How do Neurotransmitters get into the neurons? This may be a dumb question. I'm not a Neuroscientist. I'm just trying to learn more about the brain to improve my AI learning algorithms…

I understand that there are different kinds of neurotransmitters that either increase or decrease the possibility of firing an electrical impulse through the axon. I also understand that these Neurotransmitters do not actually pass through the whole cell (Correct me if I'm wrong…), so they only travel from the Cell's terminal to the next cell's body.

So my question is: How do these Neurotransmitters get into the cell's terminal? Blood? And the more important question: How are these Neurotransmitters distributed among the different neurons? It cannot be at random, or equally distributed, because we have different "reactions" to different Neurotransmitters. For example if Dopamine is produced it gets sent to these different cells in our brain which makes the activation of its cell more likely (if I understood correctly). Dopamine is also known to increase our feelings of lust and makes us more focussed (and more). But if Dopamine got sent to ALL of the Neurons in our brain, thus make the activation of EVERY cell more likely, it would bring total chaos to our brain. (Eg. Make our fear-part of the brain activate more easily, but this is not the case.). So how are these Neurotransmitters distributed?

Thanks in advance

The general rule (though like much of biology there are exceptions) is that each neuron releases a specific neurotransmitter: neuron types are often named by this principal neurotransmitter plus the suffix -ergic: a cholinergic neuron releases acetylcholine.

There are also similar molecules that do in fact act throughout the body, but we don't call these neurotransmitters, we call them hormones. Sometimes they are exactly the same molecule: epinephrine, also known as adrenaline, is both a neurotransmitter and a hormone; it can act as both because different receptors have different affinities, and the circulating hormone levels are typically much lower concentration than the amount that can be released in a more confined space.

Additionally, neurons have receptors for different neurotransmitters, so for example dopamine does not affect all neurons, only neurons that have dopamine receptors. Different cell types can also have different types of dopamine receptors, and those receptors can do different things to the cell. The same neurotransmitter could be excitatory to one cell and inhibitory to another.

Broad simplifications of nervous function such as:

  Dopamine is also known to increase our feelings of lust

really don't say anything broadly about the function of dopamine. I could similarly say that computers control airplanes: that statement is true even though you will fine airplanes not controlled by computers and because you will find the vast majority of computers don't control airplanes. However, if I turned off all the computers in the world, a lot of airplanes would have their function impacted.

How do neurotransmitters get into neurons?

Most neurotransmitters are synthesized within neurons from other ingredients. GABA, for example, is derived from an amino acid glutamate. Glutamate itself is also a neurotransmitter. All neurons that release neurotransmitters have pumps that concentrate these neurotransmitters into vesicles. Neurons often also have transporters to pull released neurotransmitter back into the cell so it can be reused, for example a common class of psychoactive drugs are the serotonin reuptake inhibitors: these drugs inhibit the protein that pumps serotonin back into serotonin-releasing cells.

General statement

Use of knowledge from neuroscience to improve AI algorithms has moved far beyond what a novice can contribute to. If you want to utilize biology in AI algorithms, you have to be prepared to become an expert in both. I'd suggest starting with a basic neuroscience textbook if you want to learn about neuroscience, for example books by Purves' Neuroscience or Kandell's Principles of Neural Science.


Can a new Y-chromosome be created? The major gene of the Y-chromosome is SRY. Would it be possible to get the X-chromosome and add SRY to create a "fuller" Y-chromosome?

What advantage does the skinny Y-chromosome give an individual anyway? Females only use one X-chromosome (via the Barr body) so they don't seem to gain as much from having the pair.

SRY translocation to the X chromosome clinically exists and characterizes the De La Chapelle Syndrome. The phenotype associated to this syndrome demonstrates the necessity of other components on the Y chromosome to develop full masculine characteristics.


What did Francis Crick and James Watson discover that Rosalind Franklin didn't? I've recently been introduced to the history of DNA research from Miescher to Franklin, Crick, and Watson, and I've found that Franklin had figured out a great many number of things out that Crick and Watson are popularly credited for when they 'acquired' her photo, including that:

DNA has a helical shape
The distance between two base pairs is 0.34nm, and each helical turn is made up of 10 bases at 3.4nm
Nitrogenous bases protrude inwards and the sugar-phosphate backbone is on the outside

On that note, did the paper written by Crick and Watson in 1953 result in any information that Franklin herself hadn't figured out? Or were Crick and Watson redundant when it comes to the current model of DNA?

There were staff migrations and personality issues, information leaks between researchers and other factors. Her boss annoyed her. Watson and Crick used her geometry of a helix with previously known DNA nucleotides and phosphate from other researchers. She actually had discovered and photographed the helices.

Franklin had obtained the basic structure, shape and measurements of DNA.

Franklin:

She used careful hydration from 75-90% in order to obtain her best pictures. Hydration makes the DNA expand into a visible helical configuration. She used cylindrical Patterson map calculations to determing DNA's density, unit cell size and water content. From this she deduced the basic dimensions of DNA strands, and that the phosphates were on the outside of what was probably a helical structure. Her research was briefed/presented in an internal meeting/seminar at the college and was published officially in 1953 in support of Watson and Crick's presentation.

Watson and Crick:

Watson and Crick suggested a basic framework of a helical molecule for DNA,  Without elaborating precisely. Watson and Crick combine all the findings of other scientists, for the bases and acids of DNA, with Franklin's helix into a synopsis into a correct helical molecular structure. The phosphate and CAGT were already known, and they arranged it into a helix.
Judge for yourself if their research was brilliant research, if it is a discovery, or if it is laying the last pieces of a puzzle assembled by other researchers.

Watson and Crick stayed friends with Franklin after 1954 and shared friendly correspondence and some road trips, and helped with her health issue.

full pdf at .edu source here

If you check that publication, what may seem dishonest is that they iamge a photo by Franklin in support of their work, but only as a blurred photo, when they actually had access to all of her best photos. I haven't been able to find if Franklin published her photos independently in Nature or another magazine.

It was obviously not her best work.

Franklin obtained undenatured DNA gel from a Swiss researcher at Berne university, Rudolf Signer.

She used careful hydration from 75-90% in order to obtain her best pictures. Hydration makes the DNA expand into a visible helical configuration. She used cylindrical Patterson map calculations to determing DNA's density, unit cell size and water content. From this she deduced the basic dimensions of DNA strands, and that the phosphates were on the outside of what was probably a helical structure.
Her research was briefed/presented in an internal meeting/seminar at the college and was published officially in 1953 in support of Watson and Crick's presentation.

The Nobel Prize in Physiology or Medicine was awarded to Watson, Crick and Wilkins in 1962. The prize was not awarded to Franklin; she had died in 1958, and although there was not yet a rule against posthumous awards, the Nobel Committee generally does not make posthumous nominations. Watson suggested that she should have won the nobel prize for chemistry in his book, and Franklin is known through his distorting lenses. Ideally it would be interesting to know what Franklins personal letters and documents told of her research. Perhaps there is an autobiography of franklin? if not there should be one! She had differences with the lab director, professional or personal, we don't know, so she changed labs after only 2 years, leaving Watson and Creek and the research at King's. In july 25,2020 it will be the centenarian of her birth... She is older than Watson and Crick and would be 99 today. Perhaps she was not fond of helices?


Why do flipped cockroaches sometimes lose their heads? Sometimes I see in my house there are flipped cockroaches whose lose their heads. I used to have a cat, but there is no pet in my house anymore so I think it's only ants can be involved in this. But if so, the headless cockroach should be preyed already. Is there any explanation for this?

In all likelihood, it is your cat who crunches the cockroach's head once it catches it and/or finishes playing with it.

Ants do eat bugs but they are usually not so selective that they'll carry off the head alone. With more manageable insects, they carry the whole thing off; otherwise they take it apart and carry it away in pieces if they're interested in it as a food source.

If you watch a cat with a mouse, chipmunk, bird, large insect, etc, they often seek to kill the animal with a throat or nape bite if they are done 'playing' with it. I've found headless prayer mantises and other large insects in my garage many times, and have seen my cats beheading them.

The techniques that cats use to kill prey vary with prey size


How does amiodarone act as an alpha and beta blocker? Amiodarone is potassium channel blocker but also voltage-gated Na+ channel blocker according to Pubchem. However, upon reading my notes I discovered

  Amiodarone blocks potassium channels and block alpha and beta channels.

I think it must be alpha and beta receptors here, instead of channel. Pubchem proposes that there may beta-blocker-like properties in amiodarone.
However, its alpha-like properties are obscure to me as I cannot find any sources. How is amiodarone working as alpha and beta blocker?

Amiodarone inhibits sodium, potassium and calcium currents. Its major antiarrhythmic properties are thought to be related to prolongation of the
action potential duration. Amiodarone also exerts an antiadrenergic
effect by non competitively inhibiting alpha- and beta-receptors (Ghuran & Camm, 2000).

Alpha blockers relax certain muscles and help small blood vessels remain open by antagonizing norepinephrine's tightening effects on the muscles in the walls of smaller arteries and veins, which improves blood flow and lowers blood pressure (Mayo Clinic). Beta blockers decrease the effects of epinephrine (adrenaline), reducing heart rate and reducing its force, thereby reducing blood pressure. Beta blockers also help blood vessels open up to improve blood flow (Mayo Clinic).

Alpha-adrenergic receptors and Beta-adrenergic receptors are G-protein coupled receptors (Wallukat, 2002). Hence, they do not form channels and your notes are incorrect. The ion currents are mediated by channels, though.

References
- Ghuran & Camm, J Clin Basic Cardiol (2000); 3: 206
- Wallukat, Herz (2002); 27(7): 683-90


Can a non-disjunction event occur in meiosis II (in the paternal gametes) to result in an XXY male? My professor stated that non-disjunction in meiosis II of the father cannot produce an XXY male. However, a disjunction event in meiosis II of the mother can. I'm not understanding why this is (?)

