H is the set of all possible Diplotypes that are consistent with genotype data I am new to Biology.SX. I have a statistics background, and have almost zero knowledge in genetics. I am trying to understand some things related to genetics in a certain paper of biostatistics.

Haplotype data were simulated using the haplotype patterns and frequencies (shown below) for 5-SNPs along a dabetes susceptibility region on chromosome 22, reported in FUSION study.

I know that haplotypes can be represented as binary sequences. I wonder why all the possible $2^5$ are not present here. (?)
The paper also says that

Let $G=(g_1,\ldots,g_M)$ denote the unphased genotype data for the $M$ loci. $\mathcal{H}_G$ denote the set of all possible diplotypes that are consistent with the genotype data $G$.

If a subject carries at most one copy of the causal haplotype '01100', it belongs to dominant genetic model, if it carries two copies of this haplotype, it belongs to recessive model.

The set $\mathcal{H}_G$ is not clear to me. While computing the likelihood, I need to know $\mathcal{H}_G$. Any help or suggestions?

Disclaimer: Like the OP, I know very little about genetics and I suppose other people in the site can give better answers than me. Anyway, since the question has been unanswered for months I'm posting my answer. Hopefully someone will improve it.

Just beware that "possible" in this context doesn't mean all haplotypes that we can imagine. As the paper says, "$\mathcal{H}_G$ denote the set of all possible diplotypes that are consistent with the genotype data $G$" and that is an additional restriction that allows just some diplotypes - the seven ones listed, not the 32 we can imagine.

Furthermore, please notice that sum of frequencies in the table equals 1, therefore there can be no more haplotypes in the set.

However, it would help if you linked the source where you got those data and quotes.


Relation between biomass and radius of roots system Is there a known relation between the mass of a plant to the size of its roots?

For example, can I take the root size to be proportional to the biomass of the plant like in this relation: $$R = R_0 (1+EB) $$, where $R_0$ is the minimal size of the root (i.e. the diameter of the seedling), $B$ is the biomass of the plant, $E$ is some parameter, and $R$ is the length of a typical root?

Your question specifically asks for an equation which gives root radius and your sample equation is for typical root length, neither of which I'm aware of. However, there is a known relation between the above-ground biomass and the below-ground biomass of a plant, which varies with species and environmental factors. This is the root:shoot ratio.

This is a linear model where the constants represent differences in starting conditions (the intercept) and biomass partitioning (slope).

  Roots and shoots are functionally interdependent and these two systems
  maintain a dynamic balance in biomass which reflects relative
  abundance of above-ground resources (light and CO2) compared with
  root-zone resources (water and nutrients). Whole-plant growth rate and
  root : shoot ratio are thus an outcome of genotype × environment
  interaction, but source of control is ambiguous.

The actual size of the roots - as in their extent - will depend on the soil characteristics, water table, the plant species, etc.

Source: http://plantsinaction.science.uq.edu.au/edition1/?q=content/6-3-1-biomass-distribution


What is this 5"-across spider found in my bedroom in France? As the subject-line says, what is s/he? I've removed more spiders than I remember over the years, but one that almost fills a pint-glass was approached with some trepidation!

It looks like a type of Wolf spider https://en.wikipedia.org/wiki/Wolf_spider


Is there any biological basis for the emphasis on the value of the firstborn son? Is the firstborn son biologically different in any way from the sons that follow?

Perhaps his epigenome is different? I have heard that a man's testosterone levels decrease when he becomes a father -- could this then have implications for the epigenetics of subsequent sons?

There are lots of cases reported now that suggest that overall the firstborn child is usually more intelligent. The articles supporting this are based on behavioural and economic study though, so the biological basis is a little lacking.
It's also not clear if this is nature or nurture. The firstborn may benefit from their parents undivided attention disproportionately.
Here's the press release for it. And the coverage from the Independent
and Forbes
I read somewhere that the firstborn is more likely to be overweight too, but I can't find the article now. Other people may know other traits that are supposed to differ between children.


Does GTP-γS (GTP gamma S) bind all GTP-binding proteins? I've just read an article Rab10 GTPase regulates ER dynamics and morphology - Nature Cell Biology 15, 169–178 (2013) doi:10.1038/ncb2647. In this paper, to identify Rab proteins in ER, first they isolated ER vesicles. Then washed them to remove cytosolic proteins. After washing, these vesicles were solubilized by detergent. Then, it was loaded on to a GTP-agarose column (to bind GTP binding proteins to the column). In the last step GTP binding proteins were eluted with GTP and analysed by SDS-PAGE.

As a control (before loading on to the column) they used GTP gamma S, because it prevents GTP-binding proteins from binding onto the column.
When I looked at their figure; on the control lane, there are lots of bands! So I'm confused :(If it prevents GTP-binding proteins from binding onto the column, after eluting from GTP agarose column why there are bands? And what can these bands be?)

This is the figure the question is about. On the right is the control experiment with GTP-γS, on the left without it:

The bands that are visible in both experiments are unspecific binding. If GTP-γS doesn't affect their presence, the mechanism by which they bind to the column can't be specific to the GTPase functionality.

The proteins the authors were after are those that are present in the experiment without GTP-γS, but are not eluted in the experiment with GTP-γS. Those are binding via an GTPase functionality to the GTP on the column. They are marked with arrow heads in the figure.

The general idea behind this control experiment is to distinguish specific binding from unspecific binding to the column. Being able to do that means that the authors had fewer proteins they needed to investigate further, saving them some work.


Can you use a cell in meiosis to create a karyotype? Why might it be problematic to use a cell undergoing meiosis to create a karyotype?

Yes, you can, but it's way more difficult.

First of all, in order to see meiotic chromosomes, you need to colect young floral bud in the right stage of development (not too young, since you don't want microspore mother cell, and not too old, since you don't want polen), and that's not that easy.
Then, once you found the right stage and made a slide, you need good knowledge on all the phases of meiosis to understand what you are looking at. Bivalents and translocation rings can make it very difficult to really understand the chromosomes set you have in the cell, so you need a good sized sample and a lot of observation and analysis. If the species you are analyzing has small chromosomes, it's even more difficult to understand what you are looking at.


Which enzyme catalyzes transcription and which translation? My attempt:

Transcription - RNA polymerase
Translation - aminoacyl tRNA synthetase

I know that the ribosome almost runs translation, but I don't think ribosomes are enzymes, which is why I went with aminoacyl tRNA synthetase.  Is this right?

Sorry, but you started on the right track. What you're looking for is called the central dogma of protein synthesis.

Genomic DNA is transcribed in the nucleus into messenger RNA (mRNA) by RNA polymerase. RNA polymerase is DNA-dependent; it needs a DNA template to make an RNA version of the message.

The messenger RNA moves into the cytoplasm where it gets translated by ribosomes into an a polypeptide (protein). Ribosomes are the enzyme that do the translating, and perhaps your confusion is because ribosomes are made up of both RNA molecules and proteins (a ribonucleotide complex).

Aminoacyl tRNA synthetases are the enzymes that make aminoacyl tRNAs (tRNA for short). These tRNA bring individual amino acids to the ribosome as the ribosome is extending the polypetide product of the mRNA message.


Eyelids interconnected? I've seen a patient who had a Vitrectomy (eye surgery) done on a single eye manifest massive swelling on both eyelids.

That seems like having my left hand swell after punching a wall with my right one.

Is this example in the eyes rare? How and why does it happen in the eyes? Does it happen anywhere else?

I cannot obviously speak for the specific case you mention (and, anyway, I am not a medical doctor so I would not make a diagnosis in any case), but one thing that comes to mind is that eyes are part of the immunologically privileged sites of the body. This means that an inflammatory response is not elicited in case of the introduction of an antigen.

I quote from Immunobiology by Charles Janeway

  Some body sites are immunologically privileged. Tissue grafts placed in these sites often last indefinitely, and antigens placed in these sites do not elicit destructive immune responses.
  Paradoxically, the antigens sequestered in immunologically privileged sites are often the targets of autoimmune attack; for example, brain autoantigens such as myelin basic protein are targeted in multiple sclerosis. It is therefore clear that this antigen does not induce tolerance due to clonal deletion of the self-reactive T cells. Mice only become diseased when they are deliberately immunized with myelin basic protein, in which case they become acutely sick, show severe infiltration of the brain with specific TH1 cells, and often die.
  Thus, at least some antigens expressed in immunologically privileged sites induce neither tolerance nor activation, but if activation is induced elsewhere they can become targets for autoimmune attack (see Section 13-25). It seems plausible that T cells specific for antigens sequestered in immunologically privileged sites are more likely to remain in a state of immunological ignorance. Further evidence for this comes from the eye disease sympathetic ophthalmia (Fig. 13.36). If one eye is ruptured by a blow or other trauma, an autoimmune response to eye proteins can occur, although this happens only rarely. Once the response is induced, it often attacks both eyes. Immuno-suppression and removal of the damaged eye, the source of antigen, is frequently required to preserve vision in the undamaged eye.


Which X-Y chromosomes have the developmental genes for mammals? I know that for a given mammal, half the chromosomes come from father and half from mother. This is typically denoted as x-y. I've recently read about "toolkit" genes that control how a cell develops into an embryo into an organism. I'm interested which set of chromosomes(x,y or both) contains these toolkit genes for development of an organism from a fertilized cell?

In other words, does an X chromosome know how to build a female and Y chromosome how to build a male, or is it some "overriding" of developmental instructions that Takes place when Y is present?

First, while half the chromosomes come from each of the two parents, these two sets of chromosomes are not termed X and Y (they would usually be called maternal and paternal).  The terms X and Y refer to potential members of just one pair of the 23 pairs (in humans) of chromosomes, and X chromosomes can come from either the mother or the father.  The presence or absence of a Y chromosome determines sex in mammals.

The Y chromosome contains one gene, SRY, which determines sex, and almost no nother genes.  SRY simply switches on the "make a male" program in the cells.

Essentially all other genes, including any toolbox genes, come from both parents, one copy from each.  (An exception, in males, are those genes on the X chromosome, which in males are present in only one copy and which came from the mother.  Another exception is mitochondrial genes.)


