Can men also become only bald on their legs? Often hair loss that primarily affects the top and front of the scalp will happen to men (and female) during aging. Male pattern hair loss is believed to be due to a combination of genetics and the male hormone dihydrotestosterone.

Men with androgenic alopecia typically have higher 5-alpha-reductase, lower total testosterone, higher unbound/free testosterone, and higher free androgens, including DHT.

The question is whether this kind of balding is only present in the hair of the scalp or can this proces also happen on the legs (or other parts of the body)?

Hair loss is known as alopecia, and is often associated with hair loss on the head. This type of hair loss is most noticeable, but hair loss can occur in nearly any part of the body, including the legs (source: Healthline). As an anecdote - my father in law (65+) has lost all his hair on his legs. This hair loss is referred to as anterolateral leg alopecia

About 35 percent of older men have this condition. The exact causes of anterolateral leg alopecia are unknown, but there may be a genetic component.

Age related hair loss in men is referred to as male pattern baldness, or androgenic alopecia. This type is related to hormones and certain genes.


Which parts of the cerebral cortex don't belong to the neocortex? In the Wikipedia article on the cerebral cortex one reads:

  »Most of the cerebral cortex consists of the six-layered neocortex.«

Accordingly, in the Wikipedia list of regions in the human brain, one finds "cerebral cortex" and "neocortex" as almost synonyms.

But assuming that they are not perfect synonyms – but that there are some parts of the cerebral cortex that are not part of the neocortex – I wonder which parts this might specifically be.

To make my question specific, I list here all parts of the cerebral cortex as listed at Wikipedia:

Cerebral cortex (neocortex)
Frontal lobe
    Primary motor cortex
    Supplementary motor cortex
    Premotor cortex
    Prefrontal cortex
    Orbitofrontal cortex
    Dorsolateral prefrontal cortex
    Superior frontal gyrus
    Middle frontal gyrus
    Inf. frontal gyrus
    Brodmann areas
Parietal lobe
    Primary somatosensory cortex (S1)
    Secondary somatosensory cortex (S2)
    Posterior parietal cortex
    Postcentral gyrus (Primary somesthetic area)
    Precuneus
    Brodmann areas
Occipital lobe
    Primary visual cortex (V1)
    V2
    V3
    V4
    V5/MT
    Lateral occipital gyrus
    Cuneus
    Brodmann areas
Temporal lobe
    Primary auditory cortex (A1)
    secondary auditory cortex (A2)
    Inf. temporal cortex
    Posterior Inf. temporal cortex
    Superior temporal gyrus
    Middle temporal gyrus
    Inf. temporal gyrus
    Entorhinal cortex
    Perirhinal cortex
    Parahippocampal gyrus
    Fusiform gyrus
    Brodmann areas
    Medial superior temporal area (MST)
Insular cortex
Cingulate cortex
    Anterior cingulate
    Posterior cingulate
    Retrosplenial cortex
    Indusium griseum
    Subgenual area 25
    Brodmann areas

If there are parts of the cerebral cortex missing here, a hint would be welcome!

The hippocampus is considered archicortex rather than neocortex. Sometimes hippocampus is considered "sub-cortical" but I think this is only really fair if you really mean "sub-neocortical"; it's common for "cortical" to be used as a shorthand for neocortex in human neurobiology. Writers will be more specific when necessary.

The piriform cortex and related olfactory structures are considered paleocortex.

Some also delineate an in-between periallocortex that includes entorhinal cortex and limbic structures around the hippocampus.

Neocortex is mostly a six-layered structure and found only in mammals. The other, non-neocortical types of cortex have fewer layers, and are shared by an older common ancestor that includes other vertebrates.


Evolution question on speciation? Really confusing! Okay, my teacher assigned this homework question, but nothing like this was ever given in our textbook.
Suppose that a type of tree tends to speciate over 10 million years and a species of fly tends to speciate over 1 million years. In the event of a mass extinction, which of the following predictions would LIKELY be true?

A) It is impossible to determine how many niches or species the trees and flies would lead to over time.
B) The trees would fill more niches and create more species than the flies.
C) The flies would fill more niches and create more species than the trees.
D) They would both lead to the same number of species.

I am stuck between A, B, and D because A would have merit, as speciation period may not always correlate to have many changes occur, B may have merit because it could be showing a Gradual model of speciation, and D may have merit because they might both just end up as the one species described? Any help, not even an answer but guidance would be really great.

The answer is C

Because it explicitly tells you the fly speciates faster than the tree (1my vs 10my). That means after the extinction event, all things being equal, the fly will speciate into more niches/species in the same amount of time. While other outcomes could occur, with the information given C is by far the most likely outcome.

This is no different than a physics question asking you which of two object will reach some arbitrary marker first give two different known velocities.


Mouse H2 allele sequences I've been trying to find complete sequences of mouse (Mus musculus) MHC H2 locus haplotypes for quite some time now with limited success. The EBI IMGT database has a table of mouse H2 haplotypes, yet IMGT only provides haplotype sequences for human HLA genes via an FTP sever. I've found similar data for several other species at EBI's IPD-MHC, but Mus musculus is not on the list. The MGI database provides access to H2 SNPs, but I haven't found a mapping from SNP combinations to reconstruct happlotype sequences given reference genes.

I have also hit this issue. I was interested in full length amino acid sequences for the classical class I mouse MHC alleles. I was able to find a number of them on uniprot but not all. Here is my list below. Interested if anyone knows additional sequences to extend this:

H-2 D

H-2 Db
H-2 Dd
H-2 Dp
H-2 Dk
H-2 Dq

H-2 K

H-2 Kb
H-2 Kd
H-2 Kk
H-2 Kq

H-2 L

H-2 Ld
H-2 Lq


Why does ionizing radiation cause only DNA double strand breaks? It's known that ionizing radiation such as X-ray and $\gamma$-ray, cause DNA damage, specifically double strand break. Why is it so? I mean, why not single strand break, why not pyrimidine dimer?

Ionizing radiation does cause single-strand breaks and other kinds of DNA lesions that are not double-strand breaks.  However, double-strand breaks are the most difficult to repair and are thus the most likely DNA damage type to result in mutation and / or cell death.  See Fig 1. from DNA damage response signaling pathways and targets for radiotherapy sensitization in cancer:

DNA damage induced by ionizing radiation. The major types of DNA damage induced by IR include base and sugar damage, single-strand breaks, double-strand breaks, clustered DNA damage, and covalent intrastrand or interstrand crosslinking


What are the molecular mechanisms that make the turtle brain more resistant to hypoxia? I know that turtle brains, particularly those of individual species that hibernate and burrow are particularly resilient to hypoxia and any tissue damage secondary to a hypoxic event.

What are the known molecular mechanisms behind this resiliency?  Does it have to do with the ability of their blood to store/release oxygen over extended periods, or is it molecular factors in the neural tissue that protect it from insult?

There is a bunch of literature on the topic. A good starting point is probably a short description with lots of references in this thesis (page 8), not to talk about other articles, which pop up in google scholar: 1, 2.

The mechanisms are multifaceted and involve principally decrease in oxygen and ATP demands: reduced neuronal activity, lower density of ion channels (but hyper-polarization of the membranes) and so on. Concerning blood flow: "Brain blood flow was continued or increased, and oxygen and creatine phosphate (PCr) stores offered some immediate protection. As PCr declined, turtle brain became increasingly reliant upon anaerobic glycolysis."


Why is living muscle tissue seemingly able to restore its shape under force, while dead tissue is not? When I press my finger, even with relatively little force, into beef or chicken (say, at a grocery store), the indentation remains.

When I poke a cow with my finger, the indentation does not remain. When I squeeze my own arm, even with the same (or greater) amount of force used to alter the shape of meat with my finger, my arm remains the same shape afterwards.

What is the difference between dead and living muscle tissue, with respect to mechanisms that allow it to maintain its shape? Does living muscle tissue somehow actively maintain its shape while dead tissue cannot? Is it something more passive, such as a breakdown of something in dead muscle tissue that makes it more malleable (and if so, what)?

Capillary refill time is defined as the time taken for the capillaries to refill after the blood in them has been squeezed out by pressure. It is widely used as a quick way to determine the effectiveness of the circulatory system in humans by doctors.

In a normal living organism, the capillaries will take time to refill after they have been emptied. Muscle volume consists of the cell volume (which is fixed in the absence of lysis), the blood, as well as lymph and other intracellular fluids (which will be displaced elsewhere when it is deformed by pressure).

When the organism is dead, there is no more circulation in both the blood and lymphatic systems, and therefore any fluids squeezed out by pressure will remain elsewhere, and the deformation is permanent without any regulatory effect by the circulatory system.


How to obtain a tardigrade? The tardigrade is often mentioned as one of the most "alien" lifeforms on Earth. This video speaks for itself:

 (from this article)

I have long wanted to see a tardigrade with my own eyes. I have a small microscope. How do I obtain a tardigrade? I know they inhabit mosses and lichen, but is there a concrete procedure an amateur can follow that will reliably net at least one specimen?

Tardigrades can be found in almost every habitat! The easiest way to find them is probably to look in lichens or mosses (although it depends where you live).

serc.careton.edu website suggests a procedure:

  Collect a clump of moss or lichen (dry or wet) and place in a shallow dish, such as a Petri dish.
  Soak in water (preferably rainwater or distilled water) for 3-24 hours.
  Remove and discard excess water from the dish.
  Shake or squeeze the moss/lichen clumps over another transparent dish to collect trapped water.
  Starting on a low obejctive lens, examine the water using a stereo microscope.
  Use a micropipette to transfer tardigrades to a slide, which can be observed with a higher power under a compound microscope.

Just FYI, the tardigrades are a sister clade to the Arthropoda (insects, spiders and others). You can find them there on tolweb.org


What is the blood ejection speed outward from human body vein? At what height blood can eject from human vein ?
I see, sometime there is direct blood transfer from one person to patient.
So sometime blood bottle is kept at certain height and blood is transfered from person to upper bottle and then from that bottle to patient directly.
At what height blood can go ?

EDIT

For example, I had not mentioned before,
What would be the blood pressure outside from body after cutting certain nerve or vein or whatever which carries blood-speedily, when we go inside vacuum chamber ?
Consider any chamber where you will be able to remove air/atmosphere inside it and a person is provided with oxygen cylinder. Now what will be the blood ejection speed outward from the body ? At what height ? You will have to consider atmospheric pressure also when we leave normally on earth. So question is, at what height in vacuum (where there is no pressure from outside world) ?

