Analogy-creep in hyping science

Via Instapundit by way of Popular Mechanics, I just saw this press release from UW-Madison hyping a new paper studying the host-virus interactome between humans and influenza.

In a comprehensive new study published today in the journal Cell Host and Microbe, the University of Wisconsin-Madison’s Yoshihiro Kawaoka and a team of researchers have set the stage for an entirely different approach. They have revealed methods for thwarting the hijackers by shutting down the cellular machinery they need, like cutting the fuel line on a bank robber’s getaway car.

When this got translated by Popular Mechanics we get the headline

Potential New Flu Treatment Would Starve the Virus, Limiting Resistance

which is the text blogged by Instapundit. This caught my eye because “starve the virus” is an odd claim since a virus is only metabolically active in the host, and the metabolites it uses are generally things the host needs too. From what I can tell from the abstract (apparently we don’t get on-campus Cell Host and Microbe here), the study is a large scale interactome to identify host proteins that coimmunoprecipitate with influenza proteins. Some of these were validated as affecting virus growth in culture by doing siRNA knockdowns. I’m not sure whether they then showed that known drug inhibitors also affected virus growth.

Here’s my guess about what happened:

  • The researcher told a UW PR person that the study catalogs host proteins that might be needed by influenza to propagate itself, and points out that resistance to drugs that target the host can’t easily arise in the virus.
  • The UW PR person tries to come up with something that is not part of a bank robber and comes up with a getaway car.
  • Continuing the analogy, the UW writer picks an essential part in the getaway car: the fuel line.
  • The Popular Mechanics headline writer saw “fuel” and thought the study was about reducing fuel for the virus
  • We get the headline suggesting that the study is about starving viruses.

Of course, if the virus is a bank robber, the host cell is not the getaway car; it’s the bank. Inhibiting virus infection with drugs that target host proteins is not like cutting the fuel line in the getaway car; it’s more like preventing bank robberies by killing bank tellers.  And it’s not just killing the tellers in the bank that’s being robbed, it’s killing all the tellers in all the banks in the community, whether they are being robbed or not.  Maybe that’s a reasonable strategy if the tellers are really nonessential in an age of ATMs. But that analogy is a lot less attractive.

The abstract mentions two potential “targets”, GBF1 and JAK1. I’m not sure how promising those are in terms of being therapeutic targets, based on the phenotypes of mouse knockouts.

Learning Artemis

For editing genome annotations, many of my colleagues use Artemis while others use Apollo. For my own use, I’ve usually just made scripts that generate GFF and visualized that in Gbrowse, Jbrowse, or IGV. For the genomics class I co-teach, we’ve had students edit GFF in a text editor (emacs!) and display it in IGV. But this year we shifted to doing more stuff that we used to do on the command line to our local teaching Galaxy, so after many years of avoiding them, I need to quickly get up to speed with Artemis and/or Apollo (in the long run, we’re going to use WebApollo, but that isn’t happening before the next homework assignment). Desktop Apollo stopped development and it’s not clear what the status of Artemis is, so this learning exercise may not be that useful.

To teach the kinds of things that MAKER does as a complete workflow, we are showing students how to take pieces of ab initio and data-driven evidence and assemble by hand the kind of evidence stack that MAKER automates. This means that we want to start with an undecorated fasta file of our artificial genome and load a bunch of gff, gtf, and bam files.

Everything below was done on a MacBook Air running OSX 10.9 (Mavericks).

Loading a fasta file

It seems like there are a couple of ways to do this. I was able to load my fasta file using either File > Read an entry or by invoking a project manager (which only seems to be available from the File menu if nothing else is opened). I initially opened a copy of my fasta file from a directory I had used with IGV, but found that this caused saves to fail because there was also a fasta index file present. Copying the file into my artemis working directory, I was able to open and save. This is what the viewer looks like.

ArtemisScreenSnapz001

 

The top line of the viewer shows a selector for feature sets, aka “Entries” in Artemis’ jargon. Below the entry bar (which can be hidden), the viewer shows an overview and a detailed view. Scroll bars on the right allow you to adjust the zoom of each; you can make the lower panel more of an overview than the top if you want. Double clicking on either panel jumps the other to the area you are viewing. A variety of graph options for things like GC content are available and open as additional panels. As you zoom out, Artemis shows stop codons in all 6 reading frames. As you zoom in, you get amino acid and DNA sequences.