Database for drug-target relation I'm writing a thesis on bioinformatics and looking for drug-target databases. I'm implementing a open-source application for a tool called Cytoscape and so far I've used a open-source database called DrugBank to retrieve drug-target data, but I've read a paper on a database called Drug2Gene that combines multiple open databases into a unified format. The paper is from 2014, but all websites are down and I was wondering if someone here knows of any other databases/resources that does this and is maybe up-to-date? I want to utilize as much open-source data on drug to target relation as possible to provide a simple way of accessing all these resources. Drugbank is regularly updated and a good source, but with so many different databases with a decreasing overlap of data I was happy to stumble across Drug2Gene database only to realize I can't get it and it's probably not up-to-date.

I will be very thankful for any tips as I'm purely a Informatician and feeling helpless in finding thing related to biology.

Source: Drug2Gene paper

There are quite a lot drug databases. I think DGIbd is a good place to start (see below). Further there are a lot of databases which describe drugs and their targets, take a look at these (and the links at the bottom) hopefully you can use several of these in your implementation.

SIDER

  SIDER contains information on marketed medicines and their recorded
  adverse drug reactions. The information is extracted from public
  documents and package inserts. The available information include side
  effect frequency, drug and side effect classifications as well as
  links to further information, for example drug–target relations.

DrugCentral

  DrugCentral provides information on active ingredients chemical
  entities, pharmaceutical products, drug mode of action, indications,
  pharmacologic action. We monitor FDA, EMA, and PMDA for new drug
  approval on regular basis to ensure currency of the resource. Limited
  information on discontinued and drugs approved outside US is also
  available however regulatory approval information can't be verified.

Therapeutic Target Database

  Therapeutic Target Database (TTD) is a database to provide information
  about the known and explored therapeutic protein and nucleic acid
  targets, the targeted disease, pathway information and the
  corresponding drugs directed at each of these targets. Also included
  in this database are links to relevant databases containing
  information about target function, sequence, 3D structure, ligand
  binding properties, enzyme nomenclature and drug structure,
  therapeutic class, clinical development status. All information
  provided are fully referenced.

Potential drug target database (PDTD)
NOTE: I think this one is coupled to DrugBank however you can take a look here

  PDTD is a dual function database that associates an informatics
  database to a structural database of known and potential drug targets.
  PDTD is a comprehensive, web-accessible database of drug targets, and
  focuses on those drug targets with known 3D-structures.

PharmGKB

  The PharmGKB is a pharmacogenomics knowledge resource that encompasses
  clinical information including dosing guidelines and drug labels,
  potentially clinically actionable gene-drug associations and
  genotype-phenotype relationships. PharmGKB collects, curates and
  disseminates knowledge about the impact of human genetic variation on
  drug responses through the following activities: Annotate genetic
  variants and gene-drug-disease relationships via literature reviews
  Summarize important pharmacogenomic genes, associations between
  genetic variants and drugs, and drug pathways Curate FDA drug labels
  containing pharmacogenomic information Enable consortia examining
  important questions in pharmacogenomics Curate and participate in
  writing pharmacogenomic-based drug dosing guidelines Contribute to
  clinical implementation projects for pharmacogenomics through
  collaborations Publish pharmacogenomic-based drug dosing guidelines,
  very important pharmacogene summaries and drug-centered pathways
  Display all information on the website and provide comprehensive
  downloads

STITCH

  To facilitate access to this data, STITCH (‘search tool for
  interactions of chemicals’) integrates information about interactions
  from metabolic pathways, crystal structures, binding experiments and
  drug–target relationships. Inferred information from phenotypic
  effects, text mining and chemical structure similarity is used to
  predict relations between chemicals. STITCH further allows exploring
  the network of chemical relations, also in the context of associated
  binding proteins. Each proposed interaction can be traced back to the
  original data sources. Our database contains interaction information
  for over 68 000 different chemicals, including 2200 drugs, and
  connects them to 1.5 million genes across 373 genomes and their
  interactions contained in the STRING database.

SuperTarget and Metador

  An easy-to-use query interface enables the user to pose complex
  queries, for example to find drugs that target a certain pathway,
  interacting drugs that are metabolized by the same cytochrome P450 or
  drugs that target the same protein but are metabolized by different
  enzymes. Furthermore, we provide tools for 2D drug screening and
  sequence comparison of the targets. The database contains more than
  2500 target proteins, which are annotated with about 7300 relations to
  1500 drugs; the vast majority of entries have pointers to the
  respective literature source. A subset of these drugs has been
  annotated with additional binding information and indirect
  interactions and is available as a separate resource called Matador.

Pharos

  Pharos is the user interface to the Knowledge Management Center (KMC)
  for the Illuminating the Druggable Genome (IDG) program funded by the
  National Institutes of Health (NIH) Common Fund. (Grant No.
  5U54CA189205-02). The goal of KMC is to develop a comprehensive,
  integrated knowledge-base for the Druggable Genome (DG) to illuminate
  the uncharacterized and/or poorly annotated portion of the DG,
  focusing on four of the most commonly drug-targeted protein families:
   G-protein-coupled receptors (GPCRs); nuclear receptors (NRs); ion
  channels (ICs); and kinases. For more information on opportunities in
  the druggable human genome see this poster

KEGG drug

  KEGG DRUG is a comprehensive drug information resource for approved
  drugs in Japan, USA, and Europe unified based on the chemical
  structures and/or the chemical components, and associated with target,
  metabolizing enzyme, and other molecular interaction network
  information. All the marketed drugs in Japan, not only the
  prescription drugs but also the OTC drugs, are fully represented in
  KEGG DRUG and integrated with the package insert information (labels
  information). These include crude drugs and TCM (Tradictional Chinese
  Medicine) drugs.

The IUPHAR/BPS Guide to PHARMACOLOGY (database)

  The information in the database is presented at two levels: the
  initial view or landing pages for each target family provide
  expert-curated overviews of the key properties and selective ligands
  and tool compounds available. For selected targets more detailed
  introductory chapters for each family are available along with curated
  information on the pharmacological, physiological, structural, genetic
  and pathophysiogical properties of each target. The database is
  enhanced with hyperlinks to additional information in other databases
  including Ensembl, UniProt, PubChem, ChEMBL and DrugBank, as well as
  curated chemical information and literature citations in PubMed.

DGIbd

  The druggable genome can be defined as the genes or gene products that
  are known or predicted to interact with drugs, ideally with a
  therapeutic benefit to the patient. Such genes are of particular
  interest to large-scale cancer profiling efforts such as TCGA, ICGC
  and others that identify lists of potential cancer driver genes from
  high-throughput sequence and other genome-wide data. In cancer
  therapy, the increasing number of targeted drugs--those designed to
  inactivate proteins carrying activating amino acid changes as
  determined by mutational analyses--make more compelling the need for a
  searchable database of drug-gene interactions, available here.

There are a lot more databases, maybe these links will help you:

Drug to Target/Gene/Protein Interaction Databases
Question: Database Of Drugs Targeting Genes
Drug Databases


Biodiversity is restricted by genome combinatorics? Me and some friends are interested in opinions for the following:

Conjecture

  The maximum number of species must be limited by the maximum
  combinatorial/permutational space that can be occupied by DNA. Thus if
  there is a maximum physical genome size this is what will determine
  the maximum number of species that can possibly exist.

Explanation

E.G. say maximum number of DNA base pairs able to fit in a genome was $3$, each base pair can be one of either ${A,G,T,C}$. Then there are $4^3 = 64$ possible combinations of genomes. Extrapolate to genome sizes of $x$ base pairs, then there are $4^x$ combinations.

Questions

Would it be possible to claim that the underlying "blueprint" that codes for living diversity sets the absolute maximum for the total "diversity space"?

**Does it make sense to define the total number of species life can achieve with the simple function:

$S < 4^x$, where X is the maximum genome size measured in DNA base pairs?**

Notable Comments

  @Shigeta: for $S<4^x$ the combinations involved quickly dwarf the
  number of atoms in the universe at ~10^80.

  @rg255: Even at this simplification of: $S<20^{x/3}$ there are
  $1.024e+13$ possible combinations with just 10 codons, many many more
  than there is likely species in the world.

Yes, we can say the number of species is limited as you conjecture.  However, quick estimation shows that the limitation has no apparent usefulness:

A reasonable estimate of the largest known genome is 150 GB (150,000,000,000 or 1.5e11 nucleobases).  The limit would be 4 raised to that power.  That limit is so high that it is too large for most calculators to calculate.  For instance. Wolframalpha.com fails to calculate 4 raised to 1e11, its maximum being about 4 raised to 1e9.  The result of 4 to the 1.0e9 power is about 1.0e602059991 or 10 raised to the 602059991'th power.

That rough result, 1.0e602059991, is so enormous that it is exponentially greater than the number of atoms in the universe (which is less than 1.0e100).  Hence, assuming the definition of species requires an organism to use at least one atom for its body, there is no consequence to saying the number of species must be less than this number.

The number of possible combinations of nucleotides is so outrageously large that it does not constrain the number of unique individual organisms or species.


How "old" is a specific snake venom? This is a World Building question, but it's biology specific (I think).

I'm looking for an approximate answer on how long, evolutionary, a specific venom has been roughly the same.  Is it pretty much species based (although I know that's a problematic term), so it would be the same as the "age" of the snake's evolutionary tree since it last branched?  Or is it based on something else?

Specifically looking for information on the Eastern Diamondback.  I am ok with extremely approximate/vague answers, or even just a hypothesis/educated guess.

If it helps, a possible rephrase of this question would be:

How far back in time could you time travel before a modern anti-venom starts to lose effectiveness?

According to the following sources, venom resistance has evolved in both snake prey and predators. Also, resistance can be just regional/confined to a certain population. That suggests that arms races occur, where the composition of the venom of a certain species is constantly changing, and so are the defenses of the prey and/or predators who get bitten. In that case, a snake venom is not the same in chemical composition for very long, and might not be the same across populations of the same species of snake. But those differences might be on a smaller scale than you are looking for. I don't know anything about how this affects effectiveness of antivenom. However long it is until the antivenom loses effectiveness, it might be much shorter than the divergence time since that snake species branched off from the evolutionary tree.

