With another Yapsi release behind me, I now turn back to the last and much-awaited post to publish and summarize the solutions of the Perl 6 coding contest.
it's clear who "won" p5.
<masak> I think you'll agree.
<colomon> but you're not going to tell us yet?
p5 didn't look hard to judge, not like p4. But after having gone through all the preparation for this post, I'd say it's just about comparable. Sorry for delaying this post; it turns out I needed a several-day hackathon to even find the time to write it. But here we go.
common substring of the two strings.
stopping after finding the first one is fine.
The algorithm loops through every possible combination of positions in the two strings, checking the length of the two common substrings starting from those positions.
The algorithm keeps a table of the lengths we've seen so far, building new rows of the table from old rows.
The algorithm concatenates the two strings, builds a suffix tree in linear time from the concatenated string, and then uses the scary voodoo of suffix trees to just pluck out the LCS in linear time.
matthias does the brute-force one. fox, moritz_, and Util do a table-driven thing with varying degrees of additional tricks applied. colomon goes all-out with the suffix tree.
Now let's get one thing clear. The brute-force algorithm is bad, basically cubic in time complexity because there is one nested loop per string, and then one more for iterating through the common substring. The table-algorithm is quadratic, because... well, because it's a two-dimensional table. The suffix tree solution is linear. So it should be clear that colomon won this one based on algorithmic niceness.
And then we turn to the statistics. Oh man.
The three columns respectively contain the string lengths tested, whether there was a common substring, and the time in seconds the algorithm took. Let's summarize what the statistics tell us.
fox and Util's algorithms end up being the slowest ones. Expected, since they're cubic.
moritz's algorithm is doing quite well against colomon's, which is a surprise. Two factors seem to play out here: for smaller values, moritz's algorithm has less setup to do. And then for larger values, colomon's algorithm is quite GC heavy. Somewhere in the middle, colomon's algorithm wins.
matthias's algorithm just blows all the others out of the water.
Reading this graph, keep in mind that the Y axis is logarithmic, so straight line trends in the graph translate into exponential trends in the data. (Which is kinda what we expect, since the strings keep doubling in length, and we don't expect to get off cheaper than linear.) But having trends as approximate lines allows us to estimate the time complexity of each algorithm by looking at the slope of the lines.
fox, moritz, and util seem to have about the same slope. This conforms to theory.
colomon's trend starts higher up, but is less steep. It looks a wee bit bent, which is either an illusion or due to the weight of the objects created.
I'd summarize things like this: colomon wins the moral victory in formulating the most scalable algorithm on paper. matthias, however, puts the fastest algorithm on the table.
I'm loath to let the moral of this be "ignore theory". I think under some circumstances, colomon's algorithm would overtake matthias's. I'm not sure those circumstances can be acheived on Rakudo, though. Already in preparing these statistics, I started hitting upon the limits of what Rakudo can handle.
Maybe the message should instead be that while O() is a fine tool, those little constants that the notation abstracts away really do matter when it comes to the practical application of algorithms. And that settling on an algorithm before benchmarking for those little constants counts as premature optimization.
Update: Seems I was using terribly one-sided data. colomon++ has the scoop here and here — essentially, the landscape is much more detailed than the above statistics reveal. I expect to be doing a followup post myself, if for no other reason than to make a new diagram and to re-assess people's algorithms.
I'll leave it at that. Please also see my reviews of the solutions.
I'm supposing you're all expecting a winner at this point. I'll give it a day or two of deep thought (and preparation), and then I'll post an announcement.


LIVE STREAMING – Download Periscope and follow @suckzone to be notified when streams begin.
Okay, so here's the deal. This is kind of a last-minute thing.
I had plans to be in Dayton, Ohio for the Hamvention – the biggest, dirtiest, most infamous ham radio convention in existence – on the weekend of May 16. So what's another week on the Plains?
After Dayton, Jess and I will fly to Kansas City and take a rental car from there for a week. On May 24 we fly back home from Kansas City.
It's really nerve-wracking to schedule these Chasecations in advance. In 2011, we were chasing the same exact week in May, but it was very slow going. We could hit the jackpot, or we could catch a sunburn. There's no way to tell but to make plans, expect the worst, and hope for the best.
I'm taking the technology in a new direction this year. With my own vehicle, I could make custom mounts for everything in advance. However, we're in a rental car this time, so whatever I bring has to fit in my luggage, and has to be flexible enough to accomodate different mounting scenarios.
As for streaming, I'd like to keep it simple as possible. I don't want to muck around with GPS uploaders and worrying about keeping a reliable stream going. There's enough going on during a chase as it is. If it works, it works.
I'll probably use Twitter Periscope for streaming. Follow @suckzone or watch the sidebar on this page for when I go live. Or, more preferrably, download Periscope on your favorite iOS device and follow @suckzone for real-time notifications.
I will post more about the technology pieces as I get everything together this week.
All content © 2015 Rockwell Schrock. Powered by Jekyll.


Looking for a job is a difficult task, but finding a career can be even more difficult. Maybe you're closer to finding your career than you think. I started at United Fire Group in 1984 as an underwriter in our home office. Throughout the years I have served in a variety of positions and undertook my fair share of difficult challenges, but I never doubted that I had found my career at United Fire.
I have always believed that United Fire's culture is one of its greatest strengths. Our culture translates into many business advantages, including good relationships, excellent customer service and a tenured, well-trained workforce. In fact, our employees average nearly 14 years at our company.
Since starting as a small automobile insurance company in 1946, United Fire has always used a combination of conservative management, progressive leadership and competitive products to find our success as a leading regional insurance carrier.
Throughout the years, as our company developed, so did the careers of our employees. Without our committed employees, we never would have become the publicly traded, multi-billion dollar company we are today.
And, most importantly, the comfort that a real person will always answer the phone.
Jobs at United Fire, aren't just jobs...they are careers. At United Fire Group, you have an opportunity to grow your career, and your success depends on what you want for your future. Your attitude, enhanced by your skills and abilities, all contribute to the success of not only you, but our company, too.
There are a lot of talented people at United Fire who have all created their careers behind its doors. If you are looking for more than a job, I encourage you to look at United Fire. You've taken the first step by searching our Careers section online. Now, take the next step and apply. You never know—your career could be closer than you think. I know mine was.


Squeezebox : Community : Forums > User Forums > General Discussion > Automatically connecting to squeezenetwork when slimserver computers shutsdown?
View Full Version : Automatically connecting to squeezenetwork when slimserver computers shutsdown?
Is it possible to setup the sb so that when the slimserver computer shutsdown the sb connects itself to the squeezenetwork.
We have a sb in the livingroom and when it does not play it functions as a clock. It would be cool when our server shuts itself down after one hour idle time the sb could reconnect itself to the squeezenetwork instead of the slimserver so that the diplay will still be able to show the clock.
Is this possible right now? And if not any chance this could be added?


text:
import datetime
import mock
import os.path
import anyjson

from nose.tools import eq_
from django.test import Client, TransactionTestCase, TestCase
from django.core.urlresolvers import reverse
from django.utils import timezone

from allmychanges.auth.pipeline import add_default_package
from allmychanges.parsing.pipeline import (
    filter_versions_by_source,
    filter_versions_by_attribute)
from allmychanges.models import (Version,
                                 User,
                                 Changelog,
                                 Preview)
from allmychanges.utils import (
    dt_in_window,
    change_weekday,
    first_sentences,
    discard_seconds)
from allmychanges.downloaders.fake import download as fake_downloader
from allmychanges.changelog_updater import (
    update_changelog_from_raw_data3)
from allmychanges.parsing.pipeline import get_files
from allmychanges.env  import Environment

from allmychanges.source_guesser import guess_source

from allmychanges.views import get_digest_for

from .utils import refresh, check_status_code, create_user

def test_update_package_from_basic_structure():
    root = Environment()
    structure = [
        root.push(version='0.1.0',
                  content='v1 content',
                  processed_content='v1 processed content'),
        root.push(version='0.2.0',
                  content='v2 content',
                  processed_content='v2 processed content')
    ]

    art = create_user('art')
    changelog = Changelog.objects.create(
        namespace='python', name='pip', source='test')
    art.track(changelog)

    update_changelog_from_raw_data3(changelog, structure)

    eq_(2, changelog.versions.count())
    v = changelog.versions.all()[0]
    eq_('0.2.0', v.number)
    eq_('v2 processed content', v.processed_text)

def test_update_package_leaves_version_dates_as_is_if_there_isnt_new_date_in_raw_data():
    root = Environment()
    structure = [
        root.push(version='0.1.0',
                  content='content',
                  processed_content='processed content')]

    art = create_user('art')
    changelog = Changelog.objects.create(
        namespace='python', name='pip', source='test')
    art.track(changelog)

    update_changelog_from_raw_data3(changelog, structure)

    v = changelog.versions.all()[0]
    discovered_at = v.discovered_at
    assert v.date is None
    assert discovered_at is not None

    with mock.patch('allmychanges.changelog_updater.timezone') as timezone:
        timezone.now.return_value = datetime.datetime.now() + datetime.timedelta(10)
        update_changelog_from_raw_data3(changelog, structure)

    v = changelog.versions.all()[0]
    # neither date not discovered_at were changed
    assert v.date is None
    eq_(discovered_at, v.discovered_at)

def test_update_package_changes_date_if_it_was_changed_in_the_raw_data():
    root = Environment()
    structure = [
        root.push(version='0.1.0',
                  content='content',
                  processed_content='processed content')]

    art = create_user('art')
    changelog = Changelog.objects.create(
        namespace='python', name='pip', source='test')
    art.track(changelog)

    update_changelog_from_raw_data3(changelog, structure)

    v = changelog.versions.all()[0]
    discovered_at = v.discovered_at
    assert v.date is None
    assert discovered_at is not None

    new_date = datetime.date(2013, 3, 27)
    structure[0].date = new_date
    update_changelog_from_raw_data3(changelog, structure)
    v = changelog.versions.all()[0]

    # package's date has changed
    eq_(new_date, v.date)
    # but discovery date didn't change
    eq_(discovered_at, v.discovered_at)

def test_fake_downloader():
    art = create_user('art')
    changelog = Changelog.objects.create(
        namespace='python', name='pip', source='test+samples/very-simple.md')
    art.track(changelog)
    path = fake_downloader(changelog.source)
    assert path
    with open(os.path.join(path, 'CHANGELOG')) as f:
        content = f.read()
        eq_("""0.1.1
=====

  * Some bugfix.