Layers of annotations are “Entries”, so I can load additional files in different formats or create them using Artemis’ built-in tools. For example, Create > Mark Open Reading Frames gives this:ArtemisScreenSnapz002Several things have changed.

  • We have a new entry “ORFS_100+” (I used the default lower limit of 100 aa for ORF calling) on the entries bar.
  • The panels are now decorated with aqua blocks showing CDS features
  • The bottom panel shows a textual list of CDS features

More tracks/entries

I loaded a couple more entries as gff files:

  • Augustus gene prediction
  • Blastx parsed with a bioperl script I wrote

 

To get this view I tried some additional options from the Display menu. I tried Display > Show One Line Per Entry View. This is Display > Feature Stack View. These two create another panel above the overview genome panel.

ArtemisScreenSnapz004

 

There are some nice things about the display, but other parts are kind of a mess:

  • I like how the coding exons are linked across different reading frames
  • The parent-child feature relationships seem to be incomplete. CDS features are linked within a transcript, but parts of the same gene feature are displayed separately, and are stacked onto each other in a way that is hard to see.

Create a new set of annotations

Create > New Entry adds an entry to the entry bar called “no_name”. Yes, really. There’s no field to name the entry when you create it. You have to use Entries > Set Name of Entry and pick the no_name entry before you can rename it.

Features can be copied from the evidence entry sets to your custom entry and then edited. But I think I haven’t found the right way to copy a feature set (e.g. gene, transcript, introns, cds etc.) together.

That’s where I am so far… more later, perhaps.

More info

Artemis manual (ftp/pdf)

Artemis tutorials:

 

 

Wendy Davis never had a chance, but she was a terrible candidate

When Wendy Davis lost to Greg Abbott last Tuesday, it was not surprising. But what would have been surprising looking at her campaign from the perspective of her initial rise to fame was the scale of the loss. But by election day I had seen the train wreck develop here in Texas based on how bad the Davis campaign was. Today, Ross Douthat in the NY Times reflected from the outside and made a devastating comparison

The Christine O’Donnell thing really did happen more or less by accident, because she happened to be in the right place at the right time to catch an anti-establishment wave and win a primary in which she was supposed to be a protest candidate. Whereas the Davis experiment was intentionally designed: She was treated to fawning press coverage, lavished with funding, had the primary field mostly cleared for her, and was touted repeatedly as part of an actual party strategy for competing in a conservative-leaning state. Of course she had a much more impressive resume than O’Donnell, with less witchcraft and real political experience, and in that sense she made a more credible candidate overall. (Though, ahem, O’Donnell actually outperformed Davis at the polls in the end …)

Ouch.

Remarkably, the morning after, longtime Texas Monthly political writer Paul Burka wrote

Davis didn’t run a bad race. She raised a lot of money and she chipped away at Abbott’s weaknesses with some effectiveness.

The Texas Tribune’s Jay Root disagrees.

Davis probably never had a modicum of a chance to win the Texas governor’s race. The 2014 election turned out to be another wave election that cost Democrats the U.S. Senate, governor’s races in heavily Democratic states and competitive legislative races across the land, including here.

But for more than a year, Democrats were crowing that with a well-funded turnout operation, Davis was the kind of candidate who could at least move the needle for the bedraggled party, which hadn’t won a statewide election since 1994. In one sense they were correct: She moved the needle, all right — backward.

Root talks about how Davis failed to utilize her inspiring personal story

When the curtain came down on Team Davis, the campaign had not aired a single English-language TV ad focusing on the Fort Worth senator’s up-from-the-trailer-park narrative once seen as her campaign’s thematic foundation. In the final days, Davis couldn’t afford to effectively air such an ad, despite her campaign’s own claims of raising almost $40 million, a top official acknowledged.

We probably don’t watch as much TV in the prime advertising slots as most prospective voters, and I time shift past commercials when I can. I did see some of the gubernatorial ads when I couldn’t avoid them during live events like sports, and I saw some of the online coverage in blogs and social media. I didn’t watch any of the debates, but I glanced at some of the news stories about them. My perspective on the race is thus pretty limited, but I suspect that it’s not that different from what an average Texas likely voter actually saw.

