text:
Yule Heibel's Post Studio © 2003-2014
Articles published in FOCUS Magazine, Victoria, Canada
Action and-or talk-talk
August 31, 2003 at 10:08 am | In yulelogStories | 4 Comments
Both The River and Wood's Lot point to a couple of interesting Noam Chomsky links. One is on the Interactivist Info Exchange, in which, among other things, Chomsky addresses the following question: "When you talk about the role of intellectuals you say that the first duty is to concentrate on your own country. Could you explain this assertion?" The other is an article by Arundhati Roy in The Hindu, The loneliness of Noam Chomsky, which shines a light on what it means to cultivate awareness of how public opinion in "free market" democracies is manufactured just like any other mass market product. In the Interactivist article, Chomsky reiterates the argument that jargon-y, complex speech, which makes the ideas presented opaque and difficult for the non-specialized reader, is typical of power-critiquing theory produced by theorists who remain ensconced in power structures and institutions. Ok, let me simplify that sentence: if you have something critical to say, do so in a language that non-specialists can understand. If you do it a language that only post-graduate specialists within the ivory tower "get," you've cut yourself off from the base — the people — that might put your critique into action, and instead kept it at the level of theory-only, and you have thereby restricted your critique to an ivory tower ghetto. Ok? Foucault might be very complicated and have some interesting things to say, but if you have to study deconstructionist theory at the graduate level for 3 years before you get it, what exactly is being reinforced here? If you answered "the power of the institution which disseminates that specialised knowledge," you move to the head of the deconstructed class. "But, but, but….," you stammer, "But I want to be in the embrace of power so that I may feel powerful myself, because if I leave the institution, I am bereft of power…. I will be afraid…." Exactly. This is another one of Chomsky's points: too many people are afraid, and the feeling of fear — a subjective one — contributes to the objective growth of fascism in democracies where liberalized capital calls the tune. Here, listen: "People in the United States work really hard, much harder than any other advanced industrial society, and this causes a lot of stress. People are always concerned about their work and they live in fear. Although there is a lot of crime in the United States, it is approximately the same as comparable societies, but fear of crime is far higher. In many ways, this is the most frightened nation in the world!" Part of the fear (fear of losing your job, fear of being excluded, fear of poverty, fear of crime, fear of others) comes from economic insecurity, and from the disconnect we feel in the face of lost democracy. We all know, intuitively and concretely, that what Chomsky and others have called the virtual senate, that is, international organizations and treaties like the IMF, trade agreements, world banks, copyright laws, mass media, and so forth, that these virtual entities, unelected and not representative of any populace, permeate our lives as surely and perhaps even more exactingly than the laws made by the people we elected to serve us. A long time ago, the critique coursing through the institutions was "who may speak?" — to pose the question was an act of criticism that could actually lead to consequences. Women weren't allowed to speak, children weren't allowed to speak, minorities weren't allowed to speak: simply pointing out that this was a social construct, vs. a "natural" state of affairs, was to poke at power structures. But while speech has by and large been set free, action is increasingly restricted. Sure, let those others talk, but let's hope the hell they don't get to act — we're afraid they'll make a mess of it. Hence, keep the jargon; remember, the masses are revolting. I guess I'm pissed off because I read the Arundhati Roy article and I'm reminded of Adorno, who was an ivory tower jargon specialist par excellence, but who — along with Horkheimer & the rest of the Frankfurt School — had already nailed so much of this in the late 1930s and 40s when European fascism learned to throw its weight around. How can it be, I wonder, that we're at such a congruent turning point again? Here's Roy: "Today, thanks to Noam Chomsky and his fellow media analysts, it is almost axiomatic for thousands, possibly millions, of us that public opinion in 'free market' democracies is manufactured just like any other mass market product — soap, switches, or sliced bread. We know that while, legally and constitutionally, speech may be free, the space in which that freedom can be exercised has been snatched from us and auctioned to the highest bidders. Neoliberal capitalism isn't just about the accumulation of capital (for some). It's also about the accumulation of power (for some), the accumulation of freedom (for some). Conversely, for the rest of the world, the people who are excluded from neoliberalism's governing body, it's about the erosion of capital, the erosion of power, the erosion of freedom. In the 'free' market, free speech has become a commodity like everything else — justice, human rights, drinking water, clean air. It's available only to those who can afford it. And naturally, those who can afford it use free speech to manufacture the kind of product, confect the kind of public opinion, that best suits their purpose. (News they can use.)" Adorno and Horkheimer said pretty much the same thing 60 years ago. And then Adorno busily retreated into academia's ivory tower. He never did like the rabble who might implement his critique, and the rowdy students of '68 pretty much killed him (they, and all the female students who exposed him by exposing themselves at the infamous final lecture). Sometimes I think fascism has gotten much worse than it was. After all, we have technologies and pharmaceuticals today that allow us to alter our inner structure as radically as the outer. If my job, for example, is unreasonably stressful, if I'm killing myself trying to live up to the American dream of having it all (you know, career and kids, beautiful home, 24-hour shopping, work-out time, private time, friends time, quality time, fantastic sex, true love, success, success, success in measurable amounts, puh-lease because you sure don't want to be called a loser, which is the worst thing of all, because winning is even more important than telling the truth), and it's depressing me because my body is trying to stop me, well, hey, if that happens, I can, instead of retreating and reassessing, or becoming a functional drunk, or beating my kids (options previously available to the elites and the masses alike), I can take medication so I can keep going. Not because I'm mentally ill, but to quell the protest in my bones. That takes fascism to a whole new level, namely the level of the dream.
There's a sadly funny passage in one of Richard Feynmann's books where he describes being invited to a sociologist's conference. After listening to a few people drone on in jargon, he said "OK, so what you are saying is that people hang out with other people because they like each other."
Oh yes. That's right. Explication rattled off in jargon.
"So why don't you just say that?"
Oh….explanation rattled off in more jargon.
I think your take is right. Academics have seized a piece of the pie and God forbid that anyone discover that the things they talk about can be discussed by anybody in simple English!
I find it interesting that, in our own ways, we've pretty much talked about the same things these last twenty four hours and expressed similar concerns. Except I talk about how the "little people" of the web are out for their share of power and how threatened they are by people like me who say "Hey, just do!"
Comment by Joel — September 1, 2003 #
Incidentally, I am an authentic major depressive. Having lived in this state most of my life, I must agree with you that there are far more depressives than there should be.
Hi Joel, I'm glad that you're not offended by my suggestion that pharmaceutical intervention can be either overused or abused, because I know you're in the trenches and have an upclose and personal perspective. There's nothing I can say about mental illness that won't sound like a cliche, since the only thing I've ever experienced was fairly significant depression (in myself, which was alleviated by a lifestyle change). I had a mother who was pathologically depressed, who may have been manic at some point earlier — and who should have had a lifestyle change, or at least for my benefit (!!??) been given medication; but a lifestyle change would have worked similar wonders. I know people — friends — who need medication to stay safe. That's significant: if they're not safe, they might harm others. I won't talk about harming yourself, because that can take so many forms as to look "normal": have another drink, go on another shopping binge, scream & rage, the list goes on. Endless hits. Sometimes literally. That gets into harming others, of course. I knew a child who hated his parents (bad boy! bad-bad-bad-bad-bad boy!!!), and his parents, within a 15-minute first-time consultation with a psychiatrist, accepted a diagnosis of bipolar syndrome, and subsequently medicated their little boy into zombie status (seriously: it was terrible to see the change). They moved away and I don't know how things developed subsequently. But who can tell me whether that 8-year-old boy really was bipolar and needed his meds to keep the pathways from burning too deeply into his brain permanently, or whether his parents were overly controlling? Maybe they did the right thing, but for everyone of him, there are 20 who get Ritalin or something else like that to get them to shut the fuck up.
I'll go on record to say that I think medication gets overused to quell what could be protest. There's pressure to adapt, and sometimes (temporary) depression or mental illness is a symptom to say, "this is bullshit. This isn't worth adapting to." And if medication is given at this point to help in the "adaptation," there's a problem. The point is, I suppose, that it's a really tough call, and has to be worked out on a case-by-case individual basis.
As to Feynman, he's the best, isn't he? Cuts through the crap, zoom!
Now, I've just gone online for the first time in 24 hours, so I must check out your blog and read about the little people. (I always think of fairies, elves, and the like, but that's a different story….)
Comment by Yule Heibel — September 2, 2003 #
Traveling Wilburies
Comment by Traveling Europe — October 28, 2005 #
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Diana Cowie a Senior Heritage Consultant, holds a Bachelor of Arts with First Class Honours, majoring in archaeology and palaeoanthropology from the University of New England. Diana has worked on a broad range of projects of varying scales across Australia and beyond.
Diana Cowie is an archaeologist with expertise in the identification and assessment of Indigenous heritage and historical sites, both in Australia and abroad. Diana has experience in a highly professional consulting company undertaking a range of projects and dealing complex heritage issues.
Diana is skilled in the preparation of heritage studies, interpretation plans, historical and Aboriginal archaeological assessments, research designs and excavation reports. Diana has experience in historical research, social values analysis, landscape, and curtilage assessment. Her expertise in site recording, mapping and GIS have been further enhanced through involvement in international projects in Jordan, Cambodia and Turkey. Diana is highly skilled in directing Aboriginal archaeological excavations, undertaking community consultation, preparing Aboriginal plans of management, post-excavation analysis, cataloguing, research and archiving. She is also well versed in state and federal heritage legislation; including best practice policies and guidelines.
Diana has been involved in built heritage assessments, interpretation, comparison, and conservation studies. She also has an understanding of movable heritage assessment, museum collection management and exhibition development.
Diana has successfully forged excellent working relationships with Aboriginal communities, clients and other heritage stakeholders in the many local consultative projects she has been involved in.
Refer to Diana's CV and/or LinkedIn Profile for an interesting and helpful array of key experience examples.
Owen, T.D. and Cowie, D.R. 2015, Stories from Kaurna, GML Heritage, Sydney.
Cowie, DR 'Federated Archaeological Information Management System (FAIMS): A Report on a New User's Field Experience,' Australian Archaeological Association and Australasian Society for Historical Archaeology Conference, Cairns, 2014.


