neuroscience - Are there neuronal firing artifacts produced by head movement?

There are certainly head-orientation cells (e.g. in the hippocampus). But neurons are reasonably immune to the kind of mild physical stresses that come from turning the head around; computing head orientation requires complex analysis of input from e.g. the visual system (optic flow) and vestibular system.

However, the electrical activity of muscles tends to swamp that of (nearby) neurons, so various muscle-related artifacts are often visible in an EEG if not carefully filtered out. And, of course, if the contact is poor you'll get artifacts from that: you're just measuring the variability in resistance between the sensor and your skin, not anything interesting about what faint potential changes are visible at your skin as a result of neuronal activity.

genetics - What accounts for size variation in breeds of dogs?

This is a fascinating bit of genetics.

Dogs are especially variable in size and many appearance, behavioral and temperamental phenotypes. It was long expected that variations in developmental genes were the reason that dog breeds were responsible for the amazing flexibility of dog sizes. One early locus found was IGF1 (insulin like Growth Factor 1).

This 2011 PLOS paper actually review the specific genotypes of dog breeds and identifying loci that are strongly associated with breed phenotype supports this idea.

... (we scanned) the genome for signatures of selective sweeps in single breeds, characterized by long regions of reduced heterozygosity and fixation of extended haplotypes. These scans identify hundreds of regions, including 22 blocks of homozygosity longer than one megabase in certain breeds. Candidate selection loci are strongly enriched for developmental genes. We chose one highly differentiated region, associated with body size and ear morphology, and characterized it using high-throughput sequencing to provide a list of variants that may directly affect these traits.

Emphasis added.

This theory has an intuitive appeal as well - no dog breeds (I think) are larger than the wolf, the stock from which all dog breeds are descended. All such breeds being derived from earlier developmental stages of the wolf makes an intuitive, if imprecise description of the effect here.

Regardless, dogs remain an important model organism for so many traits because relatively few genomic regions can cause so many important phenotypes, including size, but also behavioral and morphological variations.

In the below figure you can see how few genomic regions are responsible for the 46 breeds Vaysee et al. examined.

biochemistry - Why pouring salt in the wounds is painful?

De salt particles are alien bodies and can damage the tissue by mechanical means (This would also happen if you pour sand into an open wound). Also, the exposed tissue is vulnerable to dehydration, wich happens faster if the osmotic pressure is higher. Finally, nerve tissue is particulary sensible to changes in the ion composition of its sorroundings, so the added sodium may affect the action potential of the nociceptors.

genetics - What determines the colors and patterns of a clam shell?

Earlier this week I was looking at some bivalve shells that had ornate patterns which ranged in color from a light orange-pink to a deep orange-red. Here is an image I found online that seems to be of the same type of shell:

The friend who was with me said, "I wonder where the color comes from." We were trying to look for two shells with similar colors, patterns, and approximately equal sizes, and it was hard, even though we were looking through a large collection of similar shells.

What determines this ornate pigmentation? Is it influenced by environmental factors such as the minerals in the water? Does it have anything to do with the age or health of the organism? Or is it purely genetic? Is this determined by the same basic biological principle that determines the color of human hair, or is there something different at work in shells?

evolution - Why aren't antheridia and archegonia touching?

Antheridia and archegonia are the two male and female gametangia, respectively, and they are found in bryophytes. To cause fertilization, usually a thin film of water must be present for the sperm from the antheridia to reach the archegonia. Why hasn't evolution trivialized this process? I have the same question for flowers that primarily undergo self-fertilization. How is this not inefficient?

amino acids - Why are Taurine and Arginine essential components of the feline diet?

From the Taurine Wikipedia article:

The absence of taurine causes a cat's retina to slowly degenerate, causing eye problems and (eventually) irreversible blindness – a condition known as central retinal degeneration (CRD), as well as hair loss and tooth decay. Decreased plasma taurine concentration has been demonstrated to be associated with feline dilated cardiomyopathy.

Arginine is an Essential Amino Acid for cats (and many other mammals - including Humans while we're infants). That is, they cannot synthesize it on their own and must obtain it entirely from their diet. A 10lb. (5kg) cat will require about .86g of Arginine - which is abundant in all meats and can be met with a few ounces of food.

I could not find anything particularly special about Arginine as opposed to other EAA's for cats.

genetics - Origin, or source, of rhesus negative in human blood

This is my first post here, so please be gentle. I recently learned that I have Rh- blood (I'm A-), and was idly looking into blood types on Wikipedia. I was surprised to find that relatively few (~15% of all) humans have it, and most of those seem to be European. Looking just a little further, I found a bunch of crackpot-looking sites that try to explain how people got Rh- blood, and what weird abilities they possess as a result.

I managed to find one site that seemed at least less laughable, which suggested that interbreeding with Homo neanderthalensis (or possibly Homo sapiens neanderthalensis, since the site seemed to indicate that there was some question about how different H. s. sapiens were from H. neanderthalensis) might have accounted for the introduction of the condition.