Ground squirrels and rattlesnakes:

"Snakes win: Coevolution of venom function and prey resistance in a rattlesnake-squirrel arms race;

"Coevolution of venom function and
venom resistance in a rattlesnake predator
and its squirrel prey"

"How is rattlesnake venom like fine wine? Both have regional varieties"

(I wanted to make this a comment but don't have the rep for that).


Enzootic vs Epizootic? I'm studying microbiology and I see these words - epizootic and enzootic, often but there are no clear explanations for them online. Can someone help please?

Enzootic and epizootic are analogous to endemic and epidemic, respectively.

Enzootic means something that affects a population of non-human animals  in a limited spatio-temporal region whereas epizootic is relatively more widespread.

Endemic and epidemic are more general terms and do not, technically, apply to only humans.


Human Stem Cells and Disease Can human stem cells be stored for use by future family members as a way to combat generational diseases like diabetes

Stem cells can be stored but that is an expensive alternative to generating them freshly. It has been shown that you can make stem cells from skin cells.

Theoretically, it would be much less expensive to store a piece of epidermis from a recently deceased relative than to make fresh stem cells and store those.

However, the research for generating stem cells from deeply frozen tissues is not there yet. Furthermore, the concept of using stem cells to 'combat disease' is not the right paradigm. It might even be said that some diseases (cancer) are the result of dedifferentiation gone awry.

Where stem cell transplants are used is in the replacement of bone marrow after total body radiation/chemotherapy to destroy marrow (in those cases where the disease has arisen in the marrow). In these cases we rely on the poorly defined process that allows cells to target their microenvironment.

For example, it would not work if marrow replacement cells decided to grow wherever they landed (lungs, liver,etc).

So stem cell storage is an option whose time has passed ,as our tech now allows us to make them.


Formaldehyde turns plantar region of feet red? I'm a freshman med student and I've noticed that on all the feet (and hands) of deceased people that I've worked with, the bottom of the feet always turns red and also the inside of the palm? Why is this?

Thank you.

It might be due to livor mortis, also called postmortem lividity, which is the settling of the blood in the lower parts of the body which in your case might have been the limbs. By time the color can be interpreted as either blue or purple, but given, that not much time has passed it can very well be the reddish color you might have asked, as stated here on page 39:

  The first manifestation of livor mortis can be expected 20-30 min following the irreversible cardiovascular arrest, initially as bright-red spots that subsequently become confluent and turn bluish-violet.

Which might better describe your case is the fact, that cold conditions can cause bright red color in livor mortis, as it can also be found on page 39:

  Cold conditions, such as keeping a body in cold storage, cause ... bright-red livor mortis.

You can read more about it here or here.

EDIT

I have added references thanks to @Kendall, who provided them.


Hominidae is to hominid as Poaceae is to what? I considered asking this on English.SE, but decided against it, since it strictly applies to biological nomenclature, which not many of them will know about - particularly that of plants.

So, in animals, all families end in the suffix  -idae - e.g. Hominidae, Apidae, Canidae or Laridae. When referring to members of a family, you can use the suffix -ids - e.g. hominids, apids, canids or larids.

However, plant families are usually named with the ending "aceae" - such as Poaceae, the grass family. If I want to refer to members of Poaceae (without just saying the common name), what do I say?

Since Poaceae is the plural of Poacea in Latin - like aquae is the plural of aqua - I would say a Poacea, but I'm not a native English speaker so I don't know if this form would be acceptable in English. My guess is that you will have to use the long form a member of Poaceae. In languages like Italian and French it's easier because the Latin nomenclature and grammar are translated. So in Italian you will say una Liliacea for the singular and due Liliacee for the plural, while in French it would be une Liliacée and deux Liliacées respectively.


What are these tiny creatures swimming around my aquarium? I was checking out my aquarium today, and decided to scoop out a water sample and take a look at it more closely. What I discovered were numerous, very, very tiny white worms (?) swimming around in the water.

The worms hover around 1 mm or smaller, almost invisible to the naked eye, with some exceptional specimens reaching nearly 2 mm in length. They swim very fluently, not by wiggling or waving their bodies around, but simply, effortlessly gliding through the water.

I checked them out under a microscope, and recorded some videos. I apologize in advance for the lackluster quality, as I'm not working with expensive equipment here. It took me hours to locate the worms under the microscope, made no easier by how surprisingly fast they are.

Here's a picture:

When I first saw this, I wasn't sure I was looking at the right thing. As you can see in this video, it appears to stay rooted at the tail, while wiggling its head (?) around in various directions. Its most notable characteristic is the two ball-like structures on the front of its body. I have a feeling that those structures will be key here.

This next part was very poorly recorded, but boy did it surprise me when I saw it. Eventually, the worm stretched forward, its head seemingly morphing into three parts (video):

Finally, here's one more clip showing off how fast they can be when they want to (I swear it's not even sped up!). I wasn't able to get it back under the microscope at this point.

Does anyone know what these are, or at least what kinds of worms they might be related to (with respect to the ball-like structures on its head)?

For a little extra background, I found these in my native tank sourced with creatures caught in southern Alberta. The tank contains some longnose dace, which have been a source of concern due to heavy flashing (scratching) ever since I caught them. It makes me wonder if these worms are related, such as some kind of parasite. I'm happy to have them if they're some harmless detritus worm-- any members of the cleanup crew are welcome-- but if they're something to be worried about, I'd prefer to know.

Hard to tell because of the poor picture/video quality, but almost immediately the body shape, distinct "face", size and behavior made me think of a small invertebrate animal called a rotifer (Phylum Rotifera).

 Rotifer eating protists. Photo Credit: Jacqueline Ronson, 2016
There are about 2000 species occurring worldwide within this primarily freshwater phylum, each of which is fairly simple anatomically. Their name (which means "wheel bearer") comes from the two crowns of quick-moving cilia they possess on their heads:

 Source: Gifer
These cilia attempt to push food posteriorly toward the rotifer's back-set "mouth" (which is actually a modified pharynx called a mastax:

 Photo Credit: Jean-Marie Cavanihac
Rotifers are small (always < 2 mm) and so eat small planktonic and protist prey. From UC Berkeley:

As rotifers are microscopic animals, their diet must consist of matter small enough to fit through their tiny mouths during filter feeding. Rotifers are primarily omnivorous, but some species have been known to be cannibalistic. The diet of rotifers most commonly consists of dead or decomposing organic materials, as well as unicellular algae and other phytoplankton that are primary producers in aquatic communities.

As for body shape:
Although all Rotifer species are bilateral animals, they vary quite a bit in body shape. Box-like shaped rotifers are referred to as being loricate, while more flexible worm-shaped species are considered to be illoricate.

 Photo Credit: Juan Carlos Fonseca Mata
Regarding sometimes staying "rooted at the tail" as the OP observed:
Some rotifers are found usually free-swimming, while others "glue" down their posterior "toes" to anchor themselves to some substrate or debris. Again from UC Berkeley:

The final region of the rotifer body is the foot; this foot ends in a "toe" containing a cement gland with which the rotifer may attach itself to objects in the water and sift food at its leisure.

 Source: Starr et al. 2013 (Cengage Learning)
See here for further "fun facts!"


Is it possible to exclude article types in a PubMed search? I have a question about searching PubMed. I want to search for original research papers while omitting reviews. Is this possible in PubMed?
Example
If I am interested in the relation between Acute Renal Failure and Salt, I could use the following search string:

("Acute Kidney Injury"[Mesh]) AND ("Sodium Chloride"[Mesh])

Using the column on the left of the article overview list, you can select which article types you are interested in.
Question
But I wondered if it was also possible to exclude a specific article type (e.g., reviews) from the search?

I believe this will work:
((Acute Kidney Injury[MeSH Terms]) AND (Sodium Chloride[MeSH Terms])) NOT (Review[Publication Type])
Using the advanced search settings on PubMed it was easy enough to set up, here is the link in case you don't have it already:
https://pubmed.ncbi.nlm.nih.gov/advanced/


Is there a cheap and easy way to check for potentially unsafe UV exposure? My lab has an older large Fotodyne tabletop UV transilluminator for visualizing gels.  It has a UV blocking cover that hopefully reduces UV that passes through, but I've always been suspcious as to how effective it is.  Obviously this part can be replaced with a new one, but short of guessing on the recommended 50 hr lifetime, how would one know the level of UV passsing through?  I considered simply placing a gel on top, but that is far from quantitative.  I am really just curious if there is an easy to make and/or obtain sensor that could be used to know when UV expose could be considered dangerous.

The instrument you are looking for is probably an UV-meter.


Flower identification (Singapore, April) I saw some flowers growing by the roadside today, and was wondering about the species of this plant.

The plant also appeared to be fruiting, and it produced small fruits that formed small clusters.

This is called "Red Powder Puff" or botanically Calliandra haematocephala. See the images (from the Wikipedia article):

What you identified as the fruit appears to be the buds:

Some more information can be found here.


What insect could this be? There is a bush in my garden that I love to observe, as it often has large rain spiders building nests in its leaves, but I occasionally notice large groups of an orange-headed insect on the leaves, and I can only assume that they are the primary prey item of the spiders, but I can't seem to identify them, and I only managed to get a picture of one this morning, as they usually run and hide if I get close enough for a picture.

It has a very similar morphology to a cockroach, in my opinion, but after looking over common species in the area, I still have no matches, it is around 2 - 2.5 cm. I have never seen them anywhere but this bush. I live in Johannesburg, South Africa.

I would really appreciate any help in identifying the species.

It looks like two insects there, with the one in the background (top) impossible to see. But the one in the front, with its head down looks very much like the American cockroach, Periplaneta americana (Blattodea, Blattidae)


Does the arrangement of amino acids in a protein matter for nutrition? Let's say there are two diets, consisting of entirely different proteins. If you split up all of the proteins from one day of each diet, you'll get the same set of amino acids and the same count of each. Assume everything else about the diets is the same.