text:
Alice Dreger
Bioethicist; Author; Historian
East Lansing, MI, USA
Business Growth, Business Leaders, Communication, Communication Speakers, Futurists, Innovation, Inspirational Speakers, Internet, Leadership Speakers, Sales, Marketing and Branding, Science and Technology, Women's Issues, Writers and Journalists
Alice Dreger Biography
Alice Dreger is a writer, historian, and journalist, and most of her work centers on the epistemology of democracy. She is always working to find out what's true in the hope that it will lead people to treat each other better. She is the inaugural winner of the Courage Award from the Heterodox Academy, and has also won awards for research, writing, teaching and public service.
Dreger's bylines include the New York Times, Washington Post, Wall Street Journal, The Guardian, WIRED, Slate, the Atlantic, Pacific Standard, Aeon Magazine, the Chronicle of Higher Education, New Statesman, the Los Angeles Times, and the Chicago Tribune. Her best known book is "Galileo's Middle Finger: Heretics, Activists, and One Scholar's Search for Justice," which argues that the pursuit of evidence is the most important ethical imperative of our time. Funded by a Guggenheim Fellowship and published by Penguin Press, the book has been praised in reviews in The New Yorker, Nature, Science, Forbes, New York Magazine, Human Nature, and Salon.
Dreger's work is often aimed at getting past partisan politics. She I earned my Ph.D. in History and Philosophy of Science from Indiana University, and is a recipient of an Outstanding Leadership Award in Comprehensive Sexuality Education from SIECUS, Planned Parenthood, Advocates for Youth, GLSEN (the Gay, Lesbian, Straight Education Network), and the Healthy Teen Network.
Dreger frequently delivers keynotes and plenaries, and to date has given about 200 invited lectures. Her TEDx lecture, Is Anatomy Destiny, has been viewed over a million times, and she have appeared as a guest expert on media programs such as Oprah, Savage Love, Good Morning America, and NPR, and in many original documentaries, including for A&E, ABC, Discovery, PBS, and HBO.
Contact a speaker booking agent to check availability on Alice Dreger and other top speakers and celebrities.
The problem with moral outrage on the internet | Alice Dreger
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Fall Symposium Day 2016: Alice Dreger
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Galileo's Middle Finger: Heretics, Activists, and One Scholar's Search for Justice
Galileo's Middle Finger: Why Social Progress Depends on the Protection of Academic Freedom
This talk draws from the speaker's new book, Galileo's Middle Finger: Heretics, Activists, and the Search for Justice in Science, and explores the ways in which freedom of research is under assault from multiple fronts, including identity politics activism, the corporatization and branding of universities, and social media shaming campaigns. The speaker, who has twenty years' experience both as an intersex patient rights activist and as an academic historian, will use case studies to talk about the dangers researchers face today. She will also speak to how researchers can work individually and collectively to try to protect themselves. She argues they must do so not for their own sake, but for the sake of social progress in our fragile democracy.
Good Causes, Bad Acts: Scrutinizing Ends and Means in Medical Activism
This talk draws from the speaker's new book, Galileo's Middle Finger: Heretics, Activists, and the Search for Justice in Science, and focuses on cases where progressive activists have used problematic means to go after researchers whose findings they believed harmful to their identities or beliefs. It explores an important dimension sometimes ignored in today's discussions of academic freedom.
Reasons to Add—and Reasons NOT to add—an "I" to LGBTQ in Health Care
Some well-meaning people have moved to add 'I' (for intersex) to LGBTQ in health care conversations and settings. This talk explores the reasons for and benefits of such a move, and also the potential harms to patients and points of troubling confusion that may arise from it. The speaker draws on her twenty years of work in the intersex patient rights movement and also from collaborations with pediatricians who treat children born with less typical forms of sex development.
Should We Try to Engineer Physical "Normality" in Children?
Doctors are often quick to offer "normalizing" interventions when a child has a body that challenges social norms. Surgeons offer their services to "fix" children born with atypical genitals and to separate children born conjoined. Endocrinologists offer growth hormone to healthy children who are short. What's wrong with that kind of approach? This lecture answers that question and will suggest that what would work better is attention to outcomes data (to know what really "works" for these children) and attempts at changing society. The speaker draws on her background as an historian of medicine and patient advocate.
Who Should Count as a Woman on the Playing Field? The Question of Intersex and Trans in Sports
This talk begins with a review of how many sports have historically been divided by gender (man/woman), although we've generally pretended the division is by sex (male/female). The more that we learn about gender and sex, the more we know the drawing sex and gender divisions is not so easy. So what should happen in sports? This lecture explores this question, taking into account biology, the nature of sport (including the value of fairness), and social justice concerns. The speaker, who has consulted on this question with the International Olympic Committee's Medical Commission, will parse out the issues and offer a few possible solutions.
'Galileo's Middle Finger,' by Alice Dreger - The New York Times
"Galileo's Middle Finger" is many things: a rant, a manifesto, a treasury of evocative new terms (sissyphobia, autogynephilia, phall-o-meter) and an account of ...
The Big Problem With Outlawing Gender Conversion Therapies ...
Can we respect the expressions of gender-crossing children without being so " affirming" of their declarations that we accidentally steer them to a transgender ...
HOW TO BOOK Alice Dreger?
Our booking agents have successfully helped clients around the world secure talent like Alice Dreger for speaking engagements, personal appearances, product endorsements, or corporate entertainment for over 15 years. The team at All American Entertainment represents and listens to the needs of organizations and corporations seeking to hire keynote speakers, celebrities or entertainers. Fill out a booking request form for Alice Dreger, or call our office at 1.800.698.2536 to discuss your upcoming event. One of our experienced agents will be happy to help you get pricing information and check availability for Alice Dreger or any other celebrity of your choice.
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Booking fees for Alice Dreger, or any other speakers and celebrities, are determined based on a number of factors and may change without notice. Pricing often varies according to the circumstances, including the talent's schedule, market conditions, length of presentation, and the location of the event. Speaker fees listed on this website are intended to serve as a guideline only. In some cases, the actual quote may be above or below the stated range. For the most current fee to hire Alice Dreger, please fill out the booking request form or call our office at 1.800.698.2536 to speak with an experienced booking agent.
WHO IS THE AGENT FOR Alice Dreger?
All American Entertainment has successfully secured celebrity talent like Alice Dreger for clients worldwide for more than 15 years. As a full-service talent booking agency, we have access to virtually any speaker or celebrity in the world. Our agents are happy and able to submit an offer to the speaker or celebrity of your choice, letting you benefit from our reputation and long-standing relationships in the industry. Fill out the booking request form or call our office at 1.800.698.2536, and one of our agents will assist you to book Alice Dreger for your next private or corporate function.
All American Speakers is a "buyers agent" and exclusively represents talent buyers, meeting planners and event professionals, who are looking to secure celebrities and speakers for personal appearances, speaking engagements, corporate entertainment, public relations campaigns, commercials, or endorsements. We do not exclusively represent Alice Dreger or claim ourselves as the exclusive booking agency, business manager, publicist, speakers bureau or management for Alice Dreger or any other speaker or celebrity on this website. For more information on how we work and what makes us unique, please read the AAE Advantage.
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Alice Dreger Videos
"A big problem with moral outrage on the Internet is that it leads people to think they've done something when in fact they haven't done...
Alice Dreger, history of medicine and science, delivers her address, "Galileo's Middle Finger: Why Social Progress Depends on the Protection of...
Listen to the full podcast at: http://sotospeakpodcast.com Follow us on Twitter: http://twitter.com/freespeechtalk Like us on Facebook:...
Alice Dreger Books
Speaker Lists Featuring Alice Dreger
Female Pioneers in STEM: Science, Technology, Engineering, and Mathematics
The number of female scientists and engineers is growing each day. These female motivational speakers have made significant footprints in the fields of STEM and inspire young girls and women to take an interest in science,...
Alice Dreger Speaking Topics
FAQs on booking Alice Dreger
Alice Dreger is a keynote speaker and industry expert who speaks on a wide range of topics . The estimated speaking fee range to book Alice Dreger for your event is $5,000 - $10,000. Alice Dreger generally travels from East Lansing, MI, USA and can be booked for (private) corporate events, personal appearances, keynote speeches, or other performances. Similar motivational celebrity speakers are Laura Snyder, Edward Tenner, Dr. Shini Somara, Joanna Bloor and Susan Solomon. Contact All American Speakers for ratings, reviews, videos and information on scheduling Alice Dreger for an upcoming event.
Alice Dreger Speaker Videos
"A big problem with moral outrage on the Internet is that it leads people to think they've done something when in fact they haven't done something," says author Alice Dreger. Sure, you might get...
Alice Dreger, history of medicine and science, delivers her address, "Galileo's Middle Finger: Why Social Progress Depends on the Protection of Academic Freedom" at the Fall Symposium Day on Sept....
Listen to the full podcast at: http://sotospeakpodcast.com Follow us on Twitter: http://twitter.com/freespeechtalk Like us on Facebook: http://facebook.com/sotospeakpodcast Email us:...
"Galileo's Middle Finger: Why Social Progress Depends on the Protection of Academic Freedom" Dr. Alice Dreger spoke about her new book Galileo's Middle Finger: Heretics, Activists, and the Search...
http://www.ted.com Alice Dreger works with people at the edge of anatomy, such as conjoined twins and intersexed people. In her observation, it's often a fuzzy line between male and female, among...
Alice Dreger News
Provide you with the speaking fee to book Alice Dreger or other celebrity appearance fees
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redpajama_set_name: RedPajamaCommonCrawl