Ah, I'm afraid there are a near infinite number of variables that will make a general answer impossible.  Factors such as: age, sex, weight, which vein, additional damage, heart condition, cholesterol level, body position, body temperature, and how the vein was cut and exposed will all lead to different answers.

A general answer from someone with lots of trauma experience, not very far.  Rarely if ever greater than 10cm.  Veins just don't have the pressure that arteries do.


DNA described somewhere? This is not purely biological question but how do the companies making DNA analysis know what your DNA means? Is there some database describing human DNA?

I watched some documents about DNA, gene editing... and people in the documents were often working with some infographical like documents which described some chromosome or desease (I don't know what exactly that was, I am an amateur trying to make sense of it) but I was not able to find anything as they had on the internet.

It might be useful to look at how 23andme works, to see how this analysis product is generated, in general:

  The 23andMe genotyping platform detects single nucleotide polymorphisms (SNPs). A SNP is a DNA location, or "marker," in the genome that has been shown to vary among people in terms of the DNA base or bases. There are four DNA bases: adenine (A), thymine (T), guanine (G), and cytosine (C). So, for example, at the same genomic location, you might have a C and someone else might have a T. These DNA base differences are known as "variants."

These SNPs can differ by population types. Some subsets of a population type might suffer a disease and appear to have SNPs that others do not. So-called GWAS studies (discussed below) work at associating SNP distributions with diseases or other phenotypic traits.

You send some spit to 23andme, they tell you who you are likely related to and what diseases or other physical attributes you may have, based on patterns of these SNPs.

23andme uses Illumina chips for figuring out what genotypic variants you have in the spit sample you send to them. Illumina is a company that manufactures "chips" that react to the presence or absence of markers in the DNA sample you send to 23andme. Each chip in this platform calls different sets of markers.

These markers often have identifiers associated with them, each called an rsID.

  The rsID number is a unique label ("rs" followed by a number) used by researchers and databases to identify a specific SNP (Single Nucleotide Polymorphism). It stands for Reference SNP cluster ID and is the naming convention used for most SNPs.

They also map variants that do not use rsIDs, and instead use some other internal identifier.

Whatever the identifier, GWAS — Genome-Wide Association Studies — are research projects that analyze populations of people in different ethnicities or other cohorts, looking for over- or under-presence of various markers, compared with the larger human population.

For instance, here is such a GWAS study that is used by 23andme to indicate risk factors for Parkinson's disease, in sample donors who have these variants. There are other such studies for schizophrenia, for autoimmune diseases, and so on.

The power of these studies to make a positive, correct association depends on various factors, but the product 23andme sells is ultimately a packaged summary of a lot of work by researchers around the world.


Organ and Bone Marrow Transplantation? In organ transplantation the transplant is rejected by the body's immune system , but is it possible if along with organ transplant if bone marrow transplantation is carried out from the same donor , then will the Cell Mediated immunity still reject the graft ?

As Mowgli pointed out, a bone marrow transplant involves destroying the patient's own immune system with radiation and, essentially, replacing it with a new one from the bone marrow donor. If you did a double kidney/bone marrow transplant from Alice into Bob, then Bob's new immune system (which is the same as Alice's) would recognize the new kidney from Alice as self (because it is) and not attack it. Yay!

The problem is that, to the new immune system, all the rest of Bob appears to be non-self and will get attacked. This is called Graft-versus-host disease and is at least as serious a problem as organ rejection.


Identify this large (swamp) fly? Can anyone identify this large fly?

I encountered it in Okefenokee Swamp (Georgia, U.S.A.) on May 1, 2015.
Weather: 53-78°F (avg. 66°F), avg humidity = 60, dew point = 47°F.

The fly was about the size of an adult thumb (more accurately approx. 5cm long and 2cm wide) -- this fly was HUGE! It was fairly docile and allowed me to take a good close-up or 2.

Tabanus nigrovittatus as my initial guess. "Greenhead horse fly."

Source

This is probably the biggest give-away for the genus Tabanus (namely the features of the veins at the wing tip, denoted R4 and R5, versus other Diptera orders), still searching out a good identification key to solidify the ID. Furthermore, also known as the salt marsh greenhead, a swamp is a good candidate to find these (1).

So what's particular is entomologists have gone through and collected many specimens, and data about their wing venation, and based on the Comstock-Needham system, you can pin presence/absence of major veins, and branching of said veins to specific types on insects. In this case, R refers to the Radius or 3rd longitudinal vein, and the number refers part of the branching that reaches the margin of the wing. Pg 156 here helps us ID Tabanus vs other orders.

Problematic with identifying these spp. is you need to get a good look at the sternites on the under side as well, if you look at how they ID Tabanus sudeticus here, but the photos tend to match nicely with those of T. nigrovittatus you can widely find.


What's the longest intron in the human genome? What's the longest intron in the human genome? Discarding isoforms were a long intron spans more than one exon, i.e. what's the longest distance between two exons without another exons in between.

Short answers: Based on gencode the longest intron for protein coding transcripts, is the intron 3-4 of the transcript ENST00000465127.1 with 1,240,120 bases.

Long answer:

Download the main annotation gff3 file from gencode first. Then run this script:

zcat gencode.v29.annotation.gff3.gz \
| awk -v FS="\t" -v OFS="\t" '$3=="exon" && $9 ~ /transcript_type=protein_coding/ {match($0, "transcript_id=([^;]+)", transcript); print $0,transcript[1]}' \
| sort -k1,1V -k10,10 -k4,4g -k5,5g \
| awk -v FS="\t" -v OFS="\t" 'BEGIN {transcript=""; max_d=0; max_line=""} \
 $10 != transcript  {transcript = $10; end = $5; next;} \
 {d=$4-end-1; end=$5; if(d>max_d) {max_d=d; max_line=$0"\t"d;}} \
 END {print max_line}'

It will:

decompress the file
filter only lines that describes exons of protein coding transcripts
append the transcript id at the end of the line
sort by chromosome, transcript and position
calculate the distance between two exons of the same transcript
save the current maximum distance and the annotation line that belongs to it
print out the line of the exon which follows the longest intron. The last column contains the distance.

The output will be:

chrX    HAVANA  exon    38666121    38666309    .   +   .   ID=exon:ENST00000465127.1:4;Parent=ENST00000465127.1;gene_id=ENSG00000250349.3;transcript_id=ENST00000465127.1;gene_type=protein_coding;gene_name=AF241726.2;transcript_type=protein_coding;transcript_name=AF241726.2-201;exon_number=4;exon_id=ENSE00003644052.1;level=2;protein_id=ENSP00000417050.1;transcript_support_level=5;tag=basic,appris_principal_1,readthrough_transcript;havana_gene=OTTHUMG00000161009.1;havana_transcript=OTTHUMT00000363378.1  ENST00000465127.1   1240120

fin swimmer

EDIT:

gencode also includes transcripts that are only predicted, but never seen, or those where it is not sure that they exists. So you maybe want to just include transcripts having a certain transcript support level. For this you have to change the first awk line. E.g. to include only trasncripts with TSL1 change it to:

awk -v FS="\t" -v OFS="\t" '$3=="exon" && $9 ~ /transcript_type=protein_coding/ && $9 ~ /transcript_support_level=1/ {match($0, "transcript_id=([^;]+)", transcript); print $0,transcript[1]}'

You can also define a range, e.g 1-3:

awk -v FS="\t" -v OFS="\t" '$3=="exon" && $9 ~ /transcript_type=protein_coding/ && $9 ~ /transcript_support_level=[1-3]/ {match($0, "transcript_id=([^;]+)", transcript); print $0,transcript[1]}'

In both cases the result will change to intron 4-5 of ENST00000402655.6 with 1096453 bases.


Methods of nuclear transfection - nuclear transport I am reading through the ENCODE papers, which is taking me well out of my comfort zone in terms of modern laboratory techniques. At the risk of asking a question which may well be thoroughly answered somewhere else on the internet, I was hoping for a brief explanation of nuclear transfection.

In Whiteld et all, they describe the direct assay of transcription factor binding site efficacy in human cells.  To do this, they transfect a luciferase plasmid, presumably into the nucleus of the cell (because they subsequently observe that the luciferase plasmid is transcribed).

Reading through Materials and Methods and getting to the supplementary file, they disclosed their transfection protocol. The relevant reagants appear to be:

FuGene 6

  a nonliposomal formulation designed to transfect plasmid DNA into a wide variety of cell lines with high efficiency and low toxicity.

(From Promega's website.)

Lipofectamine LTX

  efficient reagent for plasmid delivery and protein expression

(From Invitrogen's website.)

PLUS reagent

  PLUS™ Reagent is used in conjunction with transfection reagents, such as Lipofectamine™, to enhance transfection in adherent cell lines.

(From Invitrogen's website.)

Apparently, the protocol is to combine the DNA plasmid with transfection reagent, wait a few minutes, and then add in the cells, and incubate at 37ºC for 24 hours. That's all that is required to get the plasmid into the nucleus.

I have consulted Wikipedia and Strachan and Read's Human Molecular Genetics 4th edition, but been unable to answer my question about this technique.

I think I have a pretty clear understanding of how these reagents are able to get through the cell's lipid membrane, but I don't have a similar understanding of how the DNA then passes to the nucleus.

In Human Molecular Genetics 4th edition, I can find only one paragraph about plasmid transfer across a nuclear membrane, page 704: "Transport of plasmid DNA to the nucleus of non-dividing cells is very inefficient because the plasmid DNA often cannot enter nuclear membrane pores. Various methods can be used to faciliate nuclear entry such as conjugating specific DNA sequences or protein sequences (nuclear localization seuqences) that are known to facilitate nuclear entry, or compacting the DNA to a small enough size to pass through the nuclear pores."

But nothing in the materials and methods section of Whiteld et. all mentions any of these techniques. I'm sure they would have mentioned if their plasmid included a DNA conjugation sequence, so that can't be it. Perhaps these reagents implicitly include some sort of DNA compaction polycation, such as PEG-CK30?

Isn't the cytoplasm an extremely hostile place for DNA plasmids? Shouldn't they just flail around in the cytoplasm until they are digested?