Would these diets have the same effect on the protein composition in your body? Different polypeptides, but overall the monomers are identical. Does your body break down proteins entirely, or will it reuse some chains of amino acids?

Arrangement of amino acids determines the protein structure which in turn can determine how easy it is to digest the protein. I cannot think of an example right now; never really checked if two entirely different proteins have identical composition. However, it is not really surprising. In chemistry, it is known that different isomers have vastly different physical properties.

So if the two proteins have different digestibility then they will have different nutritive values.

Regarding, protein digestion and nutrition. New proteins are built from individual amino acids and not pre-formed oligomers. Read about translation. So at some point the ingested protein has to be completely broken down into amino acids.


Do the primers used for Covid-19 test work with all new strains? We keep reading news of new Sars-CoV-2 strains, some of them allegedly able to evade vaccine-induced Igs. That's not unexpected, specially for a single-stranded RNA virus. However, it seems to me that the tests (RT-PCR) are being done exactly as they've been since early 2020, all around the world.
Therefore, my question is about the primers used: how can we be sure that there are not new strains with sequences not complementary to the primers? Does the current covid19 test target highly conserved RNA regions? If that is correct, how do we know that those regions are highly conserved?

I TRY to answer. First of all, no we cannot be 100% sure that the primers are effective against all strains.
However, the strains that are under media attention right now are due to variants in the spike protein, while RT-PCR primers are designed on different genes.
One WHO document (I do not know if it's the official guideline) targets RdRp (RNA-dependent RNA polymerase) and a gene called E gene.
While the document itself nor the paper on which it is based explicitly addressed conservation of the target genes, I found evidence for relatively high conservation of at least RDRP in this paper.
Personal opinion here: in looking for RT-PCR primers, you always need a balance between targeting genes that do not vary in the species, and targeting genes that may aspecifically amplify in different species (e.g. SARS-CoV).
Final answers:

how can we be sure that there are not new strains with sequences not complementary to the primers?

We cannot. However, as far as the variants media are talking about, we know that RT-PCR has some ability to detect them, since they have been sequenced as a consequence of some patient testing positive to RT-PCR.
We cannot exclude the existence of unknown strain. They could be identified by e.g. sequencing patients with COVID-2 symptoms testing negative to RT-PCR (and possibly testing positive to the antigenic test). I don't know if such cases have been observed.

Does the current covid19 test target highly conserved RNA regions?

Yes, the current RT-PCR based tests target conserved genes (although I wouldn't call the highly conserved, because of the caveat I expressed above as a personal opinion)

If that is correct, how do we know that those regions are highly conserved?

Mostly by sequence similarity. Regions that have the same sequence in all the individuals of a species and in related (or distant) species are conserved.


Is the amount of blood that flows through every vein and artery per minute really a constant? I was listening lectures from Mark Saltzman via Open Yale Courses. Now, if I did not understand him wrong, he said that the amount of blood that travels through every vein and artery in our bodies per minute is a constant. Five liters of blood go through the aorta every minute, and since the blood circulation is a closed system, also every other vein/artery must pass that amount of blood per minute. Is this true? How could I (mathematically) show that it is true?

I think the question is not whether the blood flux is constant in time, but rather in space: if 5L/min is the flux through aorta (in given physiological conditions), then at the same moment 5L/min will cross the capillaries. This is volume conservation, for a closed system filled with an incompressible fluid, see this sketch:

If 5L are pushed through the main pipe, the same volume needs to be pushed through the system downstream of it.

Then comes the fact that the system is not perfeclty closed, and some water (and solutes) will "leak" in and out, as @inf3rno points, so this is only approximatively true. Another limitation is that vessel walls are actually elastic, so a change in vessel radius does occur during blood flow. However I believe it is a fair approximation.


What measures are commonly used for the complexity of an organism? I'm aware of measures like number of distinct cell types being used as a measurement of complexity in biology, for example in the G-value paradox. But this doesn't really help for unicellular organisms. Is it possible to define a unit of complexity to make comparisons between different organisms?

This is a very interesting question. Not sure if there is any way to answer without specifying a definition for complexity.

It is clear that everything is made of only the same few elements, so complexity must involve more than that. Do the number and position of identical molecules matter? If so, size matters and we would label a large jelly-fish as more complex than a cat and the air in a large hot-air ballon as more complex than any single living organism (assuming it is bigger).

I think it is clear that this is not what is meant by biological complexity. Molecules acting identically should not count multiple times; the number of different molecules matters more than the mere number of molecules. But are immune cells really more complex simply because of a relatively minor difference that allows them to generate a wide variety of genetic variants?

What about the variable coat color of a calico cat. Does the complex and non-repeatable (even with cloning) pattern mean it is complex, or does the fact that a simple genetic process underlies it mean it is simple.

The difference in complexity of different representation of the same thing is a classic problem in information theory (see Kolmogorov complexity). The ratio of the circumference of a circle to its diameter requires an infinite number of decimal digits to describe, but it is just a single geometric concept and it can be represented with one or two characters, as pi or π. This applies to the problem of using phenotypes to measure complexity -- the language and definitions we use to describe or to differentiate phenotypes determines what is complex and what is simple.

Moving beyond a simple static snapshot case, biological complexity involves time-dependent evolution. The "game of life" demonstrates how simple rules + initial conditions yield apparent complex behaviors, and the beauty of fractals arises the same way. Many apparently complex organisms grow from small seeds plus time-evolved exposure to simple things like water and light and CO2. Are trees only as complex as the seed they grow from?

Finally, what about higher order complexity? One human brain is very similar in general makeup to another, but the concepts and memories stored seem complex and very different. Comparing the complexity of stored information between two people is the whole complexity problem over again.

It seems to me that complexity can only be cleanly measured within a specific context, and then only relatively. One can measure the relative genomic complexity of two organism as the edit distance between the alphabetic sequences representing their genomes. The relative regulatory complexity can be measured as mentioned above by @user1682. Each of these says something about an organisms complexity. But what if organism A has higher genomic complexity and organism B has higher regulatory complexity? It might be possible to derive something like a principle component "basis set" from several of these kinds of measurements using a training set and a list of organisms with predefined complexity values. Applying this "standard" scoring metric to another organism would allow ranking it on a "standard" scale, but it would be difficult to generate and obtain consensus on the initial "expert" ranked organism scale. Such a standard might have some value, but is not really theoretically satisfying in that it describe an organisms complexity in the same way that the average of a small sample describes the distribution of a large population.


Identify this smooth-cocoon worm from Southern India I couldn't identify which species these worms belong to. I believe they're insect larvae.
They measure approximately 5 to 10 mm in length, and are common in the southern states of India. They carry cocoons, open at both ends, which the worms can wriggle inside and alternate their direction of movement. These cocoons are perfectly smooth except for the openings.
Another post shows something similar, but the cocoon of that worm looks more woven, while this one doesn't.

This is definitely the larvae of one of a many number of case-bearing moth species. As noted in comments and elsewhere, these case-bearing moths show up fairly frequently on Bio.SE (e.g., see here, here, here, here and here for some examples).

Most of these moths are members of one of two families: Coleophoridae (the case bearing moths) or Tineidae (the fungus moths).

Some of these species even build cases that they carry around with them.

Your specific example is possibly Tinea pellionella (case-bearing clothes moth).

[

T. pellionella has a cosmopolitan distribution and occurs nearly worldwide (Cheema 1956). As the Wikipedia article summarizes, the larva feeds mainly on fibrous keratin (e.g., hair and feathers) as well as carpets, furs, upholstery, and woolen fabrics. The larvae remain inside a case it constructs from debris such as hairs and fibers (e.g., from clothing, upholstery, carpets, etc.).


Heterozygosity and overdominance Consider $m$ loci with heterozygote advantage (overdominance) such that the fitness of the two homozygotes is $1-\frac{s}{2}$ and the fitness of the heterozygotes is $1+\frac{s}{2}$, where $s>0$. We'll assume that the fitness of an individual is given by the multiplication of the fitness component on each locus. In consequence, the fitness of the best possible genotype is given by $\left(1+\frac{s}{2}\right)^m$.

According to this book, an individual is heterozygote at $j$ of these $m$ loci with probability

$${m\choose j}\left(\frac{1}{2}\right)^m$$

and the equilibrium population mean fitness $\hat w$ is

$$\hat w = \sum_{j=0}^m {m\choose j}\left(\frac{1}{2}\right)^m  \left(1+\frac{s}{2}\right)^j  \left(1-\frac{s}{2}\right)^{m-j} = 1$$

I don't understand any of these two equations! Can you help me to understand how they have been calculated?

For the moment I just enjoyed proving that $\hat w = 1$. We can reformulate $\hat w$ as

$$\hat w = \left(\frac{1}{2}\right)^m  \sum_{j=0}^m {m\choose j} \left(1+\frac{s}{2}\right)^j  \left(1-\frac{s}{2}\right)^{m-j} = 1$$

,then using the binomial identity

$$ \hat w = \left(\frac{1}{2}\right)^m \left(\left(1+\frac{s}{2}\right) + \left(1-\frac{s}{2}\right)\right)^{\space m}$$
$$\hat w = \left(\frac{1}{2}\right)^m 2^m$$
$$ \hat w = 1 $$

If the fitness of a heterozygote is $(1+s/2)$ and of a homozygote is $(1-s/2)$ then why is the probability for a given state $(1+s/2)^j(1-s/2)^{m-k}$

$$\binom mj (1/2)^j(1/2)^{m-j}= \binom mj (1/2)^m~~ ?$$

As you pointed out earlier, in the general case it need not be true that $p = q = 1/2$ but that is what the form of the probability above implies. So the threshold question is why this particular heterozygous-dominant model implies equilibrium probabilities $p = q = 1/2.$ I think the ideas below begin to address this.

The simplest case is for one locus, two alleles, and there are many good derivations online. I think if you understand the situation for one locus you can generalize to higher numbers. (Hopefully I will supplement this answer, time allowing. I think a shortcut would be to assume $p = q = 1/2$ and use your fitness weights. That gives us $\bar{w}=1$ as a denominator. Now for reasons of symmetry I think you can show that the relative frequencies of $p$ and $q$ are equal and so $p' = p.$ Then you have to show that this equilibrium solution is unique.)