0.1.0
=====

  * Initial release.""", content)

def test_environment_cloning():
    env = Environment()
    env.some = 'value'

    env2 = env.push()
    eq_('value', env2.some)

    env2.some = 'another'
    eq_('another', env2.some)
    eq_('value', env.some)

    # checking another way of creating child environment
    # and setting the values simultaneously
    env3 = env2.push(some='new value',
                     other='item')
    eq_('new value', env3.some)
    eq_('item', env3.other)
    eq_('another', env2.some)

def test_environment_comparison():
    eq_(Environment(), Environment())

    env1 = Environment()
    env1.type = 'blah'
    env2 = Environment()
    env2.type = 'blah'
    eq_(env1, env2)

    # first env inherits it's type
    # second have it explicitly
    env1 = Environment()
    env1.type = 'blah'
    env2 = Environment().push(type='blah')
    eq_(env1.push(), env2)

    # first env have two vars
    # second only one
    env1 = Environment().push(type='blah', foo='bar')
    env2 = Environment().push(type='blah')
    assert env1 != env2

def test_get_env_keys():
    eq_(['bar', 'baz', 'foo'],
        Environment() \
            .push(foo=1) \
            .push(bar=2) \
            .push(baz=3) \
            .keys())

def test_source_guesser():
    content = """Some text with package description
    which have urls like that
    and that

    But also it could include links to the bitbucked
    To some raw materials.
    And raw at bitbucket.
    """
    with mock.patch('allmychanges.source_guesser.requests') as requests:
        response = mock.Mock()
        response.content = content
        requests.get.return_value = response
        urls = guess_source('python', 'pdb')

        eq_(['https://bitbucket.org/antocuni/pdb'], urls)

class UserTests(TestCase):
    def test_two_users_can_have_blank_emails(self):
        User.objects.create(username='bob', email='')
        User.objects.create(username='karl', email='')
        eq_(2, User.objects.count())

    def test_but_two_users_should_have_different_emails(self):
        User.objects.create(username='bob', email='mail@me.com')
        self.assertRaises(ValueError,
                          User.objects.create,
                          username='karl', email='mail@me.com')

class ProfileTests(TransactionTestCase):
    def setUp(self):
        self.user = create_user('art')
        self.user.save()

        self.cl = Client()
        self.cl.login(username='art', password='art')

    def test_timezone_update(self):
        url = '/account/settings/'
        response = self.cl.post(
            url,
            dict(
                email='some@example.com',
                timezone='Europe/Moscow',
                send_digest='daily',
                slack_url=''
            )
        )
        check_status_code(302, response)
        assert url in response['Location']
        user = refresh(self.user)
        eq_('Europe/Moscow', user.timezone)

def test_tz_window():
    dt = datetime.datetime
    now = dt(2014, 05, 19, 6, 0) # system datetime (UTC)

    eq_(False,
        dt_in_window('Europe/Moscow',        # user's timezone
                     now,
                     9))                     # desired hour in user's timezone

    # Kiev 1 hour ealier than Moscow
    eq_(True, dt_in_window('Europe/Kiev', now, 9))

def test_new_user_have_allmychanges_in_digest():
    user = create_user('art')
    eq_(0, user.changelogs.count())

    add_default_package(None, is_new=True, user=user)

    eq_(1, user.changelogs.count())
    eq_('allmychanges', user.changelogs.all()[0].name)

def test_old_user_can_have_zero_packages():
    """We wont add a default package to old users."""
    user = create_user('art')
    eq_(0, user.changelogs.count())

    add_default_package(None, is_new=False, user=user)

    eq_(0, user.changelogs.count())

def test_digest_for_today_includes_changes_from_last_9am():
    user = create_user('art')
    today = datetime.datetime(2014, 1, 1, 9, 0, tzinfo=timezone.UTC()) # 9am
    one_day = datetime.timedelta(1)
    one_minute = datetime.timedelta(0, 60)

    foo = Changelog.objects.create(namespace='test', name='foo', source='foo')
    foo.versions.create(number='0.1.0',
                        discovered_at=today - one_day - one_minute)

    bar = Changelog.objects.create(namespace='test', name='bar', source='bar')
    bar.versions.create(number='0.3.0',
                        discovered_at=today - one_day)

    user.track(foo)
    user.track(bar)

    digest = get_digest_for(user.changelogs,
                            after_date=today - one_day)
    eq_(1, len(digest))

def api_get(handle, **kwargs):
    cl = Client()
    response = cl.get(reverse(handle), kwargs)
    if response.status_code >= 200 and response.status_code < 300:
        if response.content_type == 'application/json':
            return anyjson.deserialize(response.content)
    return response

def test_namespace_name_validator():
    Changelog.objects.create(namespace='foo',
                             name='bar')

    eq_({'result': 'ok'},
        api_get('validate-changelog-name-list',
                 namespace='foo',
                 name='blah'))

    eq_({'result': 'ok'},
        api_get('validate-changelog-name-list',
                 namespace='blah',
                 name='bar'))

    eq_({'errors': {'name': ['These namespace/name pair already taken.']}},
        api_get('validate-changelog-name-list',
                 namespace='foo',
                 name='bar'))

    eq_({'errors': {'namespace': ['Please, fill this field'],
                    'name': ['Please, fill this field']}},
        api_get('validate-changelog-name-list',
                 namespace='',
                 name=''))

    eq_({'errors': {'namespace': ['Field should not contain backslashes'],
                    'name': ['Field should not contain backslashes']}},
        api_get('validate-changelog-name-list',
                 namespace='fo/o',
                 name='ba/r'))

def test_landing_digest_keeps_tracked_in_cookie():
    cl = Client()
    response = cl.get(reverse('landing-digest') + '?changelogs=1,2,3')
    eq_('1,2,3', response.cookies['tracked-changelogs'].value)

def test_get_files_respect_ignore_and_search_lists():
    def walk(root):
        return [('samples/markdown-release-notes/', ['docs'], ['unrelated-crap.md']),
                ('samples/markdown-release-notes/docs',
                 [], ['0.1.0.md', '0.1.1.md'])]

    env = Environment()
    env.dirname = 'samples/markdown-release-notes'
    env.ignore_list = []
    env.search_list = []
    result = [item.filename for item in get_files(env, walk)]
    eq_(['samples/markdown-release-notes/unrelated-crap.md',
         'samples/markdown-release-notes/docs/0.1.0.md',
         'samples/markdown-release-notes/docs/0.1.1.md'],
        result)

    env.ignore_list = ['unrelated-crap.md']
    env.search_list = []
    result = [item.filename for item in get_files(env, walk)]
    eq_(['samples/markdown-release-notes/docs/0.1.0.md',
         'samples/markdown-release-notes/docs/0.1.1.md'],
        result)

    env.ignore_list = ['docs']
    env.search_list = []
    result = [item.filename for item in get_files(env, walk)]
    eq_(['samples/markdown-release-notes/unrelated-crap.md'],
        result)

    env.ignore_list = []
    env.search_list = [('unrelated-crap.md', None)]
    result = [item.filename for item in get_files(env, walk)]
    eq_(['samples/markdown-release-notes/unrelated-crap.md'],
        result)

    env.ignore_list = []
    env.search_list = [('doc', None)]
    result = [item.filename for item in get_files(env, walk)]
    eq_(['samples/markdown-release-notes/docs/0.1.0.md',
         'samples/markdown-release-notes/docs/0.1.1.md'],
        result)

def test_filtering_versions_by_source():
    # now check if CHANGELOG.md is preferred to large number of versions
    # from docs/ subdirectory
    versions = []
    versions.append(Version(filename="CHANGELOG.md", number="1.3.0"))
    versions.append(Version(filename="CHANGELOG.md", number="1.2.0"))
    versions.append(Version(filename="CHANGELOG.md", number="1.1.2"))
    versions.append(Version(filename="CHANGELOG.md", number="1.1.1"))
    versions.append(Version(filename="docs/sources/installation/ubuntulinux.md", number="14.04"))
    versions.append(Version(filename="docs/sources/installation/ubuntulinux.md", number="13.04"))
    versions.append(Version(filename="docs/sources/installation/ubuntulinux.md", number="12.04"))
    versions.append(Version(filename="docs/sources/installation/debian.md", number="8.0"))
    versions.append(Version(filename="docs/sources/reference/api/hub_registry_spec.md", number="6.2"))
    versions.append(Version(filename="docs/sources/reference/api/hub_registry_spec.md", number="4.4"))
    versions.append(Version(filename="docs/sources/reference/api/docker_remote_api_v1.5.md", number="3.3"))
    versions.append(Version(filename="docs/sources/reference/api/docker_remote_api_v1.1.md", number="3.2"))
    versions.append(Version(filename="docs/sources/reference/api/docker_remote_api_v1.1.md", number="3.1"))
    versions.append(Version(filename="docs/sources/reference/api/docker_remote_api_v1.1.md", number="2.3"))
    versions.append(Version(filename="docs/sources/reference/api/docker_remote_api_v1.1.md", number="2.2"))
    versions.append(Version(filename="docs/sources/reference/api/docker_remote_api_v1.1.md", number="2.1"))