The reason maternal non-disjunction during meiosis II can produce XXY offspring.

In this case, meiosis I occurs as normal so that after the first division the replicated homologous chromosomes, each consisting of two chromatids connected at a centromere, have separated. If a non-disjunction occurs at this point, haploid cells will not be formed. Instead, the sister chromatids of a replicated chromosome will not be separated and a gamete containing two X chromosomes will be formed. When this gamete combines with a sperm containing a Y chromosome, the offspring has the XXY genotype.

The reason paternal non-disjunction during meisosis II cannot produce XXY offspring.

This is similar to the maternal case except that after meiosis I, in one cell will be two YY chromosomes while the other cell will be two XX chromosomes. When non-disjunction occurs (assuming it occurs in both divisions), these chromosome arrangements remain the same and two cells are formed. One with two XX chromosomes and one with two YY chromosomes. If either of these gametes combines with a female X gamete, either XYY or XXX will be formed but never XXY.


Hopfield-like neuron assemblies There seems to be general agreement that theoretical Hopfield networks (consisting of artifical neurons, namely McCulloch-Pitts neurons) are biologically rather implausible, among other reasons because of their (rather strictly) symmetric synaptic weights. On the other side, some authors claim that there are neural assemblies in the brain that qualitatively behave like Hopfield networks, i.e.

they are strongly interconnected
they synaptically store a limited number of (activity) patterns
which they reach as attractors when fed with noisy or incomplete input patterns
they "learn" (mainly) by the Hebb rule

The system of hippocampal CA3 neurons is suggested to be one such assembly.

My questions:

Is there an agreement among experts that hippocampal CA3 neurons really behave similar to a Hopfield network?
Which other assemblies (possibly nuclei?) are believed to behave similar to a Hopfield network, too? (Some examples would be welcome.)

I think it really depends on the level of detail and accuracy needed.

Giving a quick look on Google Scholar, it appears that indeed there is (or at least was) a belief that hippocampal networks could be reasonably modelled by Hopfield networks (e.g. see Neuromodulatory control of hippocampal
function: towards a model of Alzheimer’s disease by Menschik and Finkel, and its references). However, many of these papers are somewhat old (though this certainly does not invalidate them!) and computational neuroscience moves fairly fast.
So yes, to a certain extent, after reading some papers that corroborate it, it might appear that some macroscopic behaviour of CA3 neurons can be reproduced by Hopfield networks.

That being said, in more recent works, I have personally never seen anyone model biological neurons with such simple neurons, when cellular level accuracy is required (often it isn't). At least stochastic Hodgkin-Huxley or integrate-and-fire, for instance, are used, even if as point processes (so that it is a system of ODEs/SDEs, not PDEs/SPDEs). Even the neurons used in today's deep neural networks (which make no effort towards biophysical plausibility) are (or at least can be) more complex than sigmoiding a linear combination of inputs!
Also, for slightly larger scales, as you note, the connectivity structure is extremely unrealistic. (Just look at the histology!)

So anyway, it depends on the goal. For simple macroscopic, qualitative similarities it may suffice. But if the goal is biophysical accuracy of simulation then I would look at newer papers and see what they do.
Check out Synaptic mechanisms of pattern completion in the hippocampal CA3 network by Guzman et al.

As for your second question, just searching for papers on Hopfield networks finds a number of them. However, they appear to be largely computational or mathematical, rather than neuroscientific modelling papers.
Maybe others can find better ones though!

Disclaimer:
I am not in the field of hippocampal modelling nor have I worked much with Hopfield networks, so take my thoughts with a grain of salt.
My suggestion is to do an extensive literature search, and post what you find as an answer here :)


How does ecology differ from biology? What precisely is ecology? How does it differ from biology? Because I never studied biology after high school, please explain as if I were 10 years old. I only know that ecology is a subset of biology
I tried some dictionaries but they  didn't  adequately discriminate. I tried to find an explanation from a scientist: the following appears to claim that only ecology concerns some organism's external interactions with other entities? But how? Biology must also? For example, suppose that someone studies prions' interactions with humans, and not just prions. Then this is biology, not ecology?
Source: by  Matthew Fraser, PhD Candidate (Marine Ecology) at University of Western Australia

So what makes us fully fledged marine ecologist different from our biologist counterparts?  Well, I think that marine ecology is even cooler than marine biology because as marine ecologists we link what we know about the biology of a given species with other plants/animals and the environment as well. [...]
If we were splitting hairs, ecology is technically a form of biology, but I felt the need to write this post given how passionately I see some researchers stating that they are in one camp or another. [...]  But as an ecologist (albeit a biased one!) what gets me excited isn’t just finding out how the amazing plants and animals we find in the ocean work, but how they interact with each other and their environment, explaining why we see certain species in some places and not others!

Ecology has two meanings. The popular and the scientific meaning.

Ecology: the popular definition: Here the term ecology is probably quite poorly defined. To my gut feeling, the concept relates to the concept of global change. It encompass many fields such as biology (ecology (in the scientific sense), evolutionary biology and conservation biology especially), ethics and moral, politics, meteorology, public policy, ...

Ecology: the scientific definition: Ecology is a subfield of biology and earth sciences that studies interactions among organisms and their environment. interaction is an important word here.

Biology has a much broader meaning. Biology is the science that studies life. Biology studies the structure, the ecology (impact on their surrounding), the evolution, development biochemical processes, etc.. of living things. Biology is a very big field of science. A researcher in biology will probably not really consider him/herself as a biologist but rather as a molecular geneticist, a neurologist, a epidemiologist, a plant physiologist, a biochemist, a bioinformatician, a system biologist, etc.. For example, I would appreciate to consider myself as a population geneticist rather than as a biologist as there are many fields of biology I know nothing about. For example, I am a pretty bad naturalist.

In short, ecology is to biology what optics is to mechanics is to physics. Some people may not like this comparison as mechanics might take a larger part of physics that what ecology does to biology. Earth scientists may not like this comparison as well, as they are part of ecology without necessarily feeling like being part of biology. But anyway.

From the text you cite

  [..] as an ecologist [..] what gets me excited isn’t just finding out how the amazing plants and animals we find in the ocean work, but how they interact with each other and their environment [..]

It shows that indeed ecologist are interested in the interaction between organisms and between organisms and their abiotic environment. Matthew Fraser says "he's not only interested in how they work". 'How they work' is obviously an extremely inaccurate sentence. A less misleading reformulation would be: I am not interested in everything about the biology of marine animals, "I am especially interested in how animals interact with each other and how they interact with the environment", but obviously that is less exciting for the reader. The goal of Matthew I guess was to create the interest and the excitation of the reader (or audience) on ecology and for this purpose he kinda implied as ecology being more than biology, while ecology is only a subfield of biology.

For more information, wikipedia is your friend!


What is the difference between a DPY-10, DPY-11, and DPY-13? My TA mentioned these three mutations of C. elegans since we started working with the worms but seems to skip over what the differences are...

Dpy is a class of genes. Usually they're written in lowercase when referring to a mutant allele. The name Dpy itself stands for dumpy and comes from the morphological change that occurs when one or more of the genes are mutated: the worms appear short and fat, or dumpy.

Another big class is Unc. Mutations in those genes cause uncoordinated movement.

For a description of the genes, see http://www.wormbase.org


Is it possible to do chip-seq on a specfic region? Is it possible to do Chip-Seq on specific region of the genome. The idea is to enrich before the sequencing step to have more sensitivity.

If the question here is to perform an assay that only sequences from a specific set of segments of the genome, you probably could, but it would be a lot of work and you'd need a good reason to want to go through that trouble.

Not sure how you would limit the nucleotides you get back to a specific region of the genome say.  The entire point of a CHP-Seq experiment is to get as unbiased a set of nucleotides read and so using specific primers designed against only a specific set of the genome would be hard.

Usually CHP experiments focus the readout they are getting by only focusing on a specific transcription factor for instance.  The number of variants of short binding sequences that usually come out will easily be read by a sequencing lane.  You'd have to have a strong reason not to take all the data genome wide.  Generally the results for many such pulldown sequences are pretty short and frequently can't be found uniquely on the genome, esp if there are lots of binding sites for the protein to be found.

I could speculate that you might synthesize labelled primers from random segments of a cut up library coming from a chromosomal segment you cloned somehow.  That again that seems like a lot of work to cut back on the data you get from the experiment without a big reason for doing this.

Using a CHP-CHP experiment that only has specific regions tiled can make do something like this - this makes the chip itself more economical, making the experiment more accessible.

Hope this helps...


Why electroporator need a cuvette? I have never obtain an Electroporator for my home-lab. Because it's very expensive, I'm trying to create a diy cheap version for myself. In all commercial design, I see that we need to put the sample to a 0.1cm-0.2cm cuvette to doing an electroporation, can I just replace it with an eppendorf plastic tube and put my 0.1->0.2cm alumium electrode inside?

Generally I would advise against making a home-brew electroporator: the voltage needed for electroporation is so high, that even with professional equipment you can easily get arc lightning. In an self-built device that would pose a serious fire hazard.

However even theoretically there are problems with the design you propose:

1) It is important that ALL bacterial cells in the cuvette get exposed to electrical field induced by the high voltage spike. If you use simple electrodes you will only affect the few cells directly between them, which will drastically reduce efficiency of the electroporation. For your design to work properly you would need electrodes that exactly match the dimensions of an eppendorf tube to make sure all bacteria will be squeezed between them.

2) With your device you can only do one electroporation, then you have to thoroughly clean the electrodes. This has to be done for two reasons: first you don't want any carry over bacteria (or as Chris pointed out DNA) from one batch to another. Secondly the electrodes need to be clean of any salts (or other molecules that increase conduction in a solution) to prevent arc lightning between them.


Why are there 2 copies of RNA in the HIV virion? There are two copies of the RNA in the HIV virion. These are retroviruses. So, they can make cDNA from even just one copy using reverse transcriptase.

