I understand Fall Ball (baseball practice and intrasquads) starts next week.

(09-25-2020 08:15 AM)Hambone10 Wrote:  

(09-24-2020 06:32 PM)Tomball Owl Wrote:  So what’s different today than a month or six weeks ago?

Are there limits on the number of practices you can have?

NCAA rules are the same as they were 6 weeks ago.
20 hours a week max.
Practicing. 11.5 hours during the week and ~8.5 on weekends.

(09-25-2020 08:54 AM)OwlSquared Wrote:  

(09-25-2020 08:15 AM)Hambone10 Wrote:  

(09-24-2020 06:32 PM)Tomball Owl Wrote:  So what’s different today than a month or six weeks ago?

Are there limits on the number of practices you can have?

NCAA rules are the same as they were 6 weeks ago.
20 hours a week max.
Practicing. 11.5 hours during the week and ~8.5 on weekends.

I'm not sure about Sundays, but I believe there is practice every day between now and the MTSU game.

I meant total number of practices during a season or number of days before your first game or similar. I believe there is a rule about the first game, and I don't know how COVID has impacted that.

Thought just hit me. SMU got the death penalty and did not play football in 1987-88. During those two years, the Mustangs won exactly the same number of SWC games as did Rice--zero.

(09-25-2020 09:04 AM)Hambone10 Wrote:  I meant total number of practices during a season or number of days before your first game or similar. I believe there is a rule about the first game, and I don't know how COVID has impacted that.

It's 29 days before the first game (which was yesterday).
I believe there is no limit, thus 29 practice days can take place as long as the team doesn't go over the 20 hours per week cap.
For instance, the team is only practicing 1 hour a day on MWF.

(09-25-2020 12:00 AM)Almadenmike Wrote:  

(09-24-2020 02:24 PM)ruowls Wrote:  

(09-23-2020 06:44 PM)Almadenmike Wrote:  Coming out in this week's Science Magazine:

Quote:The family of seven known human coronaviruses are known for their impact on the respiratory tract, not the heart. However, the most recent coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has marked tropism for the heart and can lead to myocarditis (inflammation of the heart), necrosis of its cells, mimicking of a heart attack, arrhythmias, and acute or protracted heart failure (muscle dysfunction). These complications, which at times are the only features of coronavirus disease 2019 (COVID-19) clinical presentation, have occurred even in cases with mild symptoms and in people who did not experience any symptoms. Recent findings of heart involvement in young athletes, including sudden death, have raised concerns about the current limits of our knowledge and potentially high risk and occult prevalence of COVID-19 heart manifestations. ...

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2770911/

Here is an article from Mayo from 2009 discussing myocarditis and the causes. It is interesting in that there are common viral infections and bacterial infections that can cause it. It looked back over 2 decades (3 decades now even going back to when I played). The gist of the article is what I said earlier. The means of detecting viral myocarditis have improved and when they looked for it they found it. The things that stand out are that enteroviruses (the ones that cause gastroenteritis or "stomach flu"), influenza, coxsackie viruses, strep throat, and staph aureus can cause it. There wasn't a big incentive to do cardiac testing on every athlete that got a fever, nausea, vomiting or diarrhea in the past. But with the polarization of the COVID pandemic, myocarditis from COVID has become a contentious topic and a means to overstate the relative risk compared to other historical viral infections.

I don't want to minimize myocarditis as it obviously is a medical issue of concern. But to think that this a new issue related to COVID or that COVID is significantly more harmful is a bit presumptuous.

Thanks! Interesting that the Science article didn't give more context/background. All of its references are from 2020!

Its reference 15, however, does itself include a reference (a December 2015 article in Circulation) that contains this sentence that acknowledges viruses as "often" being the cause of myocarditis: "The pathogenesis of myocarditis consists of 3 overlapping phases: acute injury, often caused by a virus; the host innate and acquired immunologic response; and finally, recovery or a transition to scar and DCM."