Or perhaps these vectors sneak into the nucleus during mitosis? (This is a theory that just occurred to me when contemplating the "non-dividing" qualification in the Strachan quote.)

Since the question isn't addressed in the paper, I can only assume the answer is elementary and something that a professional cell biologist would be expected to know. I've run out of obvious next steps for finding the answer, so I beg pardon in advance for asking it.

My attempt to find an answer has suggested that no-one knows how the DNA gets into the nucleus.

This fairly recent paper reports attempts to track the pathway of DNA entry and transfer to the nucleus.

  Le Bihan et al. (2010) Probing the in vitro mechanism of action of cationic lipid/DNA lipoplexes at a nanometric scale. Nucl. Acids Res. 39:1595-1609

The technique used was transmission electron microscopy. Complexes of plasmid DNA + cationic lipids (lipoplexes) were labelled with silica-based nanoparticles to allow visualization.

The authors describe a transfection pathway with five steps:

  (i) binding of the lipoplexes to the cell surface;
  (ii) entry of the lipoplexes into the cells mainly via endocytosis (a direct fusion with cell membrane cannot be excluded);
  (iii) DNA release into the cytosol;
  (iv) transport through the cytosol; and
  (v) entry of DNA into the nucleus and nuclear transcription.

The authors were able to follow each of the first four steps but:

  our data show nanoparticles close to, but not within, the nucleus.

They speculate about what this might mean, but they do not refer to any previously published data. My conclusion is that the answer to your question is, as I said at the beginning of my answer: no-one knows how the transfected DNA enters the nucleus.


Periods of Heavy Speciation I have a set of microRNA ages with corresponding labels suggesting which clade they first emerged from. For instance, for hsa-mir-1, let's say, it would have an age of Eutheria. I have several peaks in the distributions of my age. One idea I had was to check to see if these peaks correspond to periods of intense specialization. For instance, the Eutheria clade saw a vast diversification of species relative to other clades. I'd like to determine this from a more computational perspective rather than Googling each clade.

My guess (as your question need heavy editing!!) would be MiRdup.

  MiRdup Goals:

  Validation of pre-miRNAs predictions
  Prediction of mature miRNA

  Abstract: MicroRNAs (miRNAs) are short RNA species derived from hairpin-forming miRNA precursors (pre-miRNA)
  and acting as key post-transcriptional regulators. Most computational
  tools labeled as miRNA predictors are in fact pre-miRNA predictors and
  provide no information about the putative miRNA location within the
  pre-miRNA. Sequence and structural features that determine the
  location of the miRNA, and the extent to which these properties vary
  from species to species, are poorly understood. We have developed
  miRdup, a computational predictor for the identification of the most
  likely miRNA location within a given pre-miRNA or the validation of a
  candidate miRNA. MiRdup is based on a random forest classifier trained
  with experimentally validated miRNAs from miRbase, with features that
  characterize the miRNA-miRNA* duplex


Is the Andraka pancreatic cancer test real? In the wikipedia article about Andraka's pancreatic cancer test there are some controversial statements.

On one hand there are many glorious words about the method, also some awards, also some astonishing comparisons with other methods.

On the other hand, there is no proof, and also some evidence against its efficacy.

Also, I can't find any signs of Andraka's test in reality. For example, there is no such product in drug stores.

What is the proof or evidence that Andraka's method is really working and can feasibly exist in the near future?

Basically, Andraka's method measures mesothelin. There's two key questions being asked about it (as it stands right now), falling into two categories:

1) There is some doubt as to the significance of serum mesothelin levels as a biomarker in pancreatic and biliary cancers. Some studies (e.g. Sharon et al (1)) suggest that there is no significant difference in levels - others (e.g. Hassan et al (2)) suggest that mesothelin may be a valid biomarker in some conditions but not others.

2) There are questions around the test itself. Andraka's work is promising and quite impressive. There are, however, some claims about it are being made that there's just not the evidence to support. I suspect that any fault for this lies with the journalists reporting on the story or PR people for various companies or institutions. The device may stand up to clinical trials and testing and be as revolutionary as it's claimed to be, but it does need to be fully tested.


SNPs in the Human Genome I read online that they have found around 10 million single nucleotide polymorphisms (SNPs) across individuals in the human genome [1]. However, this number includes all SNPs found in all people who have been sampled and does not tell us much about SNPs in any single person.

I was wondering instead how many SNPs there are in a single person on average. I had trouble finding trustworthy evidence about this question.

I was wondering how many SNPs there are in a single person on average

A SNP is a polymorphism in the population, it is not a thing a haplotype can carry. Each individual has a given variant for any given of the SNPs (except for cases of sequence deletion).

It is possible though to say how many SNP a diploid individual in between its two haplotypes but I doubt this is where you interest was. Ewens smapling formula gives expectation and distribution under an infinite alleles model, panmictic population and absence of selection.

Other statistics that make sense include the average number of deleterious mutations pre individual or a few other things or how many new mutations a couple transmit to their offspring,... But asking how many SNPs an individual carry on average makes little sense.

Note as @Chris said, by stating 10k SNPs in the human genome, you seem to under-estimate the number of SNPs.

EDIT

In the comments, you further

  Would it make more sense to consider a rough minimum and maximum?

The answer is no, it would not make more sense. Consider the definition of SNP by wikipedia

  A single nucleotide polymorphism, often abbreviated to SNP (pronounced snip; plural snips), is a variation in a single nucleotide that occurs at a specific position in the genome, where each variation is present to some appreciable degree within a population [My emphasis]

The term population is key here. The concept of SNPs (or of polymorphism to be more general) makes only sense if you can make comparisons. A single individual does not have any polymorphism (to the exception of the one between his two sets of chromosomes).

If we step back and think of different species it might become more intuitive. Think of the number of pairwise differences between two species. It does not make any sense to ask "how many pairwise differences is there between a blue whale?" You need to say "how many pairwise differences is there between a blue whale and a wolf". Similarly, you cannot say "How many SNPs is there 'between a single individual'" (to the exception again of the consideration of the differences between the two sets of chromosomes), you need to consider a group of individuals.


What determines the perceived pitch (frequency) of tinnitus? I noticed that every time I suffer temporary tinnitus after going to a very loud concert, the frequency I perceive is identical. I'd put it somewhere around 17 kHz, but it's difficult to pin down with any real accuracy due to the dulling effect it has on external sound sources.

Is this frequency constant across all humans? If not, what determines the frequency? Note that I'm only interested in tinnitus caused by exposure to loud sounds, not other types of tinnitus such as idiopathic tinnitus or tinnitus caused as a side-effect of medication.

Short answer
Perceived tinnitus pitch tends to resemble the frequency content of the loud sound that induced the tinnitus.

Background
Solid, laboratory-controlled studies to the perceived pitch of temporary, noise-induced tinnitus ("ringing in the ears") are ethically questionable, because researchers have to deliberately expose study subjects to potentially damaging loud sounds. Therefore, data on temporary noise-induced tinnitus are scarce and confined to a small handful of studies done in the 1960's (Henry & Meikle, 2000).

In one of these studies (Atherly et al., 1968) the authors exposed the study subjects to loud acoustic stimuli of various pure tones. The subjects reported to experience tinnitus pitched within a certain frequency band around the tonal stimuli received. The stimulus frequency and perceived pitch approached a 1:1 relationship, such that the tinnitus pitch was e.g. 4 kHz when the noise frequency was 4 kHz. Between-subject variability was, however, considerable. For example, at a stimulus of 6 kHz, the range of perceived pitch was 4-9 kHz.

The other study I found based on the review by Henry & Meikle (2000) showed that the perceived tinnitus pitch increased when the frequency of the loud tonal stimulus or frequency content of broadband noise increased (Loeb & Smith, 1967). Basically this confirms the data from Atherly et al. (1968). However, the perceived pitch did not coincide with the stimulus frequencies, and there was considerable variability between subjects. For example, some subjects reported multiple frequencies in their tinnitus, some reported a hissing tinnitus, while others did not develop any tinnitus at all (Loeb & Smith, 1967).

In all, your suggested perceived tinnitus pitch of 17 kHz is unexpected, given that noise-induced hearing loss (by loud music exposure etc.) typically results in a 4-kHz notch in the audiogram where hearing loss is greatest. Hence, tinnitus would be expected to occur around this frequency as well. But again, variability is very high and it may well be possible it is higher pitched in your case. Also note that 17 kHz is very high and near the upper audible frequency limit for humans (e.g., the sound an old CRT screen makes, i.e., hardly perceivable for many adults).

Most research on tinnitus has been done regarding patients with chronic tinnitus complaints that suffer from sensorineural hearing loss (i.e., damage to the hair cells in the cochlea). Typically, the perceived tinnitus pitch in this group is associated with their hearing loss. In other words, the pitch of the tinnitus generally matches a frequency range within the region of frequency loss (Eggermont & Roberts, 2004).

References
- Atherly et al., JASA 1968;44:1503-6
- Eggermont & Roberts, Trends Neurosci 2004;27:676-82
- Henry & Meikle, J Am Acad Audiol 2000;11:138-55
- Loeb & Smith, JASA 1967;42:453-5

Further reading
- What's the Frequency of the ringing in my ear?
- Can humans perceive sounds above 20 kHz?


Photosynthesis: What Powers the Splitting of Water? The splitting of water is an endergonic (non-spontaneous) reaction, and thus would require energy (chemical work to be done) in order to happen.

In Photosystem II, an enzyme catalyzes this splitting, but where does it get the energy from? Does it use ATP?

Catalysis is about reducing the free energy barrier (aka. activation energy) of a reaction, so it does not require any energy. In photolysis (e.g. splitting water) you get the energy from the absorbed photons.

The exact process is called the Joliot-Kok cycle:

Figure 1 - Joliot-Kok cycle - source

So the photon separates the charges on the P680, after that the activated P680 activates the Yz intermedier, which forces the enzyme to the next step (Sx) in the reaction.