    new = filter_versions_by_source(versions)
    filenames = {v.filename for v in new}
    eq_(['CHANGELOG.md'], list(filenames))

def test_filtering_versions_by_source_on_separate_release_notes():
    versions = []
    versions.append(Version(filename='dist/kafka/0.8.2.1/RELEASE_NOTES.html', number='0.8.2.1'))
    versions.append(Version(filename='dist/kafka/0.8.0/RELEASE_NOTES.html', number='0.8.0'))

    new = filter_versions_by_source(versions)
    filenames = {v.filename for v in new}
    eq_(['dist/kafka/0.8.0/RELEASE_NOTES.html',
         'dist/kafka/0.8.2.1/RELEASE_NOTES.html'], list(filenames))

def test_filtering_versions_by_attribute():
    root = Environment()
    versions = [
        root.push(title='RELEASE_NOTES.html', number='0.8.2.1'),
        root.push(title='Version 0.8.0 release notes', number='0.8.0')]

    new = filter_versions_by_attribute(versions,
                                       search_list=[(ur'[title=Version \d.*]', None)])
    eq_(['0.8.0'], [v.number for v in new])

    new = filter_versions_by_attribute(versions,
                                       ignore_list=[ur'[title=.*\.html]'])
    eq_(['0.8.0'], [v.number for v in new])

    new = filter_versions_by_attribute(versions,
                                       search_list=[],
                                       ignore_list=[])
    eq_(set(['0.8.0', '0.8.2.1']), {v.number for v in new})

def test_digest_does_not_include_preview_versions():
    today = datetime.datetime(2014, 1, 1, 9, 0, tzinfo=timezone.UTC()) # 9am
    week = datetime.timedelta(7)
    day = datetime.timedelta(1)

    foo = Changelog.objects.create(namespace='test', name='foo', source='foo')
    foo.versions.create(number='0.1.0',
                        discovered_at=today - week)

    preview = Preview.objects.create(changelog=foo)
    preview.versions.create(changelog=foo,
                            number='0.1.0',
                            discovered_at=today)

    digest = get_digest_for(Changelog.objects.filter(pk=foo.pk),
                            after_date=today - day)

    eq_(0, len(digest))

def test_active_changelogs_filtering():
    ch1 = Changelog.objects.create(namespace='test',
                                   name='foo1',
                                   source='foo1',
                                   downloader='foo')
    Changelog.objects.create(namespace='test',
                             name='foo2',
                             source='foo2',
                             downloader='foo',
                             paused_at=timezone.now())
    Changelog.objects.create(namespace='test',
                             name=None,
                             source='foo3',
                             downloader='foo')

    response = list(Changelog.objects.only_active())
    eq_(1, len(response))
    eq_(ch1.id, response[0].id)

def test_first_sentences():
    eq_(u'Blah.', first_sentences(u'Blah.', max_length=5))
    eq_(u'Blah minor.', first_sentences(u'Blah minor. Again!', max_length=11))
    eq_(u'Blah mino…', first_sentences(u'Blah minor. Again!', max_length=10))
    eq_(u'Again!', first_sentences(u'Again! Blah minor.', max_length=7))
    eq_(u'Blah minor.', first_sentences(u'Blah minor.\nAgain!', max_length=11))
    eq_(u'Blah minor. Again!', first_sentences(u'Blah minor.\nAgain!\nAnd again.', max_length=20))

def test_change_weekday():
    # this date has weekday==2
    now = datetime.datetime(2016, 3, 2)

    eq_(now, change_weekday(now, now.weekday()))
    eq_(datetime.datetime(2016, 3, 1), change_weekday(now, 1))
    eq_(datetime.datetime(2016, 2, 29), change_weekday(now, 0))

    eq_(datetime.datetime(2016, 3, 3), change_weekday(now, 3))
    eq_(datetime.datetime(2016, 3, 4), change_weekday(now, 4))
    eq_(datetime.datetime(2016, 3, 5), change_weekday(now, 5))
    eq_(datetime.datetime(2016, 3, 6), change_weekday(now, 6))

redpajama_set_name: RedPajamaGithub


FC Hoffenheim was founded in 1899 as part of a sport community that also included volleyball, gymnastics and wrestling divisions but was not in the favor of community's management at that time. The club represents the village of Hoffenheim with population of 3,000 people. Nowadays Hoffenheim belongs to the city of Sinsheim (Baden-Wurttemberg region). Since 2008 FC Hoffenheim has been playing in German Bundesliga.
Hoffenheim spent most of its time in amateur and regional leagues. Till 1989 the club played in the 7th German division (Bezirksliga). In 1989 the team finished last and was relegated deeper to the Kreisliga. That was the breaking point in the history of the club. Billionaire Dietmar Hopp, who had played for the team when he was young, launched financial support to the club. To begin with he provided the team with 10,000 German marks to be spent on training equipment and balls. In 1990 the team won Kreisliga A and came back to the 7th division to win it in first season that got them promoted to Landesliga. It took Hoffenheim 6 years to get through the league for Verbandsliga. In 2000 the team advanced to Oberliga and the following year further on to Regionalliga Sud.
In 2003 the club forced to the 1/16 finals of the German Cup to be beaten by Koln. In 2004 the team was widely discussed in Germany after beating Eintracht, Bayer Leverkusen and Karlsruhe in the same German Cup. Sadly the club was stopped by Lubeck in quarterfinal.
In 2007 the club finished the season on the second position and went directly to Bundesliga 2. In 2008 the club got the new stadium and, inspired, made a tremendous achievement by reaching the German elite division.


text:
Cosafa Cup 2016 tournament launched with new sponsor
Soccer24 on 5 Nov, 2015
The 2016 Cosafa Cup tournament will be hosted by Namibia according to the organisers of the tournament.
Castle Lager has also returned as a title sponsor of the tournament. Speaking at a function to unveil the 2016 tournament COSAFA President Suketu Patel paid tribute to the Castle Lager brand for their investment in football in the region over the years
'We are delighted that the future of the COSAFA CUP is secure and would like to extend our sincere thanks to Castle Lager for believing in the excellent development role that the competition plays in Southern Africa, recognising the value of the platform which the annual tournament provides to the Brand and displaying their confidence in COSAFA as an organisation.
Namibia are the current holders of the tournament after winning the 2015 edition. The tournament will be staged from May 15-29 and be hosted at two venues in Windhoek – the Sam Nujoma Stadium and Independence Stadium.
Get news delivered straight to your mobile phone via the Soccer24 app available on the Google Play Store below:
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redpajama_set_name: RedPajamaCommonCrawl


text:
Q: Why is this very simple UPDATE so much slower than the SELECT it contains? In MariaDB 10.3.9:
SELECT COUNT(*) FROM photos
vs
UPDATE counts SET countValue = (SELECT COUNT(*) FROM photos) WHERE countName = 'photos';
The select takes 1.1s vs the update which takes 2.6s.  3million rows in table photos, 3 rows in table counts.
ANALYZE format=JSON output:
{
  "query_block": {
    "select_id": 1,
    "r_loops": 1,
    "r_total_time_ms": 1299.6,
    "table": {
      "table_name": "photos",
      "access_type": "index",
      "key": "PRIMARY",
      "key_length": "4",
      "used_key_parts": ["photoId"],
      "r_loops": 1,
      "rows": 3178665,
      "r_rows": 3.25e6,
      "r_total_time_ms": 1085.7,
      "filtered": 100,
      "r_filtered": 100,
      "using_index": true
    }
  }
}

vs
{
  "query_block": {
    "select_id": 1,
    "r_total_time_ms": 2764.7,
    "table": {
      "update": 1,
      "table_name": "counts",
      "access_type": "range",
      "possible_keys": ["countName"],
      "key": "sCount",
      "key_length": "1023",
      "used_key_parts": ["countName"],
      "rows": 1,
      "r_rows": 1,
      "r_filtered": 100,
      "r_total_time_ms": 0.0756,
      "attached_condition": "counts.countName = 'photos'"
    },
    "subqueries": [
      {
        "query_block": {
          "select_id": 2,
          "r_loops": 1,
          "r_total_time_ms": 2764.6,
          "table": {
            "table_name": "photos",
            "access_type": "index",
            "key": "PRIMARY",
            "key_length": "4",
            "used_key_parts": ["photoId"],
            "r_loops": 1,
            "rows": 3178665,
            "r_rows": 3.25e6,
            "r_total_time_ms": 2541.8,
            "filtered": 100,
            "r_filtered": 100,
            "using_index": true
          }
        }
      }
    ]
  }
}

Why is the subquery in the update query so slow?  I can easily fix this by doing a separate manual update with the result of the select query, but I'd like to know why this is slowing down so much.
On further examination, even THIS takes over twice as long as the simple select:
SET @foo = (SELECT COUNT(*) FROM photos);
What?  Why?!

