determine longest poly-purine tract how to determine/ find the longest poly-purine tract in any genome  and this needs to be on the E. coli genome . is it to figure out the polypurine tract and then figure out the longest chain ? or is it to splice the introns and exons away from the DNA ? since E. coli's genome is 4.6 million BP long, i need some help in breaking this down ?

Code Golf!

This is my Python script, avoiding regex and not at all prettified.

def gettract(strand):
    #if strand is 1 then replace C with T and split on T
    #else replace A with G and split on G

    if strand==1:
        print 'top strand purine tracts:'
        aseq=seq.replace('C','T')
        tracts=aseq.split('T')
    elif strand==2:
        print 'top strand pyrimidine tracts:'
        aseq=seq.replace('A','G')
        tracts=aseq.split('G')
    sortedtracts=sorted(tracts,key=len,reverse=True)
    for i in range(5):
        print len(sortedtracts[i]), sortedtracts[i]

f=open('ec_dna.txt','r')
l=f.readlines()
print 'Sequence analysed is %s' % l[0][1:] #the header line
f.close()
seq=''.join([i.rstrip() for i in l[1:]])
print 'sequence length is %i' %len(seq)
print
gettract(1)
print
gettract(2)

And here is the output:

  Sequence analysed is E. coli K-12 MG1655 U00096.2 (1 to 4639675 = 4639675 bp)

  sequence length is 4639675

  top strand purine tracts:

  28 AGAGAGAAAAGAAGAAGAGAAAAGAAAA

  22 GGGGGAGAAAGGGGGGAAAAGG

  20 AAAGAGGAAAGGGGGGGGGG

  20 GAAGAGGAAAAGAAAGAAGG

  20 AAAAAAGAAGAGAAAAAAGA

  top strand pyrimidine tracts:

  29 TTTTTCTCTTTCCCTTTTCCCTTCCCTCT

  22 CCCTCCTCTTCTCTCCCTCCCC

  21 TTCTCCTCCTTCTCTTTTCTT

  21 TTTTTCTTCTCTCTTTTCCTC

  21 CTCCCCTTTTCCCTTTTCTCC

The longest purine tract is 29 bases long, and is on the bottom strand.

This script doesn't handle the problem that the E. coli genome is a circular molecule, so if the longest tract was split at the origin it would be missed - I leave that and obtaining the coordinates of the longest tract as an exercise.


This strange looking thing was on the leaf, can you identify what this is? I found this today on one of the plant that I grow in the container at home. I cannot identify what kind of insect it is.

That is a butterfly chrysalis. Since it is clear, and you can see the wings, it is about to emerge. A chrysalis is the naked pupal stage of a butterfly, as opposed to a "cocoon", which is covered in silk.


How to promote acorn maturation I have acorns from an oak tree. They look like:

but I would like to speed up their maturation so they split and I can separate the caps:

How can I speed up this maturation process?

I would suggest putting them in the ground and watering them (Factors affecting acorn production and germination and early growth of seedlings and seedling sprouts).


Log-tranformation and GWAS Before doing any GWAS (genome-wide association study) it is necessary to check for the normality of the phenotypic distribution. If the phenotype is normally distributed only once it is log-transformed, what phenotypic data do I have to use while doing the GWAS? The non-transformed one or the log-transformed?

Yes, use the log-transformed phenotype. if you want to use a normally distributed error term, and this will only occur if the phenotype is log-transformed, then you must log-transform the phenotype.

The phenotype should be distributed in the same manner as the error term in your regression model of the GWAS.

$pheno = \beta_1 X_D + \beta_2 X_A +\epsilon$

$\epsilon = \mathcal{N}(x | \mu,\sigma)$

Following the central limit theorem, most of phenotypes are normally distributed.  However, there are cases where a Bernoulli distribution is correct, and a logistic style regression should be used.


Could a mammal convert ingested dissolved CO2 to usable energy? I'm trying to find out if it's possible that a mammal could orally ingest dissolved CO2 and convert it to energy for body heat, organ function, etc.

Unfortunately, most of the scientific sources I've been able to find talk instead of CO2 gas inhaled by mammals. All the sources speaking to orally ingested dissolved CO2 begin their argument with the assumption that all of it is converted to (and expelled as) gas in the digestive tract, but they never bother to prove that or cite anything.

It seems like this would rarely be observed in nature, and therefor not really be studied or documented, so I'm curious what degree of chemical or biological certainty there is about this, and what research has been done.

There isn't any biologically useful energy in CO2. In fact, humans and all other animals produce CO2 as a waste product at the end of metabolism specifically because it is low-energy. You don't need to ingest it or breath it in as a gas, and if you didn't breathe it out you would die.


Beta Sheets vs Alpha Helix - Strength Is there a hard and fast rule of which one is stronger than the other, or does it depend on their context in a protein?

The mechanical stability of a protein (I am assuming by strength you mean mechanical stability) depends greatly on the general context and there is no clear connection between alpha helix or beta-sheet content and stability. For example fibroin, one of the main components of spider silk and one of the strongest proteins known, consists mainly of beta sheets while keratin another very stable structural protein (the stuff hair and fingernails are made of) consists of four alpha helices alternating with three beta turns is believed to get most of its strength from hydrophobic interactions within its alpha helices. Also, actin and myosin muscle fibers consist mainly of alpha helices. The list goes on and on with no clear pattern which secondary structure forms more stable proteins.


What are the exceptions to Mendel's laws? What are the exceptions to the $-$

Law of dominance
Law of independent assortment
Law of segregation

My knowledge:

Exception of law of dominance:

Incomplete dominance

In incomplete dominance when a red snapdragon flowered plant is crossed with a white flowered plant an intermediate phenotype appears in the F1 hybrid instead of a parental phenotype.
Codominance

Unlike dominance in codominance when a A ($I^AI^A$) blood group individual mates with B ($I^BI^B$) blood group individual the offsprings have blood group AB ($I^AI^B$) instead of A or B.

Exception of law of segregation:

Nondysjunction

During meiosis homologous chromosomes/sister chromatids and hence genes may move to a common gamete violating law of segregation.

Exception of law of independent assortment:

Linkage

When genes are present on the same chromosome they tend to remain together and enter into the same gamete. This is the reason behind deviation of dihybrid test cross ratio from 1:1:1:1 and occurrence of parental combination in high frequencies.

Am I correct? Are there any more exceptions to these laws?

You are right but the list is certainly not exhaustive. Here are a few more concepts you may want to consider.

Exception of law of dominance:

epistasis

Allelic effect at a given locus depend on the variants at other loci
environment dependence and specific case of frequency dependence

The concept of dominance can be used for any quantitative trait. Typically, when the quantitative trait of interest is fitness, then the trait often depend on the environment. A typical and interesting case is when the fitness depends on the frequency of alleles in the population. Depending of the frequency of the allele at a given locus, the relationship might be a relationship of dominance, additivity or dominance for the other allele.

Exception of law of segregation:

meiotic drive

from wiki: "Meiotic drive is a type of intragenomic conflict, whereby one or more loci within a genome will affect a manipulation of the meiotic process in such a way as to favor the transmission of one or more alleles over another, regardless of its phenotypic expression. More simply, meiotic drive is when one copy of a gene is passed on to offspring more than the expected 50% of the time."

Exception of law of Independent assortment:

epistasis for fitness

Imagine a case where a given combination of allele is lethal at very young age, then you would never see these two alleles together in an individual. It is per se, not a case of exception to independent assortment but it gives the feeling of such exception. A case more extreme when a given combination of alleles prevents fecundation could however be considered as an exception to independent assortment.


What is the fastest growing bacterium? E. coli has a generation time of about 20 min, and a single CFU will generate a colony a few millimeters in diameter after 16 hours of incubation.

Is this the upper limit? How much faster can bacteria grow? How much faster can colonies grow?

The article and published work here and here respectively, reveals that E. coli replication is close to thermodynamic limits of efficiency having modelled this process using mathematical equations. However an interesting article and published work here and here, respectively reports a bacteria (homologous to Thermobrachium celere and Caloramator indicus, which are closely related) with doubling times as short as 10 minutes have been discovered in areas of hot water emissions in Lake Tanganyika.

  Small chimneys emitting hot water at temperatures of 66 to 103 degrees Celsius (150 to 217 degrees Fahrenheit) have been discovered at the shallow lake bottom of Lake Tanganyika, East Africa. In a study searching for thermophilic sulfate reducing bacteria in this extreme environment, a spore-forming bacterium was discovered that grew with a doubling time as short as 10 minutes. In theory, a single cell of this bacterium in this environment can multiply to 500 million in less than 5 hours under optimal conditions (60 degrees Celcius).

EDIT: If the question is exclusively about E. coli and it takes into account laboratory conditions then I also came across this references page claiming tha E. coli doubling time is between 4-20 minutes. Based on this paper the page reports that

  Internationally renowned researcher Bernhard Palsson and other researchers from the University of California San Diego led a team of scientists from PNNL, the University of Heidelberg, and the German Cancer Research Center to study how E. coli bacteria changed and evolved from one environment to another in a laboratory setting. The team then compared proteomics, genomic, and metabolic data from the study with a computational model for bacterial growth.

The page then goes on to say

  Using high-performance liquid chromatography coupled to mass spectrometry, the team gathered data on how the bacteria changed their protein profile as they grew and reproduced in different mediums. The scientists found that the data and model were correlated to a surprising degree (more than 98% in some cases), validating the model's ability to predict the growth of E. coli bacteria under specific conditions.

This confirms the comments above that the growth rate of E. coli depends on the specific conditions in which it is in and furthermore its growth rate under specific conditions can be predicted based on the devised model.


What medical and commercial proteins are made using genetically modified animals? Recombinant technologies in micro-organisms being used to produce commercial and medically useful proteins like insulin are fairly common.

However some proteins are still produced commercially in genetically modified animals. Why are animals a better choice than microorganisms, and which are the most common proteins produced this way?

ATryn is a human antithrombin produced in the milk of transgenic goats by GTC Biotherapeutics. It has FDA approval and I believe that it is available for prescription in the USA.

Added later, after the emphasis of the question changed somewhat.