What is the use of the other? Are both integrated into host chromosomes?

My guesses are:

To ensure increased chance of getting integrated. But, if one gets in, the other also should be able to.
To increase the amount of protein translated (if both get integrated).
Two for two sets of chromosomes. (Seems juvenile but still a possibility. although, I do not think there are specific sites of preference for the viral DNA. Are there?)

You are not totally correct because these two strands don't have to be the same, they can be genotypically different, which occurs when a cell is infected by two distinct HIV strains. Also HIV uses reverse transcriptase which can "jump" from one strand to the other so sometimes pieces get repeated, skipped etc. So you will get a recombinant --> more genetic diversity(see this article) I won't go into to much detail but if you want to know more I would highly recommend to read the article I linked after genetic diversity. So to summarize:

genetic diversity, because of switching between the two strands (this makes it so hard to cure AIDS e.g.)
If one RNA strand gets damaged it can use parts of the other RNA strand as template, so to synthesize DNA
apparently the dimeric form of RNA in HIV is essential for successive replication of the virus

Source: previous mentioned article(HIV-1 RNA dimerization: It takes two to tango.)


What is the average volume of the hippocampus? I'm trying to find any information on sizes of the hippocampus?
Ideally in the average adult male & female brain

The average values of right hippocampus were recorded as follows weight 4.11572 gm, length 6.996 cm, width 1.998,volume 13.978 and surface area11.839 cubic centimetre while left hippocampus mean values were weight 3.96458gms,length 6.995, width 1.998,volume 13.976 and surface area 11.713cc. B. Narasinga Rao, K.R.S. Prasad Rao, R. Ramana Rao. 2012. Morphometric study of hippocampus in adult human brains. Int J Basic Appl Med Sci 2: 139-143.

Men and women had identical volumes of amygdala and hippocampus, as well as dorsal prefrontal cortex Ruben C. Gur, Faith Gunning-Dixon, Warren B. Bilker, Raquel E. Gur. 2002. Sex Differences in Temporo-limbic and Frontal Brain Volumes of Healthy Adults. Cerebral Cortex 12: 998-1003

Hippocampal volume change with age: Hippocampal volume diminished by 20% from 3,584 ± 136 mm3 at age 36 to 2,870 ± 220 mm3 at age of 85, corresponding to a volume loss of about 14.6 mm3/year (Schuff N., et al. 1999. Age-related metabolite changes and volume loss in the hippocampus by magnetic resonance spectroscopy and imaging. Neurobiol Aging 20: 279–285).


Why do Kupffer cells not attack malarial sporozoites? During malaria, why don't Kupffer cells (hepatic macrophages) attack  the Plasmodium sporozoites and stop schizogony, thus saving us from the disease?

Indeed the process is even more interesting than thought: sporozoites actively attack Kupffer cells and let themselves get eaten! In a 2001 research, Pradel et al found that sporozoites pass through a layer of Kupffer cells in order to enter hepatocytes for the next stage of their life cycle. They observed that in rat liver cells, Plasmodium berghei and Plasmodium yoelii sporozoites attach to and enter the Kupffer cells, but not the sinusoidal endothelia. During experiment, the number of intracellular sporozoites kept increasing for upto 12 hours, unlike hepatocytes and other non-phagocytic cells which were invaded in vitro for only the first hour of parasite exposure. The sporozoites entered the Kupffer cells via endocytosis in specialized vesicles which did not interact with lysosomal markers. From Kupffer cells, sporozoites traversed to hepatocytes where they developed into exoerythrocytic schizonts. In another 2015 research, Cha et al concluded that the sporozoites interact with CD68 receptor on the surface of Kupffer cells for endocytosis. In short, sporozoites literally pass through Kupffer cells without letting Kupffer cells doing any harm to them. See this diagram for illustration:

EDIT: What happens in Kupffer cells during traversal of sporozoites remains unkown to some extent. However, Frevert et al, 2008 has shown that sporozoites render Kupffer cells insensitive to pro-inflammatory stimuli and force them towards apoptosis (aka programmed cell death or "cell suicide"). This happens as sporozoite-exposed Kupffer cells are stimulated by lipopolysaccharide or IFN-$\gamma$, causing down-modulation of TNF-$\alpha$, IL-6 and MCP-1 and upregulation of IL-10. Nuclear factor NF-$\kappa$B is also activated, which causes apoptosis in Kupffer cells (Punsawad et al, 2014). However, if Kupffer cells are activated, in particular by immunization caused due to high antivody levels, they may phagocytoze the sporozoites and thus prevent their traversal (Krzych et al, 2015).

References:

Pradel, G. and Frevert, U. (2001), Malaria sporozoites actively enter and pass through rat Kupffer cells prior to hepatocyte invasion. Hepatology, 33: 1154–1165. doi:10.1053/jhep.2001.24237
Cha, S.-J., et al. CD68 acts as a major gateway for malaria sporozoite liver infection. J. Exp. Med., July 2015 DOI: 10.1084/jem.20110575
Klotz C, Frevert U. Plasmodium yoelii sporozoites modulate cytokine profile and induce apoptosis in murine Kupffer cells. International journal for parasitology. 2008;38(14):1639-1650. doi:10.1016/j.ijpara.2008.05.018
Viriyavejakul P, Khachonsaksumet V, Punsawad C. Liver changes in severe Plasmodium falciparum malaria: histopathology, apoptosis and nuclear factor kappa B expression. Malaria Journal. 2014;13:106. doi:10.1186/1475-2875-13-106.
Frevert U, Krzych U. Plasmodium cellular effector mechanisms and the hepatic microenvironment. Frontiers in Microbiology. 2015;6:482. doi:10.3389/fmicb.2015.00482.


50:50 sugar/fat mixture A couple of years ago I saw a BBC Horizon television documentary about sugar and fat. One section mentioned three experiments in which rats were given their ordinary rat food plus and unlimited supply of:
Experiment A. Unlimited sugar
Experiment B. Unlimited fat
Experiment C. Unlimited sugar&fat mixed together (50:50)
The stated results were that in experiment A the rats did not put on any weight, in experiment B the rats put on weight but not much and in experiment C they put on loads of weight and would eat the 50:50 mixture to the exclusion of their ordinary food. I also remember the documentary said the 50:50 ratio was critical and if the ratio was shifted too far in either direction then the weight gain effect reduced sharply.
I have two questions. 1. What was the original research paper. and 2. Have there been any related new results with other mixtures like sugar/salt fat/salt?
EDIT: I have just found this related paper. I don't know if its the exact one relied upon by the documentary, but it's certainly close... perhaps the documentary employed the results from multiple papers.
EDIT: You can see the whole documentary here: https://www.dailymotion.com/video/x1arpze - the rat experiment discussion begins around 46 minutes in.
EDIT: years later... I found this and this.

1. What was the original research paper?

This one appears close: Hyperphagia in rats produced by a mixture of fat and sugar (PubMed, 1990)

  Experimental groups were fed sugar (sucrose), fat (corn oil), or a
  sugar-fat mixture as an option to chow; options were in the form of
  water solutions or emulsions. The control group was fed only chow. The
  sugar-fat group displayed a robust hyperphagia (greater than 36%),
  relative to the control group; the hyperphagic response was greater
  than that observed in the fat group but not in the sugar group. The
  sugar-fat group selected more calories from the option than the other
  two experimental groups. Body weight gains were also greater in the
  sugar-fat group than in the fat and sugar groups. Addition of
  saccharin to the fat emulsion increased fat and total intakes to
  levels close to those of the sugar-fat mixture. In a second
  experiment, the relative palatability of the plain and sweet fat
  emulsions was assessed with two-bottle preference tests. The sugar-fat
  mixture was preferred to the saccharin-fat mixture, which in turn was
  preferred to the plain-fat emulsion. These results suggest that the
  sweetness of the sugar-fat mixture contributed to the pronounced hyperphagia and obesity obtained with this diet option.

2. Have there been any related new results with other mixtures like sugar/salt fat/salt?

A free-choice high-fat high-sugar diet induces changes in arcuate neuropeptide expression that support hyperphagia (PubMed, 2010) (a study in rats)

  Our data suggest that the specific combination of saturated fat and
  a 30% sugar solution results in hyperphagia-induced obesity.

Snack food intake in ad libitum fed rats is triggered by the combination of fat and carbohydrates (PubMed Central, 2014)

  Thus, it can be concluded that the combination of fat and
  carbohydrates is a major molecular determinant of potato chips
  triggering hedonic hyperphagia.

Fat/carbohydrate ratio but not energy density determines snack food intake and activates brain reward areas (PubMed Central, 2015)

  We conclude from our behavioural data that the ratio of fat and
  carbohydrates, but not the absolute energy density, is the major
  determinant of the palatability and intake of snack food during
  short-term two-choice preference tests in rats.

Which Foods May Be Addictive? The Roles of Processing, Fat Content, and Glycemic Load (PubMed Central, 2015) (a human study)

  In summary, the current study found that highly processed foods,
  with added amounts of fat and/or refined carbohydrates (e.g., sugar,
  white flour), were most likely to be associated with behavioral
  indicators of addictive-like eating. Additionally, foods with high
  GL [glycemic load)] were especially related to addictive-like eating
  problems for individuals endorsing elevated symptoms of “food
  addiction.”

In conclusion, it can be either a combination of fats and sweetness (due to sugar or non-sugar sweeteners) or a combination of fats and high glycemic carbs (sugar, white flour, potatoes) that can induce overeating.


Why does the proportion of transposable elements vary so much across species? Intuitively, transposable elements (TEs) are harmful as they may cause genome instability. However, some people argue that TEs are also sources of variations, especially regulatory sequences[1].

If TEs are harmful, then their proportions may be low in most species. And if they are beneficial, then their proportions should be high. Either case leads to the conclusion that their proportions should stay close to each other. However, the fact is that the proportion varies greatly across different species:

Maize: 85% [2]
Human: 45% [3]
Arabidopsis: 10% [4]
Plasmodium: absent [5]

Why is that? Is there other factors that influences the proportion of TE, such as evolutionary pressure?

