Let's say you accidentally walk into a room pressurized with pure nitrogen (or you're jettisoned into space). Within a couple of seconds, the partial pressure of oxygen within your lungs drops to 0. But there's still a (small?) reserve within your bloodstream.
Now, will the oxygenated blood travel to your lungs? If so, will the usual gas exchange reverse, with oxygen going from your blood to the oxygen-poor environment?
Probably not many side effects except in specific instances, but no benefits either. My guess is that there are potential side effects because these glasses reduce the amount of light that the eye receives and restrict the visual field. Therefore, the restricted visual field would be bad for activities such as driving, in which you need your peripheral vision. And the reduced light makes objects appear dimmer, so it is harder to see with them at night. I also imagine (just a guess) that they would be bad for very young infants, who are almost always born without perfect vision and require some visual stimulation to correct.
There are probably many reasons why optometrists use a pinhole occluder for diagnostic purposes, but never prescribe it as treatment...
There are always exceptions but you can consider some general rules.
A is 1 i.e the sequence that is perfectly complementary (2 is complementary but direction is parallel — cannot base-pair), then B would be 1 (siRNA). Reasons (some are just based on general rules of siRNA design):
See here for guidelines for siRNA design.
We suspect a bi-directional transcription event is happening at a locus in our organism where two genes are directly adjacent to each other. The annotation data is not well established. The intergenic distance is probably less than 200 base pairs.
The two genes are expressed in opposite directions towards each other. Base on the preliminary transcriptomics data, it seems like one gene is over transcribing (3' UTR perhaps?) into the adjacent gene, possibly resulting in some kind of transcriptional regulation of the adjacent gene.
Here is a rough diagram of what we think might be happening:
------------------------==========gene A================>----------------------
----------------------------------------<====gene B=====-----------------------
Of course we need to first confirm this by designing primers to see if this over transcription is actually happening.
If this is happening, we intend to do some knock down experiments. We have no transgenesis available in our organism, only RNAi by dsRNA. It is possible to specifically knock down geneA by introducing dsRNA to the 5' region of geneA that does not overlap with geneB. Perhaps this will lead to ectopic/over expression of geneB.
Is there anyway to knock down geneB specifically without knocking down geneA? It looks like designing dsRNA for geneB would knock down both A and B.
If you are talking about sound damaging the sound sensing organs in the ear, analogous to an ultrasonic heavy metal concert, I've found an interesting report just on this topic.
For ultrasonic components above 20 kHz, the limits were set to avoid hearing damage in the audible (lower) frequencies. One-third-octave band levels of 105-115 dB were observed to produce no temporary hearing loss, and were therefore judged non-hazardous in respect of permanent hearing damage.
If you are talking about high frequency sound from a explosion, or some sort of sonic cutter with intensities of such a level of compression or a high decibel range that conveys enough energy to physically damage something of course the answer would be 'yes this would damage your ears and the rest of the body too.
Operators of ultrasonic equipment with levels above 60 dB complained of headaches and fatigue, even nausea below 60 dB they felt no effect (reference table 7 in paper). But they did not seem to have any hearing loss.
One soviet experiment is both informative and maybe also entertaining to read about:
An unspecified number of subjects were exposed for an hour to a tone of 20 kHz at 110 dB. Tests were made to examine shift of hearing threshold over the frequency range 250 Hz to 10 kHz. Pulse rate, body temperature and skin temperature were also monitored. These tests showed no appreciable effect, even when the Sound Pressure Level was increased to 115 dB. These same subjects were given a one hour exposure to a 5 kHz tone at 90 dB: a considerable TTS was found. The 5 kHz tone at 110 dB produced a powerful vascular response.
...
It seems safe to infer an underlying concept: A sound which does not produce temporary
dullness of hearing cannot produce a permanent noise-induced hearing loss.
The bowel movements are influenced by a lot of factors. For example, when you eat a meal it induces a movement in your large intestines, to defecate and clear up space for new food.
Also, there is MMC, migrating motor complex, which is responsible for the bowel movements when you are fasting. It causes a flushing effect, which prevents bacteria to overproduce in intestines.