Proteins produced in a mammalian system are more likely to have post-translational modifications that are much closer to those found on the human protein. Antithrombin, for example, has four disulphide bonds and four glycosylation sites. Although it is reasonable to assume that the disulphide bonds would be correctly formed in a eukaryotic microorganism, the same isn't true of the glycosylation: microbial glycans differ from mammalian glycans, and these differences could affect the stability of the protein in the mammalian bloodstream, or the response of the mammalian immune system to the protein. Mammalian cells in culture could be used but are, of course, quite fastidious. So the holy grail of recombinant protein production has always been to get the protein secreted into an animal's milk, allowing the use of very cheap feedstocks and the easy harvest of the protein over a period of years, notwithstanding @shigeta's remarks.


Is the sex of siblings mutually independent? I am studying probability, and one of the lectures I came across (Skip to 52:00) states that the sex of siblings is not mutually independent and that there is some correlation.

Can anyone tell me why? And if so, where is the evidence?

There is at least one paper that claims this:

  A test for heritability of the sex ratio in human genealogical data is reported here, with the finding that there is significant heritability of the parental sex ratio by male, but not female offspring.

--Trends in Population Sex Ratios May be Explained by Changes in the Frequencies of Polymorphic Alleles of a Sex Ratio Gene. Corry Gellatly, Evolutionary Biology 36:190-200, 2009 DOI: 10.1007/s11692-008-9046-3.

In other words (simplistically) some families are more prone to have male offspring, which implies that the probability of male offspring is not independent.  However, this is a hypothesis, not a proven fact, and I think it's not a very strong hypothesis.

A non-scholarly, but apparently careful, discussion is here:

  The odds of having a girl seem decrease after having each boy, but only very slightly. Even after 3 boys, you are only 6.4% more likely to have a 4th boy than a girl.

What are the odds of having another boy or girl?


How did people's liking of ceremonies evolve? Habitual group activities are prevalent across many animal species, particularly in mammals, especially in primates.

However, I do not see any evolutionary benefit of this. 'Ceremonies' take time, and in many cases seem to exert more energy than they reap. Note at this point I am not talking about hunting groups, but rather about group activities that serve a purely social purpose (mourning is a  good example of this and is present in elephants, chimpanzees, bonobos, and probably more). This costs significant amounts of resources, time, and energy which apparently could be better spent hunting, foraging, traveling, mating, or grazing.

I'm interested in finding a timeline, and explanation, of why and how this phenomenon of higher social rituals (perhaps using mourning as an example) evolved throughout the mammalian kingdom.

A cursory google revealed nothing about how this 'liking' of interaction evolved.

Perhaps customs (and culture as a whole) arises to some extent as a result of relationships between individuals of the same species. For example, I think a good example of a custom is how elephants bury their dead. This does not benefit the surviving elephants in any noticeable way, and is a "waste" of energy and time. If customs do arise because of a group dynamic, then there is clear evidence supporting that social behavior in higher organisms (chimpanzees, dolphins, etc.) does increase fitness.

However, this speculation is based upon the idea that customs are a natural result of social interaction. As to why these customs arise, perhaps it is because it enforces the group dynamic over the participating individuals.


Did we first have swimming birds or flying birds? Looking at the swimming birds building nests just across my garden, I suddenly wondered how evolution came to swimming birds and whether flying birds started swimming or whether swimming bird like animals started flying.

What came first and when and why?

Flying came first, as far as we know. The earliest known bird (currently), Archaeopteryx lithographica, already had aerodynamic feathers (Feduccia and Tordoff, 1979). The Solnhofen Limestone, where it was discovered, is ~145 million years old, so we can place the "when" flight evolved to greater than or equal to that time.

Gansus yumenensis is regarded as the earliest aquatic bird and is dated from ~120 million years ago. The Hesperornithiformes are the sister taxon of Gansus (less derived) and also aquatic. However, they date from ~85 million years ago. It is not clear whether the ancestors of Hesperornithiformes were also aquatic. Because they branched off the main line of birds before Gansus, these ancestors would likely predate Gansus, but those relatives have not yet been discovered.


Why are so many spermatozoa produced when only one of them fertilises the ovum? During fertilisation only one sperm can fertilise the ovum. So why so many millions of sperms are produced?? Isn't this a waste of energy?

Short answer : Sexual selection with sperm competition

However this answer will vary depending on which species you are referring to. When female mates with multiple males (like in many insects), sperm competition increases male's chances of getting his genes forwarded to next generation. When there is not much rival competition with other males (like in humans) this has correlation with mate guarding behavior and quality of sperm.


What is the convention for log notation in biology? I'm reading through some oldish (1980s) papers on length-weight relationships in fish and crustaceans. Many report log-log relationships without specifying whether this is natural log, base 10, etc. In mathematics log is typically assumed to mean natural log, but the results reported in these papers make more sense if you assume "log" means "log base 10".

Is there a convention in biology that I should be aware of?

There is a reason for prevalent usage of log2 and log10 compared to loge in biology and other experimental sciences. Usually while doing measurements we are generally interested in fold changes and we generally talk in the sense of two-fold (or multiples of two) or ten-fold.

Doubling is a common phenomenon at least in case of growth and so a two-fold change would represent an event of doubling. log2 gives you the extent of "doubling". Even in computer systems memory is always in the exponents of two (because of binary); so even there log2 would make sense.

In biology you would generally not see a ten-fold change but in physics it is relatively common. Most values are represented in scientific notation which basically uses an exponent of 10. Also the metric units are in multiples of 10. Here log10 would be more suitable.

loge has a special mathematical importance i.e. it can be denoted as a series. The euler's number has other important properties too. Therefore in most theoretical studies, both in biology and physics, loge is preferred because it makes more mathematical sense.

To sum up, experimentalists prefer log2 or log10 because they are better for representing measurements whereas theoreticians prefer loge because of its mathematical importance.

W.r.t the old paper that reports log-log relationships, the base of the logarithm wouldn't make any difference to the slope. But most likely it must be log10 (I think back then log10 was the default log; log2 would be much more suitable for lengths and weights of organisms compared to log10 because these measures would not vary in multiples of 10).


Essential amino acid codons Essential amino acids also have codons.Still they are needed by humans through diet?Will those codons do synthesize amino acids for some other purposes in humans or not?If so, what is the purpose?e.g?

You are mixing things. First: Codons have nothing to do with the synthesis of amino acids.

A codon is the sequence of nucleotides on the DNA (or RNA) which code for a certain amino acid. For example UGU and UGC code for the amino acid Cysteine and given these codons it will appear in the protein being synthesized. The codons are basically a way to code the sequence of a protein with the smallest amount of information (simply by the sequence of the four nucleotides in DNA/RNA). For further information have a look at the Wikipedia page on Codons.

This look like this (image from the Wikipedia):


Why do live crabs in a bucket prevent each other from escaping? It has been observed that crabs in a bucket will stop others from easily escaping. This observation has lead to the English language colloquialism crabs in a bucket. Has this phenomena been studied? What are some animal psychology explanations of this?

There should be a dictum somewhere that states, "Never ascribe to psychology what is caused by instinct."

By that I mean, the captured crab has a survival instinct. It's not going anywhere on the bottom of the bucket; it needs (I don't even know if I would say, "It wants") to get out. Out means "up", since "sideways" doesn't get them out, which doesn't prevent them from trying that as well (as shown by scuttling around the bottom repeatedly.)

The sides of the bucket are slick; there's nothing to grab onto. So if one crab climbs atop another, suddenly there's something "above" (a shadow? An outcropping? Another crab?) to grab onto to hoist itself up the side. So the crab instinctually grabs onto something above it. Unfortunately for the higher crab, there's nothing for it to hold onto above it, so he falls back into the bucket.

If only they would work together, a few of them might make it out. If they were chivalrous, the females and the young ("women and children") would go first.

I don't really know crab psychology, nor do I know any crustacean psychologists. All kidding aside, however, there have been some attempts to study stress in crustaceans. Science Daily published an article about stress in declawed crabs. What you and I think of as "stress" may be different than how the author thinks of it, but from the article, it's pretty clear that Dr. Elwood means psychological stress. However, there is no evidence to support that; the increased mortality of declawed crabs is more likely to be due to physiological stress (as in the second cited paper.) He has been called out on this by fellow biologists.

Crabs are invertebrates. If you want to learn about invertebrate psychology, the octopus is your animal.

Declawing Crabs May Lead To Their Death
Assessing Stress and Predicting Mortality in Economically Significant Crustaceans


First genomic survey of human skin fungal diversity "The researchers found that a single type of fungus, belonging to the genus Malassezia, is predominant on the head and trunk. Hands, which harbor a great diversity of bacteria, are home for relatively few types of fungi. In contrast, feet, including toenails, heels and toe webs contain tremendous diversity.

"Applying DNA sequencing to a study of the skin's fungi is the natural progression in understanding microbial life that co-exists on our bodies," said NHGRI Scientific Director Daniel Kastner, M.D., Ph.D. "Along with recent genome sequencing to define bacterial diversity, this analysis of fungal diversity provides a more complete human microbiome picture."

"Fungal communities occupy complex niches, even on the human body," said Heidi Kong, M.D., co-senior author and an investigator in the dermatology branch of NCI's Center for Cancer Research. "By gaining a more complete awareness of the fungal and bacterial ecosystems, we can better address associated skin diseases, including skin conditions which can be related to cancer treatments.""

Source

Is there another reference for this research please?

The link is given at bottom of the article that you linked to. It's a Nature paper so you need to have access rights.


Microscope scale bar In some microscopic images, there is a bar scale at one of the corners or near a specific object. How are they added to the images? Does the slide have some markers, or are they digitally added? If so, how are they computed? I am planning to buy a microscope and wondering is there something I should look for. Thanks for any help!

There are two common ways to generate a scale bar:

Measure it.  You can take a picture of an object with known spacing such as a grid target and then measure the size of each pixel.
Compute it.  If you know the magnification of your objective, and the magnification of any relay optics after the object but before your camera, you can compute the total optical magnification.  Then using the pixel size on your camera, you can get the actual pixel size.  For example, suppose you have a camera with 7.4 micron pixels, a 20x objective, and a 0.5x adapter lens before your camera, then you would have a pixel size in your image of 7.4/20/0.5 = 0.74 microns.