text:
package io.jenkins.blueocean.blueocean_github_pipeline;

import com.cloudbees.plugins.credentials.common.StandardUsernamePasswordCredentials;
import io.jenkins.blueocean.rest.hal.Link;
import io.jenkins.blueocean.rest.impl.pipeline.scm.Scm;
import io.jenkins.blueocean.rest.impl.pipeline.scm.ScmRepositoryContainer;
import org.kohsuke.github.GHOrganization;

/**
 * @author Vivek Pandey
 */
public class GithubOrganization extends AbstractGithubOrganization {

    private final GHOrganization ghOrganization;
    private final Link self;
    private final StandardUsernamePasswordCredentials credential;
    private final Scm scm;

    public GithubOrganization(Scm scm, GHOrganization ghOrganization, StandardUsernamePasswordCredentials credential, Link parent) {
        this.scm = scm;
        this.ghOrganization = ghOrganization;
        this.credential = credential;
        this.self = parent.rel(ghOrganization.getLogin());
    }

    @Override
    public String getName() {
        return ghOrganization.getLogin();
    }

    @Override
    public String getAvatar() {
        return getAvatarWithSize(ghOrganization.getAvatarUrl());
    }

    @Override
    public ScmRepositoryContainer getRepositories() {
        return new GithubRespositoryContainer(scm, ghOrganization.getUrl().toString(), getName(), credential,this);
    }

    @Override
    public Link getLink() {
        return self;
    }

}

redpajama_set_name: RedPajamaGithub


Now that it is officially Spring, Off The Shoulder tops are a must have! This blush pink ruffle OTS Top is seriously the cutest. It also comes in a mustard yellow color (which I love!) and even looks cute with a pair of shorts and some wedges.


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ISS retains all copyrights for the Serbian standards and related documents, in accordance with the law that prescribes copyright and related rights.
Reproduction in whole or in part, as well as the distribution of Serbian standards and related documents are only permitted with the consent of ISS.


text:
set work work
vlib work

# compile all of the files
vcom -work work ../../implement/results/routed.vhd
vcom -work work clkGen_tb.vhd

# run the simulation
vsim -c -t ps +transport_int_delays -voptargs="+acc" -L secureip -L simprim -sdfmax clkGen_tb/dut=../../implement/results/routed.sdf +no_notifier work.clkGen_tb


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Why does it always take away gas and how does it go?
Our today topic is how to cure gastric problem permanently?We will talk about how to cure gastric problem permanently? We will share the solution of how to cure gastric problem permanently?Excessive gas can be a condition related to the food we eat or swallow. Sometimes medication may be necessary, but changing the diet will provide adequate efficacy for most cases.
Why Does It Take to Remove Gas?
To chew on items such as pencils, sticks, pipettes, etc.
Too much gas can be caused by undigested carbohydrates. As a result of the bacterial degradation of these carbohydrates, gases such as hydrogen, carbon dioxide, methane come out.
How to Remove Gas Continuously?
Food containing indigestible carbohydrates can be reduced.
Artificial sweeteners should be avoided.
Consumption of acidic beverages should be restricted.
Instead of three meals a day, six portions of reduced meals can benefit. After you have chewed plenty of greenery, you swallow it.
However, since each person's digestive metabolism is different, these foods can cause farts in some people too. You can keep a note of your influence for follow up.
Coal Tablets: These drugs absorb gas in the digestive system and will prevent much gas from escaping. But they can reduce the effectiveness of another medicine. Consult your pharmacy before use.
Simetikon: It is another drug that solves gas problems. It can be recommended especially in the treatment of bloating.
Probiotic Drugs: The beneficial bacteria in the digestive system can increase the population and prevent the release of many gases. Especially if sensitive bowel syndrome is the case, it can be very helpful.
Alpha Galactosidase (Beano): It is a food supplements that relieve digestion.
It has also been proven that ginger or mint tea consumed in small quantities is also good for the problem of gas extraction.
Healthy LifeStyle ayurvedic home remedies for gastric problem, how to cure acidity and gastric problem, how to cure acidity permanently naturally, how to cure gas problem immediately, how to cure gastric problem naturally, how to cure gastric problem permanently. permalink.
What to Eat to Drink the Oils in the Abdominal Zone?


text:
Q: git clone - fail instead of prompting for credentials When cloning git repositories in automated tools - web front ends, CI systems, sometimes the git clone invocation opens up a prompt asking for the username and password (for example, when cloning a non-existent Github repo or on a new node missing ssh keys).
How do I make git just fail (preferably with a sensible error message and exit code) instead of waiting for the server process to give it a username and password?

A: In git version 2.3 there's an environment variable GIT_TERMINAL_PROMPT which when set to 0 will disable prompting for credentials.
You can get more info about it in man git (after updating to git version 2.3) or in this blog post on github.
Examples:

*

*git clone https://github.com/some/non-existing-repo will prompt for username & password

*GIT_TERMINAL_PROMPT=0 git clone https://github.com/some/non-existing-repo will fail without prompting for username & password

A: If you are using ssh authentication, and on linux, then you can create an ssh command replacement to disable this.
Create a file called "sshnoprompt.sh" with:
ssh -oBatchMode=yes $@
Make this file executable with chmod +x sshnoprompt.sh
Then when starting git:
GIT_SSH="sshnoprompt.sh" git clone foo@dummyserver:not_a_repo
And it will not allow any interactive git prompts or questions - it shouldn't be able to ask the user for anything.

A: How to skip, ignore and/or reject git credentials prompts
The answers above only worked partly for me when using Git-for-Windows: two different applications there were vying for my attention from the automated git pull/push scripts:

*

*git-credentials-manager (developed by the GfW team AFAICT; has a clean, grey Windows interface look)

*another dialog, which' ancestry has some definitely (crappy looking) X-Windows genes.