So, within that window, Wendy Davis started as someone who was pro-choice and against regulation of abortions at 20 weeks or later. She then told me that she was:

Really? I mean, Ted Nugent is a loon, but his groupie history and Abbott’s defense of sex toy laws as AG never seemed like things that are priorities for Texas. And while Root says Davis didn’t have the resources to run positive ads, the Kirby Vacuum salesman ad was one that I saw a lot more than anything else from Davis.

Setting aside problems with the up from the trailer park narrative, and the general problem of trying to base your narrative on overcoming adversity when running against the guy in a wheelchair, Davis never established a positive agenda that I could detect. There were lots of things that Davis could have used on the negative side against Abbott, but it seems to me that a smarter campaign would have realized that for average voters, Greg Abbott is still a nonentity. The place to attack Abbott was not for anything specific about Abbott himself: it was as a continuation of the bad parts of one-party rule and the continuation of Rick Perry’s time as Gov. I would have gone after:

  • dysfunction in the lege that meant that initiatives tapping the Rainy Day Fund were needed to deal with funding for basic things like roads and water over the past few elections
  • cronyism and its effects on things like CPRIT and the Texas Enterprise Fund.
  • the ways in which Perry’s appointments and The TPPF agenda have been hurting higher ed in Texas. Ted Nugent is a loon, but perhaps it would have been better to point out the looniness of Wallace Hall.  Despite the dislike for us pointy-headed pinko academics, I think that between sports and economics, even some conservative Texans are uncomfortable with where Perry’s Regents have been taking the UT and TAMU systems. The defenestration of Bill Powers was recent news.

Davis was perhaps never the best candidate to make these points. But she was the anointed candidate and while I agree that she was doomed from day 1, moving the needle forward required showing that there was more to her than pink sneakers and abortion celebrity.  Instead, she showed us that there was less.

Ebola transmission

I did some reading on this topic a week ago, and this has been sitting in my drafts for about a week.

In the last post I noted that NEJM recently stated

Health care professionals treating patients with this illness have learned that transmission arises from contact with bodily fluids of a person who is symptomatic — that is, has a fever, vomiting, diarrhea, and malaise. We have very strong reason to believe that transmission occurs when the viral load in bodily fluids is high, on the order of millions of virions per microliter.

The question of whether patients are contagious before they become symptomatic has come up in debates about whether quarantine is appropriate or hysteria. The judge’s decision in the case of Mayhew v. Hickox, where a returning MSF nurse contested Maine’s State Dept of Health and Human Services quarantine request repeats this. Citing an expert from the states equivalent of the CDC, the judge wrote:

Individuals infected with Ebola Virus Disease who are not showing symptoms are not yet infectious.

But others are not as sure:

Moreover, said some public health specialists, there is no proof that a person infected — but who lacks symptoms — could not spread the virus to others.

“It’s really unclear,” said Michael Osterholm, a public health scientist at the University of Minnesota who recently served on the U.S. government’s National Science Advisory Board for Biosecurity. “None of us know.”

[Dr. Philip K] Russell, who oversaw the Army’s research on Ebola, said he found the epidemiological data unconvincing

What is the actual data? Not being an epidemiologist nor a virologist, I’m not already familiar with the literature, and I am likely to miss things and not fully understand the field-specific issues and language. But I think I can at least get a superficial sense of what’s out there, and what questions I would want to ask a real expert. Bottom line: the expert opinion that only the symptomatic are significantly contagious looks pretty good to me.

The first thing I noticed was that the literature on transmission of Ebola includes lots of computer modeling and that like most other fields, the citations for facts that are regarded as well established are often to reviews that cite other reviews. In some cases papers cite things like the CDC website, where the information lacks references. But this 1999 review seemed like a pretty good introduction and starting point. Authors CJ Peters and JW Peters from the CDC summarize the history of Ebola outbreaks, and point out the difficulty of reconstructing what happened in many of the early cases. Baron, McCormick and Zubeir looked at the spread of Ebola in a 1979 outbreak in the southern Sudan.

Every case,except that of the index patient,could be traced to a human source of infection…
Details of exposure to infection were not available for 2 secondary cases; the other 27 were associated with physical contact. Of these, 24 had provided nursing care to other patients in the family; for the remaining 3 patients (including the 2 children) the history indicated that the physical contact had been less intimate.