A: Change to:
SELECT @ct := COUNT(*) FROM photos;
UPDATE counts SET countValue = @ct WHERE countName = 'photos';

Either have autocommit = ON, or at least don't put both statements in the same transaction.  This is to avoid locking counts while counting.
Also, countName should be the PRIMARY KEY.

redpajama_set_name: RedPajamaStackExchange


text:
Measuring and Accounting for Innovation in the Twenty-First Century
Measuring the Impact of Household…
Measuring the Impact of Household Innovation Using Administrative Data
Javier Miranda & Nikolas Zolas
Published Date April 2021
CONFERENCE HELD March 10-11, 2017
Book: Measuring and Accounting for Innovation in the Twenty-First Century
Book organizers: Carol Corrado, Jonathan Haskel, Javier Miranda & Daniel Sichel
PUBLISHER: University of Chicago Press
Series: Studies in Income and Wealth
We link USPTO patent data to US Census Bureau administrative records on individuals and firms. The combined dataset provides us with a directory of
patenting household inventors as well as a time-series directory of self-employed businesses tied to household innovations. We describe the characteristics of household inventors by race, age, gender and US origin, as well as the types of patented innovations pursued by these inventors. Business data allows us to highlight how patents shape the early life-cycle dynamics of nonemployer businesses. We find household innovators are disproportionately US born, white and their age distribution has thicker tails relative to business innovators. Data shows there is a deficit of female and black inventors. Household inventors tend to work in consumer product areas compared to traditional business patents. While patented household innovations do not have the same impact of business innovations their uniqueness and impact remains surprisingly high. Back of the envelope calculations suggest patented household innovations granted between 2000 and 2011 might generate $5.0B in revenue (2000 dollars).
We would like to thank Scott Stern, Shawn Klimek, Eric von Hippel, Mark Leach and Dan Sichel for valuable comments. We also thank participants in the CRIW conference Measuring and Accounting for Innovation in the 21st Century and two anonymous referees for their comments. All errors or omissions are our own. Any opinions and conclusions expressed herein are those of the authors and do not necessarily represent the views of the U.S. Census Bureau or the National Bureau of Economic Research. All results have been reviewed to ensure that no confidential information is disclosed. The views expressed herein are those of the authors and do not necessarily reflect the views of the National Bureau of Economic Research.
Javier Miranda
In compliance with the requirement of the Journal's disclosure policy, I would like to state that I, Javier Miranda, am an employee of the U.S. Census Bureau. I have received no direct financial support from any organization but I am one of the Principal Investigators on the grant from the Kauffman Foundation that we note in the acknowledgements section. The support from the Kauffman Foundation is directly related to this research as they have supported the development of the data infrastructure used in this paper as well as research analysis related to the topics in this paper. We are also using proprietary data in this paper housed at the U.S. Bureau of the Census. As we note in the acknowledgements section "All results have been reviewed to ensure that no confidential information is disclosed."
Published From Paper
November 2018 - Working Paper
Author(s): Javier Miranda & Nikolas Zolas
We link USPTO patent data to U.S. Census Bureau administrative records on individuals and firms. The combined dataset...


text:
HomeFrank Tucker2022-01-25T10:53:03-05:00
MicroHealth provides customers with the right information to promote better decision-making to improve our Nation's health and wellness. This is achieved by harnessing the combined knowledge and expertise from our seasoned team of health professionals, researchers, informaticists and technologists who specialize in health information management and technology.
Health Analytics, Research, and Informatics
Our solutions uses many best practices techniques from data mining, statistics, modeling, and machine learning, and artificial intelligence to analyze current data to make predictions about future.
Program Management and Technical Assistance
MicroHealth delivers program management leveraging the Project Management Institutes (PMI)'s best practices for program management, which improves the potential for the delivery of work products that are on time, within budget, and compliant to specifications.
Requirements, Systems Engineering, and Software Development
Requirements management encompasses those tasks that go into determining the needs or conditions to meet for a new or altered product, taking account of the possibly conflicting requirements of the various stakeholders, such as beneficiaries or users.
System Integration, Implementation, and Sustainment
Integration patterns are the key to conformity to standards and successful interoperability. They simplify the overall interoperability, yet are abstract enough to apply to most of technologies, but at the same time specific enough to offer practical guidance to architects and designers.
Independent Verification and Validation (IV&V) and Testing
Our testing and evaluation approach is conducted to provide stakeholders with information about the quality of the product or service under test.
PEO DHMS
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We are a Center for Veteran Enterprises (CVE) Service Disabled Veteran Owned Small Business (SDVOSB) and Small Business Administration 8(a) firm with process maturity appraised at CMMI-DEV Level 3, CMMI-SVC Level 3,and certified in ISO 27001:2013, ISO 20000-1:2018 and ISO 9001:2015.
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Simply put – we put Health back into Health Information Technology by
Empowering PEOPLE with information to make better decisions
Providing VALUE to patients, providers, public health and payers
Delivering INNOVATION that improves outcomes
By Diwa Reyes|2021-08-26T21:53:30-04:00August 26th, 2021|
VIENNA, Va., Aug. 25, 2021- MicroHealth, LLC is among the nation's fastest-growing private companies in 2021. This is according to Inc. Magazine's
Vienna, Virginia – 16 August, 2021 – MicroHealth LLC was named the winner of a Gold Stevie® Award in
By Diwa Reyes|2021-06-22T14:06:48-04:00June 22nd, 2021|
MicroHealth LLC has been named one of The Washington Post's 2021 Top Workplaces in the Washington, D.C. area. Selection