To shut all of them up, without uninstalling the credentials manager as mentioned in some answers here: https://stackoverflow.com/questions/37182847/how-do-i-disable-git-credential-manager-for-windows, here's what now works, sitting on top of the automated (bash) shell scripts:
# https://serverfault.com/questions/544156/git-clone-fail-instead-of-prompting-for-credentials
export GIT_TERMINAL_PROMPT=0
# next env var doesn't help...
export GIT_SSH_COMMAND='ssh -oBatchMode=yes'
# these should shut up git asking, but only partly: the X-windows-like dialog doesn't pop up no more, but ...
export GIT_ASKPASS=echo
export SSH_ASKPASS=echo
# We needed to find *THIS* to shut up the bloody git-for-windows credential manager:
# https://stackoverflow.com/questions/37182847/how-do-i-disable-git-credential-manager-for-windows#answer-45513654
export GCM_INTERACTIVE=never

What did NOT work

*

*All the incantations of git config credential.modalprompt false -- mentioned as a solution in answers to that linked SO question. no dice for me.

*fiddling with that GIT_SSH_COMMAND environment variable: nothing worked but keeping it as I suspect it'll kick in when running this stuff on a Linux box instead of Windows.

*GIT_TERMINAL_PROMPT=0: no worky either. Kept it in for the same reason, but no dice on Windows.

Oh, and uninstalling the git credentials manager as suggested in other answers in that SO link was decided a no go option as it would definitely impact other repository trees where this thing may be useful one day. Though it was considered for a bit, before I decided against doing this.
What DID work

*

*messing with those two *_ASKPASS env.vars., oddly enough shut up the 'X-Windows looking' login prompt on (automated) git push. Yay!

*GCM_INTERACTIVE=never was the magic ingredient to finally shut up that git-for-windows credential manager dialog. Thanks to that particular answer (https://stackoverflow.com/questions/37182847/how-do-i-disable-git-credential-manager-for-windows#answer-45513654), which isn't near the top of the list, but definitely was the most important one for my case.

My git version
$ git --version
git version 2.30.1.windows.1

Parting note
<rant> Been looking for this info on-and-off for years: this time apparently I was lucky and maybe persevered longer(?), wading through the zillion pages yakking about setting up your credentials: google clearly is not intelligent. At least it does not listen very well to minority questions, that's for sure. </rant>
The title is added in hopes that google indexing places this page higher for the next one looking for answers to these questions or variations therefor...

A: GIT_TERMINAL_PROMPT=0 git clone https://github.com/some/non-existing-repo

Work for me on Mac.

A: Working from git version 1.8.3.1;
git clone -c core.askPass $echo url/or/path/to/git/repo
The configuration core.askPass works by passing the control of handling credentials to the aforementioned program. However since $echo cant do anything except output, the clone attempt promptly fails and respective bash redirection applies. This code is only invoked in the event that the git repository happens to be private, and will pipe error output stating that authentication failed for the particular repository. You can test this against the https://github.com/git/git public repository against a private repository you know about.
To sweeten the deal, you wouldn't even need to reference a program like echo in the first place. Simply passing git configuration -c core.askPass with no following input would still cause failure in the event the repository happens to be private as the code will not know what program to offload credential handling to. While this is certainly an older and simpler method than the others mentioned here, I do not know if it will have the same effect in older versions of git.

A: When you only have control over the git configuration:
git config --global credential.helper '!f() { echo quit=1; }; f'

Gives
$ git clone https://github.com/edx/drf-extensions.git/
Cloning into 'drf-extensions'...
fatal: credential helper '!f() { echo quit=1; }; f' told us to quit

The idea comes from the original committer of GIT_TERMINAL_PROMPT after following @user243345's link.

A: Depending on how you're running git, redirecting stdin or stdout so that they are not connected to terminals will stop git from prompting for details and just cause it to error.
This would also allow you to surface errors (or at least logs) to the webservice.

redpajama_set_name: RedPajamaStackExchange


It is important to know that it can do anything with the user interface, it doesn't care about the model or database. It was designed from the ground up to be incrementally adoptable. This makes it very easy to integrate into an existing project. At the same time, it is strong enough to build powerful single page applications.
When compared to other frameworks, vue.js has its own pros and cons. The main advantage is that it is very light weight and easy to use. vue.js doses score higher in some benchmarks when comes to performance. vue.js offers us to build reactive interfaces. It also provides a large set of directives. Data binding, template logic, event handling and much more.
In this post, we present you some useful vue.js frameworks to help you build your applications much faster.