For a single locus the derivations of `heterozygote advantage' I have found,(1)(2), assign fitness weights as follows:

AA = (1 - s),     Aa = 1,       aa = (1 - t )

in which $s,t > 0, s \neq t$ in general, from which they derive as a condition for equilibrium

$$\Delta q = \frac{pq(sp-tq)}{\bar{W}}  = 0$$

so

$$\hat{p} = \frac{t}{s+t} ~~~\text{and}~~~ \hat{q} = \frac{s }{s+t}$$

in which $\hat{p}, \hat{q}$ are equilibrum frequencies for each allele, respectively, and s and t are rates of mutation. Nowhere did I see a model in which they had assigned the same fitness to both homozygous cases (AA, aa) but it's just a special case of the heterozygote advantage model.

fitness (AA) = fitness(aa) = (1 - s/2), fitness(Aa) = (1+ s/2).

So if we subtract s/2 from each fitness score (or normalize with respect to Aa to the same effect), we get:

fitness(AA) = fitness (aa) = (1- s ) and fitness (Aa) = 1 as in the two references above, except that now the two homozygous states have equal fitness.

But then we have $$\Delta q = \frac{pq(sp-sq)}{\bar{W}} =  \frac{pqs(p - q)}{\bar{W}} $$

and the only nontrivial solution is $p = q = 1/2.$

So what I am suggesting is that when you assign the same fitness to both $AA$ and $aa$ you no longer have the general case. As for the value of s being forced, the following seems relevant.

The full expression from (2) for the equilibrium condition is

$$p' = \frac{p^2 W_{AA}+ pq W_{Aa}}{\bar{W}} \hspace{10mm}(1)$$

in which$ W_{AA} = W_{aa} =  1- s$ and $W_{Aa} = 1$ and

$\bar{W} = p^2 W_{AA}+2pqW_{Aa}+q^2W_{aa}$

If the homozygotes are assigned the same fitness and $p = q = 1/2$ , equation (1) above becomes:

$$p' = \frac{\frac{1}{4} + \frac{1}{4}(1-s)}{\frac{1}{2} + \frac{1}{2}(1-s)} $$

The program on page 583 of (1) is helpful. Let h:= heterozygous and m:= homozygous. If $p = q = 1/2$ then as long as fitness(h) and fitness(m) are equal the system is in equilibrium immediately.

If $p\neq 1/2$ then as long as f(h) = f(m) the system reaches equilibrium at $p = 1/2$ asymtotically. If $p = 1/2$ but f(h) $\neq$ f(m) the asymtotic limit has to be calculated.

See also http://evol.bio.lmu.de/_teaching/evogen/Evo8-Summary.pdf


Why bacteria and viruses are so much smaller than animal cells? Why are bacteria and viruses so much smaller than animal cells? -
I don't have more information about the question, sorry if this is too vague.

Cells/viruses vary in size mainly according to their function, components & requirements imposed by cell division/virus replication.

Bacterial cells are so small because they need a large surface area to cell volume to take in nutrients. Bacteria accumulate nutrients from the environment by diffusion alone, and so adopt certain sizes and shapes so they can import nutrients most efficiently. other evolutionary advantages are also existent in response to the demands of the environment and predators

Viruses function is pretty minimalistic. they pretty much consists of nucleic acid surrounded by a protective coat of protein called a capsid. this is the primitive virus, all it nedds is to infect cells and pass the information stored inside them.

The size of animal cells however depends partially on the type of cell and its function. Red blood cells are pretty small in comparison to other animal cells, they don't need to divide (so do not own a nucleus) and need a large surface area in order to diffuse Oxygen efficiently. Egg cells for example serve to store nutrients and don't need to carry out active metabolism, and so they are much bigger.

I took some of the examples from here, and for more technical information about the upper limits of cell size and plant cells click here.


What to call a trait that has current utility but unclear evolutionary origin? I'm looking for a commonly used term to describe a trait that has clear current utility but an evolutionary origin that is uncertain and that we do not necessarily wish to emphasize in our description (e.g. to avoid unnecessary speculation):

Adaptation emphasizes an origin driven by natural selection.
Exaptation emphasizes an origin driven by co-option.
"Aptation" fits the bill, but it seems cryptic and rarely used.

Thank you for your help.

As you point out, people have sampled other terms like "aptation" but these terms are not commonly used.

In order to not imply anything about the evolutionary history, since it is unknown, I think it makes most sense to refer to these simply as traits or phenotypes (or genotype for that matter, depending on the approach you are taking). If you wish to emphasize that these traits are beneficial to the organism, it is sufficient to call them beneficial traits or use other adjectives like useful, positive, etc.


If people with colorblindness lack one type of cone cells, shouldn't they be unable to recognize one particular color? The 3 types of cone cells in normal humans allow them to view 3 types of colors and any color made from mixing and matching those 3.

So, 2 types of cone cells should only allow to view just 2 types of colors and any colors made from those two.

But that is clearly not the case.

https://en.wikipedia.org/wiki/Color_blindness#Red.E2.80.93green_color_blindness

  Protanopes, deuteranopes, and tritanopes are dichromats; that is, they can match any color they see with some mixture of just two primary colors (whereas normally humans are trichromats and require three primary colors).

Also, from personal experience, I'm colorblind and can see and differentiate all 3 red, green, and blue. It's just the hues between red-green and green-blue I can't distinguish much...

How exactly do dichromats see all three colors when they lack one type of cone cell?

Cones do not literally interpret colors.  The three cones work together to encode a signal that is abstractly interpreted by your brain in higher processing centers.  Here is what neuroscientists currently think the decoding scheme looks like:

This leads to what's called opponent process, an antagonist mechanism whereby the perception of green/red are a matter of the contrast between the two.  In a deuteranopes, the mechanism of antagonism is missing, so the colors can not be differentiated.

What this implies is that (to some extent) a single color has no meaning.  Colors are only meaningful in the context of other colors.


Ni-NTA purification, problem with the chaperone protein I'm trying to purify the protein by Ni-NTA affinity chromatography. It seems that my protein (size about 54 kDa) is co-purified with chaperone protein (probably GroEL  - as the band is around 57kDa).
I tried the method where 4M glycerol and ATP is added to the wash buffer 1 and then I incubated this with the resin for 2 hrs in 4C, but it did not help.
Has anyone met such a problem before? I will be grateful for any advices.

If chaperone proteins are not an expected binding partner to your protein/peptide fragment then you need to use imidazole in your lysis and wash buffer ranging from 1 to 10 mM depending on how stringent you want but 1 mM worked for me. Can go higher than 10 mM if the problem does not resolve but don't go too high since imidazole is also used to get the purified proteins off the nickel beads as an elution buffer!


Why is the variance of the Wright-Fisher model not equal p(1-p)/(2N)? I was looking at the properties of the Binomial probability distribution and it says that the variance is np(1-p). In population genetics, n = 2N. So I would expect to see that the variance is 2Np(1-p).

But when looking at the Wright-Fisher model, I often see that the variance is $p(1-p)/(2N)$ (see this presentation page 6).

How to derive the variance of the Wright-Fisher model to get this variance from $Prob\{X=i\}=\frac{n!}{i!(n-i)!}p^i(1-p)^{n-i}$?

The binomial variance $2N p (1-p)$ is for the number of individuals $n'$ carrying the allele in the next generation. The frequency of the allele in the next generation is $p'=n'/(2N)$, so its variance is $$\text{Var}[p'] = \text{Var}[n'/(2N)] = \text{Var}[n']/(2N)^2 = p(1-p)/(2N).$$


What are the physiological effects of retinal exposure to 380–400nm light? There are two categories of sunglasses: UV380 sunglasses block all light with wavelength 380nm or lower, while UV400 sunglasses block all light with wavelength 400nm or lower.
This made me wonder, what are the physiological effects of retinal exposure to the 380–400nm band of light, which is not covered by UV380 sunglasses?
Also, assuming that the 380–400nm UV light does cause eye damage, does any potential pupil dilation caused by the dark tint of such glasses have an effect on the amount of damage caused?

Answering my own question after thorough research:
Definitions
First, I noticed that there is no consensus on where the UV spectrum ends and the blue portion of the visible light spectrum begins.
According to the WHO, as well as to most other sources, the UV spectrum covers the wavelength range 100–400nm (1). However, a few other sources, notably the SCENIHR, define visible light as starting at 380nm (2), hence UV light would be 100–380nm.
Another source, the ICNIRP, directly mentions that the boundary is not clear-cut, “the band 315 to 380–400 nm is designated as UVA” (3) . At least one source refers to the 385–405nm band as the “UV/Visible Radiation Boundary Region” (4).
Tinted Lenses
To address the part about the dark tint of lenses causing pupil dilation, it is first worth noting that not all lenses that filter out UV light have a dark tint.
In fact, clear lenses can actually offer up to UV400 protection (5). There is even some research specifically on UV protection by clear lenses (6).
Back reflection of UV light
UV380 and UV400 are not the only eyeglass specifications relevant to UV protection. There is also eye-sun protection factor (E-SPF®), which was introduced in order to also account for back reflection of UV light from eyeglass lenses to the eyes (7). Therefore, this back reflection should also be taken into account when examining the effects of 380–400nm light exposure on the eye.
The 380–400nm Band
Now let’s get to answering the question.
According to the Texas Technical University Health Sciences Center, 40% of the radiation harmful to our eyes falls within 380–400nm, which they call the “UV protection gap” (8). Another source states that, while 100–380nm light is “very harmful”, 400–460nm blue light can still cause retinal damage and macular degeneration (9). The American Optometric Association also states that blue light, which they define as the range 380–500nm, may cause eye damage (10).
An article by ZEISS Vision Care explains that the UV380 standard was a “pragmatic choice” by the ophthalmic industry, and does not reflect “biomedical realities” (11). The article refers to the 380–400nm spectrum as the “most intense portion of solar UVR on Earth”. I assume the author is referring to the physical definition of intensity of radiant energy, which is the power transferred per unit area, however I am not 100% sure that this is the intended meaning of “most intense”.
I also found an article claiming that the WHO recommends UV protection up to 400nm (12), which again implies that 380–400nm does cause significant retinal damage. However, I couldn’t find the actual WHO publication stating the recommendation.