How was birth control realized in ancient days? In ancient days, there were no birth control methods like condoms or contraceptive pills available. How did they control pregnancy?

The need for birth control has been a concept for thousands of years and remains an important issue for men and women today, the need for contraception helped humans to achieve control over our population and healthy sexual relationships without having the fear of pregnancy.
The medieval contraception methods mostly relies on plant based oral contraceptives and also plant based suppositories. There is always an element of myth in the usage of these medicines to control child birth, but due to the overusage of Silphion, the plant was gone extinct.

Silphion was a plant that grew in the hills near the Greek city-state of Cyrene located in North Africa. This plant was one example of an oral contraceptive in ancient times, based partly on Pliny's statement that it could be used "to promote the menstrual discharge" but since then has been harvested into extinction.
Reference

Asafoetida is widely used as a  contraceptive in medieval period, Asafoetida or asafetida is the dried latex exuded from the rhizome or tap root of several species of Ferula.

One of the earliest contraceptive pioneers was Soranus of Ephesus, a Greek physician of the 2nd century C.E. who practiced in Rome and wrote extensively on obstetrics, gynecology and pediatrics. Many of his texts exist to this day which describes plants that were recommended for use as oral contraceptives, suppositories and abortifacients: galbanum, silphium, opopanax, myrtle, rue, white pepper, cow parsnip and pomegranate.
Reference

Also condom is not a modern mechanism it was used in ancient times, but the usage was to protect oneself from sexually transmitted diseases, but an unknown chemical used  which is a spermicide and this resulted in contraception.

Records of condom use dates back to 3000 B.C. where King Minos of Crete, son of Zeus and Europa, utilized the bladders of goats to protect himself during intercourse.
In the 1500s, a syphilis epidemic spread across Europe. It was at this time that Gabriel Fallopius,created a linen
condom as a means to protect from the continuing spread of disease . This proved especially effective when soaked in an unknown chemical solution acting as a spermicide.
Reference

The medieval contraception methods includes,

Condoms
Female Barrier Methods
Herbs and Rituals
Intrauterine devices
Male methods
The Pill

These methods are widely described in this article.


Are earthworms edible? Just that. It seemed weird for me not to find anything on Google. But I still think that they might be edible.

Yes, they’re edible and even eaten in some places.
https://culinarylore.com/food-science:are-earthworms-edible/


How to find a Cancer PPI network data I need a Protein Protein Interactions network of Cancer (any type - just I want a PPI of any type cancer), I search and see DIP PPI and ....

How to specify that is  Cancer PPI and how to get a PPI of Cancer ?

I assume that your are looking for human data. Take a look at these papers:

Human Cancer Protein-Protein Interaction Network: A Structural Perspective

From the abstract:

  Protein-protein interaction networks provide a global picture of cellular function and biological processes. Some proteins act as hub proteins, highly connected to others, whereas some others have few interactions. The dysfunction of some interactions causes many diseases, including cancer. Proteins interact through their interfaces. Therefore, studying the interface properties of cancer-related proteins will help explain their role in the interaction networks. Similar or overlapping binding sites should be used repeatedly in single interface hub proteins, making them promiscuous. Alternatively, multi-interface hub proteins make use of several distinct binding sites to bind to different partners. We propose a methodology to integrate protein interfaces into cancer interaction networks (ciSPIN, cancer structural protein interface network). The interactions in the human protein interaction network are replaced by interfaces, coming from either known or predicted complexes. We provide a detailed analysis of cancer related human protein-protein interfaces and the topological properties of the cancer network. The results reveal that cancer-related proteins have smaller, more planar, more charged and less hydrophobic binding sites than non-cancer proteins, which may indicate low affinity and high specificity of the cancer-related interactions. We also classified the genes in ciSPIN according to phenotypes. Within phenotypes, for breast cancer, colorectal cancer and leukemia, interface properties were found to be discriminating from non-cancer interfaces with an accuracy of 71%, 67%, 61%, respectively. In addition, cancer-related proteins tend to interact with their partners through distinct interfaces, corresponding mostly to multi-interface hubs, which comprise 56% of cancer-related proteins, and constituting the nodes with higher essentiality in the network (76%). We illustrate the interface related affinity properties of two cancer-related hub proteins: Erbb3, a multi interface, and Raf1, a single interface hub. The results reveal that affinity of interactions of the multi-interface hub tends to be higher than that of the single-interface hub. These findings might be important in obtaining new targets in cancer as well as finding the details of specific binding regions of putative cancer drug candidates.

Tools for protein-protein interaction network analysis in cancer research

From the abstract:

  As cancer is a complex disease, the representation of a malignant cell as a protein-protein interaction network (PPIN) and its subsequent analysis can provide insight into the behaviour of cancer cells and lead to the discovery of new biomarkers. The aim of this review is to help life-science researchers without previous computer programming skills to extract meaningful biological information from such networks, taking advantage of easyto-use, public bioinformatics tools. It is structured in four parts: the first section describes the pipeline of consecutive steps from network construction to biological hypothesis generation. The second part provides a repository of public, user-friendly tools for network construction, visualisation and analysis. Two different and complementary approaches of network analysis are presented: the topological approach studies the network as a whole by means of structural graph theory, whereas the global approach divides the PPIN into sub-graphs, or modules. In section three, some concepts and tools regarding heterogeneous molecular data integration through a PPIN are described. Finally, the fourth part is an example of how to extract meaningful biological information from a colorectal cancer PPIN using some of the described tools.


what type of insect is this? is this a moth? (southeast asia - Malaysia) i found this insect in the garden behind my house a few months ago.This is the first time i saw this insect.On that day the weather is very hot.I found the insect in the afternoon.I am from Kelantan,Malaysia.The climate in Malaysia is equatorial, hot and humid, heavy rain falls in the monsoon season between november and february.

Oleander Hawkmoth (Daphnis nerii)
Same fellow? (From oocities.org)

And a better picture from ukmoths.org.uk:

For more reading, here's a wiki article.


Why do some internal organs regenerate? I have been reading about the human liver and zebra fish heart muscle having the ability to regenerate. It seems to me that these organs have very little chance to become damaged or worn out. At the very least their chances of being damaged are comparable to other internal organs. So why those particular organs have the regenerative capability?

It is not really essential that all vital organs should have regenerative potential (for example brain).

The cellular composition of a tissue is a big factor in deciding if the organ/tissue will regenerate or not. Some cells divide while others do not; highly specialized and polarized cells like neurons do not divide perhaps because the act of division itself will compromise their function. That doesn't mean these tissues cannot regenerate; they would need stem cells that can differentiate into the type of cells that died.

So regeneration can happen via:

Division of the tissue cells (skin healing, liver regeneration)
Differentiation of stem cells (erythropoesis, muscle regeneration)

Organs that do not have non-dividing cells can regenerate by simply proliferating whereas others would need to maintain a stem cell niche- which is not possible in all tissues. Maintenance of stem cells also adds up to the cost of metabolism; so there is some tradeoff.


How is haemophilia dominant in human females? In human females one X chromosome is inactivated forming a Barr Body. Then how is it that haemophilia is dominant?

Suppose a female has one normal X chromosome and one chromosome with the haemophilia gene. Now suppose that the normal X chromosome is inactivated — will the female show haemophilia?

X-linked Hemophilia is caused by the lack of production of the clotting factors VIII or IX. It is not inherited dominantly, but instead inherited in an X-linked recessive manner.
These proteins are produced in multiple regions around the body. In a female heterozygous for the gene coding for Factor VIII or IX, X-inactivation would randomly prevent one of the chromosomes from expressing its allele. Therefore, the production of active Factor VIII or IX would only occur in half the cells which have the faulty allele inactivated.
However, half the production of the relevant factor results in a close to normal phenotype, as the hemophilic phenotype would not manifest unless the clotting factor activity levels are very low.
This Medscape article on hemophilia states that:

Normal values for FVIII assays are 50-150%. Values in hemophilia are as follows:
Mild: >5%
Moderate: 1-5%
Severe: < 1%

Therefore, despite X-inactivation reducing the production of clotting factors by 50%, the heterozygous female still displays the healthy, non-hemophilic phenotype.
While the clotting factor concentration can only be reduced to approximately 50% of normal, it is still possible for heterozygotes to suffer from mild hemophilia. This is because other genetic factors may also affect the hemophilia phenotype.
For example, the gene encoding FVIII may have point mutations which reduce the effectiveness of the protease, therefore reducing activity levels below the expected 50%. Mutations in regulatory elements or interacting proteins may also result in hemophilia due to the regulatory elements downregulating the expression or activity of the protein.

Approximately 40% of cases of severe FVIII deficiency arise from a large inversion that disrupts the FVIII gene. Deletions, insertions, and point mutations account for the remaining 50-60% of the F8C defects that cause hemophilia A.
Low FVIII levels may arise from defects outside the FVIII gene, as in type IIN von Willebrand disease, in which the molecular defect resides in the FVIII-binding domain of von Willebrand factor.


What happens to drug metabolism when CYP450 enzymes are presented with two substrates What happens when two substances, both substrates for Cytochrome P450 metabolism, are both present in the bloodstream?

For example, with sertraline and cannabidiol (CBD), if someone took a sertraline tablet and later used CBD, how does the presence of two CYP substrates affect drug metabolism? Does one drug inhibit the metabolism of the other? What happens to blood levels of the drugs? Does the order of administration matter?

I think the OP is asking the following:

  If an enzyme is not specific one substrate, but is simultaneously presented with a pair of substrates, which one 'wins' and how do we decide?

For example, if an enzyme is presented with a racemate such that the D-form has a 10-fold lower $K_m$ than the L-form, but the L-form has a 5-fold higher $k_{cat}$, which one is preferentially metabolized, and how do we decide?

