text:
Oslo and the Motivation for Evil
I'm going to Oslo for the launch of the International Association of Freethought next week. With others, I'll be speaking under the topic "Atheism in the 21st Century". I'm looking forward to being with hundreds of rational people and hearing their thoughts. But "Oslo" has a terrible resonance in people's minds at the moment, because approximately 76 people were killed by Behring Breivik in Oslo on 22 July.
Breivik has been described as a Christian fundamentalist. He is also Norwegian, male, anti-Muslim, anti-multiculturalism, anti-womens' rights and anti-socialism. We may never know what exactly motivated Breivik but it seems to be a deranged mix of factors. For atheists it may be tempting to at least partially blame the Christian influence for Breivik's rampage. Maybe religious influence is partly to blame, as I discuss further below, but atheists should be wary of playing the illogical "body count" game that sees some religious people point to Hitler (actually a Catholic) and Stalin (a dictator who was educated in a seminary) as examples of the negatives of atheism. Even if it was possible to measure accurately, a count of deaths caused by religious people relative to atheists is unlikely to tell you more than who happened to be the most effective at perpetuating evil. There are good and bad religious people, good and bad atheists, good and bad people across the political spectrum as well as good and bad left-handed people. The critical issue is why people commit atrocious acts, their underlying motivation.
The Bible is a book that has been interpreted to justify a broad range of actions, across a spectrum that would generally be considered to include "good" or "bad" designations by most people. If a Christian is looking for guidance on being a good person they could find it in the Bible – so long as they conveniently ignore all the non-good-person bits. They could also probably find such guidance in the fairytale Cinderella if they wanted to. It's a sad situation if someone needs to rely on a book (or the promise of heaven / the threat of hell) to be a good person, but it's conceivable that someone might. However, most people, religious or otherwise, are "nice" people. Humans have evolved to be cooperative because it benefited our genes to live within a supportive social structure. It's good marketing for religion to claim some credit for humans' evolved cooperative behaviour and basic "niceness", but it isn't accurate. If all the Christians found out tomorrow that the Hindus were actually right and there is no God, the vast majority of them would still be nice people. While maybe well-intentioned, those who advocate that "religious faith makes people do good things" are implying that faith is a reasonable basis for actions. It is not. It's just that the outcome is less harmful than bad actions motivated by religious faith.
Similarly, if someone is looking to justify harmful actions then they can find relevant guidance in the Bible. Unfortunately the Bible also alleges authority and a final judgement. Intellectually this is highly dubious, but at least not particularly dangerous for others in the context of good actions. However, it is very dangerous in the context of harmful actions. If there is a higher power that can trump any inconvenient human laws or social attitudes, if there is some kind of reckoning and afterlife of reward and punishment based on a religious system of right and wrong, then that facilitates an abdication of responsibility for living within the laws and attitudes of our society. Some people who have committed atrocious acts – the 9/11 hijackers, people who kill doctors who perform abortions in the US – have explicitly religious motivations, and proudly proclaim them. For others – probably including Brevik – the motivations appear varied.
In contrast to seeking guidance in old books, atheists think for themselves. If I do good things it is not because I'm an atheist. It is because logic tells me that the world will be a better place if people do good things; I am one person among many; I should do good things if I want others to do the same. And if I do bad things it won't be because atheism encouraged me to do them, it will be because I'm selfish or thoughtless. My actions, my responsibility.
No doubt some of the horrific crimes committed by humans over time have been perpetrated by atheists. One day there will be a high-profile killer who happens to be an atheist. Someone religious will probably try to claim that this killer lacked a good moral grounding because they didn't accept the teachings of [insert their preferred god/prophet/holy person here]. But they are missing the point of atheism. The absence of a belief (in a god or anything else) is not a foundation for any kind of action or inaction. There is no holy book for atheists to interpret, no one to preach that certain actions are right or wrong. Atheism doesn't tell you what to think, it just tells you to think. To use reason and logic. To base decisions and views on evidence. Some day some twisted person could construct a path from "I don't believe in any god" to "killing people is a good idea" – maybe someone already has – but atheism will not provide a rationale, excuse or absolution. Religion cannot claim the same.
Tags: #AAIPresident, #IAFT, #Oslo


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Results of the Autumn Alliance Contest!Journal Entry: Thu Dec 6, 2012, 11:22 AM
Hello my beautiful Allies! It's time to announce the winners of our Autumn Alliance Contest!
What is the Alliance, you ask?
The Alliance is a project group intended to encourage visual and literary artists to work together. I've felt for some time that the
dA Literature Community can at times be somewhat insular - to its detriment. We in the Lit Community are also sometimes prone to griping
about the lack of exposure our work receives when compared to that of visual artists. So in the spirit of ^thorns brilliant
Complaint Challenge I thought I would try to do something about that. And so the Alliance was born!
We didn't have an extraordinary amount of entries, but the entries we did receive were extraordinary.
We had a tough time choosing the winners, but choose we did. And here they are.
In First Place
The White Lady of the NorthShe among the grass did briefly dwell,
The White Lady, Forerunner of the North Wind,
But she is the end of Autumn's gold.
Her touch is ice. Her kiss is cold.
I will greet her with fire in my hands,
And whisky in my mouth.
by Synnic
based on
The judges agreed that the author really
took the original photo and made the idea their own,
wringing every last ounce of imagery and inspiration
and weaving it into the poem.
In Second Place
by Missvirginia
based on
I am as autumnI am as autumn,
dropped barefoot into some fleeting role,
self-destructing in the sterile cold
while passersby note only
the colours,
their ephemeral beauty.
I was meant
as an actress, diaphanous and
bridging the small gap between
summer and
I was born to wither and
without blooming,
to sink and
without struggling.
obedient as a child,
I tried to die
in that space before snowfall,
that melancholy breach
but there must be something in me
that is not yet dead,
that refuses to rot.
when the snow finally came,
I was stale and stagnant,
wretchedly vernal
when all else was newly
now, in the dim half-light before
springtime, I am thin
and fragile, waiting only for
another chance
The judges felt that this image was very evocative
of the inspiring poem, had a similar feel,
and that the influence of the
poem was readily apparent.
In Third Place
Nuclear FallThe world of man had passed; in his ignorance he'd died,
Despite his expectations, though, nature would not subside
An arrogant harvester, gave himself absolute worth
Oh, but if only he could have heard dear Nature's mirth
Man's creations crumbled, his poison dissipated,
Bodies beset by scavengers, pecked at, eviscerated,
And nature's gentle cycles kept on spinning even still,
The trees had leaves of amber once the air began to chill
For all of mankind's worry,
Himself alone did he kill
by Owari999
based on
by ElenaNaylor
The judges were impressed with how well the author
interpreted the inspiring image, especially
in a fixed form.
Honorable Mention
based on
AfforestThe last darkness will fall like autumn leaves
Dusky ground covered with many coloured twilights
(do you see all the lovely greys?)
Underneath which ghosten happiness lays buried
(spring was too far away. Alas)
The last darkness is falling like autumn leaves
Dusky ground covered with beaten light's corpse
(do you see all the dimmed colours?)
Underneath which darkened May Day lays buried
(spring is too far away. Alas)
The last darkness has fallen like autumn leaves
Dusky ground covered with still-frozen time
(do you see all the solemn blacks?)
Underneath which doomed Freya lays buried
(spring will be to far away. Alas)
by lunanne
The judges loved the originality in form and style
in this image, and how it captured the dark
atmosphere of the inspiring poem.
Our other entries were also fantastic! And so we shall feature them here as well.
based on
by LadyOfSilver
This piece has such a wonderful fall feeling.
The original prose piece obviously
inspired the artist greatly.
Autumn SorrowStill dark water flows by, dotted by autumn leaves. The orange has faded, now, wilted, turned brown as the season has passed. Trees stretch their dark, naked arms towards the sky, praying for sunlight, for warmth, for life. But their prayers will go unheeded for months to come as snow and frost cover all in a thick, cold, soft blanket. The world stands at Winter's door.
Silent steps descend the stairs, the sound hidden by the mournful singing of the small river. Naked feet, red with cold, step on grey stone painted with frost. Dead, brown grass crunches and breaks as the person, dressed in robes of grey, kneels before the wailing statue by the river.
Mourning grey. That is what the color is called, the one the person's robes are. They cover everything but hands, face and feet, rag-like and torn. They cannot hide the shaking shoulders as the mourner prays to the statue, the grey stone frozen in grief, both hands covering the face.
Naked feet, red with cold, step silently onto the stone.
by Lizardhound
based on
by AncientKing
The whimsical, fantasy style
of the drawing is lovely; much of the
poem made it into the image, while the artist
still made it her own interpretation.
by Auzureii
based on
Leaves and LeavingTurning leaves remind me that some people change along with the seasons.
Leaf. Leaves. Leaving.
Hush. If you listen real close, you can hear leaves laughing as they let go of the twigs that adore them. They flutter quietly to the ground, their graceful suicides silent to everyone except their beloved branches.
Look, the world is orange and jagged and rusted. It is decadence and leaves and leaving. It is home, it is heaven, and it is hell.
One by one, the trees ignite themselves and we watch their soundless self-destruction unfold. Whole forests seem to go up in flames without smoke. Sometimes we take pictures.
We are only left with black and brown skeletons that patiently wait to be buried under white.
I spend my entire autumn watching things die.
The artist took inspiration from both
a visual and a literature deviation
to create this vibrant image.
Thank you so much to everyone who entered! We are thrilled to see our members inspired by one another and hope that you'll continue to create inspired art
and submit it to our featured folder. Our Winter Contest will be announced in a few days!
Until next time...
I'm honored to have placed. Thank you very much!
wow, thanks so much for the honorable mention and your lovely words!!!!
You're most welcome!
Congrats to the winners!
Somehow the last two entries have the same text?
Somehow the last two entries have the same text?
...it was not intentional. Thanks for catching that for me!
Yay! :applaud: Congrats to all our winners!