RNA isolation- role of pH Why does RNA alone go into the aqueous phase when treated with phenol-chloroform at lower pH? At a neutral or basic pH, both DNA and RNA would escape into the aqueous phase. So how is DNA held back at acidic pH?

In this case there are two properties that determine the behaviour of RNA:

Its polarity;
Its acidity.

Because of its polarity, RNA tends to escape the phenol-clorophorm phase; actually, it can go into the aqueous phase even if the pH is neutral [1], but with a lower efficiency than if the pH is acidic. Here comes the second property, RNA acidity. Because of that, when RNA is in a neutral solution, it has a negative charge: the $-OH$s of the phosphate group dissociate to $-O^-$ and $H^+$. However, this does not happen in an acidic solution, where there are already too many $H^+$. Thus, at basic pH the $-OH$ groups are intact and have a neutral charge; this stabilizes the system.
Think about it: if the aqueous phase is at neutral pH and fills up with negatively charged RNA molecules, after a while no more negative molecules can enter that solution. On the other hand, if the RNA molecules that enter the aqueous phase stay electrostatically neutral, the number of molecules which go into the solution will be limited only by the availability of water molecules to dissolve them.

That is why you use acidic* pH, it is simply a matter of efficiency.

Disclaimer: This answer is based upon a comment by the OP under the OQ.

[1] You would never use a high-pH solution to extract RNA because such condition hydrolyses RNA.


What are the biochemical interactions between human body and Polyethylene? Our waterways and oceans are showing increased levels of plastic contamination. These plastics are breaking down into smaller pieces. When one goes to the beach and plays in the surf they often swallow some seawater and thus some amounts of plastics, including Polyethylene.

What are the biochemical pathways or effects of plastic, specifically Polyethylene, in the human body? I am looking for toxicity of both a large amount scenario (plastic bag milkshake) and a small amount (some in ocean water).

PE is not bothered by acids and there is no way humans have a pathway for it, except that for choking or being obstipated. But neither do bacteria or fungi make a dent in the molecule. That's why it's not degraded and collects in the oceans.


Commensalism with Virus bacteria Why people die of infection from microorganism, when germs can keep breeding for longer if they dont kill host?
Would not millions of years of evolution make germs evolve to not to kill human but feed on them just enough to not to kill them ?

Great question! In fact, some of the most successful pathogens (Herpes viruses are a excellent examples) have evolved with precisely this strategy. Herpes viruses have very low virulence, but infect nearly every human on the planet, and stick around for life.

But there's an evolutionary trade-off to this strategy. Herpes viruses have giant genomes (for a virus), because they need a ton of genes that counteract the immune system and perform other feats of cellular control so that they can stay dormant for long periods of time. While dormant (the technical term is "latent"), the virus is not transmissible, so while it persists  for a long period of time, they actually don't transmit very often.

Other viruses (influenza is a good counter example), are readily transmissible throughout most of their life cycle, but end up being cleared in a few weeks by most people. And yet influenza also spreads around the globe each year, so this also seems to be a pretty effective strategy.

It's really hard to ask questions like "why doesn't influenza behave like herpes?" When it comes to evolution, there are many successful strategies. Might as well ask, "why don't fish have feathers?" "Why don't sea birds have gills so that they can stay under water?" "Why aren't humans single-celled organisms?"


What species of flying insect is this? Resembles a fly with the wings of a dragonfly Locus: Vienna, Austria

Local Time : 12:24 today, 6th of January

Size: length approximately a large thumb. Width much smaller (pic).

Behaviour: possibly attracted by honey in my medicine, along with flies.

Insect ID from photos is difficult, but this is definitely in Syrphidae. The alternating thick and thin stripes on the abdomen resemble very much those in a picture I found here: https://alchetron.com/Episyrphus-balteatus
I would say that it is likely in the genus, Episyrphus, which is present in Austria.


How quantitative is the theory of evolution right now? We developed complex structures like eyes and brain, whose mechanisms rely on specific species of molecules and relevant chemical reactions. But we did not develop an enhanced night vision, the ability to fly, or a built-in silicon-based integrated circuit.

As I understand, we did not develop the latter set of abilities because they are either not so much needed, cost too much energy to be beneficial, or that they required so many information to be coded into our genome that it would take forever for the mankind to produce sufficient mutations. But could this be quantified? Can we tell if a species will develop a specific character, based on the environment they're in?

Can we tell if a species will develop a specific character, based on the environment they're in?

This is a major part of what quantitative genetics does. Or more detailedly, quantitative genetics can predict, for a population, changes in a trait given a selection pressure. First of all, for evolution to occur there must be variation in the trait you are making predictions about. Secondly the accuracy of the scale of the predictions matter greatly for the evolutionary model to be tested (eg, "Will body size increase?" vs "Will incisors increase 3mm in 300 generations?").

Several things have to be known to predict the evolution of a given trait:

The number of genetic sites controlling this trait (QTL, or quantitative trait loci). If the all the loci for a trait are known, the nucleotide heterogeneity within the population of those sites can be quantified. The number of genetic loci are important for estimating how often they will change from new mutations.
The effect of each genetic locus on contributing to variation to the trait (additive genetic effects).
The heritability of the genetics controlling this trait, (does the environment contribute to variation in the trait (low heritability) or do genetic differences cause more variation in the trait).
The strength and consistency of selection  (how fit are individuals in that environment along to phenotypic distribution compared to previous generations). Is this trait being selected in isolation, or are other traits which share the same QTL also under selection.
The effective population size.
The rate of migration between this and other populations.

So yes, given the our knowledge of quantitative and population genetic theory, predicting evolution of a given trait is possible. Just as predicting the future is possible with the laws of physics if you know the position of every atom in the universe. It's important to remember that organisms are constellations of 'traits', so predicting the evolution of all traits which make up the individuals within a species could be similar to predicting the futures of several multiverses.


Within and Between Allelic Class Diversity I am reading Charlesworth et al. 1997. They talk about diversity within and between allelic classes.

Nucleotide diversities ($π$) at each neutral site were estimated from the mean of $2 \sum z_t (1-z_t)$, over replicated introductions at the site of single variants, where zt is the frequency of the neutral variant at time t, and summation is over all times until either fixation or loss occurs.
The total genetic diversity at the neutral sites ($π_T$) was also decomposed into that within and between allelic classes at the polymorphic locus. Diversity within allelic classes, which will be written here as $π_A$, was estimated from the mean of $2 \sum \left( x_t(1-x_t)+y_t)(1-y_t) \right)$ where $x_t$ and $y_t$ are the frequencies of the neutral variant within the first and second allelic classes, respectively. Diversity between allelic classes with respect to the polymorphic locus was calculated as the difference between the total diversity values and $π_A$

Note that the parentheses don't match up but this this is what is written in the paper!
Why am I confused about this text?
I am confused about the term allelic class. I first think there is anything fancy in here and I think we can simply replace the term "allelic class" by "allele". but then when I saw the equation for $\pi_A$ I realize that the frequency of the two allelic classes does not necessarily adds to 1 (even though we consider only two allelic classes).
I also got also a little confused about the difference between $\pi$ and $\pi_T$ but I think that they just used two notations for the same think ($\pi = \pi_T$)
In population genetics's jargon, diversity just mean expected heterozygosity. $\pi_T$ makes sense to me. It is just the average heterozygosity $\left(2 z(1-z)\right)$ calculated over all time steps. Maybe a more intuitive to put it would to integrate rather than summing over time rather than time steps.
Question
I can read the equation for $\pi_A$ but I fail to get any intuition behind what it means. For example, I have no idea why it should be called within-allelic class diversity. Where does $2(x(1-x)+y)(1-y)$ come from? My whole issue might boil down to the definition of allelic class.
EDIT
The term allelic class is defined in Innan and Tajima (1997)

Suppose that there are two nucleotides, say A and T, in a particular site. Then, we can divide DNA sequences into two classes: one class includes sequences with A and the other includes sequences with T in this site. We call such a class an allelic class

(Slatkin 1996 might help as well).
I am still not quite sure what the within allelic class variance. Maybe it is: Take the most common sequence in the considered allelic class. For each, sequence, calculate the number of pairwise differences to the most common sequence and square this value. Sum over all sequence and divide by the number of sequences. In math form it would be: $\frac{1}{2N}\sum_i^{2N} (D_i)^2$, where $N$ is the population size and $D_i$ is the number of pairwise difference between the sequence $i$ and the most common sequence in the considered allelic class. Does it sound right to you?

The term allelic class is defined in Innan and Tajima (1997)

  Suppose that there are two nucleotides, say A and T, in a particular site.Then, we can divideDNA sequences into two classes: one class includes sequences with A and the other includes sequences with T in this site. We call such a class an allelic class

Two elements that were misleading (for me at least) in the article

Implicitly, in the paper of interest (Charlesworth et al. 1997), they define allelic classes for a site that is known to be under selection (and that can only be bi-allelic). The concept of allelic class is not for a polymorphic neutral site they look at but always for the same site (the one under selection).
The formula has an extra parenthesis. The real formula should be $2 \sum x_t(1-x_t) + y_t(1-y_t)$.

What is $x$ and $y$?

Consider a polymorphic (bi-allelic) locus (that is not under selection) and calculate the frequency of one allele in the first allelic class (defined for the site under selection) (this is $x$) and calculate the frequency of the same allele in the other allelic class this is $y$. In other words, consider the selected has two alleles $A$ and $B$ and the neutral locus has two alleles $a$ and $b$. $x$ is the frequency of sequences containing $A$ that also contain $a$ and $y$ is the frequency of sequences containing $B$ that also contains $a$.