So, the daily bowel movements are mainly influenced by the timing and content of the food that you eat. But as I said there are many other factors. The gastrointestinal system has a very complex nervous system. Even psychological factors can effect the bowel movements greatly, for example extreme physical pain may induce the symphatetic system and cause constipation.
Also caffeine may affect it, like many drugs do.
Your approach to translate the AA sequence, codon by codon, was correct. This was a bit of a trick question because to recognize it, you had to read the sequence backwards.
UGG-CAA-GGT-CAC etc is read directly off of the 3'->5' strand of the circled answer, reading from right to left.
The bottom left is a red herring because it starts with a start codon, ATG, but reading beyond the start codon, the sequence wouldn't match.
The answer to this could be that there are many factors contributing to the length of the life of tree species.
Climate: You can see that trees that have a reputation of becoming really old live in environments that have low moisture levels and much sunlight over the course of the year.
For example, you can see that the most long-lived trees in America are located in California, where the temperatures are relatively high, while moisture levels are low. If you have one without the other trees don't tend to live that long. Cold climates make growth
harder for each individual, yet hot and moist climates tend to help trees grow easier, but also die easier. Think of the amazon. It is one of the richest forests in the world, yet the growth of bacteria and high competition in the areas of the equator make life a lot harder for the longest living and slowest growing species.
As you can see, the vast majority of the longest-living trees are located in California, or other regions of the same latitude!
http://en.wikipedia.org/wiki/List_of_oldest_trees
Other species and the life around it/Its Ecosystem: Individual trees tend to be less likely to be destroyed by a fire, as they are less likely to catch fire. At some instances, forest trees or dried-out grass can catch fire and pass it on to other individuals.
Microbes and bugs found in some parts of the world are known to their abilities to destroy trees!
Current size of the tree: Larger trees are generally less likely to die of causes like drought or damage to their trunks, as they have greatly extensive nets of roots and thick trunks and thus are able to, even partly, recover these incidences.
If a rockfall for example causes damage to one side of the tree, some of the brunches will probably die, but the rest of them, that have their own network to the roots, will probably survive.
This means that luck is involved and if the tree is lucky enough to avoid dying for a certain amount of time, regular fluctuations in the environment do not kill it as they would kill a younger, less robust tree.
Biology of tree species: Debate is held as to whether tree cells have telomeres working the same way as they do in animals. Research published in 2001 suggests that telomeres don't work the same way, as plants developed without telomeres after six generations continue living and growing without problems. But even if they do use telomeres, they may use them in a different way. This is an area where research is still being conducted, though, and you may find controversies in the bibliography!
For example in the paper "Analysis of telomere length and telomerase activity in tree species of various life-spans, and with age in the bristlecone pine Pinus longaeva"
Barry E. Flanary & Gunther Kletetschka which can be found in the rep
we can see that sometimes, short lived trees have longer telomeres than long lived ones!
(Look in the second paragraph of the section "Results"). This means that actually, nobody really knows!! It may be the telomeres, it may be something else, it may be a combination of factors.
http://www.madsci.org/posts/archives/2002-04/1019349924.Bt.r.html
(notice that this post has links to pages that are no longer available).
Distillation and the most important point: The way that the tree is adapted to its environment determines its longevity in it. Planting an olive tree in the amazon is a great way of making sure it will not survive! Some trees are better at surviving in a certain climate (even if it is at your own garden) simply because they have evolved to live there.
That means that the trees probably don't have a defined lifetime in general, but the life expectancy is defined in each environment, depending on the circumstances!
This means that species we currently think of as short-lived can reach get really old:
http://www.ncbi.nlm.nih.gov/pubmed/11295506
What some companies may have done is try to combine characteristics of individuals through selective breeding - and yes, it works for trees as well!- to match the climate and terrain characteristics found in the certain country or region! Or they may have selected for resistance against the most common pests in your area!
I hope I answered you question adequately!