subset: commoncrawl


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Chat replay: A D-FW Sports Talk With Rick Gosselin (4/7/14)
I feel pretty good about this up and coming year,even if we lost a few really good players this year,if we can have a great draft like last year,and picking up melton,if we can get him back to probowl form.It is about time that we stop over paying for players at the end of their carrer,OR THEY HAVE A GREAT CONTRACT YEAR AND WE SIGN THEM TO A LONG BIG DOLLOR CONTRACT EXTENSION AND THEY NEVER REPEAT THAT KIND OF PERFORMANCE AGAIN AND THEN WE CUT THEM TWO OR THREE YAERS LATER,WHAT IS YOR THOUGHTS
Any reason for optimism should stem from the fact the Cowboys are finally doing right by the salary cap. They have become more wise in their spending and roster assessment. Whether you agree or nt with the decisions to part ways with Jay Ratliff, DeMarcus Ware and Jason Hatcher, it was the right thing to do. You couldn't carry players at their ages at those price tags in a salary cap world. Signing a young, Pro owl-caliber talent like Henry Melton at a club friendly contract was another step in the right direction. The key, now, is that the Cowboys have to draft well. Every time you miss on a draft pick, you wind up overspending to correct the mistake in free agency. The Cowboys have too many misses on draft day and too many overcompensations in free agency. That's how they got into this mess. There's only one way now to get out -- draft well.
When you have the worst defense in the NFL -- arguably the worst defense in the history of your franchise -- you don't fix it by focusing on offense in the draft. When they Cowboys go on the clock at 16, there will probably 3-4 candidates for the pick, all with roughly the same grade. I'd be surprised if they don't pull a defender out of that grouping. When you lose a Ware, a Hatcher and a Ratliff all in the last six months -- impact players for this franchise -- you need to replace them with impact players. You get impact in the first round. I'd go DL with my first three picks. You win in the NFL up front.
I really like Barr, but you'd be asking him to make a position switch. He was a linebacker in college with pass rush skills. Rod Marinelli would want that guy at end in this scheme. The position switch would slow him down a tad as a rookie, but he's going to be a good player at the next level.
If Johnny Football is available when the Cowboys pick, don't you think the prudent move is for Jerry to trade Tony Romo (he could probably get a couple of first round picks for him!!!) and draft JFF to be the Cowboys franchise quarterback. He looks like the next Brett Favre to me and we need him to wear a STAR on his HELMET!
Hi Goose,
Really appreciate all the sports knowledge you bring to the scene. I have a Rangers question for you. The Rangers are middling along at .500, and it seems like their biggest deficit is in the leadership department. I know the stat geeks don't care about those "intangibles," but they matter a lot. With that in mind, do you think the Rangers could coax Michael Young out of retirement to fill that role (and play some wicked 2B!)? Thanks the Goose.
If SMU is able to land Euless Trinity big man Myles Turner to pair with Emmanuel Mudiay they will have signed two of the top 5 prospects in the country. SMU returns key starters and reserves from a very good team. If they get Turner do you think SMU could potentially start next year in the Top 10?
I'd guess SMU would start the season ranked but I'd be surprised if the Mustangs are in the Top 10. Those spots usually go to the traditional basketball powers -- the Kentuckys, Dukes and North Carolinas. Sign those two players and I think SMU would start the season ranked somewhere between 16-21.
I don't ever see it happening. I could see him turning the post over to his son Stephen if and when the Cowboys win another Super Bowl under Jerry's watch. But not until then. Jerry wants to be at the front of the parade when the Cowboys win their next Super Bowl.
Jackson will make the Washington offense better and RG III a better quarterback. This team won the division two years ago and Jackson will help them compete again. hey are hoping Philadelphia's loss is their gain. But I still like the Eagles in the East in 2014. Jackson is 28 this season. The Redskins would like to get two seasons out of him. It's not like he's 23 and you're hooping to get 7-8 years out of him. Like TO, I would expect Jackson to be on his best behavior in his first season with a new team.
It's still way to early in a 162-game season. I think the Rangers need to stay afloat the first month of the season through their injuries. We saw how a slow start killed the Angels in this division last season. The Rangers have to stay near .500 after the first month, not after the first week. This first month is all about survival until the healthy troops can return.
All the experts say the Giants and Redskins did well this offseason because of how many free agents they were able to sign. But you've always said that every time a team misses on a pick they have to fill it in FA. So does that mean the Giants and Skins aren't drafting well? Shouldn't that be a cause of concern rather than rejoice?
The Giants filled a lot of holes in their roster without spending a whole lot of money. They signed 13 players and 10 of them will be making less then $3 million per year. And only one of those players will be in his 30s this season. The Giants are a team that got old overnight and they were able to apply a lot of patches this offseason. The Redskins also signed 10 players and, again, most figure to be short-term patches. These two franchises feel the sense of urgency in chasing the Eagles.
I prefer to sit upstairs at virtually every sporting event I attend as a fan because you can see the entire field, court or ice. You see plays develop and what's going on away from the play. But if you're trying to impress, get seats downstairs on the first base side. Most lineups are heavier on right-handed hitters, so the batter is facing you at your seat.
Rick - thanks for taking time out of your day to talk sports with us. Do you think the Rangers should be really worried that the Astros are about to overtake them as Texas's team? We all know Nolan Ryan got them to the two world series and that jerk Daniels took all the credit. Is Nolan going to work his magic in Houston again? Talk me off the ledge!!!
I think it would be healthy for Texas if both teams are competitive. That would develop a nice rivalry that could be good for the state, good for attendance. Daniels wasn't just along for the ride on those World Series teams. And I don't see Nolan having final say with that's happening in Houston. The Rangers will be fine in the short term and so will the Astros in the long term.
Lots of Cowboys draft talk, but question about Mavs draft prowess (or lack thereof). Mavs clearly have not valued building through the draft in the past 10 years...do you think that will come back to haunt them when Dirk retires? Spurs have been successful adding pieces with the draft, why not the Mavs?
Clearly the Mavericks need to get a young championship piece in place before Dirk hangs up his shoes. You get those players in the draft, not free agency. I've never felt the Mavericks have taken the draft too seriously. It will grow in importance every year going forward that Dirk ages. The Mavericks need some hits, especially in the mid- and later rounds as the Spurs have done. The next face of the franchise needs to emerge soon.


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There's nothing quite like a summer evening at a good old-fashioned county fair, like the one this week in Bedford.
Friday night features the weekly draw of stock car racing at the Bedford Speedway. But In addition to the fun food, carnival rides and displays, the fair brings back to life a unique brand of "farm sports."
The Bedford County Fair celebrates the culture of agriculture in Central Pennsylvania. The state's largest industry, farming is, like most businesses, trying to power through the struggling economy. The fair is a chance to put the stress on the back burner and celebrate the county's heritage, with competitions more likely to be found in a corn field than on a football field.
Jeff Foxworthy might have a field day at the fair, but that's what makes it so much fun. The fair is a forum for testing the power of your tractor John Deere goes grill to grill against International Harvester and others in a grandstand tractor pull. It's like watching two heavyweights do battle for a boxing belt with rugged tires digging into the rain-packed dirt.
The 4-by-4 truck pull tests the strength and power of the pick-up in classic Ford vs. Chevy showdowns.
The demolition derby events are always a fan favorite. Drivers try to out-maneuver each other in the confines of the race track infield. Smashmouth takes on a whole new meaning in this "sport" as cars, trucks and even mini-vans are destroyed before your very eyes.
Every day brings a new competition of one kind or another. There are even smackdowns for vegetables, maple products, flowers and Christmas trees, with winners taking home blue ribbons and bragging rights.
County fairs are like game days for area 4-H clubs, which shine while showing the products of their year-round work, from raising livestock to air pistol and rifle contests.
Fans can sit in the grandstand every night to enjoy the marquis shows: tractor pulls, 'Bullride Mania,' auto racing and demo derbies. It's family-friendly summertime fun with an historic undertone.
But for those who work on farms every day, it's even more. It's a celebration of their heritage and their hard work, a chance to showcase the fruits of their labor, like local apples and peaches, Holsteins and hogs.
Celebrating the 136th edition of the Bedford County Fair, the Holbert family, who runs the week-long event, works year-round to provide this special showcase for an under-celebrated sector of our state's workforce. The Fair's series of competitions may not earn a spot on the sports pages, but they should win a place in the hearts of all of us.
The farm sports give guests a glimpse at what goes into the day-to-day work that puts food on our tables and roofs over our heads.
Kellie Goodman Shaffer can be reached at email@example.com. Her column appears on Tuesdays.