It was Fersht who first provided the definitive answer, at least for single-substrate enzymes (Fersht, Enzyme Structure and Mechanism, 1977; see also here)

  The kinetic parameter determining the specificity for competing substrates is neither $K_m$ nor $k_{cat}$, but the (so-called) specificity constant: $$\frac{k_{cat}}{K_m}$$

If it assumed that both substrates, considered in isolation, obey the Michaelis-Menten kinetics, then it is very easy to derive (starting with the ratio of the respective Michaelis-Menten equations) the following expression for the initial velocities when both substrates are present simultaneously.

$$  {
  {{{v_{i}^1}}\over{v_{i}^2}}} =  {{{{k_{cat}^1}}\over{K_{m}^1}[S_1]}}  \times{{{{K_{m}^2}[S_2]}\over{k_{cat}^2}}} \ \ \ \ \ (1)$$

(The equation is derived by, among others, Cornish-Bowden (2004, pp 36-39):

If $V_{max}$ is preferred to $k_{cat}$:
 $$  {
  {{{v_{i}^1}}\over{v_{i}^2}}} =  {{{{V_{max}^1}}\over{K_{m}^1}[S_1]}}  \times{{{{K_{m}^2}[S_2]}\over{V_{max}^2}}} \ \ \ \ \ (2)$$

${{k_{cat}}}\over{K_m}$ has units of a second-order rate constant and, giving it a symbol (${k_{1}^{\prime}}$ for $S_1$ and ${k_{2}^{\prime}}$ for $S_2$) to reflect its status as a fundamental kinetic constant and not just a ratio, allows the following equation to be written:

$$  {
  {{{v_{i}^1}}\over{v_{i}^2}}} =  {{{{k_{1}^{\prime}}}\over[S_1]}}  \times{{{[S_2]}\over{k_{2}^{\prime}}}} \ \ \ \ \ (3)$$

This equation provides the answer to the OP question. For the racemate described above, we need only calculate the ratio of the specificity constants to get the answer:

$${
    {
     {
      {v_{i}^{D_{form}}
     }
     }\over{
             v_{i}^{L_{form}}}
            }
    }   =
{
    {
     {
      {k_{D_{form}}^{\prime}\times{[D_{form}]}
     }
     }\over{
             k_{L_{form}}^{\prime}}\times{[L_{form}]}
            }
    } = {
    {
     {
      {k_{D_{form}}^{\prime}
     }
     }\over{
             k_{L_{form}}^{\prime}}
            }
    } =  2 \ \ \ \ \ (4)$$

Much could be written about the specificity constant (diffusion control, enzyme 'perfection', Haldane relationships), but I'll make just one. Considering the single-substrate Michaelis-Menten enzyme, the following holds AT ALL SUBSTRATE CONCENTRATIONS

$$  {
  {{{v_{i}}}}} =  {{{{k_{1}^{\prime}}}}[{S_o}][E]}   \ \ \ \ \ (5)$$

When $S_o$ is very low, $[E]$ = $e_o$ (approx) and the following may be written (where,unlike $[E]$, $e_o$ is usually known or may be determined)
 $$  {
  {{{v_{i}}}}} =  {{{{k_{1}^{\prime}}}}[{S_o}]e_o}   \ \ \ \ \ (6)$$

  But it is Eqn (5) that is the important one: $k^{\prime}$ (the so-called specificity constant) may be thought of as the second-order rate constant governing the combination of ('free') enzyme with substrate at all substrate concentrations, not just when $S_o$ << $K_m$

Much could be written about this as well

Definitions

I think it is reasonably obvious what everything means. Nevertheless, here is a list:

$K_{m}^1$  is the Michaelis Constant for substrate 1
$K_{m}^2$  is the Michaelis Constant for substrate 2
$k_{cat}^1 $ is catalytic constant for substrate 1
$k_{cat}^2 $ is the catalytic for substrate 2
$V_{max}^1 $ is the maximum velocity for substrate 1
$V_{max}^2 $ is the maximum velocity for substrate 2
$k_{1}^{\prime} $ is the specificity constant for substrate 1
$k_{2}^{\prime} $ is the specificity constant for substrate 2
$v_{i}^{1} $ is the initial velocity due to substrate 1
$v_{i}^{2} $ is the initial velocity due to substrate 2

Reference

Cornish-Bowden (2004) Fundamentals of Enzyme Kinetics 3rd Edn. Portland Press (London)


Facultative Cannibalism? I heard about Larger cats eating the cubs. Is it some kind of facultative cannibalism or they can eat there own kind like that?

What are the facultative cannibalism present in animal kingdom?

What is the genetic origin?

Lions

Lions are a classic example of cannibalism. To understand why this occurs we have to understand their mating system.

Males have a harem of females and males fight in order to access a harem (Note: females may also take part in the battle depending on which male they prefer). When a male takes over a new harem, he kills the young ones of the previous male if these young ones are still dependent on their mother. The reasons are:

The mother is not fertile while she is taking care of a young baby while the male would appreciate that the female is ready to raise his own kids.
The mother needs to invest quite a lot of energy to feed/milk their young while the new male would prefer this energy to be invested in his own offspring.

In short, a male kills the young ones when he takes over a new harem because these young ones do not carry his genes and prevent this new male to optimally pass on his own genes as the offsprings of the previous male consume time and energy from the females of the harem.

And well… once the offsprings are killed, it would be a shame to waste all this good and fresh meat. Better to eat them!

In the cases of lions, cannibalism does not result from food shortage but from "not wasting food". I think that the "not wasting food" hypothesis is the most explanation for cannibalism (I am not sure though). I guess that most often the "not wasting food" occurs after death due to competition as it is the case in lions.

Other Examples

There are many cases of cannibalism in the animal kingdom. Chimpanzees eating other chimpanzees and bear eating other bears. In the tiger salamander, there are cannibal morph and normal morphs. In this species cannibalism is very frequent as in nature one offspring over 5 is eaten through cannibalism (if I am not mistaken). Cannibalism is very common in prairie dogs as well (Reference). In Dragonflies cannibalism represents 95% of the total mortality (Reference).

Sibling sharks eat each other in their mum's womb. Here is a video on the subject. This type of cannibalism is called siblicide.

In Praying mantis the female may eat her mate after copulation. This is referred to as sexual cannibalism. The subject is slightly controversial, please have a look to the wiki article for more info.

In many species (including the dragonflies example above) the old individuals eat the young. This is referred to size-structured cannibalism.

Fillial cannibalism is a type of cannibalism when the adults eat their own offsprings as it is the case in the prairie dogs example I cited above.

Have a look to the Wikipedia links for filial cannibalism, sexual cannibalism and siblicide, they go further than my answer.


Does the SMUG1 enzyme break single-stranded DNA? The SMUG1 gene codes for the enzyme single-strand selective monofunctional uracil DNA glycosylase.  This enzyme can remove uracil from single-strand (unpaired) DNA.  (Uracil can occur in DNA due to deamination of cytosine.)

What happens when this enzyme removes uracil?  It seems what would be best is that a cytosine would replace the uracil in the DNA strand to restore the original DNA sequence, but I haven't found mention of this.  The alternatives would seem to be that the enzyme simply splits the strand into two strands by removing the uracil (which are then unconnected since this is single-strand DNA), or it joins the two adjacent bases together, deleting the uracil but keeping the strand intact.

I think you needed to click just one more link: https://en.wikipedia.org/wiki/Base_excision_repair

It just cuts out the base so there's an empty spot on the ribose. I was looking for a picture and the top hit was actually this site (at A):

What is the mechanism of monofunctional glycosylases?


What do breeders call the effect when a breed resists modification? It is impossible to breed a blue rose or a cat with a bulldog shape. This is because breeding is limited by gene variations in the population.

What do breeders call this effect?

UPDATE

I guess this term is from medieval and/or handicraft breeders, not modern and hi-tech.

UPDATE 2

I am speaking not about principal impossibility but just about observable or tangible barrier. We can be sure that it is possible to turn dog into cat in billion years, but it is much harder than turn German Shepherd to Yorkshire Terrier, which is possible for hundreds of years.

So, there are are two main types of changes, ones take hundreds of years, others take hundreds of millions of years. Former require genetic recombination while latter require genetic mutation.

This barrier was felt by breeders in practice and caused some versions of anti-evolution beliefs.

I need to know how this barrier is named.

I'm honestly not sure if one exists. They simply lack the gene/allele - the only specific term I can think of when it comes to lacking a gene is referencing Knockout variations where a researcher purposefully removes a gene from a subject in order to observe the effect.

However, "Knockout Mice/etc." imply intent on behalf of the researcher, not a result of breeding or natural lack of an allele. Perhaps "Genetically Incapable" would be a phrase meaning the same thing - but I'm not aware of any 'official' shorthand for 'Cannot because it's not in their genes.'


Covid-19: Is it possible to get to r0 < 1 through social distancing measures? I'm trying to wrap my head around some of the information I'm reading about how to fight Covid-19  and conflicting opinions about how much "social distancing" is required to avert a disaster, or whether social distancing works at all. (I am a data scientist, not a biologist or medical professional)

First I want to check if some of my assumptions are correct or not:

Flattening the curve doesn't reduce the overall number of infections, only the average rate of infection for a given time period, e.g. Flattening the curve doesn't take you from 1000 infected people to 100 infected people, it takes you from 1000 infected people in a week to 1000 infected people in 3 months (numbers are just examples):  True or False?
The purpose of social distancing is to flatten the curve, not to reduce the number of overall cases: True or False?
If $r_0 > 1$ than growth is exponential: True or false?
Sub-exponential growth can only happen if $r_0 \leq 1$: True or false?
Flattening the curve cannot reduce exponential growth in number of cases to sub exponential growth, it only leads from steep exponential growth, e.g. $r_0 \approx 2.5$ or $r_0 \approx 3$, to "not so steep" exponential growth $r_0 \approx 1.5$ or $r_0 \approx 1.2$: True or False?

Assuming 1-5 are correct, here are the more complex questions I am trying to figure out:

Can social distancing (without hard quarantines, tracking as many cases as possible, and instantly isolating any new cases discovered, etc...) actually lead to $r_0 < 1$ and therefore reduce the number of infections as opposed to just spreading them out to a manageable rate?
I think the answer is "No", because of small world network theory: The majority of people respect prefect social distancing, i.e. they maintain zero social contact with anybody outside of their immediate family and the the people they interact with for procuring life essentials. Because the number of people who cannot practice social distancing due to their essential role in society (grocery and pharmacy employees, health care professionals, law enforcement, etc...) will still experience very high transmission rates, a small world phenomenon occurs, where the average chain of transmission is still very short between any two individuals in an impacted area. What is wrong with this line of reasoning?
In general, is $r_0 < 1$  achievable without a cure, a vaccine, herd immunity, or the ability to track infections with very high accuracy and isolating them instantly?