text:
ACCEPTED

#### According to
The Catalogue of Life, 3rd January 2011

#### Published in
Révis. gramin. 1:369, t. 98. 1830

#### Original name
null

### Remarks
null


text:
Hong Kong 7s: @Eagles7s Analysis, Tournament Picks
April 7, 2016 Junoir Blaber 7s, Junoir Blaber, Men's 7s, USA, USA Rugby Men's Eagles 0
HONG KONG, CHINA – The World Rugby HSBC 7s rolls into the island city of Hong Kong. Hong Kong has a very unique place in 7s lore. Though Scotland is the birthplace of rugby, Hong Kong is remains the most glorious of all the 7s tournaments. Long before the 7s series became a circuit, this was the 7s tournament that captured the world's attention. The way the tournament engrossed all of Hong Kong, it awed so many on-lookers and made cities want to have a circuit so they could have a stop on it, hoping they could create a party just like the one in Hongers. This year, Hong Kong will be the 7th leg in the extended 10 city tour series.
The USA's showing in the last tournament in Vancouver was very positive. The side dealt with key players unable for selection due to injury and managed to finish sixth. The Eagles were missing 4 regulars including 3 tour veterans that normally are crucial to success in big time playmaker Maka Unufe, Sevens Dream Team member Zach Test and the fastest man in rugby, Carlin Isles as well as developing talent Will Holder. The USA has not been able to get over the hump and regularly defeat top sides but they are consistently winning games against everyone else and they are doing it by executing the basics. USA 7s Head Coach Mike Friday said "We need to improve accuracy and consistency together with maintaining the standards we expect from all that are a part of this environment." The hope is that Friday's Charges can keep it going.
Let's look at the 3 key issues going into this tournament:
Team changes (+/-): There are 4 changes to the USA squad from Vancouver. Pat Blair, Seth Halliman, Ben Leatigaga, and Thretton Palamo failed to make the cut. In come two stalwarts in Test and Unufe. After becoming an Eagles 7s player while still in college, Peter Tiberio has been on the outside looking in for the past couple of years. He has been working hard on his fitness, adding weight and after captaining the Falcons (Eagles 7s B-side) team in Las Vegas, he has made the squad for the Asian swing. Isles was expected to be back with the team this week and traveled to Hong Kong. However in the final pre-tournament warm-up he suffered a knock that made him unavailable for the tournament. In steps Nate Ebner, who was in Hong Kong playing the GFI 10s as he works his way back to Rugby and a shot at Rio.
Chemistry: Coach Friday has been a big proponent of guys competing for spots. But after having to make 4 injury forced changes and receiving a solid performance maybe two would have been best this round. Anytime you make so many changes timing, handling and trust and all the little things that matter become an issue. And it is these little things that often make the difference between winning and losing.
Getting over the hump: At some point, the USA will have to knock off at least one of the top 4 teams to get a into the Cup or win it. You have to run with the big dogs at some point or else the view never changes. So in the Cup round the USA will have to put together a perfect performance and make a cup final or accept 4th place as the best they can do.
Optimist's View: With some of the momentum from Vancouver and returned stars the USA finish fourth.
Cynic's View: The Eagles show their ability and talent but still can't get over the hump and lose in the Plate final.
My View: It is easy to want to believe the optimist but I just don't see it. They will take the Plate but that is about as positive as I can be.
HONG KONG 7s:
It is shaping up to be an interesting round. Fiji, have taken the lead but are still being pursued by South Africa and New Zealand. There are still sides like Australia, England and the USA that are not out of it and are putting pressure on top 3 in every tournament. This continues to be the most open series ever.
Here are our pool previews:
Pool A:
This is easily the toughest group to predict. New Zealand is pure class and should have no problem topping this group. The challenge begins in picking who finishes second and continues to the Cup round. Kenya has been improving so you want to believe they will take second while Samoa are notoriously slow starters so them finishing third is believable and France started the series well but faded after losing Virimi Vakatawa to the 15s team. However he is back so they are unpredictable but their recent struggles mean they are projected to finish last.
Pool B:
I can confidently predict that South Africa will win this group. It may take them pulling away late in matches but they will win. England have been in a horrendous run of form and if it was not for the large English ex-pat presence to help lift the team, they would be predicted to finish third. We predict that Scotland, with their own ex-pats in attendance, will also play well but be nipped to second. Despite Russia's improvements they are in a tough group and finishes fourth is the most likely result.
Hong Kong Fans know how to party
Pool C:
Australia will win this group though they will face a stern challenge from the USA. An always dangerous Argentina are going to give both the top two sides a quality workout. Despite how much we truly like Portugal they will unfortunately be bringing up the rear.
Pool D:
Fiji are head and shoulders above all the other pool members so they will take first. Coming in second will be Canada who will be eager to top Wales and return the favor after losing out on the Cup playoffs in Vancouver to Wales courtesy of points difference and a try at the death in their head to head. Wales will finish third and South Korea will be merely canon fodder in this group.
2014-2015 Qualifier Winner – Russia
2015 – 2016 Core Team Qualifier Tournament
These next three pools are important because these 12 teams will play to be one of the regulars on the circuit for the 2016-16 season. Russia, as I predicted, were promoted to core team status as they were the winners of the qualifier last year, in Hong Kong. Japan were relegated and lost their status as a core team for the 2015–16 season since they finished last in the 2014-15 season. The qualifier will have 12 teams, winners of regional qualifiers (2 from each continental area union) that will battle for the one promotion place on offer. So here is a look at the twelve teams and how we think each pool will finish.
Pool E:
Hong Kong will be at home and you would think that, that will be more than enough to carry them through. However, Zimbabwe fell just short of winning the whole thing last year and they seem to be hungrier this year. Germany will have some of it 15s players back but it just seems hard to fathom them doing better than third. Cayman Islands, well thanks for showing up and here is your parting gift, fourth place in this pool.
Pool F:
Zimbabwe 7s: Now is the time for the Cheetahs
You want to say that Spain should top this group because they were a core team very recently. However, Papua New Guinea had a good run last year and if they don't win this win this pool they will be very formidable in the knock-out stages. Chile is having its troubles on the field and off the field in terms of administration and stuff so finishing third here would be par for the course. Mexico is getting better each year but they are still far from relevant in a tournament like this so last place seems apropos.
Pool G:
Japan are looking to become a core nation again and are well ahead of most of the other non-core nations in this qualifier. They will cruise by in this group. After seeing the Brazil backline play in the ARC, it is easy to believe than can finish second in this group. Tonga were one of our sides to watch in the Southern Hemisphere in 2015 but still can't seem to get their act together. They have achieved so much on the 15s stage that you have to figure their 7s program will catch-up sooner or later but that doesn't look like the case. Morocco will be able to play a physical game but their skills in space will let them down and they will finish fourth in this group.
A live stream will be provided to viewers who want to watch the action on World Rugby's website. And now, here are our predictions for playoffs and the team that wins promotion to core status will be.
Cup: Fiji
Second: New Zealand
Third: South Africa
Plate:USA
Bowl: Scotland
Shield: France
Promotion: Zimbabwe
That is it for now. Feel free to comment below, look for and "Like" our Facebook Rugby Wrap Up Page and follow us on Twitter@: RugbyWrapUp, Junoir Blaber, James Harrington, Jamie Wall, Nick Hall, DJ Eberle, Jake Frechette, Scheenagh Harrington, Ronan Nelson, Kyle Phillips and Declan Yeats, respectively
All Black 7s
Canada 7s
Dubai 7s
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Mike Friday
Sevens World Series
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It's on! Nate Ebner Called Into USA 7s Hong Kong Squad
Kerr-Barlow, Worcester, NG Dragons, Cuthbert, USA Rugby and World Rugby News
#LA7s Prep Day
The Rugby Odds: MLR Conference Finals, Layfield's Cheap Shots, Flap Jackals, Egbelu v Seawolf Rucky
MLR Weekly: Old Glory DC New Head Coach Josh Syms & Rugby Morning's Major League Rugby Headlines
MLR Weekly: Tel Aviv Heat CEO Pete Sickle, Memphis Inner City's Devin O'Brien, Nick Rowe & 9/11