The 2009 Mayo article talked about the differences in the initial immunological response and outcomes. Paradoxically, the greater initial inflammatory response, what they called fulminate, caused less prolonged inflammation and subsequent cardiac function decline. The non-fulminate cases seemed to have a lower level of inflammation initially but for a prolonged period of time. This lead to the "scarring" of the myocardium and the lasting cardiac dysfunction. This would tend to suggest that the athletes at greatest risk for lasting dysfunction would be the ones with more indolent symptoms initially.
So why haven't we tested athletes with mild viral cases in the past the same way we are doing now with COVID? Why is the concern so great now when it has been a risk for decades? It is interesting to ponder and discuss.
You would think that Rice would have someone who could recognize inconsistencies in action plans.

(09-25-2020 12:06 PM)ruowls Wrote:  

(09-25-2020 12:00 AM)Almadenmike Wrote:  

(09-24-2020 02:24 PM)ruowls Wrote:  

(09-23-2020 06:44 PM)Almadenmike Wrote:  Coming out in this week's Science Magazine:

Quote:The family of seven known human coronaviruses are known for their impact on the respiratory tract, not the heart. However, the most recent coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has marked tropism for the heart and can lead to myocarditis (inflammation of the heart), necrosis of its cells, mimicking of a heart attack, arrhythmias, and acute or protracted heart failure (muscle dysfunction). These complications, which at times are the only features of coronavirus disease 2019 (COVID-19) clinical presentation, have occurred even in cases with mild symptoms and in people who did not experience any symptoms. Recent findings of heart involvement in young athletes, including sudden death, have raised concerns about the current limits of our knowledge and potentially high risk and occult prevalence of COVID-19 heart manifestations. ...

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2770911/

Here is an article from Mayo from 2009 discussing myocarditis and the causes. It is interesting in that there are common viral infections and bacterial infections that can cause it. It looked back over 2 decades (3 decades now even going back to when I played). The gist of the article is what I said earlier. The means of detecting viral myocarditis have improved and when they looked for it they found it. The things that stand out are that enteroviruses (the ones that cause gastroenteritis or "stomach flu"), influenza, coxsackie viruses, strep throat, and staph aureus can cause it. There wasn't a big incentive to do cardiac testing on every athlete that got a fever, nausea, vomiting or diarrhea in the past. But with the polarization of the COVID pandemic, myocarditis from COVID has become a contentious topic and a means to overstate the relative risk compared to other historical viral infections.

I don't want to minimize myocarditis as it obviously is a medical issue of concern. But to think that this a new issue related to COVID or that COVID is significantly more harmful is a bit presumptuous.

Thanks! Interesting that the Science article didn't give more context/background. All of its references are from 2020!

Its reference 15, however, does itself include a reference (a December 2015 article in Circulation) that contains this sentence that acknowledges viruses as "often" being the cause of myocarditis: "The pathogenesis of myocarditis consists of 3 overlapping phases: acute injury, often caused by a virus; the host innate and acquired immunologic response; and finally, recovery or a transition to scar and DCM."

The 2009 Mayo article talked about the differences in the initial immunological response and outcomes. Paradoxically, the greater initial inflammatory response, what they called fulminate, caused less prolonged inflammation and subsequent cardiac function decline. The non-fulminate cases seemed to have a lower level of inflammation initially but for a prolonged period of time. This lead to the "scarring" of the myocardium and the lasting cardiac dysfunction. This would tend to suggest that the athletes at greatest risk for lasting dysfunction would be the ones with more indolent symptoms initially.
So why haven't we tested athletes with mild viral cases in the past the same way we are doing now with COVID? Why is the concern so great now when it has been a risk for decades? It is interesting to ponder and discuss.
You would think that Rice would have someone who could recognize inconsistencies in action plans.

More important for officials to CYA.