I believe r0 is an exponent...

It is the average number of individuals who become infected by each infected individual.

If one infected individual infects exactly one other individual (r0 = 1), the progress will be straight line; the rate will be a flat line based on "mean time between infections"; total number of infections over time will be linear sloping upwards.

If r0 > 1, then it will be an exponential increase; how rapidly/steeply it curves up depends again on the mean time over which that propagation of infection occurs.

If r0 < 1, then it will be an exponential decay. New infections continue to occur, but the overall rate of infection decreases toward but never quite reaching zero.


Why does the arch of aorta coils? My study materials use the word vesselcompression chamber of aorta to emphasize aorta's elastic property.

The arch of the aorta only coils, not its straight part.
I think the reason why the arch coils is the elasticity of aorta (artery) is high.
If the elasticity is too low, then the aorta is more stiff.
This means that heart has to work harder so higher systolic pressure and lower diastolic pressure.

Why does the arch of the aorta coils?

The main question can be answered in a very dumb way: because the lower part of the body also needs blood... and this configuration is the surest way of doing that because of reasons given below (among many others, I am sure).

If you want an anatomical reason, well the most pertinent one would be that embryologically, the heart and vascular system are derived from a single straight tube, that then begins contracting and folding over itself to form the heart chambers, the aorta, and the pulmonary trunk.
If you want a physiological explanation, the aorta curves slowly because it is a point of the circulatory system where pressure is high. Apart from the fact that sharp kinks would cause a massive and useless loss of kinetic energy on blood flow from shear stress over the aortic walls (and therefore more heart workload), the induced shear stress would also damage the aortic walls much more quickly than in the actual configuration.

The third reason is just theory on my part, but it seems the vascular system is designed by priorities: you could imagine a system with two aortas. One for the upper body going up, and a second going down. However, such a configuration makes it mechanically impossible to balance perfusion to the organs, and especially ensure brain perfusion. For example, how would the body compensate if the upper aorta got clogged while the other stayed wide open? The single aorta configuration allows the heart to adapt to such mechanical perturbation scenarii using, for example, left ventricular hypertrophy.

However to add to some elements of your question:

the reason of the aortic coiling has certainly very little to do with elasticity and the vessel compression chamber principle.
Higher elasticity means the aorta is less stiff, not more.
When the aorta gets stiff (elasticity decreases) as it is often the case with age and calcification of the aortic walls, it is correct that the heart will need to work more, that systolic pressure will get higher, and diastolic pressure lower. This gives the classical clinical symptom of "cannonball" or "gunshot" pulse


How many possible codons? Consider a codon of the form NNK (where N = Adenine, Cytosine, Guanine or Uracil & K = Uracil or Guanine).  How many codons are now available? I know if all were available there would be 4^3 = 64 codons. How many are possible now? When I have tried combinations manually I got it to be 32, is this correct?

Yes, it is.

Gerardo Furtado has already provided a short answer in the comments, but allow me to explain why.

The 4^3 = 64 if all bases can be chosen freely comes down to 4*4*4=64, because you can choose from 4 options for each of the 3 bases.

If you restrict the possibilities of one of the bases, e.g. there are only 2 options for the third base (as in your example), the formula changes to 4*4*2=32, as you can choose from 4 options each for the first 2 bases and from 2 options for the 3rd base.

Edit:
If the 2 'N's from 'NNK' have to be the same, you can choose the first base freely (4 options), the second base is already defined (it has to be the same as the first base, 1 option) and there are 2 options for the 3rd base as described above. Thus, we get 4*1*2=8 possible codons

I hope I could clear this up.


Purifying a linear plasmid after restriction digest? I expressed a yeast vector in E.coli and purified about 13µg of it. I then linearized it using a restriction enzyme, and attempted to gel purify it. I attempted this twice. The gel showed a clear bright band at the right spot, but after gel purification I end up with only 0.7µg of linear plasmid. I doubt I made the same mistake twice. What is the best way to purify a linear plasmid after digest?

Edit:

The plasmid is about 3.5 kb. I incubate an overnight culture of E. coli, miniprep the following morning, elute into water. I end up with 13µg of DNA in 200µl of H2O. I add the PmeI (10µl) and the CutSmart buffer (23µl) from NEB, incubate overnight. The following day, I run the 230µl through a 1% gel and get a single band around 3.5 kb. I excise the band, and perform a gel purification using the Biobasic kit, add denaturant (probably guanidine hydrochloride), wait for 10 minutes for the gel to dissolve, run through column, wash 2X with wash buffer with ethanol added, elute in water.

Thanks,
Max

Can't exactly say what problem you are facing but you can follow these steps for efficient restriction digestion and elution.

Never set up a digestion reaction with more than 1µg DNA per 20µl; if you require more digested DNA, then set up multiple 20µl reactions with maximum of 1µg DNA in each (500-700ng is ideal).
10µl enzyme for a 230µl reaction: bad idea. Set up 10×20µl reactions with not more than 0.5µl enzyme per reaction tube.
Avoid overnight incubations; 4 hours should be sufficient (NEB PmeI is 10 units/µl and 1 unit is the amount required to cleave 1µg DNA in 1h in a 50µl reaction. You are adding 5 units in 20µl. Overnight incubation is too much)
Deactivate the enzyme after the reaction.
Just run a little bit of sample from one tube in the gel to see if digestion has happened. After confirming digestion simply use the PCR purification kit. You can pool your tubes.
Optional: Elute in Tris-Cl pH 7.5 instead of water or use warm (60⁰C) water.


Indirect pathway of movement and Parkinson's? So Parkinson's disease leads to the loss of dopaminergic neurons. I understand how the direct pathway (an excitatory pathway) is inhibited, leading to a loss of movement. However, how can the loss of dopamine neurons cause enhancement of the indirect pathway (which enhances its inhibitory effect, leading to a loss of movement)?

I assumed that loss of neurons would decrease stimulation of both pathways.

The dopaminergic neurons of the substantia nigra pars compacta are a part of neither the direct nor the indirect pathway. The dopaminergic system rather acts as a modulator between those two pathways. More dopamine steers the system towards the direct pathway, less dopamine towards the indirect pathway.

One of the best explanations of the basal ganglia that I've ever seen were video lectures by Dr. Najeeb on youtube.

explanation of the basal ganglia pathways

pathologies involving the basal ganglia

At the beginning of the second video there is a short review of the pathways he explains in the first one. At 5:06 he starts talking about Parkinson's disease.

A paper about the topic:

Functional organization of the basal ganglia: Therapeutic implications for Parkinson's disease (Obeso et al. (2008)


What is the biological age of grafted plants? Suppose you graft a piece of an existing 'old' plant onto a host plant. Will the graft continue to grow having the same biological age as its parent? In other words, would the graft die at the same time as its parent plant? Or would the process of grafting result in some sort of rejuvenation of the grafted daughter plant? Or alternatively, would the host plant carrying the graft determine the biological age of the graft primarily?

PS: Personal experience-based (anecdotal) answers are more than welcomed

In my experience (in common with the experience of everyone I've talked to who could be considered an expert on the subject), taking old wood and using that as a scion when grafting new trees rejuvenates them, and they grow as new trees.

I'll take apple trees as an example. As you can see from the table here, there is a distinct age after which the tree begins to decline. Now, that's not concrete (I've seen some apple trees last over 100 years (didn't plant those myself btw)), but generally, an apple tree will lose vigor and productivity before it reaches 50 years of age. This tree's 'immune system' also goes down, and it becomes susceptible to many diseases. You'll rarely see such a tree, as orchardists generally replace them rather fast.

But to the point of your question. When you will graft an apple tree, you will generally bud graft it, as described here. That article (which is spot-on) says:

  Select a healthy branch of this year's growth from your desired variety of tree. Look for a plump leaf bud about halfway down the branch. Leaf buds are close to the branch where fruiting buds tend to stand out more.

Note that it says nothing about the tree's age, simply stating that the wood must be healthy. That's because old wood/young wood produce the same result in the new trees. I was using a 40 year old razor russet to graft onto all the Malling V rootstocks I had for that variety. And of course they grew as expected, as a young sapling should. I've heard of a nearby nursery taking budwood from a 100 year old tree that still looked good.

Additionally, you can use a rootstock taken from an old plant, and also a scion from an old plant, and the new plant created will grow as a young sapling. Here's how the rootstocks I use are created: You cut down a tree at ground level, and it sends out a lot of shoots. You pile soil over it, but allow the ends of the shoots to stick through. These shoots will root into the soil, and can be cut at the base, and planted out for grafting later. This way, you can have 1000's of identical (cloned) rootstocks. You can also get rootstocks from old trees. Here's a diagram of the process.

About herbaceous perennials, I've found (to some people's surprise) the same thing. The scion grows as a young plant again once grafted. I found this out because I graft heirloom tomatoes onto hybrid tomato rootstocks (the latter are seedlings). Usually, the scions will be from seedlings, but at times I take the scions from a large mature plant.

Just so you know, an indeterminate tomato plant will, once mature, flower and fruit until frost. A determinate tomato variety will produce a large crop all at once, and then die back (this is the kind preferred by owners of mechanised (machine harvested) fields).

In my tests, you could take the scion from an old determinate plant that was through fruiting, right before it started dying back, and successfully use that for grafting the new plants. These new plants' growth was identical to the growth of grafted plants whose scions came from seedlings, and they began to flower and produce fruit at the same time. Of course, actual seedlings did not have the vigor of the grafted plants, and were behind in growth.

Off-topic for your question, but possibly still of interest, I've found that cuttings and layers (not scions) taken from old plants (both woody and herbaceous), and rooted, would grow as young plants again.


Can a mathematical function be assigned to ECG diagram? This is a 12 lead electeocardiogram of a 26 year old male:

This is the graph of function $5sin(7x)sin(.5x)cos(3.25x)$
 This graph look quite similar to the ECG diagram.After sketching this graph, I thought whether ECG diagram could be assigned roughly to a mathematical function.

