Mystery Rays from Outer Space

Meddling with things mankind is not meant to understand. Also, pictures of my kids

March 17th, 2014

Influenza subtypes in birds

What subtypes of influenza are found in birds?

Influenza is naturally a disease of wild waterfowl; humans, like dogs, chickens, and whales, are occasional victims of mutated viruses from this vast global reservoir of viruses.  In wild birds, flu viruses reassert and recombine wildly, mixing almost all the known subtypes promiscuously.

There are 18 known hemagglutinin subtypes and 11 known neuraminidase subtypes. Two of each are only known from bats, so there are 16 and 9 that could occur together in birds, for a total of 144 possible combinations.  Some subtypes of each are rare, and some HA and NA types don’t play well together. Which combinations have been found, and how common are each?

Mainly because I was playing with Plotly,1 I tried making a bubble chart of HA and NA subtypes found in waterfowl throughout history.  I used sequences in the influenza databases, sorted by HA and NA, and plotted them with HA on the X axis, NA on the Y, and size of each bubble representing how common they are.

Of course, this is not really a representative look.  It’s wildly distorted by surveillance trends; people intensely test birds for H5N1 (because it’s lethal to humans), and H7N7 was surveyed mainly after multiple people were infected in the 2003 outbreak in the Netherlands, so those are probably over-represented compared to their actual prevalence in birds.  Still, it helps give a sense of the complexity of the viruses circulating out there.

Flu in birds

 


  1. My conclusion: Plotly is pretty cool, but doesn’t offer me very much.[]
February 24th, 2014

What can we expect from Daniel Nava?

Daniel Nava is a player for the Boston Red Sox (that’s baseball, by the way) who has had a pretty unusual career.  Too small to play when he started college, a late growth spurt and a ferocious work ethic wasn’t enough to induce any interest from the major-league teams.  He played with independent-league teams for year, until the Red Sox bought his contract for $1.00.  He hit a grand slam on the first pitch he saw in the majors, then didn’t make the team the next year, was added as a backup outfielder the following year, and platooned and played fairly regularly in 2013 (winning a World Series in the process).

As a regular, Nava actually hit pretty well last year (.303/385/.831), with the 5th-highest OBP in the AL.  The question is, What can we expect from Nava going forward?  Was this year a fluke, or is he genuinely this good a hitter who just followed a weird path to the majors?

I downloaded the Lahman Baseball Database and use Python, iPython Notebook, and pandas to ask what historical comparisons could show us.

I looked at players who, like Nava:

  • Made their major-league debut at the age of 27 or older.
  • Played at least 3 seasons of major-league baseball,
  • With at least 150 at-bats in at least one season.  (I chose the 150-AB cutoff arbitrarily, mostly to get rid of pitchers and pinch-runners without being too exclusive otherwise. )
  • Made their debut since 1960 (again, a rather arbitrary cutoff, but if I go much further back the game was significantly different from today)

This gave me 50 players.  I only looked at OPS; I know it’s not perfect, but it’s a pretty decent way of summarizing batting value in a single number.  Rather than include a large table here I’ll link to it.

A quick glance shows some familiar faces besides Nava.  There are a number of Japanese players who joined the majors after playing in Japan – Ichiro and Hideko Matsui being the most famous.  Davey Lopes played for 16 years in the majors despite not starting until he was 27!   But overall, I think it’s fair to say that the majority of these players were more or less journeymen.

Average OPS hovered in the low .700s for most of the players, over most of the seasons (and then exploding up — Davey Lopes! Who also stole 35 bases that year, in part-time play at the age of 41).  But after4-5 years the number of players begins to drop: The OPS is staying the same because the lowest achievers were being dumped out of the majors.

OPS over 27

The players tend to be fairly variable, as you can see from the bottom chart (note, this is only including seasons with over 150 AB, or the variability would be much more dramatic).  Champ Summers had one season with a .580 OPS in — naturally — limited playing time, then shot up to .957 two years later.  Mike Difelice went from .815 to .504 in two years.   Part of that is because many of these players were part-timers, barely making the 150 AB cutoff, which makes variability easier.  Part of it is probably that once one of the guys has a good season they’re more likely to be kept a round a little bit too long in the hope they can repeat it.

Daniel Nava is pretty much right in the middle of these guys.  He’s less variable than many, but then he’s only been in the majors for the 3 years I used as my cutoff.  Some of the other players who look a little like him had some pretty decent seasons, but only a handful had really impressive careers (Hideki Matsui, Davey Lopes, Melvin Mora, um … ).   On the other hand, Nava is just 30 years old, and lots of these players stuck around longer than that; the big dropoff is roughly around age 33 or so.  So just based on what I see here,  Nava has a reasonable chance of playing baseball for several more years, and might well have a pretty nice season or two in there, but probably hoping for him to break out and become much more than a platoon player is overoptimistic.

Good luck to him, though.