2012 - Transmembrane Electric Potential Difference in the Protein–Pigment Complex of Photosystem 2
2006 - The Manganese-calcium oxide cluster of Photosystem II and its assimilation by the Cyanobacteria

  The overall process comprises three types of reaction sequences: (a)
  light-induced charge separation leading to formation of the radical
  ion pair P680+QA(-) ; (b) reduction of plastoquinone to plastoquinol
  at the QB site via a two-step reaction sequence with QA(-) as
  reductant and (c) oxidative water splitting into O2 and four protons
  at a manganese-containing catalytic site via a four-step sequence
  driven by P680+ as oxidant and a redox active tyrosine YZ acting as
  mediator.

2007 - Photosystem II: structure and mechanism of the water:plastoquinone oxidoreductase.

So the process does not involve ATP or NAD or something like that just the "redox active tyrosine YZ". ATP and NADPH are created after the PS2 part of photosynthesis.

Figure 2 - Light-dependent reactions of photosynthesis - electron transport chain - source

The photolysis of water is about storing the energy coming from the photons (light) in ATP and NADPH. In the Calvin cycle the cells use the stored energy to reduce CO2 into carbohydrates. For instance glucose can be delivered to the cells in the root, which can use it as food.


What is the connection between sleep requirement and age? By this question: Is the human biological clock genetically programmed or learnt? we discussed that the sleep requirement depends on the age of the individual.

- Figure 1. - Sleep requirements by age - ref

I thought I ask the question, why?

I believe the current theory is that it is related to cell loss in the intermediate nucleus of the human hypothalamus. They have shown sleep disruptions due to lesions of the hypothalamic ventrolateral preoptic nucleus in rodents, and found that the intermediate nucleus in humans is homologous and shows a reduction in size in older adults that is correlated with sleep disruptions. http://brain.oxfordjournals.org/content/137/10/2847


Why is it often the case that an enzyme is favorable only towards one direction of a reaction and not both directions? In class when we're studying enzymes like amylase or protease it only works well when you're using it to break down compounds like polysaccharides.  I'm just curious but why is it not possible for enzymes to work efficiently in a reverse reaction?  I mean a formula like

$\ce{amino\ acid + amino\ acid + energy<=>H2O + protein}$

does imply that our reaction can go both ways , right?  But why is it that the enzyme favors the catabolic reaction?

Reactions have their set equilibrium constants, which are determined by the free energy of the reactants involved, and this cannot be changed by catalysts, including enzymes. Let's look at your example of peptide bond formation between two amino acids A and B,

A + B + energy $\leftrightharpoons$ H$_2$O + AB

This reaction might proceed in both directions; the rates of forward and reverse reactions depend on the free energy of A,B and the dipeptide AB, as well as how much "energy" we are talking about in the left-hand side. Let's ignore the energy term to start with, and just consider

A + B $\leftrightharpoons$ H$_2$O + AB

As it turns out, this reaction is not favorable: the $ \Delta G$ is about 10 kJ / mol (it depends a bit on which amino acids we're talking about). So this reaction goes in the reverse direction; dipeptides actually spontaneously decompose in water. But the rate of this reaction is very slow, because the peptide bond is quite stable. We say that there is an "energy barrier" between the substrates and products. Catalysts, including enzymes, lower this barrier, which increases the rate of reaction in both directions. It is physically impossible for enzymes to change the equilibrium by catalysis alone. There are plenty of enzymes that catalyze the above reaction, causing peptides to break down rapidly (peptidases, for example trypsin).

But enzymes don't just provide catalysis: an important role of enzymes is to couple two (or more) reactions together, so that a favorable one can drive an unfavorable one. This is how we obtain the "energy" term in the first reaction. The most common mechanism is to couple the unfavorable reaction to ATP hydrolysis,

ATP + H$_2$O $\leftrightharpoons$ ADP + P$_i$

which itself is highly favorable ($\Delta G$ around 40-50 kJ / mol). The coupled reaction is then

A + B + ATP + $\leftrightharpoons$ AB + ADP + P$_i$

which is now both favorable (due to ATP) and fast (due to catalysis). This is pretty much what ribosomes do (well, the actual mechanism is much more complex, but the principle is the same).

So, catalysts cannot change the equilibrium of a given reaction, but enzymes can couple reactions together to come up with something that is favorable. This is a central theme in biochemistry, allowing cells to drive reactions in the desired direction; but there is always a "price" to pay, often in the currency of ATP.


For a recombinant pUC19 plasmid with cut sites at Hind III and EcoO109i, does lactose need to be present for the gene of interest to be expressed? I am growing E. coli transformed with the plasmid pUC19 with an insert of an enzyme in rat brain between the mentioned cut sites (EcoO109i and HindIII). I have isolated and created the recombinant molecule with custom gene synthesis so that the gene encoding for the enzyme easily ligates into the plasmid.
It is after the lac promoter and lac operator, so will I need lactose in the growth media for the enzyme to be made?

I would rather use the synthetic analogon IPTG for induction of genes behind a lac promoter, as they are not getting degraded (or at least much slower than lactose) and thus give a much stronger induction signal.

You will need to test the optimal IPTG concentration, but as a starting point I would use and endconcentration of 1mM. If this is not optimal (to much unsoluble protein or not enough), you can change the concentration in either direction. To start, use an overnight culture to inocculate a fresh culture in the morning and follow up the OD600 until it reaches 0.6-0.8 before adding the IPTG.


Gastro-intestinal physiology reference I am a physicist but I have always wanted to understand how my digestion takes place in as much detail as possible. I have no idea about books or reference on the subject of Gastro-intestinal and digestive physiology. Can you help me?

If you have no medical background at all, you will need a general text that teaches more than just digestive physiology. That is because you need to understand the function of other systems that have an influence over the digestive system (for example, the peripheral nervous system).

Here are a few good general references to get you started:

Physiology by Linda Costanzo, arguably the most synthetic. Extremely good, but I am unsure of its value for someone who has no medical background.
Vander's Human Physiology, arguably the simplest, used in first year of medical school.
Medical Physiology by  Walter F. Boron, arguably the most complex, I would not recommend it as a first try.

You can start by trying to read the digestive physiology chapters, and look up the knowledge you lack in other chapters.


Herd immunity without vaccines? (corona question) Obviously there is herd immunity against many viruses such as measles because of vaccines.

Can we say that there is herd immunity against any particular virus even though people are not getting vaccinated, and what virus would that be?

Do you typically get herd immunity without vaccines against viruses without vaccines or do the viruses just linger around and infect fewer people because many have already become immune after catching the virus and developing anti-bodies?

What is "normal" virus behaviour?

This is not just a corona related question, this is true for each disease which is can be transmitted easily and which builds up a lasting immunity.

Herd immunity per se means that a large proportion of a given population is immune to a given disease, either because of vaccination or because the population went through the disease, survived it and built up lasting immunity. This means that even when this disease comes around again, it will only infect few people who have no immunity, but will not spread through the population. This can be seen in the figure below (from here), which implies vaccination, but works as well with getting the disease.

The first case is what happens right now with SARS-CoV-2, it is a new disease to which no one has immunity, so everybody who gets in contact will get the disease (either more or less severe).

If no vaccine would be available, this infection would go on, until a big enough proportion of the population has gone through the infection, developed immunity and thus stops the spread (go to the third part of the figure). At this point a big pandemie would stop.

However, this strategy has one problem: People who are coming into the population (newborns for example) who have no immunity are susceptible for the disease. This ensures low level infection rates and will make sure that the disease will stay in the population, but mostly not noticable. Over time the number of not immune people will rise until there are enough of them to feed another big breakout.

As @bryankrause pointed out, in the past getting to the point to reach herd immunity (at least partly) for diseases like smallpox or measles and to maintain it, cost a lot of lifes.

This is exactly what can be seen in the number of measles cases before the introduction of the vaccine in 1967. Before vaccination every 18 - 24 months enough people without immunity where present, causing another wave of cases. After introducing the vaccination this pattern changes and case numbers went down drastically. See the figure (from reference 1) for illustration. This figure uses data from the US, but you see similar pattern in the rest of the world.

For some more information have a look at reference 2.

Reference:

Evolution of measles elimination strategies in the United States.
Vaccination and herd immunity: what more do we know?


Color van der waals bonds in swiss PdbViewer I'm trying to color certain amino acid's van der waals bonds as in the following picture:

can anybody please describe the steps to accomplish that?

If I'm right in assuming you are trying to get colouring like the purple AA VDW bonds then I can only specifically colour VDW bonds in solid 3D view (under display, Render in solid 3D) in SPDBV but not when solid 3D view is not activated, as in the example in your picture. One option is to use POV-Ray but I haven't worked with it.

If the purple colouring is not photoshoped by the authors of the paper you got the picture from, then the chances are they have written a custom script for it in the software, which allows them to do this. So I would just contact the corresponding author and ask them how they managed it and if they have done it through a script or some other software. Most of the time people are happy to share their methodology once they have published it!

Also have you tried the Jalview software? Although it's designed primarily as an alignment tool but it has a nice 3D Jmol view. You can load up your sequence and the associated PDB file and you can play around with it. The graphics output are quite publication friendly. I'm not an expert at it and I've only been playing around with it for a bit but when you get the hang of it, it's quite nice graphically. Although the VDW view is still space fill 3D but it's a bit nicer as it has opacity etc etc. Just download it and as soon as you open it up, you are presented with an example alignment and Jmol view. Just play around with the alignment section and the Jmol view and see if you like the aesthetics. The only tricky part in the software is getting the residues you want selected but once you manage that, you can get the program to display VDW only for the selected residues.

Hope this helps.


Does the NMDA antagonist, Memantine that's used to prevent Excitotoxicity cause brain damage? Does the NMDA antagonist, Memantine that's used to prevent excitotoxicity in Alzheimer's disease (AD) and Dementia with Lewy Bodies (DLB) cause brain damage? I know that in rodents NMDA antagonists like ketamine and phencyclidine (PCP) cause a form of brain damage known as Olney's lesions. Despite Olney's lesions never being directly observed in primates like humans, permanent brain damage from chronic ketamine exposure has been observed in adolescent cynomolgus monkeys.1

Reference List

Sun, Lin; Qi Li, Qing Li, Yuzhe Zhang, Dexiang Liu, Hong Jiang, Fang Pan, David T. Yew (2012). "Chronic ketamine exposure induces permanent impairment of brain functions in adolescent cynomolgus monkeys". Addiction Biology. doi:10.1111/adb.12004. PMID 23145560.

Yes, it does cause lesions in rats, although I don't think it's been observed to do so in humans.