Reference

[1] Rita R, et al. 2012. Transposable elements: an abundunt and natural source of regulatory sequences for host genes. Annu. Rev. Genet 46:21-42
[2] Schnable PS, et al. 2009. The B73 maize genome: complexity, diversity, and dynamics. Science 326:1112-15
[3] International Human Genome Sequencing Consortium. 2001. Initial sequencing and analysis of the human genome. Nature 409:860-921
[4] Arabidopsis Genome Initiative. 2000. Analysis of the genome sequence of the flowering plant Arabidopsis thaliana. Nature 408:796-815
[5] Biemont C, Vieira C. 2006. Genetics: junk DNA as an evolutionary force. Nature 443:521-24

I can think of two factors that would influence this, but there are probably more.

1) How do transposable elements (TE) get into the genome in the first place?  The answer is both vertically and horizontally.  Vertical transmission needs no explanation.  Horizontal transmission of TE has been documented in several cases.  In some cases, infectious agents can transfer them between species individuals, for instance, viruses can package transposable elements in addition to their own DNA.

http://www.cell.com/trends/ecology-evolution/abstract/S0169-5347(10)00123-0

2) How efficient can the TE replicate?  For example, in the human genome there are a variety of different types of retrotransposons, but only the L1 element can replicate.  Others like Alu and SINEs parasitize their replication machinery and therefore replicate also but at much lower frequencies.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2884099/

So, the difference between species has to do with both of these and probably other factors.  I would imagine in the 2nd case, the selective pressures put upon a given species at any point in time, due to infections or inter-species competition, would surely impact the efficiency of TE replication because they are so important to genomic evolution and adaptation.


How does kissing burst a person's ear drum? A young Chinese woman was left partially deaf following a passionate kiss from her boyfriend.

..

  The kiss reduced pressure in the mouth, pulled the eardrum out and caused the breakdown of the ear.

Source - BBC News

How exactly does this work though? With me not immediately being familiar with the inter-mechanisms of the mouth/jaw/ears, I'm not able to so easily discern the cause-effect of this; also, most all literature I come across is anatomically oriented, like this, as apposed to perhaps more "functionally" oriented.

Follow-up / Accenting question: is there any kind of anatomical disposition that would make the woman more susceptible to this happening? I mean, there are millions of people that partake in "passionate kissing" every day, however, this is the first I've ever heard of it bursting someone's ear drum.

"The kiss reduced pressure in the mouth, pulled the eardrum out and caused the breakdown of the ear"

All you really need to understand the mechanism given this statement is anatomy: the nasal cavity and ears are connected through the https://en.wikipedia.org/wiki/Eustachian_tube so pressure changes in the mouth can be communicated to the ears. A typical individual would experience this when having the ears 'pop' in response to changes in outside pressure due to elevation or swimming underwater.

  is there any kind of anatomical disposition that would make the woman more susceptible to this happening

Although I have not conducted a survey with a sufficient sample size, I don't believe most peoples' passionate kissing involves forming a mouth-to-mouth seal and then sucking/inhaling forcefully to create enough of a vacuum to damage someones' eardrum. It seems that the anatomical disposition most likely to make a woman or man more susceptible to this happening is having a kissing partner with this unorthodox approach. As commenter @kmm points out, you would also need to seal the nose, so having a partner who plugs your nose during kissing or having nasal congestion would also be necessary.

With 7 billion+ humans, though, there is a large enough sample that statistically rare events occur all the time, in part because there is also a near-infinite set of possible rare events.


Histone marks mechanism I am slightly confused about the mechanisms that makes histone modifications associate with gene expression.

That is, H3K36me3 is believed to be present in actively transcribed genes, H3K27me3 in repressed regions, etc. What is the mechanism that makes the presence of H3K36me3 to be in active regions, etc.? Is it causal or just an association?

First we must remember what a nucleosome is: a segment of DNA packed with proteins called histones. This is the initial step to turn the DNA a more compact structure. Citing the advantages of an extremely compact but flexible structure like chromosomes would make this answer a little longer (if you want, I can add them later), and to answer your question faster, we'd better keep moving on the discussion. Epigenetics and gene expression are so beautiful that they have many mechanisms to regulate or change gene expression, and you mention one, which is done by reversible covalent modifications on histones. Such modifications are executed by especific proteins, that can do methylation, acetylation, phosphorilation in some aminoacids of histones. When an aminoacid of a histone is linked with charged groups (e.g: methyl, acetyl) its charge is altered, and depending of the resulting charge (negative or positive), it can reduce or increase the afinity between the histone tail and the adjacent nucleosomes, and therefore, make the nucleosome more compact and less accessible or less compact and more accessible, respectively. But the main effect of these covalent modifications on histones is that the groups added to the aminoacids act like markers indicating for proteins involved in expression (like transcriptional factors and RNA polymerase) that some genes are switched on or switched off. The patterns of this modifications (which one repress or estimulate gene expression) is not completely understood yet.An example of how a certain region is chosen to be marked for expression or repression: Consider an organism that has received a repressed gene related to obesity from its parents and this organism is lazy, eats a lot, has a sedentary life. As a result of all this stimulation, the proteins responsible for altering the histones of the gene related to obesity can be activated or recruited by others proteins, and make covalent modifications in a way that the histones of that gene now are marked for it to be expressed. This organism can pass the new mark to the its children and they will have propensity to obesity due to the activated gene. (This final example was an experiment of epigenetics using rats, I saw a long time ago, so I can't remember the reference).And about if it's casual or not, the marks of regulation in a sequence of DNA can't be casual. For each one or two modifications of histones there is an enzyme that will only do its function if some event is already triggered or if it's triggered during the cell life depending on the environment the cell is exposed to. So millions of cells of a same tissue that have the same function would not have the same pattern of expression for the main genes related with that function by chance. Therefore, regulation of gene expression is very refined and histone marks are one of the many mechanisms that together dictate if a gene is repressed or expressed.


Does the renal vein have a greater glucose concentration than the renal artery? My IGCSE markscheme says that the renal vein has a lower concentration of glucose? I would expect the renal artery to have lower glucose concentration as water is lost from the kidneys. Why is it so?

The kidneys use glucose from the blood as a nutrient, so, this is the reasoning behind your source saying there is less glucose in the renal veins than in the arteries.

If the renal vein contains both less of water and glucose than the renal artery, the concentration of glucose in the renal vein still be lower. This agrees with Bioninja.com.au:

  Blood in the renal vein (i.e. after the kidney) will have:

  Less urea (large amounts of urea is removed via the nephrons to form urine)
  Less water and solutes / ions (amount removed will depend on the hydration status of the individual)
  Less glucose and oxygen (not eliminated, but used by the kidney to generate energy and fuel metabolic reactions)
  More carbon dioxide (produced by the kidneys as a by-product of metabolic reactions)

On the other hand, an article in Scielo.br says:

  Unlike the proximal nephron, cells in the distal nephron are fully
  capable of glucose utilization. In physiologic conditions, the amount
  of glucose utilized in the distal segments of the nephron equals that
  derived from the renal gluconeogenesis in proximal tubules. This is
  confirmed by the common finding that the arterial-renal vein blood
  glucose concentration difference in the post-absorptive state is near
  zero.

In conclusion, your source can still be right.


What triggers programmed cell death in humans (from outside the cell)? What triggers programmed cell death in humans? Is it decided by the brain (for the entire body)? Or is it a local decision of a cell by its environment? Something else?

I realize that there might be different cases. But I'd like to get a general idea of where (and why, actually) does this happen.

EDIT

As linked to by a comment below - one type of cell-death (Necrosis) just "happens" to a cell. And perhaps there are other types that are decided by the cell.
What I'm asking about (and trying to understand more) is about the idea that cell-death might be initiated externally to the cell because it would be beneficial to the whole organism. Such as "the separation of fingers and toes" mentioned in Wikipedia  .   "Who" would initiate it? Are there examples of the CNS initiating it? Notifying the cell by nerves? By hormones? Are they initiated by neighboring cells? (And if so - what cells have the "clout" to send such signals?)

What I'm trying to understand is who decides when a cell dies in those cases where it's not the cell itself.

The answer is, in part, it depends. Let's think of the PI3K/AKT pathway. Akt actively phosphorylates BAD which abrogates the Bax/Bak apoptosis pathway. RTK's at the plasma membrane activate this pathway when bound with survival factors. In the absence of survival factors, Akt would become dephosphorylated and you'd have a net movement toward apoptosis. In a particular form of cell death called anoikis, this could be as simple as detaching from the extracellular matrix. So anything that halts the binding of survival factors could play a role.

In the case of immune response, activated Tc cells can induce apoptosis by secreting pore-forming enzymes as well as enzymes that directly activate caspases. The Tc cells also express Fas on their membrance which is involved in the extrinsic apoptosis pathway. TNF (tumor necrosis factor) may also bind cell surface receptors as sort of a death factor, and push towards apoptosis.

These are just examples, some generic searches about apoptosis, necroptosis, entosis, and a myriad of other programmed death mechanisms will yield a very comprehensive overview.


Is there a difference between an organizer and inducer substance? There is a question in my Embryology textbook's exercise that asks about an organizer and inducer substance. I found their definitions and now I am wondering if they are the same things?

According to Merriam-Webster they are synonyms:

  [An organizer is]  a region of a developing embryo or a substance produced by such a region that is capable of inducing a specific type of development in undifferentiated tissue —called also inductor

Lifemap and Biology Today support the terms being synonymous as well.