It seems that from more reputable (medical) sources, the only difference between Rh+ and Rh- is that complications can arise during pregnancy if the mother is Rh- and the fetus is Rh+. Indeed, most sites (e.g., WebMD) seem to explicitly state that there are no other differences of note.

I am not a biologist, or an anthropologist, or a life-science kind of guy at all. However, as a computer scientist, I like to think that I have both an open mind but one which demands scientific and/or logico-mathematical evidence for claims. Lots of the pseudo-scientific, paranormal, etc. theories on the web I basically dismiss out of hand, as explanations which are almost certainly fantasies, but most definitely baseless and untestable.

My question:

What, if any, is the current scientific understanding of the origin, or source, of rhesus negative blood in human beings? Do individuals with Rh- blood have any common (in a statistically significant sense) characteristics or health issues, aside from the issue with pregnancy and tending to be more European than not? Is there anything to continuing to look into this?

For context, I got started down this rabbit hole while looking into different dieting strategies, and found the "blood type diet". Just as an aside, I don't think there's a lot of merit to that diet... sounds like a fad thing. Any sources or information or help on this subject are appreciated.

EDIT:

I have been looking a little more, and I stumbled across a paper entitled, "The influence of RhD phenotype on toxoplasmosis and age-associated changes in personality profile of blood donors" which looks at the effect of the Rh- trait on personality changes caused by toxoplasmosis (if you Google the title, you should be able to download). Using Cloninger's and Cattel's personality factors, they seem to show a variety of things, including (a) personality differences between Rh+ and Rh- individuals not affected by toxoplasmosis, and (b) different reactions to prolonged toxoplasmosis affection in Rh+ and Rh- individuals.

I didn't even know that parasites could affect your behavior; that seems frightening on the one hand, but on the other, it's fascinating if it's for real, especially since the incidence of toxoplasmosis is not insignificant in most people. Anybody who knows anything about this or who reads the paper and can help me understand what it's saying would be doing me a great favor to answer/comment/chat. Thanks!

evolution - Does a fully-resolved phylogenetic tree have to be dichotomous?

In theory, yes, every tree has to be dichotomous. You can understand a trichotomy in a tree as the summatory of two dichotomies that had happened so close in time that you cannot know wich was first.

Given a certain population, assume that some individuals colonize a new environment, got reproductively isolated and form a new specie. This is the typical speciation process. In this case, the two species, share a common ancestor. If you go back in time, all the individuals of the new specie will descend of only one individual. The same goes for the original specie. If you go back further, this individuals will share an ancestor, too. This is the conceptual meaning of the dichotomy, but normally it is impossible to determinate wich was exactly the common ancestor.

Now imagine that the original population formed not one, but two new species. And that this process happened about the same time as the one described before. It is conceptually possible that a set of three brothers were the origin of three different species (wich will be a true trichotomy), but not only it's very unlikely, but it's virtually impossible to prove. Since two close dichotomies are far more probable than a trichotomy, it's assumed that every tree has to be dichotomous, and that a trichotomy is in fact due to lack of resolution.

pathology - What mechanisms do animals living in groups (herds, packs, swarms) have against spreading contagious diseases?

Almberg ES, Mech LD, Smith DW, Sheldon JW, Crabtree RL (2009) A Serological Survey of Infectious Disease in Yellowstone National Park’s Canid Community. PLoS ONE 4(9): e7042. doi:10.1371/journal.pone.0007042

The authors found that the majority of Yellowstone wolves had been exposed to a number of different viruses (evidence from antibodies in blood samples).

They also found evidence for historical outbreaks of canine distemper virus in wolves, coyotes and red foxes in 1999 and 2005. These outbreaks correlated with peaks in wolf pup mortality.

This evidence suggests that wolves have no mechanisms for avoiding the spread of these viral diseases. Perhaps periodic episodes of increased mortality are the price that has to be paid for a longer-term 'herd immunity'?

Edit - in response to OP comment below:

The data indicate very high levels of seropositivity to the viruses. I would say that 'not 100% successful' is an understatement. But I must admit that I am way out of my area of expertise here!

From the abstract:

We found high, constant exposure to canine parvovirus (wolf seroprevalence: 100%; coyote: 94%), canine adenovirus-1 (wolf pups [0.5-0.9 yr]: 91%, adults [>or=1 yr]: 96%; coyote juveniles [0.5-1.5 yrs]: 18%, adults [>or=1.6 yrs]: 83%), and canine herpesvirus (wolf: 87%; coyote juveniles: 23%, young adults [1.6-4.9 yrs]: 51%, old adults [>or=5 yrs]: 87%) suggesting that these pathogens were enzootic within YNP wolves and coyotes.

evolution - How much can you learn about species variation from a skeleton?

It seems as if this article is purely speculative. They didn't mention any DNA testing, but instead discussed physical features.