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Beaudoin, Greg MSc*; Diker, Bilge MSc*; Angel, Jonathan B MD*†; Copeland, Karen F T PhD*
From the *Molecular Medicine Program, Ottawa Health Research Institute, Ottawa, Ontario, Canada; and †Infectious Diseases Division, The Ottawa Hospital, Ottawa, Ontario, Canada.
Received for publication September 20, 2005; accepted May 30, 2006.
Supported by the AIDS Program Committee of the Ontario Ministry of Health and Long-Term Care (grant PA00103).
J. B. Angel is an Ontario HIV Treatment Network Career Scientist. K. F. T. Copeland is an Ontario HIV Treatment Network Scholar.
Reprints: Karen Copeland, PhD, Molecular Medicine Program, Ottawa Health Research Institute, 501 Smyth Road, Ottawa, Ontario, Canada K1H 8L6 (e-mail: email@example.com).
Summary: To date, the relation between the CD8+ antiviral factor (CAF) and clinical indicators of disease progression in HIV-1 infection (CD4+ T-cell counts and viral load [VL]) is inconclusive. Particularly, the effect of antiretroviral therapy and immune recovery on CAF production remains unclear. Using a transient transfection assay and a reporter gene activated by the HIV-1 long terminal repeat (LTR), we analyzed CAF production in CD8+ T cells of HIV-1-positive individuals divided into 3 groups: patients on protease inhibitor (PI)-based therapy, patients on nonnucleoside reverse transcriptase inhibitor (NNRTI)-based therapy, and patients receiving no therapy. We found that within the untreated group, CAF activity inversely correlated with VL and high CAF was associated with lower VLs over a period of 0.5 to 3 years. Furthermore, patients who were drug-naive demonstrated significantly higher CAF than untreated patients who had previously undergone antiretroviral therapy. CAF activity in treated patients was similar to CAF in drug-naive patients and higher than in off-treatment patients. There seemed to be a trend toward higher CAF in patients on NNRTI-based therapy compared with those on PI-based therapy. These results suggest that immune recovery after highly active antiretroviral therapy (HAART) contributes to the normalization of CAF levels in HIV-1-positive individuals. Furthermore, we have distinguished between CD8+ T-cell-mediated suppression of HIV-1 replication and gene transcription.
CD8+ T cells were first shown to suppress HIV-1 replication almost 2 decades ago,1 yet the protein factor(s) involved in CD8+ antiviral factor (CAF) activity is unknown. CAF suppresses viral replication at the level of transcription,2-7 and it has been shown that CAF activity, particularly the inhibition of long terminal repeat (LTR)-mediated gene expression,8 is not mediated by chemokines.8-11 CAF has also been found not to affect reverse transcription or provirus integration.12
In the context of clinical HIV-1 infection, data are inconclusive as to the effects of infection on CAF activity. Blackbourn et al13 showed that CAF activity in lymphoid tissue-derived CD8+ T cells positively correlated with control of viral replication in the lymphoid tissues, but no such correlation was observed in peripheral blood.13,14 In another study, a negative correlation was found between CAF and viral load (VL) in baboon peripheral blood.15 Others have shown that before antiretroviral therapy, CAF inversely correlates with VL, but that after therapy, the 2 are positively correlated.16 The association between immune status and CAF is also unclear. CAF has been shown to decrease with disease progression,17,18 and other studies have shown a positive19-21 or negative22 correlation between CAF and CD4+ T-cell counts in untreated HIV-1-positive individuals. Improved clinical status was shown not to be a determinant of CAF levels, however.23 This is corroborated by Kootstra et al,24 who showed that there was no correlation between CD4+ T-cell counts and CAF.
The effects of highly active antiretroviral therapy (HAART) on CAF activity within HIV-1-positive individuals have recently been studied, and conflicting results have arisen. In a longitudinal study, CAF was shown to decrease significantly in 76% of patients on HAART but increased or was maintained in untreated patients.25 In addition, CAF from HIV-1-positive individuals undergoing HAART was found to decrease to levels associated with HIV-1-negative individuals in another study.16 Conversely, Kottilil et al26 showed higher CAF in HAART-treated patients compared with untreated controls, and Chun et al27 showed that patients who commenced HAART shortly after acute infection had significantly higher β-chemokine-independent CAF than long-term nonprogressors, untreated patients, and patients who commenced treatment during chronic infection. This is reflective of findings by Oxenius et al,28 who found that HIV-1-specific CD8+ T-cell function was preserved in patients who commenced HAART during primary infection or concurrent to seroconversion; in patients in whom HAART commencement was delayed, HIV-1-specific CD8+ T-cell function was lost. Replication-based assays were used to determine CAF, and most do not control for confounding factors that might inhibit steps of the infection cycle other than that of gene transcription. Our goals were to determine the effects of HAART on CAF in HIV-1-positive individuals and whether there was any association between CAF and clinical profiles using an assay that defines CAF activity as the ability of cell-free supernatants from phytohemagglutinin (PHA)-stimulated CD8+ T cells to suppress LTR-driven gene expression.
Primary CD8+ T cells were cultured in RPMI 1640 (Gibco, Carlsbad, CA) supplemented with 20% fetal calf serum, 200 U/mL of penicillin (Gibco), 200 μg/mL of streptomycin (Gibco), and 20 U/mL of interleukin (IL)-2 (National Institutes of Health [NIH] AIDS Research and Reference Reagent Program) at 37°C and 5% co2. Jurkat T cells were cultured in RPMI 1640 supplemented with 10% fetal calf serum.
HIV-1-positive patients attending the Ottawa Hospital Infectious Diseases Unit provided informed consent to provide blood for this study. Age-matched patients were divided into 3 groups depending on their treatment regimen: protease inhibitor (PI)-containing therapy (n = 12), nonnucleoside reverse transcriptase inhibitor (NNRTI)-containing therapy (n = 13), and an untreated group consisting of patients who had been off treatment for more than 6 months (n = 8) or who were drug naive (n = 8). In both treated groups, selection criteria (to ensure effective treatment) included an undetectable VL (<50 copies/mL) and a CD4+ T-cell count of >200 cells/mm3. T-cell counts and VL data were assessed between 0 and 3 months before CAF analysis.
Peripheral blood mononuclear cells (PBMCs) were separated from whole blood by Ficoll-Paque PLUS (Pharmacia Fine Chemicals, Piscataway, NJ) gradient separation, washed twice with phosphate-buffered saline (PBS), and cultured at 1 × 106 cells/mL. CD8+ T cells were isolated from cultured PBMCs using magnetic affinity cell sorting (MACS) CD8 microbeads and MS+/RS+ columns (Miltenyi Biotec, Auburn, CA) according to the manufacturer's instructions. Briefly, cells were washed twice with MACS buffer (5% bovine serum albumin and 2 mM of ethylenediaminetetraacetic acid [EDTA] in PBS) and incubated for 20 minutes at 4°C with CD8-specific microbeads. Cells were passed through the magnetic separation column, washed, eluted with MACS buffer, and washed twice with PBS. Cells were then cultured at 1 × 106 cells/mL and activated with 5 μg/mL of PHA for 3 days, washed and resuspended at 1 × 106 cells/mL in fresh media in the absence of PHA, and cultured an additional 3 days. After pelleting the cells, CD8+ T-cell supernatants were removed and their volumes were adjusted with media so the amount of supernatant originating from 0.5 × 106 cells would equal 1 mL. Cell-free supernatants were then heat-inactivated (56°C for 60 minutes), and stored at −80°C.
Jurkat T cells were grown to confluence, resuspended at 1 × 106 cells/mL in fresh media for 18 hours, and then pelleted and resuspended in an equal volume of fresh media for 2 to 3 hours. Cells were washed twice in serum-free RPMI 1640 and resuspended at 6 × 106 cells/mL in transfection buffer containing 250 μg/mL of diethylaminoethyl (DEAE)-dextran (Sigma, Oakville, Ontario, Canada) and 50 mM of Tris, pH 7.3, in serum-free RPMI 1640. We then added 1 μg/mL of a vector in which the LTR of HIV-1 drives the expression of chloramphenicol acetyltranferase (pLTRCAT)29 with an LTR sequence of a clinical isolate (HIV-1BRU) to position +77, and 0.5 μg/mL of a vector in which Tat expression is controlled by the SV40 promoter (pSVtat)30 to activate the LTR. Cells were incubated in a 37°C water bath with shaking at 50 rpm for 45 minutes. Transfected cells were pelleted, washed twice with serum-free RPMI 1640, and cultured at 3.75 × 106 cells/mL. Each transfection was performed on a maximum of 30 × 106 cells. Freshly transfected Jurkat T cells were aliquoted in 12-well tissue culture plates (1.875 × 106 cells per well), and 1 mL of CAF-containing cell-free CD8+ T-cell supernatants was added to each well. Cells were cultured for 24 hours and then activated with 25 ng/mL of PMA (Sigma) and 2 μM of ionomycin (Sigma) to enhance baseline reporter gene expression further. After 18 hours of activation, cells were washed twice with PBS and resuspended in 0.5 M of Tris. Cells were lysed using 3 freeze-thaw cycles, and lysates were cleared of cell debris by centrifuging at 14,000g for 15 minutes. Protein concentrations in cleared lysates were determined using the BioRad Protein Reagent (BioRad, Mississauga, Ontario, Canada). For CAF determination, 10 μg of total lysate protein was loaded into a CAT enzyme-linked immunoassay (ELISA) plate (Roche, Laval, Quebec, Canada), and volumes were adjusted to normalize total protein concentration to 50 μg/mL. CAF activity for each CD8+ T-cell supernatant was determined as percent suppression of CAT expression relative to a media-treated control.
Interferon (IFN)-γ and IL-16 concentrations in cell-free supernatants were determined using ELISA kits (IFN-γ ELISA; BD Biosciences, Mississauga, Ontario, Canada; IL-16 ELISA: Biosource International, Camarillo, CA), according to the manufacturer's instructions.
Jurkat T cells were activated with 25 μg/mL of PMA and then treated with 2 μg/mL of polybrene for 1 hour. The cells were washed and then infected with a 300 tissue culture infectious dose (TCID50) of HIVIIIB) of HIVIIIB) correct as written? Please revise to clarify meaning. -->, a β-chemokine insensitive strain. After 5 days, Jurkat cells were resuspended at 5 × 106 cells/mL in fresh media and aliquoted in a 96-well round-bottom tissue culture plate (0.75 × 106 cells per well) for determination of HIV-1 suppressive activity.
Cell-free CD8+ T-cell supernatants, with volumes normalized as discussed previously, were added to HIV-1-infected Jurkat T cells, and cells were cultured for 24 hours. Jurkat supernatants were then measured for p24 concentrations using a p24 Antigen Capture Assay Kit (SAIC-Frederick, Inc., Frederick, MD). HIV-1 suppressive activity was determined with the same method as CAF determination, as percent suppression of viral replication relative to a media-treated control.
Significant differences between groups were determined using the Student t test or the Mann-Whitney rank-sum test. Correlations between CAF activity and various immunologic or virologic parameters were determined using the Spearman rank-order correlation test. Calculations were performed using SigmaStat 3.0 software (SPSS, Inc., Chicago, IL).
We found no significant differences in T-cell counts between the PI and NNRTI groups at the time of sample acquisition (Table 1) or before treatment commenced (data not shown). Mean pretreatment VLs of each group were compared, and the NNRTI group demonstrated a lower log10 VL (4.2) than the PI group (5.0). This difference was statistically significant (P = 0.009).
To determine CAF activity, cell-free supernatants of PHA-activated CD8+ T cells of HIV-1-positive patients on HAART and untreated controls were assessed for their relative abilities to suppress LTR-driven gene expression. After assessing CAF activity in all patient samples, we determined whether there was any association between CAF and T-cell levels, VL, and HAART profiles. Clinical data from all patients are shown in Table 1. We found no correlation between CAF activity and CD4+ or CD8+ T-cell counts. Furthermore, we found no association between CAF and the specific drug regimen or the amount of time an individual was treated (Table 2). We also found no correlation between CAF and pretreatment T-cell counts or VL (data not shown).
In the untreated group, a negative correlation was observed between CAF and VL (P = 0.004, r = 0.848; Table 3). When the untreated group was subdivided into patients that were drug naive (NAIVE, n = 8) or were off treatment for at least 6 months (OFF, n = 8), we observed that the NAIVE group demonstrated significantly higher CAF activity than the OFF group (30.0% and 9.3%, respectively; P = 0.027; Fig. 1A). We examined VL over time (up to 3 years before and/or after sample acquisition) for each of the patients in the untreated group to determine whether individuals with a higher CAF at the time of our study were able to maintain lower VLs over a long period in the absence of antiretroviral treatment. Some of the untreated patients began HAART shortly after we collected their blood samples, and thus were not included in this analysis. We found that individuals in the NAIVE group with the highest CAF activity were able to maintain lower VLs over a period of 0.5 to 3 years compared with 5 of 8 individuals in the OFF group. Also, NAIVE individuals with a lower CAF (patients C7 and C11) had VLs similar to the 6 OFF patients with the highest VLs (Fig. 2). Average VLs below and above a log10 value of 4 were compared with each other, and all noted differences were significant (P ≤ 0.001). CAF activity, average VLs, and the amount of time over which data were collected are given in Table 3. CD4 counts before the resumption of treatment for the OFF group and prior treatment of these subjects are summarized in Table 4.
We compared CAF activity from patients in each of the study groups to determine whether HAART had any effect on CAF levels. The median values of CAT suppression in each group were: 22.5% (range: 0%-55.6%) for the PI group, 46.0% (range: 0%-90.2%) for the NNRTI group, 24.9% (range: 0%-65.6%) for the NAIVE group, and 6.75% (range: 0%-27.2%) for the OFF group (see Fig. 1A). As with NAIVE group, CAF from NNRTI group was significantly higher than that of the OFF group (P = 0.018). Results were further interpreted to reflect only individuals who effectively suppressed LTR activity (>50% suppression), similar to interpretations by others.31 We found that a higher proportion of the NNRTI group (5 of 13 persons) effectively suppressed LTR activity compared with the other groups (1 of 12 persons in the PI group, 2 of 8 persons in the NAIVE group, and 0 of 8 persons in the OFF group; see Fig. 1B). This trend was also observed when using 20% as the lower limit of effective suppression. IFNγ and IL-16 suppress LTR activation, and concentrations of these cytokines were assessed in CD8+ T-cell supernatants by ELISA to determine whether the LTR suppression observed in our system could be attributed to one or both of these cytokines. No correlation between CAF and IFNγ levels was observed. A positive correlation was observed between CAF and IL-16 levels in the PI group only (P = 0.007, r = 0.718); however, the highest of the IL-16 concentrations in our system was approximately 1000-fold lower than required for HIV-1 inhibition32 and likely did not contribute to LTR suppression here.
CAF activity inhibits HIV-1 replication at the level of transcription, but it is not clear whether CD8+ T-cell-mediated inhibition of viral replication in an acute infection assay accurately reflects suppression of the LTR by CAF. We sought to determine whether levels of suppression observed in our transient transfection system were mirrored in an acute infection assay. Jurkat T cells were infected with HIV-1 IIIB and treated with the same cell-free CD8+ T-cell supernatants as in the transcription-based assay or with media as a control. After 24 hours, viral replication was measured by p24 ELISA and replication suppression was assessed. We performed Spearman rank-order correlation tests on each subgroup and found no correlation between levels of CAF and levels of suppression of HIV-1 replication (Fig. 3).
The relation between CAF and disease progression, in terms of T-cell counts and VLs, in HIV-1-positive individuals is not clear. Using a transcription-based system to evaluate CAF, we have shown that within each group studied, there is no correlation between CD4+ T-cell counts and CD8+ T-cell-mediated LTR suppression, in agreement with a previous study.24 Others have shown a positive19-21 or negative22 correlation between CD4+ T-cell counts and CD8+ T-cell-mediated suppression of viral replication in acute infection assays. In addition, no correlation was observed between CD8+ T-cell counts and CAF. We have also demonstrated that within untreated HIV-1-positive individuals, there is an inverse correlation between VL and CD8+ T-cell-mediated LTR suppression. This is in agreement with a study of baboon-derived CD8+ T-cell-mediated suppression of viral replication.15 This contradicts other findings, however, where no correlation was seen between blood VL and CAF.13,14
CAF activity in the drug-naive subgroup (NAIVE) was significantly higher than that of the off-treatment subgroup (OFF). This associated strongly with relative VLs for the 2 groups, such that NAIVE patients with the highest CAF activity were able to maintain lower VLs continually than most OFF patients, without antiretroviral treatment, over a span of 0.5 to 3 years. Furthermore, NAIVE individuals with lower CAF demonstrated higher VLs in the same range as OFF individuals. This indicates a possible relation between CAF and disease progression in vivo. There are few data available that describe an actual antiviral role for CAF in vivo, with the exception of high CAF levels seen regularly in long-term nonprogressors21,33-35 and exposed uninfected individuals.36-40 Our data show that in untreated HIV-1-positive individuals, higher levels of CAF can be associated with lower VLs for at least 0.5 to 3 years. This suggests that CAF may be partly responsible for suppression of viral replication in vivo. Nevertheless, we cannot exclude the reverse situation, where VL and disease progression have a negative effect on CAF levels in HIV-1 infection. Certain immunologic factors, such as CD28 costimulation, IL-2, and IL-15 derived from mature dendritic cells, are known to be involved in CAF production and have also been shown to be decreased in advanced HIV-1 infection.41-46 It is therefore possible that general immune dysregulation associated with higher VLs and advanced disease progression might subsequently diminish an individual's ability to produce CAF. This notion is supported by the fact that drug-naive individuals demonstrating lower CAF tend to have VLs in the same range as the OFF group, suggesting that VL may be an important determinant of CAF activity. CAF activity in the naive group may be higher for several reasons, such as better general health or higher CD4 counts. In addition, lower CAF production in the OFF group may result from irreversible changes that may have been induced by prior therapy, which could affect CAF production. For example, antiretroviral therapy has been demonstrated to induce irreversible changes in metabolism in HIV-infected individuals.47,48
The effects of antiretroviral therapy on CAF production are not well established. Others have shown CAF to be increased26,27 or decreased16,25 in patients on HAART, using replication inhibition-based systems to determine CAF activity. In our transcription-based system, we have shown that there is no significant difference in CAF-mediated suppression of the LTR between treated individuals and those in the NAIVE group and that both are higher than in the OFF group (only the NNRTI group was significantly higher). This suggests that HAART might return CAF to a level similar to that of untreated individuals capable of maintaining lower VLs. CAF has been shown by some to decrease with disease progression.17,18,21 It is therefore possible that by reducing VL and subsequently restoring immune functions, HAART reverses this trend.
There seems to be a trend towards higher CAF in patients on NNRTI-based therapy. A slight but nonsignificant difference in CAF (P = 0.074) was observed between the PI and NNRTI groups. The lack of significance was attributable to a high degree of variability within each group. Analysis of the proportions of individuals in each group who effectively suppressed LTR activity (>50% suppression) showed that 38.5% of individuals in the NNRTI group demonstrated effective suppression compared with 7.7% of individuals in the PI group. A similar trend was seen when the limit of effective suppression was set at 20%, showing that the observed differences were not attributable to suppression levels in the PI group falling just below 50%. Interestingly, we observed that the NNRTI group had significantly lower pretreatment VLs than the PI group, and, as previously mentioned, we found an association between lower VL and higher CAF in untreated individuals. There was no correlation between lower VL and high CAF within the NNRTI group, however; thus, it is unlikely that lower pretreatment VLs had any effect on posttreatment CAF levels. It is not clear why the NNRTI group demonstrates a higher proportion of effective suppressors, because little is known about the comparative effects of PI- and NNRTI-based therapy on CD8+ T-cell function. Smith et al49 showed that CD8+ T cells from NNRTI-treated patients expressed higher levels of CD38 and human leukocyte antigen-D-related (HLA-DR) than PI-treated patients. An activated phenotype involving elevated expression levels of CD38 and/or HLA-DR has been associated with higher CAF activity.18,50 Therefore, this might explain why a higher proportion of the NNRTI group in our system demonstrated effective suppression of LTR activity. This contrasts with a study in which patients switching from PI-based to NNRTI-based HAART experienced a decrease in CD38+ CD8+ T cells.51 Moreover, others have found that there is no difference in CD8+ T-cell activation in either type of treatment52,53 and that when patients switch from PI- to NNRTI-based therapy, there is no change in CD8+ T-cell activation.54
CAF activity is mediated by at least 1 unknown CD8+ T-cell-derived soluble factor that suppresses viral replication by inhibiting LTR activation. The LTR suppression observed in our system can be attributed to CAF activity, because we excluded the possibility of interference by IL-16 and IFNγ, which are known to inhibit LTR activation.55,56 Furthermore, β-chemokines (macrophage inflammatory protein-1α [MIP-1α], MIP-1β, and regulated on activation, normal T-cell expressed and secreted [RANTES]) that block viral entry57,58 do not inhibit LTR-mediated gene expression;8 therefore, controls for these chemokines were not included. Taking these controls into consideration, it is most likely that the LTR suppression seen in our system was the direct result of CAF activity.
We investigated whether the data collected in our LTR suppression system would be mirrored in an acute infection assay. We showed a different pattern of inhibition of viral replication compared with that of LTR suppression. No correlation was found between LTR suppression and HIV-1 suppression in our system. Furthermore, no correlations were observed between HIV-1 suppression and IFNγ and IL-16. Taken together, these findings indicate that CD8+ T-cell-mediated suppression of viral replication in vitro could occur independently of chemokines and known LTR suppressors and that these levels of replication suppression do not always reflect CAF-mediated LTR suppression.
Previous studies of the effects of HAART on CD8+ T-cell noncytotoxic antiviral activity were performed using replication inhibition-based assays.16,25-27 Although these studies describe CD8+ T-cell-mediated inhibition of viral replication, they do not specifically demonstrate the effects of HAART on CAF-mediated LTR suppression. We have shown that cell-free supernatants derived from activated CD8+ T cells differentially modulate HIV-1 gene transcription and viral replication. Taken together with previous published data, this lends support to the possibility that more than 1 type of CD8+ T-cell antiviral activity exists. To date, CAF-mediated LTR suppression is the best characterized of these activities, whereas the mechanisms of action of other potential antiviral activities remain to be determined.
CD8+ T cell; chemokine; HIV-1; replication; transcription
© 2006 Lippincott Williams & Wilkins, Inc.
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Randy Mayor
"I wanted an easy and delicious way to prepare fish with exotic flair. After returning home from a trip to Jamaica with a suitcase full of spices, I went to work, and this is the result." -Karen Harris, Castle Rock, CO
4 servings (serving size: 1 steak)
Nutritional Information
Calories 241
Caloriesfromfat 30 %
Fat 8.5 g
Satfat 2.8 g
Monofat 3 g
Polyfat 1.7 g
Protein 35.5 g
Carbohydrate 3.8 g
Fiber 0.7 g
Cholesterol 72 mg
Iron 1.8 mg
Sodium 406 mg
Calcium 69 mg
3/4 cup plain yogurt
1 tablespoon Jamaican jerk seasoning (such as Spice Islands)
1 tablespoon fresh lemon juice
1 teaspoon garlic powder
1 teaspoon ground cumin
1 teaspoon chili powder
1/2 teaspoon ground cinnamon
1/2 teaspoon ground ginger
4 (6-ounce) swordfish steaks (about 3/4 inch thick)
Cooking spray
Combine the first 8 ingredients in a large bowl. Add fish, turning to coat. Cover and refrigerate for 1 hour, turning the bag occasionally.
Prepare grill.
Place fish on grill rack coated with cooking spray; grill 4 minutes on each side or until fish flakes easily when tested with a fork or until desired degree of doneness.
MyRecipes is working with Let's Move!, the Partnership for a Healthier America, and USDA's MyPlate to give anyone looking for healthier options access to a trove of recipes that will help them create healthy, tasty plates. For more information about creating a healthy plate, visit www.choosemyplate.gov.
May 2006