The biological environment in every cell and tissue of your body is an extremely complex, tightly controlled system. There are tens of thousands of genes in a typical eukaryotic genome, and depending on tissue types and environmental conditions, these genes are turned on and off in a very controlled manner. There is regulation at every point in the flow of genetic information: nucleosome disruption to expose DNA; RNA transcription from the DNA; protein translation from the RNA; and in some cases, additional modifications of proteins or intermediate mRNAs. At early stages in development, regulation of RNA and protein levels is even more crucial than, say, when an organism is fully developed and healthy.
All living organisms share some basic building blocks--DNA, RNA, and proteins work pretty much the same in all of life (there are a few rare variations of the genetic code but the basic premise is identical). However, the way that specific genes, transcripts, and proteins work together to sustain life varies widely between different organisms.
For a very rough analogy, imagine you want to bake a batch of cookies. Then consider the three following scenarios.
The first example we can relate to two individuals of the same species mating. Of course there is natural variation in the population, but this doesn't typically lead to lethality during development. The second example we can relate to individuals of two related species (such as a horse and a donkey). Sometimes these matings can produce viable offspring, although these offspring are often sterile. The third example we can relate to individuals of two very divergent species (such as donkey and dog in your original question). The biological systems inside donkeys are just so different from those inside dogs that this mating cannot produce a viable offspring.
Admittedly this is a rough analogy, but hopefully is sheds some light on the issue.
Free radicals are damaging because their unpaired electrons (or not fully filled valence shell) makes them highly reactive species. They are often considered together with highly oxidizing "reactive oxygen species" (ROS) such as peroxides. They are especially problematic for cell membranes and DNA. In the latter they can react with (oxidize) heterocyclic bases.
As suggested first by Gerschmann et al. (1954), since oxidative damage to cells and cell structures is seen to accumulate with age, the corollary of this could be that aging is a result of oxidative damage. The very fact that cells have antoxidant enzymes such as superoxide dismutase (SOD) suggests that suppression of these species is important in the cell.
Many (but not all) ROS originate from mitochondria during cell metabolism. Therefore, it has been suggested that by regulating metabolism (that is, reducing the metabolic rate) the "rate of living theory" (Harman 1981) the rate of oxidative damage can be reduced. One way to do this may be calorie restriction.
This idea seems to fallen out of favour though. Another possibility is that the rate of mitochondrial ROS has nothing to do with metabolic rate per se; rather it might simply be a longevity determinant.
However, having said all this there is evidence that ROS are actually crucial in a number cellular pathways. It may be that it is the deregulation of pathways managing ROS that can contribute to aging rather than simply damage accumulation with age.
Gerschman, R., Gilbert, D. L., Nye, S. W., Dwyer, P., and Fenn, W. O. (1954). "Oxygen poisoning and x-irradiation: a mechanism in common." Science 119(3097):623-626.
Harman, D. (1981). "The aging process." Proc Natl Acad Sci U S A 78(11):7124-7128.
Yes it is possible, and as far as I can see, there should not be any plant which would be impossible to grow in a such an environment, just more or less difficult, although this is just my speculation.
I have myself grown tomatoes from only a liquid solution of minerals and nutrients, but you have to change the solution from time to time to prevent bacteria and fungi growing starting to grow in it. The reason why this is not a method used in industrious growing is because it is a lot more expensive than using soil and fertilisers, and more work.
TL;DR:
There is a dearth of actual experimental evidence. However:
there is at least one study that confirmed the process ([STUDY #7] - Myxococcus xanthus; by Fiegna and Velicer, 2003).
Another study experimentally confirmed higher extinction risk as well ([STUDY #8] - Paul F. Doherty's study of dimorphic bird species an [STUDY #9] - Denson K. McLain).
Theoretical studies produce somewhat unsettled results - some models support the evolutionary suicide and some models do not - the major difference seems to be variability of environmental pressures.
Also, if you include human predation based solely on sexually selected trait, examples definitely exist, e.g. Arabian Oryx
First of all, this may be cheating but one example is the extinction because a predator species specifically selects the species because of selected-for feature.