text:
JACC Journals
JACC: Basic to Translational Science
JACC: CardioOncology
JACC: Cardiovascular Imaging
JACC: Cardiovascular Interventions
JACC: Case Reports
JACC: Clinical Electrophysiology
JACC: Heart Failure
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Source -- All Journals --JACC: Basic to Translational ScienceJACC: Cardiovascular ImagingJACC: Cardiovascular InterventionsJACC: Case ReportsJACC: Heart FailureJACC: Clinical ElectrophysiologyJournal for the American College of Cardiology
Source -- All Journals --JACC: Basic to Translational ScienceJACC: Cardiovascular ImagingJACC: Cardiovascular InterventionsJACC: Case ReportsJACC: Heart FailureJACC: Clinical ElectrophysiologyJournal of the American College of Cardiology
Journal of the American College of Cardiology
Volume 50, Issue 24, December 2007 DOI: 10.1016/j.jacc.2007.08.044
Preclinical Study
Broad and Specific Caspase Inhibitor-Induced Acute Repression of Apoptosis in Atherosclerotic Lesions Evaluated by Radiolabeled Annexin A5 Imaging
Masayoshi Sarai, Dagmar Hartung, Artiom Petrov, Jun Zhou, Navneet Narula, Leo Hofstra, Frank Kolodgie, Satoshi Isobe, Shinichiro Fujimoto, Jean-Luc Vanderheyden, Renu Virmani, Chris Reutelingsperger, Nathan D. Wong, Sudhir Gupta and Jagat Narula
Author + information
vol. 50 no. 24 2305-2312
https://doi.org/10.1016/j.jacc.2007.08.044
Received April 10, 2007
Revision received August 23, 2007
Accepted August 24, 2007
Published online December 11, 2007.
Copyright & Usage:
American College of Cardiology Foundation
Masayoshi Sarai, MD⁎,1,
Dagmar Hartung, MD⁎,†,1,
Artiom Petrov, PhD⁎,⁎ (adpetrov{at}uci.edu),
Jun Zhou, MD⁎,
Navneet Narula, MD⁎,
Leo Hofstra, MD, PhD‡,
Frank Kolodgie, PhD§,
Satoshi Isobe, MD⁎,
Shinichiro Fujimoto, MD⁎,
Jean-Luc Vanderheyden, PhD∥,
Renu Virmani, MD, FACC§,
Chris Reutelingsperger, PhD‡,
Nathan D. Wong, PhD⁎,
Sudhir Gupta, MD, PhD⁎ and
Jagat Narula, MD, PhD, FACC⁎
⁎
∥
↵⁎Reprint requests and correspondence:
Dr. Artiom Petrov, University of California, Irvine, School of Medicine, C116 Medical Science I, Irvine, California 92697.
Masayoshi Sarai, Dagmar Hartung, Artiom Petrov, Jun Zhou, Navneet Narula, Leo Hofstra, Frank Kolodgie, Satoshi Isobe, Shinichiro Fujimoto, Jean-Luc Vanderheyden, Renu Virmani, Chris Reutelingsperger, Nathan D. Wong, Sudhir Gupta, Jagat Narula
Apoptosis contributes to the vulnerability of atherosclerotic plaques to rupture. We evaluated the role of caspase inhibitors on acute resolution of apoptosis by imaging with technetium-99m–labeled annexin A5 in an atherosclerotic rabbit model. Tracer uptake in atherosclerotic animals was significantly higher than that in unmanipulated rabbits and significantly lower in those given broad caspase inhibitors and caspase-1, -3, or -9 inhibitors. Uptake was not affected by caspase-8 inhibition. A substantial decrease in foam cell apoptosis was observed in caspase-inhibited groups. Broad and specific caspase inhibitors reduced apoptosis in atherosclerosis, which may allow the development of novel therapeutic strategies in acute vascular events in humans.
Objectives The purpose of this study was to evaluate the role of caspase inhibitors on acute resolution of apoptosis in atherosclerotic lesions as evaluated by imaging with annexin A5.
Background Extensive apoptosis of macrophages has been reported at the site of plaque rupture in patients dying of acute coronary syndrome.
Methods Of 31 New Zealand White atherosclerotic rabbits, 6 received broad caspase, 3 received caspase-1, 3 received caspase-3, 3 received caspase-8, and 4 received caspase-9 inhibitors; 12 animals did not receive any caspase inhibitors (treatment control group). Six unmanipulated rabbits were used for comparison (disease control group). Technetium-99m–labeled annexin A5 was used for imaging atherosclerotic lesions; 6 of the 12 uninhibited atherosclerotic rabbits received 99mTc-labeled mutant annexin A5 (radiotracer control group). Gamma images were obtained, and quantitative radiotracer uptake was compared with pathologic findings.
Results Atherosclerotic lesions were best visible in untreated atherosclerotic rabbits. Quantitative annexin uptake, defined as the percent of injected dose per g of abdominal aorta tissue, was significantly higher in untreated atherosclerotic animals (mean ± SD = 0.0515 ± 0.0099) compared with the normal rabbits (0.0065 ± 0.0008; p < 0.0001) or atherosclerotic rabbits receiving mutant annexin (0.014 ± 0.0024; p < 0.0001). Among all caspase inhibitor-treated rabbits, uptake was 39% lower (0.0314 ± 0.0151) than in untreated atherosclerotic animals (p < 0.01). Uptake was also significantly lower in rabbits receiving broad caspase (0.0206 ± 0.0058; p < 0.0001) or caspase-1, -3, or -9 (0.0272 ± 0.0088, p < 0.01; 0.0286 ± 0.0095, p < 0.01; 0.0300 ± 0.0021, p < 0.01, respectively) inhibitors. Caspase-8 inhibitor did not affect apoptosis (0.0618 ± 0.0047; p = NS). Upon histologic characterization, a substantial decrease in macrophage apoptosis was observed in caspase-inhibited animals.
Conclusions Molecular imaging, using radiolabeled annexin A5, allows the detection of acute resolution of apoptosis as a result of caspase inhibition in experimental atherosclerosis. If proven clinically, this may allow development of novel intervention strategies in acute vascular events.
Autopsy studies have revealed a high prevalence of apoptosis in vulnerable and ruptured atherosclerotic plaques, which is associated with activation of caspase-1 and -3 (1,2). Apoptosis of smooth muscle cells leads to attenuation of the fibrous cap (3,4), and apoptosis of foam cells results in enlargement of the necrotic core (5); both thin caps and large cores are important determinants of plaque vulnerability. In addition, extensive apoptosis of foam cells is seen at the site of fibrous cap rupture (1,2). Therapeutic interventions known to substantially reduce acute coronary events, such as dietary modification and statin treatment, reduce the prevalence of apoptosis in atherosclerotic lesions (6,7). However, a recent clinical trial of high-dose statin treatment, immediately following acute coronary syndrome, demonstrated that the benefit of statins may be observed only after a lapse of 4 to 5 weeks, a period when recurrent events are most frequent (8). Therefore, it is logical to assume that if apoptosis contributes to plaque rupture, acute repression of apoptosis in acute coronary events should help prevent early recurrent coronary events. It should be possible to inhibit apoptosis acutely by pharmacologic interventions targeted at the signaling cascade of apoptosis.
There are 2 major signaling pathways of apoptosis (Fig. 1):the death receptor pathway (9–11) and the mitochondrial pathway (12,13). In the death receptor pathway, the signal is provided by the interaction between the ligand and death receptor, recruitment of adapter proteins, and activation of proximal (caspase-8) and executioner caspases. In the mitochondrial signaling pathway, a number of molecules (including cytochrome c) are released from the mitochondrial intermembrane space into the cytoplasm. There they interact with adapter proteins and activate a distinct initiator caspase (caspase-9) that then activates common executioner caspases, resulting in apoptosis. Caspase-3 is a prototype of the executioner caspases, and it cleaves a number of cytoplasmic and nuclear substrates, which results in the morphologic and biochemical characteristics of apoptosis (11). Activation of proximal caspases distinguishes between death receptor (caspase-8) and mitochondrial (caspase-9) pathways of apoptosis.
Pathways of Apoptosis and Possible Involvement of Caspase-1 in Apoptosis
In the present study, inhibitors of caspase-8 and -9 were used to differentiate between involvement of the death receptor and mitochondrial pathways of apoptosis. IL = interleukin; ROS = reactive oxygen species.
Caspase-3 activation is closely associated with phosphatidylserine (PS) expression on the apoptotic cell surface (14). Annexin A5, a naturally occurring protein, binds to PS with high affinity and has been used as an early marker of apoptosis. Radiolabeled annexin A5 has been successfully employed for the noninvasive detection of macrophage apoptosis in experimental atherosclerotic lesions in rabbit (15) and mouse aorta (16), porcine coronary arteries (17), and carotid arteries in patients who had suffered transient ischemic episodes (18).
The present study was performed to evaluate if acute repression of apoptosis was possible by the using caspase inhibitors, as determined by noninvasive imaging with technetium-99m (99mTc)–labeled annexin A5. For inhibition of apoptosis, we employed intravenously infused broad caspase inhibitors, executioner caspase-3–specific inhibitor, and inhibitors of proximal caspases-8 and -9 to distinguish between death receptor and mitochondrial pathways of apoptosis. Inhibitor of caspase-1 was used because activated caspase-1 has been observed in vulnerable plaques and ruptured lesions in patients dying of acute coronary events (2).
The experimental protocol was approved by the Institutional Animal Research and Care Committee at the University of California-Irvine. Thirty-seven male New Zealand White rabbits were obtained from Western Oregon Farm (Philomath, Oregon). After a 1-week quarantine, 6 unmanipulated animals were set aside as disease controls, and they received normal rabbit chow for 16 weeks (Fig. 2).These animals were imaged with 99mTc-annexin A5 16 weeks later.
The Timeline and Experimental Design of the Study
Annexin A5 uptake in 19 animals treated with broad and specific caspase inhibitors was compared with 6 animals each of treatment (Rx), disease, and radiotracer control groups.
Atherosclerotic lesions were induced in the remaining 31 rabbits. These animals were fed a 0.5% cholesterol diet custom-mixed in 6% peanut oil. One week after the start of the high-cholesterol diet, they underwent balloon de-endothelialization of their infradiaphragmatic aortas and continued on a high-cholesterol, high-fat diet for 15 additional weeks (6). Of these, 25 atherosclerotic animals were imaged with 99mTc-annexin A5 at 16 weeks and classified as follows. Six of these 25 atherosclerotic animals were imaged in the absence of any caspase inhibitor (treatment control), and 19 animals received caspase inhibitors. The caspase inhibitors were administered by intravenous push for 6 h (3 mg) and 1 h (4 mg) before radiolabeled annexin A5 injection: broad (nonselective) caspase inhibitor (n = 6), caspase-1 inhibitor (n = 3), caspase-3 inhibitor (n = 3), caspase-8 inhibitor (n = 3), or caspase-9 inhibitor (n = 4). The remaining group of 6 atherosclerotic rabbits was imaged with mutant annexin A5 at week 16 (radiotracer control); mutant annexin A5 has ineffective PS-binding sites (6).
We used a cell-permeable nonselective caspase inhibitor (ZVAD-fmk; BIOMOL International, LP, Plymouth Meeting, Pennsylvania), caspase-1 inhibitor (YVAD-cho; BIOMOL International, LP), caspase-3 inhibitor (DEVD-cho; BIOMOL International, LP), caspase-8 inhibitor (ZIETD-fmk; Calbiochem, San Diego, California), and caspase-9 inhibitor (ZLEHD-fmk; BIOMOL International, LP) for acute suppression of apoptosis. The inhibitors were dissolved in dimethylsulphoxide and diluted with saline for intravenous administration. For radionuclide imaging, human recombinant annexin A5 was obtained from Theseus Imaging Corporation (Boston, Massachusetts), and mutant annexin A5 was from Mosa Medics (Maastricht, the Netherlands).
Noninvasive imaging of atherosclerotic lesions
Radiolabeling of Annexin A5 With 99mTc
Human recombinant annexin A5 was produced by expression in Escherichia coliand was labeled with 99mTc, as described (19). Recombinant annexin A5 has been shown to retain PS-binding activity equivalent to that of native annexin A5. Before radiolabeling, annexin A5 was derivatized with the nicotinic acid analog hydrazinonicotinamide (HYNIC) (AnorMED, Incorporated, Langley, Canada) at a 0.9 mol/mol ratio by gentle mixing. Hydrazinonicotinamide is a bifunctional molecule with an affinity for lysine residues of proteins on 1 moiety and for the conjugates of 99mTc on the other; the stable complex formed by this molecule does not affect protein bioreactivity. For binding 99mTc to the HYNIC-annexin A5 conjugate, a reduced tin (stannous ion) and tricine solution was added to 99mTc pertechnetate with an aliquot of HYNIC-annexin A5 under anoxic conditions. The final specific radioactivity was 10 to 200 μCi/μg protein (1 μCi = 37 kBq). Thin-layer chromatography using the solvent NaCl showed a radiopurity between 92% and 97%.
Imaging Protocol