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For the first time ever, the Victor Pirates enter the Class C state tournament as the Western C divisional champions. It will be only the third time that Victor has competed at the state tournament. Victor earned the trip by defeating Ennis, 51-33, in the championship game.
"We're tough to beat," said first year coach Drew Lewis of the Pirates after their opening game against Gardiner.
That proved to be the case throughout the Western C Divisional in Hamilton. Every game gave the Pirates more confidence and that, in turn, earned them another victory.
Kyle Ball, the Pirates' go to guy, got off to a shaky start in their opening game against Gardiner. While he rarely picks up more than a couple of fouls a game, first game jitters got the best of him and he had three fouls before the first half was over.
"Picking up three fouls is out of character for him," said Lewis. "But the rest of the boys, they stayed steady and came to play."
Victor had a six point lead at the end of the first half against Gardiner in their opening game of the Western C Divisional. They continued to build on the lead and went on to win, 68-52. Ball finished with 20 points including two treys and 10 rebounds. Randy Miller added 15 more points and also had 10 rebounds. Corey Deering added 11 points. Lewis also credited Nate Bishop for coming off the bench and playing tough defense.
Victor 68, Gardiner 52
Victor – Kyle Ball 20, Corey Deering 11, Randy Miller 15, Derrick Cavill 5, Matt Kittel 6, Nate Bishop 9, Michael O'Leary 2.
Gardiner – Kremer 26, Reihart 4, Wines 9, Coy 6, Darr 7,
The Pirates advanced to the semi finals where they met Manhattan Christian. Victor jumped out to a 12-point lead at the end of the first quarter and cruised to a 56-42 victory and a trip to the championship game. Ball finished with 30 points. Miller battled for 10 rebounds.
Victor 56, Manhattan Christian 42
Manhattan Christian – C. VanDyken 20, Kamps 1, B. VanDyken 8, Daines 5, Heidema 4, Blanksma 2, N. Kroon 2.
Victor – Ball 30, Deering 1, Miller 10, Cavill 6, Kittel 5, Bishop 4.
Ennis had been the top team from the eastern districts in the division until Gardiner won the championships. The Mustangs were bigger than Victor but that didn't matter to the Pirates. Victor took an early lead and never trailed in the game. They handled the larger team with speed and scoring and went on to win, 51-33.
Victor 51, Ennis 33
Ennis – Goodman 4, Farnes 2, B. McKittrick 6, Bullock 10, Sullivan 10, W. McKittrick 1.
Victor – Ball 23, Deering 3, Miller 4, Cavill 7, Kittel 11, Bishop 3.
On the girls' side of the Western C Divisional, Darby had a tough time against Gardiner in their opening game of the tournament. Darby lost to Gardiner, 61-40. Keely Ehmann finished with 13 points, including two three pointers, to lead the Lady Tigers.
The Lady Tigers then matched up against Superior in loser out action. Although Darby stayed close in the game, Superior pulled ahead in the final quarter and took the 57-50 win. Lacey Dolcater had 11 points and Keely Ehmann and Julie Abrahamsen each had 10 points.