The most obvious case is when the predator species is human. As a random example, Arabian Oryx was nearly hunted to extinction specifically because of their horns.
Please note that this is NOT a simple question - for example, the often-cited in unscientific literature example of Irish Elk that supposedly went extinct due to its antler size may not be a good crystal-clear example. For a very thorough analysis, see: "Sexy to die for? Sexual selection and risk of extinction" by Hanna Kokko and Robert Brooks, Ann. Zool. Fennici 40: 207-219. [STUDY #1]
They specifically find that evolutionary "suicide" is unlikely in deterministic environments, at least if the costs of the feature are borne by the individual organism itself.
Another study resulting in a negative result was "Sexual selection and the risk of extinction in mammals", Edward H. Morrow and Claudia Fricke; The Royal Society Proceedings: Biological Sciences, Published online 4 November 2004, pp 2395-2401 [STUDY #2]
The aim of this study was therefore to examine whether the level of
sexual selection (measured as residual testes mass and sexual size dimorphism) was related to the risk of extinction that mammals are currently experiencing. We found no evidence for a relationship between these factors, although our analyses may have been confounded by the possible dominating effect of contemporary anthropogenic factors.
However, if one takes into consideration changes in the environment, the extinction becomes theoretically possible. From "Runaway Evolution to Self-Extinction Under Asymmetrical Competition" - Hiroyuki Matsuda and Peter A. Abrams; Evolution Vol. 48, No. 6 (Dec., 1994), pp. 1764-1772: [STUDY #3]
We show that purely intraspecific competition can cause evolution of extreme competitive abilities that ultimately result in extinction, without any influence from other species. The only change in the model required for this outcome is the assumption of a nonnormal distribution of resources of different sizes measured on a logarithmic scale. This suggests that taxon cycles, if they exist, may be driven by within- rather than between-species competition. Self-extinction does not occur when the advantage conferred by a large value of the competitive trait (e.g., size) is relatively small, or when the carrying capacity decreases at a comparatively rapid rate with increases in trait value. The evidence regarding these assumptions is discussed. The results suggest a need for more data on resource distributions and size-advantage in order to understand the evolution of competitive traits such as body size.
As far as supporting evidence, some studies are listed in "Can adaptation lead to extinction?" by Daniel J. Rankin and Andre´s Lo´pez-Sepulcre, OICOS 111:3 (2005). [STUDY #4]
They cite 3:
The first example is a study on the Japanese medaka
fish Oryzias latipes (Muir and Howard 1999 - [STUDY #5]). Transgenic males which had been modified to include a salmon growth-hormone gene are larger than their wild-type counterparts, although their offspring have a lower fecundity (Muir and Howard 1999). Females
prefer to mate with larger males, giving the larger
transgenic males a fitness advantage over wild-type
males. However, offspring produced with transgenic
males have a lower fecundity, and hence average female
fecundity will decrease. As long as females preferentially
mate with larger males, the population density will
decline. Models of this system have predicted that, if
the transgenic fish were released into a wild-type
population, the transgene would spread due to its mating
advantage over wild-type males, and the population
would become go extinct (Muir and Howard 1999).
A recent extension of the model has shown that
alternative mating tactics by wild-type males could
reduce the rate of transgene spread, but that this is still
not sufficient to prevent population extinction (Howard
et al. 2004). Although evolutionary suicide was predicted
from extrapolation, rather than observed in nature, this
constitutes the first study making such a prediction from
empirical data.
In cod, Gadus morhua, the commercial fishing of large
individuals has resulted in selection towards earlier
maturation and smaller body sizes (Conover and Munch
2002 [STUDY #6]). Under exploitation, high mortality decreases the
benefits of delayed maturation. As a result of this,
smaller adults, which mature faster, have a higher fitness
relative to their larger, slow maturing counterparts
(Olsen et al. 2004). Despite being more successful
relative to slow maturing individuals, the fast-maturing
adults produce fewer offspring, on average. This adaptation,
driven by the selective pressure imposed by
harvesting, seems to have pre-empted a fishery collapse
off the Atlantic coast of Canada (Olsen et al. 2004). As
the cod evolved to be fast-maturing, population size was
gradually reduced until it became inviable and vulnerable
to stochastic processes.