For molecular imaging, each preparation of annexin A5 (0.1 mg) radiolabeled with 5.5 ± 1.3 mCi of 99mTc was injected into the left marginal ear vein of rabbits. Three hrs later animals were anesthetized with ketamine and xylazine (0.1 mg/ml each, 10:1 vol/vol). Radionuclide imaging was performed using a Vertex PLUS gamma camera (ADAC Laboratories, Milpitas, California) for planar imaging (n = 30) or a dual-head gamma camera (n = 7) with micro-computed tomography (CT) X-SPECT (Gamma Medica, Inc., Northridge, California) for SPECT images. Planar images of the abdomen were obtained for 30 min in a 128 × 28 matrix using a 1-mm pinhole collimator. Single photon emission computed tomography (SPECT) images of the abdomen were acquired in a 64 × 64 scaffold, 32 steps at 120 s/step on a 140-keV photopeak of 99mTc with a 15% window. After SPECT acquisition, a micro-CT image of the rabbit abdomen was acquired without moving the animal position. The micro-CT used an X-ray tube operating at 50 kVp and 0.8 mA, and images were captured for 0.5 s/view for 256 views in 360° rotation. The micro-SPECT images were converted to a 256 × 256 scaffold, and micro-CT studies were fused, allowing the achievement of simultaneous molecular and anatomic information in all tomographic scans in 3 different spatial axes. After in vivo imaging, animals were sacrificed with an overdose of sodium pentobarbital (120 mg/kg). Aortas were carefully dissected, and planar images of ex vivo aortas were obtained for 15 min in a 128 × 128 matrix using a 1-mm pinhole collimator.
Quantitative radiotracer uptake in tissue specimens
After ex vivo imaging, each aorta was segmented at 1-cm intervals. These segments were weighed and counted in an automatic well-type gamma counter (1480 Wizard 3″, Wallac, Turku, Finland) for determination of the percent injected annexin dose per gram (%ID/g) of tissue. Biodistribution in the blood, lung, liver, spleen, kidney, and skeletal muscles was also evaluated. Aortas were preserved for histologic and immunohistochemical investigations, as reported earlier (15).
Histologic assessment of experimental atherosclerosis
The aortic segments were fixed with HEPES-buffered formalin (4%) containing an additional 2 mmol/l Ca2+. Histologic and immunohistochemical characterization was performed in 10 atherosclerotic (4 untreated and 2 broad caspase, 1 caspase-1, 2 caspase-8, and 1 caspase-3 inhibited) animals and 2 normal controls. Each aorta was segmented at 1-cm intervals, and each 1-cm segment was subdivided into 3 equidistant sections and embedded on edge in paraffin. The tissue was then dehydrated in a graded series of ethanol. Serial 4-μm-thick sections were cut and mounted on charged slides (Superfrost; Fisher Scientific, Waltham, Massachusetts). Tissue sections were stained with hematoxylin-eosin and Movat pentachrome elastin stains. Atherosclerotic lesions were characterized using a classification scheme based on the recommendations of the American Heart Association (20).
For the immunohistochemical characterization of the cellular composition, primary antibodies directed against macrophages (using marker RAM-11, dilution 1:200 overnight incubation; Dako, Carpinteria, California) and smooth muscle cells (using a primary antibody against actin α and β isotopes, HHF-35, dilution 1:200 overnight incubation; Enzo Biochem, New York, New York) were employed as described previously (15). Primary antibodies were tracked with a biotinylated link anti-mouse antibody using a peroxidase-based labeled streptavidin biotin kit (Dako) and visualized by an 3-amino-9-ethylcarbazole substrate-chromogen system (Dako). The presence of apoptotic cells was evaluated by histologic detection of DNA fragmentation by terminal deoxyribonucleotide transferase TdT-mediated nick-end labeling (TUNEL) staining using an in situ apoptosis detection kit (TACS, Trevigen, Inc., Gaithersburg, Maryland) as described previously (15). A positive reaction was visualized with the chromogen substance diaminobenzidine tinted with CoCl2, which produces a black reaction product. The sections were counterstained with methylgreen (blue-green nuclei).
Based on our previous article (15), annexin uptake in untreated atherosclerotic animals was 0.054 ± 0.0095 %ID/g. With a sample of 6 untreated animals (treatment control group) in the present study, 3 animals per caspase inhibitor treatment group would provide 94% power (1-tailed alpha = 0.05) to detect a 40% reduction in annexin uptake (≤0.0324 %ID/g uptake). We felt this to be an important magnitude of reduction to demonstrate, based on our previous observation showing chronic statin treatment and dietary modification to reduce annexin update by this magnitude (6).
The gamma scintillation counts were calculated as %ID/g of tissue or blood. Results were expressed as mean ± standard deviation. The Student ttest was initially used to compare uptake between untreated atherosclerotic rabbits and all caspase inhibitor-treated groups combined. To determine the statistical significance of differences between individual caspase inhibitor and control groups, 1-way analysis of variance was performed followed by Scheffe's post hoc test for multiple comparisons. An alpha level <0.05 after adjustment for multiple comparisons was considered statistically significant.
In vivo annexin imaging
Gamma imaging allowed noninvasive visualization of atherosclerotic lesions in the abdominal aorta; best visible were the untreated atherosclerotic plaques (Fig. 3).No annexin uptake was observed in normal (nonatherosclerotic, disease control) animals. Similarly, no tracer uptake was seen in atherosclerotic rabbits imaged with mutant annexin A5 (radiotracer control). Annexin uptake was significantly lower in the groups of animals treated with broad caspase inhibitor and caspase-3 inhibitor compared with the untreated atherosclerotic rabbits. Inhibition of caspase-1 and -9 was also associated with substantial reduction in annexin uptake. The uptake was not affected in the caspase-8 inhibitor-treated group. The ex vivo gamma images of the explanted aortic specimens verified the in vivo results.
Noninvasive Imaging of Apoptosis in Experimentally Induced Atherosclerosis With Radiolabeled Annexin A5
The images were obtained in both control (nonatherosclerotic) and atherosclerotic (athero) rabbits with or without caspase (Casp) inhibitor therapy. The top paneldemonstrates planar gamma images, and the bottom panelpresents micro-single photon emission computed tomography (CT) images superimposed on a morphologic background of micro-CT images. (A)Lack of annexin uptake in the region of the abdominal aorta as denoted by arrowsin the normal rabbit with no atherosclerotic lesions. The annexin metabolism and excretion results in variation burden to liver (L), spleen (S), and kidney (K). (B)Compared with the negative control, significant radiotracer accumulation can be seen in the abdominal aorta (shown by arrowsin front of vertebral column activity) of the animal with experimental atherosclerotic lesions. The animals receiving (C)nonselective caspase inhibitor or (D)selective caspase-1 inhibitor demonstrate total abrogation of annexin uptake. (E and F)The bottom panelreveals superimposed nuclear and CT images after treatment with selective caspase-3 inhibitor and caspase-8 inhibitor. The images are present in the set of 2 projections, transverse and sagittal. Whereas the caspase-3 inhibitor completely prevented annexin A5 uptake (arrowspointing to aortic area in front of vertebral uptake), caspase-8 inhibition did not affect annexin uptake or apoptosis. In caspase-8 inhibitor-treated animals, vivid uptake of radiotracer is seen in the abdominal aorta.
Quantitative annexin A5 uptake in treated and untreated lesions
The quantitative annexin uptake in the atherosclerotic specimens, calculated as %ID/g of aortic tissues, should represent the extent of apoptotic activity in the lesions. Maximum annexin uptake was observed in the untreated atherosclerotic lesions (0.0515 ± 0.0099%), which was 10-fold higher than that in the aortic specimens obtained from disease control rabbits (Fig. 4).Among all caspase inhibitor-treated animals (combining broad and caspase-1, -3, -8, and -9 groups; n = 19), there was an overall 39% lower annexin uptake (0.0314 ± 0.0151%; p < 0.01 compared with untreated atherosclerotic rabbits). Among individual caspase inhibitor groups, the annexin uptake was significantly reduced in broad caspase (0.0206 ± 0.0058%; p < 0.0001) and caspase-3 inhibitor (0.0286 ± 0.0095%; p = 0.0034) groups (compared with untreated atherosclerotic lesions). Annexin uptake in the broad caspase inhibitor group was not significantly different than the annexin uptake in normal aortic specimens (p = NS), suggesting almost complete (and acute) abrogation of apoptosis in atherosclerotic lesions. The uptake also was reduced markedly in caspase-9 (0.03 ± 0.0021%; p = 0.0024) and -1 inhibitor (0.0272 ± 0.0088%; p = 0.0016) groups. Annexin uptake remained unchanged for the caspase-8 inhibitor group (0.0618 ± 0.0047%; p = NS compared with the untreated group and p < 0.0001 compared with the disease control group). Together, these data suggest involvement of the mitochondrial pathway of apoptosis in atherosclerosis. Finally, there was no uptake of mutant annexin in atherosclerotic lesions, and quantitative uptake was as low as annexin uptake in normal rabbit aortas (0.014 ± 0.0024%; p = NS). The biodistribution of radiotracer in nontarget organs showed maximal radiation burden in the renal cortex (6.2 ± 1.1 %ID/g), spleen (0.37 ± 0.14%), and liver (0.15 ± 0.05%).
The Extent of Apoptosis in Various Animal Groups Represented by Quantitative Annexin A5 Uptake and Histologic Characterization of Untreated and Broad Caspase-Inhibited Animals
The left paneldemonstrates the uptake of annexin A5 in abdominal aortas. Disease control animals (C) with no atherosclerotic lesions are represented by an open barand the remaining atherosclerotic animals by solid bars. Atherosclerotic animals imaged with mutant annexin were used as tracer controls (gray bar), and the remaining atherosclerotic animals were either untreated (black bar)or treated with various caspase inhibitors (colored bars). Broad and caspase-3 inhibition bars are shown in pink, caspase-8 and -9 inhibitors differentiating between mitochondrial and extramitochondrial pathways are in blue, and capase-1–specific inhibition is represented by a green solid bar. The statistical significance of caspase inhibition, in comparison with the disease control and untreated atherosclerotic animals, is shown above and below the bars, respectively. The uptake is significantly higher in the abdominal aortas of untreated atherosclerotic animals compared with that in the disease and tracer control groups. Treatment with a broad caspase inhibitor or selective caspase-1, -9, or -3 inhibitor significantly reduced the apoptotic activity as represented by lower annexin uptake. On the other hand, selective caspase-8 inhibition did not affect apoptosis. The right panelcompares histologic characterization of atherosclerotic lesions in atherosclerotic untreated animals and atherosclerotic animals receiving the broad caspase inhibitor. Movat pentachrome (M5Ch), smooth muscle cell (α-actin), and macrophage (Ram-11) staining (×200) in untreated atherosclerotic animals (left)and broad caspase inhibitor-treated animals (right)demonstrate similar cholesterol crystal-rich necrotic core, foam cell-rich, and smooth muscle-deficient lesions. The morphologic characteristics of the lesions in untreated and caspase-treated atherosclerosis are unchanged. However, terminal deoxyribonucleotide transferase-mediated nick-end labeling (TUNEL) reveals evidence of marked apoptotic nuclei in untreated atherosclerotic animals but marked resolution in the atherosclerotic lesions in caspase-inhibited animals.
Histology of atherosclerotic lesions
Our previous study had shown that specific annexin uptake preferentially occurred in the advanced American Heart Association type IV atherosclerotic plaque; the uptake was traced to the apoptotic foam cells by dual immunohistochemical staining techniques (15). Similarly, in the present study, the lesions were predominantly foam cell rich with minimal smooth muscle cell content and showed extensive apoptosis (Fig. 4). The animals treated with the broad caspase inhibitor also revealed foam cell-rich lesions histopathologically similar to those in untreated rabbits; however, almost no TUNEL-positive apoptotic nuclei were observed (Fig. 4). The lipid cores with predominant cholesterol clefts and abundant macrophages were visible in the lesions and remained unaffected after administration of caspase inhibitors. A similar phenomenon was observed in the animals treated with selective caspase-1 and -3 inhibitors. However, apoptosis was unaffected in the selective caspase-8 inhibitor group and was found to be similar to untreated animals (Fig. 5).