(09-25-2020 12:22 PM)OptimisticOwl Wrote:  

(09-25-2020 12:06 PM)ruowls Wrote:  

(09-25-2020 12:00 AM)Almadenmike Wrote:  

(09-24-2020 02:24 PM)ruowls Wrote:  

(09-23-2020 06:44 PM)Almadenmike Wrote:  Coming out in this week's Science Magazine:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2770911/

Here is an article from Mayo from 2009 discussing myocarditis and the causes. It is interesting in that there are common viral infections and bacterial infections that can cause it. It looked back over 2 decades (3 decades now even going back to when I played). The gist of the article is what I said earlier. The means of detecting viral myocarditis have improved and when they looked for it they found it. The things that stand out are that enteroviruses (the ones that cause gastroenteritis or "stomach flu"), influenza, coxsackie viruses, strep throat, and staph aureus can cause it. There wasn't a big incentive to do cardiac testing on every athlete that got a fever, nausea, vomiting or diarrhea in the past. But with the polarization of the COVID pandemic, myocarditis from COVID has become a contentious topic and a means to overstate the relative risk compared to other historical viral infections.

I don't want to minimize myocarditis as it obviously is a medical issue of concern. But to think that this a new issue related to COVID or that COVID is significantly more harmful is a bit presumptuous.

Thanks! Interesting that the Science article didn't give more context/background. All of its references are from 2020!

Its reference 15, however, does itself include a reference (a December 2015 article in Circulation) that contains this sentence that acknowledges viruses as "often" being the cause of myocarditis: "The pathogenesis of myocarditis consists of 3 overlapping phases: acute injury, often caused by a virus; the host innate and acquired immunologic response; and finally, recovery or a transition to scar and DCM."

The 2009 Mayo article talked about the differences in the initial immunological response and outcomes. Paradoxically, the greater initial inflammatory response, what they called fulminate, caused less prolonged inflammation and subsequent cardiac function decline. The non-fulminate cases seemed to have a lower level of inflammation initially but for a prolonged period of time. This lead to the "scarring" of the myocardium and the lasting cardiac dysfunction. This would tend to suggest that the athletes at greatest risk for lasting dysfunction would be the ones with more indolent symptoms initially.
So why haven't we tested athletes with mild viral cases in the past the same way we are doing now with COVID? Why is the concern so great now when it has been a risk for decades? It is interesting to ponder and discuss.
You would think that Rice would have someone who could recognize inconsistencies in action plans.

More important for officials to CYA.

I see it now.

(09-25-2020 09:35 AM)Owl 69/70/75 Wrote:  Thought just hit me. SMU got the death penalty and did not play football in 1987-88. During those two years, the Mustangs won exactly the same number of SWC games as did Rice--zero.

I actually thought that those 2 seasons where when Rice FB hit absolute bottom (actually i think a case could be made for athletics in general), but I never dreamed that we would be as awful as we were the last 2-3 years under Bailiff in a conference filled with schools that we would have scheduled as a guaranteed win years ago (of course acknowledging that we lost to USL, twice, and SW Tx State in the 80's).

What a mess. What is really sad as I have lost the ability to be mad anymore...

Santa Clara was the opening game for Rice Stadium in 1950. Rice won 27-7. U of Chicago won national championships in football 1905 and 1913. They dropped football in 1939 and brought it back as D3 in 1973.

(09-21-2020 05:40 PM)Almadenmike Wrote:  

(09-21-2020 01:15 PM)Owl 69/70/75 Wrote:  Nobody as fallen as far as Rice. Nobody. Not even close.

I suspect that the only schools who'd come close would be those who ended up dropping football altogether.

I'd thought about Santa Clara (alma mater of Oiler QB Dan Pastorini), but their greatness was more distant than I'd realized.

They are 3-0 bowl games: The Broncos beat LSU (9-0-1 & 9-1) in consecutive Sugar Bowls (1937 & 1938) and upset Bear Bryant's 9-2 Kentucky Wildcats in the Jan, 2, 1950, Orange Bowl. (But soon thereafter their coach jumped to Pitt. Their second game of the subsequent 1950 season under the new coach was a 27-7 loss to Rice in the first game at the soon-to-be Historic Rice Stadium.)