See: http://www.druglib.com/druginfo/namenda/description_pharmacology/


Do transposons usually jump from one chromosome to another? If it is usual occurrence, does it mean that my one gene can change its location from one chromosome to another?

Yes of course; they are not like tandem duplications.

However, some transposons have site preferences; for example the Tn7 transposon.

EDIT:

I don't know what you mean by original location. Some transposons, especially LINEs, have expanded a lot in the human genome. For any individual you can check the germ cells for a reliable estimate on the original positions. There are mechanisms such as piRNA mediated silencing that suppress transposon activity in germ cells. The genome of the germ cells also tells you what exactly will be inherited by the offsprings.


Which server to use for volume and accessible surface area calculation of proteins I want to find the accessible surface area and the volume of a protein, giving PDB file as the input for the protein. I used two servers, 3vee and Vadar. For the PDB id, 1LTM, the websites are giving me different volume and surface area measures as follows:
3vee (vol: 50951 A^3; Surface area: 10837 A^2)
Vadar(vol: 40937.8 A^3; Surface area: 14680.6 A^2)
Can anyone tell me which server to use, which server is more accurate? If you know of any other server giving accurate result, please let me know that too.

Note: Both the publications are from Nucleic Acids Research, I guess I do not need to validate them. 3vee has been published in 2010 with citation of 164 and Vadar was published in 2003 with citations of 416. Is it okay if I take 3vee since it is the latest tool?

You can use PDBSum and PDBe-PISA servers for calculating accessible surface area and buried surface area and Castp server for finding pockets within your protein molecule. If your protein is globular, you can measure the diameter in pymol and calculate its volume. Hope it helps.


What is Oncogene, and how do you get it? I was looking at my family tree and it said that one of my family members died by Oncogene. What is it and how do you get it?

An oncogene is a gene that has the potential to cause cancer. If an oncogene is activated, it will contribute towards cancer, though there are typically many other factors necessary before cancer becomes noticeable and potentially lethal.

In short, your family member presumably died of cancer, though writing the cause of death as "oncogene" is highly abnormal.

Many normal and healthy genes can cause cancer when they are overly active. For example, PDGF produces a growth factor required for normal health, but if too much growth factor is produced it can cancer like breast cancer.


What kind of fly is this? I found this dude hanging out in my sink, but he didn't fly away when I put a dish in the sink. Turned out it was dead. The front part looks exactly like a housefly. But, I've never seen the back end (abdomen) look like this. Any ideas?

This is probably a fly killed by the fungi Entomophthora muscae (or closely related) or maybe a Cordyceps fungus. These kinds of fungi mainly attacks insects, and you sometimes see attacks as white, swollen abdomens in flies.

(Picture of common infection, from bugguide.net)

These fungi are also known to change the behaviour of infected individuals, so that they e.g. climb up tall plants to die (sometimes called "zombie-insects"), to allow for better dispersal and transmission of the fungal spores. Lots of information about the behavioural modifications of hosts by fungi can be found in Roy et al. (2006), but they can involve both climbing to exposed locations and special mechanisms for host attachement at death:

  In many cases the final interactions, or endgames, between a host and pathogen involve complex behavioral modifications such as the infected insect seeking an elevated position where wind currents can effectively disseminate conidia. Elevation seeking by insects at late stages of infection is a common phenomenon that was recognized by early insect pathologists who noted that diseased lepidopteran larvae, such as Lymantria monacha (the nun moth), infected with baculoviruses migrated to the tops of trees where they died (94). This host-altered behavior was named “Wipfelkrankheit” or “Wipfelsucht” (meaning tree top disease in German) for viral diseases (41) and “summit disease” for fungal diseases (24, 57, 106).

and

  Some fungi do not produce rhizoids, but the host is held in situ by host structures alone, namely the legs or mouthparts (mandibles or stylets). The pose of the dead insect is generally characteristic of the pathogen species involved. For instance, E. grylli-infected grasshoppers (Figure 3a) and E. scatophagae–infected yellow dung flies (Figure 3b) seek elevated positions on grasses or other vegetation and cling tightly (death grip) with their legs (96). Tipulids infected with fungal species from the genera Eryniopsis and Entomophaga also attach to grasses with their long legs, often overhanging water (Figures 5b,c).

If you do google image searches on "Entomophthora fly abdomen" or "fly Cordyceps" you can see some examples of infections. I don't know about the fly species, but Musca domestica is probably likely.

For some more examples and information on Entomophthora muscae and related fungi see:

Roy et al. 2006. Bizzare Interactions and Endgames: Entomopathogenic Fungi and Their Arthropod Hosts. Annual Review of Entomology 51(1) (pdf)
Biological Control: Entomophthora muscae, webpage from Cornell Uni.
Harmon. 2012. Fungus that controls zombie-ants has own fungal stalker. Nature
Mind-controlling fungus turns insects into zombies (blog post)


psychological database with sequenced DNA records I'm looking for an epigenetic database which includes for each example the psychological history of the persons DNA. Right now I can only find DNA and epigenetic databases. Sadly none of the databases provide "thick data" (qualitative data eg. history of person) to the sequenced DNA.

I want to investigate the effects of psychology on epigenetic and vice versa.

You might want to look at the Danish Data archive:

http://www.sa.dk/content/us/about_us/danish_data_archive

I have never used their data and I don't know what barriers there might be to accessing it, but the impression I got at a talk by Soren Brunak (http://ctbr.hunter.cuny.edu/Brunak), was that this was one of the most complete databases for studying relationships between people's DNA records and other health information that might be available about them.


Why do cells in meristematic tissues lack vacuoles? Cells located in meristematic cells in plants lack vacuoles. However, this contradicts with the fact that plant cells have large vacuoles to store water and keep the plant in an upright position. I would also like to add that meristematic tissues are generally found in roots and stems of plants. Finally, I would like to ask why do meristems lack vacuoles?
Sources

Turgor pressure exerted by the vacuole is also essential in supporting plants in an upright position: Wikipedia

Apical mertisem is present at the growing tips of stems and roots and increases the length of the stem and the root. The girth of the stem or root increases due to lateral mertisem (cambium): Science for Class 9 by National Council of Educational Research & Training, page number 69

Cells of meristematic tissue are very active, they have dense cytoplasm, thin cellulose walls and prominent nuclei. They lack vacuoles: Science for Class 9 by National Council of Educational Research & Training, page number 70

Meristematic tissues or meristems contain cells which can rapidly divide or reproduce and is responsible for the overall growth of the plant. Apical meristems and lateral meristems are found in the roots and stems of the plants. Please note that the whole stem or root is not laded with these tissues. Plant cells usually have a large central vacuole which applies turgor pressure to keep the plant upright, as mentioned in one of your sources.
The tips do not require to be very stiff and straight. So, a central vacuole is just not required. Also, meristematic cells grow various organelles as they mature.


How long does it take to form a peptide bond? What is the time taken to form a peptide bond in vivo or in vitro? It isn't mentioned in my course on protein structures. I was just curious to find out  if any  time scale is known?

Given that prokaryotic and eukaryotic cells have difference ribosome structures, is there any chance that the time might vary between species or even within species?

Alberts et al, Molecular Biology of the Cell, say that eukaryotic ribosomes add about 2 amino acids per second, and bacterial about 20 per second (5th edition, p 275). These should be taken only as ballpark estimates: the rate certainly will vary from species to species, from cell to cell, from protein to protein. Some cells (reticulocytes, for instance) are professional protein synthesizers. Others, for instance bacterial endospores, do almost no protein synthesis at all.

These authors estimate the translation rate in mouse embryonic stem cells at around 5.5 amino acids/second. There is a lot of variation from gene to gene, even within this one cell type. They even see systematic variation depending on where you are in the gene.


What is the Definition of Homologous Chromosomes? length, gene position are the same or similar? what is the Definition of Homologous Chromosomes?

this post says

  Homologous chromosomes are chromosome pairs (one from each parent)
  that are similar in length, gene position, and centromere
  location.

and then

  The position of the genes on each homologous chromosome is the same.

are length, gene position of a pair of chromosomes the same or similar?

if exactly the same (I guess not), job well done.

if just similar, What is the Definition of similar? 99% same?

in the case of a pair of human Chromosome 1, what is the exact number of base pairs that are the same?

Unfortunately despite the impression given by the many poor explanations available (including the one you quoted), homologous is not a synonym for similar.

Homology is defined as the existence of shared ancestry1,2.  Thus, structures being homologous simply means they had a common ancestor — i.e. homology is a relationship not a property of an individual structure.

The "definition" you quote is actually a description of what you typically see when comparing two homologous chromosomes within a species. High levels of sequence similarity suggest homology, but are not sufficient to prove it.  (To test that requires building phylogenetic trees.)

(One classic example of this is the superficial similarity between dolphins and sharks, which is an example of convergence not homology.  Another is the homology between bird and bat wings — they are not homologous as wings, though they are homologous as tetrapod forelimbs.)

Consequently, for two chromosomes to be homologous they must have descended from a (potentially much earlier) chromosome that has been duplicated possibly for many generations (the ancestral chromosome might even have existed in a now extinct ancestral species).

So, if an inversion happens within a chromosome (and changes the ordering of the genetic loci) that chromosome is still homologous to the parental type chromosome that didn't undergo inversion.

ETA: Note that chromosomes don't need to be in the same cell (or even the same species) to be homologous and chromosomes can be homologous even if the cell they are in is not diploid.  For example, the human chromosome 1 is homologous to the chimpanzee chromosome 1.

Similarity is a measurement of "distance" between sequences, but while very similar sequences are likely to be homologous there is no magical value of similarity that proves (or disproves) homology.

Individual humans are about 99.9% identical (depends on how you measure this) at the nucleotide level, so that will also be true for chromosome 1.

Finally, the UC Berkeley Museum of Paleontology also has useful resources for understanding evolution including some material on homology — e.g.:
https://evolution.berkeley.edu/evolibrary/article/lines_04

References:
1: Brigandt, Ingo, "Essay: Homology". Embryo Project Encyclopedia (2011-11-23). ISSN: 1940-5030 http://embryo.asu.edu/handle/10776/1754.

2: Mindell, D. P., & Meyer, A. (2001). Homology evolving. Trends in Ecology & Evolution, 16(8), 434-440.