The only strictly experimental evidence for evolutionary
suicide comes from microbiology. In the social
bacterium Myxococcus xanthus individuals can develop
cooperatively into complex fruiting structures (Fiegna
and Velicer 2003 - [STUDY #7]). Individuals in the fruiting body are
then released as spores to form new colonies. Artificially
selected cheater strains produce a higher number of
spores than wild types. These cheaters were found to
invade wild-type strains, eventually causing extinction of
the entire population (Fiegna and Velicer 2003). The
cheaters invade the wild-type population because they
have a higher relative fitness, but as they spread through
the population, they decrease the overall density, thus
driving themselves and the population in which they
reside, to extinction.
Another experimental study was "Sexual selection affects local extinction and turnover
in bird communities" - Paul F. Doherty, Jr., Gabriele Sorci, et al; 5858–5862 PNAS May 13, 2003 vol. 100 no. 10 [STUDY #8]
Populations under strong sexual selection experience
a number of costs ranging from increased predation and
parasitism to enhanced sensitivity to environmental and demographic
stochasticity. These findings have led to the prediction that
local extinction rates should be higher for speciespopulations
with intense sexual selection. We tested this prediction by analyzing
the dynamics of natural bird communities at a continental
scale over a period of 21 years (1975–1996), using relevant statistical
tools. In agreement with the theoretical prediction, we found
that sexual selection increased risks of local extinction (dichromatic
birds had on average a 23% higher local extinction rate than
monochromatic species). However, despite higher local extinction
probabilities, the number of dichromatic species did not decrease
over the period considered in this study. This pattern was caused
by higher local turnover rates of dichromatic species, resulting in
relatively stable communities for both groups of species. Our
results suggest that these communities function as metacommunities,
with frequent local extinctions followed by colonization.
This result is similar to another bird-centered study: Sexual Selection and the Risk of Extinction of Introduced Birds on Oceanic Islands": Denson K. McLain, Michael P. Moulton and Todd P. Redfearn. OICOS Vol. 74, No. 1 (Oct., 1995), pp. 27-34 [STUDY #9]
We test the hypothesis that response to sexual selection increases the risk of extinction by examining the fate of plumage-monomorphic versus plumage-dimorphic bird species introduced to the tropical islands of Oahu and Tahiti. We assume that plumage dimorphism is a response to sexual selection and we assume that the males of plumage-dimorphic species experience stronger sexual selection pressures than males of monomorphic species. On Oahu, the extinction rate for dimorphic species, 59%, is significantly greater than for monomorphic species, 23%. On Tahiti, only 7% of the introduced dimorphic species have persisted compared to 22% for the introduced monomorphic species.
...
Plumage is significantly associated with increased risk of extinction for passerids but insignificantly associated for fringillids. Thus, the hypothesis that response to sexual selection increases the risk of extinction is supported for passerids and for the data set as a whole. The probability of extinction was correlated with the number of species already introduced. Thus, species that have responded to sexual selection may be poorer interspecific competitors when their communities contain many other species.
This seems to be an interesting and ambiguous topic.
On one hand, the collagen as any other protein is cleaved into small-sized chunks (oligopeptides) and single aminoacids before absorption. The chunks of proteins which were not completely digested before absorption are broken up further in the body and cannot be selectively used for collagen re-building in the body. Therefore, there should be no difference between the collagen of different types and, basically, no difference between the supplements containing collagen and just a mixture of aminoacids. This also explains the fact why collagen supplement is in most cases taken in the lysate (pre-cleaved) form.
On the other hand, a quick search in PubMed and I found an interesting article on the topic (source), where the authors claim:
At 6 months, the proportion of clinical responders to the treatment,
according to VAS scores, was significantly higher in the collagen
hydrolysate (CH) group 51.6%, compared to the placebo group 36.5%
(p<0.05).