However, I think the most commonly used terminology here is that the organizer [used as a noun] induces [used as a verb] the differentiation of embryonic tissue. For example, consider the following quote (Arizona State University):

  The Spemann-Mangold organizer, also known as the Spemann organizer, is
  a cluster of cells in the developing embryo of an amphibian that
  induces development of the central nervous system


Optimization of Signal Peptides We are looking at modifying the signal peptide of a receptor in a common immortalized human cell line.  The cell line already expresses an unusually high amount of the protein, but much of it is not surface expressed.

When we compared the sequence of the signal peptide in the cell line (in this specific case the first 19AA), we found 2 mutations vs the wild type (WT) sequence.  One obvious idea, which we will do, is to restore the peptide to the WT version.

But I've been curious about options that increase trafficking to the plasma membrane over WT.  When I've looked up groups that have actually done this, it's normally been with large screens against every possible mutation in the signal peptide.

Are there targeted approaches to choosing a small number of signal peptides to increase surface expression?

I'm playing around with swapping it out some viral peptides that are totally unrelated to see if we can get increased expression with a receptor that's still (semi) functional.

You could upregulate the transcription of the receptor gene you are interested in. More receptors being produced = more receptors being expressed on the cell's surface.


Can anyone identify this species of spider? These spiders are all over everything on my padio in New Hampshire. Can anyone help me identify what they are?

Based on your area and this pest control site I believe that the bugs in your picture are not spiders, they are clover mites. I have found that some clover mites are a darker brown color and also slightly larger. This image gives a better view of the features of a clover mite, including the longer pair of front legs and oval shaped body:  Clover mites don't pose a threat to people or animals as they live off of either plants or fungi, but smashing them can leave stains on furniture and clothing.


Visualisation of phylogeography I am working on phylogeography on one model species and I am a beginner. You can imagine one species that came on locality more than 5 mya (million years ago). It was a good environment, so the species expanded very quickly. After climatic changes this model species split in two refugiums (isolated locations for a once widespread species) and evolved into two species. This happened several times and now we have from that one ancestral species six valid species.

I have data from MrBayes and BEAST molecular clock. Can you recommend some phylogeographical program which can consider also expansion and contraction of model species?

My input data:

molecular identification (sequences)
coordinates (lat, lon) for each species
geographical data of a continent (altitude, precipitation etc.)

My goal:

Create a map where will be polygons (areas) of each species. These areas will expand and contract (step-by-step not like a do not want create video).

My problem:

I am able to make polygons by MCP, or kernel density, but unable to incorporate barriers into model. For example, polygons of species which lives in mountain region created by MCP include areas of lowland inside...

I think Spread will be best for this work.

SPREAD: Spatial Phylogenetic Reconstruction of Evolutionary Dynamics

Authors: Filip Bielejec, Andrew Rambaut, Marc A. Suchard & Philippe Lemey

Homepage: http://www.phylogeography.org

License: LGPL


Organisms using thermal energy as their sole energy source After seeing this question I remembered that in secondary school we watched a documentary stating something along the lines of "all organisms derive their energy directly or indirectly from the sun. *pause* Well, except a couple of organisms in the deep sea cultures that get their energy from small undersea volcanoes" . Now, after doing a lot of searching I was able to find the 'giant tube worm', however that still indirectly relies on energy from the sun as well as it relies on free Oxygen being available that in the end comes from photosynthesis (if my understanding is correct). So my question is two fold, am I correct in my understanding of the giant tube worm and if so, are there any organisms that function in a way that does not require any energy source beyond geothermal energy?

I had to re-read your last sentence a few times to make sure I understood it correctly, but I think that now I do, and I can answer your question.

What you're talking about are thermophiles. They're small organisms that love hot conditions - up to nearly 250 degrees Fahrenheit. They can be found places with a lot of hot water, such as hot springs - and, yes, ocean vents. Many use sulfur as a fuel during chemosynthesis, oxidizing it to make sulfuric acid. They take the energy from the heat source to do this.

Not all thermophiles use chemosynthesis. Those in hot springs may get a lot of sunlight, and they can use photosynthesis. However, those in the deep sea cannot undergo photosynthesis, and are forced to use the energy from the vents to undergo chemosynthesis. In fact, entire ecosystems can be built off them!

Thermophiles may even have been some of the first organisms on Earth. Around the time that life is thought to have first formed, Earth wasn't a very hospitable place. As Ashwini Kumar Lal writes of the first forms of life,

  Many of them are evolutionary relics called “archaea”, believed to be among the first homesteaders on the Earth 3.8 billion years ago. They are presumably
  the first version of life on our planet when its atmosphere was devoid of oxygen, and comprised largely of ammonia, methane, water vapour and carbon dioxide. They are microorganisms similar to bacteria in size and simplicity of structure, but continue as an ancient group intermediate between bacteria and eukaryotes. Heat – loving microbes, or “thermophiles”, are among the best studied of the extremophiles that can reproduce or grow readily in temperatures exceeding 45º C, and some of them, referred to as “hyperthermophiles”, are capable of thriving even thrive in temperatures as high as 110º C – more than boiling water temperature.

While we do not know (and may never know) the truth of this hypothesis, it is certainly plausible, given the locations where some extremophiles have been found.

References:

1: Microbial Life in Extremely Hot Environments

2: http://en.academic.ru/dic.nsf/enwiki/18641 (link no longer works, for some reason)

3: Origin of Life

Note: While I list several Wikipedia articles throughout the answer, I did not use them for the information in this answer. I think they're a good starting point to lead you to other sources, though.


Photosynthesis and thermosynthesis(?) in plants/organism A while back I thought to myself: if plants could absorb the entire(or most of) light spectrum as opposed to a narrow range, would it be better/absorb more energy/etc. Recently i read that was not the case because any higher on the spectrum and it could knock electrons loose(or something like that) and any lower and it would generate heat instead. Also the article said that plants focus on specific wavelengths for photosynthesis, hence the colors.

If heat is the main issue, then is it possible to turn the heat energy into usable chemical energy? Potentially allowing plants to absorb a much larger range on the light spectrum? And if the plant could absorb heat as well, would it be cool/cold to the touch?

Theoretically it should be possible for an organism to use hat to produce a chemical that it can then use to make useable energy however at present we know of none that do this. If it is possible though it would allow for life in the warm, dark oceans of Europa and if life is not there already it would make it pretty easy to introduce life permanently to a planet like the moon Europa. However in deep sea vents types of anaerobic respiration are most effective and on the surface light is and so if any organisms ever did use thermosynthesis on earth they were probably outcompete do by other forms of energy production and forced to extinction.


How can I measure the population growth of yeast? I will soon have to carry out an experiment. I want to estimate the rate of growth of a population of yeast, although I don't know if it is possible to at least estimate the number of yeast bacteria in a set yeast population. Does someone know of a way this can be carried out? Thanks.

The standard way to measure growth in a liquid culture is to measure the optical density (OD) of the solution – basically, how cloudy it is. Bacteria or yeast in a solution will absorb light that passes through it, making it more cloudy (or turbid). Within a certain range of turbidity, the OD of the solution is directly proportional to the concentration of organisms in the solution, and you can use it to accurately estimate the population in your sample. Outside of this range, you'll need to accurately dilute your sample to get it into this linear range.

Generally, we use a spectrophotometer to measure absorbance of red-orange light (this is called OD 600, for optical density for light with a wavelength of 600nm). A google search turns up a number of plans to make cheap, homemade spectrophotometers that could let you take these measurements without having access to a lab, though I can't speak to how accurate they may be. You might also look at home-brewing supplies, as brewers are also interested in measuring yeast growth and tend to have lower budgets than molecular biologists.

You only need a spectrophotometer that uses visible light to measure bacterial/yeast growth. Many specs also work in the UV spectrum which allows them to measure DNA concentration, but you won't need that.


Area under the curve in a drug concentration curve I am not from a background on pharamacokinetics and trying to learn some concepts.

I noticed that the definition for AUC involve the first 24 hours. For example in here AUC is defined as "the area under the concentration–time curve over 24 h
divided by the MIC."

Is there any reason why this 24 hours is selected?
Say I test 2 treatment strategies. Strategy 1: 500 mg tablets given 3 times a day (500m g×3, 8 hours apart) and Strategy 2: 500 mg tablets given 3 times a day for 2 days (500 mg×6, 8 hours apart).
In this case if I simulate the change in the drug concentration over time assuming exponential decay, then the two concentration curves would have the same values for the first 24 hours. Therefore the AUC obtained in the first 24 hours for these two strategies are the same. But strategy 2 performs better than strategy 1. So, in this case isn't the total area under the curve above MIC a better index than consdiering AUC in the first 24 hours?
Is it wrong to inform why a particular dosing strategy is effective than the other one using 'Total area under the curve (rather than of the first 24 hours)'?

This definition of AUC is non-standard.
The usual definition does not involve the MIC or 24h: it is the area (~ integral) of the plasma concentration curve as a function of time, from first administration time $t_0$ time to infinity. (You will sometimes see it subscripted as $\mathrm{AUC}_{0 \to \infty}$)
In the case of so-called time dependant antimicrobials (beta-lactams, macrolides, vancomycin), the bacteria are inhibited from replicating as long as the concentration stays above the MIC (minimal inhibitory concentration). Often a second threshold, the MBC (minimal bactericidal concentration) is defined corresponding to the required concentration to kill rather than just inhibit replication.
As you stated, the second strategy has indeed a longer duration above MIC. It is more effective from a purely kinetic standpoint. Whether than translate to clinically relevant effects depends on the antibiotics, the bacteria and the tissue under consideration.
A second point is whether a higher AUC is beneficial if the time spent above MIC or MBC is the same (nb: not the case here). However this also depends on factors beyond just pharmacokinetics.
As an aside, some antimicrobials like the aminoglycosides display a "concentration dependant" effect where the peak drug concentration determines the effect, dictating different dosing schedules.


Can paper/plastic currency serve as a medium for pathogens? http://www.nytimes.com/2009/12/15/health/15real.html seems to indicate for a surface, to serve as a medium, the following properties are relevant

animation
humidity
temperature

The article however does not elaborate on the properties a surface must possess to serve as a medium - albeit i would figure it may vary from one virus/bacterium to another.