text:
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Soft tissue sarcomas (STS) are a rare group of heterogeneous malignancies with >50 histologic subtypes that have varying biological behaviour and responsiveness to systemic therapy. The mainstay of therapy for metastatic STS in recent decades has been doxorubicin. To improve survival outcomes, numerous agents have been combined with doxorubicin; however, no combination has led to a survival benefit over doxorubicin alone until the recent use of olaratumab, a monoclonal antibody targeting platelet-derived growth factor-α. In addition to olaratumab, several other new drugs have surfaced as promising treatment options. Marine-derived chemotherapy agents, eribulin and trabectedin, are active in selecting STS subtypes. Both agents are effective in liposarcoma, while trabectedin also has activity in leiomyosarcoma. Further understanding of the importance of STS subtype-directed therapy, as well as the genomic complexities of STS, has led to development of several small molecule inhibitors for specific STS histologies. Agents targeting vascular endothelial growth factors, platelet-derived growth factors, and cyclin-dependent kinases 4 and 6 have all shown some efficacy in various STS subtypes. Similar to the selective activity of cytotoxic agents and small molecule inhibitors, immunotherapy, which has revolutionised management of numerous cancers, has also demonstrated activity in select STS subtypes. Collectively, these novel therapies highlight the importance of histology-directed approaches and of a greater understanding of the genomic landscape of STS. This review describes advances in chemotherapy, molecularly targeted, and immunotherapy agents for STS.
Soft tissue sarcomas (STS) are a rare group of heterogeneous malignancies with >50 histologic subtypes that have varying biological behaviour and responsiveness to systemic therapy. Doxorubicin has been the mainstay of treatment in numerous subtypes of metastatic STS for decades, achieving response rates (RR) of 12–29% and average life expectancies of 12–18 months (Table 1).1-7 Until recently, numerous agents have been combined with doxorubicin with limited benefit. Olaratumab, a fully human IgG1 monoclonal antibody that targets platelet-derived growth factor receptor (PDGFR)-α, combined with doxorubicin resulted in a near doubling of overall survival (OS) compared with doxorubicin alone.4 Aside from doxorubicin-based regimens, novel chemotherapy agents, eribulin and trabectedin, have demonstrated efficacy in the L-sarcomas, liposarcoma (LPS), and leiomyosarcoma (LMS), highlighting the role of histology-directed therapy for these malignancies.
Table 1: Chemotherapy studies in advanced soft tissue sarcoma.
LMS: leiomyosarcoma; LPS: liposarcoma; OS: overall survival; PFS: progression-free survival; RR: response rate; STS: soft tissue sarcoma.
Further understanding of the importance of subtype-directed therapy and the genomic complexities of STS has led to the development of small molecule inhibitors for certain STS histologies (Table 2).8-13 Tyrosine kinase inhibitors (TKI) (imatinib, sunitinib, and regorafenib) have dramatically changed the treatment landscape and outcomes for gastrointestinal stromal tumour (GIST), one of the most common STS subtypes.14-16 Imatinib, cediranib, and pexidartinib have also demonstrated activity in some of the rarest, chemo-refractory STS subtypes, including dermatofibrosarcoma protuberans,17,18 alveolar soft part sarcoma (ASPS),19 and tenosynovial giant cell tumour.20,21 The increased efficacy of these agents is due to the complex STS genomic landscape, including alterations to KIT, PDGFR-β, vascular endothelial growth factor receptors (VEGFR), and colony stimulating factor-1. Other more common STS also demonstrate potentially targetable aberrations in VEGFR, PDGFR-α and β, and cyclin-dependent kinases (CDK), suggesting a need for study of additional targeted therapies.
Table 2: Targeted agents in soft tissue sarcoma.
DDLPS: dedifferentiated liposarcoma; LMS: leiomyosarcoma; LPS: liposarcoma; NR: not reported; OS: overall survival; PFS: progression-free survival; RR: response rate; SS: synovial sarcoma; STS: soft tissue sarcoma; WDLPS: well-differentiated liposarcoma.
Similar to the selective activity of cytotoxic agents and small molecule inhibitors, immunotherapy, which has revolutionised the management of numerous cancers, has also demonstrated activity in select STS subtypes. Immunotherapy trials have shown activity in undifferentiated pleomorphic sarcoma (UPS) and LPS (Table 3).22-25 Factors such as tumour microenvironment, tumour mutational burden, and the transcriptome have been associated with response to immunotherapy; however, the data for these factors in STS are limited.26,27 Correlative work to understand the relevant factors for predicting response in STS is ongoing. Numerous studies, including combinations of immunotherapy agents or immunotherapy combined with radiotherapy and/or chemotherapy, are also in progress.
Table 3: Immunotherapy studies in sarcoma.
AS: angiosarcoma; ASPS: alveolar soft part sarcoma; bid: twice daily; CS: chondrosarcoma; GIST: gastrointestinal stromal tumour; LMS: leiomyosarcoma; LPS: liposarcoma; MFS: myxofibrosarcoma; NR: not reported; NYR: not yet reached; OS: overall survival; OST: osteosarcoma; PFS: progression-free survival; q: every; qow: every other week; RR: response rate; SFT: solitary fibrous tumour; STS: soft tissue sarcoma; UPS: undifferentiated pleomorphic sarcoma; wk: week.
As in other cancers, the understanding of the genomic complexity of STS has expanded over the past decade and spurred development of novel agents. The treatment paradigm for STS has shifted from treating all subtypes similarly towards a more histology-directed approach. In this review, the authors summarise recent developments in the treatment of non-GIST STS, as well as ongoing studies within the realms of chemotherapy, targeted therapies, and immunotherapy.
Doxorubicin has been the backbone of treatment for advanced STS for >40 years. The addition of ifosfamide (and its analogues evofosfamide and palifosfamide) and dacarbazine has resulted in improved RR but lacked a significant survival benefit and with increased toxicities.1,3,28-30 Olaratumab, a monoclonal antibody that targets PDGFR-α, was the first agent to be combined with doxorubicin and demonstrated an OS benefit in patients with metastatic STS. Olaratumab targets PDGFR-α by blocking the binding of PDGF ligands and preventing receptor activation. PDGFR-α is overexpressed in some STS subtypes31,32 and preclinical work in LMS cell lines has demonstrated antitumour efficacy,33 providing rationale for investigation in STS patients. A Phase I/II study4 enrolled varied STS subtype patients and randomised them 1:1 to doxorubicin with olaratumab versus doxorubicin alone. The progression-free survival (PFS) was 4.1 months and 6.6 months in the monotherapy and combination arms, respectively (p=0.0615), and the OS nearly doubled following combination therapy (26.5 months compared with 14.7 months with doxorubicin alone [p=0.0003]). The reason for the survival improvement with olaratumab remains unclear and preliminary analysis of the PDGFR-α expression status suggested no association with outcomes. Further investigation of the mechanism of action of olaratumab is needed to understand how the drug alters the tumour microenvironment and potentially improves the efficacy of doxorubicin. Olaratumab–doxorubicin combination therapy increased rates of neutropenia (58% versus 35%), mucositis (53% versus 35%), nausea (73% versus 52%), vomiting (45% versus 18%), and diarrhoea (34% versus 23%) compared with doxorubicin alone. However, despite increased neutropenia, there was no difference in the rates of febrile neutropenia or infection between the study arms. Infusion reactions, including two Grade 4 events, occurred in 13% of patients treated with combination therapy, but no cases were reported in those treated with doxorubicin alone.4 This study led to conditional approval of olaratumab in 2016 by the European Medicines Agency (EMA) and accelerated approval by the U.S. Food and Drug Administration (FDA) for the treatment of patients with STS not amenable to curative treatment with radiotherapy or surgery and with a histologic subtype for which an anthracycline-containing regimen is appropriate.
Data from the ANNOUNCE study,34 a Phase III trial comparing outcomes of STS patients treated with doxorubicin and olaratumab or doxorubicin alone, are expected in late 2019, and the results will determine whether the survival benefit withstands in a larger population. The results may also identify subtypes that have the greatest benefit and the mechanism of this survival benefit. Other ongoing studies are investigating neoadjuvant olaratumab as well as combinations with other sarcoma chemotherapy (gemcitabine–docetaxel,35 doxorubicin–ifosfamide,36 and doxorubicin–trabectedin37) and immunotherapy (pembrolizumab)38 agents, which may identify additional roles for olaratumab in STS. Trabectedin is a synthetically derived tetrahydroisoquinoline alkaloid originally isolated from the marine ascidian Ecteinascidia turbinata. Trabectedin binds to the minor groove of DNA, resulting in a conformational change of the DNA, bending towards the major groove and altering transcription regulation.39 The first Phase II studies of trabectedin in patients with advanced STS demonstrated a RR of 4–17%, median PFS of 1.9 months, and median OS of 9.2–12.8 months.40-43 Given the paucity of treatment options for STS and the clinical activity and tolerability, the drug received approval by the EMA in 2007 for the treatment of patients with advanced STS after failure of anthracyclines and ifosfamide or for those who were unfit to receive these agents.
In these initial Phase II studies, patients with L-sarcomas, particularly LMS and myxoid round cell LPS, showed the greatest benefit.40-44 Therefore, a multicentre Phase III trial45 compared trabectedin 1.5 mg/m2 every 3 weeks to dacarbazine 1,000 mg/m2 every 3 weeks in L-sarcoma patients after prior anthracycline treatment and at least one additional regimen. The median PFS was improved, measuring 4.2 months versus 1.5 months (p<0.001) with trabectedin and dacarbazine, respectively. In addition, the median PFS improvement was greatest in the myxoid round cell LPS group, totalling 5.6 months versus 1.5 months with trabectedin and dacarbazine, respectively. There was no difference in RR or OS. Trabectedin was also well tolerated, with the most common serious adverse events (AE) being myelosuppression and transient liver function test elevation.5 This study led to FDA approval for trabectedin in 2015 for the treatment of patients with unresectable or metastatic LPS or LMS who had received a prior anthracycline-containing regimen. Trabectedin became the third FDA-approved drug for STS treatment after doxorubicin (1974) and pazopanib (2012).45 The approval of trabectedin, based on improvement in PFS, demonstrates the acceptance of disease stability as a meaningful endpoint in metastatic STS and highlights that disease response by Response Evaluation Criteria in Solid Tumors (RECIST) is uncommon in STS, underscoring the need for novel systemic therapies.
Eribulin mesylate is a synthetically derived analogue of halichondrin B, which was originally derived from a marine sponge. It is a non-taxane microtubule inhibitor that prevents mitotic spindle formation, inducing cell cycle arrest.46 Eribulin was initially FDA-approved to treat advanced or metastatic breast cancer. Similar to trabectedin, a Phase II study47 of eribulin in multiple STS subtypes demonstrated activity solely in the L-sarcomas. The proportion of LMS and LPS patients who were progression-free at 12 weeks was 31.6% and 46.9%, respectively, which compared favourably to historical controls.47 Due to the activity in L-sarcomas, a Phase III study6 compared the efficacy of eribulin 1.4 mg/m2 on Days 1 and 8 of a 21-day cycle with dacarbazine 850–1,200 mg/m2 every 3 weeks only in these patients. The OS was improved, totalling 13.5 months versus 11.5 months with eribulin and dacarbazine, respectively (p=0.0169), and there was no difference in PFS or RR.6 In a preplanned subgroup analysis, the primary benefit of eribulin was in LPS, with improved OS (15.6 months versus 8.4 months, respectively [p<0.001]) and PFS (2.7 months versus 1.9 months, respectively [p=0.0015]) in the eribulin group compared to the dacarbazine group. Notably, there was no difference in RR.7 In both cohorts, eribulin was associated with a greater incidence of AE Grade ≥3 (67%) than dacarbazine (56%). Most severe AE were haematologic; however, the incidence of neutropenic fever was low.6 Collectively, these data led to the approval of eribulin by the EMA and FDA in 2016 for patients with unresectable or metastatic LPS after a prior anthracycline-based regimen, but not for patients with LMS. This agent provides a reasonable second-line option for treating advanced LPS because it demonstrated a 2-month survival benefit and was reasonably well tolerated.
Pazopanib is an oral, synthetically derived indazole pyrimidine that inhibits VEGFR 1–3, PDGFR-α and β, and c-kit.52 VEGF and PDGF are factors in STS angiogenesis, providing a rationale to study pazopanib as a treatment option. An initial Phase II study evaluated daily 800 mg pazopanib in 142 advanced STS patients in a Simon two-stage design.53 Patients were stratified into four cohorts: adipocytic sarcoma, LMS, synovial sarcoma (SS), and other sarcomas. The adipocytic cohort closed after the first stage, but the other three cohorts completely accrued. The PFR at 12 weeks for the LMS, SS, and other sarcomas was 44%, 49%, and 39%, respectively. PFS and OS compared favourably to historical controls; in the LMS, SS, and other sarcomas, the median PFS and OS were 91 and 354, 161 and 310, and 91 and 299 days, respectively.53 These data provided the basis for the Phase III study of pazopanib in patients with advanced STS except the adipocytic subtypes.8 Patients were randomised 2:1 to receive either daily 800 mg pazopanib or a placebo. The median PFS was improved with pazopanib, recorded as 4.6 months versus 1.6 months with placebo (p<0.0001). However, the OS was not significantly different with pazopanib and placebo (12.5 months versus 10.7 months, respectively [p=0.25]) and the RR were 6% with pazopanib and 0% in the placebo group. The most common severe AE were fatigue (13%), hypertension (7%), anorexia (6%), and diarrhoea (5%).54 Overall quality of life was not significantly worsened by pazopanib.54 This study led to the approval of pazopanib in 2012 by the EMA and the FDA for patients with advanced STS, except adipocytic sarcomas, who have received previous chemotherapy. This approval again demonstrates the value of stable disease in the treatment of metastatic STS.
Regorafenib is an oral TKI that targets VEGFR 1–3, PDGFR, KIT, RET, and Raf, and is EMA and FDA-approved to treat GIST, colorectal cancer, and hepatocellular cancer. REGOSARC10 was a double-blind, placebo-controlled Phase II study of four cohorts of STS: LPS, LMS, SS, and other sarcomas. Patients were randomly assigned to receive 160 mg daily regorafenib on Days 1–21 of a 28-day cycle or placebo. There were no significant differences in RR or OS; however, the median PFS was significantly improved in all cohorts except for LPS. The most common Grade 3/4 AE included asthenia (13%), hand and foot skin reaction (15%), hypertension (19%), and hypophosphataemia (13%). There was one Grade 5 hepatitis-induced liver failure that was related to regorafenib.10 This study demonstrates the activity of regorafenib in non-adipocytic STS, and further investigation in a Phase III study against an active agent is warranted.
The TKI described thus far have limited or no activity in adipocytic sarcomas, suggesting that alternative targets are needed. Palbociclib is an oral inhibitor of CDK4 and CDK6 that prevents phosphorylation of the retinoblastoma protein and can result in tumour stasis or regression.58 CDK4 is overexpressed in two subtypes of adipocytic sarcoma, well-differentiated LPS (WDLPS) and dedifferentiated LPS (DDLPS), as compared to normal fat cells.59 Preclinical work demonstrated the antitumour activity of palbociclib in WDLPS/DDLPS cell lines and in xenografts.60 Two Phase II studies11,12 confirmed antitumour activity of palbociclib in 90 patients with WDLPS/DDLPS. The studies evaluated different dosing regimens, either 200 mg daily on Days 1–14 of a 21-day cycle (high dose) or 125 mg daily on Days 1–21 of a 28-day cycle (low dose). The primary endpoint was met in both studies, achieving a PFS at 12 weeks of 66% in the high-dose and 57% in the low-dose group. The median PFS was 18 weeks in both studies and the low dose was slightly better tolerated. Grade 3/4 AE were primarily haematologic: anaemia (17% versus 22%), thrombocytopenia (30% versus 7%), neutropenia (50% versus 36%), and febrile neutropenia (3% versus 0%) with the high and low doses, respectively.11,12 Correlative work from paired tumour biopsies demonstrated that benefit from palbociclib treatment was associated with downregulation of MDM2,61 suggesting a potential biomarker that could be used to predict response to CDK4 inhibition.
Immunotherapy was first described as a potential anticancer strategy in the 19th century in sarcoma patients. Streptococcal antigens (Coley's toxins) were injected into sarcomas and resulted in tumour shrinkage.63 However, there was doubt about these findings, and investigation of chemotherapy and radiation took precedence over further investigation of immunotherapeutic options. More recently, immunotherapy agents targeting T cell checkpoint molecules, such as cytotoxic T lymphocyte-associated protein 4 and programmed death receptor (PD-1) and its ligand (PD-L1), have revolutionised the treatment of numerous malignancies.64-68 However, the success of immunotherapy agents in sarcoma in the modern era has been limited (Table 3).
One of the initial investigations of immunotherapy in sarcoma was SARC028,22 a two-cohort, single-arm, open-label Phase II study of pembrolizumab, an anti-PD-1 monoclonal antibody, administered intravenously (IV) every 3 weeks at a dose of 200 mg. Forty patients were enrolled into each of the bone and soft tissue cohorts. The STS cohort was split into 10 patients with each of the following histologies: UPS, LPS, LMS, or SS. RR were highest in the UPS and LPS cohorts, measuring 40% and 20%, respectively. No responses were seen in LMS patients. In the bone cohort, the RR were 5% (1 out of 22) in osteosarcoma, 20% (1 out of 5) in chondrosarcoma, and 0% (0 out of 13) in Ewing's sarcoma. The median PFS and OS were 18 and 49 weeks in the STS cohort, and 8 and 52 weeks in the bone cohort, respectively. Treatment was well tolerated, with treatment-related serious AE occurring in 11% of patients. AE included pneumonitis (4%), adrenal insufficiency (4%), pulmonary embolism (2%), interstitial nephritis (2%), infectious pneumonia (2%), bone pain (2%), hypoxia (2%), and pleural effusion (2%). There were no Grade 5 AE. The study concluded that pembrolizumab was promising in UPS and LPS and recently completed enrolment of additional patients into these cohorts. Select results from correlative work were included in the initial analysis. PD-L1 expression was identified in 5% (2 out of 40) of the STS samples, both cases were from UPS patients who had responded to therapy. However, responses were also noted in non-PD-L1-expressing LPS patients, suggesting that predicting response to anti-PD-1 therapy is based on more than PD-L1 expression.22 Additional correlative work from this study is pending and will offer further insight into the role of immunotherapy in sarcoma.
Combining immunotherapy agents, such as ipilimumab, an anti-cytotoxic T lymphocyte-associated protein 4 monoclonal antibody, and nivolumab, is an effective strategy in melanoma and renal cell carcinoma.72,73 As a result of the potential synergy of these agents, a Phase II study evaluated two treatment strategies: nivolumab with or without ipilimumab in sarcoma. Treatment included 3 mg/kg IV nivolumab every 2 weeks or 1 mg/kg IV ipilimumab with 3 mg/kg nivolumab every 3 weeks for four doses, followed by 3 mg/kg nivolumab every 2 weeks for up to 2 years. The study was not designed to compare results between treatment arms. The RR was 5% with nivolumab and 16% with combination therapy. In the monotherapy arm, responses were seen in ASPS and non-uterine LMS, while, in the combination treatment arm, responses were seen in LMS (n=2), UPS (n=2), myxofibrosarcoma, and angiosarcoma. The median PFS and OS were 1.7 and 10.7 months and 4.1 and 14.3 months with monotherapy and combination therapy, respectively. Given that the monotherapy did not reach its target RR, nivolumab alone is considered inactive; however, the combination has activity similar to other approved sarcoma therapies and is being further investigated in UPS and LPS. Treatment-related serious AE occurred more frequently with combination therapy (26% versus 19%) than in the monotherapy arm. AE included adrenal insufficiency, elevated alanine and aspartate aminotransferase, hyponatraemia, anaemia, fatigue, pain, and pruritus with dual agent therapy, and anaemia, thrombocytopenia, anorexia, dehydration, diarrhoea, fever, elevated creatinine, and pleural effusion in the monotherapy cohort. Correlative work, including PD-L1 expression, tumour-infiltrating lymphocytes, mutational burden, neoantigen analysis, and T cell receptor clonality, is in progress.24 Results of these studies will help determine factors that predict response or suggest a role for further study of combination immunotherapy in sarcoma.
STS are a highly heterogeneous group of tumours with varying responses to treatment. Given their variable genomic makeup, histology-directed therapy should be regarded as the future of treatment. Currently, combined doxorubicin and olaratumab is the first-line treatment regimen for numerous STS subtypes; however, results of the Phase III study may discern subtypes that derive the greatest benefit. Trabectedin and eribulin have demonstrated efficacy in the L-sarcomas, but further investigation is needed to understand why these subtypes have the greatest success. Targeted therapies, such as pazopanib, have an established role in treating non-adipocytic STS. Novel agents, anlotinib, palbociclib, and selinexor, have shown promise in Phase II studies; however, larger, confirmatory Phase III studies are awaited to determine whether new options for LMS, SS, ASPS, and DDLPS will become available. The role of immunotherapy in STS remains uncertain and is currently only recommended within the context of a clinical trial. Responses in UPS and LPS are encouraging; however, additional studies evaluating more patients, combination strategies, and correlative work are needed. Collectively, the results of recent studies demonstrate the ability of the sarcoma community to enrol histology-tailored trials, which will allow for the development of more subtype-specific therapies.
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Wolchok JD et al. Nivolumab plus ipilimumab in advanced melanoma. N Engl J Med. 2013;369(2):122-33. Pembrolizumab superior to ipilimumab in melanoma. Cancer Discov. 2015;5(6):568. pembrolizumab has antitumor activity in advanced head and neck cancer. Cancer Discov. 2016;6(7):693. De Marinis F, Passaro A. [Nivolumab in second-line treatment of squamous non-small cell lung cancer.]. Recenti Prog Med. 2016;107(12):634-40. (In Italian). First-line atezolizumab effective in bladder cancer. Cancer Discov. 2016;6(8):OF7. Ganjoo KN et al. The prognostic value of tumor-associated macrophages in leiomyosarcoma: A single institution study. Am J Clin Oncol. 2011;34(1): 82-6. George S et al. Loss of PTEN Is associated with resistance to anti-PD-1 checkpoint blockade therapy in metastatic uterine leiomyosarcoma. Immunity. 2017;46(2):197-204. Pollack SM et al. 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Oncologists face multiple challenges when treating patients with cancer, especially if patients are elderly or if they experience adverse events (AEs).