More importantly, the large numbers of family members who did not get Ebola suggested that the virus is not easily transmitted without direct contact with bodily fluids. Antibodies in asymptomatic family members (who had contact) suggested infactions that never turned into symptomatic cases. There were no cases where these were the source of another infection. But the numbers were relatively small.

In January of 1995, a charcoal worker who probably got Ebola from a natural reservoir was admitted to the Kikwit General Hospital. Retrospective analysis showed that he infected his family in the area of Kikwit, and some of the secondary and tertiary patients went to the Kikwit II Maternity Hospital over the following months. The official index patient of the outbreak was a 36 year old male who worked in the Kikwit II Maternity Hospital as a lab tech. The lab tech presented fever and intestinal symptoms that led to surgery for a suspected perforated bowel.

He underwent laparotomy at Kikwit General Hospital for a suspected perforated bowel after protracted fever. Postoperative abdominal distention increased, and an abdominal puncture revealed bloody peritoneal fluid. The patient underwent a new laparotomy, which showed massive intraabdominal hemorrhage. Three days later, on 14 April 1995, the patient died.

By that time, medical personnel who had cared for the index patient were getting sick. Only then was a viral hemorrhagic fever suspected. CDC confirmed that it was Ebola on May 10 after getting samples from Zaire the day before. Even before the confirmation, the government had declared an epidemic. By the end of the Kikwit outbreak, 316 people were known to have gotten Ebola, and 285 deaths were attributed to Ebola. This provided another opportunity to look at who gets Ebola and who doesn’t during an outbreak.

Dowell et al looked at risk factors for transmission of Ebola within families in the Kikwit outbreak. The results are overall in agreement with what was seen in Sudan.

The exposure that was most strongly predictive of risk for secondary transmission was direct physical contact with an ill family member, either at home in the early phase of illness or during the hospitalization. Of 95 family members who had such contact, 28 became infected, whereas none of 78 family members who did not touch an infected person during the period of clinical illness were infected (RR, undefined; P < .001). Nevertheless, the 78 family members who did not report direct physical contact with an ill person during the clinical phase of illness participated in a variety of activities that would have exposed them to fomite or airborne routes of spread. During the incubation period, all 78 shared meals with their ill family member, 26 reported direct physical contact, 15 shared their bedroom, and 6 shared their bed. In the early phase of illness, 62 slept in the same house and 42 shared meals. During the late phase of illness, 24 visited the hospital and 18 spoke with their ill family member.

Of the 316 patients, the majority had a known source of exposure, but 55 were initially unexplained. Roels et al went back and reexamined the available epidemiological information for 44 of these 55 (8 couldn’t be found and 3 refused to participate).

The probable source of exposure was identified for 32 (73%) of the 44 patients. Seventeen had visited an ill friend or relative with symptoms suggestive of EHF, 9 had been admitted to a health center in the 3 weeks preceding onset of EHF symptoms, and 6 had both risk factors. Of the 23 who had visited an ill friend or relative with symptoms suggestive of EHF, 4 (17%) resided in the same household as the ill patient and were their caregivers, 14 reported touching the ill patient, and 5 visited without touching the patient.

This leaves 12 people unaccounted for, and these 12 are sometimes cited as a problem for the conventional wisdom.

we identified an exposure source for 32 of 44 patients for whom no source was originally reported. Of the 12 patients who did not have an identified exposure source, no sociologic, occupational, or dietary risk factors for illness were found. Direct person-to-person contact was the likely mode of transmission for most EHF cases during this outbreak. However, our findings suggest that other EHF transmission modes cannot be excluded and may account for infection in those individuals for whom no previously recognized mode of transmission could be documented.

Although the alternative transmission cannot be formally eliminated, it is important to note that the 12 should also not be taken as proof of alternative transmission. In fact, none of them were actually confirmed as even having Ebola based on culturing the virus (See Table 3). There are also questions of the ability of the researchers to really reconstruct the contacts for each of these 12 people.