The same article also states

... when objects in a hotel room — light switches, telephones — were contaminated
with a  cold virus, 60 percent of healthy volunteers picked up the virus when they
touched one of the objects an hour later. Eighteen hours later, the transmission rate
was cut in half.

When currency changes hands we rarely ever know whether it may , within a reasonable timespan, have passed through an agent/carrier.

Sir Dumpty loves to sneak off with a currency note to get me to chase him. He is protected; another member of his species may not be so protected. For that matter a person infected with, say, the common cold virus may have passed a note/coin/card to the vendor at the store within a minute of sneezing/coughing into his/her hand. What if the same person , instead, suffered from TB?

So ... can currency serve as a medium for transmission of pathogens?

TB is an extremely poor example, because as has been mentioned, it usually requires prolonged contact.
But lets go with something with a low required infectious dose, that's friendly to surface contamination, and persists in the environment: Norovirus.
Can norovirus serve as a medium for pathogens? Absolutely. To be blunt, almost anything will serve as a medium for the right pathogen with some level of efficacy. This is a presentation from the New York Federal Reserve on what contaminates money, but given the outlandish things that can be contaminated with infectious material, there's no reason to suspect money isn't among them.
Wash your hands.


Will the N- or the C- terminal soluble domain be on the extracellular side? Here is a homework question

A single-pass transmembrane protein is destined to be transported to the plasma membrane. In the wild-type protein, a lysine flanks the transmembrane domain on the N- terminal side, and a glutamic acid flanks on the C-terminal side. Both the N- & C-terminal soluble domains carry sequences that can by glycosylated by oligosaccharyltransferase.
After the protein is transported to the plasma membrane, will the N- or the C- terminal soluble domain be on the extracellular side?

My answer is

N-terminal with lysine will be towards the extracellular side and C-terminal will be towards the cytoplasm.

Does this seem right to you?

Luminal/cytoplasmic orientation of single-pass transmembrane proteins is mostly dictated by positively charged residues residing on the cytoplasmic side (positive-inside rule) and negatively charged residues being suppressed on the cytoplasmic side/preferred on the luminal side (negative inside depletion/outside enrichment rule).

Since your molecule has a positively charged Lys residue on its N-terminus and a negative negatively charged Glu residue on its C-terminal side your protein would most likely acquire a type II integral membrane protein topology, i.e. the C-terminal part would be directed towards the extracellular space while the N-terminal part is in the cytosol.

Further references can be found here:

Baker JA et al., Charged residues next to transmembrane regions revisited: “Positive-inside rule” is complemented by the “negative inside depletion/outside enrichment rule” BMC Biol. 2017 pubmed

Ott CM and Lingappa VR, Integral membrane protein biosynthesis: why topology is hard to predict. J. Cell. Sci. 2002 pubmed


tissue-specific expression of homolog genes Two or more genes are homolog if thay have similar sequences. homolog sequences between species are called orthologs (caused by speciation events) and homolog sequences in an species are called paralogs (caused by duplication events).

I would like to know what is expression pattern of paralogs or orthologs in an specific tissue. Are paralog (or ortholog) genes have same expression in a tissue or they express different?

I hope my question is clear, but if it has mistakes I appreciate your corrections.

The evolution of new genes is frequently associated with gene duplication. The paralogous genes are then free to evolve on their own into new functions over time. Sometimes (usually) the paralog will end up with a frame shift, or stop codon that inactivates it. But your question is lacking the element of time. At the instant of gene duplication, each copy is identical. However, one copy may lack the control elements (usually upstream), and not be transcribed. Or one copy may eventually evolve a new, tissue specific function. But whether the copy is inactivated, or evolves a new function, or remains active is not the same for every instance. It depends on how each copy changes under the influences of mutation and selection.


What are the fibers and small droplets on the surface of dividing HeLa cells in the figure? I did some literature searching but could not find any info probably because I did not know how people name them.

The figure is from the wikipedia entry HeLa


What magnification do I need to see blood cells? If I want to buy a microscope for my kids to be able to view single celled creatures and blood cells, about what magnification is required?  A Celestron Pentaview digital scope claims up to 600×. Is that going to be sufficient? I somehow get the impression that I'd need 2000× or better, but I'm having trouble verifying any information about magnifications via my good friend Google.

Just my 2-cents worth as visual add-on to @MattDMo 's answer:

Blood smear showing red blood cells and two white blood cells at 400x. Source: Microscope Master

Human red blood cells 1000x. Source: Wikipedia

Human white blood cells 2000x. The small dots (red arrow) are Diplococcus gonorrhea bacteria (Neisseria gonorrhoeae), each ~0.5 micrometers in diameter. Some of the neutrophils have phagocytosed bacteria. Source: Waynes World

Red blood cells visualized by scanning electron miscroscopy. Source: Pinterest.
Note: for illustrative and comparative purposes only; electron microscopy is not the most advisable method for home use.


What is the difference between effective and efficient selection? I always thought of the efficiency of natural selection in the context of molecular evolution. I.e. that linked selection and smaller population size cause less efficient selection. It took me a while before I even noticed that people also say the efficacy of selection.
When researching the answer myself, I found that older papers talk more often about efficacy (like this one). I also found that besides the natural-selection context, it seems efficiency of selection is also used in the context of breeding (like here). However, you can certainly find cases when used in the context of natural selection. Finally, there are about 4x more papers that contain the words "efficiency" and "natural selection" compared to "efficacy" and "natural selection".
So, is effective and efficient natural selection the same thing? Is "efficacy of selection" and "efficiency of selection" be used interchangeably?
-- EDIT --
I am interested in the use of these two words in the context of natural selection only. Unlike in other contexts, in natural selection dictionary definitions of the two words do not make much sense.

You have a word problem here, not really biology.
Efficacy means "power to produce the desired result/effect"
Effective means "producing the desired result", stressing the ability to produce that result
Efficiency means "degree of being efficient"
Efficient in turn means "ability to produce desired result with little waste"
Efficacy and efficiency are not interchangeable as they have different meanings, albeit a subtle difference. You could on the other hand us efficacy and effective as synonyms, though properly the synonym of efficacy is effectivness.


Do human neurons in a petri dish do different things from chimpanzee neurons I want to know if qualitative experiments have been done growing chimpanzee neurons and human neurons in vitro and have any differences emerged, such as the amount of connections per neuron or anything else.

I have came across several studies indicating large similarities between chimpanzee and humans. A study by Bianchi et al., 2013 used immunohistochemistry, electron microscopy, and Golgi staining to characterise synaptic density and dendritic morphology of pyramidal neurons in primary somatosensory (area 3b), primary motor (area 4), prestriate visual (area 18), and prefrontal (area 10) cortices of developing chimpanzees (Pan troglodytes). They found that synaptogenesis occurs synchronously across cortical areas, with a peak of synapse density during the juvenile period (3–5 y). Moreover, similar to findings in humans, dendrites of prefrontal pyramidal neurons developed later than sensorimotor areas. These results suggest that evolutionary changes to neocortical development promoting greater neuronal plasticity early in postnatal life preceded the divergence of the human and chimpanzee lineages. This study however does note that

  Despite sharing these neurodevelopmental similarities, it is important to note that cognitive ontogeny in chimpanzees differs from humans in several respects. Behavioral studies suggest that the different social and environmental contexts in which humans and chimpanzee develop may have also been important in the evolution of human-specific socio-cognitive abilities. For example, whereas young chimpanzees do not fully wean until 4–5 y of age and remain closely attached to their mothers during the early years of development, human infants often interact with multiple caregivers and engage in joint attention.

In another study by Bianchi et al., also published in 2013 regional variation in the morphology of pyramidal neurons in the cerebral cortex of great apes, humans' closest living relatives were investigated. The study used the rapid Golgi stain to quantify the dendritic structure of layer III pyramidal neurons in 4 areas of the chimpanzee cerebral cortex: Primary somatosensory (area 3b), primary motor (area 4), prestriate visual (area 18), and prefrontal (area 10) cortex. The study showed that

  Consistent with previous studies in humans and macaque monkeys, pyramidal neurons in the prefrontal cortex of chimpanzees exhibit greater dendritic complexity than those in other cortical regions, suggesting that prefrontal cortical evolution in primates is characterized by increased potential for integrative connectivity.

However

  Compared with chimpanzees, the pyramidal neurons of humans had significantly longer and more branched dendritic arbors in all cortical regions.

These studies show that despite significant morphological and developmental similarities between human and chimpanzee neurons, there are still notable observable differences.


Have bacteria evolved antibiotic resistance in a laboratory setting? Is it possible to breed a strain of bacteria in a laboratory setting so that it gains resistance to an antibiotic, replicating the kinds of resistance seen in wild, and has that been done?

Yes, many times.

For just one example, see this paper; you could also see this review for numerous examples.

These are examples of spontaneous mutations that lead to antibiotic resistance, so this is sort of an extreme version of evolution of antibiotic resistance. You could also say that antibiotic resistance "evolves" in terms of selection any time an experiment is done that uses a resistance gene to mark a subset of cells, which occurs on a daily basis in labs all over; fortunately these experiments use antibiotics that aren't used to treat patients.


Antibacterial soap impacts on septic system? What impacts do antibacterial soaps have on septic systems?

I know that septic systems rely heavily on bacteria (especially regarding the breakdown of wastes by bacteria), so it seems as though antibacterial agents surely could do some harm to septic systems. Is that the case?

One of my students in my Environmental Science class asked me this question, and it seemed very much worthwhile to post the Q&A to Bio.SE!