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Cardano Founder Partners With Polymath To Build A Compliant Securities Blockchain (forbes.com)
Polymath, the leading security token platform, has announced today at Consensus 2019 that they will build "Polymesh," the world's first security token blockchain. Charles Hoskinson, co-founder of Ethereum and Founder of Cardano, will collaborate with Polymath, taking on the title of Polymesh's co-architect.
Until now, Polymath has built its technology solution for security tokens on Ethereum. While there have been over 120 Security Tokens created using the Polymath Token Studio, adoption of security tokens has been minimal. Polymath believes this is due to compliance issues. "Polymesh is a new security token layer one blockchain.
It is purpose built, since security tokens have unique needs and characteristic that demand a specific foundation. Ultimately, we want to marry issuers, investors and regulators together, which is what the layer one architecture is designed to do," Trevor Koverko, co-founder of Polymath told me.
According to Polymath, Ethereum lacks regulations and compliance, making it better suited to enable "unstoppable applications". By contrast, Polymesh is being built from the ground up, taking in mind certain considerations to ensure that it will eventually become the underlying infrastructure for the world's capital markets.
"After co-founding Ethereum and Cardano, two of the most widely used blockchains in the world, I am looking forward to working on Polymesh. There are quadrillions of dollars of financial securities, and building a blockchain to secure them is an incredibly exciting task," said Charles Hoskinson, co-founder of Ethereum and founder of IOHK and Cardano.
Moreover, according to Hoskinson, it's important to differentiate the construction of a security token from the ecosystem that it resides in.
All kinds of data are associated with a security that you wouldn't want associated with a cryptocurrency. It's not a good idea for security tokens to live in a completely open system. For instance, every time something is done in an open system it becomes a shared resource. However, security tokens are data intensive protocols, which means operating costs will be high, and this won't scale if we are talking about millions of securities, which we will eventually see. Moreover, things need to be done that you wouldn't want to be done on Ethereum, like freeze or reverse transactions. So we are at odds with the standard Bitcoin ethos here," Hoskinson told me.
And while Polymath initially launched on Ethereum, the team was well aware that a layer one blockchain would eventually be needed.
"All the best features of Ethereum are actually bugs for security tokens. We see a coming stampede of security tokens, but it's more complicated then the first wave of utility coins due to all the regulations, compliance issues, and data," Koverko told me.
However, while Polymesh isn't an entirely open system, it's not a private permissioned network either.
It's a false dichotomy to say that Polymesh is a private permissioned network or that is has be one or the other. Rather, this is a hybrid network in which we layer systems together. For instance, we can take multiple ledgers and put them together in a way were some of those can have closed settings, but still augment them on to an open system where transactions can occur," explained Hoskinson.
Providing Liquidity For Trillions Of Dollars Of Assets
Moreover, Polymath has made clear that the issuers on the Polymath platform are responsible for knowing the regulations behind the securities they are creating. While Polymath provides issuers with the logic to build these assets, the next step has been to create a framework to bring these assets to market.
The sole purpose of Polymesh is to build a special purpose framework for being that environment for securities, regardless of the jurisdiction that they live in. And it's a huge market opportunity, since there are trillions of dollars of assets in emerging economies that are illiquid right now. However, they will be securitized in the next 10-15 years. Polymesh is a perfect example of how we can build a system with equivalent or even better efficiencies then the western markets, while operating at a lower cost and giving regulators more control over particular assets," said Hoskinson.
Hosinson also notes that they have been in discussion with regulators, both in the U.S. and in other parts of the world, about securities. "Most regulators know that regardless of the law they have to understand certain key facts about transactions and the actors behind that. We understand this. However, the biggest challenge regulators obsess about is compliance. A lot of commissioners appreciate that we have to innovate in this space," said Hoskinson.
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Rachel Wolfson
I am an entrepreneur and writer based in San Francisco, California. I cover financial topics related to cryptocurrency, blockchain technology and women disrupting the wo... Read More
May 14 (edited) by Admin in Blockchain News