What is a Mitochondrial Eve and Y-chromosomal Adam I've read this question:
What kind of event would cause the current Mitochondrial Eve to be replaced by a new one?

And the values in Wikipedia about Mitochondrial Eve and Y-chromosomal Adam and I am not sure I understand the concept behind them.

When talking about a maternal unbroken linage and a paternal unbroken linage, is the meaning that Mitochondrial Eve had a linage of only women reaching every person today, and the same with Y-chromosomal Adam and men? So that other humans that lived in their age, didn't have an unbroken line of linage consisting of only same sex descendants?

How is the specific "identity" or time period of those persons is known, assuming that researchers didn't check the Mitochondrial DNA or Y-chromosome of every single living human being today, how can they know for sure that there aren't some tribes in the Amazons, which have a direct female linage to Mitochondrial Eve's sister?

When talking about a maternal unbroken linage and a paternal unbroken linage, is the meaning that Mitochondrial Eve had a linage of only women reaching every person today, and the same with Y-chromosomal Adam and men?

Kind of, yes. The concept behind Mitochondrial Eve and Y-Chromosomal Adam has to due with cell replication and basic genetics.

The Mitochondria ("Power Generators" of the cell) are directly inherited from mother to daughter cell. That is, new cells do not start with 0 and are forced to make them de novo. Some Mitochondria are replicated before division and some are 'given' to the daughter cell to start with.

Because of the unique way that Mitochondria are inherited, when it comes to creating new humans it means that only the Mother's Mitochondria are given to any children she gives birth to regardless of the sex of the child. So I, being male, have my Mother's Mitochondria - which the same as my Grandmother's - and the same as my Great-Grandmother's - etc. etc. etc. until you can trace that line back to "Mitochondrial Evel" whose Mitochondria are the origin for all humans on the planet and are inherited Maternally.

In that sense it is an unbroken lineage of genetic information as inherited from mothers, though not exclusive to women.

"Y-Chromosomal Adam" is a similar concept - Women do not have a "Y"-Chromosome, so every Y-Chromosome men have today had to originate from somewhere. It's trickier to do than tracing Mitochondrial DNA because while Mitochondria are inherited exclusively from mother to child, there could have been multiple Fathers to Mitochondrial Eve's children and other similar complications that muck things up.

  How is the specific "identity" or time period of those persons is known, assuming that researchers didn't check the Mitochondrial DNA or Y-chromosome of every single living human being today?

For "Y-Chromosome Adam" it's still more or less in the data-gathering phase as far as I was last aware. It's not as concrete as "Mitochondrial Eve", which has a very solid body of work supporting her.

The "identity" is known because the more in common a person's genes have with the genes of another, the more closely they are related. The researchers took a lot of genes from very divergent populations, and compared them. The researchers were then able to tell which portions were common among all of the Mitochondrial DNA, which had changed the most, and which had changed the least from each other. Using that data, you can construct a rough image of what the originator (or LCA - Last Common Ancestor) had for their own genetic makeup.

You can construe a time period because portions of your DNA (either Mitochondrial or Nuclear) acquire/tolerate mutations at an expected rate - say 1 mutation every 1.5 Million Years. So as long as you have a rough idea of what your LCA's genes looked like (see above), then a modern day sample with 5 mutations is 7.5 M.Y. away from the LCA.

  how can they know for sure that there aren't some tribes in the Amazons, which have a direct female linage to Mitochondrial Eve's sister?

They didn't when they started testing. That's part of the fun of the project.

The "Out of Africa Hypothesis" rose in prominence partially due to the findings of the research. It basically posits that the ancestors of humans evolved once in Africa, and then spread from Africa to the rest of the world. Because the Mitochondrial Eve research concludes that "Eve" was around before we spread throughout the rest of the world, it implies that every ancestor already had Eve's legacy when they started migrating into Europe, Asia, the Philippines, etc. Thus every human on Earth, no matter where they are today, shares traits with Mitochondrial Eve.

For the Amazonian tribes, they would have inherited it from their ancestors in North America, which were ancestors of tribes in Asia who crossed an ice bridge into North America, and the tribes in Asia came out of Africa.


Molecular cause of cramps, spasms and strengthening in muscles? (incl. intro to muscle contraction) When motor neurons are stimulated to trigger an action potential, this potential propagates down the spine, eventually reaching a neuromuscular junction, causing the release of acetylcholine (ACh).

ACh binds to nicotinic ACh receptors (nAChR) on the muscle fibers, leading to an action potential. The nAChR is a non-selective, ligand-gated ion channel, permeable to sodium-, potassium- and calcium ions. This means sodium ions will flow in, leading to depolarization, but potassium will flow out, working towards hyperpolarization.

If enough of these channels are opened, the post-synaptic membrane potential will be drawn towards $E_{Na}$ enough to reach a threshold, so that voltage-gated sodium channels open on the post-synaptic membrane, causing a post-synaptic action potential.

This action potential travels down inward extrusions of the plasma membrane, called transverse (T) tubules. Is the membrane continuous along these tubules, or does the tubule just end somewhere inside the muscle fiber? Anyway, the action potential comes in contact with the muscle fiber version of an endoplasmic reticulum: The sarcoplasmic reticulum (SR).

Upon contact with the action potential, the calcium ion channels in the SR open, causing calcium ions to flow into the cytosol. Here they bind to troponin complexes on the tropomyosin protein - a regulatory protein, that twists around the thin filaments of the muscle fiber. In short, when calcium ions bind to troponin, it reveals binding sites for myosin on the thin filaments, letting the muscle contraction cycle of the myosin heads proceed, and the muscle contracts!

When the stimulus goes away, calcium ions are transported back into the SR, and myosin has nowhere to bind, thus the cycle is halted, and the muscle relaxes.

When the muscle is twitching... is this neurological of nature, or is it related to a molecular cause in the muscle itself?

When the muscle is cramping... I'm almost certain this arises in the muscle. What causes it? A malfunction with regard to the calcium ions?

Lastly, and on a slightly different subject, what are the microlesions in the muscles that occur during strength training, and what is the overcompensation that happens? The basis of this might not be entirely on the molecular level I feel.

I think a lot of your questions try to split the hair; is this happening at the chemical or the histological level and I do get what you're asking, but you should know that the distinction is often not worth making. Pretty much whenever a neuron's involved, the interesting biology is multi-scale.

  Is the membrane continuous along these tubules, or does the tubule just end somewhere inside the muscle fiber?

The membranes are continuous.

  When the muscle is twitching... is this neurological of nature, or is it related to a molecular cause in the muscle itself?

Most things you'd call a muscle twitch are at the whole-muscle-group scale, involving the coordinated contraction of many individual motor units, so it's basically neurological.

  When the muscle is cramping... I'm almost certain this arises in the muscle. What causes it? A malfunction with regard to the calcium ions?

A muscle cramp is a colloquialism for a couple of things that are quite different from each other. Overall, as with the previous question, if someone's experiencing a muscle cramp that means it's a fairly macroscopic phenomenon and it likely involves a whole group of muscle filaments, so it's neurological. Most spasms and cramps are neurologically mediated.

The connections with electrolyte balances (cramps from low sodium, potassium, magnesium, or calcium) also hint at the neurological basis because neurons act on each other (and on muscles) by forming or dissipating ion gradients. You may know that low dietary calcium can lead to muscle cramps; if this was relevant to the calcium release within the myocyte (from the sarcoplasmic reticulum) then the calcium-starved muscles wouldn't be expected to chronically contract (which requires calcium) but to chronically relax.

That being said, there's a lot of room for feedback mechanisms. So, let's say a person experiences a muscle tear; the tear is small enough that it doesn't compromise the function of the entire muscle group. In this case it's adaptive for the local damage to 'signal' to the rest of the muscle group to initiate spasm so as to stabilize the damaged structures as they're repaired. In this scenario the local damage would 'inform' a neurological (and/or endocrine) response that actually effects the spasm.

  Lastly, and on a slightly different subject, what are the microlesions in the muscles that occur during strength training, and what is the overcompensation that happens?

Last time I was updated on this (not my bag), there were some large questions remaining. The tricks used by growing muscle to establish large, regular arrays of contractile machinery, that is organized over many spatial orders of magnitude, are poorly understood. There are structures that monitor the overall organization and that detect any large deformations. Regarding overcompensation, let's play through a generic scenario. A muscle cell is loaded too much and becomes physically damaged. It has to stop taking orders (stop responding to contraction/relaxation signals) and to initiate repairs. The overcompensation results because muscle cell's not really capable of knowing how large it was before the damage, so the safe amount of repairs to do is extra. Probably there are epigenetic processes that let a muscle cell 'count' the number of times its been greatly damaged and to scale-up the response appropriately.

If you just consider two likely sources of damage -- mechanical strain and lactic acidosis -- you can see that there are widely different mechanisms that would be required to detect the damage and to initiate repairs.


In what fluid does the sperm swim in the oviduct? We know that after sexual intercourse, sperm enters the female body and continues to pass through the oviduct by swimming. "Swimming" implies the presence of fluid.

I want to know what that fluid is called. Also could you please tell me the color of that fluid? Is it yellow/off-white?

Specifically in the fallopian tubes, the fluid is called tubal fluid, and is produced by the innermost mucosal layer of the tubes (specifically, the peg cells in the epitelium)

In the follicles, there is the follicular fluid, liquor folliculi.
In the uterus, the endometrial fluid.
In the cervix, cervical fluid.

I don't know about the color. For what it's worth, cervical fluid varies from white to yellowish, but it's transparent when it's best for spermatozoa to swim.


Can mutation rate be selected for? Can the mutability of DNA be selected for in a population? I don’t mean selection for the phenotype that is the result of a mutation. Rather, can the rate of mutations in a population be increased by natural selection?

Yes.