The quick answer is: Yes, it can cause harm.
Think about it...The septic system (both the tank and your "drain field") rely on bacteria, and antibacterial soap is not designed to kill only specific species of bacteria. In other words, antibacterial soap can kill a whole range of bacteria, and that certainly includes the bacteria needed in your septic system.
According to University of Arizona Cooperative Extension (Farrell-Poe, 2018):

The use of “antibacterial,” “disinfectant,”or “sanitizing” products in the home can and do destroy both good and bad bacteria in septic treatment systems. “Normal usage” (according to directions) of these products will destroy some beneficial bacteria. Fortunately, the normal bacteria population within the septic system is sufficient and adequate to quickly recover. Significant treatment problems, with conservative use, should not occur. Excessive use of these products in the home can cause significant and even total destruction of the bacteria population. Normally, the use of any single product or single application will not cause major problems.
However, the accumulative affect of using too many such products and excessive application may cause serious problems and damage to the septic system.
It appears that some alternative systems may be more affected by “antibacterial” products than other systems. Additional and more conclusive research is needed.

You can find additional info about antibacterial agents in septic tanks as well as discussion about the effects of the common antibacterial agent, triclosan, on septic tanks here: Svenningsen et al. (2011) and Kirjanova et al. (2014).

 Works cited:
Farrell-Poe, K., 2018. Antibacterial Products in Septic Systems. The University of Arizona Cooperative Extension fact sheet
Svenningsen, H., Henriksen, T., Priemé, A. and Johnsen, A.R., 2011. Triclosan affects the microbial community in simulated sewage-drain-field soil and slows down xenobiotic degradation. Environmental pollution, 159(6), pp.1599-1605.
Kirjanova, A., Rimeika, M., Vollertsen, J. and Nielsen, A.H., 2014. Retainment of the antimicrobial agent triclosan in a septic tank. Water science and technology, 70(4), pp.586-592.


Is episome a plasmid or a virus? A plasmid is a small DNA molecule that is physically separate from, and can replicate independently of, chromosomal DNA within a cell.

In general, in eukaryotes, episomes are closed circular DNA molecules that are replicated in the nucleus. Viruses are the most common examples of this, such as herpesviruses, adenoviruses, and polyomaviruses. Episomes in eukaryotes behave similarly to plasmids in prokaryotes in that the DNA is stably maintained and replicated with the host cell.

Source is wikipedia.

(Reposting my comment as an answer since it seems to be what was required.)

A DNA molecule that replicates independently of chromosomal DNA is an episome. By this definition a plasmid is (usually) an episome. If a plasmid integrates into a chromosome by some mechanism (as for example in Hfr strains of E. coli where the F plasmid is integrated) the plasmid loses its episomal status.

The term "episome" was first coined by Joshua Lederberg to describe the nature of the F element in E. coli.


Why did many odd-toed ungulates become extinct? There were a lot of odd-toed ungulate animals in the ancient times but now just few of them survived. What is the reason for that?

there are two suborder under perissodactyla that are still suvival, Hippomorpha and Ceratomorpha. many perissodactyla species become extinct may bacause the member of perissodactyla animals have sample stomach, compared with artiodactyla, so after the plant change on the earth, they cannot adapt it. and also hinting was one part of reason.
http://en.wikipedia.org/wiki/Odd-toed_ungulate


How did viruses come to be? My question is out of curiosity and got me thinking. How did viruses with the head, tail and tail fibres actually evolve? These viruses look more like machines than biological entities. Are there any theories to how these viruses evolved?

I found a book chapter for you here

Quick summary:
3 hypotheses to Origin of viruses

From pre-cellular world (virus first hypothesis)
From reductive evolution of parasites (reduction hypothesis)
From fragments of cellular genetic material (escape hypothesis)

Drawbacks:

virus require cells (to infect) so how can they come first
virus do not look like known reduced parasites from Bacteria/Eukarya/Archaea
unlikely that genetic fragments form complex viral structures for viral function

  Because of these drawbacks, the problem of virus origin was for a
  long time considered untractable and not worth serious consideration

The rest of the chapter looks more in-depth into the 3 hypotheses


Why would Aspergillus Oryzae produce lactase when no lactose is present? Studies [1] have shown that lactase is produced by A. oryzae when grown on wheat bran and spent beer grains.

Why would A. oryzae produce lactase when these substrates have no lactose?
In [1], it's shown that A. oryzae produces more lactase when grown on wheat bran vs when grown on whey, which has lactose in it - what might explain that?
Since lactose is found in mammals and is not common elsewhere, how/why could A. oryzae have evolved the ability to produce lactase in the first place?

[1] Bailey, M. J., & Linko, M. (1990). Production of β-galactosidase by Aspergillus oryzae in submerged bioreactor cultivation. Journal of Biotechnology, 16(1-2), 57–66. doi:10.1016/0168-1656(90)90065-j

"Although beta-galactosidase is mainly produced for utilization in the hydrolysis of lactose in milk or whey, in natural systems this enzyme is also involved in the breakdown of galactan-based hemicelluloses. Wheat bran contains almost 30% hemicellulose, including considerable amounts of galactose residues (Salo and Kotilainen, 1970). Similar residues are presumably also present in spent grain (wheat). "

From the paper linked in the question.


Base Substitution Probabilities Derivation In Felsenstein's 1981 Paper Evolutionary Trees from DNA Sequences: A Maximum Likelihood Approach, he describes (in equations (6) and (7)) a derivation of the equation of the probability of a particular base substitution.  I am having trouble making the connection between equations 6 and 7.  That is, going from

$$P_{ij}(dt) = (1- u\  dt)\ \delta_{ij} + u\ dt \ \pi_j \quad\quad [6]$$

to

$$P_{ij}(t) = e^{-ut}\ \delta_{ij} + (1- e^{-ut}) \pi_j \quad\quad [7]$$

where $u$ is the rate of base substitution per unit time, $\pi_j$ is the probabiltiy of observing a particular base and $\delta_{ij}$ is the Kronecker delta function (1 if i=j, 0 if i != j).

In the paragraph that follows these equations there is an explanation as to why the exponential term makes sense (if you already know thats what it is), but I'm not understanding how to get from the first equation to the second. Any insights?

In case anyone is ever interested (or perhaps if I eventually forget), it appears that Felsenstein is using a Poisson Process approximation for equation [7], although even with this new information I still do no see the connection between equations [6] and [7].

Page 9 of this thesis had a pretty good explanation of this.

(1) There are two cases. For the first equation (6), the case $i \neq j,$

$$(1) \hspace{13mm} P_{ij}(dt) = u~dt ~\pi_j $$ if we have a transition from one base to another (for example G to C). In the case $i = j,$

$$(2)\hspace{10mm} P_{jj}(dt) = (1 - u~dt) + u~dt~\pi_j $$ holds for a same-base transition (G to G) or a non-transition (say, G and no change). Intuitively, we expect that, all things being equal, the probability of a base to same-base situation is slightly higher: it is the sum of probability that the base changes to itself plus the probability the base sits and does nothing in time $dt$ (with the same net result).

(2) Now we look at the equation(s) (7). Again there are two cases.

$$(1a) \hspace{10mm} P_{ij}(t) = (1 - e^{-ut})\pi_j $$

For case 2 (base to same base transition, $i = j$):

$$(2a)\hspace{13mm} P_{jj}(t) = e^{-ut} + (1 - e^{-ut})\pi_j. $$

(3) The author uses  $P(dt),$ $P$ at a very small (infinitesimal) quantity $dt.$ He tells us the leap from (1) to (1a) follows "almost immediately" when we see that $e^{-ut}$ is the probability that no base transition occurs. Well, then $(1 - e^{-ut})$ is the probability that a transition occurs.

Now $e^{-ut} \approx (1 - ut) $ (a truncated Taylor series) or $ut\approx (1 - e^{ut}).$ So for short times $dt$ we have $u~dt \approx (1 - e^{-u dt})$ and this explains his first equality $P(dt) = u~dt~\pi_j.$

So we have to recognize when he tells us about $e^{-ut}$ that $u t$ is the [truncated] Taylor series representation of $(1-e^{-ut})$ for $t$ very near 0. That is how he gets from 1 to 1a and (6) to (7).

(4) $(1 - u)$ is the probability that no transition from one base to another occurs in some short time $t_i.$ The probability that this happens over n consecutive time intervals is $(1 - u)^{(nt_i)}.$ Let $nt_i = T.$

Note that  $u \ll 1.$ We can write $(1 - u)^T = (1 - \frac{uT}{T})^T $ and
$$\lim_{T \to \infty} (1 - \frac{uT}{T})^T= e^{-uT}.  $$ This reasoning comes directly from that used to derive the Poisson distribution which is used to study rare events. See, for example, Deonier, Computational Genome Analysis, p.74.


Is it the theory of the 5 senses obsolete? An enigmatic topic in traditional science was labelled as the mystery of the 5 senses, and how to best group senses by type.

Is that theory now meaningless?

Do Scientists still agree that that there are 5 types of sense, and no salient new 6th sense which can't be classed with the others?

There was widely accepted merit for that summary classification, because it was the best logical process to approach a complex subject.

The theory questioned the controversial logic of these groups: Soundwaves, Photons, Chemical scent of the air, chemical scent of taste and touch which represents any nerves found in the rest of the body.

It depends who's counting and according to what criteria.

Some neuroscientists argue that smell and taste are one sense because altering one produces substantial changes in the other.

Conversely, if you break down the senses to receptors, you get at least 5 different for taste and 1000 or more for smell.


Why do Guinea Pigs chirp / sing? Ok, so this appears to be quite a mystery. Me and my girlfriend have 2 Guinea Pigs, 1 male and 1 female.

My girlfriend once picked up the female one and took her outside into our garden. The Guinea got scared for some unknown reason and jumped out of my girlfriend's arms and fell down hard.. That night, the female Guinea woke us up with some very strange sounds. She sounded like a chirping bird.

Since then, she sometimes repeats these sounds (most often at night, but not always). Mostly, we are puzzled as to why as there is often no apparent reason for her sounds. Also, when she makes the sounds, she appears to be in a trance-like state, making no movements at all.