Question: Has anyone ever tried to even roughly assign the diagram to a mathematical function? Is it even possible?


Identifying the inheritance pattern GrandParents                  -- 1
                            |
                            |
                -------------------------
                |S                      |D          -- 2
            ---------                ----------
            |S(A)   |D               |S(A)    |S(A) -- 3
            |S      |D                              -- 4

S = Son
D = Daughter
(A) = Affected with a degenerative disease.

The question is how to identify the type of inheritance of the disease - whether
X-based, Autosomal dominant or recessive. Which sex of fourth generation are likely to have the disease? Does it depend on the disease?

Short answer

As said @Biogirl, "This pedigree can not lead to one absolute answer". We miss information in order to answer this question.

Long answer

Should we make the assumption that the allele causing the disease (A) necessarily come from the lineage you draw or can it come from the partners of the second generation (offspring of GrandParents)?

Then, depending on your answer to this question...

If yes (= if the allele causing (A) comes from the GrandParents):

This genealogy is impossible if the type of inheritance is as simple as you suggested (either recessive or dominant, no epigenetics, no epistasis, no effect of the environment, no protein-mediated disease via the vomb,... even if it can be autosomal, sexual or mitochondrial genes)

If no (= if the allele causing (A) do not come from the GrandParents only)

Everything is possible (from the space of possibilities that you suggested)

some possibilities would be more probable than others (depending especially on the allele frequencies)


Can cancer grow forever if supplied with unlimited resources? If somehow a human could give a tumor unlimited resources, would the cancer grow forever?  It seems like it would until it gets so large that it physically affects vital organs.  Is what would likely happen?

Yes. The very first cells used to study cancer are still around (HeLa Immortal Cells - Named for the subject Henrietta Lacks) and are basically immortal as long as they're fed.

As for tumors, whether cancerous or not they most definitely can continue to grow until they become a serious medical issue (WARNING: GRAPHIC - 3 Largest Tumors Recorded). One of the largest recorded tumors was 300lbs (~140kg) in a woman's abdomen that sprouted off of an ovary. They had to operate with her laying on her side, otherwise it would have crushed her abdomen and killed her.

Not all forms of cancer are immortal or produce large tumors (the 300lb tumor was benign), but it's definitely within the realm of plausibility.


Why do hummingbirds build nests with live ferns instead of dead materials? Hummingbirds prefer to build their nests with spore-bearing ferns, and mosses. This is helpful for the reproduction of the ferns, which are then better able to spread their seeds. But how is this beneficial for hummingbirds? Building in this manner is more difficult and energy-consuming.

Do live ferns make for better building materials? Is there a scent that these ferns are giving off to attract the hummingbirds? What kinds of research exist on this question?

References:

Carl Zimmer's National Geographic article, "A Living Nest?" (Feb 4, 2014) http://phenomena.nationalgeographic.com/2014/02/04/a-living-nest/

Question by Twitter-user Jessica: @LadyJaya

From the article titled "Evidence of mutualistic synzoochory between cryptogams and hummingbirds", the specific advantage for the hummingbird is that it gets good nest building material through the selection of cryptograms. The cryptograms though have its seeds dispersed over large distances by birds which is a process called synzoochory.


Can someone identify this worm? The first time I saw these was in an old cooler full of water by my shed, there were 3 of them about 2 weeks ago. Now tonight I found one crawling up my door. Can anyone offer some insight? I have dogs and I'm horrified that it may be some kind of parasitic worm that they can contract.
This was observed in northwestern Pennsylvania, US. Rainy, cool fall weather currently, as it's the end of October. They're about 2 inches long. Very thin, blackish red in color and extra wiggly.

The "bump" on an earthworm (i.e., a worm species of the order Opisthopora) is a clitellum. Clitella are only visible on earthworms when they're sexually mature [Sources: 1, 2, 3]. So the absence of a clitellum does not preclude your specimen from being a member of this order.
The species in your photo is almost undoubtedly some species of earthworm. Without clearer images or more detail, I can't imagine someone taking the time to try to ID to species.
There are many species of earthworms present in Pennsylvania (though likely none of them are native to the US: see here). Keep an eye out for a recent invader, the "Asian Jumping Worm" [read more].


Ligaments at the posterior superior iliac spine In Causes of Back Dimples, it was determined that these 'Dimples of Venus' are created by

  a short ligament stretching between the posterior superior iliac spine and the skin. They are thought to be genetic. (@Johnny)

The linked article in the answer to my original question says nothing more other than the fact that dimples of venus are normal dimples (not medically significant).

DrLumbago.com states:

  The sacroiliac joints move together as a single unit.  From the back it is common to see a pair of dimples on the buttock near the base of the spine.  These are sometimes called the “dimples of Venus” and they are a landmark for the top portion of the sacroiliac joints.

Posterior superior iliac spine (PSIS) marked in red

Image made by DBCLS (Polygondata is from BodyParts3D) CC BY-SA 2.1 jp, via Wikimedia Commons

Ligaments of the PSIS

Cooperstein & Hickey (2016) has an image of ligaments connected to the PSIS, but unless I am mistaken, the image doesn't seem to have the ligament(s) involved with the dimples of venus.

It seems from the description in Kumar, et al. (2014) that the "dimples of venus ligament(s)" are connected to the skin, and seeing that ligaments are fibrous connective tissues that normally connect bones to other bones, I am intrigued to know more.  What is the name of these "dimple of venus ligaments" and what is their purpose?

References

Cooperstein, R., & Hickey, M. (2016). The reliability of palpating the posterior superior iliac spine: a systematic review. The Journal of the Canadian Chiropractic Association, 60(1), 36.PMCID: PMC4807681

Kumar, A., Kanojia, R. K., & Saili, A. (2014). Skin dimples. International journal of dermatology, 53(7), 789-797. DOI: 10.1111/ijd.12376

It seems from the description in Kumar, et al. (2014) that the "dimples of venus ligament(s)" are connected to the skin, and seeing that ligaments are fibrous connective tissues that normally connect bones to other bones, I am intrigued to know more. What is the name of these "dimple of venus ligaments" and what is their purpose?

First, re: what a ligament is, you're correct in your understanding that ligaments generally bind bones to bones (vs. tendons), but the term is used more broadly as connective tissue that binds things together, holds them in place, is a remnant of a fetal structure, or a mesenteric fold. Your wikipedia link acknowledges this. Some examples are:

Round ligament of the liver: a remnant of fetal structure
Broad ligament of the uterus: a mesenteric fold
Median arcuate ligament: this one actually binds two muscles together
Sternopericardial ligament: binds the pericardium to the sternum

The unnamed short ligaments Kumar describes (and wikipedia, quora, and stack exchange have repeated), are probably unnamed because they are difficult to isolate and study, and they are not clinically relevant. They may even be theoretical. There are no studies on them indexed in medline, and they aren't discussed in any anatomy text I've read. Dimples are generally thought to be caused by fibrous connections between the skin and muscle, bone, or other deep tissue. If you ever cut into the back of a cadaver or surgical patient, you'll see that there are a great number of unnamed fibrous connections to the skin. It's not unreasonable for Kumar to invoke them as the cause for these dimples.


Would tinnitus be explained by perpetually-bent/opened hairs in the cochlea? When I look around for what causes tinnitus and the like, the usual response is "Well, loud sounds and hearing damage" but I feel like that's a little plain and I am curious about the underlying mechanism / explanation on a physiological level.
My previous understanding of how the ear works can be found in my previous question (with a terrific answer by AliceD).
So my question is this: Let's say a really loud, fierce sound occurs - the sort of thing that is said to cause tinnitus. This is equivalent to a really strong pressure wave approaching the eardrum. I imagine it would hit the eardrum, causing it to move violently / harshly, causing a similarly strong movement in the stapes, which is already providing something like a 20x pressure amplification to the cochlea.
So the stapes hammers hard on the oval window of the cochlea, causing a harsh pressure wave through the perilymph / endolymph, also causing the basilar membrane to move very harshly and violently. To me this would imply a fierce smashing/dragging of the hair cells against the tectorial membrane above, possibly causing sufficiently harsh wear-and-tear along the tops of the hair cells, leaving them bent or maybe even chopped, allowing their channels to remain perpetually open.
If these channels are always open, they're always accepting potassium, always creating the action potentials, always triggering the nerves underneath, which would mean the person is always hearing that particular tone all day, every day, 24/7.
Is this more or less what happens, or am I way off in my little thought experiment daydream here? Is this why tinnitus is difficult to cure, because it would require somehow rebuilding / closing up hair cells that are always open?

What you're describing would likely cause hearing loss, which could later result in tinnitus, but not by the mechanism you describe.
Hair cells transduce sound via remarkably fragile connections between stereocilia. The channels are closed until tension pulls the channels open (see Fettiplace 2011 for a review that covers pretty much all of sound transduction including a detailed description of the tip links and channels involved). Disconnection would result in the channels being perpetually closed, not perpetually open.
Anything like the trauma you describe would irreversibly damage the tip links and sound transmission would fail. There are mechanisms in the ear to prevent this sort of damage, but for sufficiently loud sounds the damage is not avoidable.
@AliceD has another excellent answer on tinnitus specifically here for more realistic mechanisms proposed for tinnitus: What is the mechanism behind tinnitus?. These are all centrally derived in some way. In short, the absence of proper input to the auditory processing parts of the brain results in compensation that induces an illusory perception. Similar sensations are experienced in other parts of the body as well, such as phantom limb.

Fettiplace, R. (2011). Hair cell transduction, tuning, and synaptic transmission in the mammalian cochlea. Comprehensive Physiology, 7(4), 1197-1227.


Are there gaps in what our ears can hear? I know about the hair cells in our Cochlea and it is the movement of the fluid that makes them vibrate. And it is this that activates the transmission of electrical signals to the brain that become sound.

But I've heard that hair cells are each built to detect specific pitches of sound. And if they don't get that particular pitch then they don't transmit.
So as I understand it, we have cells that each respond to one particular pitch and nothing else. Since we have many that each respond to a different pitch, this is what gives us a wide spectrum of hearing.

What I've been wondering is this, if each hair cell responds to one particular pitch, what happens if we try to hear a sound that is in between two hair cells?