Immunohistologic Characterization of Atherosclerotic Lesions in Selective Caspase Inhibitor-Treated Animals
Movat pentachrome (M5Ch), smooth muscle cell (α-actin), macrophage (Ram-11), and terminal deoxyribonucleotide transferase-mediated nick-end labeling (TUNEL) staining (×200) in representative sections of aorta from nonatherosclerotic control animals, untreated atherosclerotic (Athero) animals, and those treated with selective caspase (Casp)-1, -3, and -8 inhibitors are shown. The pentachrome stains demonstrate atherosclerotic lesions with large necrotic cores, and the immunostains show intense macrophage infiltration and low smooth muscle cell content in all treated and untreated animals. Therefore, caspase treatment did not change the morphologic characteristics of the atherosclerotic lesions. The TUNEL staining showed evidence of marked apoptotic nuclei in untreated atherosclerotic animals, but treatment with caspase-1 and -3 resulted in decreased apoptotic nuclei in neointima; treatment with caspase-8 did not affect the number of TUNEL-positive nuclei.
The present study demonstrated the feasibility of acute resolution of apoptosis in atherosclerotic plaques with broad and selective caspase inhibitors. This study also demonstrated the feasibility of employing radioactive annexin A5 for evaluation of apoptosis resolution by noninvasive imaging. Because apoptosis of macrophages contributes significantly to plaque rupture, it is logical to presume that acute repression of apoptosis may be of therapeutic benefit in acute coronary events.
The data support efficacy of broad caspase and caspase-9 and -3 inhibitors for acute repression of apoptosis in atherosclerosis. Because caspase-8 inhibition had no significant effect on apoptosis and caspase-9 inhibition significantly blocked it, the apoptosis of foam cells is likely to involve the mitochondrial pathway and not the death receptor pathway. In an earlier in vitro study, caspases-3 and -9 played a critical role in the apoptosis of cultured vascular smooth muscle cells in atherosclerotic lesions, and the inhibitors of both caspase-9 and -3 markedly reduced apoptosis (21).
We observed that the caspase-1 inhibitor also blocked apoptosis to a level similar to the broad caspase and specific caspase-3 inhibitors, suggesting that caspase-1 may also be involved in apoptosis in atherosclerotic lesions (Fig. 1). A previous autopsy report also demonstrated the role of caspase-1 activation in acute coronary syndrome (2). Activation of caspase-1 in apoptosis in atherosclerosis is intriguing (22,23). The pro-domain of caspase-1 enhances caspase-8 activation during CD95 (fas)-mediated apoptosis (24), the specific caspase-1 inhibitor blocks CD95-mediated apoptosis in rat acinar cells (25), and caspase-1–deficient mice are resistant to CD95-mediated apoptosis (26). These studies suggested that caspase-1 may be involved in the death receptor or extrinsic pathway of apoptosis. However, we observed no effect of the caspase-8 inhibitor on apoptosis in atherosclerotic lesions, excluding an involvement of the extrinsic pathway. Caspase-1 involvement in the mitochondrial pathway of apoptosis has recently been demonstrated in traumatic brain injuries in children. Increased levels of cytochrome c, caspase-3, and caspase-1 have been observed in the cerebrospinal fluid, and caspase-3 and -1 activation have been observed in brain tissue (27). It has been proposed that reactive oxygen species generation is downstream of caspase-1 (28,29). Because reactive oxygen species generation mediates apoptosis via cytochrome c release and activation of caspase-9 and -3 (30), it is likely that caspase-1 is upstream of caspase-9 and -3. Our data may indirectly support these observations because the caspase-1 inhibitor blocks apoptosis in atherosclerotic lesion to a similar extent as the inhibitor of caspase-9. Interestingly, activation of caspase-11 has been demonstrated during ischemia-induced apoptosis in the brain (31), which was associated with subsequent activation of caspase-1 and -3. It is unclear if there is activation of caspase-11 in experimentally induced atherosclerotic lesions.
Acute resolution of apoptosis may have translational clinical implications. Because extensive apoptosis has been demonstrated in acute coronary events, acute repression of apoptosis may offer novel avenues for intervention. Such a proposal may be of added value because resolution of apoptosis has also been shown to be beneficial in limiting myocardial injury in experimental myocardial infarction.
The present study indicated that broad and specific caspase inhibitor therapy can acutely reduce the incidence of apoptosis in experimental atherosclerotic lesions. A mitochondrial pathway appears to be predominantly involved in induction of apoptosis, and a novel role of caspase-1 in apoptosis in atherosclerotic lesion is suggested. If verified in clinical trials, repression of apoptosis by specific caspase inhibitors may add to intervention strategies in acute coronary syndromes. Our findings also support the value of annexin A5 imaging as a noninvasive tool to monitor pharmacologic effects of therapies aimed to reduce apoptosis.
↵1 Drs. Sarai and Hartung contributed equally to this study.
This study was supported by the National Institutes of Health, grant #RO1 HL68657 (to Dr. Narula).
Dan Berman, MD, served as Guest Editor for this article.
%ID/g
percent injected dose per gram
single photon emission computed tomography
terminal deoxyribonucleotide transferase-mediated nick-end labeling
Received April 10, 2007.
Revision received August 23, 2007.
Accepted August 24, 2007.
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University of South Carolina archaeologists found an abundance of platinum -- an element associated with cosmic objects like asteroids or comet -- at 11 Clovis excavation sites across the United States. Credit: South Carolina Institute for Archaeology and Anthropology, University of South Carolina
Discovery Of Widespread Platinum May Help Solve Clovis People Mystery
March 13, 2017 Eurasia Review 2 Comments
No one knows for certain why the Clovis people and iconic beasts — mastodon, mammoth and saber-toothed tiger – living some 12,800 years ago suddenly disappeared. However, a discovery of widespread platinum at archaeological sites across the United States by three University of South Carolina archaeologists has provided an important clue in solving this enduring mystery.
The research findings are outlined in a new study released Thursday (March 9) in Scientific Reports, a publication of Nature. The study, authored by 10 researchers, builds on similar findings of platinum – an element associated with cosmic objects like asteroids or comets – found by Harvard University researchers in an ice-core from Greenland in 2013.
The South Carolina researchers found an abundance of platinum in soil layers that coincided with the "Younger-Dryas," a climatic period of extreme cooling that began around 12,800 ago and lasted about 1,400 years. While the brief return to ice-age conditions during the Younger-Dryas has been well-documented by scientists, the reasons for it and the demise of the Clovis people and animals have remained unclear.
"Platinum is very rare in the Earth's crust, but it is common in asteroids and comets," said Christopher Moore, the study's lead author. He calls the presence of platinum found in the soil layers at 11 archaeological sites in California, Arizona, New Mexico, Ohio, Virginia, North Carolina and South Carolina an anomaly.
"The presence of elevated platinum in archaeological sites is a confirmation of data previously reported for the Younger-Dryas onset several years ago in a Greenland ice-core. The authors for that study concluded that the most likely source of such platinum enrichment was from the impact of an extraterrestrial object," Moore said.
"Our data show that this anomaly is present in sediments from U.S. archaeological sites that date to the start of the Younger-Dryas event. It is continental in scale — possibly global — and it's consistent with the hypothesis that an extraterrestrial impact took place."
He said the Younger-Dryas coincides with the end of Clovis culture and the extinction of more than 35 species of ice-age animals. Moore says while evidence has shown that some of the animals were on the decline before Younger-Dryas, virtually none are found after it.
Moore said that would indicate an extinction event for North America.
He also says the platinum anomaly is similar to the well-documented finding of iridium, another element associated with cosmic objects, that scientists have found in the rock layers dated 65 million years ago from an impact that caused dinosaur extinction. That event is commonly known as Cretaceous-Tertiary or K-Pg by scientists.
"In both cases, the anomalies represent the atmospheric fallout of rare elements resulting from an extraterrestrial impact," Moore said.
He said the K-Pg dinosaur extinction was the result of a very large asteroid impact while the Younger-Dryas onset impact is likely the result of being hit by fragments of a much smaller sized comet or asteroid, possibly measuring up to two-thirds a mile in diameter.
"Another difference is that the Younger-Dryas impact event is not yet associated with any known impact crater," Moore said. "This may be because the fragments of the large object struck the glacial ice-sheet or exploded in the atmosphere. Several candidate craters are under investigation but have not been confirmed."
Moore said while his team's data does not contradict the Young-Dryas impact hypothesis, it also does not explain the likely effects that such an impact could have had on the environment, Paleoindians or ice-age animals.
Contributing to the study is Moore's university colleagues Mark Brooks, a geo-archaeologist who conducts research and excavations at the Savannah River Site, and archaeologist Albert Goodyear, who has spent decades documenting Clovis culture at the famed Topper site. Topper, located in Allendale County, South Carolina, along the banks of the Savannah River, is considered one of the most pristine U.S. sites for research on Clovis, one of the earliest ancient people.
Goodyear's work with Moore builds on research in which he found traces of extraterrestrial elements, including iridium, at the Younger-Dryas layer at Topper that was published in the Proceedings of the National Academy of Sciences in 2012.
Moore, Goodyear and Brooks conduct research through the South Carolina Institute of Anthropology and Archaeology in the university's College of Arts and Sciences.
In addition to Topper, the remaining 10 archaeological sites that Moore, Goodyear and others on their team conducted research in 2016 included Arlington Canyon on Santa Rosa Island, California; Murray Springs, Arizona; Blackwater Draw, New Mexico; Sheriden Cave, Ohio; Squires Ridge and Barber Creek, North Carolina; and Kolb, Flamingo Bay, John Bay and Pen Point, South Carolina.
Moore said the bottom line of the study and paper in the journal Scientific Reports is the presence of an easily identifiable hemispheric marker (platinum) in sediment layers for the start of Younger-Dryas. That discovery contributes to the body of evidence that a potential cosmic impact event occurred and warrants further scientific investigation.
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2 thoughts on "Discovery Of Widespread Platinum May Help Solve Clovis People Mystery"
Joe Hueglin
How fortunate for those of us to-day, unlike the Clovis people, have the capability of countering natural events. We cause global warming. We can halt it. Unlike the Clovis who would have had to let it run its course.
Fern Henley
Our capability of countering natural events has been considered by a few humans but to act on a plan to deflect a big extraterrestrial body impacting earth is far from our current capability. The current challenge we face is to create a global community of sovereign nation states capable of cooperating for the common good of detecting and deflecting an extraterrestrial missile from any direction. Possibly this community is being developed now by the OBOR initiative. That seems the best possibility of protecting humanity from this danger which is just now being added to our list of dangers already identified such as war, disease, poverty, pestilence, and climate change. Only a few thousand years ago did we begin to study the Golden Rule so we are making progress. The retributive justice so helpful in establishing law and order is being replaced with restorative justice but slowly.