In the recent outbreak there are cases of health care workers who have contracted Ebola despite precautions. This could mean that there is a route of transmission that bypasses the protective protocols… or the simpler explanation is that errors in following the protocols led to transmission by the accepted route of direct contact with virus-laden bodily fluids. The Spanish nurse who has now recovered says she doesn’t know how she got it, but earlier reports talk about contact with gloves as she removed protective gear. For at least one of the nurses from Dallas, there are reports that she contacted Thomas Duncan in the ER without protective gear, before it was recognized that he was an Ebola patient.

NEJM on Ebola

The New England Journal of Medicine has an Editorial criticizing the quarantines in NJ and other states.

Health care professionals treating patients with this illness have learned that transmission arises from contact with bodily fluids of a person who is symptomatic — that is, has a fever, vomiting, diarrhea, and malaise. We have very strong reason to believe that transmission occurs when the viral load in bodily fluids is high, on the order of millions of virions per microliter. This recognition has led to the dictum that an asymptomatic person is not contagious; field experience in West Africa has shown that conclusion to be valid. Therefore, an asymptomatic health care worker returning from treating patients with Ebola, even if he or she were infected, would not be contagious.

In the same issue, there is an article: Clinical Illness and Outcomes in Patients with Ebola in Sierra Leone. Take a look at the supplementary material. Figure S8 shows temperature and heart rate for fatal and non fatal cases

Panels B, C,E and F represent cases with a normal temperature-pulse association.

All of these are infected. One of the three was a fatal. Table S5 shows symptoms. 11/36 did not present fever. We don’t see if they presented other symptoms but, from the legend:

Eight fatal subjects and one nonfatal subject showed no reported symptoms on the case notification form and were excluded from these results.

AcrobatScreenSnapz003
From Schieffelin et al. (2014) Clinical Illness and Outcomes in Patients with Ebola in Sierra Leone NEJM DOI: 10.1056/NEJMoa1411680 Figure S7

Perhaps people can die of Ebola without being viremic to the level needed for infect others? I also wonder if they really meant “millions per microliter” or “millions per milliliter”. The former is 109/milliliter. Figure S7 shows viral loads in fatal and nonfatal patients, and it does look like Ebola in serum can reach that level, but two of the fatal cases are well below that. Other sources have claimed that the number of particles needed for an infection is on the order of 1-10. Even at 106/ml,a microliter would be 1000 particles. When people are exposed to infected bodily fluids, are the volumes involved in the picoliter range?

Update: the ID50 is on the order of 1-10 for animal models, but in mice the sensitivity depends on the route of introduction.

The LD50 of mouse-adapted EBO-Z virus inoculated into the peritoneal cavity was ~1 virion. Mice were resistant to large doses of the same virus inoculated subcutaneously, intradermally, or intramuscularly.

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College Football Week 6: Chaos

My teams went 0-3 in a series of frustrating losses, each of which was depressing in a different way. But these were just a small slice of a crazy weekend in sports.

Miss State d A&M

The question going into this game was whether the Arkansas game showed A&M’s grit and ability, or revealed problems. Meanwhile Miss State was coming off a bye week after their historic win at LSU. Pundits were picking the Bulldogs despite A&M’s #6 ranking, and the line moved from the Ags being slight favorites to slight underdogs.

The game was in the early slot, starting at 11AM CDT. MSU was missing starting center Stomping Dillon Day, but at gametime it was announced that they would not play one of their better receivers. The Ags revealed that the shoulder injury that Malcome Kennedy sustained against Arkansas would keep him out of the game in Starkvegas. Aggie fans were surprised that among the large numbers of receivers on the roster, walk on Boone Niederhofer was the top choice to take Kennedy’s spot.

The Ags started fast again, scoring a TD on their first drive. State answered with a TD of their own, but with their drive including a Myles Garrett sack of Dak Prescott and the need for some penalties to keep the drive alive, I was hopeful that the Ags would come away with the win.  But after starting fast again, the Ags repeated their problems of keeping drives going. A muffed punt after the second A&M possession gave the Ags an opportunity to retake the lead despite stalling on the second drive, but could not convert on 4th and 1 after a horrible spot on the 3rd down catch by Niederhofer. The D got a stop on the next MSU possession, but the Ags stalled again. The number of drops was something between 9-15 depending on who was counting. Meanwhile, although the D was able to get enough stops to win if A&M was the scoring machine we expected, MSU and Prescott got their act together, found weaknesses, and made it 21-7.