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Wednesday, October 16, 2013
The Berkeley Lady Stags 200-yard freestyle relay team earned a bronze medal with a third place finish at the Class AAA-AA-A girls' state swim meet at the University of South Carolina Natatorium in Columbia on Oct. 5.
The 200-yard freestyle relay team finished with a time of 1:44.83.
Sarah Mundy, a seventh grader led off the race and posted a time of 26.56 seconds; senior Tiffany Hennick followed with a time of 27.07 seconds; Sarah West, another seventh grader came in strong with a time of 26.66 seconds, and junior anchor Ashley Thornal brought home the bronze with a time of 24.54 seconds. The Lady Stags finished just 3.5 seconds behind James Island's winning time of 1:41.34.
Region 8AAA was well represented in the top 10 finishers as the Lady Stags finished 10th behind state champion Hilton Head and fifth place James Island.
"Our tenth place finish was our best ever," said Coach Robert Thornal as his Lady Stags previous best finish was 15th place. "For the girls this was the best season we've ever had. We exceeded all of our goals and expectations."
Thornal said the boys team showed improvement as well.
"Our boys are young," he said. "And our lone senior Tyler Mills competed in the state meet and had his best season."
Top individual finishers for the Lady Stags include Ashley Thornal with a fourth place finish in the 100-yard freestyle with a time of 56.44 and a fifth place finish in the 50-yard freestyle with a time of 24.83. Sarah Mundy with a 14th place finish in the 200-yard freestyle with a time of 2:06.99 and a 16th place finish in the 50-yard freestyle with a time of 26.74.
Tiffany Hennick placed 18th in the 200-yard intermediate medley with a time of 2:31.80. Jessica Belille finished 20th in the 500-yard freestyle with a time of 5:53.32. Sarah West finished 17th in the 100-yard backstroke with a time of 1:07.77.
The 400-yard freestyle relay team finished seventh with a time of 3:50.73.
Thornal said he gave his team the week off and then pick up the YMCA season this week with meets beginning in November.
"The Y and U.S. swim meets is where these kids get the real college exposure," he said.
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Your Daily Freak-Out: Sharks Are Falling From the SkyJoslyn Gray
I seriously can't believe people don't think golf is dangerous. I mean, those clubs are heavy (at least that's what the caddies tell me), and you have to really be on the lookout for drunk people driving those golf carts all crazy. Also, sometimes those polo shirts can be really scratchy.
And then there's the sharks that fall out of the sky onto the course. Which really is the worst kind of hazard a course could offer.
According to the Capistrano Dispatch, a 2-foot shark was found thrashing in the grass near the 12th tee of the San Juan Hills Golf Club in San Juan Capistrano, California.
"It was just wriggling around," Director of Club Operations Melissa McCormack told the Capistrano Dispatch. "Honestly, this is the weirdest thing that's happened here."
A quick-thinking course marshal picked up the shark and drove it to the clubhouse in his golf cart. Cart attendant Bryan Stizer then placed the shark into a bucket filled with water and a bit of salt. He then clocked out for his break to drive the shark to the beach, where he released it into the ocean.
Ms. McCormack theorized that the shark was dropped by a predatory bird, noting that the shark had some puncture wounds and a little bit of blood on it.
Incredibly, the shark survived the entire ordeal.
"I thought he was dead," Mr. Stizer told the Capistrano Dispatch. "When I dropped him into the water, he just lied their for a few seconds, but then he did a twist and shot off into the water."
Read the whole story at: The Capistrano Dispatch – Fish Out of the Water Live Shark Found at San Juan Hills Golf Course
(Photo Credit: Melissa McCormack, San Juan Hills Golf Club)
Read more from Joslyn at Strollerderby and at her blog, stark. raving. mad. mommy. You can also follow her on Facebook and Twitter.
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Small Mesh Hay Net
This colored Small Mesh Hay Net slows down hay consumption, allowing for healthier digestion and less boredom for non-pastured horses. Perfect for fast eaters, easy keepers, on the road, in the trailer and more! Read more...
The Small Mesh Hay Net in colors slows hay consumption rate for healthier digestion and to keep your horse busy longer. Use it daily for horses that are rapid eaters or that are overweight, and on long trips to keep horses busy during hauling. Hangs easily anywhere and holds multiple flakes of hay. 2" x 2" openings. 38" diameter with ring bottom.
Overall Rating: 5 StarsAverage Based on 5 Reviews Write a Review
I have been using these for quite sometime. My horses went from eating their hay in about 30 minutes to almost 8 hours using these nets. My horses do not have the "hay belly" look to them. The easiest way I have found to fill theses bags is with a kitchen garbage can that I put the bags into and fold over the outside of the can.
I have 3 of these and just bought 2 more. These are wonderful and work great in the winter with boredom. They have saved a good portion of my wood fence from my easily bored mare. Two of the three bags fit 4 flakes of hay in them so id say its a 3-4 flake bag.
I have 6 of these nets and they are tough. Use them in the trailer, camping and when my horses are too fat and need to slow down. I replaced the rope with a big clip so the horses can't get caught up in the rope. LOVE THESE!!!
I love these nets as they work great for my horses and are reasonably priced. I was concerned that they would eat through the net but so far all they are doing is pulling out the hay. I do plan on ordering more. We gather up all the hay that falls off the bales and stuff it into the nets and use it as a mid-day snack.
Have had this net for over a month now. So far so good. I use it for the minis. It holds 4 flakes of hay. They are eating less, losing those hay bellies and there is zero waste now, which is a first for these girls. I am not a fan of the material, wish it was cotton instead, but so far, noone has eaten it.
100% Satisfaction Guaranteed - Your Money Back Any Time, for Any Reason.
Smith Brothers is proud to offer a 100% satisfaction guarantee on all of our products. We stand behind the quality of our products, and should you not be satisfied with your purchase, simply return it and we will refund, replace or exchange it for you.