...
This study suggests that collagen hydrolysate 1200 mg/day could
increase the number of clinical responders (i.e. improvement of at
least 20% on the VAS) compared to placebo. More studies are needed to
confirm the clinical interest of this food supplement.
So, if the article is not a bogus (I failed to get the full version of it and the journal does not seem to belong to the top journal in the field of medicine), there could be some mechanisms yet to be discovered.
"There are antibiotics which contain carbohydrates, such as Gentamycin and Streptomycin (the aminoglycosides). These must be the antibiotics that could account for this phenomenon."
My conjecture that the carbohydrate moities contained within aminoglycosides account for the high energy is incorrect. Aminoglycosides are NEVER metabolized by the body, they are excreted out into the urine UNCHANGED. See here: http://www.ebmedicine.net/topics.php?paction=showTopicSeg&topic_id=43&seg_id=839
And even if it were possible to metabolize the carbohydrate molecules within them, the energy released would be far less than the energy consumed to break their linkages in the first place, thus placing a negative energy balance on the body, and thus, not providing the burst of energy that is apparently observed after taking antibiotics.
Unlike erythrocytes that have a very rigid shape and almost cannot change their size (hence the size distribution is indicative and can be used for diagnostic purposes in medicine), lymphocytes can change their size in a wider range, this is why you see the numbers 6-9 and 10-15 μm.
And they indeed cluster into several different groups: so-called "large granular lymphocytes", also known as NK-cells or "natural killers" (usually >10μm) and "small granular lymphocytes", constituted by a large family of T- and B-lymphocites(usually <10μm). But this clustering is not really distinct, for as I said above, both NK and T/B-cells can shrink (if the osmolarity of the external medium grows due to acidosis, inflammation etc.) and swell (on binding many IgE/IgG complexes, on certain cell factor released etc.). Besides, there are also some intermediate size cells, called NKT-cells, that also flatten the distribution.
So, what you can definitely say is that the typical size distribution of lymphocytes has two peaks: around 8 and 12 μm respectively.
The first step in troubleshooting is to run controls - run lanes with your protein input alone, and the conjugate alone (you may need to play with the type/percentage of the gel if the conjugate molecule is much smaller than your target protein - attaching biotin to a 50 kDa protein, for example) to see if the smear shows up. Depending on the type of conjugation you're using, the number of acceptor sites on the substrate, and the time and conditions of the conjugation reaction, you may be adding a highly variable number of conjugate molecules to your substrate. For example, when I first started working with adding fluorophores like Alexa and DyLight dyes to antibodies, the fluor/protein ratio was highly variable from reaction to reaction and between antibodies in the same reaction.
This is most likely what is happening in your case - the number of conjugate molecules being added to each substrate molecule is highly variable. If you haven't already, I'd suggest getting in touch with your conjugation kit vendor's tech support, as they likely encounter this problem all the time. You may need to change the type of conjugation chemistry, get a higher-quality conjugate, or purify the substrate before and/or after the reaction. One of the solutions to my antibody labeling problem I mentioned above was to purify the reaction products through a size-exclusion column. This had the dual effect of separating out the un-reacted antibody and fluorophore, and allowing us to pick different fractions of the conjugated product and decide which were best for our needs.
I am currently reading Richard Dawkins's book 'The Greatest Show On Earth: The proof for evolution' and in the second chapter he talks very much about the evolution of dogs.
He says centuries ago there was only such dog-like creature as the wolf, but in a matter centuries the wolf has evolved into the many breeds of dog we have through artificial selection conducted by man.
This to me seemed very peculiar and quite frankly untrue, and I may be getting the wrong end of the stick and he is in fact being analogous, although I'm pretty sure he's not.
So, did wolves evolve into the many breeds of dog we have through artificial selection conducted by man?
If so, how many centuries did this take?
(Dawkins's point was that if the wolf can evolve into the vast amount of breeds of dog we have at the moment from artificial selection over a matter of centuries, then surely over many millions of years, the evolution we claim to know of through natural selection could definitely have happened).