After three lackluster seasons (9-18-2) under the new coach, Santa Clara dropped football on Dec. 29, 1952, citing increasing financial losses due to increasing costs, such as those associated with the introduction of platoons. (BTW, Rice, Texas and Miami (Fla.) were on the Broncos' 1953 schedule; and Oklahoma was on its 1954 card.)

In 1959, Santa Clara reinstated football as a D-II program. They dropped it again after the 1991 season and have not had a varsity football team since.

The Leach version of Miss St is making LSU look very beatable....in Baton Rouge.

37-34 Miss St with 3:46 to play.

Make that 44-34 with 3:39 to play.

That’s the final. Miss St QB threw for a SEC record 623 yds.

(09-26-2020 06:24 PM)Tomball Owl Wrote:  The Leach version of Miss St is making LSU look very beatable....in Baton Rouge.

37-34 Miss St with 3:46 to play.

Make that 44-34 with 3:39 to play.

That’s the final. Miss St QB threw for a SEC record 623 yds.

Jesus... maybe coaching quality really does vary that much, even at the top

(09-26-2020 06:24 PM)Tomball Owl Wrote:  The Leach version of Miss St is making LSU look very beatable....in Baton Rouge.

37-34 Miss St with 3:46 to play.

Make that 44-34 with 3:39 to play.

That’s the final. Miss St QB threw for a SEC record 623 yds.

Costello, who was a grad transfer from Stanford. He got fed up with Shaw's run-focused offense. What a 180 degree change with Leach.

(09-25-2020 07:15 PM)texowl2 Wrote:  

(09-25-2020 09:35 AM)Owl 69/70/75 Wrote:  Thought just hit me. SMU got the death penalty and did not play football in 1987-88. During those two years, the Mustangs won exactly the same number of SWC games as did Rice--zero.

I actually thought that those 2 seasons where when Rice FB hit absolute bottom (actually i think a case could be made for athletics in general), but I never dreamed that we would be as awful as we were the last 2-3 years under Bailiff in a conference filled with schools that we would have scheduled as a guaranteed win years ago (of course acknowledging that we lost to USL, twice, and SW Tx State in the 80's).

What a mess. What is really sad as I have lost the ability to be mad anymore...

Ah, my freshman and sophomore years...when we played at SMU in the 1989 season opener, we were the only two 1-A schools not to have beaten another 1-A school in the previous two seasons. Blowing them out that day started the slow climb up to semi-respectability that marked the early '90's.

Kansas St defeats Oklahoma 38-35 in Norman. No.3 OU was up 35-14 with 2:46 to play in the 3Q.

Interesting year so far for those teams playing D1 football.

(09-26-2020 09:34 PM)Tomball Owl Wrote:  Kansas St defeats Oklahoma 38-35 in Norman. No.3 OU was up 35-14 with 2:46 to play in the 3Q.

Interesting year so far for those teams playing D1 football.

Heard some cowbells today. Last time I heard 'em was in Memphis at the beginning of a long decline for our program. The air was dun raided today.

(09-27-2020 02:58 AM)GoodOwl Wrote:  

(09-26-2020 09:34 PM)Tomball Owl Wrote:  Kansas St defeats Oklahoma 38-35 in Norman. No.3 OU was up 35-14 with 2:46 to play in the 3Q.

Interesting year so far for those teams playing D1 football.

Heard some cowbells today. Last time I heard 'em was in Memphis at the beginning of a long decline for our program. The air was dun raided today.

I guess we differ on when exactly was the beginning of a long decline. I think the decline started in the early 60’s, when we failed to adjust to changes in the football world, changes in the rules and changes in the world at large. Our ‘61 team was the last to go to a bowl until ‘06.