Meaning of the formula

The formula is just the sum of the expected heterozygosity within each allelic class. $$2x(1-x) + 2y(1-y) = 2 (x(1-x)+y(1-y))$$. Then, we just have to sum over all time step during which the neutral locus is polymorphic and we get $$\pi_A = \sum_{i=1}^T 2 (x_t(1-x_t) + y_t(1-y_t)) = 2 \sum x_t(1-x_t) + y_t(1-y_t)$$, where $x$ and $y$ are now function of the instant (time) considered and $T$ is the total number of time steps.

What values can $\pi_A$ take?

This measure takes values between 0 and $T$ as all $x_t$ and $y_t$ take values between $0$ and $1$ (and therefore $x(1-x)$ and $y(1-y)$ take values between 0 and 0.5). Dividing the whole thing by $T$ will result in a measure that is bound between 0 and 1.

I would have not been able to understand without the help of @AMR. Thank you


Calling Alterations in Exome Data What are the main technical differences between accurately calling somatic point mutations vs copy number variation (CNV) in exome data? Side note: would you need other -omic data to accurately infer CNV (exome data isn't enough)?

Exome data can be used to determine both somatic point mutations and copy number variations.  The limiting element for the power of detection for both is read count (how many reads per gene).

Exome data:  Exome data uses a reference (for a trio, that would be parents; for cancer, that would be a paired normal sample from blood or non-invasive tissue) in order to determine if a certain point is mutated or not.  Next-generation sequencing is prone to sequencing errors, so having a high enough read count is essential to properly calling a somatic mutation.  Even so, issues with highly repetitive sites can make this difficult.

Using exome data for copy number is happening a lot nowadays.  The number of reads is used as a proxy for how many copies exist, and the balance of alleles at any given gene tells you whether there has been loss of heterozygosity.  Of course, with exome data, you aren't getting truly genomic data.  But there is enough coverage using the exome to pick up the big events.

CNV data: Copy number analysis is now conventionally done using a high density SNP (single nucleotide polymorphism) array.  These are designed to be biallelic, and come in two types.  First are the copy number SNPs, which are designed to give the best information about copy number.  Then there are the genotyping SNPs, which give information about loss of heterozygosity.  Often, SNP array data is higher quality, but this is determined by your platform.  Newer platforms have extremely high coverage of the genome and can allow you to really pick out focal changes.

These arrays, based on manufacturer's recommendations, are not meant to be used for somatic mutation calling.

As far as bioinformatic pipelines, you can use similar tools for each.  For example, the Aroma package in R has pipelines for both Exome & SNP array data.  GISTIC 2.0 from Broad can be used to find focal copy number changes.

A word of caution: It is always best to validate what you find in one platform with another.  I recently worked on a paper that used both Exome sequencing and SNP array data to determine copy number.  Using GISTIC, there were no focal peaks that matched.  The broad chromosomal trends were the same, and that's what the group reported.


Inheritance patterns in individuals with triploidy If you search on the genetics of Down's Syndrome, you'll find plenty of results explaining the genetic mechanisms which can result in triploidy. However, I can't find any information on the inheritance combinations of triploidy - i.e. what are the possible genetic outcomes in the event that an individual with triploidy should reproduce.

It might seem unlikely, which is presumably why it's glossed over. However, I'm just curious about it from an academic standpoint.

So: how does one calculate the inheritance probabilities for a trait associated with triploidy, and what are the outcomes?

Triploids are characteristically sterile, but people with Down's Syndrome aren't triploid(they're anueploid technically). There's only one chromosome duplicated, and it's the smallest one. Women with Down's can have kids just fine, but men tend to be sterile(according to WebMD at least).

See here for a full coverage of triploid genetics and why triploids are nearly always sterile. In short: gametes formed during meiosis pair off but there's always one copy of each chromosome that chooses a daughter cell at random. If one daughter cell gets none of the extra copies, you have a haploid gamete and a diploid zygote and everything goes according to plan. If one daughter cell gets all of the copies you have a diploid gamete and you'll have a triploid zygote and everything will be fine-ish, but you'll have another triploid generation.

Statistically this happens for 2(1 for females with asymmetric gametes, but let's fudge it a little) of the possible sorting patterns, of which there are 2^n where n is the number of chromosomes. For a triploid human male(bear with me) mating with a diploid female(the best possible combination mathematically) instead of the more typical 200 million viable sperm he would produce about 50 viable sperm(About 2 in 8 million sperm have a chance.). If you account for 23-triploidy that number goes up to about 100, but that's still worse than a millionth of the fertility.

Other combinations are vastly worse. A human female only has about 2 million eggs lifetime total, so even in the best of circumstances a triploid female has maybe a fifty fifty shot at having a single viable egg in her entire life. The calculation for the probability of a two triploid humans(or any n=23 organism) breeding successfully is left as an exercise for the reader but it's very low indeed.

If you were working in some other organism with maybe n=2 chromosomes the numbers would be more forgiving and it might be worth thinking about making Punnet squares. They'd work much like Punnet squares for diploid creatures, but the sides would be a little longer to accommodate the larger number of gamete genotypes, and you'd have to adjust the probability of some of the squares to account for aneuploidy-related fatalities and other weirdness. For instance, with two triploid parents the probability of getting a successful triploid zygote from any random pair of zygotes is something like 1/2^n instead of the 4/2^2n or whatever it is for diploid or quadruploid offspring. This is counterbalanced by aneuploid gametes perhaps dying(or even being slightly less fit).

If n=1 the math is more tractable, however(surprisingly, this exists. haplodiploidy complicates triploidy considerations so I'm pretending it doesn't exist). Examples like AAaxAa give strange results(only 1/12 are recessively phenotyped) but AaaxAa produces 1/4 recessive phenotypes and 3/4 dominant ones, just like AaxAa.

In sum, I see why triploids are just declared infertile and not dealt with in the fullest, most complex sense.


What is the difference between sieve cells and sieve-tube elements? I looked it up and I'm still confused. Apparently, sieve cells lack sieve plates? What does that really mean? It's difficult to find a good picture of either.

All plants have sieve cells, but not all plants have sieve tube elements because they evolved after the plant family tree had started to branch. Only angiosperms have sieve tube elements.

Sieve tube elements are more specialized for their job as transport cells, and can transport more nutrients faster than sieve cells. During their development, the meristem cell divides into two cells: the sieve tube element and the companion cell. The sieve tube element loses its nucleus, vacuoles, and ribosomes when it matures in order to make it easier for its cytoplasm to flow, and so it relies on its companion cell for proteins and carbohydrates. The porous plates between sieve tube elements provide little resistance to water and nutrient flow, and so flow through the sieve tube is more rapid than it would be if there were cell membranes or small pores for it to pass through. The sieve tube elements are wide to make wide tubes, which provide less resistance to fluid flow.

Sieve cells evolved before sieve tube elements, and are a bit less specialized for their job. They still have all their organelles, and are long and thin. Some plants, such as seedless plants and gymnosperms, don't have any sieve tube elements and rely solely on sieve cells for nutrient transport.

References:
Organelles present in sieve tubes
https://en.wikipedia.org/wiki/Sieve_tube_element


What is the function of the RNA primer in DNA replication? During DNA replication, RNA primase puts an RNA primer in the lagging strand. What is the function of this RNA primer? Why can't the enzymes put DNA fragments directly?

DNA polymerases need a primer oligonucleotide (RNA or DNA) - their substrates are an existing 3'-OH group and a dNTP. The primase however is a typical RNA polymerase, capable of initiating polynucleotide synthesis de novo by positioning a complementary ribonucleoside 5'-triphosphate opposite its complementary DNA base. The primase makes an RNA primer that the DNA polymerase can then use for chain extension. The RNA primer is ultimately degraded and replaced by a DNA polymerase.

The rationale for this difference is that DNA polymerases have an active site that is geared towards proofreading and that primerless initiation would be an error-prone process. By having the primers 'tagged' by virtue of them being RNA, it is possible for the replication machinery to use them but then replace them with a high fidelity DNA copy of the template strand.

Edit in response to OP comment:
Synthesis of the leading strand consists of extending an existing DNA. However the leading strand is also originally initiated, at the ori element, with an RNA primer. Once that first initiation event has taken place the synthesis of the leading strand is simply a process of extending that original primer.

Some viruses employ ingenious variations on this theme such as using tRNA primers , or proteins - see Wikipedia.


Does digestion require hydrochloric acid? Would our digestion function any differently if we secreted something else, like sulfuric or nitric acid, instead? I'd assume an acidic environment may be required, but not sure if chloride is also required as well!

Perhaps we just use it out of convenience—e.g., presumably blood serum $$\left[\ce{SO4^2-}\right] + \left[\ce{NO3-}\right] \ll \left[\ce{Cl-}\right]$$ and channeling polyatomic ions across the membrane may be significantly more difficult than doing the same for chloride as well!

*Edit: In fact, Wikipedia states

  In the stomach, chief cells release pepsinogen. This zymogen is activated by hydrochloric acid (HCl), which is released from parietal cells in the stomach lining. The hormone gastrin and the vagus nerve trigger the release of both pepsinogen and HCl from the stomach lining when food is ingested. Hydrochloric acid creates an acidic environment, which allows pepsinogen to unfold and cleave itself in an autocatalytic fashion, thereby generating pepsin (the active form). Pepsin cleaves the 44 amino acids from pepsinogen to create more pepsin.

So, while maybe something like $\ce{H2SO4}$ or $\ce{HNO3}$ could work too, hydrochloric acid is just more convenient to use?

Parietal cells use ion pumps to expel protons and chlorine ions into the lumen, which create the necessary acidic environment to denature pepsinogen into pepsin.

It is the low pH environment that reconfigures or denatures pepsinogen into pepsin. The acid used does not matter. For example, one experiment in classifying properties of pepsinogen used a 3.5 pH solution of 0.5 N sulfuric acid to activate pepsin.

We evolved stomachs with parietal cells that use an energetically expensive process to maintain the acidic gradient necessary for digestion and protection from pathogens.