  Evolutionary success of bacteria relies on the constant fine-tuning of
  their mutation rates, which optimizes their adaptability to constantly
  changing environmental conditions. When adaptation is limited by the
  mutation supply rate, under some conditions, natural selection favours
  increased mutation rates by acting on allelic variation of the genetic
  systems that control fidelity of DNA replication and repair. Mutator
  alleles are carried to high frequency through hitchhiking with the
  adaptive mutations they generate. However, when fitness gain no longer
  counterbalances the fitness loss due to continuous generation of
  deleterious mutations, natural selection favours reduction of mutation
  rates. Selection and counter-selection of high mutation rates depends
  on many factors: the number of mutations required for adaptation, the
  strength of mutator alleles, bacterial population size, competition
  with other strains, migration, and spatial and temporal environmental
  heterogeneity. Such modulations of mutation rates may also play a role
  in the evolution of antibiotic resistance.

https://www.ncbi.nlm.nih.gov/pubmed/16677295

Large differences in mutation rates can be found among viruses: 10^-3 mutations per nucleotide per replication in RNA bacteriophage Qβ versus 10^-8 mutations per nucleotide per replication in DNA Herpes simplex virus. Generally, RNA viruses have higher mutation rate because RNA-dependent RNA polymerases lack the proof-reading capacity present in DNA polymerases. However, both increasing and decreasing these typical mutation rates leads to reduced virulence of the virus population.

https://www.ncbi.nlm.nih.gov/pubmed/16220146

https://www.ncbi.nlm.nih.gov/pubmed/16327776


genetic complementation problem I've attached the picture of the problem.

SO, based on the information I managed to assemble two large cistrons. (if the combination of two mutants yield (-) mutations are on the same chromosome)

A)so my cistrons are:

1)(1,4,5,6,7,9)

2)(2,3,4,7,8,10)

Note: somehow 4 and 7 is present in both cistrons

B) they ask us what mutation could cause two different cistrons have the same mutants

I was thinking maybe an insertion? i just dont get how it's even possible since if they have the same mutants doesnt it mean they overlap and thus are on the same chromosome??

I would appreciate if you could explain me what type mutation could cause it and check if I did the complementation correctly

bacteriophage T4 has a single chromosome (approx. 200 kb in length). The chromosomes are terminally redundant,  so the genetic map is circular, even though the physical map is linear (as I recall).
A mutation in E. coli (or its viruses) that affects two adjacent protein-coding genes is said to be 'polar'. This indicates that the two genes in question form part of an operon. A strong loss-of-function mutation in the promoter for the operon will typically affect the expression of all the genes in the operon. In your example there are two cistrons, or genes, in the rII locus of T4.

It is possible that the data for this question are taken directly from the published literature. I suggest you search PubMed for papers by Seymour Benzer, from the 1950s.


Why should we use the NA12878 dataset for benchmarking? As far as I understand, the human genome sample called NA12878 provides high confidence variants for a human sample. It is being used as a benchmark for many genomic research projects.

Q: Why exactly the NA12878 is such a popular benchmark dataset? Just because we have a set of high confidence variants? But we can also get some high confidence variants from the 1000 Genome project. Does that have something to do with the sequencing technology? Anything to do with the sample itself? Why do we want to benchmark our experiments with NA12878?

So to clarify for people unfamiliar with NA12878, that's the sample identification for a particular Utah woman. Her parents are NA12891 and NA12892. In human variation data-sets that's what we are given to identify individuals, an ID, sex and population. All the other data is removed to protect patient privacy. So the question is why was NA12878 (this Utah woman) chosen as the reference patient in genomic analysis...

I don't know the real practical answer but from what I gather it's inertia.

I don't have a full history for her but I do know somethings which make her genome a good choice for a benchmark. NA12878 is a fairly old to geneticists and her DNA is included in multiple legacy projects, specifically HapMap.

She has a genetic disease (CYP2D6 mutation) which is probably what initially included her and her family genetic analysis. This is a better reason to study this genome in detail instead of it simply being someone famous (i.e. Venter).

She's Utah mormon (small founder population with extensive pedigree information), has 11 children (can do recombination/inheritance analysis). What this means is that a deep understanding of her genome will have applications to this population.

Her lymphoblastoid cell line GM12878 was included as tier-1 ENCODE cell of study. This means there's terabytes of epignomic data for her as well.

When I choose to do human genome analysis, NA12878 is the obvious choice because of how much data is already available, which also means more data is going to be available. Thus I think the answer is largely inertia.

Also consider it this way, if you're trying to say your pipeline or sequencing technology is better then other ones, and everyone uses NA12878 to benchmark their technology, then it's wise to also use NA12878 so the results can be comparable.


How much of your stock solution should you take to make the 1000 cells/mL mixture? You need a solution containing 1000 buccal cells/mL. You count that you have 125 buccal cells in 50uL, from a total solution of 8 mL. How much of your stock solution should you take to make the 1000 cells/mL mixture? How much solvent if you would like a total volume of 5mL?

I don't even know how to approach this!!!
Help??

Oh, come on, thats simple math.
First calculate how many cells you have per ml: 50$\mu$l are $\frac{1}{20}$ of 1 ml. So multiply 125 with 20 to get the concentration per ml: $125 \times 20 = 2500 \frac{cells}{ml}$

If you want to know how many cells you have in total, multiply by 8 (for the 8ml you have) and you come to 20.000 cells in your 8ml solution.

When you want to know, how much of your solution you need, you calculate: $\frac{2500 \frac{cells}{ml}}{1000 cells} = \frac{1 ml}{x}$.

This can be transformed into $x = \frac{1}{2,5} ml = 400 \mu l$.

So you need 400 $\mu$l for each ml of your final cell solution. So if you want to have 5ml with 1000 cells/ml you need $5 \times 400 \mu l = 2000 \mu l = 2 ml$ of your cell solution. To reach 5 ml add 3 ml of your solvent/media.


Are hens and roosters the same species? I know that one is a female chicken and the other is male chicken. Are the chickens laying eggs considered the same species as those that we use for poultry meat? Or, are they different sub-species, analogous to how there are multiple breeds of dogs?

The main difference between a rooster and a hen is that the former is male and the latter is female. Their appearance differs in several ways [1].

A rooster also known as a cockerel or cock, is a male gallinaceous bird. The term usually refers to a male chicken [2]. The hen or the chicken (Gallus gallus domesticus) is a domesticated fowl, a subspecies of the Red Junglefowl [3].

And yes, the chickens laying eggs could be the same as the chickens that we use for poultry meat.

References:

Anjus Chiedozie. Rooster Vs. Hen on eHow.com
Wikipedia. Rooster
Wikipedia. Chicken


Does Sympaticus and lymphatic circulation cause feeling of thirsty after short shower? I have been reading blogs, Guyton and Pocock about what triggers the feeling of thirsty.
I am not convinced that is the fact of

warm water
time is short so not much water lost

Assume that the water's temperature is the same as body's temperature.
Of course, there is little temperature change caused by air and water, but I think it is not that much.
I think more important is the steady, continous irritation of skin as a mechanism.

I wrote my suggestion for the answer below.

Do sympaticus and stimulation of lymphatic circulation cause feeling of thirsty?

I think the mechanism is the stimulation of the skin systemically i.e. the most important endocrine organ which we have.
The irritation of skin in the shower is

mechanical turbulent stream of water in acceleration

1) hitting (start) your skin from different directions (many flows) in many different flows
it's you who causes the systemic stimulation effect!
water steam in acceleration all the time; moving its direction; in ellipsoidal tracts
water stream flowing slowly on your skin towards periphery mostly
causing smooth but continuos irritation of your skin

activation of smooth muscles in synchronous order which boost lymphatic circulation

mechanical turbulent stream of air (temperature change of skin)

this one is not in accelerative move, since there is no forces which keep the subsequent air and skin together
very little impact, unless extreme situation (etc in Alaska)

I would think that the increased lymphatic circulation irritates the walls of lymphatic circulation which causes an increase in the need of water there.
So water would diffuse from vascular space inside blood vessels (extravascular space) into the lymphatic system.
The decrease in blood pressure through baroreflexive arch and hypothalamus (some nuclei too) would then be sensed as the feeling of thirsty.

Water in shower on the skin accelerates, since it changes its direction all the time from the beginning of the stream until the end.
I think it is the steady change of irritation's location in ellipsoidal tracts that stimulates hypothalamus.
I think it is not the strength of the stream but the changing direction that is cause of the irritation.
Of course, there is little changes in the strength of the total stream.
I think this is not so significant than the change of the direction of the water flow causing the irritation.

In short, I say that accelerative water streams massage lymphatic system in ellipsoidal tracts.


What large "package" is carried by this large spider underneath itself? One night in early May in northern Taiwan a strange looking spider carrying a large white "package" underneath itself ran in front of me and stopped, so I photographed it. The package is roughly the size and shape and color of a round dental floss dispenser that one would carry in one's pocket, perhaps a little smaller, about 2.5 cm in diameter.

I took some photos with a flash and without. The total span of the spider's legs was about 10 cm.

I'm guessing this would be an egg case, but it's surprisingly large, could it be prey? I suppose if a spider didn't have a home of any kind it would have to carry its meals with itself. It seems to be well adapted to this and moved quickly even with the large load.

Question: What kind of spider is this and what is it carrying underneath itself?

It's a Huntsman spider. The genus is  Heteropoda but not sure of the species (pingtungensis?) Yes, it is an egg case she is carrying.
Ask a local if it is the white barred spider, LaYa 喇犽, Mandarin is 白額高腳蛛. If so then it may be veratorias as in below article.
Wikipedia article on one species at
https://en.wikipedia.org/wiki/Heteropoda_venatoria
If you get more good photos, put them on wikipedia or somewhere. Until then, here's Heteropoda venatoria (Fam. Sparassidae) from here:
 click for full size


A question about IPTG induction I have found the information: `In the absence of lactose, the lac repressor binds to the operator sequence on DNA and bends the DNA by 40 degrees. This blocks access of T7 RNA polymerase to the promoter site and thus prevents leaky transcription of your gene before induction.'
I am confuse about one fact.

When I add IPTG,  the lac repressor protein (from E.coli chromosome) can no longer bind the operator and native E. coli RNA polymerase begins transcribing, the T7 RNA polymerase gene engineered into its chromosome.

So if there is IPTG and lac repressor protein (from E.coli chromosome) can no longer bind the operator standing in front of the T7 RNA polymerase gene, why lac repressor protein still can bind to operator standing in front of the target gene from plasmid?

What makes you think that the lac repressor will still be bound at the target gene?

In strains with this type of regulatory configuration (usually with DE3 in the genotype) the idea is that IPTG induction turns on expression of T7 polymerase from a lac promoter on the chromosome, and then this T7 polymerase then transcribes the target gene on the plasmid. The presence of IPTG ensures that repressor will bind at neither site.

