knows what she's doing, but why she'd go out of her way to be so hurtful, Khloe doesn't get."
Apparently, this hangout was the final blow for Kylie, who had hoped that she and her former friend could rekindle their friendship after time had passed.
"Kylie was so upset when she heard Jordyn was out with James Harden, so she decided to unfollow Jordyn on Instagram," the source said. "It was the final straw for her. She still followed Jordyn because she still had just a little bit of hope that with time, they could talk and try to rebuild something."