Imagine a hair cell that only responds to 1 Hz (and based on my understanding they do) And next to it a cell that responds to a sound at 2 Hz.
What happens if there is a sound that is 1.5 Hz? Can we not hear that sound because it exists in the gap between our hair cells? Or can hair cells cover a wide range so they overlap and cover the gap?

As our ability to hear sound quantised or continuous?

I know that there are sounds so low or high they are beyond our range of hearing but what about within our range of hearing? If someone played a sound that was right in between two hair cells could we not hear it? Is there a finite number of different sounds that we can hear within our hearing range?

Short answer
No, there are no between-hair cell induced tonotopical gaps in frequency perception.

Background
Young people are able to hear over a frequency range of about 10 octaves, with a frequency resolution of about 0.3% of an octave. So we would have about 2300 resolvable frequencies. This number is dependent on the sound level, as excitation spreads at higher sound levels, but it gives a reasonable starting point to answer your question.

The human cochlea contains on the order of 3,500 inner hair cells. Hence, according to this (highly simplified) calculation, it seems that the number of hair cells is redundant.

In other words, the notion of in-between hair-cell stimulation is stretching the limits of physiological frequency resolution a tad too far.

Reference
- Elliott & Shera, Smart Mater Struct (2012); 21(6):064001

Source
- Cochlea.eu. Cochlea: function


Why is the Trendelenburg position used when placing and removing Central Venous Line catheters in the sub-clavian vein? The title says it all. Why is it that patients are placed in the trendelenburg position when a catheter is inserted in the sub clavian vein? What would happen if the patient wasn't placed in the trendelenburg position when placing the catheter?
Thanks in advance for the help.

There are 2 main reasons for using the Trendelenburg position when placing and removing a central venous line catheter into the subclavian or even internal jugular vein.

Exactly what C Rags mentioned-- to increase the size of the vein. This position utilizes the force of gravity to pool blood towards the head from the lower extremities. This makes the vein of interest easier to visualize compared to surrounding structures, to palpate since this increases pressure within the vein, and to ultimately puncture.
To avoid air embolisms, which are particularly more damaging if they get into the brain causing a stroke than if they travel inferiorly to the leg, for example. Air embolisms can be introduced when inserting or removing a line.

Ref:

http://emedicine.medscape.com/article/422189-overview#showall


Ephedrine or pseudoephedrine indirectly central alpha2 mimetic? I started to think this problem by first thinking if the alpha2 mimetism is possible in either case.
It seems to be indirectly in either one.
Ephedrine seems to have more prominent effect in CNS.
So I propose that Ephedrine has indirect central alpha2 mimetic effect.

Is ephedrine central alpha2 mimetic?
I think one evidence about that would be if there is a alpha2 receptor which is activated by ephedrine somehow indirectly.

Anongoodnurse provide an excellent comment in other discussion about how to search PubChem.

Ephedrine is not alpha2 mimetic.
Pseudoephedrine is alpha2 mimetic, source:


Is it possible to elicit transient gene silencing by using virus induced gene silencing (VIGS) in plants? I am looking for a molecular tech' which could result in transient gene silencing in plants. The objective is to not make transgenic plant, but to use these tech' to silence a gene of interest for a short time. From my limited knowledge, I found that virus induced gene silencing (VIGS) may be an option, I wonder how easy and how long such silencing last? Is there any alternative method?

I don't have any candidate gene to be silenced at this moment, but the tissue will be flower. so it would be nice if the protocol works for flower.

Thank you in advance

Virus induced gene silencing (VIGS) is definitely an option.

The ease of using VIGS depends on a lot of factors. Current VIGS vectors have limited host ranges. Depending on the species of plant that you are working with, there may or may not be suitable, pre-made VIGS vectors available and published techniques for using them. Many of the VIGS vectors that are available may be limited in terms of which tissues they can infect. Working with the vectors themselves requires that you have some way to propagate them and some way of getting them into your target plants (for example Biolistics, Agrobacterium or direct application of infectious virus).

There have been a number of VIGS vectors developed over the years, capable of infecting a diversity of plant species. Modified Tobacco mosaic virus (TMV) and Tobacco rattle virus (TRV) are two common VIGS vectors used for silencing in a variety of plants. TRV in particular is known to have a very wide host range. If your species doesn't fall within or even near the documented host range of available vectors it may be worth just trying a few different ones. Or, you could always isolate a virus specific to your target plant and build you're own. What fun!

The length of time that silencing will last is difficult to predict. In my experience, it will typically last a few weeks. But this may vary depending on a number of host factors and the VIGS vector used.

One potential alternative would be to just use Agrobacterium. It could be combined with a recombinase system to satisfy your condition of transience. To build such a system you could insert you're silencing construct into a binary vector. By including an inducible recombinase sequence adjacent to your silencing construct sequence and by flanking both of these with the recombinases recognition sequences, you would be able to remove inserted DNA at some point down the road after transforming the plant.

Again, depending on which species and variety of plant you're working on, this could require some trial and error as there may not be published techniques for Agro mediated transformation of you're target plant.

While Agro mediated transformation may not quite be what you're looking for in terms of transient silencing, it may be sufficient for a proof of concept.


What is the exact chemical composition of human body? I've just watched Breaking Bad Season 01 Episode 03. In that Walter gives the chemical composition of human body. The conversation is as follows

  Walter White: Let's break it down. Hydrogen. What does that give us?

  Gretchen Schwartz: We're looking at 63%.

  Walter White: Sixty-three, that is a big bite. My next step's gotta be
  oxygen.

  Gretchen Schwartz: Oxygen, 26%.

  Walter White: Twenty-six. There you have your water.

  Gretchen Schwartz: Carbon, 9%.

  Walter White: Carbon, 9.

  Gretchen Schwartz: For a total of 98%.

  Walter White: Right.

  Gretchen Schwartz: Nitrogen, 1.25%.

  Walter White: One-point-two-five.

  Gretchen Schwartz: That brings you to 99 and a quarter. Which only
  leaves you with the trace elements down where the magic happens.

  Walter White: Oh, wait a minute. What about calcium? Calcium's not a
  trace. Got a whole skeleton to account for.

  Gretchen Schwartz: You would think, right? Calcium's only 0.25%.

  Walter White: What? That low? Seriously? Damn, I never would've
  thought that. Okay, so where does iron fit in.

  Gretchen Schwartz: Iron. 0.00004%

  Walter White: What? You can't have hemoglobin without iron.

  Gretchen Schwartz: Apparently, it don't take take much. No doubt. Go
  figure.

  Walter White: Sodium.

  Gretchen Schwartz: Sodium, 0.04%. Phosphorus, 0.19%.

  Walter White: Point-one-nine. There we go. So the whole thing adds up
  to... 99.888042%. We are 0.111958%. Shy.

  Gretchen Schwartz: Supposedly that's everything.

  Walter White: Yeah? I don't know, it just... it seems like something's
  missing, doesn't it? There's got to be more to a human being than
  that.

  Gretchen Schwartz: What about the soul?

  Walter White: The soul? There's nothing but chemistry here.

When I searched for it, Wikipedia has something different.

Which one is correct?

That conversation is strange. While different tables exist, the very first elements seem messed up. If the body is 60 (some sources say 70)% water, then oxygen has to be the most abundant element by weight (water - H2O - has a molecular weight of ~18 g/mol, with hydrogen contributing only 2g/mol of that weight).

The usual figures are roughly Oxygen (65%), Carbon (18%), Hydrogen (10%), Nitrogen: (3%), Calcium (1.5%), etc.

However, the writers of Breaking Bad weren't stupid. So, they weren't discussing percentages of the mass of each element, but rather the frequency of that atom in the body. The number of hydrogen atoms does indeed exceed the number of oxygen atoms.

So, by atomic percent, Oxygen is 25.6%, Carbon: 9.5%, Hydrogen: 63%, Nitrogen: 1.3%, Calcium: 0.24%, etc. So yes, the numbers are approximately correct for a normal, average, youthful (more water) 70 kg male.

So here is a table incorporating both percent by weight and percent by abundance. The writers were pretty well informed.


Identify this spider I found this spider on my balcony in Sunnyvale, CA. It sat in a irregular net. The body was approx. 6mm long. Which species does it belong to?

That's a Western Black Widow subadult female.  The banded legs, with dark 'knees' and lighter brown intervals, become all black as the spider matures, just as the bands on the body disappear as it becomes all black.

Below is a slightly older one, where the center stripe is beginning to turn red.
Your first clue is the irregular web, characteristic of the Theridiid cobweb spiders.  The second clue is the robust body and legs, with especially long first and last pairs.  The key field mark, if you had seen the underside, is the red or orange hourglass.  It is clearly not any kind of orbweaver, simply from the web; and none of the several sorts of Argiope look anything like this spider.

Be aware that this spider can give quite a potent bite (although they often don't, preferring to hide, and not biting unless endangered).  Like the other Black Widows, they are best not handled, just in case.

https://bugguide.net/node/view/1458045/bgimage


Can anyone tell me what tree does this leaf belong to? I found a lovely tree in my friends yard and we do not have a clue what tree is it. The leaf texture is a but like the ginko biloba, but the shape is different. Can anyone identify it? (It's in Romania, Eastern Europe, but I suspect it's not a local tree)

maybe it is from tulip-tree (Liriodendron tulipifera)

use one of this applications to identify plant species:

http://www.plantsnapp.com/#theapp
https://itunes.apple.com/gb/app/id957861141?mt=8
https://itunes.apple.com/gb/app/flowerchecker-plant-identification/id916709270?mt=8
https://play.google.com/store/apps/details?id=cz.thran.flowercheckerplus

and many others here


What part of the cactus photosynthesizes? In general, plants photosynthesize through their leaves and, to a much lesser extent, through their stems. Cacti, however, have no visible leaves, but instead spines. In what part of the cactus does the photosynthesis take place?

In wiki there is a good answer for your question http://en.wikipedia.org/wiki/Cactus#Leaves

In plants photosynthesis takes place in chloroplasts. Chloroplasts may be in the cells of fruits, stems, but most of all in leaves. In some succulents (such as cacti), the main photosynthetic activity is associated with a stem.