It got worse when Hill threw picks on the next two possessions, squandering a forced turnover after the first interception. This made the halftime score 28-10 after the Ags added a late FG. The D got stops on the first two possessions of the second half. But the O couldn’t shift the momentum by scoring, and when MSU scored on their third possession to make it 34-10, the chances for a comeback faded.  A great catch by Speedy Noil cut it to 34-17, but we couldn’t stop State and another TD made it 41-17. The Ags scored the only points of the 4th quarter to make the final score look better, but it was still a beatdown.

As I write this, Gabe Bock and Billy Liucci are dissecting the game on the radio. The question they are addressing is whether the WR corps got surprised the last two weeks about the difference in play in the SEC West compared to the previous opponents.  This sounds right to me… dropped passes aren’t just about what a WR does with his hands at the end of the play. Everything that goes into running a good rout and creating a window affects the probability of a catch. I once read that running full speed decreases visual acuity due to the amount of head movement that happens in a full out sprint. This 2009 WSJ article about Larry Fitzgerald has some interesting thoughts about what makes a great WR in terms of vision.

Northwestern d Wisconsin

Wisconsin and Stanford both had 2:30 CDT kickoffs, and between being depressed by the Ags taking the dog out, and flipping to other games, I didn’t watch all of this game. The Badgers have had trouble with their passing game all year, which puts extra pressure on the run game. Despite the poor passing, Melvin Gordon has had an exceptional year, and Wisconsin has managed to win against weaker opponents.

If A&M fans are concerned about QB play, they only need to watch the Badgers to see how good we have it. On Saturday the Wisconsin coaches decided that a below average Joel Stave is a better choice than a horrendous Tanner McEvoy at QB. Unfortunately, this improvement includes the fact that Stave’s bad passes are close enough to the receivers to be picked off, while McEvoy tends to miss so badly that even the DBs can’t find the ball.

I missed most of Melvin Gordon’s runs on the way to a career-high 259 yards. Unfortunately for the Badgers, Northwestern’s D kept Gordon from making it into the end zone more than once. The Wildcats took a 10-0 lead into halftime. Gordon’s only TD of the game cut the lead to 10-7 and the hope was that the Badgers would get another game where the run game wears the defense out for a late win.  And when the Badgers stopped Northwestern at midfield after Gordon’s TD, it looked like that would be the script for the day.

Instead, starting deep in their own territory after a penalty on the punt return, the Badgers ran Gordon twice to make it 3rd and 5 from the 11. Instead of taking their chances with another run, the Badgers threw for the sticks… and Stave was picked off at the 16. One handoff later it was 17-7 Northwestern.

A missed Wisconsin FG and a good NW FG made it 20-7. The Badgers got down to the NW 16, but penalties and losses gave them 4th and 21 at the 27. Instead of trying another FG, the Badgers played for field position by taking a delay and punting. This looked like it had paid off when the D held and Wisconsin got the ball back at the Wildcat 44.

Most of the above is reconstructed from the online play-by-play. I only saw glimpses as I channel surfed. I did, however, watch live as the Badgers lined up with first and goal from the 3 with a chance to cut the lead to 6.  What happened next was one of the worst combinations of play calling and execution of the weekend. With everyone watching anywhere expecting the Badgers to blast into the end zone with 3 chances to make 3 yards, OC Andy Ludwig calls a pass. Stave gets chased out of the pocket and goes to the right. Instead of throwing the ball away to take 2 chances to blast Gordon or Clement into the end zone, he tries to hit a receiver for the TD and throws a pick.

Later in the 4th, Stave hit Kenzell Doe on a long TD to get the lead to 6. But now there was only 4:16 to go. The Badgers kicked deep but weren’t able to prevent Northwestern from draining the clock to 33 seconds. A final interception gave Stave 3 for the day, to go with 1 by McEvoy. Wisconsin QBs finished the day with QBRs of 10.1 and 8.8.

Notre Dame d Stanford

While the Wisconsin debacle was going on, Stanford was in South Bend playing Notre Dame in the rain. While it could be viewed as a good old-fashioned defensive game, I’m not sure if the lack of offensive production was good D or below average offense. The Irish outgained the Cardinal 370 yards to 205. With those numbers, it’s not surprising that neither team had a 100 yard rusher. Both teams tried the run 32 times (including sacks); the leading runners where Wright for Stanford with 29 yards and McDaniel for the Irish with 41.