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6293 - Troubleshooting and Supporting Windows 7 in the Enterprise


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A project of People For the American Way dedicated to monitoring and exposing the activities of the right-wing movement. Learn More >
Barton: 'It Makes Perfect Sense' that People are on Welfare Because they are not Reading the Bible
As we have noted several times in recent months, David Barton has a bit of a habit of saying things that are fundamentally and demonstrably untrue ....a tendency he continued today on "WallBuilders Live" when he praised Liberty University by claiming that the LU Law School was one of the top schools in the nation:
Every year, US News and World Report produces a list of the best law schools in America that ranks the top 150 schools and Liberty University Law School was ranked number "Rank Not Published," meaning it didn't even qualify among the top 150. Thus, it is a little hard to understand how it could be considered one of the top law schools in the nation when it doesn't even make the list of top law schools in the nation.
Later, Barton began musing about some supposed connection linking welfare to failure to read the Bible enough, saying he'd love to see some study done that examines the correlation because "it makes perfect sense":
Wouldn't it be interesting to do a study between those that are on welfare and see how much and how often they read the Bible. You know, if Booker T. Washington is right that Christianity and reading the Bible increases your desires and therefore your ability for hard work; if we take that as an axiom, does that mean that the people who are getting government assistance spend nearly no time in the Bible, therefore have no desire, and therefore no ability for hard work? I could go a lot of places with this. I would love to see this proven out in some kind of sociological study, but it makes perfect sense.
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Robber continues to wear motorcycle helmet during holdupsUPDATED 6:57 PM MDT Jul 31, 2013
About 24 hours after a Chevron clerk came face to face with a motorcycle helmet-wearing robber, he had a message for him.Video Transcript
AN ARMED ROBBER WHO WEARS A MOTORCYCLE HELMET, STRIKES AGAIN BUT THIS TIME - HE WALKED INTO A WEB OF SURVEILLANCE CAMERAS, THAT CAUGHT HIS EVERY MOVE ACTION 7 NEWS REPORTER ANNA VELASQUEZ IS HERE WITH THE LATEST A-P-D SAYS THIS LATEST ROBBERY HAPPENED AT THE CHEVRON AT 12TH AND CANDELARIA IN NORTHWEST ALBUQUERQUE YESTERDAY AFTERNOON. THE CLERK EVEN TRIED TO GET HIM TO TAKE OFF HIS HELMET BARELY 24 HOURS AFTER THIS CHEVRON CLERK CAME FACE TO FACE WITH THE MOTORCYCLE HELMET WEARING ROBBER... HE HAS THIS MESSAGE FOR HIM 1:14 show your face, chicken for real! :17 FOR THE FIRST TIME IN FOUR ROBBERIES ... A SURVEILLANCE CAMERA CAPTURES HIS MOTORCYCLE. IT'S A MAROON, OLDER MODEL HONDA. HE PARKS ON THE OTHER SIDE OF THE GAS PUMPS... AND WALKS IN. :08 he came inside the store, i asked if i could help him :11 THE CLERK SAYS THE ROBBER DIDN'T SAY ANYTHING. HE WENT STRAIGHT TO THE COOLER... AND BROUGHT A BOTTLE OF DR PEPPER TO THE COUNTER :22 i was like, that's it? and he was like nope pulled out a gun, he was like gimme all your money :25 HE SAYS HE OPENED THE REGISTER AND STARTED TO GATHER THE MONEY :34 and then he was like don't put your hands under the counter! what ever your do, don't put your hands under the counter! i was like i'm not i'm not :38 THE ROBBER ALSO ORDERED HIM TO LIFT THE REGISTER'S DRAWER AND WHEN HE SAW THERE WASN'T ANYTHING THERE ... :45 he's like alright, you have a nice day and walked out :48 TUESDAY WAS THE FOURTH ARMED ROBBERY IN SIX DAYS APD SAYS HE ALSO ROBBED THE QUIZNOS NEAR 2ND AND MENAUL... THE RAM OIL GAS STATION ACROSS THE STREET FROM QUIZNOS... AND THE ALLSUPS AT INDIAN SCHOOL AND 17TH STREET NW... WHICH IS ABOUT A MILE AWAY 1:22 eventually he's going to get caught though and then when he gets to jail he'll know what happens to him :26 SO FAR NO ONE HAS BEEN HURT BUT DETECTIVES SAY THE CONCERN WITH ARMED ROBBERS... AS THEY CONTINUE THEIR CRIME SPREES... THEIR PROPENSITY FOR VIOLENCE ESCALATES. A-P-D SAYS THEY ARE FOLLOWING UP ON LEADS, AND ARE LOOKING FOR ANY OF INFORMATION. IF YOU RECOGNIZE THE SUSPECT... CALL CRIME STOPPERS AT 843-STOP
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Nah, it started out as a cluster-fuck.
Printable View
Nah, it started out as a cluster-fuck.
[QUOTE=Blackcatbone;952592]Nah, it started out as a cluster-fuck.[/QUOTE]Yeah, the OP pretty much guaranteed that by telling everyone who disagreed with him to STFU and GTFO of "his" thread on this free public forum. :D
Not the approach most conducive to reasoned and civil discourse, IMO.
Haters win another thread
Heaven forbid someone not agree with the thread hijackers
[QUOTE=Blackcatbone;952592]Nah, it started out as a cluster-fuck.[/QUOTE]
Speaking of which, S and I were out for coffee this afternoon and we sat out on the patio. The table next to us had a guy who used fuck like this example: "I fuckin' told her to fuckin' put the fuckin' bowl fuckin' down."
We thought it was hilarious, and nearly snorted our coffees because we had just finished a conversation on the optimum times to say fuck.
By the way some people use DH or something like that, for spouses I think... I've been thinking it's strange how all these people have partners with the same initials.
[QUOTE=Blackcatbone;952567]Well, in the case of a disaster my neighbors would be in the same boat as me, my family wouldn't be able to get help to me and the churches would already be swamped. I may be fairly comfortable financially but at $10 a pop my charity would only go so far. While I would certainly do what I could to help those around me I wouldn't be dropping the thousands of dollars it would cost to help those that could be helped for much less without the price gouging. And where are the churches supposed to get the money and supplies if vendors can charge whatever they want?[/QUOTE]
If everyone is in such a sorry situation where nobody can help anyone else out, then the government isn't going to help you either.
I wasn't there in Katrina, but I heard the government did a really lousy job. Rounding up people's guns and such.
You would be much better off actually preparing for disaster yourself rather than having the money you would have spent on disaster preparation stolen from you by the government so they can pay outrageous salaries and benefits to FEMA employees who do nothing but go around and take all your guns when a hurricane strikes.
[QUOTE=kenn;952605]Haters win another thread
Heaven forbid someone not agree with the thread hijackers[/QUOTE]
They need fertility gods.
Or THIS guy.
well, i originally planned to read the first page and skip to the last. then i saw that i am one of the barren freaks who should stay away so i decided to keep reading
soo here's my thoughts, unwanted tho they may be
life for humanity isn't ideal. as a species, we are diseased and weak, yet over populated enough that we encroach on other species and drive them to extinction. i believe that we need this short (evolutionary) break from populating the species so we can heal and become genetically stronger
it's not something that can be fixed in 5 minutes
and i prefer my dogs to children too, you know, cause i'm a barren freak
[QUOTE=zoebird;952350]If we want to get into some science, there's a lot of interesting work at the Weston A Price Foundation web site about the impact of soy on fertility, as well as on sperm motility, etc. [/QUOTE]
With regards to the soy, that is a [I]severe[/I] goitrogen, and if you check out the ingredients on virtually [I]any[/I] processed food (I mean, like 97% of shit at the grocery store) then, yeah, you'll find soy is in it, some way, somehow. So I most definitely think that that could be a strong, strong component of the infertility epidemic. As a perfectly logical precautionary measure, I personally think that people should avoid soy altogether, but [I]especially[/I] people who are trying to have children.
(Here's an [URL="http://lewrockwell.com/mercola/mercola162.html"]excellent Mercola article [/URL]on the ravaging effects of processed soy.)
As far as whether soy is solely to blame, I wouldn't think so, but who knows? My guess, though, would be that many countries like Russia have less soy than the U.S., which provides subsidies for soy (and the other grains, obviously) and so, if soy were the lone culprit, than the U.S. would be the only country with this problem. But it's not. It seems to be [I]all [/I]countries (especially countries of European descent).
Obviously, many of the other things that you'd cited (such as people choosing to be childless and people being more open and vocal about their fertility problems) are more cultural things, and are unlikely to have had any impact on the 92% reduction in sperm count.
[QUOTE=bloodorchid;952652]life for humanity isn't ideal. as a species, we are diseased and weak, yet over populated enough that we encroach on other species and drive them to extinction. i believe that we need this short (evolutionary) break from populating the species so we can heal and become genetically stronger [/QUOTE]
It's funny: I was get confused when I hear people talking about, "we" when discussing things, as if we're a hivemind or something. I never talk like that, "We need to ------" or "Our problem is -----".
I guess that the libertarian ethos of self-motivation and individual thinking is so deeply embedded in my worldview that I think of myself as a person first, and don't view the world in this collectivist, communist, centralized manner.
So I see the fact that your testicles are hollowed out and useless (you likely couldn't have children even if you wanted to) as an assault on you as an individual, not some sort of, I don't know, collectivist philosophical thing.
no no, my uterus expells fetuses. my ovaries still work and are succulent and eggy
i consider myself part of the human race, when i say 'we' or 'our' i mean that on average the race i belong to is genetically weakened
you seem to feel as tho when i say 'we' i say 'you'
don't be so touchy