February 10th, 2014

How we died in 1890

From the Report on Vital and Social Statistics of the United States at the Eleventh Census: 1890

Malaria 1890
Malaria was a major killer.
Measles 1890
As was measles.
August 26th, 2013

The pace of new virus discovery

From: Search strategy has influenced the discovery rate of human viruses (Proc Natl Acad Sci U S A. 2013 Aug 20;110(34):13961-4)

Virus Discovery
 (A) The cumulative discoveries of human-pathogenic viruses in any organism (black) and their incrimination as a cause of human disease (green). (B) The cumulative discoveries of human-pathogenic arboviruses (red), and nonarboviruses (blue). (C) Yearly arboviruses and nonarboviruses discovered (red and blue points, respectively).

For arthropod-borne viruses, which comprised 39% of pathogenic viruses, the discovery rate peaked at three per year during 1960–1969, but subsequently fell nearly to zero by 1980; however, the rate of discovery of nonarboviruses remained stable at about two per year from 1950 through 2010. The period of highest arbovirus discovery coincided with a comprehensive program supported by The Rockefeller Foundation of isolating viruses from humans, animals, and arthropod vectors at field stations in Latin America, Africa, and India. The productivity of this strategy illustrates the importance of location, approach, long-term commitment, and sponsorship in the discovery of emerging pathogens.

June 24th, 2013

Neutrophil swarm

Neutrophils (red) and monocytes (green) entering an area of tissue damage.

This representative video shows the immediate response of fast-migrating neutrophils (small red cells) towards a focal tissue damage site, while monocytes (green) migrate with slower speeds and follow the developing neutrophil cluster with delay.

–Neutrophil swarms require LTB4 and integrins at sites of cell death in vivo
Tim Lämmermann et al
Nature 498, 371–375 doi:10.1038/nature12175

(See also When Neutrophils Attack)

May 13th, 2013

Deaths in 1898

“Number of deaths per 1000 deaths from known causes” — US Census Office, 1898

(Click for a larger version.)

Top tow, from left: Consumption (scale goes up to “135 and over per 1000 deaths”), diphteria (50 and over), cancer and tumors (30+), whooping cough (14+);

Middle row: Pneumonia (105+), croup (20+), malarial fever (80+), scarlet fever (11+);

Bottom row: Diarrheal diseases (100+), typhoid fever (50+), measles (20+), heart disease and dropsy (80+).

From davidrumsey.com.   

March 25th, 2013

On the Influenza Epidemic of 1892 in London

Table I
London.  Weekly Deaths from “Influenza” during Four Epidemics – 1847-48, 1890, 1891, 1891-92
Table V
London.  Causes of the Mortality due to the Influenza Epidemic of 1892

The link between influenza, and deaths from apparently-unrelated causes, has apparently been noted for well over 100 years. It’s still somewhat controversial today.

Effect on the Mortality from other Diseases.
One of the chief characteristics of an influenza epidemic is the effect it produces on the mortality from other diseases. The disorders most conspicuously affected are, as is well known, those of the respiratory system; but others are influenced in an almost equally marked degree. The annexed table gives details of the relation between the mortality due to various causes of death and that attributed primarily to influenza during the course of the 1892 epidemic.

The principal facts are contained in Table III. Besides the rise in the mortality from the respiratory diseases, the augmented fatality of phthisis, diseases of the circulatory system, and whooping-cough is noticeable, as is also the increase in the number of deaths attributed simply to “old age.”

Another diagram (No. 1) exhibits the dependence of the mortality ascribed to the two main respiratory diseases, bronchitis and pneumonia, on the presence of influenza for the whole period from October, 1889, to July, 1892. It will be seen that in every instance of the prevalence of the latter, the curves representing the mortality from, the two former rise far above the average; The peculiar significance of these curves lies in the fact that the presence of influenza as the primary cause of death was not recognised in any of the cases which they represent; otherwise they would have appeared in the Registrar-General’s returns under the head of “influenza,” and not under that of “bronchitis ” or “pneumonia ” as the case may be.

An increased mortality from all or most of the causes that have been mentioned characterises all influenza epidemics, and not that of 1892 alone. It is impossible to believe that the invariable coincidence between the rise of these various causes of death and influenza is accidental, and the conclusion seems inevitable that influenza itself is the determining cause, though it does not so appear in the returns furnished to the Registrar-General. This being the case, in estimating the mortality of any particular epidemic it is necessary to allow for the deaths returned under other heads than that of influenza.

–On the Influenza Epidemic of 1892 in London :: BMJ 2:353-356 (1892)

February 11th, 2013

Useful information about spider legs

(This post is adapted from two questions I answered on Quora.)

Why do a spider’s legs curl up when it dies?

The explanation was provided by Pritesh Kalantri: Spider legs extend due to hydraulic pressure, not muscular action, so when the hydraulics are turned off (as when the spider dies) the muscles that contract the legs have no opposing action, and the legs curl up.