If you think of our program as a series of ups and downs, certainly that Liberty Bowl was the first step in the last downward slope, but to define that as the beginning of the decline is to tacitly admit we were at something of a peak until then.

I agree that game was a nightmare in many ways, the #$&#@%#$* cowbells maybe the least. Oddly, I had ridden a bus to the game, loaded with MSU fans, and their behavior on the way back was human and respectful, which has left me as a bit of a fan for MSU.

Respectfully, I have seen the decline of Rice. It has dominated my life. I am older than seven.

(09-27-2020 09:50 AM)OptimisticOwl Wrote:  

(09-27-2020 02:58 AM)GoodOwl Wrote:  Heard some cowbells today. Last time I heard 'em was in Memphis at the beginning of a long decline for our program. The air was dun raided today.

I guess we differ on when exactly was the beginning of a long decline. I think the decline started in the early 60’s, when we failed to adjust to changes in the football world, changes in the rules and changes in the world at large. Our ‘61 team was the last to go to a bowl until ‘06.

If you think of our program as a series of ups and downs, certainly that Liberty Bowl was the first step in the last downward slope, but to define that as the beginning of the decline is to tacitly admit we were at something of a peak until then.

I agree that game was a nightmare in many ways, the #$&#@%#$* cowbells maybe the least. Oddly, I had ridden a bus to the game, loaded with MSU fans, and their behavior on the way back was human and respectful, which has left me as a bit of a fan for MSU.

Respectfully, I have seen the decline of Rice. It has dominated my life. I am older than seven.

Agree, OO.

But the Owls' 10-3 season in 2013 (before being pummeled in "the most one-sided AutoZone Liberty Bowl victory in the game's 55-year history") is surely one of the several local maxima to be celebrated along the decades-long slide.

(09-27-2020 09:58 AM)Almadenmike Wrote:  

(09-27-2020 09:50 AM)OptimisticOwl Wrote:  

(09-27-2020 02:58 AM)GoodOwl Wrote:  Heard some cowbells today. Last time I heard 'em was in Memphis at the beginning of a long decline for our program. The air was dun raided today.

I guess we differ on when exactly was the beginning of a long decline. I think the decline started in the early 60’s, when we failed to adjust to changes in the football world, changes in the rules and changes in the world at large. Our ‘61 team was the last to go to a bowl until ‘06.

If you think of our program as a series of ups and downs, certainly that Liberty Bowl was the first step in the last downward slope, but to define that as the beginning of the decline is to tacitly admit we were at something of a peak until then.

I agree that game was a nightmare in many ways, the #$&#@%#$* cowbells maybe the least. Oddly, I had ridden a bus to the game, loaded with MSU fans, and their behavior on the way back was human and respectful, which has left me as a bit of a fan for MSU.

Respectfully, I have seen the decline of Rice. It has dominated my life. I am older than seven.

Agree, OO.

But the Owls' 10-3 season in 2013 (before being pummeled in "the most one-sided AutoZone Liberty Bowl victory in the game's 55-year history") is surely one of the several local maxima to be celebrated along the decades-long slide.

I was there, as GoodOwl can attest. Worst football experience of my life. Cold, cowbells, rout, and the death of optimism. If that is what you mean by maxima, I agree.

But I have seen a lot of losses in 58 years, some horrifying, some heartbreaking, with a few highs along the way. I just think the decline started long before I got to campus.

Neely did pretty good in one platoon football. We could play heads up with anybody with a core of about 18 good players. But we did not recruit well enough or widely enough to compete. My freshman year we had 22 recruits. Texas had 75. We did not integrate the program as quickly as we should have. We were still playing 50’s ball in the 60’s.

I think of Goldsmith, Hatfield, Graham, and Bailiff as if the program was a drowning man. We Have surfaced a few times, gasped for air, but we have never made it back to shore since Neely first tossed us in. Waiting to see if Bloomgren will bring us back up for more air.