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This workshop will provide professional development for humanities and social science faculty in teaching with visual documents found on CD-ROMs and the World Wide Web. The program will also advance the teaching of visual literacy as a means to improve critical thinking, reading, writing, and oral skills for high school and college students.
Participants will discuss new (and some old) scholarship, examine new media resources, develop strategies for classroom implementation, and discuss individual and institutional implications of incorporating new technologies. Sessions will include:
Theme-related academic content will be integrated into each day's sessions along with the exploration and testing of new media resources and technologies — online syllabi, electronic archives, dialogical technologies, hypermedia and hypertext.


text:
Most recently, it was decided by the well-documented and deflected Hail Mary from Kirk Cousins to Keith Nichol that lifted Michigan State from a tie to a thrilling 37-31 win on Oct. 22.
Michigan State left guard Joel Foreman has been a member of the Spartans for the past five games, and started in four.
He expects another game that might come down to the last play, and another of what he calls classic Big Ten Conference battles.
Michigan State, champion of the Legends Division, meets Wisconsin, co-champion and representative of the Leaders Division, in the inaugural Big Ten Championship Game tonight at Lucas Oil Stadium.
"Wisconsin is always a game in that the team that is willing to go out there for 60 minutes and play tough football is the team that is going to win that game," Foreman said. "It's a really classic Big Ten matchup. It's one of those games that is a very physicial game, that you look to on the schedule and you always know it's going to be a physical game.
LAST FIVE MEETINGSMichigan State vs. Wisconsin:
• 2007 at Wisconsin 37, Michigan State 34
• 2008 at Michigan State 25, Wisconsin 24
• 2009 at Wisconsin 38, Michigan State 30
• 2010 at Michigan State 34, Wisconsin 24
• 2011 at Michigan State 37, Wisconsin 31
Michigan State coach Mark Dantonio has pushed the idea that the game will go the full 60 minutes again. He noted the Spartans falling behind 14-0 before they had two offensive plays in the Oct. 22 thriller. Then they went on a 31-3 run to take control before a furious late 14-0 rally by Wisconsin to tie the score.
His message to the Spartans this week: "Stay fresh, stay excited and understand there is going to be adversity, understand we're going to have to weather the adversity and push through that."
Wisconsin running back Montee Ball, a Heisman Trophy candidate with 1,622 yards rushing, believes the game will be great and showcase the Big Ten's brand of football.
"I honestly believe it will," he said. "We're really going to get after each other and make some noise about how good the Big Ten is. It's an honor to play in the first Big Ten Championship Game. It's a great feeling, an overwhelming feeling, and the two teams are, I believe, the powerhouse teams in the Big Ten."
Russell Wilson, Wisconsin's high-profile transfer quarterback, is new to the conference this year after transferring from North Carolina State. He expects a similar atmosphere to this season's previous meeting.
"Obviously we're playing a great team in Michigan State, and when we played them before it was a game that went back-and-forth," he said. "We had adversity in that game, and we came back and tied it with not much time on the clock. It didn't end the way we wanted, but we know we were right there.
"Obviously, no turnovers this time, stay away from penalties and we just have to be prepared to go right to that last play."
Wisconsin defensive lineman Patrick Butrym is convinced the two teams have established a great rivalry. In that vein, he expects a rivalry game.
"It's definitely competitive, and they recruit a lot of the same players," he said. "There are similarities in the programs. They've won a lot of games the last two years, and we have to. It's definitely become a rivalry, and that means another great game."
E-mail Greg Johnson: firstname.lastname@example.com and follow him on Twitter at twitter.com/gregjohnsongrp


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11:00 AM — Sunday Worship — Religious Education for children and youth
No 9:15 AM Adult Religious Education Class on 25 September 2016 — classes resume on 2 October 2016
Located at 9449 Ellerbe Road, Shreveport LA 71106 (click on address for map and driving directions)
We are a "Welcoming Congregation" and we have completed a special program of study and reflection so we can strive to be more welcoming to bisexual, gay, lesbian, and transgender persons.
- Frequently Asked Questions
- Church Newsletter
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- Congregational Mission Statement
- Our History
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- All Souls Young Adult Facebook Group (ages 18-35)
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- Our Church Staff
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During our worship time, we also offer a religious education program for children and youth along with nursery care for infants.
Please join us for Sunday worship and fellowship before and after worship so we can get to know each other better.
For more information, contact the church office by phone at (318) 868-3313 or by email at firstname.lastname@example.com.
(Updated – 23 September 2016)


text:
LC-MS Gains Favor Due To the...
Process Development Jobs Still the Most...
Quadruple Helices Appear To Have Role...
Adapting to Evolving Business Environments Is...
For $50 million up front and the potential for up to $514 million in milestones, Merck takes lead in mTOR inhibitor development.
Merck is paying Ariad Pharmaceuticals $50 million to take over full development and commercialization rights to the latter's mTOR inhibitor, ridaforolimus, which is currently in Phase III trials against sarcoma. The new deal represents a restructuring to the companies' original ridaforolimus agreement, signed in 2007.
Under terms of the amended deal, Ariad could also receive up to $514 million in regulatory and sales milestones if the drug is approved for multiple cancer indications, as well as global royalties in lieu of a profit split. Potential milestone payments of over $65 million are associated with the sarcoma indication. Merck will in addition reimburse Ariad for ridaforolimus-related expenses incurred since January 2010. Ariad estimates this to be in the region of $19 million. The firm retains an option to carry out minority co-promotion activities for ridaforolimus in the U.S.
The new deal has been under negotiation with Merck for over a year; it brings in near-term cash payments of some $69 million and removes Ariad's obligation to fund 50% of ridaforolimus-related development costs, explains Harvey J. Berger, M.D., Ariad's chairman and CEO. "This will allow us to focus our resources on commencing the pivotal trial for our next promising product candidate, AP23534, our investigational pan BCR-ABL inhibitor, and on advancing development of AP26113, our investigational ALK inhibitor." In December 2009 Ariad reported positive results from an ongoing Phase I trial with AP23534 in patients with advanced hematological cancers. In March the drug was granted orphan drug status by the U.S. and EU authorities for the treatment of chronic myeloid leukemia.
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Several years ago, I posted a message on this group.
At that time, I was such a noob that I used my very personal email to
post my question...
Consequently, if I google my "firstname.lastname", I obtain this
message as a result, which is a bit embarassing.
Is there any way to erase this post from this newsgroup ?


text:
Winter – February's Assignment
What Does Your Winter Look Like?
I heard someone refer to this winter as the "snow-pocalypse." Between snow, ice storms and freezing temperatures this has certainly has been an unusual winter Whether your world is covered in white and you are outside trying to catch snowflakes, or you live in a warm climate and winter is just another day of fun in the sun, we want you to show us. What does winter mean for you? Are you skiing, sledding, sipping hot chocolate, or were you on the first flight south in search of warmer weather?
We are going to shake it up a little. For this assignment, we just want you to photograph. No questions to answer. Just go out and enjoy your winter with your camera!
Submitting images:
Please send all submissions to email@example.com. Please submit only three images for this assignment. All images should be in jpeg format, 72 ppi, with the longest side of your image measuring 600px.
March 8, 2011
Submitted images will appear in an online gallery on Paper Airplanes, RMSP's blog on March 11, 2011. All images will be used in the online gallery for this specific assignment only and will be copyrighted to the photographer. An email confirmation that your submission was received will be sent by March 9th. If you do not receive the email confirmation, please contact firstname.lastname@example.com.