It may be that biochemical pathways to generate other acids did not evolve, because it is either energetically cheaper for these cells to make HCl, compared with other pathways that would generate other acids of sufficient strength; or the relevant chemical components involved are more abundant than others in what we eat and drink, and thus easier to make in quantities needed for digestion and defense. Chloride ions also serve a role in maintaining intra- and extracellular fluid pressure and thus play a larger part as electrolytes in the normal function of the body — they are available and cells use them.

But to answer your main question, an acidic environment activates pepsin, and it is not chemically necessary for this to be created by hydrochloric acid.


How do we call a region of low carrying capacity? I am looking for a convenient word to define a region of the landscape where the  local carrying capacity (population size) for a given species is low but different from zero. The species is still present in this zone.

How would you call such area?

If you ask about quantity/numbers only, I would suggest using "the zone of low population density" or "intermittent zone" which in turn borders the "buffer zone" and "the zone of intermediate/high population density".

The "buffer zone" is the zone between two different populations where the number of the animals in question is zero.

J.Potts, M.Lewis "How do animal territories form and change? Lessons from 20 years of mechanistic modelling"

There are other classifications based on the "main usage" of the territories.


A career in synthetic biology So I am thinking about a career in synthetic biology, but I am not sure what route should/needs to be taken. I don't want to do technician work--I want to be involved in the planning. Y'know, the exciting stuff. :)

I'm wondering whether I should go for a Master's or a PhD (or is a Bachelor's enough?)

It's a young field, so I'm having trouble finding this kind of information online. Any help would be much appreciated!

I think that "career in synthetic biology" and "involved in planning" both express very vague ideas. There are significant differences in what you will be able to do with a Bachelor's, Master's or PhD, depending on what exactly you end up doing.

I entered a PhD program in biology for no better reason than that I felt awed and fascinated with science and had done really well in science subjects as an undergrad. Grad school seemed like a natural extension of that effort.

In retrospect, my motivations for pursuing a PhD were horribly naïve and easily the greatest challenge that I faced as a grad student was that of defining why I was there and where I wanted to go with my degree. So, to address the issue of vagueness in your question, my first piece of advice is to have a firmer idea of what you want to do. Plans will change, but simply having a plan (a real plan) might provide an anchor when you need one.

As to what you can do with the various degrees, I can't precisely answer your question, the way you've phrased it, but I can give you a general idea.

A bachelor's degree in biology will not get you far in a lab setting. Among the lab techs I've worked with, even most of them have master's degrees. From what I've seen, this holds just as true for academia as for industry.

It's a little unclear what you mean by "planning", but most of the admin that I work with, who are involved in planning our various projects also hold advanced degrees, typically in science, business or public health. I see a strong representation among the management at my institution (Columbia University) of PhD scientists, who left the bench for something less life-consuming, while still wanting to have a hand in research. These people are frequently grants managers or program directors.

As I mentioned earlier, the lab techs around me generally hold master's degrees. When I was considering quitting my PhD program after the master's component, a friend in industry advised me against it, if I ever thought that I might seek work in industry. The picture that he painted was that in industry, a master's degree makes you overqualified for many of the tasks that you can expect to be hired for, but underqualified for significant future career advancement.

Obviously, you shouldn't feel limited to academic vs industrial research tracks. There are plenty of other options out there. Maybe look up people's blogs that involve synthetic biology or whatever other topics of interest you might have to get a wider view of what people who have expertise in the subject are doing.

Good luck!


Is it possible to transfer acquired hemophilia with breast milk? There is a transplacental form of acquired hemophilia: http://www.jpeds.com/article/S0022-3476%2895%2970132-X/abstract

This disease is caused by polyclonal immunoglobulins (IgG1 and IgG4) against the A2 and C2 domains of factor 8. So acquired hemophilia is an autoimmune disease. By the transplacental form the maternal IgG antibodies causing this disease in the newborn. As far as I know IgG antibodies are transferred with breast milk too. Can breast milk cause this disease?

Acquired Hemophilia is an AutoImmune Disease, hence it is possible to transfer it from mother to child through breastfeeding milk. The antibodies subjected to autoimmune disease also passes into the infant or baby from breastmilk in addition to the healthy antibodies. These abnormal antibodies will act as an inhibitor to the enzyme responsible for production of Factor VIII , a blot clotting protein. Less number of factor VIII protein results in increased amount of internal bleeding.


How are non-glucose sugars metabolized in the body? In my biology book's section on disaccharide metabolism and glycolysis, it states that sugars other than glucose must be acted upon to enter glycolysis. Let's take sucrose as an example. Sucrose is hydrolyzed in the small intestine by sucrase. The resulting fructose and glucose are absorbed and transported to the liver via the portal vein. My question concerns the fate of fructose.

To undergo glycolysis, the book states that fructose is converted into either fructose-6-phosphate (F6P) or fructose-1-phosphate (F1P). Let's say it is converted to F1P. Aldolase splits this into dihydroxyacetone phosphate and D-glyceraldehyde. Triose kinase then converts D-glyceraldehyde to glyceraldehyde-3-phosphate, a glycolytic intermediate. Where is this occurring in the body? Are we still in the liver? I can't imagine that all the fructose we consume is undergoing glycolysis in the liver. To leave the liver as a sugar, it would have had to been converted to glucose, right?

In classes I've taken, I've been told that sugars that enter the liver are pretty much all converted to glucose. Once they are converted to glucose, they can be distributed to the rest of the body, stored as glycogen, etc. If we are going straight from fructose to F1P to a glycolytic intermediate, we couldn't have left the liver. How is such a transformation even useful? Anyone care to shed some light on this?

Where is this occurring in the body?

Almost totally in the liver.

To leave the liver as a sugar, it would have had to been converted to glucose, right?

Correct, but it's not a direct conversion.
Fructose is metabolized almost completely in the liver in humans, and is directed toward replenishment of liver glycogen and triglyceride synthesis...
...Increased concentrations of DHAP and glyceraldehyde-3-phosphate in the liver drive the gluconeogenic pathway toward glucose-6-phosphate, glucose-1-phosphate and glycogen formation. It appears that fructose is a better substrate for glycogen synthesis than glucose and that glycogen replenishment takes precedence over triglyceride formation. Once liver glycogen is replenished, the intermediates of fructose metabolism are primarily directed toward triglyceride synthesis.
So, Fructose is almost entirely made into something else first, and then that something (Glycogen or the Glycerol from triglycerides) gets broken down into Glucose or an intermediate.
Fructose stays in the liver because Fructokinase has a pretty low Km (0.5 mM) compared to Glucokinase (12mM) for Fructose, so almost all of the Fructose that enters the liver is phosphorylated into F1P - which cannot leave.


Can humans eat grass? Can a human eat grass and digest it?
Could it be possible to use it as food just like other plants such as wheat or beans?

To elaborate on A random zoologist's answer, the problem is that the human digestive system does not contain any cellulase enzymes. Cellulases are a class of enzymes that break down cellulose, the chief structural component of plants.  You might be able to obtain a small amount of nutrition from grass or other cellulose-rich materials, but as the plant cell walls are made of cellulose, most of the plant material will be indigestible.


Downstream analysis after in vivo pathogen RNAseq We performed RNA-Seq of in vivo bacterial samples and identified some key up- and down-regulated pathways.

We compared bacteria during infection with conventional agar plate.

Which could be the next steps to validate our findings? We are interested in antibiotic and vaccine developemnt.

Okay, first, I would say to everyone planning a high-throughput experiment: Hypothesis first, then experiment. Otherwise you're setting up an expensive and time-consuming test that's not going to answer the questions you want answered.

In this case, the question your experiment is designed to answer is "What genes are crucial to growth in vivo that are not crucial to growth on a plate?", which is probably not the clearest model for vaccine/antibiotic design.

I guess you could say that a difference between the plate sample and the in vivo sample is the presence of a host, and therefore it's possible that upregulated pathways represent the bacteria's host adaptation, and maybe you can attack the bacteria by attacking its ability to colonize the host. A gene involved in immune evasion could make a good target.

(That's a very messy model, as there are tons of other differences going on, but since you've already run the experiment it's probably the best you've got.)

So then, use your data for a new round of hypothesis generation. Take your pathways and come up with a way that they might be allowing the bacteria to adapt to the host-- maybe a secretory pathway that could be interfering with the target immune system, or some membrane signalling molecules that get upregulated, or whatever.

Now you have a hypothesis, so design an experiment. For instance, take a key upregulated member of a pathway. The hypothesis is that it's crucial to growth in a host but not to growth in general. So, knock it down, either with chemical inhibitors or with genomic editing, and see if it's less effective at host colonization.

(Although host colonization effectiveness is pretty difficult to measure ethically if your target organism is humans. But you have some sort of proxy or model system to measure that, right?)


what is the difference between early blight of potato and late blight of potato? apart from different fungus causing these diseases in potato, how are Early Blight of potato and Late blight of potato different?

Some Differences are listed here

Please consider reading these articles (article 1, article 2)


Plasmid with ITPG and pBR322 ori I'm looking for suggestions as my internet searches aren't turning up much.

I'm trying to find a plasmid that has the pBR322 origin, as it's low(ish) copy number and can tolerate large inserts. Additionally I need the plasmid to be inducible with a system other than the pBAD setup (e.g. IPTG would be fine, but if there is one that is more tightly repressed that would be preferrable as IPTG is leaky).

Lastly, I could do with it having a potentially obscure resistance cassette, but this is less of a problem.

Any help appreciated.

The pET vectors family is what you are looking for.


How loud a sound would need to be to wake someone up? I have been researching about this and it looks like the term would be auditory arousal threshold. Imagine you fall asleep while listening to music with earbuds. Out of a sudden, the device starts playing really loud music (let´s say 40 dB higher compared to what you were listening). This sound would be quite loud that it would damage your ears.
My question is, is there any study showing which would be the minimum dB level of a sound that would make you wake up (and, well, remove the earbuds)?
I would assume this would depend on the frequency of the signals as well. But, what about the age of the person?

I think a SIREN sound with higher Decibel >110 will work. Because as a human being, a high pitch sound create alert signal to our brain.
Still, the sound to wake up a person will vary from person to person.
But a person will definitely react to eardrum piercing sound waves