Bloomington, Ind. – Physicians will now have access to Cook Medical's Word catheter, a silicone balloon catheter used to treat cysts of the Bartholin gland, company officials announced today.
Cysts in the Bartholin gland occur when the gland becomes blocked, causing a buildup of fluid in the gland and the formation of a cyst. Cysts vary in size and occasionally become infected, which causes abscesses. Treatment for cysts of the Bartholin gland can include antibiotics, drainage of the cyst or surgical removal of the gland. Once the cyst has been drained, Cook's Word catheter holds the drainage lumen open so the cyst can fully heal without closing again and risking further infection. This is a common procedure often performed in an office setting, and may help reduce the reoccurrence of cysts.
The Word catheter from Cook Medical includes a silicone balloon that is inserted into the cyst and then inflated to hold the catheter in place and allow the cyst to heal without closing again. Cook's catheter is constructed of silicone, which eliminates the issue of patient sensitivity to latex. To prevent the cyst from closing and refilling again, the catheter can remain in place for up to 28 days while the gland heals.
In response to the recent trend of cost-savings and improved efficiency in the health care industry, Cook is offering the Word catheter at a moderate price to aid health care facilities in their attempts to restrict spending.


Is it the behavior of this blessed little one and her cub?
Mothers always know what to do. Even cats. Amazing.
Re: What is the meaning of love?
What a loving being you are ... an angel l have no doubt .
The charm of every man's inner child?
Much respect for men of his ilk.
Awww shucks. Thanks again mudra!
Much love for you, too.
Surely it must be present in the Acts of Ascenion?
Is it in the missing of the smell of the dust that rose from the feet of one so full of grace? i.e. Is it in this Christ Consciousness? We need it, now.
Whatever love is, radiation cannot kill it.
Is it found in the belief of the power of creation? A "good vibration"?
Perhaps it may be found gazing upon the countenance of one who "loves" you? Is it the endless hours today on the phone, planning out our lives as if all of this craziness in the world is not happening?
Perhaps there is a certain appeal to a being needing their time alone in the garage. I "love" that.
Is it in my blood? MY Acts? My orientation? Is it in being sensual without allowing exploitation?
Was it in the chronic, compliments of Mother Gaia and The Emerald Triangle? Is "love" in the silliness of seeing us look like a couple of newts?
Loving this thread Troy. Please keep it going. I'm sure you'll (and we'll hopefully) find lots more images, videos etc that make our hearts glow with that most wonderful of feelings....Love....if we're feeling a bit sad and need reminding. Bless you for providing another such sanctuary here at the Mists.
Sanicle wrote: Loving this thread Troy. Please keep it going. I'm sure you'll (and we'll hopefully) find lots more images, videos etc that make our hearts glow with that most wonderful of feelings....Love....if we're feeling a bit sad and need reminding. Bless you for providing another such sanctuary here at the Mists.