text:
God, who said, "Let light shine out of darkness," has shone inour hearts to give the light of the knowledge of the glory of Godin the face of Jesus Christ.
2 Corinthians 4:6
This book is a cry from the heart of John Piper. He is pleadingthat God himself, as revealed in Christ's death and resurrection,is the ultimate and greatest gift of the gospel.
None of Christ's gospel deeds and none of our gospel blessingsare good news except as means of seeing and savoring the glory ofChrist. Forgiveness is good news because it opens the way to theenjoyment of God himself. Justification is good news because itwins access to the presence and pleasures of God himself. Eternallife is good news because it becomes the everlasting enjoyment ofChrist.
All God's gifts are loving only to the degree that they lead usto God himself. That is what God's love is: his commitment to doeverything necessary (most painfully the death of his only Son) toenthrall us with what is most deeply and durably satisfying-namely,himself.
Saturated with Scripture, centered on the cross, and seriouslyjoyful, this book leads us to satisfaction for the deep hungers ofthe soul. It touches us at the root of life where practicaltransformation gets its daily power. It awakens our longing forChrist and opens our eyes to his beauty.
Piper writes for the soul-thirsty who have turned away empty andin desperation from the mirage of methodology. He invites us toslow down and drink from a deeper spring. "This is eternal life,"Jesus said, "that they know you the only true God, and Jesus Christwhom you have sent." This is what makes the gospel-and thisbook-good news.
"synopsis" may belong to another edition of this title.
ECPA Gold Medallion winner John Piper is senior pastor of Bethlehem Baptist Church in Minneapolis and the head of Desiring God. He has written numerous books on topics that include personal holiness, missions and historical figures.
"About this title" may belong to another edition of this title.
Book Description Crossway Books, 2005. Book Condition: New. Brand New, Unread Copy in Perfect Condition. A+ Customer Service! Summary: Most people, when they ponder what it means to be loved by God, do not think God-centered thoughts. They think of the things that God does for us but which, in their minds, don't have God as the satisfying center. But it wouldn't be loving of God to give us everything but himself-and so his love doesn't do that. It gives us himself for our enjoyment, and it gives us other things as means of knowing him better and loving him more. In John Piper's reflective, paradigm-challenging book, he drives home the point that what is most loving about God is not his making much of us, but his enabling us, at great cost to himself, to enjoy making much of him forever. Bookseller Inventory # ABE_book_new_1581347510
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Contaminated Collections: An Overview of the Legal, Ethical and Regulatory Issues
Rebecca A. Tsosie
University of Arizona - James E. Rogers College of Law
Collection Forum, Vol. 17, p. 14, 2001
Repatriation of contaminated objects to Native Nations poses at least two distinct issues: first, the need to identify whether dangerous chemicals exist on an object prior to repatriation; and second, for those objects that are contaminated, the need to identify the particular health risk posed by the contamination. These issues fall within a complex legal framework, governed by at least two separate statutory regimes - cultural resources statutes and environmental statutes - as well as by principles of tort law. Although these legal principles influence the respective rights and duties of Native people and of museums, they are not dispositive of the issues. Rather, the issue of repatriation of contaminated objects requires a restructuring of existing law and policy directives to achieve a coherent legal solution. However, before such a restructuring is possible, it is necessary to examine the legal and
ethical dimensions of the problem through an intercultural lens. The nature of the problem is one that threatens human health and safety, requiring scientific study of the health effects of such contamination given the patterns of use employed by Native people. However, it is also one that requires recognition of cultural harm and the inadequacy of existing tort law to quantify the damages that are being suffered by Native people.
Number of Pages in PDF File: 16
Keywords: Native people, torts, repatriation
Date posted: May 9, 2009
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This was a pretty big weekend for Cincinnati basketball. It started on Saturday morning with the win over Seton Hall. It extended to Sunday when 5 star recruit Jermaine Lawrence picked Cincinnati. Take a minute to check out of the Big East standings. Cincinnati is tied for 2nd with Louisville, Notre Dame and Georgetown. They are a game in the loss column out of first place. It's hard to not want to look ahead and wonder if this team can acquire greatness. There is a damn good shot that this team could, and they will be favored to, win the next 4 games. That might put them at the top of the league. We've never been to these heights with Cincinnati basketball in the Big East. 6-3 is the best 9 game record ever. Lord knows that there are traps all over the place and every game is a battle. I trust this team.
Trust is a very important word in life. There aren't a lot of things that you can trust and rely on. I trust that this team is going to find a way to win. The 3 of 4 losing skid that welcomed in 2013 seems to have been necessary. This team needed to be tested. They needed to see what they have inside. New Mexico is a good team. Notre Dame was playing well. St John's is a little better than most people thought, and they always give Cincinnati fits. Those games seemed to strengthen the core. When it comes down to brass tax, this team has what it takes to win. Syracuse is a tricky one because they let that one get away. But I don't think they will let many more get away from them down the stretch. This team has the instinct.
What this team doesn't have is the killer instinct. Saturday showed the same problem that plagued UC against Marquette. The same problem that plagued them against DePaul to a lesser extent. They get up big and it seems like they take the foot off the gas. Marquette is not in the same class because they were shooting unbelievably bad and started making shots. But that was still a 16 point lead that was blown. DePaul was down 11 late and was able to cut it to 5 and eventually 3.
Seton Hall was down 20. They were playing awful basketball. Kevin Willard went to multiple timeouts early in the second half. The Bearcats could do no wrong. Seton Hall could do no right. The subs gave some horrible minutes. Dan Cronin, Mick's brother, predicted a run was coming when the lead was 15. He was not wrong. I don't think it is too much to ask for this team to just put someone away. The season is long. We have at least 11 games left. I don't think I can take panic attacks in every one of them.
Justin Jackson gave us a different type of game than he did against Rutgers. Different in this case doesn't mean bad. He had 3 points, 5 rebounds, 4 assists, 3 steals, 1 block and 2 turnovers. Only 1 foul. Jackson played 20 minutes. He split time evenly with Titus Rubles. Jackson doesn't have to be a superstar. He has to be an active energy boost for this team. He gets knocked on his passing because for every good pass there is a turnover to follow, but he has a lot of passing skill. Look at his face when he thinks he made a good pass. You can see how proud he is of it. Solid game from Jackson. Keep it up, 5.
Cheikh Mbodj is on a tear right now. He put up 7-7-5 blocks. He is on the highest scoring 3 game stretch of his career. He was 2-5 from the field and 3-4 at the stripe. All he has to do to be effective is score on dunks and layups. His post game is incredibly weak. 2 of his misses were on awful attempts. One of them was blocked. Mbodj cleans up the offensive glass pretty well. The biggest flaw for him is staying on the court. He was saddled with 4 fouls. Mick wants to play him 30 minutes so badly. The rotation is getting a lot tighter. Mbodj has to be on the floor longer for the team to be successful. With the way he has played on both ends, he needs to stay on the floor to take advantage of his hot streak.
Cashmere Wright has had a rough go of things since returning. He is 7-29, 4-21 from 3. Titus Rubles is telling him to stop shooting 3s right now. Cash hit 2 of those 3s in the game Saturday. They were both on wide open looks. One of them he created with some nice dribbling, the other was a spot up. I'm a little worried that he's relying too much on the 3 point shot. Especially since it has stopped falling. He has 6 games this season where he has attempted 8 or more 3 pointers. 2 of them are in the last 3 games. He's made 3-8, 5-9, 5-10, 2-8, 1-8 and 1-8. I know you were all wondering. He has not been the same shooter in Big East play. Getting to the basket more seems like it would help him.
It definitely helped him get to the free throw line. Cash was 7-7 from the stripe. He was 4-13 from the field. He had 4 assists to 2 turnovers. Wright recorded 1 steal to tie him with Darnell Burton for second most all time. I am pretty sure I said that stat incorrectly on Friday, so apologies.
Sean Kilpatrick went full volume shooter Saturday afternoon. He scored a game high 21 points. He used 19 shots to get them. He was 3-4 from 2 and 5-15 from 3. He only got to the free throw line once. Killa is a gunner. Luckily for all of us, he does more than just shoot. He had a team best 7 rebounds. He added a pair of steals. He got a steal late that led to his 3 late to ice the game. Offense on this team is going to come down to Sean Kilpatrick and Cashmere Wright scoring. Only 4 players attempted more than 2 shots. Only 3 players made at least 2 shots. Killa played 36 minutes. He's good. I like him. You probably do as well.
JaQuon Parker had trouble getting his shot to fall, but he went 6-8 at the foul line for the majority of his 9 points. He had 2 boards and 2 assists. He was also called for a travel. It seems like he is called for a travel in every game. Not a lot to say about JaQuon today.
Titus Rubles rebounds like a mad man. He had 6 in his 20 minutes. He made both of his free throws for his only points. He had an assist and a steal. I feel like what he does isn't accurately reflected in the box score. I don't think starting matters to Rubles as much as it does Jackson. Rubles comes in and does his thing no matter what. Jackson has played completely different since being placed back in the starting lineup. It's good to have guys who don't have massive egos and are willing to get their 20 minutes any way they can. Props to Titus.
That picture is both awesome and a representation of Rubles' rebounding skill.
The rebounding was outstanding in the second half. UC pulled in 25.7% of their misses for the game, which isn't great, but they had 8 offensive boards in the second half. 7 of their 8 second chance points were in that half. UC pulled in 74.4% of Seton Hall's misses. The Pirates had 0 second chance points in the second half.
UC had 9 steals. Seton Hall is known for turning the ball over a lot. They turned it over 14 times, which is below their average.
It seemed like Seton Hall scored off of every UC turnover. Sure enough, the Pirates had 8 points off of 5 first half turnovers and 9 points off of 8 second half turnovers. Nearly 29% of the Pirate points came off of UC turnovers. That's not a great thing.
Shaq Thomas and Ge'Lawn Guyn both played 5 minutes. Thomas was called for 2 fouls and had a rebound. Guyn missed a 3, pulled in a board, had a steal and turned the ball over.
Jermaine Sanders played 9 minutes. He scored a bucket. He also had a rebound and a turnover.
Kelvin Gaines once again got the early minutes over David Nyarsuk. Gaines was 1-2 for 2 points. The 1 was of a dunk. Of course. He had a rebound. In the bad category, he had 3 fouls and 2 turnovers. One of those was an offensive foul.
Nyarsuk played 1 more minute, 7-6. He had 2 points by going 2-3 from the foul line. He hit a big pair late in the game. He had 2 rebounds. One of his most inspired games in a while.
The free throw shooting was pretty excellent. 21-27, 77.8%. I could take that.
The 3 point shooting numbers are going to look bad when SK and Cash aren't making them at a high rate. They were 7-23. UC was 8-26. That stat is totally reliant on Cash and Killa.
I was pretty impressed by Brandon Mobley of Seton Hall. He had 16 points on 6-8 shooting. He was a big part of the reason they were close in the first half.
Fuquan Edwin had 14 in the second half on 4-10 shooting. He was held to 1 steal. I think Edwin is definitely going to be a pro. I like his game.
Gotta hand it to Seton Hall, they didn't quit.
I can't end this piece without talking about our good friend Carc. Ol' Carc was at the UC-Seton Hall game as the sideline reporter, which is a pretty dumb job in college basketball. He did some weird thing where he dressed up as a Pirate. That was the lead in to his epic journey. No one in the history of planet earth has done this. He started at UC-Seton Hall and went ALL THE WAY ACROSS THE COUNTRY to the Gonzaga-San Diego game. Now, he didn't even stay for the whole UC game. That's kind of lame. This was a big build the entire first half. When Carc finally left, people on twitter rejoiced. This was the worst promotion of the season. You can do better, ESPNU.
Photos via Cincinnati.com


text:
PSP Network Utility Disc (Korean Version)
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Published by: Sony Computer Entertainment
Developed by: SCEK
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