Supplementary:

I think that I understand why you are confused now. Your picture of the way this works is based on the idea that the repressor is locked on to the operator until an inducer such as IPTG comes along. In fact there is an equilibrium between bound and unbound:

  repressor/operator <=> repressor + operator

and, in the brief periods when the repressor isn't bound, the E. coli RNA polymerase can bind and transcribe the operon. This is referred to as 'escape synthesis' and it is generally assumed that it is functionally relevant in ensuring that there are low levels of lac permease expression at all times so that lactose can be taken up. If this wasn't the case, how would the natural inducer (a derivative of lactose) ever be able to induce the lac operon?

In protein expression systems it is generally considered desirable to keep escape synthesis of the foreign protein to a minimum so that there is no selection acting on the gene to negate any deleterious effects of its expression. The use of T7 polymerase as an intermediate level of regulation helps to achieve this. Even if there is a low level of escape synthesis of T7 polymerase, the concentration of T7 polymerase will be so low in the uninduced state (compared to the endogenous RNA polymerase) that the amount of escape synthesis of the target protein due to T7 polymerase gaining productive access to the T7 promoter on the plasmid will be negligible.

Read more here.


Black spider identification Location is in Canada / Ottawa

I did a web search, but I can't figure out what species it is.

This is very likely an araneid (or Orb-weaver spider) in the family Araneidae.

Without further evidence/details, it's hard to narrow down to a species.

One possibility is Larinioides sclopetarius (the bridge spider or gray cross spider).

 Source: Ed Nieuwenhuys

 Source: Eurospiders.com

Description:

  Prosoma grey to grey-brown. Opisthosoma grey to grey-brown, dorsally with pronounced, white margined pattern. [Source: University of Bern]

See University of Bern for detailed drawings of anatomical structures.

Size: females = 10-14 mm ; males = 8-9 mm.
Web: orb webs can have diameters of up to 70 cm.
Ecology: often lives on briges or near water; often found on steel structures.
Range: holoarctic including Ottawa, Canada

What it's NOT

Although visually similar, this is not
Nuctenea umbratica (walnut orb-weaver)

 Source

This species is confined to Europe, Asia and Africa.

The specimen is also unlikely Larinioides ixobolus, which generally has a black outline (vs white) on their backs And is constrained to Europe/Asia:

 Source


genomatix software linux install I have installed the genomatix software which is a jar file the name is InstallChipInspector21.jar.But now I really don;t know how do I start it ,can any one suggest me a method??

I don't know what else to say as an answer but here is a link to the user manual. If you are looking for more specific usage instructions, I would suggest that you try Biostars though I can't guarantee that you receive an answer.


Visual receptive fields What I know about centre-surround type receptive fields is that depending on whether the region is on or off, the response to being stimulated is either excitatory or inhibitory respectively. So if a light shines on the centre of an on-centre/off-surround and off-centre/on-surround fields, spikes would be detected in the first case and not the second.

To my understanding, if both centre and surround areas are simultaneously stimulated, no spikes would be detected in either of the above-given fields. However, that means that if I am staring at what is essentially a blank white wall, I shouldn't be able to see anything. But that is obviously not happening. What am I missing here?

Also, on a related note - do on-centre & surround or off-centre & surround fields exist? What function do they serve, if any? What are the other types of visual receptive fields in humans, or other animals? Is there a major difference in properties of visual fields across species?

Edit: While browsing a few resources on receptive fields, I found this very-helpful image here.

This image perfectly illustrates my question: what happens to the grey areas in the right image? How are they processed by the retinal ganglion cells?

The centre + surround do not cancel completely, as you can see from these mudpuppy recordings. [Image 1] (Werblin and Dowling, 1969, I believe)

One function of a centre-surround set-up is to highlight the contrast at borders.  Most of the useful visual information is from borders/outlines, so this is a method of ignoring redundant information.  The highlighting of contrast borders and ignoring of redundant information explains why the neural image appears different. [Image 2 - right].
Another function of centre-surround fields is to avoid saturation, but this is more complicated to explain. [Image 2 - left] (Diagrams from Cambridge MVST Part IB lecture series by Hugh Matthews)


Is there a biological urge to have children in women? Searching information about this subject often leads to personal stories from women making the choice to live childfree and women stating they either always wanted to have children or experienced a sudden 'baby fever'. Often this baby fever is understood to be a biological urge.

In this article a link between hormones and the need for own offspring is made a couple of times, but also contradicted.

  In  the  context  of  evolutionary adaptedness, all women were exposed
  to babies and infants, and the ‘default’ setting for the female  body
  is  to  have  experienced  both nurturing  and  pregnancies  by  the
  early  twenties. Rotkirch therefore suggests that longing for a baby
  develops out of hormonal changes evolved to prepare women for
  motherhood. These might be triggered by falling in love; the ‘nesting’
  behaviour associated with settling down; exposure to infants or the
  aging process. Conversely, however, Kravdal has found evidence in
  Norway of a demographically significant cohort for whom reproduction
  and finding a long-term partner and ‘settling’ down’ are quite
  exclusive (Kravdal 1997).

In the same article, the effects of hormones on human intercourse and attractiveness between men and women is briefly explained. However, to me it seems that the urge to have sex is something different from the urge to have babies or to become a parent. I would like to know if there are hormones or other biological changes in women that cause something like 'baby fever' or if it is rather more of a more psychological or social environment phenomenon.

Other relevant articles are often not accessible to me or prove too difficult to understand with basic biology knowledge.

The biological urge to find a mate means that an innate desire for children is unnecessary. Having sex with a partner pretty much guaranteed children before contraception was available.

It's hard to imagine why an urge to have children would exist, but that's not the same as saying it doesn't -- but I also can't imagine how you'd be able to pull apart biological vs social pressures in such a complex and core part of being human.


why is cellulase not found in animals? As it is really beneficial for all organisms, why are animals, especially mammals (I don't know about other vertebrates) unable to synthesize cellulase enzyme in their body? Is it linked to some DNA defects or have we not evolved from cellulase producing bacteria?

The answer to questions like this is just a guess (Primarily Opinion Based), and I've voted to close. But some food for thought too long for a comment:

  As it is really beneficial for all organisms...

Why do you think that cellulase is so very beneficial to mammals? Animals did have cellulase (some ancient invertebrates still do, like sea squirts, abalone; crayfish have it); we may well have faulty copies of the gene (as @AMR suggested in comments.) But you presume to know we'd be better off with it. That's a belief without any objective evidence.

What might happen if we could convert cellulose into sugar? This is also important to think about. If some of that surfeit glucose in out guts were fermented into alcohol (this condition does rarely occur in humans, and the living people afflicted with this are truly afflicted), because we have a gut microbiome, we would walk around drunk much of the time (ok, maybe even only some of the time), which would make escaping predators less drunk than we were difficult. Maybe the body would be incapable of handling that level of glucose ingestion, and we'd all be T2 diabetics by the time we were just out of toddlerhood.

Humans need fiber in our GI tracts. I don't know all the reasons why we developed that way, but we do. Cellulase would do away with that. Do you know for sure that this would be good for us?

The thing is, you've made an assumption (we'd all be better off with cellulase) that has no evidence to support it at all (or, at least you have not provided any.)

It's always tricky to assume that you know what's more beneficial for a mammal in the presence of billions of mammals that seem to be doing OK. There are millions of reasons that they are doing OK. We don't know all of them, but the absence of the very thing you presume would be a benefit may be what allowed vertebrates to develop at all.

Ancient Origin of Glycosyl Hydrolase Family 9 Cellulase Genes
Structure and function of a cellulase gene in redclaw crayfish, Cherax quadricarinatus


How fast can a panda run? Pandas are going extinct, mostly due to habitat destruction. This leads me to the question:  How fast can an average adult panda run? (more specifically Giant Panda)

Top speed = 20 mph (32 kmh), according to a-z animals.


What is the functional difference between hemoglobin and ferritin? I read that both hemoglobin and ferritin are for storing iron in the body. So, what is the difference between them in terms of storing/binding iron?

Hemoglobin is the protein of erythrocytes (red blood cells) which has ferrous ions (Fe2+) bound in its subunits. These are able to keep oxygen bound which enables the cell to transport oxygen through the circulation. It's not really for storage of iron, it's for using it.

Ferritin is the actual storage protein, cells express it to store iron in case of deficiency and also to regulate the amount they have in the cell. According to this, it's mainly expressed in muscle, liver and kidney cells (but I'm not too sure about the details of that study so I might have got that wrong).

Edit: just found this in one of my old lectures; unfortunately it doesn't quote sources: ferritin stores iron in liver and heart. The total iron in the body is ~3.9g, of which 2.5g are in use in hemoglobin, 500mg in stores (an additional 250mg in the liver), 150mg in bone marrow, 300mg in myoglobin and 150mg in other enzymes. The remaining 5mg are bound to transferrin in the plasma.


Can any species be bred selectively/engineered to become as diverse looking as dogs? I've done some research and it appears that dogs are the most diverse looking single species of mammals. The questions that interest me is - are dogs special in respect to genes/gene activation mechanisms related to appearance? Or does this dramatic difference in appearance have something to do with dog anatomy and how they give birth?

If dogs are not special, this makes me interested if other species of mammals can also be bred selectively (or genetically engineered) to produce such dramatic variation?

Dogs have a genomic structure that allows breeding with high variation in size, shape, coat quality, color and other qualities particular to each breed as well.

Other domesticated animals can be bred for as many qualities, but dogs in particular show a wide level of morphological traits - varying in size from just over a pound to the size of a wolf, from which dogs are derived and genetically are still compatible.  But more interesting than just size or coat color/texture and even their intelligence and personalities, the proportions of their bodies, of their skull length and breadth, are remarkable.

There are over 160 registered breeds of dogs, but this is only a measure of how much time people have put into them.  I think its possible to get nearly anything you want with animals, if you are patient enough - its not clear what is and is not possible with enough genetic manipulating. For instance, horses can be bred over nearly as great a size range for instance (the miniature horse the size of a large dog, the Shire is 3,300 pounds), but it would not be as easy to get both the size and muscularity and shape of a bulldog in a horse.  Breeding a mouse of various colors can be done, and so can interesting behaviors, but body shape seems to be harder: a Weimaraner mouse could take a tremendous amount of time and animals.