This was new to me, and I quickly found what seems to be the original paper establishing this fascinating fact:  Parry, D. A., R. H. J. Brown: The hydraulic mechanism of the spider leg. J. Exp. Biol. 36 (1959a) 423–433.

A helpful diagram should you decide to test hydraulic pressure in your own spider’s legs. This can be used with live spiders, as needed.
A more detailed view of spider anatomy

1. The blood pressure inside the leg of the house spider Tegenaria atrica has been measured. Maintained pressures of about 5 cm. Hg and transient pressures of up to 40 cm. Hg have been found.
2. The relation between the blood pressure in the leg and the extension torque at the hinge joints has been established.
3. Considerable torques can be developed at the hinge joints during extension, for example, when accelerating a mass fixed to the leg. The transient pressures found to arise in the leg are adequate to account for these torques.
4. The hydraulic mechanism is discussed. The available evidence suggests that the pressure found in the legs occurs also in the prosoma but not in the abdomen, in which case the maintained pressure must be due to the heart. This, however, requires further investigation.

We are greatly indebted to the Cambridge Instrument Company for the loan of a photo-electric transducer; and also to many friends who have supplied us with spiders.

However, a little further research suggests that hydraulic activity is not the only mechanism for spider leg movement.

In large spiders such as A. concolor, the advantage of strong leg flexion remains valid. Here, during jumps and starts, the net propulsive power is shifted more to their front legs. In contrast to jumping spiders, the ground reaction forces of the frontal legs and the second legs are as strong as those exerted by the hind legs.  … It seems that depending on the spider’s body size both hydraulics and muscular leg flexion contribute, to variable degrees, to the propulsion of the hind legs.

Hydraulic leg extension is not necessarily the main drive in large spiders.
J Exp Biol. 2012 Feb 15;215(Pt 4):578-83. doi: 10.1242/jeb.054585.
Weihmann T, Günther M, Blickhan R.

This led inevitably to the next question:  If you accidentally sever a spider’s leg, will the leg bleed?

It does bleed, but there is a special mechanism that prevents too much loss of fluid.  Here is an explanation from a 1957 paper:

Figure 3.  Anatomy of a spider leg, showing the mechanism by which fluid loss is minimized if the leg is severed

Unlike Crustacea and insects, spiders autotomize their legs at a functional
joint and an account is given of the interesting mechanism by which the joint is severed and bleeding restricted. …

THE AUTOTOMY MECHANISM
‘Autotomie’ was defined by Fredericq (1883) as ‘mutilation par voie reflexe comme moyen de defense chez les animaux’. Usage has since widened the term to embrace all cases of fracture of limbs and other structures at a specific point where structural adaptations associated with the fracture mechanism and reduction of bleeding are found to occur.

… I have shown above (see fig. 3, A-D) that in Tegenaria the coxal muscles are all inserted on to a ring of sclerites which fit into a groove in the proximal rim of the trochanter. The joint fractures between these sclerites and the trochanter, and the coxal muscles then pull the articular membrane proximally while at the same time the sclerites converge on one another (fig. 3, E) so that a comparatively small hole is left in which the blood rapidly clots and which after a day or two is sealed by a brown plate.

– Spider Leg-muscles and the Autotomy Mechanism
D. A. PARRY
Quarterly Journal of Microscopical Science, Vol. 98, part 3, pp. 331-340, Sept. 1957.

October 8th, 2012

Smallpox posters

Took my kids to the CDC museum last week.

CDC smallpox poster 1 CDC smallpox poster 2
CDC smallpox poster 3 CDC smallpox poster 4
July 16th, 2012

“Is the world becoming sicker?”

Zoonoses map
Map of zoonotic emerging infectious diseases. Number of zoonotic EID events:  

Is the world becoming sicker or are we just better able to detect disease? The last decades have seen dramatic improvements in biological disease detection with dozens of new potential pathogens anticipated by 2020. At the same time innovations in information management are increasing awareness of disease outbreaks. Perry et al. (2011)1 explore this in a recent review and conclude that there is overall evidence for increased emergence of disease in recent decades, and not just improvements in diagnosis and surveillance. The current increase in disease emergence is not historically unprecedented: major epidemiological transitions also occurred during the Neolithic when livestock were domesticated on a wide-scale, during the age of exploration when Old World pathogens were introduced to the New World, and to a lesser extent with increased global travel in the nineteenth century).

Grace, D. et al. 2012. Mapping of poverty and likely zoonoses hotspots: Report to the Department for International Development. Nairobi, Kenya: ILRI 


  1. Perry, B.D., Grace, D. Sones, K., 2011. Current drivers and future directions of global livestock disease dynamics. Proceedings of the National Academy of Sciences of the United States of America, 16 May 2011. doi 10.1073/pnas.1012953108 []