Looking for the answer online I found many discussions on the subject like this one or this one. Mostly, the sounds (and the often mentioned trance like behavior) appear to be interpreted as either (1) alarm sounds, (2) loneliness sounds or (3) happiness sounds.

There are also recordings of it one Youtube, like this one.

What I was wondering:

Does anybody know about some actual research that has been committed on this subject? If so, what were the results?

I'm just so very curious to find out!

I found this question very interesting so I did some research. Here's a brief summary of what I've found:

Researchers have found that there are 11 different call types. Some of these include a "sharp alarm cry", "sociable clucking", chutter, whining, purring etc. Using body position and behaviour, researchers attempted to associate these vocalizations with behaviour. Some vocalizations had no apparent associated action including what researchers designated the "chirrup" ( I think this is similar to what your guinea pig might have emitted.)

For more information you can read the results section of this paper by Berryman. You can find a full description of each of the 11 calls and their assumed cause or purpose. Some involve social interaction, reproduction, and distress. Much of the research regarding Guinea pig vocalization involves communication and response between mothers and pups.

In short, it seems as though this chirping behaviour your Guinea pig is exhibiting is normal, but not of any known cause.


What are the highest and lowest possible pH, paCO2 and HCO3 in the blood of living human? What are the highest and lowest possible values of pH, $paCO_2$, and $HCO_3$ in the (arterial or venous) blood of a living human being?

As discussed in the comments, there are theoretical and practical problems with arriving at such data. There have been controlled experiments using canines, but you have specifically stated your interest in humans. I offer a summary of a few observational studies that may be helpful.

In this study, 117 patients in intensive care units (who are likely to have the most abnormal blood gas parameters among the living) were monitored with continuous optode-based blood gas analysis system. Of the 1,341 measurements, the ranges were:1,2

pH: 7.14 to 7.64
PaCO2: 19 torr  - 98 torr
PaO2: 38 torr – 413 torr3

Another study included a total of 487 samples were obtained in ICU patients with severe respiratory failure and found the following ranges:

pH 7.23 – 7.55
PaCO2: 19 torr – 83 torr
PaO2 30 torr – 522 torr3

These are reasonable ranges for pseudo-stable ICU patients.
Contrast that with normal ranges (+/- 2 standard deviations):

pH: 7.35 – 7.45
PaCO2: 35 torr – 45 torr

On the other hand, you’re interested in the most extreme recorded values, which are likely going to occur during cardiac arrest. According to this case report and literature review, the lowest published arterial pH of an adult who survived cardiac arrest with neurologic recovery is 6.33. The caveat here is that this was a near-drowning victim, and the associated hypothermia provides neurologic protection. The authors go on to report several others including their own patient with pH in the range of 6.5 - 6.6 with neurologic recovery in the absence of hypothermia.

Notes

1. Bicarbonate measurements on whole blood are calculated rather than measured and so not included in such studies. The more accurate test for this measurement is serum chemistry. The bounds are usually defined by the assay. It’s possible for a living human to have HCO3 less than assay (5 mmol/L in most labs by serum chemistry) or greater than assay (~50 mmol/L by most labs).

2. All data provided are arterial. Venous blood gases are of little clinical utility except as a cop-out for obtaining an arterial blood gas.

3. These upper values are intubated patients breathing 100% FiO2. (The lower values are those about to be intubated breathing 100% FiO2....) The theoretical maximum PaO2 on room air is derived from the alveolar gas equation, ~100 torr.


Why does a worm's skin need to be wet for oxygen to diffuse across it? Pages I've read about worms' respiratory systems says that the skin needs to be wet (covered in mucus) or oxygen won't diffuse across the skin. Why? If there is more oxygen outside the worm's skin than inside, what prevents it from diffusing across the skin, even if the skin is dried out?

The quick answer: When the skin dries, the lipids in the cell membranes of the skin tissue undergo a phase transition which makes the membranes less permeable for oxygen.

Explanation: The lipids of the cell membrane can exist in different phase states. In the liquid disordered phase the lipids are relatively flexible and mobile, making this phase more oxygen permeable compared to the liquid ordered phase, in which the lipids are more rigidly packed.

The phase transition temperature of lipids increases upon dehydration (another reference), meaning that at the same ambient temperature, a dry lipid membrane is in the liquid ordered state and a wet lipid membrane is in the liquid disordered state.

Therefore, a dry cell membrane is less oxygen permeable than a wet one.


Why are some genes dominant over others? What is the mechanism behind it? If I have a brown eye gene which encodes the protein that is responsible for the brown color and have a blue eye gene as well, what is the reason that my eye color is brown? How does one gene maintain dominance over the other?

One version or allele of the gene for eye color may encode instructions to make the brown pigment, while the blue allele makes no pigment. Alternatively, it is possible, logically speaking, that the blue allele blocks the productions of brown pigment, but this is not the case.

Now, brown vs blue is not a case of one gene and two alleles. After producing pigment, it must be transported, deposited and such. Many processes are involved. So, the pigment deposition process may be functional or not, but as above, it is often found that a non-functional version is simply non-functioning and not actively inhibiting the process. There are numerous cases where an aberrant form of a protein, encoded by a variant allele, acts as an active inhibitor of a given biological or biochemical process.

The key to your question as written is blue eye color is a lack of pigmentation.


How does the cell regulate different metabolic pathways? I heard somewhere that cells use different nucleosides bound to triphosphates e.g. ATP, GTP, CTP and other modified compounds: NADH, NADPH to distinguish between different metabolic pathways and so they regulate where they use up the energy. I heard that kinases play an important role in the regulation. Is there a connection (I guess there is if I check NADPH)? Is this regulation mapped? I mean is there a simple map which contains the main processes and the energy carrier and regulatory compounds?

I am looking for something like this map (of receptor responses), but for metabolic regulation:

Figure 1 - signal transduction - wikipedia

So it possibly contains mitochondria, O2, CO2, flows, ATP, NADPH, etc... I understand that different cell types can have different energy producer and consumer organelles and it is not possible to create something that is universally true, so I would be satisfied with a map of your favorite human cell type.

I heard somewhere that cells ………………………… so they regulate where they use up the energy.

Yes NADP/H is primarily employed in anabolic pathways such as fatty acid synthesis, while NAD/H is employed in catabolic pathways such as glycolysis.

I don't think there is a general rule for other "energy-currency" molecules (pyrimidine triphosphates are not used except in some rare cases such as glycogenesis).

  I mean is there a simple map which contains the main processes and the energy carrier and regulatory compounds?

You can search for the term "metabolic network". It would be too huge so it is better to look at specific sub-networks. KEGG is a good site for finding metabolic networks. There are other representations like hive plots, to visualize very huge graphs.


Formal definition of a 'genetic trait reservoir'? I've read the tomato genome paper in Nature published recently, and they describe the tomato genetic resource as a rich trait reservoir that will provide biological knowledge and empower biodiversity-based breeding. What would be a formal definition of trait reservoir in this context?

In this context, "trait reservoir" refers to the set of all possible alleles for all the different genes in the organism. The more different alleles the organism has, the more possible genotypes it might have. The Nature paper might have referred specifically to the set of known allelic variants.


How did our bodies decide on the right enzymes and where did we get them? I have read that enzymes act as catalysts to reactions in our bodies and that they are extremely target-specific.
My question is how did our body know that a particular enzyme could act as a catalyst for a particular reaction? How did de we get the perfect combination of reactants and their catalysts?
Note:- I am not a person who is studying biology so I might not know that which is pretty obvious to you people.
Anyways, the least expected answer is that ancient aliens carried out some sort of Worldwide Enzyme Injection Programme ;-)

Edit:- By the knowledge gained after asking this question I've figured out that it might be something like this -
There were species which had a different set of enzymes than us but as these weren't the right match the species perished. Those who had the right enzymes survived. Am I right ?

I can understand why your asked this sort of question so I will clear your doubts one by one.

First of all Enzymes are not scattered inside our body, every enzyme is localised in a particular orgenelle or compartment of protoplasm in the cell, where they play their specific role.

Such as the enzymes of glycolysis ( the process by which you create ATP and breakdown glucose to pyruvate) are present in cytoplasm where as the enzymes for TCA ( Oxidative-decarboxylation of AcetylCoA) are present in mitochondria.

Enzymes are very specific.(1) If you have heard of lock and key hypothesis which states that an enzyme binds to the substrate that is complementary to its active site. Enzymes have very high specificity for their substrates the active site where reactions happen are somewhat complementary to the Enzyme substrate complex and thereby it provides the binding energy that lower downs the activation energy of that particular reactions that enzyme is going to catalyse.

I hope that helps!

References: (1) please refer to lehninger principles of biochemistry for further information!


Age-associated neurodegenerative diseases Age-associated neurodegenerative diseases encompass Alzheimer's Disease and Parkinson's Disease. What other neurodegenerative diseases could be described as age-associated? Multiple Sclerosis? Brain tumors? What might be the criteria for defining a disease as age-associated, specifically in the realm of neurobiology?

Dementia with Lewy bodies (DLB): It is characterized anatomically by the presence of Lewy bodies, clumps of alpha-synuclein and
  ubiquitin protein in neurons, detectable in post-mortem brain
  histology.[1] Lewy Body dementia affects 1.3 million individuals in
  the United States alone.

http://en.wikipedia.org/wiki/Dementia_with_Lewy_bodies

  Binswanger disease is a form of small vessel vascular dementia caused by damage to the white brain matter.[1] White matter atrophy
  can be caused by many circumstances including chronic hypertension as
  well as old age.[2] This disease is characterized by loss of memory
  and intellectual function and by changes in mood. These changes
  encompass what are known as executive functions of the brain.[3] It
  usually presents between 54 and 66 years of age, and the first
  symptoms are usually mental deterioration or stroke.[4]

http://en.wikipedia.org/wiki/Binswanger%27s_disease

To name the two with the highest prevalence after Alzheimer's and Parkinson's.