Multiple fission and spore formation I came across this question today. In the B diagram, zoospores of chlamydomonas is given. Now my doubt is, are the zoospores formed by multiple fission or spore formation? If it is by spore formation, isn't spore formation and multiple fission the same thing when it comes to unicellular organism i.e chlamydomonas? If it is the same thing, why isn't option c correct in the question I attached?

All the organisms shown in the figure reproduce asexually. (A) is Penicillium in which non-motile conidia are produced singly or in chains. Organism (B) is Chlamydomonas in which reproduction occurs by zoospores. In Hydra (C) and yeast (D), asexual reproduction takes place by budding.
Mutliple fission and Spore Formation are two distinct processes where in:

Multiple fission can be explained with the following diagram:

Multiple fission is a process of asexual reproduction in which a single organism splits up into multiple organisms or daughter cells of similar type under favourable conditions like availibity of food and suitable environmental conditions.

Spore formation can be explained with the following diagram:

Spores are tiny microscopic hard unicellular sexual bodies which are always suspended in air. Under suitable environmental conditions they settle down and grow into new plants. Above given is a structure of rhizopus(bread mould) reproducing through the process of spore formation. Each rhizopus consists of a globular structure at the top known as the sporangium which consists of spores. When the favourable conditions arrive then the sporangium bursts and the spores get suspended in the air. Soon they settle on the moist bread particles, leading to the formation of new rhizopus plants.


Lookup for transporter locations in humans I am interested in several transporters and cotransporters (eg SLC12A1/2 and many others), more precicely, in (human) organism that are made of cells containing those transporters. So does anyone know a lookup table or database where I can find information about that? My google search unfortunately left me in the dark :/ So I am thankfull about any hint!

This site can help you locate RNA expression of a particular gene (if you know the gene for the protein in context) in various tissues. Its called biogps.
http://biogps.org/#goto=welcome

Hope it helps :)


What species is most prolific? What species represents the largest biomass on earth, ie, how much does the entire population weigh? Also, what species has the most members?

This article covers your desires. Briefly, the single species that weights the most is the cow (520 million tonnes in 2011, now probably way more). About the most members, it looks like that the prize could go to the Antarctic krill (7.8 x 10^14 according to Wikipedia. [

This BBC article, instead, argues that collembola might be the most numerous group on Earth, being present in the number of 10000 per square meter (I leave the calculation to the reader). Collembola, however, are made up of ~6000 species. The same goes for ants and termites.

Regarding bacteria, the same article mentions
cyanobacteria, and more interestingly Wolbachia, an intracytoplasmic parasite that can bend the sex of the progeny of its host to spread more effectively.


Why do (some) cats chase their own tail? Is this just playful behaviour or are they unaware that it's their own body part ?

I will try to answer this. First of all we have to make a claim. This behavior can be found in many animals behaviors but it is much more common in dogs.

In cats there is a few reason for that:

Born hunter

Feline predators have a genetic desire to chase anything what is moving. So the chasing tail behavior can be just game for practising hunting skills.

OCD

But if this behavior doesn't stop after the cat grew up it might be a serious problem.  Just like any compulsion behavior in general it might indicate that your lovely cat has obsessive compulsive disorder. If this is the case, your pet can become much more aggressive, hyperactive.

Source

Perfect Paws: Predatory Behavior of Cats

Psychology Today: It's Alive! Why Cats Love Laser Pointers

Pet Place: Feline Hyperesthesia (FHS)


Can someone tell me if the example I wrote below is one possible answer? Here is an imaginary mRNA sequence:
5’- THE BIG BOY SAW THE CAT EAT THE HOT DOG – 3’
Each 3 letter-word is equivalent to the codons in real mRNA.

What would the imaginary mRNA sequence look like if there was a deletion of two bases near the 5’ end of the mRNA? Write out the example above with the two-base deletion and 3-letter “codons” to explain your answer. Label the ends of your imaginary RNA and clearly show the mutation.

I used this: 5’- TBI GBO YSA WTH ECA TEA TTH EHO TDO G-3’. However I am not sure if writing in this form answers the question, can someone tell me whether this is correct and if not how should I change it?

No your answer seems correct, but are you sure they aren't asking you to delete the two bases at the absolute 5' end? In that case it becomes:

5’- EBI GBO YSA WTH ECA TEA TTH EHO TDO G – 3’

But if they're asking you to delete any two near the end, then you're correct.


Why did abiogenesis only happen once? If the "primordial soup" theory of abiogenesis is to be believed, self-reproducing organisms spontaneously arose on Earth at least 3.5 billion years ago, surprisingly soon after the Earth cooled down enough to potentially harbor life.

It may never have happened again, however, since all lifeforms on Earth today are similar on a molecular level (DNA), suggesting a common origin.

This appears to imply at least one of the following:

Immediately after the first spontaneous abiogenesis, environmental conditions on Earth changed dramatically, making a repeat impossible.
The first organisms that arose consumed any subsequent organisms that came into being. This was suggested by Alexander Oparin, but I find it very difficult to believe since it would have to happen everywhere on Earth. Also, most single-celled organisms found today do not consume other organisms, and even where they do that does not usually lead to their complete extinction.
The common origin theory is in fact false, despite the similarities between organisms, and abiogenesis did occur multiple times in the same way.
Abiogenesis happened more than once, but only the descendants of one occurrence survived till today.
Spontaneous abiogenesis never occurred on Earth after all because the conditions never allowed it; instead, a proto-organism arrived on Earth from a planet where the conditions do (Panspermia).
The standard theory of geological history is wrong (i.e. the Earth was in a "fertile" state for much longer before the eventual origin of life than commonly thought, due to some unknown mechanism causing radiometric dating to give wrong results).

None of these seem likely to me, yet even less likely I find the idea that life arose spontaneously almost immediately (within a few hundred million years, possibly even faster) after the Earth's crust solidified, and never again afterwards.

What are the currently held theories on that matter? Can poeple provide references to relevant publications.

It may never have happened again, however, since all lifeforms on Earth today are similar on a molecular level (DNA), suggesting a common origin.

An important distinction to make here is that all extant life on Earth has a common origin.

It's completely possible that abiogenesis occurred many times, but whatever organisms emerged as a result became extinct early on or are not preserved in the fossil record.

  Immediately after the first spontaneous abiogenesis, environmental conditions on Earth changed dramatically, making a repeat impossible.

Nope. The red bands and subsequent dating techniques suggest it took a very long time for a change to occur.

  The first organisms that arose consumed any subsequent organisms...

Possible, but we have solid data suggesting the first functional organisms were autotrophs. That is, they made their own food from whatever they were exposed to, and the predator/prey relationship had yet to play a major role.

  The common origin theory is in fact false, despite the similarities between organisms, and abiogenesis did occur multiple times in the same way.

The Common Origin Theory - as you've defined it - is almost certainly true. DNA is a constant, as is RNA, mitochondria, etc.

That, however, doesn't mean abiogenesis couldn't have happened more than once. As I said above, the Common Origin Theory applies to extant (living) species, not necessarily all organisms that have ever existed. Species go extinct all the time.

  Spontaneous abiogenesis never occurred on Earth after all because the conditions never allowed it; instead, a proto-organism arrived on Earth from a planet where the conditions do (Panspermia).

That merely pushes the question of abiogensis back a bit. Why did it evolve on another world and not Earth, then? How did it survive in space? Why was it so well suited to Earth's environment if Earth-like planets are (relatively speaking) rare?

  The standard theory of geological history is wrong (i.e. the Earth was in a "fertile" state for much longer before the eventual origin of life than commonly thought, due to some unknown mechanism causing radiometric dating to give wrong results).

Estimations and conclusions have come from more than radiometric dating. We have fossil records, geological records spanning continents, and even ice-core records from the poles that both confirm radiometric dating and establish themselves as independent evidence.

  None of these seem likely to me, yet even less likely I find the idea that life arose spontaneously almost immediately (within a few hundred million years, possibly even faster) after the Earth's crust solidified, and never again afterwards.

Why?

  What are the currently held theories on that matter? Both random speculations and references to relevant publications are welcome.

This SE is not the place for random speculations. I don't have publications handy, so I may return and edit my answer when I have the impetus.

The most widely held theory is that all extant life, with a few possible exceptions, has evolved from a single organism that existed billions of years ago. That organism may or may not have been the only one to arise. If it was one among many variations of progenitors, we have yet to find the progenitors in the fossil or biological records. Given the extremely long time span between now and the beginnings of life, we don't expect fossil records to exist of all the organisms that existed some 3 B.Y.A. so the best we can do is speculate on what might have existed to account for what we see today.


Are humans evolving since their first appearance? Is the evolution a very prolonged progress, or are we going to witness further evolution of the human species?

If so, in which direction? Are there any widely predicted changes for humans?

Are humans evolving since their first appearance?

The idea of first appearance suggest an important misunderstanding. There is no such as a first appearance of humans (or any other species) that would not be arbitrary. The Homo lineage evolves and keep evolving but don't think of humans as being created at some point and then eventually evolving. Life came to existence 4.6 billions years ago and it is evolving and diversifying ever since but no species has ever been created anew.

  Is the evolution a very prolonged progress

The only, non-arbitrary definition of evolution is a change of allele (=gene variant) frequency in a population over time. Such change occurs several times every second in humans. So evolution is constantly occurring. It really does not take much time. However, I realize that when layman ask "How much time does it take for evolution to occur" they mean something of the kind "How much time does it take for a previously absent phenotypic trait to come to existence in a population?". The problem is that the answer very much depend on what phenotypic trait and what are the selection pressures on this trait.

  are we going to witness further evolution of the human spieces?

Yes, we had, we are and we will. Humans are still evolving and you might want to have a look at the post Human Evolution in Modern Times.

  If so, in which direction?

In plenty of directions in the same time. Each phenotypic trait will evolve (not completely independent of each other though). There is no single direction for a whole species. You should therefore specify the trait of interest for the question to make sense. Again I think that the post Human Evolution in Modern Times will help you.

Want to have a basic understanding of what evolution is?

Understanding Evolution (UC Berkeley) is a free online very introductory course to evolutionary biology. It will help you to very quickly raise you level of knowledge of evolutionary processes.