After a 7-7 halftime tie, both teams were futile in the third quarter. Halfway through the final period, ND broke the tie with a FG. Failure to have the holder wear gloves on an earlier attempt in the pouring rain kept them from taking the lead earlier. Stanford put together what should have been the winning drive starting with a nice Ty Mongomery kickoff return to the Stanford 42. A mix of passes and runs got the Cardinal to the ND 33, where QB Kevin Hogan converted a 3rd down by lofting a 23 yard pass to Devon Cajuste at the 10. I was kind of shocked that this was completed. The ball floated high into double coverage and the ND defenders just failed to break up the completion. After two futile running plays made it 3rd and goal from the 11, Notre Dame dropped into a pass-prevent defense, leaving a vast hole up the middle that Remound Write ran through pretty much untouched for a TD and the lead with 3 minutes to go.

With Stanford’s top ranked defense and the offensive futility displayed through the day, that should have been enough. But instead the Cardinal put in a textbook display of how to blow a late lead.  They started by booting the kickoff out of bounds, giving the Irish the ball on their own 35. They then showed why people say that prevent defense is only good at preventing victories. Using a 3 man rush, they gave ND QB Everett Golson time to find holes in the secondary and march down the field. Worse, if you’re going to drop 8, it helps if they pass defenders actually know where to go. One busted coverage led to a pass interference call, giving ND the ball on the Stanford 22. The second busted coverage came on a play that was a golden opportunity for the D to save the game: 4th and 11 from the 23. Instead, the D left a tight end wide open in the left side of the end zone. TD Irish.

Stanford got the ball back with a minute to go and managed to get to midfield. But Hogan took an intentional grounding penalty and the runoff ended the game with a whimper. From the post-game.

Stanford coach David Shaw was asked what coverage the No. 14 Cardinal were in on the play.

“There was no coverage on Notre Dame’s touchdown pass,” he said. “That sounds sarcastic but he was wide-open. There was nobody on him.”

Indeed.

Elsewhere

A lot of teams thought they had an opportunity to move up in the rankings when unranked Arizona upset #2 Oregon on Thursday night. Not so much.

 

Sous vide tandoori-style lamb chops

Debby got some leftover vegetable biryani from a Biology party.  We’re going to use as a side with some lamb chops I got from Rosenthal, so I thought I’d do something different and make them with a tandoori marinade.

Marinade

  • Yogurt
  • Garlic
  • Ginger
  • Cumin
  • Coriander
  • Cinnamon
  • Garam Masala
  • Sambal
  • Some of the goop from a jar of Indian mixed pickle
  • Salt

Mixed in a stainless bowl and put thawed lamb chops in at about 2:40 PM. The color is sort of a light chocolate brown.

Sous vide and broil

Let it warm to room temp and bagged it all. 135F for 2 hours starting at ~6PM. Finish under the broiler.

IMG_1203.JPG
It might have been better to finish in a pan or on a grill, as the broiler may have taken them past medium rare. but the marinade worked well.

College Football Week 5:Comebacks

I didn’t get around to posting last week’s results, when my teams went 3-0, but each of the wins foreshadowed problems that surfaced this week. I meant to write something last week, but got busy with actual work.

Wisconsin d S. Florida

The Badgers played an early (11AM CDT) game against S. Florida. The game was tied at 3 at halftime, as Wisconsin continued to show problems in the passing game, and was slow to get Melvin Gordon and the passing game going with Tanner McEvoy. The Badgers broke out in the third quarter. Final Score: Wisconsin 27, S. Florida 10.