There are two "types" of archaeologists: clumpers and splitters. Clumpers (like the author of this article) believe that there is wide variety among members of the same species, and so it is often wrong to categorize every new hominid fossil as being a different species. Splitters like to "split" their findings into new species, even though there is no evidence that speciation had ever occurred; they just decide that since the remains look different, they must have speciated.

In the future, I hope that archaeologists will have more sophisticated means of sequencing the DNA of ancient remains, allowing them to construct an accurate phylogeny

microbiology - How can a respiratory infection lead to a skin infection?

Example of a case: 5 children develop a bright red rash on the face and turns violet after a few days and then disappears. Then maculopapular rash appears on the trunk, buttocks and extremities. It soon fades from the trunk but persists on the thights and forearms. Two children have also had a slight fever and a sore throat, but all were not terribly sick. What is the genetic material of the most likely causative agent?

It is a skin infection. Not so severe. Little upper respiratory infection but not necessary caused by the agent. Infects many so spread probably by respiratory droplets. But how a respiratory infection can lead to a skin infection?

human biology - What are the limitations of commercial-grade DNA genotyping compared to full sequencing?

23andme briefly describes the technology they use here. They are testing the genotype of your DNA at roughly 1 million locations. The technology they use to do this is known as a microarray.

The limitations of using a microarray, as compared to sequencing, is that you will only find what you are looking for -- people often describe the disadvantages of microarrays as compared to sequencing with the streetlight effect/metaphor.

Arrays can only measure regions of the genome that they were designed to probe. Technically, if they probe 1,000,000 million locations, and the human genome is roughly 3.4 billion bases ... you can do the math.

In practice, SNPs tell you a bit more about just the nucleotide being interrogated, due to linkage disequilibrium (cf. tag/proxy SNPs), so the array might tell you more than you expect.

Of course, modulo sequencing errors, whole genome sequencing will tell you "everything" as far as recovering the NTs that make up your genome, but how much information that will provide you is another thing altogether (for now, that is).

human anatomy - Why does the sweat of children not smell like adults?

There are two types of sweat glands: (1) eccrine sweat glands and (2) apocrine sweat glands.

1. Eccrine sweat glands are present from birth in humans and secrete sweat that is mostly water and functions in evaporative cooling.


2. Apocrine sweat glands are found in the armpits and groin regions and become active in humans at puberty (although the distribution appears to be broader fetally). These sweat glands secrete an oily substance containing lipids and proteins that through interactions with bacteria on the skin (e.g., bacteria digesting lipids), lead to the "smelliness" of adults (including body odor).

So it's not really the sweat that smells, it's the action of bacteria on apocrine sweat that becomes prevalent after puberty.

genetics - Expression of plasmid genes

It would depend of the plasmid, the genes it contains and the promotors those genes have. Basically, regulation of extrachromosomal genes follow the same patterns of the rest. Bacteria, Archaea and some other organisms that can have plasmids will express the genes if the promotors of those genes are constitutive, or if they trigger by conditions that are present in a given moment. The degree of expression would be a function of the characteristics of the promoter and the number of copies of the plasmid. Finally, the number of copies of the plasmid would depend of its size and the characteristics of its replication origin.

Organisms can loss the plasmids if doing so don't suposse a negative effect (this is a big problem in industrial microbiology, since the recombinant strains may be unstable and reduce its productivity). In laboratory, a plasmid containing resistance genes towards an specific antibiotic would remain stable as long as this antibiotic is present in the media. The characteristics of its replication origin also play a big role determining the stabilty of plasmids. You can even select for the loss of plasmids, take the example of URA3 in Saccaromyces (not a bacteria, but the mechanisms are the same), wich can be used as a negative selection factor if the media contains 5-fluoroorotic acid.

So there's no particular advantage in expressing plasmidic genes all the time. When that happens, actually there exist an evolutionary pressure against the presence of the plasmid, and thus it trends to dissapear. Bacteria can survive without plasmids (with the exception of some that carry megaplasmids that acts more than little chromosomes. In some of this cases, the plasmid may contain genes for important methabolic pathways and other key elements of the cell, thought if the genes they carry are very importants, like polymerases or ribosomal RNAs, the term minichromosome is prefered). However, plasmids may contain genes that confer an important advantage to the population (like in presence of an antibiotic), and if so the plasmid spread. If at some point the ecological pressure cease, the plasmid would turn unstable again. Note that it's not impossible to have horizontal genes transfer between plasmid and chromosomes, and plasmids (alongside viruses and foreign transformed DNA) are important sources of new genetic material.

ethology - are female bonobos "always" pregnant?

In most species, females are pregnant as often as they can be. Since the availability of sex is rarely a limiting factor, it seems likely that female bonobos are as "always" pregnant as other chimps and socially living primates. The actual rate of pregnancy will be hormonally limited by things such as reduced fertility during lactation and so on.