text:
Q: Why was this uploaded image rotated 90 degrees? I recently uploaded this image in chat.

However, on upload, the image was rotated 90 degrees to the right, for no obvious reason that I can discern. I didn't ask for it!

What happen?

A: [michael@challenger:~]$ jhead DSCN0873.jpg
Header missing JFIF marker
File name    : DSCN0873.jpg
File size    : 120421 bytes
File date    : 2008:12:27 15:08:01
Camera make  : NIKON
Camera model : COOLPIX S51
Date/Time    : 0000:00:00 00:00:00
Resolution   : 600 x 800
Orientation  : rotate 90
Flash used   : No (auto)
Focal length :  7.9mm  (35mm equivalent: 47mm)
Exposure time: 0.0031 s  (1/320)
Aperture     : f/6.9
ISO equiv.   : 100
Exposure bias: -0.70
Whitebalance : Auto
Metering Mode: pattern
Exposure     : program (auto)

Looks like the rotation metadata got missed due to the missing header.
After fixing header:
cp DSCN0873.jpg DSCN0873-fixed.jpg
jhead -mkexif DSCN0873-fixed.jpg
jhead -te DSCN0873.jpg DSCN0873-fixed.jpg

But wait! Those dimensions... let's just nuke the rotation data:
jhead -norot DSCN0873-fixed.jpg

So as it turns out, imgur was acting correctly.


The large dish with moulded green overlapping leaves with puce veins with a central raised roundel with a polychrome flower bouquet. The rim with puce rococo swirls. Two tiny frits to rim invisibly repaired.
Provenance: Albert Amor Ltd.; Private collection label with WP 295.
Reference: Zorensky catalogue fig. 83. Provenance: the Rous Lench collection, Sothebys 1st July, 1986, lot 261.
This shape is relatively rare and unlike most leaf forms in English porcelain, it appears to have no Meissen prototype. For a blue and white example see fig. 615.


This is an article I wrote for my profile on Tutor Pages.
As you are likely to know if you are reading this, the grading for GCSE has been changing, with the new method phased in between 2017 and 2019. Maths, my subject, was one of the first to 'move over' to the grades from 9 to 1 from A to G.
Unless a tutor has worked in schools during this period and so picked up on training there, he or she needs to do some homework on the changes. I don't claim to have done all the work I need to on this, but I thought I would share some observations on how exam questions have changed, specifically in Maths.
The change from letters to numbers is not just cosmetic. The distribution of the grades will be different. Under the old system, grades A to C were considered as the old fashioned 'pass'. When I took my GCSE course in the 1980s, this was shortly after the GCSE qualification had been created from a merger of GCE and CSE. My lecturers on that course were keen to say that all 'letters' were a sign of attainment – a student who gained a D had found some level of success – but the idea that one should 'pass' – and that A, B and C were the pass grades – persisted. It's commonly held that you 'have a GCSE' if you attained C or higher. I'm not saying that is good or bad, but I was sure this would happen even while being told otherwise by my lecturers.
A notable feature of the 9 to 1 system is there are more pass grades. A grade 4 or above will be considered a 'pass' – which is not to say that a pass will be easier to achieve. A 4 will be roughly equivalent to a C, though the grade boundaries are not exactly the same. It's at the top end that the change is greatest, with a 7, 8 or 9 all corresponding to an A/A* grade, and differentiation between the brighter students that provides the reasoning behind the change.
For this to be achieved there needs to be an increase in the number of truly challenging questions on exam papers. There will be more questions that students targeting a respectable 4, 5 or 6 will find it difficult to attempt. There is also a different style of question even in the 4/5/6 range of question that will reward not only hard working 'book workers' but encourage a depth of understanding and problem solving skills.
Does this make the exams harder? Arguably so. But if prepared for properly by educators, will raise the level of ability as related to grade.
I'd like to look at a few examples to support my point – though I'll add here as an aside, for the non school based tutor, the change has the unwanted side effect that we won't have the bank of old paper to use. This will of course, improve with time. Exams tend to be made available 15 months or so after they are 'live', and some boards have published free samples.
Calculation of surface area and volume isn't the simplest subject area on the GCSE Maths syllabus, but neither is it the most complex. But this question really tests the exam takers reasoning powers. On the old A-G papers, this might have been 'Find the volume of a cube with surface area 150cm2'. This question puts the student in a new role, which might be unfamiliar if their tutor has not prepared well.
This is another question designed to strech the student. The three marks for part a can be earnt by understanding how to estimate. The extra mark requires an understanding of exactly what they did in part a. It's a deeper level of knowledge, and shows that grades 8 and 9 are there if one is truly at home with numbers.
I have found my able Year 10 student lapped this up – but for a student aiming for a 4 to 6 grade, I'd probably leave this alone.


Suzanne Flynn and Wayne O'Neil Massachusetts Institute of Technology I. INTRODUCTION The theory of Universal Grammar (UG) as explicated e. g. in Chomsky, 1986, has led to explosive developments in the study of natural language as well as to significant advances in the study of first language (L I) acquisition. Most recently. the theory of UG has led to important theore tical and empirical advances in the field of adult second language (L2) acquisition as well. The principle impetus for this development can be traced to the work in linguistics which shifted the study "from behavior or the products of behavior to states of the mind/brain that enter into behavior" (Chomksy. 1986:3). Grammars within this framework are conceived of as theoretical accounts of "the state of the mind/brain of the person who knows a particular language" (Chomsky. 1986:3). Research within fields of language acquisition seeks to isolate and specify the properties of the underlying competence necessary for language learning. Full development of a theory of UG demands study and understanding of the nature of both the formal properties of language and of the language acquisition process itself. However. while there is a tradition of debate and dialogue established between theoretical linguistics and Ll acquisition research. relatively few connections have been made between linguistic theory and L2 acquisition research.
A Theoretical and Historical Context for Second Language Acquisition.- Linguistic Theory: Generative Grammar.- The Ontogenesis of the Field of Second Language Learning Research.- B Parameters.- Parameterized Grammatical Theory and Language Acquisition: A Study of the Acquisition of Verb Placement and Inflection by Children and Adults.- Nature of Development in L2 Acquisition and Implications for Theories of Language Acquisition in General.- Linguistic Theory. Neurolinguistics and Second Language Acquisition.- Second Language Acquisition: A Biolinguistic Perspective.- Neurolinguistics and Parameter Setting.- C Markedness in Second Language Acquisition.- The Acquisition of Infinitive and Gerund Complements by Second Language Learners.- Island Effects in Second Language Acquisition.- On the Role of Linguistic Theory in Explanations of Second Language Developmental Grammars.- L2 Learnability: Delimiting the Domain of Core Grammar as Distinct from the Marked Periphery.- Kinds of Markedness.- D Additional Evidence for Universal Grammar.- The Categorial Status of Modals and L2 Acquisition.- UG-Generated Knowledge in Adult Second Language Acquisition.- Prosodic Phonology and the Acquisition of a Second Language.- Universal Grammar in Second Language Acquisition: Promises and Problems in Critically Relating Theory and Empirical Studies.- E Complementary Perspectives.- Pidginization as Language Acquisition.- All Paths Lead to the Mental Lexicon.- Intermorphology and Morphological Theory: A Plea for a Concession.- F Universal Grammar from a Traditional Perspective.- Second Language Acquisition and Linguistic Theory: The Role of Language Transfer.- Grammatical Theory and L2 Acquisition: A Brief Overview.- Typological and Parametric Views of Universals in Second Language Acquisition.- List of Contributors.- Index of Names.- Index of Subjects.