A&M d Arkansas

The Aggies went to Dallas for the second straight week to face an improving Arkansas team in their SEC opener (talking heads seem to forget that we had already played S. Carolina). After the usual fast start, A&M fell behind on a long run by RB Alex Collins. A&M tied it on a TD to Ed Pope, but the Ags misfired with dropped passes and a surprising FG miss by Lambo. While the Ags drives misfired, we did an OK job stopping the Razorbacks until a fake punt that went 51 yards to give Arkansas a 21-14 lead going into halftime. With Arkansas getting the ball first to start the second half, A&M fans were worried about getting into a shootout needing to break service. The D held on that first drive and A&M moved to the Arkansas 21 with a chance to tie the game. But a Kenny Hill to Ricky Seals-Jones out pattern on 4th and 1 was well covered, and the Ags gave the ball back. Arkansas got a 2 TD lead on their next drive on a play-action pass to TE AJ Derby. Derby blocked CB Devante Harris before releasing into the open with no safety help, while QB Brandon Allen did an excellent job of hiding the ball after faking a handoff. 28-14 Arkansas.

The first major turning point of the game came on a bonehead play by Arkansas tackle Dan Skipper in the 4th quarter. Arkansas ran a well-blocked play that sprang Jonathan Williams to the 2 yd line. But away from the point of attack, Skipper was knocked down and reacted by not one but at least two flails of his legs, ultimately drawing a tripping call that brought back the big play that would have led to a 3 TD lead. A&M’s next possession after a punt to the 12 yard line took 2 plays. The second was an 86 yard bomb to Pope to cut the lead to 28-21. Arkansas went 3 and out on their next drive, but Kenny Hill threw a long interception to give the Hogs the ball back with 8:34 to go. Both defenses got stops and Arkansas took over with a TD lead with 5:27 left. A pair of 17 yard runs got the ball into A&M territory. A fumbled snap was recovered by Arkansas, but the Hogs settled for a FG attempt from the A&M 31 to make it a 2 score lead with less than 3 minutes to go. Unfortunately for the Arkansans, the FG was missed. The Ags struck quickly again, with Hill hitting Josh Reynolds on the right side between two defenders. Reynolds shot through the gap and ran to the end zone to tie it up.

After stopping Arkansas again, the Ags had a chance to win in regulation, getting the ball on the 25 with 1:18 left. A&M got as far as their own 38 before opting to go to OT. The OT didn’t last long, as the Ags scored in one play on a Hill pass over the middle to Malcome Kennedy (who got away with a false start that was disguised by Hill’s acting like there was an audible after Kennedy’s twitch). The Arkansas linebacker bit on a fake WR screen to the right, and Kennedy ran straight up the middle to snag the pass and run into the endzone. Arkansas had to score a TD to keep OT going, but couldn’t convert on 4th and 1. Final Score: A&M 35 Arkansas 28. Bullet dodged.

Stanford d Washington

The Cardinal went to Seattle to play Washington. The game started while the A&M game was already going, so I only caught glimpses of it. But what I did see seemed like typical Stanford for this year: good D combined with an offense that has trouble in the red zone. Stanford had 3 turnovers, and the game was tied at 13 in the 4th quarter. I did not see the peculiar decision by Washington to run a fake punt on 4th and 9 from near midfield. It was stuffed and Stanford scored the game winning TD on the next possession.

Elsewhere

There were lots of interesting results on the field, but the story that dominated the week was a decision by Michigan’s Brady Hoke to sub in a player who was concussed during a blowout loss to Minnesota. This seemed to be a product of cluelessness and incompetence more than a manifestation of macho throwback values, but it was still appalling. Michigan handled the aftermath badly as well, leading to campus rallies against the AD and grandstanding from congresscritters.

On the field:

Sous vide halibut

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Debby bought some frozen halibut filets. Thought I’d try to cook them sous vide.
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Decided on 128F. Salted the frozen filets and put them in a bag with some butter and lemon slices. Into the bath at 7:45PM. I figure to add some time to the recommended 20-30 min for the fish to thaw.

The bag didn’t sink as much as when I do red meat, so I put a spatula in to make sure the bag was submerged.

As the Giants and Nationals went into extra innings in game 2, I took the fish out of the bag and portioned it. I had intended to pan-fry the portions to crisp up the skin, but it was too fragile. Instead, I removed the skin and served with rice and mixed vegetables.

The fish was tender and moist – perhaps to the point of being on the wet side. It was tasty but a bit on the boring side.  Despite the lemon slices and the spritz of lemon juice I added when I served them, I think this would be better with some sort of bright and spicy sauce.

But for a meal put together from what we had in the fridge and freezer on a night when we needed to go grocery shopping… not too bad.